By: Macular Degeneration In General
One of the more popular juvenile macular degeneration is the Stargardt Macular Degeneration. This category of macular degenerationi was first reported in 1901 by a German ophthalmologist, Karl Stargardt. It has the common feature of loss of central vision. In 1963, France ophthalmologist Adolphe Fransceschetti used the term Fundus flavimaculatus for a degenerative loss of central vision, but soon to be identified as Stargardt Macular Degeneration by Hadden and Gass in 1976.
This macular dystrophy affects about one in every 10,000 children. The problem may start anytime between the ages 6 and 20, but patients may not notice until they reach their 30s or 40s. First, the children may experience difficulty in reading, and complaining of some blind spots that are often gray, black or hazy at their central vision. They will need more time to adjust between the different lighting of the room too, between light and dark environments.
The dystrophy affects the retina, that sensitive tissue that lies at the back of the eye, focusing especially in the middle region called the macula. The macula is where focus is, that area that is highly sensitive and strong enough to give us the sharp central vision for tasks such as reading, driving and recognising faces.
Stargardt macular degeneration is similar to dry macular degeneration, with the build-up of abnormal yellow pigment substance called lipofuscin building up in cells underlying the macula. Patients will also experience problem with night vision, and it will be difficult for them to move around in places with low lighting. In some others, the patient may also experience colour impairment at advanced stages of the disease.
Vision loss is usually slow, until the 20/40 level. It may suddenly shoot right up to 20/200 where the patient is considered legally blind and forbidden from driving. In some cases, it may even deteriorate to 10/200 within a matter of months.
Genes are a big issue when it comes to Stargardt macular degeneration. A group of genes collectively known as the ABC genes, was found to be the culprit of this juvenile macular degeneration, a discovery made since 1997. The ABCA4 gene, responsible for the production of protein used as an energy transport to and from photoreceptor cells in the retina, mutates and produces dysfunctional protein that cannot perform such transport function. The useless ABCA4 protein then allows the accumulation of yellow, fatty material to accumulate in the retina, slowly covering the macularand ultimately causes the loss of vision. However, more studies had to be done to further understand how the mutated genes affect the biochemistry of the retina.
All is not lost for patients with Stargardt disease. It was found that patients may slow down the progression of vision loss by wearing UV protective sunglasses and avoid exposure to bright light. Although there is not yet any effective treatment for this form of macular degeneration at this moment, it is believed that the identification of the genes behind macular degeneration will help the search for new strategies and therapies. The latest is a study scheduled to begin in 2011, for the injection of embryonic stem cells into the eyes of twelve patients affected by the disease. The Advanced Cell Technology announced in November 2010 that the FDA had approved this injection and study.
Stargardt Macular Degeneration may be either autosomal or recessive trait type. A person may not have prior family history, but may have a recessive gene. If both parents carry a mutated gene, there is always a chance for the child to develop macular dystrophy. In fact, there may be more than one family member who gets Stargardt. For children who did not develop Stargardt, there is again the possibility of carrying the mutant gene, and pass on to their children instead. The chances will be 25%.
Three tests are used to check the presence of fundus flecks and the loss of cones to determine whether a patient has Stargardt Macular Degeneration. It may be fluorescein angiography, electroretinography or electrooculography. Since this problem is rare, it is not a widely studied subject. The discovery of genetic mutation in Stargardt may have encouraged the findings of genetic links for age-related macular degeneration, but further studies on the age-related macular degeneration may also become the contributing factor towards better understanding of Stargardt’s disease and its possible lead to new treatment. Whichever way it may be, it will always remain hopeful for parents and their affected children.
Showing posts with label blind. Show all posts
Showing posts with label blind. Show all posts
Sunday, January 23, 2011
Sunday, January 9, 2011
Novartis gains new indication for Lucentis in EU for vision loss due to Diabetic Macular Edema
By:Financial
The European Commission has granted Novartis a new indication for Lucentis (ranibizumab) to treat patients with visual impairment due to diabetic macular edema (DME), a leading cause of blindness in the working-age population in most developed countries.
Laser therapy, the current standard of care, has provided stabilization of vision in many patients, but generally does not improve vision. Lucentis is the first licensed therapy to significantly improve both vision and vision-related quality of life in patients with visual impairment due to DME.
"Similarly to wet age related macular degeneration, diabetic macular edema can cause disabling vision loss. While vision loss as a consequence of diabetes affects only a very small proportion of people with the disease, it is one of the most feared complications," said Don Curran, Chair, AMD Alliance International. "Visual impairment impacts everything from managing social interactions to the ability to work - thus, for most people it means a loss of independence."
The approval of Lucentis was based on data from two Novartis-sponsored clinical trials, RESTORE and RESOLVE, which showed that Lucentis was superior in providing rapid and sustained visual acuity gain versus sham (dummy) therapy or laser therapy, the current standard of care.
"In the clinical trials, Lucentis-treated patients began to recover their vision as early as eight days after the first injection on average, and vision improvement was maintained at one year," said Gabriele E. Lang, Professor, University Eye Hospital, University of Ulm, Germany. "The vision improvement for many of these patients was clinically significant, meaning that they regained the ability to carry out day-to-day activities such as driving."
The RESTORE study showed patients treated with Lucentis alone or with Lucentis plus laser therapy gained an average of 6.8 letters and 6.4 letters, respectively, in visual acuity at 12 months compared to baseline, while laser-treated patients gained an average of 0.9 letters as measured on a standard ETDRS eye chart.
The RESOLVE study showed that Lucentis-treated patients gained an average of 10.3 letters in visual acuity at 12 months compared to baseline while sham-treated patients, some of whom also received laser treatment, lost an average of 1.4 letters.
"Since its first launch in the EU in 2007, Lucentis has become the gold standard treatment of wet AMD and its use has stimulated research into other ocular conditions," said David Epstein, Division Head of Novartis Pharmaceuticals. "Our continued investment in the clinical development of Lucentis means that another group of patients who are at risk of losing their eyesight will have the option of a licensed therapy that could help save their vision."
"The pivotal data from RESTORE and RESOLVE studies are further supported by results of an independent US study examining Lucentis for the treatment of DME compared to standard of care. Conducted by the Diabetic Retinopathy Clinical Research Network (DRCR.net), this study showed that at 12 months patients treated with Lucentis plus laser gained an average of nine letters in visual acuity compared to baseline while patients treated with laser therapy alone gained an average of three to four letters. In addition, the study demonstrated superior gains in visual acuity among Lucentis-treated patients up to two years, with a reduced number of Lucentis injections required the second year compared to the first. Specifically, there was a median of only two to three injections required in the second year of treatment compared to a median of eight to nine injections required in the first year," Novartis said.
Diabetic macular edema (DME) is a consequence of diabetic retinopathy, the most common diabetic eye complication. DME is characterized by changes in the blood vessels of the retina, which is the light-sensitive layer at the back of the eye. In patients with DME, leakage from these abnormal blood vessels occurs in the central portion of the retina, called the macula. Because this part of the eye is responsible for sharp central vision, DME can lead to significant visual impairment. Visual impairment due to DME affects approximately 1-3% of patients with diabetes, and DME is a leading cause of blindness in the working-age population in most developed countries.
Lucentis offers an entirely new pharmacological approach to treatment for visual impairment due to DME compared to the current standard of care, which involves the use of laser burns to stop capillary leakage and reduce swelling. Lucentis is an antibody fragment that is injected into the eye and neutralizes vascular endothelial growth factor (VEGF), a protein that is known to increase vascular permeability, resulting in capillary leakage and macular edema in patients with diabetes.
Lucentis was generally well tolerated in DME clinical studies, either when given as monotherapy or when combined with laser treatment. Its safety profile was consistent with the well established profile in patients with wet age-related macular degeneration (wet AMD). There was an incidence of arterial thromboembolic events (<=3.5%) observed in the DME clinical trials, consistent with what was seen in the wet AMD clinical trials, with no significant difference between the groups treated with Lucentis compared to sham or laser therapy. Ocular adverse events were similar to those seen in the wet AMD trials, with an incidence of 1.4% endophthalmitis in the pooled pivotal studies.
Lucentis is currently licensed in more than 85 countries for the treatment of wet AMD. It receives continuous safety monitoring via a systematic pharmacovigilance system and there is more than 750,000 patient-treatment years of exposure to date for Lucentis.
Lucentis was developed by Genentech and Novartis. Genentech has the commercial rights to Lucentis in the United States, where Lucentis is also approved for the treatment of macular edema following retinal vein occlusion (RVO). In addition, Genentech is conducting two Phase III studies, RISE and RIDE, in patients with diabetic macular edema with results expected in 2011. Novartis has exclusive rights in the rest of the world and has filed in the European Union for approval of Lucentis for the treatment of visual impairment due to macular edema secondary to RVO.
The European Commission has granted Novartis a new indication for Lucentis (ranibizumab) to treat patients with visual impairment due to diabetic macular edema (DME), a leading cause of blindness in the working-age population in most developed countries.
Laser therapy, the current standard of care, has provided stabilization of vision in many patients, but generally does not improve vision. Lucentis is the first licensed therapy to significantly improve both vision and vision-related quality of life in patients with visual impairment due to DME.
"Similarly to wet age related macular degeneration, diabetic macular edema can cause disabling vision loss. While vision loss as a consequence of diabetes affects only a very small proportion of people with the disease, it is one of the most feared complications," said Don Curran, Chair, AMD Alliance International. "Visual impairment impacts everything from managing social interactions to the ability to work - thus, for most people it means a loss of independence."
The approval of Lucentis was based on data from two Novartis-sponsored clinical trials, RESTORE and RESOLVE, which showed that Lucentis was superior in providing rapid and sustained visual acuity gain versus sham (dummy) therapy or laser therapy, the current standard of care.
"In the clinical trials, Lucentis-treated patients began to recover their vision as early as eight days after the first injection on average, and vision improvement was maintained at one year," said Gabriele E. Lang, Professor, University Eye Hospital, University of Ulm, Germany. "The vision improvement for many of these patients was clinically significant, meaning that they regained the ability to carry out day-to-day activities such as driving."
The RESTORE study showed patients treated with Lucentis alone or with Lucentis plus laser therapy gained an average of 6.8 letters and 6.4 letters, respectively, in visual acuity at 12 months compared to baseline, while laser-treated patients gained an average of 0.9 letters as measured on a standard ETDRS eye chart.
The RESOLVE study showed that Lucentis-treated patients gained an average of 10.3 letters in visual acuity at 12 months compared to baseline while sham-treated patients, some of whom also received laser treatment, lost an average of 1.4 letters.
"Since its first launch in the EU in 2007, Lucentis has become the gold standard treatment of wet AMD and its use has stimulated research into other ocular conditions," said David Epstein, Division Head of Novartis Pharmaceuticals. "Our continued investment in the clinical development of Lucentis means that another group of patients who are at risk of losing their eyesight will have the option of a licensed therapy that could help save their vision."
"The pivotal data from RESTORE and RESOLVE studies are further supported by results of an independent US study examining Lucentis for the treatment of DME compared to standard of care. Conducted by the Diabetic Retinopathy Clinical Research Network (DRCR.net), this study showed that at 12 months patients treated with Lucentis plus laser gained an average of nine letters in visual acuity compared to baseline while patients treated with laser therapy alone gained an average of three to four letters. In addition, the study demonstrated superior gains in visual acuity among Lucentis-treated patients up to two years, with a reduced number of Lucentis injections required the second year compared to the first. Specifically, there was a median of only two to three injections required in the second year of treatment compared to a median of eight to nine injections required in the first year," Novartis said.
Diabetic macular edema (DME) is a consequence of diabetic retinopathy, the most common diabetic eye complication. DME is characterized by changes in the blood vessels of the retina, which is the light-sensitive layer at the back of the eye. In patients with DME, leakage from these abnormal blood vessels occurs in the central portion of the retina, called the macula. Because this part of the eye is responsible for sharp central vision, DME can lead to significant visual impairment. Visual impairment due to DME affects approximately 1-3% of patients with diabetes, and DME is a leading cause of blindness in the working-age population in most developed countries.
Lucentis offers an entirely new pharmacological approach to treatment for visual impairment due to DME compared to the current standard of care, which involves the use of laser burns to stop capillary leakage and reduce swelling. Lucentis is an antibody fragment that is injected into the eye and neutralizes vascular endothelial growth factor (VEGF), a protein that is known to increase vascular permeability, resulting in capillary leakage and macular edema in patients with diabetes.
Lucentis was generally well tolerated in DME clinical studies, either when given as monotherapy or when combined with laser treatment. Its safety profile was consistent with the well established profile in patients with wet age-related macular degeneration (wet AMD). There was an incidence of arterial thromboembolic events (<=3.5%) observed in the DME clinical trials, consistent with what was seen in the wet AMD clinical trials, with no significant difference between the groups treated with Lucentis compared to sham or laser therapy. Ocular adverse events were similar to those seen in the wet AMD trials, with an incidence of 1.4% endophthalmitis in the pooled pivotal studies.
Lucentis is currently licensed in more than 85 countries for the treatment of wet AMD. It receives continuous safety monitoring via a systematic pharmacovigilance system and there is more than 750,000 patient-treatment years of exposure to date for Lucentis.
Lucentis was developed by Genentech and Novartis. Genentech has the commercial rights to Lucentis in the United States, where Lucentis is also approved for the treatment of macular edema following retinal vein occlusion (RVO). In addition, Genentech is conducting two Phase III studies, RISE and RIDE, in patients with diabetic macular edema with results expected in 2011. Novartis has exclusive rights in the rest of the world and has filed in the European Union for approval of Lucentis for the treatment of visual impairment due to macular edema secondary to RVO.
Monday, December 27, 2010
Treatment For Wet Macular Degeneration in Seniors
by: Admin
The National Eye Institute (NEI) had published their facts about Age-Related Macular Degeneration (ARMD) to help patients and their family members to search for general information about the disease.
Age Related Wet Macular Degeneration
In its attempt to ensure better public understanding of the disease, it had detailed the ARMD by starting on its definition. The NEI defined ARMD as “a disease associated with aging that gradually destroys sharp, central vision.” It is then explained that central vision is important to see fine details and helps common daily tasks such as reading and driving. It has to be noted that ARMD causes no physical pain to the patients.
There are two types of ARMD, which is the dry and the wet ARMD. In most cases, elderly adults develop the dry ARMD and it is the most common form of the disease, with some of them progressing into wet ARMD when abnormal blood vessels start developing and ruptures within. Wet ARMD can be treated, but not fully cured, by laser surgery, photodynamic therapy and injections into the eye. These treatments may actually just delay the process of being legally blind, but patients need to be aware that conditions will continue to worsen over time.
Treating wet ARMD with Laser surgery is a procedure which utilizes the laser technology to destroy fragile, leaky blood vessels that had formed abnormally. A high energy light beam is directly focused on the new blood vessels, and it destroys them to prevent further loss of vision. The negative side of this treatment is that it potentially destroys other healthy cells surrounding the treatment area.
Only a small percentage of patients may use laser to treat wet ARMD. The procedure is performed at the doctor’s office or an eye clinic, and laser is more effective if the abnormal, leaky blood vessels are developed away from the middle of the macula, which is called the fovea. It does not mean that the abnormal blood vessels will automatically stop developing after laser surgery, in fact repeated treatments are necessary as the risk of developing new abnormal blood vessels post surgery is high. In some cases, the patient may still suffer vision loss progressively despite repeated treatments.
Another treatment, called the photodynamic therapy, involves the injection of a drug called verteporfin into the patient’s arm, and it travels throughout the body including the new blood vessels in the eye. The drug will attach itself to the surface of new blood vessels. After this, the doctor shines a light into the patients eye for about 90 seconds to activate the drug. The drug, once activated, will destroy the new blood vessels and helps slower down the rate of vision decline. It is topical and aims only at the new blood vessels, so it does not destroy surrounding healthy tissues and cells like the laser surgery.
However, caution has to be taken with the use of this drug. As it gets activated by lights, patient has to avoid going outdoors, or exposing skin or eye to direct sunlight or bright indoor lights for five days after treatment. Remember that the drug is administered through injection on the patient’s arm, and the fact that it travels throughout the body instead of being contained within the eye.
This treatment is basically painless, and can be performed at the doctor’s office in about 20 minutes. However, while it slows down the rate of vision loss, it does not stop vision loss, or restore the patient’s vision if it was already damaged by ARMD. Again, this technique will require repeated treatments as necessary, based on the doctor’s prescription and the progress of your condition.
