Response to letter: COVID-19 and macular edema—a necessary blindness?

Graefe's Archive for Clinical and Experimental Ophthalmology -     

Latanoprost and cystoid macular edema: is there a causal relation?

Published reports of the occurrence of cystoid macular edema (CME) in eyes being treated with latanoprost have led to concern regarding a possible causal relation between the two. Review of all published cases (28 eyes in 25 patients), plus another case reported here for the first time, indicates that all eyes had independent risk for development of CME, so that definitive conclusions about a causal relation cannot be established. In addition, controlled clinical trials and experimental studies with latanoprost have given no indication that latanoprost causes clinical CME. Pharmacokinetic considerations indicate that the concentration of latanoprost expected in the posterior segment of the eye is too low to have a pharmacologic effect, and latanoprost is not known to exhibit vasoactive or inflammatory properties. Nevertheless, reports of a possible association between CME and latanoprost use must be given serious consideration, and in eyes that are at risk for CME, an increased level of surveillance for its development is recommended.     

Cholesterol and age-related macular degeneration: is there a link?

PURPOSE: To examine the relation among serum cholesterol, apolipoprotein E genotype (APOE), and the risk of early and late age-related macular degeneration (AMD). DESIGN: The Rotterdam Study, a population based prospective cohort study. METHODS: Serum levels of total and high-density lipoprotein (HDL) cholesterol as well as APOE genotype were determined at baseline. Of 3,944 subjects, 400 were diagnosed with incident early and late AMD after a mean follow-up of 5.2 years. RESULTS: Serum HDL, but not total, cholesterol was associated with an increased risk of AMD (odds ratio/SD, 1.20; 95% confidence interval; 1.06-1.35). The association remained unchanged after adjustment for APOE genotype. When stratifying for APOE genotype, the association was strongest in persons with the e 4 allele; an inverse association seemed to be present for e 2 carriers. CONCLUSION: Elevated HDL but not total cholesterol is associated with an increased risk of AMD. Apolipoprotein E genotype does not explain this association but may be an effect modifier.     

Is there a correlation between structural alterations and retinal sensitivity in morphological patterns of diabetic macular edema?

Spectral domain optical coherence tomography (SDOCT) enables enhanced visualization of retinal layers and delineation of structural alterations in diabetic macular edema (DME). Microperimetry (MP) is a new technique that allows fundus-related testing of local retinal sensitivity. Combination of these two techniques would enable a structure-function correlation with insights into pathomechanism of vision loss in DME. To correlate retinal structural derangement with retinal sensitivity alterations in cases with diabetic macular edema, using SDOCT and MP. Prospective study of 34 eyes of 30 patients with DME. All patients underwent comprehensive ophthalmic examination, fluorescein angiography, microperimetry and SDOCT. Four distinct morphological patterns of DME were identified- diffuse retinal thickening (DRT), cystoid macular edema (CME), schitic retinal thickening (SRT) and neourosensory detachment (NSD) of fovea. Some retinal loci presented with a mixture of above patterns There was significant difference in retinal thickness between groups (P<0.001). Focal retinal sensitivity measurement revealed relatively preserved retinal sensitivity in areas with DRT (13.8 dB), moderately reduced sensitivity (7.9 dB) in areas with CME, and gross retinal sensitivity loss in areas with SRT (1.2 dB) and NSD (4.7 dB) (P<0.001). Analysis of regional scotoma depth demonstrated similar pattern. Retinal sensitivity showed better correlation to OCT pattern (r=-0.68, P<0.001) than retinal thickness (r=-0.44, P<0.001). Structure-function correlation allows better understanding of the pathophysiology of visual loss in different morphological types of DME. Classification of macular edema into these categories has implications on the prognosis and predictive value of treatment.     

Residual edema evaluation with ranibizumab 0.5?mg and 2.0?mg formulations for diabetic macular edema (REEF study)

Purpose

To compare the efficacy of ranibizumab 0.5-mg and 2.0-mg intravitreal injections for persistent diabetic macular edema (DME) previously treated with bevacizumab.

Methods

In all, 43 patients with residual center-involved DME following intravitreal bevacizumab were included in this 12-month prospective, nonrandomized, multicenter study. Enrolled patients received three monthly ranibizumab 0.5-mg injections. At month 3, patients with residual macular edema switched to three monthly injections of ranibizumab 2.0-mg. Assessments included monthly visual acuity and spectral-domain optical coherence tomography.

Results

Mean visual acuity improved by +6.4 letters at month 3 and +8.8 letters at month 6. Mean central subfield thickness (CST) decreased by –113 μm at month 3 and –165 μm at month 6. Before enrollment, 29/43 (67.4%) patients showed <10% CST reduction following monthly bevacizumab treatment. After three monthly ranibizumab 0.5-mg injections, 22/29 (75.9%) patients showed >10% reduction in CST, whereas 6 showed <10% reduction. Of these six, three (50%) showed >10% reduction in CST after switching to three monthly ranibizumab 2.0-mg doses. No serious adverse events were observed to month 6.

Conclusion

Ranibizumab 0.5-mg or 2.0-mg may improve visual and anatomic outcomes in patients with DME who demonstrated minimal or no response to bevacizumab therapy. Moreover, increased dosage of ranibizumab (2.0-mg) may provide additional benefit over ranibizumab 0.5-mg in some patients. However, 2.0-mg ranibizumab is not currently commercially licensed or available.     

Respuesta a antiangiogénicos en el edema macular secundario a necrosis retiniana aguda

A 55 year-old female patient with unilateral Acute Retinal Necrosis (ARN) developed macular oedema (MO) after the resolution of her necrosis. The macular oedema (MO) was managed and controlled for four years with intravitreal anti-VEGF injections. Anti-VEGF therapy could be useful for the treatment of MO secondary to ARN, the same as for treating MO resulting from panuveitis, where its efficacy has been already demonstrated.     

Interferon alfa-2a: a new treatment option for long lasting refractory cystoid macular edema in uveitis? A pilot study

PURPOSE: To perform a prospective pilot study to evaluate interferon alfa-2a (IFN alfa-2a) for the treatment of refractory cystoid macular edema (CME) in endogenous uveitis. METHODS: IFN alfa-2a was administered at an initial dose of 3 or 6 million IU (depending on body weight) per day subcutaneously. Afterwards IFN alfa-2a was tapered slowly over 6 months and finally discontinued. If CME relapsed IFN alfa-2a was reinstituted and tapered slowly again to evaluate the lowest maintenance dose to keep remission. RESULTS: A total of 15 eyes of 8 patients with refractory CME due to intermediate or posterior uveitis were included. Ineffective pretreatment consisted of systemic steroids and acetazolamide (all patients) and at least one additional immunosuppressant (6 patients). Six of 8 patients (11 eyes) responded well to IFN alfa-2a and CME resolved completely during 6 months treatment. One patient was lost to follow-up after IFN alfa-2a was stopped. In 1 patient (1 eye) even 19 months after cessation of IFN alfa-2a no recurrence of CME occurred. In 4 patients (8 eyes) IFN alfa-2a had to be reinstituted because CME relapsed. All 4 patients responded again. During a mean follow-up period of 16.4 months since restart of therapy we succeeded in all 4 patients to taper IFN alfa-2a to maintenance doses between 1.5 million IU every second and every sixth day without a recurrence of CME in any of the 8 eyes. CONCLUSION: IFN alfa-2a can be a treatment option for patients with otherwise treatment resistant uveitic CME.