PURPOSE: To describe 4 patients who were diagnosed with chronic central serous chorioretinopathy (cCSC), which appeared to be the presenting symptom of Cushing syndrome (CS). METHODS: In this retrospective review of charts, all patients received extensive ophthalmologic examination and endocrinologic analyses. RESULTS: A 56-year-old man and a 49-year-old woman were treated because of bilaterally active, therapy-resistant cCSC. The clinical sign indicative for CS leading to referral to the endocrinologist was muscle weakness in the man and plethora in the woman. In a 37-year-old woman with known diabetes mellitus and central obesity, bilateral cCSC was diagnosed before CS screening. Another 49-year-old woman was treated for unilateral cCSC for 4 years. Complaints of fatigue, muscle weakness, central adiposity, and skin atrophy led to referral and a CS diagnosis due to bilateral macronodular adrenal hyperplasia. In all patients, CS surgery resulted in complete resolution of subretinal fluid. During postsurgical follow-up, no reactivation of cCSC was observed. CONCLUSIONS: Chronic CSC can be the principal manifestation of relatively mildly symptomatic and unrecognized CS. In patients with cCSC, ophthalmologists should have a high index of suspicion for clinical signs of CS that warrant endocrinologic analysis. Cushing syndrome surgery can stop active subretinal fluid leakage in cCSC.
PURPOSE: To describe 4 patients who were diagnosed with chronic central serous chorioretinopathy (cCSC), which appeared to be the presenting symptom of Cushing syndrome (CS). METHODS: In this retrospective review of charts, all patients received extensive ophthalmologic examination and endocrinologic analyses. RESULTS: A 56-year-old man and a 49-year-old woman were treated because of bilaterally active, therapy-resistant cCSC. The clinical sign indicative for CS leading to referral to the endocrinologist was muscle weakness in the man and plethora in the woman. In a 37-year-old woman with known diabetes mellitus and central obesity, bilateral cCSC was diagnosed before CS screening. Another 49-year-old woman was treated for unilateral cCSC for 4 years. Complaints of fatigue, muscle weakness, central adiposity, and skin atrophy led to referral and a CS diagnosis due to bilateral macronodular adrenal hyperplasia. In all patients, CS surgery resulted in complete resolution of subretinal fluid. During postsurgical follow-up, no reactivation of cCSC was observed. CONCLUSIONS: Chronic CSC can be the principal manifestation of relatively mildly symptomatic and unrecognized CS. In patients with cCSC, ophthalmologists should have a high index of suspicion for clinical signs of CS that warrant endocrinologic analysis. Cushing syndrome surgery can stop active subretinal fluid leakage in cCSC.
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