Another treatment is the use of injection, this time with new drugs that are injected directly into the eyes. The anti-VEGF therapy will see these new drugs block the effects of the specific growth factor that triggers the abnormal blood vessels. Multiple injections will be required, and it can be a monthly affair. Before injection, the eyes are numbed. After injection, the patient will be kept at the doctor’s office for a while so that the doctor may monitor the progress of the eyes before declaring that the patient is safe to go home. It is said that this treatment helps slow down vision loss from ARMD and may also help to improve the sight of patients in some cases.
In any of these treatments, the patient should listen to the doctor because the doctor will know the best option available for each individual.
The National Eye Institute (NEI) had published their facts about Age-Related Macular Degeneration (ARMD) to help patients and their family members to search for general information about the disease.
Age Related Wet Macular Degeneration
In its attempt to ensure better public understanding of the disease, it had detailed the ARMD by starting on its definition. The NEI defined ARMD as “a disease associated with aging that gradually destroys sharp, central vision.” It is then explained that central vision is important to see fine details and helps common daily tasks such as reading and driving. It has to be noted that ARMD causes no physical pain to the patients.
There are two types of ARMD, which is the dry and the wet ARMD. In most cases, elderly adults develop the dry ARMD and it is the most common form of the disease, with some of them progressing into wet ARMD when abnormal blood vessels start developing and ruptures within. Wet ARMD can be treated, but not fully cured, by laser surgery, photodynamic therapy and injections into the eye. These treatments may actually just delay the process of being legally blind, but patients need to be aware that conditions will continue to worsen over time.
Treating wet ARMD with Laser surgery is a procedure which utilizes the laser technology to destroy fragile, leaky blood vessels that had formed abnormally. A high energy light beam is directly focused on the new blood vessels, and it destroys them to prevent further loss of vision. The negative side of this treatment is that it potentially destroys other healthy cells surrounding the treatment area.
Only a small percentage of patients may use laser to treat wet ARMD. The procedure is performed at the doctor’s office or an eye clinic, and laser is more effective if the abnormal, leaky blood vessels are developed away from the middle of the macula, which is called the fovea. It does not mean that the abnormal blood vessels will automatically stop developing after laser surgery, in fact repeated treatments are necessary as the risk of developing new abnormal blood vessels post surgery is high. In some cases, the patient may still suffer vision loss progressively despite repeated treatments.
Another treatment, called the photodynamic therapy, involves the injection of a drug called verteporfin into the patient’s arm, and it travels throughout the body including the new blood vessels in the eye. The drug will attach itself to the surface of new blood vessels. After this, the doctor shines a light into the patients eye for about 90 seconds to activate the drug. The drug, once activated, will destroy the new blood vessels and helps slower down the rate of vision decline. It is topical and aims only at the new blood vessels, so it does not destroy surrounding healthy tissues and cells like the laser surgery.
However, caution has to be taken with the use of this drug. As it gets activated by lights, patient has to avoid going outdoors, or exposing skin or eye to direct sunlight or bright indoor lights for five days after treatment. Remember that the drug is administered through injection on the patient’s arm, and the fact that it travels throughout the body instead of being contained within the eye.
This treatment is basically painless, and can be performed at the doctor’s office in about 20 minutes. However, while it slows down the rate of vision loss, it does not stop vision loss, or restore the patient’s vision if it was already damaged by ARMD. Again, this technique will require repeated treatments as necessary, based on the doctor’s prescription and the progress of your condition.
Another treatment is the use of injection, this time with new drugs that are injected directly into the eyes. The anti-VEGF therapy will see these new drugs block the effects of the specific growth factor that triggers the abnormal blood vessels. Multiple injections will be required, and it can be a monthly affair. Before injection, the eyes are numbed. After injection, the patient will be kept at the doctor’s office for a while so that the doctor may monitor the progress of the eyes before declaring that the patient is safe to go home. It is said that this treatment helps slow down vision loss from ARMD and may also help to improve the sight of patients in some cases.
In any of these treatments, the patient should listen to the doctor because the doctor will know the best option available for each individual.
Monday, December 20, 2010
Zeaxanthin For Macular Degeneration Prevention and Treatment in Dry AMD
by The Pulitzer
Most ophthalmologists recommend the antioxidants lutein and zeaxanthin for macular degeneration that is age related, commonly referred to as AMD. It is unusual for doctor’s to recommend nutritional supplements of any kind, unless a person has an outright deficiency, but AMD is a unique condition.
There are no effective treatments for one type of AMD (dry), but there are some partially effective treatments for wet AMD. Together, these two are the major causes of blindness in the elderly. The wet form is the most severe, if not treated early.
In wet AMD, blood vessels grow up and behind the retina, an area responsible for gathering light and transmitting signals to the brain, resulting in sight. The blood vessels often rupture and leak blood and protein below the macula, a very sensitive area within the retina.
Eventually, bleeding, leaking and scarring causes irreversible damage to the light receptors (rods and cones). Rapid vision loss is experienced if it is left untreated. Laser treatment and drugs that inhibit blood vessel growth are usually recommended.
Generally, doctors recommend lutein and zeaxanthin for macular degeneration that is of the dry type. Dry AMD is much more common than wet. It is caused by a build up of yellow deposits called drusen on the retina.
In nature lutein and zeaxanthin are pigments or colors. They are normally present in the retina, with zeaxanthin being concentrated in the macula and lutein more highly concentrated in the periphery of the retina. There roles within the eye are not well understood, but they seem to help reduce or prevent the build up of drusen.
Drusen is similar in composition to the deposits that are found in the brains of Alzheimer’s patients and the plaque that is present in atherosclerosis. People with either of those two conditions have a higher risk of developing dry AMD.
Some doctors recommend taking lutein and zeaxanthin for macular degeneration prevention, particularly to their patients that have a family history of the disease. But, since the drusen are similar to the deposits that cause Alzheimer’s and heart disease, other antioxidants may be beneficial, as well.
Curcumin, an antioxidant present in the spice turmeric, is currently being studied for its benefit in Alzheimer’s disease. Not only does it prevent the accumulation of the plaque, it breaks it up. It might be able to break up the drusen in AMD, too.
One study indicates that the ideal combination of nutrients is omega 3 fatty acids, beta carotene, vitamin E, lutein and zeaxanthin for macular degeneration. Omega 3 fatty acids, particularly DHA, are the most abundant fatty acids present in the retina. Beta-carotene is converted by the body to vitamin A, which is essential for good vision. Vitamin E is well-known for its antioxidant activity.
Prevention is worth a pound of cure, they say. In order to prevent AMD, people should lower their total fat intake, and increase their nutrient intake. This may help reduce the risk of many other diseases, as well. Taking zeaxanthin for macular degeneration prevention is a good idea. Taking a multi-nutritional supplement that contains it, is a great one.
Valerie Rosenbaum researches omega 3 fish oil supplements, anti aging supplements and natural skincare products. Through her research she has discovered the best anti aging supplement, in both quality and value, available today.
Most ophthalmologists recommend the antioxidants lutein and zeaxanthin for macular degeneration that is age related, commonly referred to as AMD. It is unusual for doctor’s to recommend nutritional supplements of any kind, unless a person has an outright deficiency, but AMD is a unique condition.
There are no effective treatments for one type of AMD (dry), but there are some partially effective treatments for wet AMD. Together, these two are the major causes of blindness in the elderly. The wet form is the most severe, if not treated early.
In wet AMD, blood vessels grow up and behind the retina, an area responsible for gathering light and transmitting signals to the brain, resulting in sight. The blood vessels often rupture and leak blood and protein below the macula, a very sensitive area within the retina.
Eventually, bleeding, leaking and scarring causes irreversible damage to the light receptors (rods and cones). Rapid vision loss is experienced if it is left untreated. Laser treatment and drugs that inhibit blood vessel growth are usually recommended.
Generally, doctors recommend lutein and zeaxanthin for macular degeneration that is of the dry type. Dry AMD is much more common than wet. It is caused by a build up of yellow deposits called drusen on the retina.
In nature lutein and zeaxanthin are pigments or colors. They are normally present in the retina, with zeaxanthin being concentrated in the macula and lutein more highly concentrated in the periphery of the retina. There roles within the eye are not well understood, but they seem to help reduce or prevent the build up of drusen.
Drusen is similar in composition to the deposits that are found in the brains of Alzheimer’s patients and the plaque that is present in atherosclerosis. People with either of those two conditions have a higher risk of developing dry AMD.
Some doctors recommend taking lutein and zeaxanthin for macular degeneration prevention, particularly to their patients that have a family history of the disease. But, since the drusen are similar to the deposits that cause Alzheimer’s and heart disease, other antioxidants may be beneficial, as well.
Curcumin, an antioxidant present in the spice turmeric, is currently being studied for its benefit in Alzheimer’s disease. Not only does it prevent the accumulation of the plaque, it breaks it up. It might be able to break up the drusen in AMD, too.
One study indicates that the ideal combination of nutrients is omega 3 fatty acids, beta carotene, vitamin E, lutein and zeaxanthin for macular degeneration. Omega 3 fatty acids, particularly DHA, are the most abundant fatty acids present in the retina. Beta-carotene is converted by the body to vitamin A, which is essential for good vision. Vitamin E is well-known for its antioxidant activity.
Prevention is worth a pound of cure, they say. In order to prevent AMD, people should lower their total fat intake, and increase their nutrient intake. This may help reduce the risk of many other diseases, as well. Taking zeaxanthin for macular degeneration prevention is a good idea. Taking a multi-nutritional supplement that contains it, is a great one.
Valerie Rosenbaum researches omega 3 fish oil supplements, anti aging supplements and natural skincare products. Through her research she has discovered the best anti aging supplement, in both quality and value, available today.
Monday, November 22, 2010
New Techology Detects Retinal Disease
by Martha L. Hernández
McALLEN — For years, the only way for doctors into the back of the eye for a retina inspection involved special eye drops, which dilated the patient’s pupils and required the wearing of dark glasses for hours after the exam.
Now, scientists have developed the Optomap Retinal Exam, which eliminates the need for drop. Patients only see a quick, green flash of light.
“This test is a non-invasive way of doing it. We don’t put drops in your eyes, we just take a picture of the back of your eye and under 25 seconds (later), it gives us a 3D image. We can review the image with you on the computer (immediately after),” said Dr. Fiona Kolia, a therapeutic optometrist at Astoria Vision Source.
“We can look at it with different filters. This test is very important because it allows us to tell you about the health not only of your eye — where we can detect (diseases like) glaucoma (or) macular degeneration, any holes or tears, anything that is in the eye that shouldn’t be there — it also tells us about the health of your body,” Kolia said.
The new technology has detected other medical conditions in people seeking glasses or contacts.
“For example, a young person, healthy, walked in and he had a hemorrhage in his eye that is caused by high blood pressure, and high blood pressure is a silent killer, you refer them (to their family doctor) and they can start to get treated and take care of themselves,” Kolia said. Undetected high blood pressure can lead to strokes and other serious complications, Kolia noted.
“Sometimes we are the first to detect if the people have signs of high blood pressure, diabetes, high cholesterol, any arteriosclerosis in the eye and we refer them to their family physician” Kolia said.
Kolia is the only optometrist south of Corpus Christi that has an Optomap.
“Sometimes people just don’t see well and they might think it’s just their glasses” Kolia said. “There was a gentleman that had a macular degeneration that needed to be treated … but sometime in younger people (that) kind of problem happens due to high stress and the macular area (center of the eye) can become swollen and you can lose your central vision (if you do not treat it),” Kolia said.
“What we hope to do is be able to screen a lot of people, I think that in this area it is very important for diabetics. We want to it as a tool and make people aware that an eye exam not only involves getting you a better pair of glasses, it involves looking at the interior structures of the eye and behind the eye,” which can aid in the detection of numerous health issues, Kolia said.
Insurance companies do not typically cover treatment with an Optomap. If there is a definite medical diagnosis it may be billed as a retinal photo in some instances with some insurance plans. Patients without insurance pay $37 for the test.
“In a lot of people who are nearsighted, the eyeball elongates, so it is important to look behind the eye because they can develop a retinal detachment,” Kolia said.
Kolia said the Optomap likely would be added to the regular battery of tests conducted by optometrists and ophthalmologists during routine eye exams as the technology comes into more widespread use.
McALLEN — For years, the only way for doctors into the back of the eye for a retina inspection involved special eye drops, which dilated the patient’s pupils and required the wearing of dark glasses for hours after the exam.
Now, scientists have developed the Optomap Retinal Exam, which eliminates the need for drop. Patients only see a quick, green flash of light.
“This test is a non-invasive way of doing it. We don’t put drops in your eyes, we just take a picture of the back of your eye and under 25 seconds (later), it gives us a 3D image. We can review the image with you on the computer (immediately after),” said Dr. Fiona Kolia, a therapeutic optometrist at Astoria Vision Source.
“We can look at it with different filters. This test is very important because it allows us to tell you about the health not only of your eye — where we can detect (diseases like) glaucoma (or) macular degeneration, any holes or tears, anything that is in the eye that shouldn’t be there — it also tells us about the health of your body,” Kolia said.
The new technology has detected other medical conditions in people seeking glasses or contacts.
“For example, a young person, healthy, walked in and he had a hemorrhage in his eye that is caused by high blood pressure, and high blood pressure is a silent killer, you refer them (to their family doctor) and they can start to get treated and take care of themselves,” Kolia said. Undetected high blood pressure can lead to strokes and other serious complications, Kolia noted.
“Sometimes we are the first to detect if the people have signs of high blood pressure, diabetes, high cholesterol, any arteriosclerosis in the eye and we refer them to their family physician” Kolia said.
Kolia is the only optometrist south of Corpus Christi that has an Optomap.
“Sometimes people just don’t see well and they might think it’s just their glasses” Kolia said. “There was a gentleman that had a macular degeneration that needed to be treated … but sometime in younger people (that) kind of problem happens due to high stress and the macular area (center of the eye) can become swollen and you can lose your central vision (if you do not treat it),” Kolia said.
“What we hope to do is be able to screen a lot of people, I think that in this area it is very important for diabetics. We want to it as a tool and make people aware that an eye exam not only involves getting you a better pair of glasses, it involves looking at the interior structures of the eye and behind the eye,” which can aid in the detection of numerous health issues, Kolia said.
Insurance companies do not typically cover treatment with an Optomap. If there is a definite medical diagnosis it may be billed as a retinal photo in some instances with some insurance plans. Patients without insurance pay $37 for the test.
“In a lot of people who are nearsighted, the eyeball elongates, so it is important to look behind the eye because they can develop a retinal detachment,” Kolia said.
Kolia said the Optomap likely would be added to the regular battery of tests conducted by optometrists and ophthalmologists during routine eye exams as the technology comes into more widespread use.
Monday, November 15, 2010
Limited Retinal Translocation for Wet Macular Degeneration
Posted by Administration
Limited Retinal Translocation-Limited retinal translocation is another treatment aimed at wet macular degeneration. In this procedure the retina is actually moved somewhat to allow laser treatments to be applied more successfully to abnormal blood vessel growth. The procedure is still in the macular degeneration treatments developmental stages in terms of approval for commercial applications. Surgical options for dry macular degeneration are proposed periodically. The methodologies change from procedure to procedure, but the general idea is the same.
Limited Retinal Translocation-Limited retinal translocation is another treatment aimed at wet macular degeneration. In this procedure the retina is actually moved somewhat to allow laser treatments to be applied more successfully to abnormal blood vessel growth. The procedure is still in the macular degeneration treatments developmental stages in terms of approval for commercial applications. Surgical options for dry macular degeneration are proposed periodically. The methodologies change from procedure to procedure, but the general idea is the same.
Thursday, November 4, 2010
Eye Implant breakthrough
By Andrew Hough
Eye implant breakthrough: scientific advances towards a blindness cures
An eye test is the only way to diagnose glaucoma, the leading cause of blindness in Britain.
* Stem cells grown on contact lenses could be a cure for a common cause of blindness, claim scientists. Australian researchers said that the world breakthrough could "dramatically improve" the sight of patients with damage to their cornea – the clear outer shell of the eye – caused by disease or injury.
The research team removed tissue with regenerative stem cells from patients' own eyes and then multiplied them in the laboratory on the surface of a contact lens. This was then placed back onto the damaged cornea for 10 days, during which the cells, which can turn into any other sort of cell, were able to recolonise and "patch" the damaged eye surface. Within weeks the patients saw dramatic improvements in their vision. If early findings bear out then the treatment could be affective for thousands of patients in Britain and is so cheap it could be used for millions more in the Third World.
