Hypothyroid-like regulation of the pituitary-thyroid axis in stable human immunodeficiency virus infection

Abstract

Thyroid function and regulation were studied in 14 consecutive male outpatients with asymptomatic human immunodeficiency virus (HIV) infection ( CDC II III , n = 8) or AIDS (CDC IV, n = 6) who were free of concomitant infections and hepatic dysfunction, and in eight health, age- and weight-matched male controls. Blood was sampled every 10 minutes over 24 hours for measurement of thyrotropin (TSH). Thereafter, thyroid hormones and TSH responsiveness to thyrotropin-releasing hormone (TRH) were measured. Triiodothyronine (T 3) and thyroxine (T 4) did not differ between HIV-infected patients and controls, but HIV patients had lower thyroid hormone-binding index ([THBI] HIV patients, 1.01 ± 0.02; controls, 1.11 ± 0.03; P < .02), free thyroxine (FT 4) index (94 ± 3 v 110 ± 4, P < .01), FT 4 (11.8 ± 0.4 v 14.3 ± 0.4 pmol/L, P < .01), and reverse triiodothyronine (rT 3) values (0.18 ± 0.01 v 0.26 ± 0.02 nmol/L, P < .001) and higher thyroxine-binding globulin [TBG] 20 ± 1 v 16 ± 1 mg/L, P < .02) values. Mean 24-hour TSH levels were increased in HIV patients (2.39 ± 0.33 v 1.44 ± 0.16 mU/L, P < .05), associated with increased mean TSH pulse amplitude and TSH responsiveness to TRH. No differences were observed between asymptomatic HIV-seropositive and AIDS patients. In conclusion, there is a hypothyroid-like regulation of the pituitary-thyroid axis in stable HIV infection, which differs distinctly from the euthyroid sick syndrome in non-HIV-nonthyroidal illnesses. These changes in thyroid hormones might be caused directly, as an HIV-associated impairment in thyroid function, or indirectly, as an adaptation to counteract hypermetabolism in HIV infection.