Endocrine and metabolic disturbances in human immunodeficiency virus infection and the acquired immune deficiency syndrome.

Abstract

Numerous alterations in endocrine function are observed in HIV infection. Direct destruction of endocrine organs by HIV itself or by invasive infection with opportunistic organisms resulting in loss of function is rare. When acutely ill, HIV patients can develop the metabolic derangements that accompany any severe systemic disorder. Studies of thyroid function tests emphasize that the presence of acute secondary infection must be analyzed when evaluating such patients. In addition to euthyroid sick syndrome other hormonal axes are affected by severe illness. These alterations may be cytokine mediated. As with seronegative patients, these changes can be transient and resolve with successful treatment of the intervening illness. Given the complexity of HIV disease, future reports should characterize patients by CD4 cell count, history of AIDS-indicating illnesses, and viral load. Viral burden is an independent predictor of immunosuppression and progression to AIDS. A large number of medications used in the treatment of HIV infection and related illnesses can alter endocrine function, mineral and electrolyte balance, and substrate turnover. Drug therapy must be considered in the evaluation of endocrine abnormalities in HIV-infected patients and carefully characterized in studies of these patients. The endocrine effects of medications used in the treatment of HIV infection are summarized in Table 3. Concomitant factors that affect endocrine function independent of the HIV virus can confound results in these patients. For example, opiate use affects PRL, gonadotropins, and cortisol response to ACTH stimulation. Investigations in HIV-infected patients must include careful descriptions of the study population and comparison to relevant controls. HIV-infected patients may also demonstrate more subtle alterations in endocrinological function in early, relatively asymptomatic, stages. The etiology and clinical significance of these changes, particularly their relationship to cytokines, continues to be investigated. The sequential studies of stable aldosterone levels despite decreased aldosterone response to ACTH stimulation indicate that alterations in response to provocative testing do not predict the development of hormonal insufficiency in this patient population. Similar longitudinal studies need to be done for the other hormonal axes to further delineate the endocrinological alterations in HIV infection. Finally, when the rationale for hormone replacement is debatable, double-blind, placebo-controlled studies are necessary. Transient improvement in clinical status during open-label treatment does not prove hormone insufficiency. The long-term efficacy and safety of hormonal therapy must be demonstrated.