Non-prescription cold and flu medication-induced transient myopia with uveal effusion: case report.

BACKGROUND: To report a case of non-prescription cold and flu medication-induced transient myopia with uveal effusion. CASE PRESENTATION: Bilateral high intraocular pressure, shallow anterior chambers, uveal effusion, and a myopic shift were encountered in a 39-year-old Chinese male 1 night after taking a non-prescription flu medicine three times than the recommended dose. Ultrasound biomicroscopy (UBM) showed bilateral ciliochoroidal effusions, disappearance of the ciliary sulcus, closure of the angle of the anterior chamber, and anterior displacement of the lens-iris diaphragm. Treatment with aqueous suppressants was given. Within a week, the uncorrected vision restored, and the myopia had disappeared. UBM revealed major resolution of the ciliochoroidal effusions in both eyes, deepening of the anterior chamber, return of the lens-iris diaphragm to a more posterior position. CONCLUSIONS: Overdose of non-prescription cold and flu medication may cause bilateral uveal effusions inducing acute angle-closure glaucoma and acute myopia.

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.

Efusión uveal inducido por escitalopram / Uveal effusion induced by escitalopram

CASO CLÍNICO: Mujer de 73 años en tratamiento con escitalopram que presentó glaucoma agudo de ángulo cerrado secundario a efusión uveal tras duplicar la dosis de dicho fármaco 3 días antes. Evolucionó favorablemente tras la suspensión del antidepresivo además de tratamiento hipotensor tópico y prednisona vía oral. DISCUSIÓN: La efusión uveal secundaria a fármacos es un síndrome infrecuente. Se puede acompañar de miopización y glaucoma agudo por cierre angular. El diagnóstico correcto y la suspensión del fármaco conducen a la resolución de esta nosología

CASE REPORT: A 73 year-old woman with depression treated with escitalopram developed acute secondary angle closure glaucoma related to uveal effusion after duplicating the drug dose 3 days before. She evolved favorably once the antidepressant treatment was suspended and a new treatment with topical hypotensive therapy and oral prednisone was used. DISCUSSION: The uveal effusion syndrome associated to medicines is rare; it may be associated with acute myopic shift and acute angle closure glaucoma. The correct diagnosis and discontinuation of the drug lead to the resolution of this nosology

[Uveal effusion induced by escitalopram]. / Efusión uveal inducido por escitalopram.

CASE REPORT: A 73 year-old woman with depression treated with escitalopram developed acute secondary angle closure glaucoma related to uveal effusion after duplicating the drug dose 3 days before. She evolved favorably once the antidepressant treatment was suspended and a new treatment with topical hypotensive therapy and oral prednisone was used. DISCUSSION: The uveal effusion syndrome associated to medicines is rare; it may be associated with acute myopic shift and acute angle closure glaucoma. The correct diagnosis and discontinuation of the drug lead to the resolution of this nosology.

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 as a mechanism of bilateral angle-closure glaucoma induced by chlorthalidone.

PURPOSE: To report a novel case of acute bilateral uveal effusions, angle closure, and acute myopia induced by administration of chlorthalidone. METHODS: Case report. RESULTS: Bilateral shallow anterior chambers, high intraocular pressure, and a myopic shift were encountered in a patient 1 week after initiation of chlorthalidone. Ultrasound evaluation revealed bilateral ciliochoroidal effusions, appositional angle closure, and suspected ciliary body edema. Cessation of chlorthalidone, in addition to administration of cycloplegics and ocular antihypertensives, resulted in prompt resolution of this idiosyncratic reaction. CONCLUSIONS: The antihypertensive medication chlorthalidone may cause bilateral uveal effusions inducing acute angle-closure glaucoma and acute myopia.

Indapamide-induced transient myopia with supraciliary effusion: case report.

BACKGROUND: Ingestion of sulphonamide-derived drugs has been reported to possibly have ocular side-effects. Authors aimed to present a rare case of indapamide-induced transient myopia with ciliary body edema and supraciliary effusion. CASE PRESENTATION: A 39 years old caucasian female patient presented at the Department of Neurology with headache and sudden bilateral loss of distant vision. Neurological assessment and cranial CT scans were unremarkable. For her hypertension, twice a day bisoprolol 2.5 mg and once a day indapamide 1.5 mg tablets were prescribed several days before. At her presenting, ophthalmic findings were as follows: visual acuity 0.08-7.25Dsph = 1.0 and 0.06-7.25Dsph = 1.0; IOP 25 mmHg and 24 mmHg, anterior chamber depth (ACD) 2.32 mm and 2.49 mm, lens thickness (L) 4.02 mm and 4.09 mm in the right and the left eye, respectively. By means of ultrasound biomicroscopy (UBM), thickened (720 / 700 micron) and detached ciliary body, its forward movement (ciliary body-cornea angle 108' / 114') and forward rotated ciliary processes were seen. Angle opening distance (AOD500) were 300 / 314 microns. By the following days, the myopia gradually diminished, and a week after her first symptoms, her uncorrected visual acuity was 1.0 in both eyes, IOP 13 mmHg and 17 mmHg, ACD 3.68 mm and 3.66 mm, L 3.78 mm and 3.81 mm in the right and the left eye, respectively. Ciliary body edema and detachment disappeared (ciliary body thickness 225 / 230 micron), both of the ciliary body-cornea angle 134' / 140' and the AOD500 (650 / 640 microns) increased. At this point, the patient admitted that she had stopped taking indapamide two days before. CONCLUSIONS: Our case report is the third one in the literature to present indapamide-induced transient myopia, and the first to employ UBM for describing the characteristics of this rare condition. According to the findings, authors suggest that both ciliary muscle contraction and ciliary body edema may play role in the pathomechanism. UBM seems to be a useful tool in the differential diagnosis of acute myopia. Further, authors wish to draw attention to one of the potential adverse effects of this drug which was not listed by its package insert.

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.

Escitalopram-induced uveal effusions and bilateral angle closure glaucoma.

PURPOSE: To report the onset of bilateral angle closure glaucoma resulting from ciliochoroidal effusions noted after taking escitalopram. DESIGN: Case report. METHODS: A 41-year-old woman with a medical history of depression was placed on escitalopram and presented with acute bilateral angle closure glaucoma. A medical history and ophthalmic examination (including slit-lamp photography and high-frequency ultrasonography) were performed at the time of diagnosis and at resolution of her symptoms. RESULTS: High-frequency ultrasonography revealed bilateral choroidal effusions with ciliary body detachments and angle closure. Attempts to reduce intraocular pressure with topical ocular antihypertensive drugs and subsequent laser peripheral iridotomy were unsuccessful. Over the course of four days, the use of topical cycloplegics, corticosteroids, and discontinuation of escitalopram resulted in normalization of intraocular pressures, deepening of anterior chamber depths, and resolution of her uveal effusions. CONCLUSIONS: The use of escitalopram resulted in uveal effusions, angle rotation, and acute bilateral angle closure glaucoma. Discontinuation of escitalopram and corticosteroid therapy resulted in normalization of the patient's eyes.