David H. Abramson, MD

Treatment and Outcomes of Coats’ Disease with David Abramson, MD

2025 New York State Ophthalmological Society (NYSOS) Annual Meeting

, David H. Abramson, MD, an ophthalmologist at Memorial Sloan Kettering Cancer Center, presented the results of, and his findings from, a pediatric surgery on a patient with 

Coats’ disease, historically defined by telangiectatic, exudative retinal vessels with peripheral capillary dropout, remains a diagnostic and therapeutic challenge, particularly in its advanced stages. While early-stage, localized disease—limited to approximately 90 degrees of the retina—can often be managed effectively with laser photocoagulation, more extensive cases typically progress to subretinal exudation, retinal detachment, neovascular glaucoma, and loss of the eye.

Abramson noted that anti-VEGF agents, despite widespread success in other exudative retinal pathologies, have shown limited effectiveness in Coats’ disease. Successes have been rare and unpredictable. Notably, however, this case involved combination therapy with laser and anti-VEGF and resulted in a successful outcome. Abramson hypothesizes a potential link between treatment responsiveness and underlying telomere biology disorders, though this remains speculative.

“I’ve had a suspicion – but I don’t really have anything more than a suspicion – that it’s the patients who have the telomere biology disorders causing Coats’ who are the ones that actually do respond to anti-VEGF agents,” Abramson told 

Surgical management for total retinal detachment in Coats’ disease is technically straightforward but often ineffective due to the viscous nature of chronic subretinal exudate, which Abramson likens to honey. The high rate of surgical failures has led many experienced pediatric retinal surgeons to advocate for conservative management in such scenarios. Steroid use has shown anecdotal promise, but consistent replication of positive outcomes remains elusive.

Additionally, existing treatments are prone to subfoveal, submacular, and subretinal scarring, which result in profound vision impairment. Abramson notes the necessity of this damage.

“Success here is not determined as getting good vision,” Abramson said. “Success is keeping the eye and, of course, identifying what [the disease] is.”

Abramson’s genetic findings will further complicate and enrich general understanding of Coats’ disease. Though long considered a unilateral condition, widefield fluorescein angiography now reveals bilateral involvement in many cases. Moreover, genetic studies have implicated mutations in genes such as LTBP2, though many cases remain genetically unexplained. These findings support a broader systemic context, which Abramson categorized as "Coats’ plus”, characterized by multi-organ involvement—cardiac, hepatic, pulmonary, dermatologic, neurocognitive, and hematologic—including risks of malignancy and bone marrow failure.

While no gene-targeted therapies for Coat’s disease exist to date, recognizing these systemic associations enables earlier multidisciplinary interventions and more comprehensive patient care. Ultimately, Abramson underscores the importance of evolving beyond outdated clinical paradigms, integrating both modern imaging techniques and genetic diagnostics to improve outcomes and guide long-term management strategies.

Abramson, DH. Coats' Disease: A New Gene and a New Finding. Presented at the 2025 New York State Ophthalmological Society Annual Meeting. May 16, 2025. New York, NY.

Videos

Abramson discusses the potential benefits and limitations of treatment methods for Coats’ disease and further discusses the genetic component of its pathology.

Genetic Insights into Coat's Disease with David H. Abramson, MD

The featured case study involved a child initially suspected of having retinoblastoma, who was ultimately diagnosed with Coats’ disease after detailed imaging. Notably, fluorescein angiography revealed bilateral retinal vascular changes, which contradicts the generally accepted belief that Coats' disease only appears unilaterally.

"A few years ago, we began doing fluorescein angiograms of the peripheral retina, something we really hadn't done in ophthalmology until relatively recently, and in many, maybe even all of our Coats' patients, we were seeing subtle abnormalities in the fellow eye," Abramson told 

. "Now, as we've taught for years, Coats' disease is unilateral, and clinically it is. And yet, with fluorescein angiogram, the disease appears to be bilateral."

Abramson and colleagues then conducted genetic testing, measuring the length of the patient's telomeres. Prior studies have indicated that, of the genes known to influence telomere length, ≥10 are also associated with Coats' disease. Given this, the team investigated these genes to identify a potential cause of bilateral Coats' disease.

Ultimately, these tests identified a variation in the LTBP2 gene, which has previously been associated with pseudo-exfoliation, open-angle glaucoma, and Marfan syndrome. Notably, it has not thus far been associated with Coats' disease.

Abramson notes two key takeaways from this operation. First, despite the wealth of literature indicating that Coats' disease is unilateral, evidence now indicates that symptoms can manifest bilaterally. Abramson also suggests that bilateral Coats' disease may appear far more often than previously suspected, given the limited amount of fluorescein imaging conducted until recently.

Second, the general concept that one gene causes one disease is not always true, as more and more genetic tests indicate that individual genes can contribute to a variety of diseases.

"The concept that one gene can cause many diseases is something we are more and more finding is true in ophthalmology," said Abramson. "So our concept that we all had in the past, that one gene causes one disease, is true, but not nearly as often as we think."

Abramson's presented operation indicates that Coats disease can manifest bilaterally and is potentially caused by multiple independent genes.

David H. Abramson, MD

Articles