Dr. Grossman’s Blog

Researchers have found that cataract surgery is not associated with an increased risk of age-related macular degeneration (AMD) progression in patients with non-neovascular AMD.

Surgeons enrolled 108 patients with nonneovascular AMD who were awaiting cataract surgery. Fluorescein angiography was performed preoperatively, and again at postoperative week 1, month 3, and month 12 visits.

After 12 months, neovascular AMD developed in only 3 of 65 eyes (4.6%) that did not have neovascular AMD at the preoperative visit or the one-week postoperative visit.  This statistic is consistent with an estimated one-year progression rate in the general AMD population.

Results of this study, published in the November issue of the Archives of Ophthalmology, state that the low incidence of neovascular AMD development between 1 week and 1 year after cataract surgery did not support the hypothesis that cataract surgery increases the risk of AMD progression.

Researchers also noted that  several eyes appeared to have disease progression on postsurgery week 1 fluorescein angiograms, suggesting that many cases of presumed progression to neovascular AMD following cataract surgery may have been present prior to cataract surgery, but not recognized owing to lens opacity.

Read other studies about macular degeneration at the Natural Eye Care site

SOURCE:  Progression of Age-Related Macular Degeneration After Cataract Surgery, Dong, et al, Arch Ophthalmol. 2009;127(11):1412-1419.

People with age-related macular degeneration (AMD) who are taking anticoagulant and antiplatelet drugs such as aspirin, warfarin, and clopidogrel run a significant risk of retinal hemorrhage.  

A study presented at the Retina Congress 2009 reviewed the records of 195 eyes in 195 patients, average age 83, of whom 96 were taking antiplatelets and anticoagulants on a daily basis.

Of the patients taking antiplatelets or anticoagulants, 63% developed retinal hemorrhage compared with 29% who were not taking these drugs.  It is estimated that 7.6 patients out of 100 would develop retinal hemorrhage each year when taking these drugs.  The risk of retinal hemorrhage was highest among patients who were using multiple drugs.

Since taking the patient off the blood-thinning agent is not an option, study authors suggest that ophthalmologists follow these patients closely.  It is recommended that information about a patient’s use of antiplatelets and anticoagulants should be noted prominently on the patients’ charts.

The 2009 Retina Congress is a combined meeting of the American Society of Retina Specialists, the Macula Society, and the Retina Society.

Source:  “The Association of Antiplatelets and Anticoagulants With Intraocular Hemorrhage in Patients With Exudative Age-Related Macular Degeneration,” http://www.asrs.org/

Researchers at Washington University School of Medicine in St. Louis have identified an intricate process that allows the human eye to adapt to darkness very quickly, as well as the process by which the eye can function in bright light.

This research will help scientists better understand human diseases that affect the retina, including age-related macular degeneration (AMD).

The retina’s main light-sensing cells are called rods and cones.   Cone cells allow us to see colors and can adapt to rapid changes in light intensity.   Cones use light-sensing molecules that bind together to make up visual pigments which are destroyed when they absorb light.  They must be rebuilt, or recycled, for the cone cells to continue sensing light. After exposure to light, key components of pigments called chromophores can leave the cells and travel to the nearby pigment epithelium near the retina. There the chromophore is restored and returned to the photoreceptor cells.

Researchers removed the pigment epithelium layer in salamander retinas, so that pigment molecules could not be recycled that way.  When they exposed retinal cells both to bright light and to darkness they found that the rods no longer worked, but the cones continued to function properly, even without the eye’s pigment epithelium.

Scientists treated mouse retinas with a chemical that destroyed Müller cells, which support and interact with rods and cones.  The retinas were then exposed to bright light, followed by darkness.   

When the function of Müller cells was blocked the retinal visual pathway could not function because cones ran out of photopigment and could not adapt to dark. When the Müller cells function properly, cones in the mouse, primate and human retinas are able to function in bright light and adapt to darkness, independently of the pigment epithelium.

Study authors believe that in the future it may be possible to manipulate this pathway in the retina to improve vision when the other pathway, involving pigment epithelium, has been interrupted by injury or disease, such as age-related macular degeneration.

SOURCE:  Wang, et al, “An alternative pathway mediates the mouse and human cone visual cycle”, Current Biology vol. 19 (19), Oct. 13, 2009.
“Researchers discover mechanism that helps humans see in bright and low light”, http://mednews.wustl.edu/news/page/normal/14856.html

Researchers from the University of Washington and the University of Florida have used gene therapy to cure two monkeys of color blindness. 

