Chapter 28 : Endocrine and Metabolic Aspects of Tuberculosis

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Endocrine and metabolic derangements are infrequent in patients with tuberculosis, but they are important when they occur. When infection is not isolated to the adrenals, the most common extra-adrenal manifestations are pulmonary and genitourinary tuberculosis. The potential causes of tuberculosis-associated hyponatremia include adrenal insufficiency, the syndrome of inappropriate antidiuretic hormone (SIADH), and cerebral salt wasting. The degree of hyponatremia is variable in patients with tuberculosis, and most patients are asymptomatic. In the vast majority of patients, hyponatremia resolves concurrently with response to antituberculosis therapy. In one large series of patients from Hong Kong, 6% of patients with confirmed hypercalcemia had tuberculosis. The actual prevalence of hypercalcemia in patients with tuberculosis is difficult to estimate, as concurrent serum albumin levels are not always reported. The majority of the reports of hypercalcemia are for patients with pulmonary tuberculosis, perhaps reflecting the preponderance of pulmonary infection over infection at other sites. The physiological role for macrophage production of 1,25-dihydroxyvitamin D is uncertain. According to one proposed mechanism, 1,25-dihydroxyvitamin D enhances the antimycobacterial activity of the monocyte, either as a direct effect or by enhancing cellular responses to gamma interferon. Diabetes may lead to increased susceptibility to tuberculosis through several mechanisms. Diabetic patients demonstrate impaired granulocyte chemotaxis, phagocytosis, bactericidal activity, and superoxide production. The endocrine and metabolic manifestations of tuberculosis are protean. Direct involvement of endocrine glands is only one way in which tuberculosis can affect hormonal and metabolic function.

Citation: Vinnard C, Blumberg E. 2011. Endocrine and Metabolic Aspects of Tuberculosis, p 436-447. In Schlossberg D (ed), Tuberculosis and Nontuberculous Mycobacterial Infections, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817138.ch28

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