Endocrine Abstracts

Introduction: Glucocorticoids, even endogenous or exogenous, suppress the inflammatory response therefore they are the most preferred treatment options in inflammatory diseases. Persistent hypercortisolism induces lymphopenia and lymphoid tissue atrophy. Excessive endogenous hypercortisolism might mask the active inflammatory disease. Rebound immune modulation may occur after Cushing’s syndrome (CS) remission, leading to the new onset of autoimmune diseases.

Case: Here, we report a 27-year-old female patient newly diagnosed as sarcoidosis after remission of CS. Adrenal CS was treated successfully with right adrenalectomy. The patient was free of sarcoidosis during the course of CS with normal thorax imaging and without any symptoms of sarcoidosis. After complete remission of CS she started to complain of cough and was diagnosed sarcoidosis with clinical, radiological and bronchoscopic evidence.

Conclusion: Endogenous Cushing’s syndrome is caused either by excess ACTH secretion or by autonomous cortisol release from the adrenal cortex. Glucocorticoids are the main endogenous mechanism to suppress the inflammatory response genes. Exposure to persistent hypercortisolism induces lymphopenia and lymphoid tissue atrophy resulting in immunosupression. After treatment of CS rebound immunity occurs especially in patients with overt disease. In rare cases, the treatment of CS may result in unmasking or aggravation of diseases responsive to glucocorticoid medication such as thyroid, rheumatologic and allergic diseases. Excessive hypercortisolism might suppress the active inflammatory stage of sarcoidosis. However, the disease became apparent after the reduction of cortisol levels following the treatment of CS.