Aim: To describe the diagnostic and therapeutic management of cytomegalovirus (CMV) anterior uveitis unassociated with retinal necrosis in immunocompetent patients. Methods: Patients referred between 2001 and 2003 for management of unilateral, chronic, recurrent uveitis associated with secondary glaucoma underwent extensive investigation including laboratory tests for herpes virus infections. Specific antiviral treatment was initiated in all cases and the level of ocular inflammation was evaluated during the follow up. Results: Five patients, three men and two women, were included. Median age was 50 years old (range 30-80 years). Anterior unilateral uveitis without iris atrophy was observed in all cases. Uveitis was chronic in three cases and recurrent in two cases. Glaucoma was observed in all patients with a median intraocular pressure of 30 mm Hg (range 22-43 mm Hg). Five patients responded initially to specific anti-CMV therapy. Even though glaucoma surgery was necessary in two cases, both ocular inflammation and glaucoma were controlled in all cases. Relapses occurred in three cases after cessation of therapy, requiring prolonged maintenance therapy with valganciclovir. Conclusions: CMV infection and specific antiviral therapy should be considered in all cases of relapsing or chronic iridocyclitis and secondary glaucoma. Maintenance regimens of valganciclovir may be necessary to prevent further relapses.
BackgroundSarcoidosis, a multisystem, granulomatous disorder, sometimes manifests with a neuro-ophthalmic subtype. The latter can pose a diagnostic challenge, especially when ocular symptoms appear before systemic involvement, as the clinical picture then can be non-specific and systemic laboratory and standard imaging investigations can be negative.FindingsA 71-year-old woman presented with a 4-month history of sudden-onset visual loss in the left eye. Slit lamp examination revealed anterior chamber cells, iris, and angle neovascularization. Fundoscopy showed a pale edematous optic nerve head surrounded with intraretinal hemorrhages and yellow retinal infiltrates. The vasculature was very narrow to absent. Indeed, fluorescein angiography filling was limited to the (juxta-)papillary region. An extensive systemic work-up revealed a monoclonal gammopathy and absence of any inflammatory markers. On MRI, a mass infiltration of the intraorbital and the intracranial optic nerve was visible. Additional PET-CT scan revealed hilar lymph nodes. A transbronchial biopsy demonstrating a non-caseating granulomatous lesion led to the diagnosis of sarcoidosis and thus neurosarcoidosis. Treatment with high-dose prednisone and azathioprine was started to avoid progression and subsequent visual loss in the other eye.ConclusionsA patient with neurosarcoidosis presenting with compressive ischemic optic disc edema and neovascular glaucoma is described, increasing the diversity of clinical presentations and confirming the diagnostic challenge of neurosarcoidosis.
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