Recent press releases regarding the potential adverse effects of aspirin on macular degeneration have caused patients with age-related macular degeneration (AMD) to discontinue their aspirin use without consulting their physician.1,2 There are many benefits to aspirin use, and therefore many reasons patients should continue taking the recommended aspirin dose prescribed by their primary physician or cardiologists. As with any treatment, it is important to weigh the risk/benefit ratio of aspirin use, especially in generally elderly and high-risk populations. The benefits of aspirin have long been well documented and highly recommended for the prevention and treatment of cardiovascular diseases (CVDs), such as myocardial infarction, stroke, and death. The recent retrospective epidemiological eye studies suggesting that aspirin use may exacerbate macular degeneration are based on three limited studies, while the benefits of aspirin use for macular degeneration patients have been suggested in larger studies, including Age-Related Eye Disease Study (AREDS), the Physicians Health Study (PHS), Women’s Health Study (WHS).1–4 Therefore, the data regarding the effects of aspirin on AMD are conflicting and inconclusive.
Full Paper: Macular Degeneration and Aspirin Use
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Recent practices at “stem cell clinics” in the United States have resulted in blinding complications for three patients who underwent bilateral intravitreal injection of adipose-derived stem cell injections for dry age-related macular degeneration, as recently published in the New England Journal of Medicine: patient’s vision went from 20/30 to no light perception and 20/200.
The “stem cell clinics” problem is that they provide unproven, unregulated, and costly ($50,000) treatment for a variety of disorders and raise high concern for patients.
By having studies listed on clinicaltrials.gov, “stem cell clinics” seemingly bolster their legitimacy to patients. clinicaltrials.gov website is simply a repository of clinical studies and does not judge the merits of the listed studies.
It is important to encourage patients to speak with a “trusted healthcare professional” prior to enrolling in a study. Exploring the difference between the positive stem cell research and the activities carried out at “stem cell clinics” is essential in preventing such catastrophic outcomes.
Further regulation of these “stem cell clinics” is also necessary to help prevent similar outcomes in the future.
“Implications of Stem Cell Clinics for Retina Patients and Clinical Trials” Retinal Physician, Volume 14, Issue: May 2017, page(s) 32,40: Ajay E. Kuriyan, MD, MS; Thomas Albini, MD; Harry W. Flynn, Jr., MD
“The Growing ‘Stem Cell Clinic’ Problem” American Journal of Ophthalmology, Volume 177, xix–xx: Ajay E. Kuriyan, MD, MS; Thomas Albini, MD; Harry W. Flynn, Jr., MD
Table 1. “Age-Related Macular Degeneration Clinical Trials With Oral Medications”
(Retinalphysician.com | April 2017)
Full Paper: Age-Related Macular Degeneration Clinical Trials With Oral Medications Table
Since Kelly and Wendel introduced the victrectomy technique to reattach the macular hole (MH),1 considerable advances in surgical treatment have been achieved. As a consequence, MH has now become a surgically treatable disease with standardized techniques incorporating vitrectomy, induction of posterior vitreous detachment, internal limiting membrane (ILM) peeling, and gas tamponade.2 Although there was a debate on ILM peeling in the past, ILM peeling has been established to improve surgical success rates.3–6 In addition, retinal ILM peeling has been facilitated by staining dye such as indocyanine green.7,8
The rationale for ILM peeling is that MH can occur and enlarge owing to contraction of perifoveal vitreous and cellular constituents with myofibroblastic differentiation on the surface of the ILM.2,9 Although ILM has no inherent contractile properties, it does act as a scaffold for contractile tissue to exert tangential traction on fovea. Several studies using optical coherence tomography (OCT) have reported the dynamic sealing process after MH surgery.10–13 Foveal tissue elongation and macular migration have been noted following ILM peeling after surgery for MH and diabetic macular edema.14–17 In addition, there is a significant correlation between these morphologic changes and visual function such as metamorphopsia.14
Although ILM peeling has become a widely accepted surgical technique since the introduction of MH surgery, the optimal extent of ILM peeling is not known and the anatomic and functional outcomes according to peeling extent have not been investigated. The purpose of this study was to investigate the influence of the extent of ILM peeling on anatomic and functional outcomes of MH surgery.
