Cytomegalovirus infection in a patient with endogenous Cushing's syndrome.

pportunistic infections are well described complications in patients with acquired immunodeficiency syndrome, hematopoietic and lymphoreticular malignancies and Cushing’s syndrome. The common infections in Cushing’s syndrome are mycobacterial, fungal, bacterial and rarely viral.1-3 However, patients with exogenous Cushing’s syndrome are more predisposed to opportunistic infections than patients with endogenous Cushing’s syndrome due to higher levels of circulating glucocorticoids and consequent immunosuppression. During the past decades, there have been several reports of opportunistic infections in endogenous Cushing’s syndrome. Graham et al3 in 1983 reported 23 cases of rare/unusual opportunistic infections in association with endogenous Cushing’s syndrome. Subsequently, many other reports described opportunistic infections in these patients. Cytomegalovirus (CMV) infection, though a common opportunistic infection in other immunocompromised states, is very rare in endogenous Cushing’s syndrome. To the best of our knowledge, only one case of CMV infection has been so far reported with endogenous Cushing’s syndrome in the form of CMV pneumonitis.4 We describe CMV colitis in a patient with endogenous Cushing’s syndrome. A 27-year-old man was admitted with history of rapid weight gain, striae, proximal muscle weakness and increasing pigmentation for the last 2 years. He had no history of exogenous steroid intake. On examination, his body mass index (BMI) was 33 Kg/m2, and had purple striae, proximal muscle weakness and pulp atrophy. His blood pressure was 190/110 mm Hg and had features of psychosis. Biochemistry showed serum sodium 135 meq/L, potassium 2.1 meq/L, blood glucose 21.8 mmol/L, serum cortisol at 8 am 880 nmol/L, at 10 pm >1200 nmol/L, and 10 pm adrenocorticotropic hormone (ACTH) 137 pg/ml. Serum cortisol levels following overnight dexamethasone challenge was 440 nmol/L while low dose challenge was 600 nmol/L and high dose challenge was 540 nmol/L. A computed tomography (CT) scan of the chest showed mediastinal lipomatosis and CT of adrenals revealed bilaterally enlarged adrenal glands. An MRI of the pituitary was non-contributory. Meta-iodo-benzyl gauanidine (MIBG) scan to look for any nueroendocrine tumor did not reveal any abnormality. He was treated with spironolactone, O Clinical Notes