A 62-year-old man was admitted to hospital for analysis of weight loss, nausea and loss of appetite without fever. His medical history included sleep apnoea, anaemia due to blood donations and a previous suspicion of ocular sarcoidosis. On examination, hyperpigmentation of the skin and a blood pressure of 87/62 mmHg were found. Blood tests revealed hyponatremia (131 mmol/l), normal potassium (4.4 mmol/l), a decrease in kidney function (eGFR MDRD 47 ml/min) and increased inflammation parameters (CRP 16 mg/l, ESR 52 mm/h) with normal leukocyte count (5x109/l) and differential. A CT scan showed bilateral enlargement of the adrenal glands (Fig. 1) and cervical, thoracic and abdominal lymphadenopathy. Cortisol levels indicated primary adrenocortical failure (basal cortisol 62 nmol/l, ACTH 72 nmol/l) and hydrocortisone and fludrocortisone were started. TB was considered the most likely cause, other considerations being lymphoma or metastases of an unknown primary tumour. It subsequently became clear that the patient had been born in Indonesia and had stayed in a TB clinic in the Netherlands at the age of eight. An attempt to obtain lymph node material by surgical exploration of the cervical region and axillary ultrasound-guided biopsy was unsuccessful. Subsequent adrenal biopsy specimens showed necrosis, infiltration of histiocytes and granulomas. Auramine staining of the first specimen revealed acid-fast bacteria, the microscopic features consistent with M. tuberculosis bacilli (Fig. 2).
PCR was inhibited, culture was negative. In the second specimen, PCR and culture were both negative and no bacilli were found. Enzyme-Linked ImmunoSpot (ELISPOT) on blood and brochoalveolar lavage fluid was positive for M. tuberculosis, while culture and PCR were negative. A working diagnosis of AD caused by adrenal TB was made and the patient was put on a course of tuberculostatic medication consisting of isoniazid, rifampicin, pyrazinamide and ethambutol. Doses of hydrocortisone and fludrocortisone were increased two- to threefold because of interaction between rifampicin and steroids. After 2 months of treatment, a CT scan showed decreased lymphadenopathy and a reduction in the size of both adrenal glands. Symptoms resolved and 1 year after presentation, the patient is still on hydrocortisone, fludrocortisone and tuberculostatics.