* Artificial corneas grown in the laboratory were transplanted into patient's eyes for the first time in an operation, scientists reported. The new technique involved growing human tissue or collagen in the laboratory and then shaping it using a contact lens mould.
Damaged and scarred tissue from the front of the eye is then removed and the "biosynthetic" replacement is stitched in its place. Eventually existing cells and nerves in the eye grow over the artificial cornea incorporating it fully into the eye.
* Eye cells that are sensitive to light were produced from skin in a breakthrough that could eventually lead to treatments for blindness, scientists reported in August. Researchers genetically “reprogrammed” human skin cells to possess the same properties as those that make up the retina.
The process involved first turning them into pluripotent stem (IPS) cells, which have the potential to develop into virtually every kind of tissue in the body. By exposing the IPS cells to a specific cocktail of chemicals, the scientists then caused them to grow into partially developed retina cells – the light-sensitive cells at the back of the eye which transmit nerve signals to the brain.
* Patients who were left blinded after chemical accidents have had their sight restored using corneas grown from their own stem cells, scientists claimed in June. In the largest study of its kind, Italian researchers said they restored the sight of patients left blinded or suffered severely impaired vision, after suffering chemical burns.
Experts said the study, undertaken between 1998 and 2007, offers new hope to the thousands of people who suffer chemical burns on their corneas from heavy-duty cleansers or other substances at work or at home. The research is also being hailed as a key breakthrough in scientific regeneration that could give hope to other patients with otherwise irreversible eyesight.
* Also in June, a new study suggested a simple way to stop you eyesight deterioriating - drinking red wine. Researchers have found that a substance found in grapes and other fruits could protect blood vessels in the eye being damaged by old age. It is effective because the compound, known as resveratrol, stops the blood vessels from being damaged.
The substance, which has been linked to anti-ageing and cancer protection in the past, is believed to work because it protects against abnormal angiogenesis – the formation of damaged or mutated blood vessels. This condition is linked to cancer, heart disease and eye diseases such as age-related macular degeneration. In the study, reported in the New England Journal of Medicine, researchers successfully extracted adult stem cells from healthy eye tissue before growing additional stem cells that were placed over damaged eye tissue.
* Gene therapy was used by American scientists to improve the vision of children with hereditary blindness. US doctors treating 12 patients with a rare genetic eye disorder were able to significantly improve vision in the youngest, according to medical journal The Lancet. The research, which builds on work carried out by doctors at London's Moorfields Eye Hospital, focused on Leber's congenital amaurosis (LCA), a disorder which causes gradual deterioration in vision and can lead to blindness by the time the patient is 20. It occurs when faulty genes, called RPE65, stop the layer of cells at the back of the eye working and affects approximately one in 80,000 people. It is responsible for one in 10 severe sight disorders in children.
* Scientists cured colour blindness in monkeys, in what some were signalling has new hope for millions of sufferers of the condition. Researchers reported last September that they cured the animals using a treatment called gene therapy. A harmless virus which delivers corrective genes to the retina was injected into the eyes of two squirrel monkeys, Dalton and Sam, who had been colour blind since birth. Within weeks a protein produced by the corrective genes allowed both monkeys to make out reds and greens for the first time. They can still see the colours two years later. The breakthrough could also have implications for other damaging genetic eye defects, including those which can cause blindness, after researchers proved for the first time that the brain can “rewire” itself to see things it has never been able to before.
* A new eye drop treatment was offered to help preserve the sight of thousands of people at risk of going blind due to glaucoma, scientists reported. The drops were first of their kind that avoid unpleasant side effects which deter up to a third of patients from continuing their treatment.
Many patients simply refuse to apply the drops because of the discomfort, thereby putting themselves at risk of vision loss. Regular use of the eye drops can keep the condition under control for a patient's life time. Without them, a patient can go blind in five to 10 years. When the disease becomes too advanced the only remedy is surgery, which is risky and may itself result in blindness.
Eye implant breakthrough: scientific advances towards a blindness cures
An eye test is the only way to diagnose glaucoma, the leading cause of blindness in Britain.
* Stem cells grown on contact lenses could be a cure for a common cause of blindness, claim scientists. Australian researchers said that the world breakthrough could "dramatically improve" the sight of patients with damage to their cornea – the clear outer shell of the eye – caused by disease or injury.
The research team removed tissue with regenerative stem cells from patients' own eyes and then multiplied them in the laboratory on the surface of a contact lens. This was then placed back onto the damaged cornea for 10 days, during which the cells, which can turn into any other sort of cell, were able to recolonise and "patch" the damaged eye surface. Within weeks the patients saw dramatic improvements in their vision. If early findings bear out then the treatment could be affective for thousands of patients in Britain and is so cheap it could be used for millions more in the Third World.
* Artificial corneas grown in the laboratory were transplanted into patient's eyes for the first time in an operation, scientists reported. The new technique involved growing human tissue or collagen in the laboratory and then shaping it using a contact lens mould.
Damaged and scarred tissue from the front of the eye is then removed and the "biosynthetic" replacement is stitched in its place. Eventually existing cells and nerves in the eye grow over the artificial cornea incorporating it fully into the eye.
* Eye cells that are sensitive to light were produced from skin in a breakthrough that could eventually lead to treatments for blindness, scientists reported in August. Researchers genetically “reprogrammed” human skin cells to possess the same properties as those that make up the retina.
The process involved first turning them into pluripotent stem (IPS) cells, which have the potential to develop into virtually every kind of tissue in the body. By exposing the IPS cells to a specific cocktail of chemicals, the scientists then caused them to grow into partially developed retina cells – the light-sensitive cells at the back of the eye which transmit nerve signals to the brain.
* Patients who were left blinded after chemical accidents have had their sight restored using corneas grown from their own stem cells, scientists claimed in June. In the largest study of its kind, Italian researchers said they restored the sight of patients left blinded or suffered severely impaired vision, after suffering chemical burns.
Experts said the study, undertaken between 1998 and 2007, offers new hope to the thousands of people who suffer chemical burns on their corneas from heavy-duty cleansers or other substances at work or at home. The research is also being hailed as a key breakthrough in scientific regeneration that could give hope to other patients with otherwise irreversible eyesight.
* Also in June, a new study suggested a simple way to stop you eyesight deterioriating - drinking red wine. Researchers have found that a substance found in grapes and other fruits could protect blood vessels in the eye being damaged by old age. It is effective because the compound, known as resveratrol, stops the blood vessels from being damaged.
The substance, which has been linked to anti-ageing and cancer protection in the past, is believed to work because it protects against abnormal angiogenesis – the formation of damaged or mutated blood vessels. This condition is linked to cancer, heart disease and eye diseases such as age-related macular degeneration. In the study, reported in the New England Journal of Medicine, researchers successfully extracted adult stem cells from healthy eye tissue before growing additional stem cells that were placed over damaged eye tissue.
* Gene therapy was used by American scientists to improve the vision of children with hereditary blindness. US doctors treating 12 patients with a rare genetic eye disorder were able to significantly improve vision in the youngest, according to medical journal The Lancet. The research, which builds on work carried out by doctors at London's Moorfields Eye Hospital, focused on Leber's congenital amaurosis (LCA), a disorder which causes gradual deterioration in vision and can lead to blindness by the time the patient is 20. It occurs when faulty genes, called RPE65, stop the layer of cells at the back of the eye working and affects approximately one in 80,000 people. It is responsible for one in 10 severe sight disorders in children.
* Scientists cured colour blindness in monkeys, in what some were signalling has new hope for millions of sufferers of the condition. Researchers reported last September that they cured the animals using a treatment called gene therapy. A harmless virus which delivers corrective genes to the retina was injected into the eyes of two squirrel monkeys, Dalton and Sam, who had been colour blind since birth. Within weeks a protein produced by the corrective genes allowed both monkeys to make out reds and greens for the first time. They can still see the colours two years later. The breakthrough could also have implications for other damaging genetic eye defects, including those which can cause blindness, after researchers proved for the first time that the brain can “rewire” itself to see things it has never been able to before.
* A new eye drop treatment was offered to help preserve the sight of thousands of people at risk of going blind due to glaucoma, scientists reported. The drops were first of their kind that avoid unpleasant side effects which deter up to a third of patients from continuing their treatment.
Many patients simply refuse to apply the drops because of the discomfort, thereby putting themselves at risk of vision loss. Regular use of the eye drops can keep the condition under control for a patient's life time. Without them, a patient can go blind in five to 10 years. When the disease becomes too advanced the only remedy is surgery, which is risky and may itself result in blindness.
Saturday, October 30, 2010
Telescope Implant Improves Vision in Macular Degeneration
by Kathleen Louden
(Chicago, Illinois) — People with end-stage age-related macular degeneration (AMD) have improved visual acuity and quality of life after receiving an intraocular implant containing a tiny telescope in 1 eye, new research shows. An ophthalmologist who participated in the clinical trials presented the unpublished results here at the American Academy of Ophthalmology and Middle East Africa Council of Ophthalmology 2010 Joint Meeting.
The telescope implant improves vision in "a disease in which the patient is legally blind and has no surgical or medical alternatives," the presenter, Stephen Lane, MD, told Medscape Medical News. He was a medical monitor for the pivotal trials and is an adjunct professor of ophthalmology at the University of Minnesota, Minneapolis.
In July, the US Food and Drug Administration approved the telescope implant, also called the implantable miniature telescope (VisionCare Ophthalmic Technologies), to improve vision in some patients with end-stage AMD.
Telescope Magnifies Images More Than 2 Times
"The reason why this [device] works is a magnification effect, so the central scotoma can be overcome," Dr. Lane told meeting attendees.
This pea-sized implant, which replaces the natural lens, magnifies images greater than 2 times and projects the images onto a healthy part of the retina, according to the device manufacturer. It is available in 2 models: 1 that provides 2.2 times the magnification and another that gives 2.7 times magnification. Patients use the eye that received the implant for central vision and use the untreated fellow eye for peripheral vision.
To be eligible for this class 3 medical device, patients must have bilateral geographic atrophy or "post-wet" AMD disciform scars and must not yet have had cataract surgery, although they can have cataract, Dr. Lane said. Other eligibility criteria, according to the US Food and Drug Administration, include age 75 years or older and "stable severe to profound vision impairment" resulting from bilateral central scotoma.
In a multicenter clinical trial of more than 200 patients who received the implant, the mean best corrected visual acuity before implantation was worse than 20/300, Dr. Lane said. More than 80% of patients had at least a 2-line improvement in visual acuity on the Snellen chart 1 year after surgery, and 46% of patients improved 4 lines or more at 1 year, he reported. Most of those patients, according to Dr. Lane, maintained their improved visual acuity 2 years postoperatively (75% with 2 lines or better and 43% with 4 or more lines of improvement).
"Quality of life gains also are clinically meaningful," Dr. Lane said. "Patients were less dependent, better able to recognize people, and better able to...do activities of daily living."
Endothelial Cell Loss Possible
A possible complication of the implant is the loss of corneal endothelial cells. In the study, there was a 20% loss of epithelial cells, which Dr. Lane called "a little high." He said ophthalmologists should inform their patients that substantial endothelial cell loss can lead to corneal decompensation and the need for a corneal transplant.
A Michigan ophthalmologist who did not participate in the studies, George Williams, MD, said in an interview that study investigators told him that most patients in the studies tolerated the implant well and found it very helpful.
However, the device is for "a select group of patients with end-stage AMD," said Dr. Williams, chairman of the Department of Ophthalmology at Oakland University William Beaumont School of Medicine, Royal Oak, Michigan.
He mentioned, as did Dr. Lane, that patients need to undergo an evaluation to determine whether they can benefit from this device, which involves a trial with an external telescope.
"Only 1 in 5 patients who are screened actually end up getting the device," Dr. Williams told Medscape Medical News.
After the surgery, patients must receive training with a low-vision specialist. "It's hard to walk around with a telescope in your eye," Dr. Williams said.
Patients who did not tolerate the implant were those who could not adjust to using 1 eye for near-vision tasks and the other eye for distance vision, Dr. Lane said during the meeting.
(Chicago, Illinois) — People with end-stage age-related macular degeneration (AMD) have improved visual acuity and quality of life after receiving an intraocular implant containing a tiny telescope in 1 eye, new research shows. An ophthalmologist who participated in the clinical trials presented the unpublished results here at the American Academy of Ophthalmology and Middle East Africa Council of Ophthalmology 2010 Joint Meeting.
The telescope implant improves vision in "a disease in which the patient is legally blind and has no surgical or medical alternatives," the presenter, Stephen Lane, MD, told Medscape Medical News. He was a medical monitor for the pivotal trials and is an adjunct professor of ophthalmology at the University of Minnesota, Minneapolis.
In July, the US Food and Drug Administration approved the telescope implant, also called the implantable miniature telescope (VisionCare Ophthalmic Technologies), to improve vision in some patients with end-stage AMD.
Telescope Magnifies Images More Than 2 Times
"The reason why this [device] works is a magnification effect, so the central scotoma can be overcome," Dr. Lane told meeting attendees.
This pea-sized implant, which replaces the natural lens, magnifies images greater than 2 times and projects the images onto a healthy part of the retina, according to the device manufacturer. It is available in 2 models: 1 that provides 2.2 times the magnification and another that gives 2.7 times magnification. Patients use the eye that received the implant for central vision and use the untreated fellow eye for peripheral vision.
To be eligible for this class 3 medical device, patients must have bilateral geographic atrophy or "post-wet" AMD disciform scars and must not yet have had cataract surgery, although they can have cataract, Dr. Lane said. Other eligibility criteria, according to the US Food and Drug Administration, include age 75 years or older and "stable severe to profound vision impairment" resulting from bilateral central scotoma.
In a multicenter clinical trial of more than 200 patients who received the implant, the mean best corrected visual acuity before implantation was worse than 20/300, Dr. Lane said. More than 80% of patients had at least a 2-line improvement in visual acuity on the Snellen chart 1 year after surgery, and 46% of patients improved 4 lines or more at 1 year, he reported. Most of those patients, according to Dr. Lane, maintained their improved visual acuity 2 years postoperatively (75% with 2 lines or better and 43% with 4 or more lines of improvement).
"Quality of life gains also are clinically meaningful," Dr. Lane said. "Patients were less dependent, better able to recognize people, and better able to...do activities of daily living."
Endothelial Cell Loss Possible
A possible complication of the implant is the loss of corneal endothelial cells. In the study, there was a 20% loss of epithelial cells, which Dr. Lane called "a little high." He said ophthalmologists should inform their patients that substantial endothelial cell loss can lead to corneal decompensation and the need for a corneal transplant.
A Michigan ophthalmologist who did not participate in the studies, George Williams, MD, said in an interview that study investigators told him that most patients in the studies tolerated the implant well and found it very helpful.
However, the device is for "a select group of patients with end-stage AMD," said Dr. Williams, chairman of the Department of Ophthalmology at Oakland University William Beaumont School of Medicine, Royal Oak, Michigan.
He mentioned, as did Dr. Lane, that patients need to undergo an evaluation to determine whether they can benefit from this device, which involves a trial with an external telescope.
"Only 1 in 5 patients who are screened actually end up getting the device," Dr. Williams told Medscape Medical News.
After the surgery, patients must receive training with a low-vision specialist. "It's hard to walk around with a telescope in your eye," Dr. Williams said.
Patients who did not tolerate the implant were those who could not adjust to using 1 eye for near-vision tasks and the other eye for distance vision, Dr. Lane said during the meeting.
Tuesday, October 26, 2010
Gene Therapy/ Treatment for Visual Impairment
Gene Therapy For Visual Impairment
By: Mark Burnsy
In modern society where most people are educated, eyesight problems inevitably proliferate, due to the fact that they have spent more time in reading. TV and computers are also incentives of the skyrocketed eyesight problems. Owing to the invention of eyeglasses and contact lenses, people with nearsightedness, farsightedness, astigmatism and presbyopia are able to view a clear world as well. Additionally, fast developed, eyeglass manufactures achieve advancement in glare reduction and unwanted wavelengths of light elimination.
However, eyeglasses and contacts can not serve as helps for vision improvement of people suffering from eye diseases, such as Macular Degeneration and Diabetic Retinopathy. Recently, a medical treatment is developed, which is also able to treat visual impairments. Avastin is a drug that was originally used in Colo-rectal cancer treatments but is found to have an ability to improve the vision in patients with Macular Degeneration, Diabetic Retinopathy and other vascular related retinal diseases. What's more, many other new drugs are brought about in succession as well, for example, the non steroidal anti inflammatory drugs can reduce retinal inflammation and cyst formations.
