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Central serous chorioretinopathy after solid organ transplantation. 2006
OBJECTIVE To describe the demographic and clinical characteristics of central serous chorioretinopathy (CSC) after solid organ transplantation. METHODS Case series. METHODS Fifteen patients who presented to the authors with CSC after solid organ transplantation. METHODS We performed a retrospective chart review to identify patient demographics and clinical features of disease, including angiographic changes. METHODS Patterns of CSC. These patterns were compared with type of organ received, demographics, and visual outcome. RESULTS We identified 25 eyes of 7 women (46.7%) and 8 men (53.3%) that developed CSC after solid organ transplantation. Patient ages ranged from 27 to 55 years (median, 40). Seven of the 15 patients (46.7%) were Caucasian, including 3 Hispanic patients (20%). Of the 8 remaining patients (53.3%), 2 were African American (13.3%), 2 were Filipino (13.3%), and 4 were Asian (26.7%). The organs received included 13 kidneys (86.7%), 1 liver (6.7%), and 1 heart (6.7%). Systemic hypertension was reported in 14 of 15 patients (93.3%). All patients were receiving systemic immunosuppressive drugs at presentation; 14 of 15 (93.3%) were also receiving systemic corticosteroids. Visual acuity at presentation ranged from 20/20 to counting fingers. Patterns of CSC included (1) geographic or diffuse alterations in the retinal pigment epithelium (5 eyes; 2 bilateral, 1 unilateral), (2) focal CSC (6 eyes, all unilateral), (3) multifocal CSC (6 eyes; 2 bilateral, 2 unilateral), and (4) CSC with bullous retinal detachment (8 eyes, all bilateral). Follow-up, available for 21 affected eyes of 13 patients, ranged from 1 month to 6 years (median, 12 months). Compared with other solid organ transplant recipients at our institutions, renal transplant recipients (P = 0.003), as well as Hispanic and Asian patients (P = 0.05), were more prevalent in this cohort. CONCLUSIONS Central serous chorioretinopathy after solid organ transplantation varies in presentation and severity. Our observations support a role for choroidal vascular compromise in the pathogenesis of this disorder.
