Early and late phases of fluorescein angiogram showed window defects with no evidence of leakage. == Differential Diagnosis == The differential diagnosis for inflammatory choroidal neovascularization includes infectious (toxoplasmosis, tuberculosis, and Lyme disease) and inflammatory etiologies (sarcoidosis and inflammatory multifocal chorioretinopathies).1Our patient underwent extensive evaluation to define the underlying etiology. the left eye showed multiple, round, yellow lesions with ill-defined margins in the posterior pole; there was a larger one, slightly elevated, inferior to the fovea associated with a small retinal hemorrhage (Physique 1A). No vitreous cells were detected. Examination of the right vision was normal. == Physique 1. == Left eye of patient with juxtafoveal choroidal neovascularization (arrows) secondary to punctate inner choroidopathy. A, Fundus photograph. B, Fluorescein angiogram showing early phase hyperfluorescence. C, Fluorescein angiogram showing midvenous phase hyperfluorescence. D, Indocyanine green angiogram showing areas of hyperfluorescence. E, Optical coherence tomography (OCT). == Ancillary Testing == Fluorescein angiography showed well-demarcated, small, areas of early- and late-phase hyperfluorescence (Physique 1B). The larger macular lesion was hyperfluorescent, with blurred contours and markedly increased hyperfluorescence over Diethyl aminoethyl hexanoate citrate the course of the imaging consistent with a juxtafoveal choroidal neovascular membrane (Physique 1C). Indocyanine green angiography showed several areas of hypofluorescence in the right eye (Physique 1D), which corresponded to the visible subretinal lesions observed during Diethyl aminoethyl hexanoate citrate fundus examination; the juxtafoveal lesion was hyperfluorescent, which confirmed the activity of the neovascular membrane. Time-domain optical coherence tomography revealed a macular thickness of 246 m in the left eye; there was no subretinal fluid (Physique 1E). A complete work-up, including chest X-ray, serology for syphilis, immunoglobulins (IgM and IgG) forToxoplasmaandBorrelia burgdorferiand angiotensin-converting enzyme levels, was normal. == Treatment == The patient was treated with two monthly intravitreal injections of 0.05 mL/0.5 mg ranibizumab, without ocular or systemic complications. Four months after presentation, her visual acuity had improved to 1 1.0 and the metamorphopsias had resolved. Fluorescein angiography showed resolution of the choroidal neovascular lesion and complete resolution of the hemorrhage (Physique 2). Fluorescein angiography at 18 months follow-up showed no recurrence of the choroidal neovascular membrane and her vision remained stable. No systemic or ocular adverse events were noted. == Physique 2. == Fundus photographs and fluorescein angiograms of left vision before and 1, 4, and 18 months after intravitreal ranibizumab injections showing resolution of the hemorrhage and the choroidal neovascular membrane. The pretreatment fundus photograph shows a juxtafoveal choroidal neovascular membrane with multiple small chorioretinal lesions. Early and late phases of fluorescein Mouse monoclonal to SORL1 angiogram showed window defects with no evidence of leakage. == Differential Diagnosis == The differential diagnosis for inflammatory choroidal neovascularization includes infectious (toxoplasmosis, tuberculosis, and Lyme disease) and inflammatory etiologies (sarcoidosis and inflammatory multifocal chorioretinopathies).1Our patient underwent extensive evaluation to define the underlying etiology. Her work-up was unfavorable for infectious and inflammatory conditions. Inflammatory chorioretinopathies are often difficult to differentiate. Punctate inner choroidopathy (PIC), multifocal choroiditis and panuveitis (MCP), and presumed ocular histoplasmosis syndrome (POHS) are the subtypes most frequently associated with choroidal neovascularization; however, any other form of posterior uveitis, for instance, acute posterior multifocal placoid pigment epitheliopathy, birdshot Diethyl aminoethyl hexanoate citrate retinochoroidopathy, multiple evanescent white dot syndrome, Vogt-Koyanagi-Harada syndrome, and sympathetic ophthalmia, can be complicated by choroidal neovascularization.1 PIC is an idiopathic inflammatory disorder that typically occurs in young (1555 years), white, myopic women. Presenting symptoms are blurred vision and scotomas with or without flashes of light. 2The symptoms are usually unilateral, but most patients show bilateral fundus involvement.2,3PIC is characterized by multifocal choroidal lesions (yellow-white lesions of Diethyl aminoethyl hexanoate citrate the inner choroid and retinal pigment epithelium of approximately 100300 m in size), usually distributed throughout the posterior pole but sparing the peripapillary region.2,4There are no other signs of ocular inflammation elsewhere in the eye. Visual prognosis is generally good since the lesions usually evolve into atrophic scars; however, choroidal neovascularization may develop in 17% to 40% of patients, potentially threatening central vision if untreated.47 MCP is an inflammatory disease that occurs in healthy young patients in their fourth decade, predominantly in white women. MCP is characterized by the presence of multiple small, yellow-gray choroidal lesions that, as the disease becomes inactive, are replaced by well-demarcated chorioretinal scars.4Patients with MCP typically have inflammatory cells in the anterior chamber or vitreous cavity at the time of presentation.1MCP may be complicated by choroidal neovascularization in 32% to 46% of the patients.1Choroidal neovascularization can occur more frequently in inflamed areas, although it may originate from an old chorioretinal scar.4 POHS is a bilateral immune reaction to an infectious agent,Histoplasma capsulatum, that affects the choroid and retina. It usually occurs in young patients. Men and women are equally affected. POHS is usually characterized by discrete atrophic choroidal scars in the macula and midperiphery.