Uveal Effusion After Immune Checkpoint Inhibitor Therapy.

Importance: Immune checkpoint inhibitors, including antiprogrammed cell death protein-1 (anti-PD-1) and antiprogrammed cell death ligand-1 (anti-PD-L1) monoclonal antibodies, have recently been introduced as a promising new immunotherapy for solid cancers. The adverse effects typically include inflammation of the skin, endocrine, and gastrointestinal systems. Objective: To describe 3 patients who developed uveal effusion after initiating anti-PD-1 and anti-PD-L1 monoclonal antibody therapy. Design, Setting, and Participants: This case series was conducted in a university-based ocular oncology practice. The participants were a 68-year-old African American man with metastatic adenocarcinoma of the lung and 2 white men, aged 52 years and 85 years, with metastatic cutaneous melanoma; all were taking anti-PD-1 and anti-PD-L1 monoclonal antibody therapy. Main Outcomes and Measures: Ocular findings of 3 patients. Results: We identified 3 patients who developed uveal effusion within 1 to 2 months after initiating anti-PD-1 and anti-PD-L1 monoclonal antibody therapy. Uveal effusion resolved completely in 6 to 12 weeks after discontinuation of systemic therapy in 2 patients and persisted in 1 patient who continued the therapy. Conclusions and Relevance: Uveal effusion should be considered in patients taking anti-PD-1 and/or PD-L1 monoclonal antibody therapy. Because of the role of the PD-1 pathway in the inhibition of self-reactive T cells, PD-1 inhibition might lead to inflammation because of immune-related adverse effects.

Posterior segment toxicity after gemcitabine and docetaxel chemotherapy.

PURPOSE: To report outer retinal disruption and uveal effusion after gemcitabine and docetaxel combination therapy. CASE REPORT: A 78-year-old woman presented with blurry vision after two cycles of gemcitabine and docetaxel combination chemotherapy for stage IV sarcoma. At presentation, visual acuity was finger counting and 20/25 in the right and left eyes, respectively. Slit-lamp examination and B-scan ultrasonography revealed severe uveal effusion in the right eye and choroidal folds in the left eye. Spectral domain optical coherence tomography showed disruption of photoreceptor inner segment ellipsoid band in the right eye. The patient was monitored weekly with ophthalmic examination and B-scan ultrasonography, while continuing with gemcitabine monotherapy. At 8 weeks follow-up, uveal effusion improved considerably and visual acuity was 20/40 and 20/20 in the right and left eyes, respectively. CONCLUSIONS: Uveal effusion and outer retinal disruption were reported after gemcitabine and docetaxel chemotherapy. Early detection and close ophthalmic monitoring may allow concurrent cancer treatment and prevention of possible chemotherapy-induced ocular side effects.

Uveal effusion induced by topical travoprost in a patient with Sturge-Weber-Krabbe syndrome.

PURPOSE: To report a case of uveal effusion with subtotal exudative retinal detachment induced by topical administration of travoprost. CASE REPORT: A 20-year-old woman with a medical history of right-sided Sturge-Weber-Krabbe syndrome and bilateral aphakia secondary to congenital cataract extraction was referred to our department for retinal detachment associated with uveal effusion of the right eye. The ocular manifestations of Sturge-Weber-Krabbe syndrome in her right eye were glaucoma and diffuse choroidal hemangioma. Antiglaucomatous medications using topical travoprost 0.004%/timolol 0.5% (fixed combination) had been begun 1 week before. An adverse effect of travoprost was suspected and the drug was discontinued. Three weeks later, a fundus examination showed total disappearance of the uveal effusion. CONCLUSIONS: Interaction of the effects of topical prostaglandin analogs (blood-aqueous barrier disruption, enhancement of uveoscleral outflow) with both the diffuse choroidal hemangioma and the elevated episcleral venous pressure may lead to uveal effusion in Sturge-Weber-Krabbe syndrome. In spite of their efficiency, prostaglandin F2 analogs (latanoprost, travoprost and bimatoprost) should be used with caution in Sturge-Weber-Krabbe syndrome and particularly in cases of proved diffuse choroidal hemangioma.

Drug-induced transient myopia and angle-closure glaucoma associated with supraciliary choroidal effusion.