There are some people whose eye diseases arise from within the patients, genetic and congenital disorders. They pose a great challenge to eye doctors and surgeons. Luckily, gene therapy is found to be able to dramatically improve those patients' vision. The procedure is performed at the Scheie Eye Institute in Philadelphia and the patients formerly suffering from Leber's Congenital Amaurosis claim that he could read letters on an eye chart already after such a procedure. Then the news was published in the New England Journal of Medicine, on which the cause of Leber's Congenital Amaurosis and how the surgery achieves an success are recorded. It is stated that a lack of RPE 65 gene prevents protein production which is required for the retinal tissue to absorb and process the light into vision. A normal RPE is injected in the gene therapy to restore the protein production. After two weeks, the patients can mostly view more clearly than they did before. Possible complications of gene therapy include sensitivity to light.
In spit that it is just a successful case of Leber's Congenital Amaurosis treatment, it gives hopes to other eye diseases originated from gene disorders. Researches concerned are under procession. The application of gene therapy in visual impairment will be a great success in the near future.
By: Mark Burnsy
In modern society where most people are educated, eyesight problems inevitably proliferate, due to the fact that they have spent more time in reading. TV and computers are also incentives of the skyrocketed eyesight problems. Owing to the invention of eyeglasses and contact lenses, people with nearsightedness, farsightedness, astigmatism and presbyopia are able to view a clear world as well. Additionally, fast developed, eyeglass manufactures achieve advancement in glare reduction and unwanted wavelengths of light elimination.
However, eyeglasses and contacts can not serve as helps for vision improvement of people suffering from eye diseases, such as Macular Degeneration and Diabetic Retinopathy. Recently, a medical treatment is developed, which is also able to treat visual impairments. Avastin is a drug that was originally used in Colo-rectal cancer treatments but is found to have an ability to improve the vision in patients with Macular Degeneration, Diabetic Retinopathy and other vascular related retinal diseases. What's more, many other new drugs are brought about in succession as well, for example, the non steroidal anti inflammatory drugs can reduce retinal inflammation and cyst formations.
There are some people whose eye diseases arise from within the patients, genetic and congenital disorders. They pose a great challenge to eye doctors and surgeons. Luckily, gene therapy is found to be able to dramatically improve those patients' vision. The procedure is performed at the Scheie Eye Institute in Philadelphia and the patients formerly suffering from Leber's Congenital Amaurosis claim that he could read letters on an eye chart already after such a procedure. Then the news was published in the New England Journal of Medicine, on which the cause of Leber's Congenital Amaurosis and how the surgery achieves an success are recorded. It is stated that a lack of RPE 65 gene prevents protein production which is required for the retinal tissue to absorb and process the light into vision. A normal RPE is injected in the gene therapy to restore the protein production. After two weeks, the patients can mostly view more clearly than they did before. Possible complications of gene therapy include sensitivity to light.
In spit that it is just a successful case of Leber's Congenital Amaurosis treatment, it gives hopes to other eye diseases originated from gene disorders. Researches concerned are under procession. The application of gene therapy in visual impairment will be a great success in the near future.
Monday, October 4, 2010
Combination PDT, anti-VEG effective for choroidal neovascularization due to AMD
October 4, 2010
A customized combination of photodynamic therapy and intravitreal ranibizumab treatment for choroidal neovascularization due to age-related macular degeneration achieved good visual results with a decreased need for re-treatment, a study found.
"Combined customized PDT and ranibizumab treatment can achieve visual results similar to those obtained with intravitreal monotherapy with the advantage of fewer intravitreous injections and reduced potential for adverse effects," the study said.
In the nonrandomized, prospective, interventional study, 53 eyes of 53 patients with subfoveal and juxtafoveal choroidal neovascularization secondary to AMD were treated with PDT and intravitreal Lucentis (ranibizumab, Genentech).
At the end of the 12-month follow-up period, subjects' mean visual acuity had improved by 7.2 letters, and 78.8% maintained or improved their initial vision.
"The central retinal thickness and choroidal neovascularization size decreased to 118 µm and 0.26 disc areas, respectively, from baseline to 12 months," the study authors said.
Sixty-five PDT treatments (mean of 1.22 per patient) were performed, and 126 doses of ranibizumab were injected (mean of 2.37 per patient).
In 21 cases, only a single initial dose of PDT and ranibizumab was required.
A customized combination of photodynamic therapy and intravitreal ranibizumab treatment for choroidal neovascularization due to age-related macular degeneration achieved good visual results with a decreased need for re-treatment, a study found.
"Combined customized PDT and ranibizumab treatment can achieve visual results similar to those obtained with intravitreal monotherapy with the advantage of fewer intravitreous injections and reduced potential for adverse effects," the study said.
In the nonrandomized, prospective, interventional study, 53 eyes of 53 patients with subfoveal and juxtafoveal choroidal neovascularization secondary to AMD were treated with PDT and intravitreal Lucentis (ranibizumab, Genentech).
At the end of the 12-month follow-up period, subjects' mean visual acuity had improved by 7.2 letters, and 78.8% maintained or improved their initial vision.
"The central retinal thickness and choroidal neovascularization size decreased to 118 µm and 0.26 disc areas, respectively, from baseline to 12 months," the study authors said.
Sixty-five PDT treatments (mean of 1.22 per patient) were performed, and 126 doses of ranibizumab were injected (mean of 2.37 per patient).
In 21 cases, only a single initial dose of PDT and ranibizumab was required.
Saturday, September 18, 2010
Advanced Cell Technology Obtains Broad Patent covering use of Stem Cell
Sep 14, 2010 by Advanced Cell Techno;ogy
Advanced Cell Technology, Inc. ("ACT"; OTCBB: ACTC), a leader in the field of regenerative medicine, announced today that it will be issued U.S. Patent Numbers 7,795,025 and 7,794,704 on Tuesday, September 14th, which continue to extend the company's patent portfolio covering its retinal pigment epithelial (RPE) cell programs. In particular, the claims that will issue in patent number 7,794,704 broadly cover methods for treating retinal degeneration using human RPE cells differentiated from human embryonic stem cells (hESCs). Issuing with 68 claims, this patent covers methods of treatment with hESC-derived RPE cells that includes, but is not limited to, Stargardt's disease, retinitis pigmentosa, and macular degeneration. The 41 claims issuing in US Patent 7,795,025 contribute to the development of the company's protection of the processes for manufacturing RPE cells from human ES cells. The patent covers fundamental methods for generating transplantable cells for treatment of human patients.
"Another wonderful milestone for ACT! These patents continue the recognition of the inventions and innovations resulting from our scientific team's ongoing research, and further protects the platform technology underlying our RPE program, one of our key therapeutic programs," said William M. Caldwell IV, ACT's Chairman and CEO. "A valuable addition to our strong intellectual property portfolio, these patents should help position ACT as the dominant player in this potentially very large market. Our RPE technology is safe and scalable, and has tremendous potential for treating some 200 or more diseases of the retina."
"ACT is developing first-in-class treatments for degenerative disorders of the retina," said Robert Lanza, M.D., ACT's Chief Scientific Officer. "The use of RPE cells created from human embryonic stem cells should open the door to potential treatments for many diseases of the retina that impact sight. According to the World Health Organization, macular degeneration alone is known to affect 30-40 million people worldwide, and this represents only a handful of the 200 diseases that may be treated using our RPE cells. We have worked hard to develop an efficient method for producing a renewable source of transplantable RPE cells that can be used to target diseases such as Stargardt's Disease and Age-related Macular Degeneration. For many of these patients there are no available treatments. We have demonstrated that our stem cell-derived RPE cells can rescue visual function in animals that otherwise would have gone blind. We are looking forward to starting our clinical trials with the hope that these cells will be similarly efficacious in patients."
"We believe that these patents are especially important as they extend the company's patent coverage of the scalable manufacturing of human RPE cells for therapeutic use, which are core to our technology and product portfolio," continued Mr. Caldwell. "This IP further expands our patent estate with respect to protecting the use of RPE cells in a wide range of treatments, offering additional validation of the strength and breadth of our patent portfolio. This development also dovetails nicely with the prospect of initiating our human clinical trial for our RPE program. We are optimistic that the methods-of-treatments and the culturing processes covered by these two new patents, along with the Company's proprietary detection technique for final product release, will establish a formidable barrier to entry for any potential competitors. Once we have begun to treat Stargardt patients, we plan to initiate another clinical trial relating to the use of RPE cells in the treatment of dry Age-Related Macular Degeneration (AMD). At present there is no approved treatment for dry AMD, despite the fact that it represents a $20-30 billion potential market."
ACT's Single Blastomere technology used for isolating hESCs does not require the destruction of embryos. The RPE and other hESC-derived cells the company intends to produce for clinical use all begin with these "embryo-safe" stem cells. ACT does not rely on government funding for any of its research or development efforts, and accordingly has not been impacted by the recent court injunction against federal funding of hESC research. Nevertheless, the company's hESC lines and cells made for those lines (such as RPE cells) should fall outside the scope of the court order. While the injunction has been stayed, it is widely believed that this is only a temporary reprieve, with a permanent injunction a real possibility perhaps as early as the end of this month. Should that come to pass, ACT stands ready to offer its human stem cell lines to the research community, pending their approval by the National Institutes of Health (NIH).
About Advanced Cell Technology, Inc.
Advanced Cell Technology, Inc. is a biotechnology company applying cellular technology in the field of regenerative medicine. For more information, visit http://www.advancedcell.com.
Forward-Looking Statements
Statements in this news release regarding future financial and operating results, future growth in research and development programs, potential applications of our technology, opportunities for the company and any other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Any statements that are not statements of historical fact (including statements containing the words "will," "believes," "plans," "anticipates," "broad," "expects," "estimates," and similar expressions) should also be considered to be forward-looking statements. There are a number of important factors that could cause actual results or events to differ materially from those indicated by such forward-looking statements, including: limited operating history, need for future capital, risks inherent in the development and commercialization of potential products, scope and enforceability of our intellectual property, and economic conditions generally. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in the company's periodic reports, including the report on Form 10-K for the year ended December 31, 2009.
Forward-looking statements are based on the beliefs, opinions, and expectations of the company's management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. Forward-looking statements are based on the beliefs, opinions, and expectations of the company's management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change.
Advanced Cell Technology, Inc. ("ACT"; OTCBB: ACTC), a leader in the field of regenerative medicine, announced today that it will be issued U.S. Patent Numbers 7,795,025 and 7,794,704 on Tuesday, September 14th, which continue to extend the company's patent portfolio covering its retinal pigment epithelial (RPE) cell programs. In particular, the claims that will issue in patent number 7,794,704 broadly cover methods for treating retinal degeneration using human RPE cells differentiated from human embryonic stem cells (hESCs). Issuing with 68 claims, this patent covers methods of treatment with hESC-derived RPE cells that includes, but is not limited to, Stargardt's disease, retinitis pigmentosa, and macular degeneration. The 41 claims issuing in US Patent 7,795,025 contribute to the development of the company's protection of the processes for manufacturing RPE cells from human ES cells. The patent covers fundamental methods for generating transplantable cells for treatment of human patients.
"Another wonderful milestone for ACT! These patents continue the recognition of the inventions and innovations resulting from our scientific team's ongoing research, and further protects the platform technology underlying our RPE program, one of our key therapeutic programs," said William M. Caldwell IV, ACT's Chairman and CEO. "A valuable addition to our strong intellectual property portfolio, these patents should help position ACT as the dominant player in this potentially very large market. Our RPE technology is safe and scalable, and has tremendous potential for treating some 200 or more diseases of the retina."
"ACT is developing first-in-class treatments for degenerative disorders of the retina," said Robert Lanza, M.D., ACT's Chief Scientific Officer. "The use of RPE cells created from human embryonic stem cells should open the door to potential treatments for many diseases of the retina that impact sight. According to the World Health Organization, macular degeneration alone is known to affect 30-40 million people worldwide, and this represents only a handful of the 200 diseases that may be treated using our RPE cells. We have worked hard to develop an efficient method for producing a renewable source of transplantable RPE cells that can be used to target diseases such as Stargardt's Disease and Age-related Macular Degeneration. For many of these patients there are no available treatments. We have demonstrated that our stem cell-derived RPE cells can rescue visual function in animals that otherwise would have gone blind. We are looking forward to starting our clinical trials with the hope that these cells will be similarly efficacious in patients."
"We believe that these patents are especially important as they extend the company's patent coverage of the scalable manufacturing of human RPE cells for therapeutic use, which are core to our technology and product portfolio," continued Mr. Caldwell. "This IP further expands our patent estate with respect to protecting the use of RPE cells in a wide range of treatments, offering additional validation of the strength and breadth of our patent portfolio. This development also dovetails nicely with the prospect of initiating our human clinical trial for our RPE program. We are optimistic that the methods-of-treatments and the culturing processes covered by these two new patents, along with the Company's proprietary detection technique for final product release, will establish a formidable barrier to entry for any potential competitors. Once we have begun to treat Stargardt patients, we plan to initiate another clinical trial relating to the use of RPE cells in the treatment of dry Age-Related Macular Degeneration (AMD). At present there is no approved treatment for dry AMD, despite the fact that it represents a $20-30 billion potential market."
ACT's Single Blastomere technology used for isolating hESCs does not require the destruction of embryos. The RPE and other hESC-derived cells the company intends to produce for clinical use all begin with these "embryo-safe" stem cells. ACT does not rely on government funding for any of its research or development efforts, and accordingly has not been impacted by the recent court injunction against federal funding of hESC research. Nevertheless, the company's hESC lines and cells made for those lines (such as RPE cells) should fall outside the scope of the court order. While the injunction has been stayed, it is widely believed that this is only a temporary reprieve, with a permanent injunction a real possibility perhaps as early as the end of this month. Should that come to pass, ACT stands ready to offer its human stem cell lines to the research community, pending their approval by the National Institutes of Health (NIH).
About Advanced Cell Technology, Inc.
Advanced Cell Technology, Inc. is a biotechnology company applying cellular technology in the field of regenerative medicine. For more information, visit http://www.advancedcell.com.
Forward-Looking Statements
Statements in this news release regarding future financial and operating results, future growth in research and development programs, potential applications of our technology, opportunities for the company and any other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Any statements that are not statements of historical fact (including statements containing the words "will," "believes," "plans," "anticipates," "broad," "expects," "estimates," and similar expressions) should also be considered to be forward-looking statements. There are a number of important factors that could cause actual results or events to differ materially from those indicated by such forward-looking statements, including: limited operating history, need for future capital, risks inherent in the development and commercialization of potential products, scope and enforceability of our intellectual property, and economic conditions generally. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in the company's periodic reports, including the report on Form 10-K for the year ended December 31, 2009.
Forward-looking statements are based on the beliefs, opinions, and expectations of the company's management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. Forward-looking statements are based on the beliefs, opinions, and expectations of the company's management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change.
Sunday, September 12, 2010
How to prevent age-related macular degeneration
by Dr Pandula Siribaddana
Age Related Macular Degeneration or ARMD is a common condition seen in the elderly population and can be named as one of the commonest causes of visual loss among the same age group. The condition is characterized by the gradual loss of central vision and could be recognized as having two major categories.
In one form, which is the ‘dry’ macular degeneration, the retina and the layer below in the back of the eye would be separated by cellular debris and in the second form, which is the ‘wet’ macular degeneration, the two layers will be separated by enlarging blood vessels under the retina. In both instances, the peripheral vision would be spared and therefore, these individuals would be able to carry out their daily activities, although the functions such as reading would be impaired to a significant extent.
How to prevent ARMD in the elderly?
The prevention strategies related to ARMD would include avoiding the risk factors which would cause the condition in the first place. Therefore, following prevention strategies can be named as the most useful in order to achieve better vision in the elderly age.
Control blood sugar levels
This has shown to have an influence in the manifestation of macular degeneration and since it is prevalent abundantly, adhering to good glycaemic control would be essential to reduce the disease burden of ARMD.
Avoid smoking
Among the many influences it makes on health, macular degeneration is one and therefore its avoidance would greatly help susceptible individuals to maintain better visual health. According to statistics, there seems to be a threefold risk among the smokers than in non-smokers to develop ARMD during the elderly life.
Control hypertension and cardiovascular diseases
Researchers have identified these two as influencing the occurrence of macular degeneration and controlling of the same would reduce the risk of ARMD in susceptible individuals.
Avoid direct sun light
Sun light, particularly the blue light in the sun’s rays, have shown to influence the functioning of the retina and thus can lead to the development of ARMD. Therefore, using special eye glasses and avoiding such exposure would be recommended for people whom are constantly at risk of being exposed.
