Treatment of Secondary Full-Thickness Macular Holes with Topical Therapy.

PURPOSE: To report the outcomes of secondary full-thickness macular holes (FTMHs) treated with topical therapy. DESIGN: Retrospective case series. PARTICIPANTS: Patients with secondary FTHMs initially treated with topical therapy in a referral-based retina practice. METHODS: Patients evaluated between April 14, 2016, and February 22, 2019, for secondary FTMHs who underwent topical therapy were included. Patient demographics, ocular history, type of drops used, duration of therapy, and duration of follow-up as well as anatomic features on OCT, including hole diameter and presence of vitreomacular traction, epiretinal membrane (ERM), and cystoid macular edema (CME), were analyzed. MAIN OUTCOME MEASURES: Closure rate of FTMHs and change in visual acuity. RESULTS: A total of 123 FTMHs were seen during the study, of which 12 were secondary macular holes. Topical therapy was attempted in 9 eyes (8 patients). Six of these 9 FTMHs were associated with prior retinal detachment (RD). Previous pars plana vitrectomy (PPV) had been performed in 3 eyes (1 for RD, 2 for ERM). One eye had vitreomacular traction and a remote history of blunt trauma. Average initial hole diameter was 79.6 µm (range, 44-132 µm). Average follow-up was 53 weeks (range, 5-153 weeks). All FTMHs had some element of ERM and CME. All patients received difluprednate with the addition of a topical carbonic anhydrase inhibitor in 6 eyes and nonsteroidal anti-inflammatory drug (NSAID) drops in 2 eyes. Eight eyes (89%) achieved successful hole closure and resolution of CME with concurrent improvement in visual acuity after an average of 6 weeks of therapy (range, 2-19 weeks). Average vision among all 9 eyes improved from 0.69 to 0.37 logarithm of the minimum angle of resolution (Snellen equivalent from approximately 20/100 to approximately 20/50). No episodes of corneal melts or ulcers occurred. One patient showed mild keratopathy and elevation of intraocular pressure with topical NSAID and steroid therapy that resolved when the topical NSAID was stopped and difluprednate was tapered down to once weekly. CONCLUSIONS: Topical therapy achieved high closure rates in secondary FTMH and can be considered as an initial treatment option especially in those with small holes and CME.

Prevalence of Hepatocyte Growth Factor and Autoantibodies to α-HGF as a New Etiology for Bilateral Diffuse Uveal Melanocytic Proliferation Masquerading as Neovascular Age-Related Macular Degeneration.

OBJECTIVE: The goal was to test the hypothesis that high serum hepatocyte growth factor (HGF) and retinal autoantibodies against α-HGF contribute to the pathology of bilateral diffuse melanocytic proliferation (BDUMP). METHODS: Case report of an elderly diagnosed with neovascular age-related macular degeneration (n-AMD) treated with bilateral Bevacizumab injections. Examination included comprehensive ophthalmic examination and images obtained by fundus photography, fundus autofluorescence, fluorescein angiography, spectral-domain optical coherence tomography (OCT), and B-scan ultrasonography. The levels of HGF and circulating HGF receptor (c-MET) were measured in the serum by ELISA and anti-retinal autoantibodies by western blotting. RESULTS: Patient received Bevacizumab injections for presumed n-AMD and had a history of papillary renal cell carcinoma stage 4 with a tumor containing gene mutation Y1230C in the mesenchymal-epithelial transition factor (MET). Visual acuity was 20/200 OD and CF OS. Multimodal imaging was consistent with BDUMP. Plasma exchange therapy was recommended but could not be started until 10 months later due to deterioration in his medical condition. Pre- and post-plasma exchange sera demonstrated anti-retinal autoantibodies against 69-kDa protein of the same molecular weight as the α-HGF. Serum autoantibodies reacted with purified recombinant α-HGF on the blot. CONCLUSIONS: BDUMP can mimic n-AMD, which can delay treatment. Plasma exchange resulted in resolved inflammation, resolution of exudative detachments and improved vision after cataract surgery. Consideration of the tumor genetics led to the recognition of elevated HGF levels and autoantibodies to α-HGF (anti-69-kDa), which suggested a new pathogenic mechanism of BDUMP. We believe that therapy with tyrosine kinase inhibitors and a checkpoint inhibitor may contribute to the high HGF levels and subsequent immune response.

Diagnosis of limited ophthalmic Wegener granulomatosis: distinctive pathologic features with ANCA test confirmation.

PURPOSE: To describe the clinical and histopathologic finding of very limited ophthalmic Wegener granulomatosis (WG). METHODS: Thirteen patients with scleritis, orbitopathy, episcleritis, and panuveitis were studied. They presented without evidence of lung or kidney disease, though eight had sinus involvement. We reviewed the biopsies for histopathologic findings consistent with WG, and tested for antineutrophil cytoplasmic antibodies antineutrophil cytoplasmic antibody (ANCA). RESULTS: WG was suggested by granulomatous foci, collagen necrosis, neutrophils/nuclear dust, plasma cells and infiltrating eosinophils. Granular degeneration of the interstitial collagen; mummification of the collagen with disappearance of fibroblastic nuclei; and a polymorphous infiltrate exhibiting plasma cells, lymphocytes, neutrophils, and eosinophils within the epithelioid granulomas should suggest the diagnosis. ANCA test results supported the diagnosis of WG in all cases. CONCLUSION: The described histologic characteristics are highly suggestive of WG. These findings along with clinical or laboratory findings, allow the diagnosis of very limited ophthalmic WG in the absence of systemic involvement.