PURPOSE: We investigated the mechanism of drug-induced transient myopia, anterior chamber shallowing, and secondary angle-closure glaucoma in a young woman. METHODS: Ultrasound biomicroscopy was performed and the effects of cycloplegic eyedrops and unilateral laser iridotomy were evaluated. RESULTS: Cycloplegic eyedrops and unilateral laser iridotomy had no effect. Ultrasound biomicroscopy identified the presence of a supraciliary choroidal effusion that caused forward displacement of the lens-iris diaphragm, resulting in increased myopia, anterior chamber shallowing, and angle-closure glaucoma. Discontinuance of trimethoprim and sulfamethoxazole combination led to the complete resolution of the condition. CONCLUSIONS: Idiosyncratic drug reactions may produce a supraciliary choroidal effusion, resulting in myopia and secondary angle-closure glaucoma from the induced forward shift in the position of the crystalline lens and ciliary body.

Six cases of central serous choroidopathy induced by systemic corticosteroid therapy.

We report 6 cases of central serous choroidopathy (including pigment epithelial detachment in one case) which appeared in the course of systemic corticosteroid administration conducted to cure concurrent general diseases, and in one patient with a steroid-releasing pituitary adenoma. The majority of cases arose within about one month following the administration of more than 200 mg of prednisolon. It is postulated that corticosteroids operate as a kind of stress intervening in the hypophysis-adrenal system, leading eventually to the development of central serous choroidopathy.

Histopathological and laboratory assessment of visual dysfunction.

The currently available methods of assessing ocular toxicity are discussed. Manifestations of ocular toxicity are best described clinically; histopathological examination of the eye is beset with problems of preparing the eye for morphological examinations. Electron microscopy is essential to look for chemically induced side effects at the cellular level. Mechanisms of ocular toxicity are poorly understood, and the limitation of animal studies in predicting side effects in man must be appreciated.

Experimental ciliochoroidal detachment. Effect on intraocular pressure and aqueous humor flow.

Ciliochoroidal detachments were produced in rhesus monkeys by injecting glutathione bicarbonate Ringer's solution, autologous serum, or silicone oil into the anterior suprachoroidal space. Silicone oil detachments, like sham operations, caused a transient 2 mm Hg reduction in intraocular pressure. Detachments with glutathione bicarbonate Ringer's solution or serum caused a 6 mm Hg reduction in intraocular pressure, which normalized in three weeks. Aqueous humor flow in serum-detached eyes was normal, indicating that the hypotonia does not result from reduced aqueous humor formation. Blood was present in Schlemm's canal in most eyes with hypotonia, which suggests that hypotonia is not the result of enhanced conventional aqueous humor outflow. Therefore, it is postulated that hypotonia might result from enhanced aqueous humor outflow from the anterior chamber into the suprachoroidal space and out of the eye through the emissarial channels of the sclera (uveoscleral outflow).

[Plexiglas (PMMA) in the anterior chamber. An experimental study on biological compatibility]. / Plexiglas (PMMA) in der Vorderkammer. Eine experimentelle studie zur biologischen Verträglichkeit

For six months the anterior chambers of rabbits were examined at regular intervals with the slit-lamp photograph. The reactions of iris, aqueous, and cornea were observed after implanting one PMMA-disc (0.25 mm thickness and 1.5 mm diameter) through a lancet incision. At the place where the disc touched the iris one could see during the half year period hyperaemia iridis, ciliary injection, atrophia iridis, and foreign-substance-granuloma of the iris with partial adhesion of the iris wrinkles. The cause for these reactions is a toxin in the PMMA. Mechanical irritation and plastic alteration could be excluded by the experimental method.

Miotic drugs: a review of ocular, visual, and systemic complications.

Cholinergic drugs and anticholinesterases have caused ocular complications including cataracts, iris cysts, retinal detachment, iritis, increased intraocular tension, allergic and toxic reactions, and hypermia. The visual complications include accommodative spasm; myopia and reduced visual acuity; changes in vision sensitivity, dark adaptation, and visual fields; and discomfort. The systemic complications are those common to cholinergic drugs and anticholinesterases. This review is intended as a ready reference to the drugs that cause such effects and source material.