Include carotenes in the diet
Carotenes containing foods or else supplements have shown to be effective to a certain extent in reducing the risk of macular degeneration and therefore steps should be taken to include such foods and to take a balanced diet as much as possible.
Add omega 3 fatty acids
Similar to carotenes, omega 3 fatty acids are suggested as being supportive in the prevention of ARMD and should be included in the diets of all ages.
Lastly, due to the fact that there are other factors which are not modifiable and may lead to the development of ARMD, it is always best to screen and initiate treatment as early as possible in order to prevent progression of the disease and to avoid the occurrence of complete blindness.
Age Related Macular Degeneration or ARMD is a common condition seen in the elderly population and can be named as one of the commonest causes of visual loss among the same age group. The condition is characterized by the gradual loss of central vision and could be recognized as having two major categories.
In one form, which is the ‘dry’ macular degeneration, the retina and the layer below in the back of the eye would be separated by cellular debris and in the second form, which is the ‘wet’ macular degeneration, the two layers will be separated by enlarging blood vessels under the retina. In both instances, the peripheral vision would be spared and therefore, these individuals would be able to carry out their daily activities, although the functions such as reading would be impaired to a significant extent.
How to prevent ARMD in the elderly?
The prevention strategies related to ARMD would include avoiding the risk factors which would cause the condition in the first place. Therefore, following prevention strategies can be named as the most useful in order to achieve better vision in the elderly age.
Control blood sugar levels
This has shown to have an influence in the manifestation of macular degeneration and since it is prevalent abundantly, adhering to good glycaemic control would be essential to reduce the disease burden of ARMD.
Avoid smoking
Among the many influences it makes on health, macular degeneration is one and therefore its avoidance would greatly help susceptible individuals to maintain better visual health. According to statistics, there seems to be a threefold risk among the smokers than in non-smokers to develop ARMD during the elderly life.
Control hypertension and cardiovascular diseases
Researchers have identified these two as influencing the occurrence of macular degeneration and controlling of the same would reduce the risk of ARMD in susceptible individuals.
Avoid direct sun light
Sun light, particularly the blue light in the sun’s rays, have shown to influence the functioning of the retina and thus can lead to the development of ARMD. Therefore, using special eye glasses and avoiding such exposure would be recommended for people whom are constantly at risk of being exposed.
Include carotenes in the diet
Carotenes containing foods or else supplements have shown to be effective to a certain extent in reducing the risk of macular degeneration and therefore steps should be taken to include such foods and to take a balanced diet as much as possible.
Add omega 3 fatty acids
Similar to carotenes, omega 3 fatty acids are suggested as being supportive in the prevention of ARMD and should be included in the diets of all ages.
Lastly, due to the fact that there are other factors which are not modifiable and may lead to the development of ARMD, it is always best to screen and initiate treatment as early as possible in order to prevent progression of the disease and to avoid the occurrence of complete blindness.
Monday, August 23, 2010
Macular Degeneration Surgery
By Joven Villanueva
While the quest in searching for the cure of macular degeneration is on going. Many national eye centers are investigating new ways to treat the said illness. There are different options in managing macular degeneration as the illness has two types. The wet form which usually results to loss of vision due to no reliable treatment yet to be developed and the dry form accounting 90% of cases can still be managed and controlled if diagnosed at an early stage and by eating the right food rich in vitamins A, C, E and other supplements such as zeaxanthine and zinc - proven to be effective in slowing down the disease
Here are some optional treatments available for patients having the wet form of macular degeneration. First is Photodynamic therapy which uses a combination of both cold laser and light-sensitive drug destroying abnormal blood vessels as the drug travels to the unwanted vessels after it was injected from the arm. Another option is Laser therapy where high energy lights are used to destroy abnormal growing blood vessels.
The Cole eye institute is conducting experimental treatments such as a surgery to remove abnormal blood vessels and blood. A genetically engineered enzyme is used by the surgeon to dissolve blood clots under the macula. Another procedure is called Macular translocation.This is performed using a laser therapy to treat abnormal blood vessel. To prevent the formation of scar tissue and damage to retina, the surgeon rotates the retina in a healthy area.
The healing process may take three to six weeks. The doctor may request for an angiogram after the macular surgery to make sure that there are no additional blood leakage in the area. An additional laser treatment maybe performed if a problem was observed.
Macular degeneration is a medical condition resulting to loss of vision making it difficult to read and recognize faces. To better understand the patient's condition, print out some letters six inches high and try to identify them while looking it at straight ahead. Hold the paper slightly to the side. This visual impairment does not lead to total blindness and in most cases some vision remains.
This disease mostly affects older and adults 50 years old and above. In a recent study for macular degeneration it was found out that those patients aging sixty six to seventy four suffer from this illness. Mostly women are prone to macular degeneration compare to men and smokers of any gender are also part of the growing list as tobacco increase the risk in three folds due to the toxic effects in retina. It is even 50% risky for those who have relatives with muscular degeneration to develop the illness compare to those who doesn't have with only 12% probability. Caucasians are more prone to develop macular degeneration compare to other races.
Other than age and family history, there are factors that cause macular degeneration. These includes hypertension or commonly known as high blood pressure, obesity, and high fat intake.
Ophthalmologists diagnose macular degeneration by looking at the abnormal vessels under the retina. A dye is injected in the arm of the patient where pictures are taken by a special camera until it reaches the eye. Any changes in the retina as shown from the photographs taken will serve as a guide for treatment.
While the quest in searching for the cure of macular degeneration is on going. Many national eye centers are investigating new ways to treat the said illness. There are different options in managing macular degeneration as the illness has two types. The wet form which usually results to loss of vision due to no reliable treatment yet to be developed and the dry form accounting 90% of cases can still be managed and controlled if diagnosed at an early stage and by eating the right food rich in vitamins A, C, E and other supplements such as zeaxanthine and zinc - proven to be effective in slowing down the disease
Here are some optional treatments available for patients having the wet form of macular degeneration. First is Photodynamic therapy which uses a combination of both cold laser and light-sensitive drug destroying abnormal blood vessels as the drug travels to the unwanted vessels after it was injected from the arm. Another option is Laser therapy where high energy lights are used to destroy abnormal growing blood vessels.
The Cole eye institute is conducting experimental treatments such as a surgery to remove abnormal blood vessels and blood. A genetically engineered enzyme is used by the surgeon to dissolve blood clots under the macula. Another procedure is called Macular translocation.This is performed using a laser therapy to treat abnormal blood vessel. To prevent the formation of scar tissue and damage to retina, the surgeon rotates the retina in a healthy area.
The healing process may take three to six weeks. The doctor may request for an angiogram after the macular surgery to make sure that there are no additional blood leakage in the area. An additional laser treatment maybe performed if a problem was observed.
Macular degeneration is a medical condition resulting to loss of vision making it difficult to read and recognize faces. To better understand the patient's condition, print out some letters six inches high and try to identify them while looking it at straight ahead. Hold the paper slightly to the side. This visual impairment does not lead to total blindness and in most cases some vision remains.
This disease mostly affects older and adults 50 years old and above. In a recent study for macular degeneration it was found out that those patients aging sixty six to seventy four suffer from this illness. Mostly women are prone to macular degeneration compare to men and smokers of any gender are also part of the growing list as tobacco increase the risk in three folds due to the toxic effects in retina. It is even 50% risky for those who have relatives with muscular degeneration to develop the illness compare to those who doesn't have with only 12% probability. Caucasians are more prone to develop macular degeneration compare to other races.
Other than age and family history, there are factors that cause macular degeneration. These includes hypertension or commonly known as high blood pressure, obesity, and high fat intake.
Ophthalmologists diagnose macular degeneration by looking at the abnormal vessels under the retina. A dye is injected in the arm of the patient where pictures are taken by a special camera until it reaches the eye. Any changes in the retina as shown from the photographs taken will serve as a guide for treatment.
Wednesday, August 18, 2010
Epidemiolgy and Burden of Retina Disease
By Nancy M. Holekamp, MD
Age-related macular degeneration. The Eye Disease Prevalence Group has estimated that 1.75 million people in the United States have advanced age-related macular degeneration (AMD), including neovascular AMD or geographic atrophy, but not necessarily involving the foveal center, with the highest prevalence in adults older than 80 years of age.1 These numbers are estimated to increase substantially in the coming decades.
The numbers are huge, but what impact does AMD have on our patients? AMD is associated with an increased incidence of depression, mortality, and a greater need for assistance for daily tasks. In a quality-oflife study that was part of the Submacular Surgery Trials (SSTs), patients were asked to rate their current vision during phone interviews. Patient scores were converted to a preference value scale ranging from 1 (perfect health with perfect vision) to 0 (death). A mean preference value of 0.64 for subfoveal choroidal neovascularization (CNV) suggests a profound impact on quality of life. The impact is reported as greatest in those with the most severe loss of vision, but even patients with visual acuity of at least 20/40 in one eye had relatively low preference values.2 This is striking because it is right between having chronic renal failure and symptomatic HIV/AIDS (Figure 1). Clearly, AMD has a significant impact on the quality of life of individuals.
Diabetic retinopathy. It is well known that we are in the midst of an epidemic of obesity and diabetes in the United States. The rates of both have increased dramatically from 1990 to 2001, particularly in the southeast (Figure 2) and the increase in people with diabetes directly correlates to the rise in obesity.3 An estimated 18.2 million people had diabetes in the United States in 20023 and diabetes has been estimated to affect 151 million people worldwide, and is projected to increase to 324 million by 2025.4 It is also estimated that 35% of any diabetic population will have diabetic retinopathy.5 We know this from the Beaver Dam Eye Study. In terms of costs, the direct and indirect costs for diabetes were estimated at $132 billion in 2002.6 Almost $1 out of every $5 in the United States spent on healthcare is for patients with diabetes. Diabetes has an enormous impact on patients’ quality of life and represents a large economic issue.
Retinal vein occlusion. Retinal vein occlusion (RVO) is the second most common retinal disease after diabetic retinopathy. The Beaver Dam Study reported a prevalence of 0.6% in patients older than 43 years and the same study reported a 15-year cumulative incidence of BRVO of 1.8%.7 Although these numbers may sound low, the average age of these patients is 65 and this age group may have a host of comorbidities (eg, hypertension, vascular disease, diabetes). RVOs share risk factors with myocardial infarction (MI),8 stroke, and other arterial thrombotic events.9 In a study that is currently in press,10 we reviewed the records of 4,500 patients with RVO and compared them with 13,500 patients who were age-matched controls. We found that patients with RVO had significantly higher likelihood of having angina, cardiac arrhythmia, congestive heart failure, diabetes, heart disease, MI or stroke, hyperlipidemia, and hypertension (P=.001) The incidence of RVOs continues to increase as the incidence of diabetes increases and the population ages.
EVIDENCE-BASED MEDICINE
Evidence-based medicine is the practice of medicine based on the best scientific data available. The questions are, “How much evidence do you need?” and “How much science is behind it?”
These are the various levels of evidence. The weakest is the single-case report, which is level 5 evidence. The second weakest is the case series without a comparison group (level 4). Level 3 evidence consists of nonrandomized clinical trials that may compare two groups that are not concurrent or randomized. A level 2 clinical trial is similar to a phase 2 US Food and Drug Administration (FDA) clinical trial—it is randomized and controlled but it has a high type-1 error, where a trend is apparent and may be significant, but the number of patients is insufficient. A type-2 error is when a treatment difference likely exists but, again, there are not enough patients to isolate the difference.
Level 1 evidence is from randomized, prospective, controlled trials, with a low type-1 and type-2 errors. These are the phase 3 clinical trials that eventually lead to drug approval by the FDA. The key to level 1 evidence is a well-designed study and a large number of patients.
CLINICAL TRIAL DESIGN: WHY IS IT IMPORTANT?
In medicine we prefer level 1 trials because of random assignment to treatment or control; the concurrent enrollment that ensures patients are being treated in a similar manner; the large numbers of patients; and the masking of the investigators. The standardized follow up is also important to the significance of outcomes. By controlling these variables, we are able to clinically treat patients in the most scientific manner. My colleague Kuldev Singh, MD, who is a glaucoma specialist has said, “This term [randomized, controlled] allows the investigator to disarm the novice scientific critic, while impugning lesser prospective and all retrospective studies, not to mention case series and reports.” The randomized, controlled study is at the top of the food chain.
A case example of using low-level evidence-based medicine upon which to base treatment decisions is that of bevacizumab (Avastin, Genentech) for treating AMD. In August 2005, there was one case report (level 5 evidence) demonstrating improvement on optical coherence tomography (OCT) for a patient nonresponsive to pegaptanib sodium (Macugen, Eyetech/Pfizer) for AMD in the published literature.11 Simultaneously, Philip Rosenfeld, MD, PhD, one of the authors of the aforementioned case report, presented a paper (level 4 evidence) at the American Society of Retina Specialists in Montreal on a series of patients with exudative AMD who benefited from intravitreal bevacizumab. Clearly, the “bevacizumab for AMD” era was ushered in using the least convincing type of evidence.
Unlike bevacizumab, ranibizumab (Lucentis, Genentech) was subject to two phase 3 randomized, controlled clinical trials sponsored by industry (MARINA ANCHOR) that resulted in FDA approval. The extent to which the efficacy and safety of ranibizumab has been scrutinized is to the highest level.
But can you have a randomized, controlled trial for every disease and treatment? Paul Lichter, MD, said, “Authors of case reports, retrospective studies, and other manuscripts covering the gamut of imperfect clinical projects often conclude their papers by calling for a randomized, controlled, collaborative clinical trial. While I have no idea how many times such statements are made, there is no question that these pronouncements are abundantly more frequent then the clinical trials that result from them.”
CRITERIA FOR CONDUCTING A LEVEL 1 CLINICAL TRIAL
Clearly, a level 1 clinical trial cannot be conducted for every clinical situation. My four criteria for conducting a randomized, controlled clinical trial include the following:
* The disease must represent a significant health problem. An example of what can be called an questionable effort is in 1993 when the Canadian Ophthalmology Study Group conducted a multicenter randomized, controlled clinical trial to compare the argon green vs krypton red laser for choroidal neovascularization (CNV) in AMD.12 The comparison of these lasers was not a burning issue for the health care system.
* There must be scientific plausibility of benefit. In other words, there has to be some biologic basis for believing that a treatment works. An example from the AMD literature is subfoveal laser for CNV.13 There was no basis to suggest that applying laser to a patient’s fovea would be beneficial.
* A plausible, biologic benefit must exist. In other words, the early data on a new treatment should suggest the possibility of benefit. A good example of this is the Submacular Surgery Trials in AMD where early pilot data did not show any benefit to submacular surgery over laser photocoagulation.14 The eventual the long-term data supported this conclusion.
* Sufficient numbers of patients must be enrolled. If a study cannot recruit enough patients, it will not succeed. For example, it was almost impossible to recruit patients into the Macular Translocation clinical trial because they were randomized to either photodynamic therapy—a relatively painless 15-minute office-based laser procedure— or to macular translocation, which had a 25% complication rate at the time they were trying to enroll.15
The clinical trials’ registry, www.clinicaltrials.gov, currently lists 530 clinical trials for the treatment of AMD. Of those 200 trials are open and actively recruiting patients. Eighty-seven of these are randomized and controlled. Those of us in the field of ophthalmology and the subspecialty of retina are fortunate to be part of a profession that is committed to providing the best scientific evidence for its members. We have a long, proud history of practicing evidence-based medicine and performing randomized clinical trials in our field.
NON-INFERIOR CLINICAL TRIALS
There are basically three types of trial design: superiority, equivalence, and non-inferiority. The Comparisons of Age- Related Macular Degeneration Treatments Trials (CATT) is a non-inferiority trial comparing intravitreal ranibizumab to intravitreal bevacizumab. The margin of non-inferiority must be pre-specified in the design protocol to construct a two-sided, 95% confidence interval (CI) to determine the true difference between the agents. To be able to declare bevacizumab non-inferior, that interval must lay entirely on the positive side of the non-inferior margin.
Figure 3 helps illustrate how the results of a non-inferiority trial are interpreted. Applied to the CATT, if proved non-inferior, bevacizumab is either almost as good as, equivalent to, or better than ranibizumab. If bevacizumab fails non-inferiority then it is either equivalent, almost as good as, or inferior to ranibizumab. All of those possibilities exist.
