Human immunodeficiency virus infection and the thyroid gland

Abstract

Human immunodeficiency virus (HIV) infection and the resulting acquired immunodeficiency syndrome (AIDS) may involve, directly or indirectly, virtually every endocrine organ system, including the thyroid gland (1–3). A variety of potential pathogenetic mechanisms may account for thyroid dysfunction in HIV disease. These include alterations of thyroid tissue by hemorrhagic, infectious or neoplastic processes, changes in thyroid hormone secretion or action due to HIV infection, interference with hormone secretion and binding and effects of antibodies, cytokines or other biologically active molecules (Table 1). A further cause of thyroid dysfunction in patients with HIV disease is therapy with drugs that can disturb various endocrine systems and affect thyroid gland integrity or function, as well as hepatic metabolism of thyroid hormones (4). Interpretation of thyroid function tests and thyroid status in patients with HIV infection is complicated further by the well-recognized effects that any acute or chronic illness may have on thyroid function (5). Interactions between HIV disease and the thyroid gland may cause a broad spectrum of changes ranging from subtle abnormalities in hormone secretion, transport or metabolism to rare instances of overt thyroid gland failure with profound consequences unless recognized and treated appropriately. In this article, we review the spectrum of thyroid abnormalities currently known to occur in HIV disease and discuss possible underlying pathophysiological mechanisms. In addition, we present practical guidelines to assist clinicians in the evaluation, interpretation and management of thyroid dysfunction in patients with HIV infection.