Full Paper: Extent of Internal Limiting Membrane Peeling and its Impact on Macular Hole Surgery Outcomes: A Randomized Trial
A 59-year-old patient with bilateral worsening diabetic macular edema received intravitreal injection of aflibercept (Eylea; Regeneron, Tarrytown, NY) to the left eye only. On 1-month follow-up, there was noted bilateral improvement of visual acuity and diabetic macular edema on spectral-domain optical coherence tomography imaging, reflecting bilateral effect of unilateral treatment with aflibercept.
Full Paper: Reduction of Diabetic Macular Edema in the Untreated Fellow Eye Following Intravitreal Injection of Aflibercept
Diabetic Macular Edema (DME) is the leading cause of visual impairment in patients with diabetic retinopathy.1 In 2010, approximately 20.6 million out of a projected 92.6 million adults with diabetic retinopathy worldwide were estimated to have concurrent DME.2 This global healthcare burden will likely continue to increase at alarming rates, as some models estimate the number of diabetics will double by the year 2030.3
With the Early Treatment Diabetic Retinopathy Study (ETDRS) in the 1980s,4 macular laser photocoagulation became the mainstay of DME management, and it remained the standard of care in the decades that followed. The advent of intravitreal pharmacotherapy agents, primarily driven by the class of vascular endothelial growth factor (VEGF) inhibitors, has since revolutionized how this condition is treated. Validated through the RISE and RIDE phase 3 clinical trials,5 ranibizumab (Lucentis; Genentech, South San Francisco, California, USA) became the first VEGF inhibitor approved by the Food & Drug Administration (FDA) for this indication in 2012.
While off-label, bevacizumab (Avastin; Genentech) has been evaluated through smaller trials, such as the BOLT study.6 Most recently, aflibercept (Eylea; Regeneron, Tarrytown, New York) gained FDA approval to treat DME in July 2014 with the VIVID and VISTA phase 3 clinical trials.7,8
While there is ample evidence supporting the safety and efficacy of the 3 anti-VEGF agents in the management of DME, a head-to-head comparison only recently became available when the Diabetic Retinopathy Clinical Research Network (DRCR) published the 1-year outcomes of its Comparative Effectiveness Study of Intravitreal Aflibercept, Bevacizumab, and Ranibizumab for DME (Protocol T).9 The results demonstrated that when baseline visual acuity (VA) loss was mild (›20/ 40), there was no clinical difference between the 3 medications. However, when the initial acuity loss was more severe (‹20/50), a greater visual benefit was derived from aflibercept.9
Since the FDA approval of aflibercept for DME, and in light of Protocol T’s findings, many retinal specialists are converting eyes from ranibizumab or bevacizumab to aflibercept with the goal of optimizing treatment outcomes, particularly in cases of refractory DME. In the current study, we evaluated the short-term functional and anatomic responses of patients with persistent DME after multiple previous anti-VEGF injections that were converted to aflibercept therapy.
Full Paper: Conversion to Aflibercept After Prior Anti-VEGF Therapy for Persistent Diabetic Macular Edema
Anti-VEGF therapies in many patients with wet age-related macular degeneration go on to develop atrophy. The speculation for causes of this are:
- Natural progression of underlying age-related macular degeneration driving the atrophy.
- Atrophy is associated with choroidal neovascularization.
- Atrophy is associated with anti-VEGF therapy independent of choroidal neovascularization.
No answers to these theories are yet available, so we should not change how we treat patients. We should, however, advise patients that treating wet age-related macular degeneration may not stop the progression of their underlying dry age-related macular degeneration.