The major criteria for non-inferiority clinical trials are:
1) historical evidence that the reference drug works (ie, MARINA and ANCHOR);
2) trial design must be the same as the reference trial (ie, the CATT has same design as MARINA and ANCHOR);
3) trial conduct must be the same (ie, many of the clinical sites from MARINA and ANCHOR are also sites for the CATT);
4) the non-inferior margin (minus delta) must be acceptable (ie, six letters for the CATT).
In addition to the CATT, there are two other non-inferiority trials in AMD: HARBOR (A Study of Ranibizumab Administered Monthly or on an As-Needed Basis in Patients With Subfoveal Neovascular Age-Related Macular Degeneration) and VIEW I (VEGF Trap-Eye: Investigation of Efficacy and Safety in Wet AMD). These are both similar to MARINA and ANCHOR in historical evidence, trial design and trial conduct, and have an acceptable non-inferior margin.
SUMMARY
The best way to practice evidence-based medicine is with phase 3, randomized, and controlled trials. The requirements for level 1 clinical trials do not necessarily constitute a “cookbook” for successful trials; rather, they provide guidelines for those who are designing and participating in clinical trials.
Finally, evidence alone is never sufficient information to make a clinical decision—there are many factors to be taken under consideration. When treating our patients, we consider several factors including a patient’s values, socio-economic status, and age; however we should rely on three main components: our years of clinical experience, the patient’s particular circumstances, and what we have learned from evidence-based medicine.
1. Friedman DS, O’Colmain BJ, Muñoz B, et al; The Eye Diseases Prevalence Research Group. Prevalence of age-related macular degeneration in the United States. Archives of Ophthalmology. 2004;122:564-572.
2. No authors listed. Submacular surgery trials randomized pilot trial of laser photocoagulation versus surgery for recurrent choroidal neovascularization secondary to age-related macular degeneration: II. Quality of life outcomes submacular surgery trials pilot study report number 2. Am J Ophthalmol. 2000;130(4):408-418.
3. National Institute of Diabetes and Digestive and Kidney Diseases. National Diabetes Statistics Fact Sheet: General Information and National Estimates on Diabetes in the United States. Bethesda, MD, US Department of Health and Human Services, National Institutes of Health, 2003.
4. King H, Rewers M. Global estimates for prevalence of diabetes mellitus and impaired glucose tolerance in adults: WHO Ad Hoc Diabetes Reporting Group. Diabetes Care. 1993;16:157–177.
5. Beaver Dam Eye Study.
6. Hogan P, Dall T, Nikolov P; American Diabetes Association. Economic costs of diabetes in the US in 2002. Diabetes Care. 2003;26(3):917-932.
7. Klein R, Klein BE, Moss SE, Linton KL. Beaver Dam Eye Study. Retinopathy in adults with newly discovered and previously diagnosed diabetes mellitus. Ophthalmology. 1992;99(1):58-62.
8. National Heart Lung and Blood Institute. Heart attack. Available at http://www.nhlbi.nih.gov/health/dci/Diseases/HeartAttack/HeartAttack_WhatIs.html.
9. Thom T, Haase N, Rosamond W, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Committee. Circulation. 2006;113:85-151.
10. Holekamp N. Arch Ophthalmol. In press.
11. Rosenfeld PJ, Moshfeghi AA, Puliafito CA. Optical coherence tomography findings after an intravitreal injection of bevacizumab (avastin) for neovascular age-related macular degeneration. Ophthalmic Surg Lasers Imaging. 2005;36(4):331-335.
12. The Canadian Ophthalmology Study Group. Argon green vs krypton red laser photocoagulation of extrafoveal choroidal neovascular lesions. One-year results in age-related macular degeneration. Arch Ophthalmol. 1993;111:181-185.
13. Macular Photocoagulation Study Group. Visual outcome after laser photo- coagulation for subfoveal neovascularization secondary to age-related macular degeneration. The influence of initial lesion size and initial visual acuity. Arch Ophthalmol. 1994;112:480–488.
14. Bressler NM, Bressler SB, Hawkins BS, Marsh MJ, Sternberg P Jr, Thomas MA; Submacular Surgery Trials Pilot Study Investigators. Submacular surgery trials randomized pilot trial of laser photocoagulation versus surgery for recurrent choroidal neovascularization secondary to age-related macular degeneration: I. Ophthalmic outcomes submacular surgery trials pilot study report number 1. Am J Ophthalmol. 2000;130(4):387-407.
15. Hawkins BS, Bressler NM, Miskala PH, et al; Submacular Surgery Trials (SST) Research Group. Surgery for subfoveal choroidal neovascularization in age-related macular degeneration: ophthalmic findings: SST report no. 11. Ophthalmology. 2004;111(11):1967-1980.
Age-related macular degeneration. The Eye Disease Prevalence Group has estimated that 1.75 million people in the United States have advanced age-related macular degeneration (AMD), including neovascular AMD or geographic atrophy, but not necessarily involving the foveal center, with the highest prevalence in adults older than 80 years of age.1 These numbers are estimated to increase substantially in the coming decades.
The numbers are huge, but what impact does AMD have on our patients? AMD is associated with an increased incidence of depression, mortality, and a greater need for assistance for daily tasks. In a quality-oflife study that was part of the Submacular Surgery Trials (SSTs), patients were asked to rate their current vision during phone interviews. Patient scores were converted to a preference value scale ranging from 1 (perfect health with perfect vision) to 0 (death). A mean preference value of 0.64 for subfoveal choroidal neovascularization (CNV) suggests a profound impact on quality of life. The impact is reported as greatest in those with the most severe loss of vision, but even patients with visual acuity of at least 20/40 in one eye had relatively low preference values.2 This is striking because it is right between having chronic renal failure and symptomatic HIV/AIDS (Figure 1). Clearly, AMD has a significant impact on the quality of life of individuals.
Diabetic retinopathy. It is well known that we are in the midst of an epidemic of obesity and diabetes in the United States. The rates of both have increased dramatically from 1990 to 2001, particularly in the southeast (Figure 2) and the increase in people with diabetes directly correlates to the rise in obesity.3 An estimated 18.2 million people had diabetes in the United States in 20023 and diabetes has been estimated to affect 151 million people worldwide, and is projected to increase to 324 million by 2025.4 It is also estimated that 35% of any diabetic population will have diabetic retinopathy.5 We know this from the Beaver Dam Eye Study. In terms of costs, the direct and indirect costs for diabetes were estimated at $132 billion in 2002.6 Almost $1 out of every $5 in the United States spent on healthcare is for patients with diabetes. Diabetes has an enormous impact on patients’ quality of life and represents a large economic issue.
Retinal vein occlusion. Retinal vein occlusion (RVO) is the second most common retinal disease after diabetic retinopathy. The Beaver Dam Study reported a prevalence of 0.6% in patients older than 43 years and the same study reported a 15-year cumulative incidence of BRVO of 1.8%.7 Although these numbers may sound low, the average age of these patients is 65 and this age group may have a host of comorbidities (eg, hypertension, vascular disease, diabetes). RVOs share risk factors with myocardial infarction (MI),8 stroke, and other arterial thrombotic events.9 In a study that is currently in press,10 we reviewed the records of 4,500 patients with RVO and compared them with 13,500 patients who were age-matched controls. We found that patients with RVO had significantly higher likelihood of having angina, cardiac arrhythmia, congestive heart failure, diabetes, heart disease, MI or stroke, hyperlipidemia, and hypertension (P=.001) The incidence of RVOs continues to increase as the incidence of diabetes increases and the population ages.
EVIDENCE-BASED MEDICINE
Evidence-based medicine is the practice of medicine based on the best scientific data available. The questions are, “How much evidence do you need?” and “How much science is behind it?”
These are the various levels of evidence. The weakest is the single-case report, which is level 5 evidence. The second weakest is the case series without a comparison group (level 4). Level 3 evidence consists of nonrandomized clinical trials that may compare two groups that are not concurrent or randomized. A level 2 clinical trial is similar to a phase 2 US Food and Drug Administration (FDA) clinical trial—it is randomized and controlled but it has a high type-1 error, where a trend is apparent and may be significant, but the number of patients is insufficient. A type-2 error is when a treatment difference likely exists but, again, there are not enough patients to isolate the difference.
Level 1 evidence is from randomized, prospective, controlled trials, with a low type-1 and type-2 errors. These are the phase 3 clinical trials that eventually lead to drug approval by the FDA. The key to level 1 evidence is a well-designed study and a large number of patients.
CLINICAL TRIAL DESIGN: WHY IS IT IMPORTANT?
In medicine we prefer level 1 trials because of random assignment to treatment or control; the concurrent enrollment that ensures patients are being treated in a similar manner; the large numbers of patients; and the masking of the investigators. The standardized follow up is also important to the significance of outcomes. By controlling these variables, we are able to clinically treat patients in the most scientific manner. My colleague Kuldev Singh, MD, who is a glaucoma specialist has said, “This term [randomized, controlled] allows the investigator to disarm the novice scientific critic, while impugning lesser prospective and all retrospective studies, not to mention case series and reports.” The randomized, controlled study is at the top of the food chain.
A case example of using low-level evidence-based medicine upon which to base treatment decisions is that of bevacizumab (Avastin, Genentech) for treating AMD. In August 2005, there was one case report (level 5 evidence) demonstrating improvement on optical coherence tomography (OCT) for a patient nonresponsive to pegaptanib sodium (Macugen, Eyetech/Pfizer) for AMD in the published literature.11 Simultaneously, Philip Rosenfeld, MD, PhD, one of the authors of the aforementioned case report, presented a paper (level 4 evidence) at the American Society of Retina Specialists in Montreal on a series of patients with exudative AMD who benefited from intravitreal bevacizumab. Clearly, the “bevacizumab for AMD” era was ushered in using the least convincing type of evidence.
Unlike bevacizumab, ranibizumab (Lucentis, Genentech) was subject to two phase 3 randomized, controlled clinical trials sponsored by industry (MARINA ANCHOR) that resulted in FDA approval. The extent to which the efficacy and safety of ranibizumab has been scrutinized is to the highest level.
But can you have a randomized, controlled trial for every disease and treatment? Paul Lichter, MD, said, “Authors of case reports, retrospective studies, and other manuscripts covering the gamut of imperfect clinical projects often conclude their papers by calling for a randomized, controlled, collaborative clinical trial. While I have no idea how many times such statements are made, there is no question that these pronouncements are abundantly more frequent then the clinical trials that result from them.”
CRITERIA FOR CONDUCTING A LEVEL 1 CLINICAL TRIAL
Clearly, a level 1 clinical trial cannot be conducted for every clinical situation. My four criteria for conducting a randomized, controlled clinical trial include the following:
* The disease must represent a significant health problem. An example of what can be called an questionable effort is in 1993 when the Canadian Ophthalmology Study Group conducted a multicenter randomized, controlled clinical trial to compare the argon green vs krypton red laser for choroidal neovascularization (CNV) in AMD.12 The comparison of these lasers was not a burning issue for the health care system.
* There must be scientific plausibility of benefit. In other words, there has to be some biologic basis for believing that a treatment works. An example from the AMD literature is subfoveal laser for CNV.13 There was no basis to suggest that applying laser to a patient’s fovea would be beneficial.
* A plausible, biologic benefit must exist. In other words, the early data on a new treatment should suggest the possibility of benefit. A good example of this is the Submacular Surgery Trials in AMD where early pilot data did not show any benefit to submacular surgery over laser photocoagulation.14 The eventual the long-term data supported this conclusion.
* Sufficient numbers of patients must be enrolled. If a study cannot recruit enough patients, it will not succeed. For example, it was almost impossible to recruit patients into the Macular Translocation clinical trial because they were randomized to either photodynamic therapy—a relatively painless 15-minute office-based laser procedure— or to macular translocation, which had a 25% complication rate at the time they were trying to enroll.15
The clinical trials’ registry, www.clinicaltrials.gov, currently lists 530 clinical trials for the treatment of AMD. Of those 200 trials are open and actively recruiting patients. Eighty-seven of these are randomized and controlled. Those of us in the field of ophthalmology and the subspecialty of retina are fortunate to be part of a profession that is committed to providing the best scientific evidence for its members. We have a long, proud history of practicing evidence-based medicine and performing randomized clinical trials in our field.
NON-INFERIOR CLINICAL TRIALS
There are basically three types of trial design: superiority, equivalence, and non-inferiority. The Comparisons of Age- Related Macular Degeneration Treatments Trials (CATT) is a non-inferiority trial comparing intravitreal ranibizumab to intravitreal bevacizumab. The margin of non-inferiority must be pre-specified in the design protocol to construct a two-sided, 95% confidence interval (CI) to determine the true difference between the agents. To be able to declare bevacizumab non-inferior, that interval must lay entirely on the positive side of the non-inferior margin.
Figure 3 helps illustrate how the results of a non-inferiority trial are interpreted. Applied to the CATT, if proved non-inferior, bevacizumab is either almost as good as, equivalent to, or better than ranibizumab. If bevacizumab fails non-inferiority then it is either equivalent, almost as good as, or inferior to ranibizumab. All of those possibilities exist.
The major criteria for non-inferiority clinical trials are:
1) historical evidence that the reference drug works (ie, MARINA and ANCHOR);
2) trial design must be the same as the reference trial (ie, the CATT has same design as MARINA and ANCHOR);
3) trial conduct must be the same (ie, many of the clinical sites from MARINA and ANCHOR are also sites for the CATT);
4) the non-inferior margin (minus delta) must be acceptable (ie, six letters for the CATT).
In addition to the CATT, there are two other non-inferiority trials in AMD: HARBOR (A Study of Ranibizumab Administered Monthly or on an As-Needed Basis in Patients With Subfoveal Neovascular Age-Related Macular Degeneration) and VIEW I (VEGF Trap-Eye: Investigation of Efficacy and Safety in Wet AMD). These are both similar to MARINA and ANCHOR in historical evidence, trial design and trial conduct, and have an acceptable non-inferior margin.
SUMMARY
The best way to practice evidence-based medicine is with phase 3, randomized, and controlled trials. The requirements for level 1 clinical trials do not necessarily constitute a “cookbook” for successful trials; rather, they provide guidelines for those who are designing and participating in clinical trials.
Finally, evidence alone is never sufficient information to make a clinical decision—there are many factors to be taken under consideration. When treating our patients, we consider several factors including a patient’s values, socio-economic status, and age; however we should rely on three main components: our years of clinical experience, the patient’s particular circumstances, and what we have learned from evidence-based medicine.
1. Friedman DS, O’Colmain BJ, Muñoz B, et al; The Eye Diseases Prevalence Research Group. Prevalence of age-related macular degeneration in the United States. Archives of Ophthalmology. 2004;122:564-572.
2. No authors listed. Submacular surgery trials randomized pilot trial of laser photocoagulation versus surgery for recurrent choroidal neovascularization secondary to age-related macular degeneration: II. Quality of life outcomes submacular surgery trials pilot study report number 2. Am J Ophthalmol. 2000;130(4):408-418.
3. National Institute of Diabetes and Digestive and Kidney Diseases. National Diabetes Statistics Fact Sheet: General Information and National Estimates on Diabetes in the United States. Bethesda, MD, US Department of Health and Human Services, National Institutes of Health, 2003.
4. King H, Rewers M. Global estimates for prevalence of diabetes mellitus and impaired glucose tolerance in adults: WHO Ad Hoc Diabetes Reporting Group. Diabetes Care. 1993;16:157–177.
5. Beaver Dam Eye Study.
6. Hogan P, Dall T, Nikolov P; American Diabetes Association. Economic costs of diabetes in the US in 2002. Diabetes Care. 2003;26(3):917-932.
7. Klein R, Klein BE, Moss SE, Linton KL. Beaver Dam Eye Study. Retinopathy in adults with newly discovered and previously diagnosed diabetes mellitus. Ophthalmology. 1992;99(1):58-62.
8. National Heart Lung and Blood Institute. Heart attack. Available at http://www.nhlbi.nih.gov/health/dci/Diseases/HeartAttack/HeartAttack_WhatIs.html.
9. Thom T, Haase N, Rosamond W, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Committee. Circulation. 2006;113:85-151.
10. Holekamp N. Arch Ophthalmol. In press.
11. Rosenfeld PJ, Moshfeghi AA, Puliafito CA. Optical coherence tomography findings after an intravitreal injection of bevacizumab (avastin) for neovascular age-related macular degeneration. Ophthalmic Surg Lasers Imaging. 2005;36(4):331-335.
12. The Canadian Ophthalmology Study Group. Argon green vs krypton red laser photocoagulation of extrafoveal choroidal neovascular lesions. One-year results in age-related macular degeneration. Arch Ophthalmol. 1993;111:181-185.
