Introduction:
Addison’s disease (AD), or primary adrenocortical insufficiency, was first described by Thomas Addison in patients with adrenal tuberculosis (TBC). Over the past several decades, along with the introduction of antituberculous chemotherapy, the incidence of TBC and AD have declined. The most common symptoms are non-specific and diagnosis is therefore often delayed and patients may first present with a life-threatening crisis.

Objective:
To describe clinical symptoms and signs, as well as diagnosis and treatement of Addison’s disease due to adrenal tuberculosis.

State of knowledge:
At present in developed countries, about 75-80% of cases of AD are caused by autoimmune destruction, i.e. autoimmune adrenalitis, whereas TBC is the other most common cause and accounts for 7-20% of cases; however, it still remains the main cause of Addison’s disease in the developing countries. TBC is more commonly associated with the bilateral glands than the unilateral glands. CT and MR are useful to differentiate between tuberculous Addison’s disease and the other causes of adrenal insufficiency with high specificity. The CT or MR features of adrenal TBC are bilateral mass-like enlargement, peripheral rim enhancement and calcification on CT scans.

Summary:
Although tuberculous Addison’s disease has been decreasing markedly in recent years, the possibility of adrenal insufficiency should be considered when hyponatremia is observed in patients with active tuberculosis, or in those having a past history of TBC. A combination of clinical symptoms, laboratory results, pathological findings and CT or MR features can help to establish a final diagnosis. Prompt treatement with antituberculous chemotherapy, biochemical monitoring of adrenal function, and appropriate steroid therapy are essential for the management of adrenal TBC which may even be reversible if detected in early stages.