A 51-year-old man who lived in Trabzon, Turkey, was admitted to the hospital because of anorexia, dizziness, nausea, vomiting, diarrhea, and weight loss. During the previous few months, he had developed dark skin pigmentation noted by his family and lumbar back pain. He had knee surgery for a torn meniscus 5 months before admission; the past medical history otherwise was negative. Examination showed low blood pressure (90/50 mm Hg), severe orthostatic hypotension, and inguinal lymphadenopathy. Laboratory studies showed high erythrocyte sedimentation rate (50 mm/h), high C-reactive protein (14.5 mg/L), low-serum sodium (121 mmol/L), high-serum potassium (7.5 mmol/L), high-serum creatinine (2.2 mg/dL), and low-serum cortisol (5 mug/dL).
The diagnosis of acute adrenal crisis was made, and the patient was started on intravenous fluid replacement and methylprednisolone. Microscopic examination of the stool showed leukocytes and erythrocytes, and ciprofloxacin was started; however, stool cultures showed no pathologic microorganisms and the diarrhea resolved within 2 days. After 2 days of intravenous steroids, the serum sodium and creatinine levels became normal. Fludrocortisone was added because of resistant hyperkalemia.
Further studies showed a low adrenocorticotropic hormone (ACTH) level (5.41 pg/mL) under treatment. Magnetic resonance imaging (MRI) of the upper abdomen showed asymmetrically enlarged adrenal glands (coronal diameter: right, 9 mm; left, 11 mm), consistent with bilateral adrenal hyperplasia (Figure 1). Possible reasons that may cause adrenal insufficiency by infiltrating adrenal glands were sought throughly. Considering tuberculosis; the patient could not produce a sputum sample, and chest radiography was normal. 
 Inguinal sonography showed multiple, enlarged (diameter, 1.5 to 2 cm), hypoechoic, nonreactive right inguinal lymph nodes with thickened cortex; excisional biopsy of an inguinal lymph node showed caseating granulomas, consistent with granulomatous lymphadenitis (Figure 2). Lumbar MRI showed loss of vertebral body height and the presence of pathologic signal in L1 and L2, consistent with compression fracture, metastasis, or infection (Figure 3); lumbar vertebral biopsy, performed by an open surgery, showed chronic, necrotic, caseating granulomas consistent with tuberculous osteomyelitis (Figure 4). Polymerase chain reaction assays of homogenates of the lymph node and vertebral specimens were negative for Mycobacterium tuberculosis. Further evaluation was negative for other chronic diseases, diabetes mellitus, human immunodeficiency virus infection, and malignancy.
The patient was treated with isoniazid, rifampicin, and pyrazinamide for 1 year, in addition to steroids (5 mg/day, fludrocortisone 0.1 mg/day). Two months after antituberculous therapy was completed, the glucocorticoid and mineralocorticoid drugs were stopped, and the patient was monitored closely as an inpatient. After 1 week of discontinuing steroid therapy, the morning serum cortisol was (7.3-9 mug/dL), and ACTH was high (874-665 pg/mL). A Synacthen stimulation test was not performed as the level of ACTH was already very high. MRI of the adrenal glands showed bilateral asymmetric adrenal hyperplasia, similar to that observed 1 year earlier. The patient was begun again prednisolone (5 mg/d) and advised to increase the dosage during stressful conditions including fever, surgery, dental extraction, strenuous exercise with sweating, during extremely hot weather, and with gastrointestinal upsets such as diarrhea.