13. Macular Photocoagulation Study Group. Visual outcome after laser photo- coagulation for subfoveal neovascularization secondary to age-related macular degeneration. The influence of initial lesion size and initial visual acuity. Arch Ophthalmol. 1994;112:480–488.
14. Bressler NM, Bressler SB, Hawkins BS, Marsh MJ, Sternberg P Jr, Thomas MA; Submacular Surgery Trials Pilot Study Investigators. Submacular surgery trials randomized pilot trial of laser photocoagulation versus surgery for recurrent choroidal neovascularization secondary to age-related macular degeneration: I. Ophthalmic outcomes submacular surgery trials pilot study report number 1. Am J Ophthalmol. 2000;130(4):387-407.
15. Hawkins BS, Bressler NM, Miskala PH, et al; Submacular Surgery Trials (SST) Research Group. Surgery for subfoveal choroidal neovascularization in age-related macular degeneration: ophthalmic findings: SST report no. 11. Ophthalmology. 2004;111(11):1967-1980.
Monday, August 9, 2010
Retinitis pigmentosa treatment
As human beings, there is very little more universally feared than the dark, and few disabilities more frightening than blindness which would leave us trapped in it. Retinitis pigmentosa is a condition which, to many people, might sound like a nightmare. Retinitis pigmentosa refers to a group of genetic conditions in which the eye progressively degenerates over time. The first symptoms of retinitis pigmentosa are night blindness. This night blindness worsens over time, eventually developing into tunnel vision which little by little narrows the sufferer’s peripheral vision until finally they become legally – and perhaps totally – blind.
Progression is different in each case of retinitis pigmentosa. The night blindness phase of the disease can proceed tunnel vision by years or even decades, and many people with retinitis pigmentosa do not legally go blind until their forties or fifties. Some never retain some level of vision throughout their lives. At the same time, others may go blind as early as during childhood.
Retinitis pigmentosa diagnosis come as a fearful shock to some people, which is why retinitis pigmentosa treatments are so important.
Since time out of mind, people have struggled to treat the diseases around them. They have relied on everything from superstition, prayer, spells and religious chants to herbal remedies, surgeries and medicines, some of which are still in use today. Unfortunately for people before the modern era, there was very little to be done for loss of sight. Our ancestors had very few options in terms of treatment for retinitis pigmentosa. Retinitis pigmentosa is caused by abnormalities in the receptors in the eye, the rods and cones which allow us to see color, light and movement. As these abnormalities increase over time, the sufferer’s eyesight diminishes. There was very little for even our grandfathers and grandmothers to do when faced with this sort of disease. It has only been recently that our understanding of how the eye works, our understanding of how the body as a whole operates, and our technology has reached a point where retinitis pigmentosa treatments have become something of a reality and moved out of the realms of witchcraft and hope.
Retinitis pigmentosa treatments are still relatively few. There is no true cure for retinitis pigmentosa, only treatments which may help to slow the progression of this degenerative disease.
Among the first treatment options for people diagnosed with retinitis pigmentosa are medications and supplements. For example, vitamin A therapies can support eye health and slow the progression of this disease. People who receive these should have their liver enzymes checked annually, since in too great of doses, vitamin A can become toxic to the system. Other retinitis pigmentosa treatment options include omega-3 polyunsaturated fatty acid and antioxidant, docosahexaenoic acid, acetazolamide, lutein, and calcium blockers.
In the event that medication proves an ineffective retinitis pigmentosa treatment, there are also surgical treatments to consider. What kind of surgical options a patient may have for their retinitis pigmentosa treatment depends on many factors, as the progression of the disease varies greatly from person to person, and as the disease is associated with a number of other genetic and structural conditions. For some people, partial retinal transplants can be a useful retinitis pigmentosa treatment. The possibility of a retinal prosthetics
have also been under consideration for several years now. While there are currently no prosthetics available for clinical use as retinitis pigmentosa treatment, they may present a promising future for those with this degenerative disease.
Since retinitis pigmentosa is a genetic disorder, it should not be surprising that when considering retinitis pigmentosa treatments, speculation might turn to the possibilities of gene therapy and stem cell research. These treatments are, as yet, still in the research and investigation phases, but may well represent the future of retinitis pigmentosa treatment.
Progression is different in each case of retinitis pigmentosa. The night blindness phase of the disease can proceed tunnel vision by years or even decades, and many people with retinitis pigmentosa do not legally go blind until their forties or fifties. Some never retain some level of vision throughout their lives. At the same time, others may go blind as early as during childhood.
Retinitis pigmentosa diagnosis come as a fearful shock to some people, which is why retinitis pigmentosa treatments are so important.
Since time out of mind, people have struggled to treat the diseases around them. They have relied on everything from superstition, prayer, spells and religious chants to herbal remedies, surgeries and medicines, some of which are still in use today. Unfortunately for people before the modern era, there was very little to be done for loss of sight. Our ancestors had very few options in terms of treatment for retinitis pigmentosa. Retinitis pigmentosa is caused by abnormalities in the receptors in the eye, the rods and cones which allow us to see color, light and movement. As these abnormalities increase over time, the sufferer’s eyesight diminishes. There was very little for even our grandfathers and grandmothers to do when faced with this sort of disease. It has only been recently that our understanding of how the eye works, our understanding of how the body as a whole operates, and our technology has reached a point where retinitis pigmentosa treatments have become something of a reality and moved out of the realms of witchcraft and hope.
Retinitis pigmentosa treatments are still relatively few. There is no true cure for retinitis pigmentosa, only treatments which may help to slow the progression of this degenerative disease.
Among the first treatment options for people diagnosed with retinitis pigmentosa are medications and supplements. For example, vitamin A therapies can support eye health and slow the progression of this disease. People who receive these should have their liver enzymes checked annually, since in too great of doses, vitamin A can become toxic to the system. Other retinitis pigmentosa treatment options include omega-3 polyunsaturated fatty acid and antioxidant, docosahexaenoic acid, acetazolamide, lutein, and calcium blockers.
In the event that medication proves an ineffective retinitis pigmentosa treatment, there are also surgical treatments to consider. What kind of surgical options a patient may have for their retinitis pigmentosa treatment depends on many factors, as the progression of the disease varies greatly from person to person, and as the disease is associated with a number of other genetic and structural conditions. For some people, partial retinal transplants can be a useful retinitis pigmentosa treatment. The possibility of a retinal prosthetics
have also been under consideration for several years now. While there are currently no prosthetics available for clinical use as retinitis pigmentosa treatment, they may present a promising future for those with this degenerative disease.
Since retinitis pigmentosa is a genetic disorder, it should not be surprising that when considering retinitis pigmentosa treatments, speculation might turn to the possibilities of gene therapy and stem cell research. These treatments are, as yet, still in the research and investigation phases, but may well represent the future of retinitis pigmentosa treatment.
Monday, July 26, 2010
Commencement of CABERNET clinical trial
NeoVista, Inc announced the official commencement of the CABERNET (Cnv Secondary Amd Treated with BEta RadiatioN Epiretinal Therapy) clinical trial for the treatment of subfoveal choroidal neovascularization associated with wet age-related macular degeneration (AMD). Neovascular AMD is the leading cause of irreparable blindness in the elderly population, afflicting over 200,000 individuals each year in the U.S.
Dr. Nelson Sabates, Professor and Chairman, Department of Ophthalmology, University of Missouri-Kansas City (UMKC)/Truman Medical Centers and Director of Vision Research Center, University of Missouri-Kansas City at Truman Medical Centers performed the procedure on the first patient enrolled in the CABERNET study. When asked for initial feedback on the procedure, Dr. Sabates commented, "The procedure was no different than performing a common vitrectomy and the Epi-Rad device allowed me to deliver a well focused dose of radiation to the lesion. Treating neovascular AMD using a multi-faceted approach like the use of radiation and anti-VEGF therapy may well be the next frontier in combating this sight threatening disease."
The CABERNET clinical trial will involve clinical sites in the United States, Europe, Israel, and South America. The CABERNET trial protocol is divided into two treatment arms - investigational and control.
The investigational treatment arm consists of concomitant delivery of Beta radiation, via the proprietary NeoVista technology (Epi-Rad90™), and an FDA approved anti-VEGF agent. The investigational treatment is administered during an outpatient surgical procedure and delivers Beta radiation directly to the area of the retina that has been compromised by the disease. An injection of the anti-VEGF agent is administered at the time of surgery with one additional injection administered 30 days after surgery. The control arm is utilizing the FDA approved anti-VEGF agent alone.
The surgery was performed in collaboration with, Saint Lukes Hospital in Kansas City. Dr. Terry J. Wall, J.D., M.D. of the Saint Lukes Cancer Institute was the attending radiation oncologist involved with the procedure.
"This is a very good day for NeoVista employees and the investors who are supporting our work," stated John N. Hendrick, President and CEO of NeoVista. "More importantly, it is a potential harbinger of hope for those suffering from wet AMD." We remain optimistic that our treatment approach will provide maximum benefit to this patient population."
Dr. Nelson Sabates, Professor and Chairman, Department of Ophthalmology, University of Missouri-Kansas City (UMKC)/Truman Medical Centers and Director of Vision Research Center, University of Missouri-Kansas City at Truman Medical Centers performed the procedure on the first patient enrolled in the CABERNET study. When asked for initial feedback on the procedure, Dr. Sabates commented, "The procedure was no different than performing a common vitrectomy and the Epi-Rad device allowed me to deliver a well focused dose of radiation to the lesion. Treating neovascular AMD using a multi-faceted approach like the use of radiation and anti-VEGF therapy may well be the next frontier in combating this sight threatening disease."
The CABERNET clinical trial will involve clinical sites in the United States, Europe, Israel, and South America. The CABERNET trial protocol is divided into two treatment arms - investigational and control.
The investigational treatment arm consists of concomitant delivery of Beta radiation, via the proprietary NeoVista technology (Epi-Rad90™), and an FDA approved anti-VEGF agent. The investigational treatment is administered during an outpatient surgical procedure and delivers Beta radiation directly to the area of the retina that has been compromised by the disease. An injection of the anti-VEGF agent is administered at the time of surgery with one additional injection administered 30 days after surgery. The control arm is utilizing the FDA approved anti-VEGF agent alone.
The surgery was performed in collaboration with, Saint Lukes Hospital in Kansas City. Dr. Terry J. Wall, J.D., M.D. of the Saint Lukes Cancer Institute was the attending radiation oncologist involved with the procedure.
"This is a very good day for NeoVista employees and the investors who are supporting our work," stated John N. Hendrick, President and CEO of NeoVista. "More importantly, it is a potential harbinger of hope for those suffering from wet AMD." We remain optimistic that our treatment approach will provide maximum benefit to this patient population."
Friday, July 16, 2010
Gene Therapy for Eye Diseases
The pharmaceutical giant Genzyme has started a clinical trial to see whether a drug to treat macular generation could be delivered via long-lasting gene therapy rather than monthly injections.
Eye colors: Drusen, the yellow flecks in this image of the retina, are common in people with age-related macular degeneration. These flecks are made up of proteins involved in the part of the immune system called the complement system, which has also been implicated in the disease by genetic studies.
A drug called Lucentis, made by Genetech, has proved effective at treating the wet form of age-related macular degeneration, which can lead to blindness. Some 200,000 Americans a year are diagnosed with the disease. But Lucentis has to be injected into the eye every month or two, a burden for patients and doctors.
Lucentis binds to and neutralizes a wound-healing growth factor known as VEGF. This binding action stalls the excess growth of blood vessels in the eye that characterizes age-related macular degeneration. Genzyme's gene therapy drug, officially called AAV2-sFLT01, would insinuate itself into the patient's retinal cell to produce the same VEGF-binding protein as Lucentis over far longer periods--up to several years.
A phase 1 clinical trial of Genzyme's gene therapy treatment began at the end of May. Three patients received the treatment, according to Sam Wadsworth, a Genzyme group vice president in charge of gene and cell therapy. Preliminary results should be available in about a year.
The trial is one of a handful worldwide seeking to prove the effectiveness of gene therapy for eye diseases. The Genzyme trial also involves using new type of virus as the delivery mechanism. Early results of a federally funded trial to deliver normal-functioning genes to patients with a rare retinal disease known as type 2 leber congenital amaurosis, or LCA, have confirmed that this "viral vector" has merit for eye treatments, several researchers say.
The LCA trials "demonstrated success both in terms of safety and ability to introduce the gene and have efficacy and success," said Jeffrey S. Heier, an assistant professor at Tufts University School of Medicine and director of retinal research at Ophthalmic Consultants of Boston, a private practice group, who is involved in the Genzyme research. "This study is taking the virus vector that they used, and [Genzyme has] taken what has really been the success of the anti-VEGF story and they've packaged the two together."
Eyes have been an early target for gene therapy because they are small--meaning they require relatively little active dose, they are self-contained, and because the tools of eye surgery have advanced enough to make the treatments possible. The drug has to be delivered to the retina, a thin film lining the inner wall of the eye. Instrumentation has improved in recent years to allow injections through the retina without piercing it, said Shalesh Kaushal, chairman of ophthalmology at University of Massachusetts Memorial Medical Center and UMass Medical School.
To Kaushal, who is involved in the Genzyme study as well as the LCA research, the big challenge will be broadening the use of gene therapy to dozens more diseases, and using that understanding to eventually reach beyond the eye. "If one could understand those fundamental cellular, biochemical events and identify targets, you might have the chance to treat many diseases with a single gene-therapy construct," Kaushal said.
Earlier gene therapy programs used a type of virus called adenovirus to target genes, but both the LCA and Genzyme trials are using adeno-associated virus, which is far less inflammatory and which expresses itself over longer periods than adenovirus, therefore making the treatment last longer, Wadsworth said. Viruses are used to deliver gene therapies because they are adept at getting through cell walls.
VEGF is involved in vascular cell growth throughout the body, and its expression increases in the presence of a wound. Studies have shown that with Lucentis, virtually all the VEGF-binding protein stays within the eye, and does not significantly affect VEGF levels elsewhere in the body, Wadsworth says. Genzyme's drug will provide even lower levels of the VEGF-binding protein, so it's expected that the drug will not have any adverse affects throughout the body, he said.
The trick will be getting the cells to produce enough VEGF-binding protein to help patients, said Peter Campochiaro, a professor at the Wilmer Eye Institute at Johns Hopkins Medicine, who is involved in the research. In addition to establishing safety, the current phase 1 trial will explore four different doses of the study
Eye colors: Drusen, the yellow flecks in this image of the retina, are common in people with age-related macular degeneration. These flecks are made up of proteins involved in the part of the immune system called the complement system, which has also been implicated in the disease by genetic studies.
A drug called Lucentis, made by Genetech, has proved effective at treating the wet form of age-related macular degeneration, which can lead to blindness. Some 200,000 Americans a year are diagnosed with the disease. But Lucentis has to be injected into the eye every month or two, a burden for patients and doctors.
Lucentis binds to and neutralizes a wound-healing growth factor known as VEGF. This binding action stalls the excess growth of blood vessels in the eye that characterizes age-related macular degeneration. Genzyme's gene therapy drug, officially called AAV2-sFLT01, would insinuate itself into the patient's retinal cell to produce the same VEGF-binding protein as Lucentis over far longer periods--up to several years.
A phase 1 clinical trial of Genzyme's gene therapy treatment began at the end of May. Three patients received the treatment, according to Sam Wadsworth, a Genzyme group vice president in charge of gene and cell therapy. Preliminary results should be available in about a year.
The trial is one of a handful worldwide seeking to prove the effectiveness of gene therapy for eye diseases. The Genzyme trial also involves using new type of virus as the delivery mechanism. Early results of a federally funded trial to deliver normal-functioning genes to patients with a rare retinal disease known as type 2 leber congenital amaurosis, or LCA, have confirmed that this "viral vector" has merit for eye treatments, several researchers say.
The LCA trials "demonstrated success both in terms of safety and ability to introduce the gene and have efficacy and success," said Jeffrey S. Heier, an assistant professor at Tufts University School of Medicine and director of retinal research at Ophthalmic Consultants of Boston, a private practice group, who is involved in the Genzyme research. "This study is taking the virus vector that they used, and [Genzyme has] taken what has really been the success of the anti-VEGF story and they've packaged the two together."
Eyes have been an early target for gene therapy because they are small--meaning they require relatively little active dose, they are self-contained, and because the tools of eye surgery have advanced enough to make the treatments possible. The drug has to be delivered to the retina, a thin film lining the inner wall of the eye. Instrumentation has improved in recent years to allow injections through the retina without piercing it, said Shalesh Kaushal, chairman of ophthalmology at University of Massachusetts Memorial Medical Center and UMass Medical School.
