Anti-vascular endothelial growth factor in the treatment of macular edema in epidemic retinitis.

PURPOSE: To study efficacy of anti-vascular endothelial growth factor (anti-VEGF) in resolution of macular edema in epidemic retinitis (ER). METHODS: In this retrospective, comparative study, patients diagnosed as ER with central macular thickness (CMT) ≥ 600 µm on SD-OCT at presentation were studied. Eyes which did not receive intravitreal anti-VEGF formed group A and eyes receiving additional anti-VEGF formed group B. Eyes receiving anti-VEGF monotherapy were studied separately. Cases with subsequent OCT scans with interval of more than 20 days and cases without OCT scan at the resolution were excluded. Treatment details, visual outcome, and days to resolution of macular edema were studied. RESULTS: Mean CMT in group A (n = 8) was 820.1 µm (range 607-1004 µm) and in Group B (n = 4) was 756.0 µm (range 603-1000 µm). Macular edema resolved in 34.8 days (range: 16-65) and 39.0 days (range: 21-45) in group A and B, respectively. Two eyes with anti-VEGF monotherapy recovered in 45 and 18 days, respectively. Mean corrected distance visual acuity (CDVA) at presentation in group A was 19.1 (range: 0-61) ETDRS letters and in group B was 14.3 (range: 0-35) ETDRS letters. Mean CDVA improved to 65.7 (range: 0-85) and 50.8 (range: 20-76) ETDRS letters in group A and B, respectively. Anti-VEGF monotherapy eyes improved from 35 and 46 ETDRS letters to 70 and 85 ETDRS letters, respectively. CONCLUSION: Additional anti-VEGF therapy has no added advantage in speed of resolution of macular edema due to ER. A randomized controlled trial with steroids sparing "anti-VEGF monotherapy" may verify our observations.

Aqueous humor tyrosinase activity is indicative of iris melanocyte toxicity.

Antibiotics such as fluoroquinolones (FQLs) are commonly used to treat ocular infections but are also known to cause dermal melanocyte toxicity. The release of dispersed pigments from the iris into the aqueous humor has been considered a possible ocular side effect of the systemic administration of FQLs such as Moxifloxacin, and this condition is known as bilateral acute iris transillumination (BAIT). Bilateral acute depigmentation of iris (BADI) is a similar condition, with iris pigment released into the aqueous, but it has not been reported as a side effect of FQL. Iris pigments are synthesized by the melanogenic enzyme tyrosinase (TYR) and can be detected but not quantified by using slit-lamp biomicroscopy. The correlation between dispersed pigments in the aqueous and the extent of melanocyte toxicity due to topical antibiotics in vivo is not well studied. Here, we aimed to study the effect of topical FQLs on iris tissue, the pigment release in the aqueous humor and the development of clinically evident iris atrophic changes. We evaluated this process by measuring the activity of TYR in the aqueous humor of 82 healthy eyes undergoing cataract surgery following topical application of FQLs such as Moxifloxacin (27 eyes, preservative-free) or Ciprofloxacin (29 eyes, with preservative) or the application of non-FQL Tobramycin (26 eyes, with preservative) as a control. In addition, the patients were questioned and examined for ocular side effects in pre- and post-operative periods. Our data showed a significantly higher mean TYR activity in the aqueous humor of Ciprofloxacin-treated eyes compared to Moxifloxacin- (preservative free, p < 0.0001) or Tobramycin-treated eyes (p < 0.0001), which indicated that few quinolones under certain conditions are toxic to the iris melanocytes. However, the reduced TYR activity in the aqueous of Moxifloxacin-treated eyes was possibly due to the presence of a higher drug concentration, which inhibits TYR activity. Consistently, immunoblotting analysis of the aqueous humor from both Ciprofloxacin- and Moxifloxacin-treated eyes showed the presence of soluble TYR enzyme, thus reflecting its toxicity to iris melanocytes and corresponding to its activity in the aqueous humor. Intriguingly, none of these patients developed any clinically appreciable ocular side effects characteristic of BAIT or BADI. Overall, our results suggest that topical antibiotics cause different levels of iris melanocyte toxicity, releasing dispersed pigments into the aqueous humor, which can be measured through TYR enzyme activity. Hence, we conclude that topical FQLs may cause subclinical toxicity to the iris melanocytes but may not be the sole cause of the development of BAIT or BADI.