An article published online in the journal Nature discusses the potential for this type of gene therapy to treat adult vision disorders involving cone cells, including color blindness and other retinal diseases.

Color blindness is an inherited disorder caused by a single defective or absent gene.  Jay Neitz, a professor of ophthalmology at the University of Washington (U.W.) School of Medicine and senior study author and his wife Maureen Neitz, also in the U.W. ophthalmology department, have identified this particular gene and developed a working virus vector to carry a functional copy of it.

Researchers injected the gene-carrying virus into the monkeys’ eyes. In about 20 weeks the monkeys attained full color vision and have shown no harmful side effects.

Color-blindness is a common genetic disorder, affecting more than 3.5 people in the United States, including about 8% of Caucasian men, leaving them unable to distinguish between red and green hues.

The research team hopes to be able to translate the findings into clinical trials for humans. The team used human genetic material in the monkeys in the interest of expediting future research.

SOURCE:  Colour blindness corrected by gene therapy, Nature doi:10.1038/news.2009.921

Scientists have determined that glaucoma patients who have damage to both hemifields (half of the visual field) of their eye will experience more rapid progression of the disease than patients who have damage to a single hemifield.

The study, published in the September 2009 journal Archives of Ophthalmology, reviews data from 205 patients.  79 were found with an initial superior defect, 61 with an initial inferior defect, and 65 with both hemifields affected.  

Analysis showed significantly higher baseline intraocular pressure and thinner central corneal thickness in patients with initial damage to both hemifields.

The study authors concluded that initial damage to both hemifields increases the risk of glaucoma progression, and that doctors should consider more aggressive therapy for these patients.

Learn more about glaucoma, including natural ways to help prevent and care for glaucoma at the Natural Eye Care website

SOURCE:  Glaucoma With Early Visual Field Loss Affecting Both Hemifields and the Risk of Disease Progression, De Moraes, et al,  Arch Ophthalmol. 2009;127(9):1129-1134.

Researchers at the University of Wisconsin have successfully grown light-sensing retinal cells from human skin cells. 

The ability to grow retinal cells may someday be used to treat degenerative eye diseases such as macular degeneration and retinitis pigmentosa by enabling doctors to repair damage to the retina with new cells generated from the patient’s skin.

Scientists at the University of Wisconsin manipulated human skin cells to act like embryonic stem cells, which can be used to grow into any tissue in the body. 

The study, published in the journal Proceedings of the National Academy of Science, indicates that the ability to create human retinal cells helps researchers better understand how eyes develop, enabling them to better treat genetic eye conditions.

SOURCE:  Modeling early retinal development with human embryonic and induced pluripotent stem cells, Meyer, et al, Proceedings of the National Academy of Science, http://www.pnas.org/content/early/2009/08/24/0905245106.abstract

Researchers at the University of Alabama at Birmingham believe that thyroid disorders may increase the risk of glaucoma.  Their study, published in the British Journal of Ophthalmology, reviewed data from the 2002 National Health Interview Survey to quantify the association between a self-reported diagnosis of glaucoma and a self-reported history of thyroid problems.

Of the 12,376 survey participants, 4.6% reported glaucoma, and 11.9% reported a history of thyroid problems.  The prevalence of glaucoma among those who reported thyroid problems was 6.5% compared with 4.4% among those who did not report thyroid problems.  This association between glaucoma and thyroid problems remained after adjusting for differences in age, gender, race and smoking status.

The results of this study lend support to the hypothesis that thyroid disorders may increase the risk of glaucoma.   Although further research on the topic is expected, study authors suspect that hypothyroidism may diminish outflow in the eye.

Learn more about glaucoma, including prevention and treatment options at the Natural Eye Care website

SOURCE:  The association between thyroid problems and glaucoma, Cross, et al, British Journal of Ophthalmology 2008;92:1503-1505.

In this dry eye study, it shows that the GLA group showed a significant improvement in the specific symptom of ‘dryness’ at 3 and 6 months (p <0.01) as well as significant improvement in overall lens comfort at 6 months (p<0.01). Tear meniscus height was increased in the GLA group at 6 months relative to baseline (p<0.01), although all other objective signs were unchanged.