To Kaushal, who is involved in the Genzyme study as well as the LCA research, the big challenge will be broadening the use of gene therapy to dozens more diseases, and using that understanding to eventually reach beyond the eye. "If one could understand those fundamental cellular, biochemical events and identify targets, you might have the chance to treat many diseases with a single gene-therapy construct," Kaushal said.
Earlier gene therapy programs used a type of virus called adenovirus to target genes, but both the LCA and Genzyme trials are using adeno-associated virus, which is far less inflammatory and which expresses itself over longer periods than adenovirus, therefore making the treatment last longer, Wadsworth said. Viruses are used to deliver gene therapies because they are adept at getting through cell walls.
VEGF is involved in vascular cell growth throughout the body, and its expression increases in the presence of a wound. Studies have shown that with Lucentis, virtually all the VEGF-binding protein stays within the eye, and does not significantly affect VEGF levels elsewhere in the body, Wadsworth says. Genzyme's drug will provide even lower levels of the VEGF-binding protein, so it's expected that the drug will not have any adverse affects throughout the body, he said.
The trick will be getting the cells to produce enough VEGF-binding protein to help patients, said Peter Campochiaro, a professor at the Wilmer Eye Institute at Johns Hopkins Medicine, who is involved in the research. In addition to establishing safety, the current phase 1 trial will explore four different doses of the study
Wednesday, July 7, 2010
Tyrosine Kinase inhibitor shows promise for AMD treatment
A new study finds that inhibition of CXCR4 may be useful in preventing neovascularization but does not appear to have an effect on already established angiogenesis, whereas a multiple receptor tyrosine kinase inhibitor (SU14813) reduced the size of previously formed lesions.
Endothelial precursor cells (EPCs) derived from hematopoietic stem cells (HSCs) have been shown to contribute to choroidal neovascularization (CNV) by signaling through the SDF-1 and its receptor, known as CXCR4. Hematopoietic stem cells are implicated in the formation of new pathologic vessels observed in wet AMD. Recruitment of endothelial precursor cells to the site of neovascularization is mediated, in part, by the chemokine SDF-1, and its receptor, CXCR4. CXCR4 is a G-protein-coupled receptor found on lymphocytes, monocytes, hematopoietic, endothelial progenitor cells, and mature endothelial cells.
Methods and Results
CNV in rats was generated by focal rupture of Bruch's membrane with an 810-nm diode laser. In the prevention mode, a CXCR4 antagonist (AMD3100) was delivered via an osmotic pump 1 day after laser induction. In the intervention mode, AMD3100 delivery commenced 14 days after laser induction. Inhibition of CXCR4 was determined through leukocyte and SDF-1 actin polymerization blood biomarker assays. Leakage was assessed by fluorescein angiography, and CNV lesion size was quantified after isolectin B4 endothelial cell staining. SU14813, an anti-VEGFR, PDGFR-beta, KIT, and FLT3 inhibitor, was also assessed in an intervention study protocol.
Related News
CCR3 is a target for AMD diagnosis and therapy
Integrin α5β1 inhibitor JSM6427 combats CNV in animal study
Stem cells show promise to restore vision
Inhibition of CXCR4 was demonstrated by an increase in the number of blood leukocytes, and diminished SDF-1 induced actin polymerization in whole blood. CNV leakage and neovascularization were inhibited when the dose regimen was initiated 1 day after laser-induced CNV induction. AMD3100 did not show efficacy when administered 14 days after lasering. Treatment with SU14813 significantly decreased CNV leakage and lesion size in an intervention modality.
Discussion and Conclusions
In this study, CXCR4 inhibition was efficacious in the prevention of CNV, but failed to reduce choroidal leakage and angiogenesis in the intervention modality. This finding suggests that therapies targeting the SDF-1/CXCR4 axis may be beneficial in blocking the induction of ocular neoangiogenesis, but are unlikely to reduce already established angiogenesis.
There is strong evidence that CXCR4 inhibition disrupts the recruitment of endothelial precursor cells (EPCs) to sites of angiogenesis, most likely the major mechanism leading to efficacy in the prevention model.
In addition to suppressing CNV, CXCR4 inhibition reduced choroidal vascular leakage in the prevention modality (but not in the intervention modality). It is not known whether CXCR4 inhibition decreases leakage directly or as a secondary effect of the reduction of the angiogenic vessel area.
The observation that CXCR4 inhibition did not decrease choroidal leakage or angiogenic lesion size in the intervention modality suggests that after a 2-week generation of laser-induced CNV, there is limited, if any, contribution of EPC cells to the already established vessels
A multiple receptor tyrosine kinase (RTK) inhibitor may still be an effective monotherapy, as SU14813 reduced the size of previously formed lesions. In treatment mode, both leakage and angiogenesis decreased even after the pathologic effect was given 14 days to fully establish before drug intervention. This study suggests that blockade of the VEGF receptor is an effective alternative method of inhibiting the VEGF pathway compared to conventional anti-VEGF strategies.
SU14813 is a small molecule with broad target RTK selectivity, inhibiting the VEGF receptor (VEGFR), PDGFR-β, KIT, and FLT3. Although the primary mechanism that reduces preexisting angiogenesis and leakage is the blockade of the central VEGF pathway, the additional inhibition of PDGFR-β may augment efficacy in this model over single anti-VEGFR agents.
The investigators conclude that inhibition of CXCR4 may be useful in preventing neovascularization but does not appear to have an effect on already established angiogenesis. A multiple receptor tyrosine kinase inhibitor (SU14813) approach shows promise for the treatment of wet age-related macular degeneration.
Endothelial precursor cells (EPCs) derived from hematopoietic stem cells (HSCs) have been shown to contribute to choroidal neovascularization (CNV) by signaling through the SDF-1 and its receptor, known as CXCR4. Hematopoietic stem cells are implicated in the formation of new pathologic vessels observed in wet AMD. Recruitment of endothelial precursor cells to the site of neovascularization is mediated, in part, by the chemokine SDF-1, and its receptor, CXCR4. CXCR4 is a G-protein-coupled receptor found on lymphocytes, monocytes, hematopoietic, endothelial progenitor cells, and mature endothelial cells.
Methods and Results
CNV in rats was generated by focal rupture of Bruch's membrane with an 810-nm diode laser. In the prevention mode, a CXCR4 antagonist (AMD3100) was delivered via an osmotic pump 1 day after laser induction. In the intervention mode, AMD3100 delivery commenced 14 days after laser induction. Inhibition of CXCR4 was determined through leukocyte and SDF-1 actin polymerization blood biomarker assays. Leakage was assessed by fluorescein angiography, and CNV lesion size was quantified after isolectin B4 endothelial cell staining. SU14813, an anti-VEGFR, PDGFR-beta, KIT, and FLT3 inhibitor, was also assessed in an intervention study protocol.
Related News
CCR3 is a target for AMD diagnosis and therapy
Integrin α5β1 inhibitor JSM6427 combats CNV in animal study
Stem cells show promise to restore vision
Inhibition of CXCR4 was demonstrated by an increase in the number of blood leukocytes, and diminished SDF-1 induced actin polymerization in whole blood. CNV leakage and neovascularization were inhibited when the dose regimen was initiated 1 day after laser-induced CNV induction. AMD3100 did not show efficacy when administered 14 days after lasering. Treatment with SU14813 significantly decreased CNV leakage and lesion size in an intervention modality.
Discussion and Conclusions
In this study, CXCR4 inhibition was efficacious in the prevention of CNV, but failed to reduce choroidal leakage and angiogenesis in the intervention modality. This finding suggests that therapies targeting the SDF-1/CXCR4 axis may be beneficial in blocking the induction of ocular neoangiogenesis, but are unlikely to reduce already established angiogenesis.
There is strong evidence that CXCR4 inhibition disrupts the recruitment of endothelial precursor cells (EPCs) to sites of angiogenesis, most likely the major mechanism leading to efficacy in the prevention model.
In addition to suppressing CNV, CXCR4 inhibition reduced choroidal vascular leakage in the prevention modality (but not in the intervention modality). It is not known whether CXCR4 inhibition decreases leakage directly or as a secondary effect of the reduction of the angiogenic vessel area.
The observation that CXCR4 inhibition did not decrease choroidal leakage or angiogenic lesion size in the intervention modality suggests that after a 2-week generation of laser-induced CNV, there is limited, if any, contribution of EPC cells to the already established vessels
A multiple receptor tyrosine kinase (RTK) inhibitor may still be an effective monotherapy, as SU14813 reduced the size of previously formed lesions. In treatment mode, both leakage and angiogenesis decreased even after the pathologic effect was given 14 days to fully establish before drug intervention. This study suggests that blockade of the VEGF receptor is an effective alternative method of inhibiting the VEGF pathway compared to conventional anti-VEGF strategies.
SU14813 is a small molecule with broad target RTK selectivity, inhibiting the VEGF receptor (VEGFR), PDGFR-β, KIT, and FLT3. Although the primary mechanism that reduces preexisting angiogenesis and leakage is the blockade of the central VEGF pathway, the additional inhibition of PDGFR-β may augment efficacy in this model over single anti-VEGFR agents.
The investigators conclude that inhibition of CXCR4 may be useful in preventing neovascularization but does not appear to have an effect on already established angiogenesis. A multiple receptor tyrosine kinase inhibitor (SU14813) approach shows promise for the treatment of wet age-related macular degeneration.
Sunday, May 10, 2009
New Medical Study Establishes First-Ever Long-Term Benefits for Macular Degeneration Sufferers Using Macular Health Vitamin Supplement
New Medical Study Establishes First-Ever Long-Term Benefits for Macular Degeneration Sufferers Using Macular Health Vitamin Supplement
Eye disease product has the potential to preserve vision for millions
BIRMINGHAM, Ala., April 28 /PRNewswire/ -- As many as 17.8 million people will suffer from age-related macular degeneration (AMD) by 2050 and 1.57 million will be blind from the disease, according to the U.S. Centers for Disease Control and Prevention. However, a new medical study by a group of retina specialists at the Callahan Eye Foundation Hospital at the University of Alabama Birmingham (UAB) indicates that with the use of the Macular Health vitamin supplement there is a way to reduce these numbers and potentially preserve the vision of millions.
The second phase of the Multifocal Electroretinogram (MERG) study recently revealed that patients suffering from AMD experienced long-term benefits from taking Macular Health, a special combination of supplemental vitamins, minerals and carotenoids. Phase I of the MERG study, completed in 2005, confirmed an average of 16 percent improvement in vision after taking Macular Health for only 12 weeks. Phase II measured the vision function of the same patients two years later and found an average improvement in vision of 17 percent.
"The outcome of this study is extremely encouraging for sufferers of age-related macular degeneration," says John O. Mason, III, MD, researcher and retinal specialist at the Callahan Eye Foundation Hospital. "These new findings prove that Macular Health can slow vision loss and actually improve vision function over time."
MERG testing was used to gauge the vision of AMD patients before and after using the Macular Health supplement. The test results of patients taking Macular Health were compared to results of a control group that did not take the supplement. Phase II of the study was accepted by the Association for Research and Vision in Ophthalmology (ARVO) for poster presentation. Mason and a team of retina specialists will continue to monitor study participants to evaluate improvement in eye health and vision with the use of Macular Health.
Jeffery McAnnally, President of Macular Health, LLC, says, "On behalf of the Macular Health Company, I am pleased to share this additional proof of Macular Health's effectiveness. Not only is Macular Health the most affordable product of its kind on the market today, it is the easiest to take."
An estimated 9 million people currently suffer from AMD, and one-third of adults over 70 are afflicted with this incurable disease. AMD is the leading cause of blindness in Americans 50 years of age and older. AMD is a breakdown of the macula of the eye that typically occurs during the aging process. Damage of the macula increases the difficulty of seeing fine details and even faces clearly.
To learn more about age-related macular degeneration or the Macular Health vitamin supplement, visit www.macularhealth.com. To speak with John O. Mason, III, MD, please contact Julie Ward at 205.503.5955 or julie@styleadvertising.com.
Website: http://www.macularhealth.com/
Eye disease product has the potential to preserve vision for millions
BIRMINGHAM, Ala., April 28 /PRNewswire/ -- As many as 17.8 million people will suffer from age-related macular degeneration (AMD) by 2050 and 1.57 million will be blind from the disease, according to the U.S. Centers for Disease Control and Prevention. However, a new medical study by a group of retina specialists at the Callahan Eye Foundation Hospital at the University of Alabama Birmingham (UAB) indicates that with the use of the Macular Health vitamin supplement there is a way to reduce these numbers and potentially preserve the vision of millions.
The second phase of the Multifocal Electroretinogram (MERG) study recently revealed that patients suffering from AMD experienced long-term benefits from taking Macular Health, a special combination of supplemental vitamins, minerals and carotenoids. Phase I of the MERG study, completed in 2005, confirmed an average of 16 percent improvement in vision after taking Macular Health for only 12 weeks. Phase II measured the vision function of the same patients two years later and found an average improvement in vision of 17 percent.
"The outcome of this study is extremely encouraging for sufferers of age-related macular degeneration," says John O. Mason, III, MD, researcher and retinal specialist at the Callahan Eye Foundation Hospital. "These new findings prove that Macular Health can slow vision loss and actually improve vision function over time."
MERG testing was used to gauge the vision of AMD patients before and after using the Macular Health supplement. The test results of patients taking Macular Health were compared to results of a control group that did not take the supplement. Phase II of the study was accepted by the Association for Research and Vision in Ophthalmology (ARVO) for poster presentation. Mason and a team of retina specialists will continue to monitor study participants to evaluate improvement in eye health and vision with the use of Macular Health.
Jeffery McAnnally, President of Macular Health, LLC, says, "On behalf of the Macular Health Company, I am pleased to share this additional proof of Macular Health's effectiveness. Not only is Macular Health the most affordable product of its kind on the market today, it is the easiest to take."
An estimated 9 million people currently suffer from AMD, and one-third of adults over 70 are afflicted with this incurable disease. AMD is the leading cause of blindness in Americans 50 years of age and older. AMD is a breakdown of the macula of the eye that typically occurs during the aging process. Damage of the macula increases the difficulty of seeing fine details and even faces clearly.
To learn more about age-related macular degeneration or the Macular Health vitamin supplement, visit www.macularhealth.com. To speak with John O. Mason, III, MD, please contact Julie Ward at 205.503.5955 or julie@styleadvertising.com.
Website: http://www.macularhealth.com/
Sunday, May 3, 2009
Possible Cure on Horizon
It's a sight for sore eyes.
Stem cell therapy to cure blindness is being developed by British scientists, and surgeons believe it could become a simple procedure that will be available in six or seven years' time, the London Times reported.
The process involves replacing a layer of dying cells with fresh ones created from embryonic stem cells.
It targets age-related macular degeneration (AMD), one of the most common causes of blindness, which involves the loss of eye cells.
"This is a huge step forward for patients," Tom Bremridge, chief executive of the Macular Disease Society, told the Times. "We are extremely pleased that the big guns have become involved, because, once this treatment is validated, it will be made available to a huge volume of patients."
Embryonic stem cells have the ability to develop into all types of body tissue.
Their use is controversial, however, because it involves the destruction of human embryos.
Lab tests done by the British team have shown that stem cells can prevent blindness in rats, and similar elements work on pigs.
A clinical trial is expected within two years.
It will most likely be the second in the world to use embryonic stem cells on humans. The first, spinal cord injury sufferers, will start later this year in the United States.
Stem cell therapy to cure blindness is being developed by British scientists, and surgeons believe it could become a simple procedure that will be available in six or seven years' time, the London Times reported.
The process involves replacing a layer of dying cells with fresh ones created from embryonic stem cells.
It targets age-related macular degeneration (AMD), one of the most common causes of blindness, which involves the loss of eye cells.
"This is a huge step forward for patients," Tom Bremridge, chief executive of the Macular Disease Society, told the Times. "We are extremely pleased that the big guns have become involved, because, once this treatment is validated, it will be made available to a huge volume of patients."
Embryonic stem cells have the ability to develop into all types of body tissue.
Their use is controversial, however, because it involves the destruction of human embryos.
Lab tests done by the British team have shown that stem cells can prevent blindness in rats, and similar elements work on pigs.
A clinical trial is expected within two years.
It will most likely be the second in the world to use embryonic stem cells on humans. The first, spinal cord injury sufferers, will start later this year in the United States.
Subscribe to:
Posts (Atom)