GLA (gamma-linolenic acid), an omega-6 fatty acid with anti-inflammatory properties can be found in oils derived from black currant seeds and the evening primrose plant. Several small trials testing GLA and linoleic (LA) oil in dry eye syndrome with an inflammatory component report reduced ocular surface inflammation and symptom improvement.

Related Studies:
1. Barabino, M et al. Systemic linoleic and gamma-linolenic acid therapy in dry eye syndrome with an inflammatory component. Cornea 22:97?101, 2003.
2. Aragona P, et al. Systemic omega-6 essential fatty acid treatment and PGE1 tear content in Sjogren’s syndrome patients. Invest Ophthalmol Vis Sci 46:4474?9, 2005
3. Kokke KH, et al. Oral omega-6 essential fatty acid treatment in contact lens associated dry eye. Contact Lens Anterior Eye 31:141-6, 2008.
4. Macri A, et al. Effect of linoleic acid and gamma-linolenic acid on tear production, tear clearance and on the ocular surface after photorefractive keratectomy. Graefes Arch Clin Exp Ophthalmol 241: 561-6, 2003.

For natural remedies for dry eye syndrome, go to Natural Eye Care

Oral supplementation with lutein and zeaxanthin with coantioxidants may improve vision at 36 months for those at high risk for progression to late age-related macular degeneration (AMD).

In the Carotenoids and Co-Antioxidants in Age-Related Maculopathy (CARMA) study, presented at the Association for Research in Vision and Ophthalmology (ARVO) 2009 Annual Meeting, researchers examined the effects of supplementation with serum lutein and zeaxanthin plus coantioxidants (vitamins C and E and zinc) on visual function and the progression from early to late stages of AMD.

A total of 433 participants in the United Kingdom with early AMD in at least one eye, or any level of AMD in the study eye and late-stage AMD in the fellow eye, received either carotenoids plus coantioxidants or a placebo.

Study participants were examined at 12, 18, 24, 30, and 36 months. Although no statistically significant difference was seen in best corrected distance visual acuity (BC DVA) at 12 months, at the 36 month follow-up researchers did note an improved BC DVA.

Investigative team member Usha Chakravarthy, MD, PhD, from Queens University of Belfast in Northern Ireland concluded that supplementation with lutein and zeaxanthin results in better macular function in patients with early AMD. He also noted that the eyes of people who had high serum (lutein) demonstrated a less severe early AMD change over time, and suggested that supplementation may prove beneficial in preventing progression to late AMD.

Learn about self-help for macular degeneration, including recommended diet and supplements containing lutein and zeaxanthin at the Natural Eye Care website

SOURCE: ARVO 2009: Lutein, Zeaxanthin Supplements May Result in Better Macular Function in Early AMD, Chakravarthy, et al, The Association for Research in Vision and Ophthalmology (ARVO), May 4, 2009.

Researchers at the University of North Carolina at Chapel Hill School of Medicine and the University of Kentucky have identified a new target for the diagnosis and treatment of age-related macular degeneration.

In a study published by the journal Nature, researchers demonstrate that blocking the activity of a specific protein, called CCR3, can reduce the abnormal blood vessel growth that leads to macular degeneration. Targeting this new protein may prove to be safer and more effective than the current treatment for the disease, which is directed at a protein called vascular endothelial growth factor or “VEGF.”

When researchers blocked CCR3, either with drugs or through genetic engineering, they saw a decrease in the generation of abnormal blood vessels. Drugs targeting CCR3 were significantly more effective than those targeting VEGF, which could represent a new therapy for the two-thirds of patients who do not respond to current treatment.

Study authors hope that this discovery may enable physicians to catch the disease in its earliest stages, before blood vessels have fully infiltrated and destroyed the central portion of the eye’s retina (the macula) to cause vision loss.

“It would be much better to prevent the disease in the first place,” said study co-author and principal investigator of the UNC study site, Mary Elizabeth Hartnett, M.D., a professor of ophthalmology in the UNC School of Medicine. “An exciting implication of this study was that the CCR3 protein could be detected in early abnormal blood vessel growth, giving us the opportunity to prevent structural damage to the retina and preserve vision.”

Learn more about macular degeneration at the Natural Eye Care web site

Read other studies about macular degeration

Source: Study suggests new approach to common cause of blindness, Hartnett, et al, June 14, 2009, href=”http://www.unchealthcare.org/site/newsroom/news/2009/June/hartnett?searchterm=macular+degeneration