Unique Alterations of Thyroid Hormone Indices in the Acquired Immunodeficiency Syndrome (AIDS)

Abstract

Study Objective: To determine alterations in serum thyroid hormone indices in patients with human immunodeficiency virus (HIV) infection.

Design: Prospective, single-blind study.

Setting: Large metropolitan hospital where 20% of all patients with the acquired immunodeficiency syndrome (AIDS) in Los Angeles are treated.

Patients: Twenty-six inpatients with bronchoscopy-proven Pneumocystis carinii pneumonia and AIDS. Outpatients included 10 persons seropositive for HIV, 10 with AIDS-related complex, and 10 with AIDS.

Main Results: There were 19 survivors and 7 nonsurvivors of P. carinii infection. Serum triiodothyronine (T3) values generally remained normal until hospitalization, with nonsurvivors having lower values than survivors (0.56 ± 0.1 nmol/L compared with 1.3 ± 0.1 nmol/L, P < 0.002, respectively). Reverse triiodothyronine (rT3) levels were low in persons with AIDS-related complex (0.21 ± 0.02 nmol/L, P < 0.001) and in AIDS outpatients (0.17 ±0.02 nmol/L, P < 0.001). Normalization of rT3 occurred after patients were hospitalized (0.28 ± 0.01 nmol/L). Serum thyroxinebinding globulin values rose with progression of HIV infection (seropositive, 369.7 ± 18.1 nmol/L, P < 0.005; AIDS-related complex, 419.1 ± 37.0 nmol/L, P < 0.005; AIDS, 423.3 ± 31.9 nmol/L, P < 0.005; survivors, 476.3 ± 24.6 nmol/L, P < 0.001), whereas nonsurvivors had normal values. All values are compared with normal values (T3, 2.3 ± 0.04 nmol/L; rT3, 0.28 ± 0.01 nmol/L; thyroxinebinding globulin, 288.2 ± 6.9 nmol/L).

Conclusions: Infection with HIV produces unique alterations in thyroid function. A progressive decline in rT3 and elevation in thyroxine-binding globulin accompany advancing HIV infection. The persistence of a normal T3 despite progression of HIV infection may contribute to weight loss. A low serum T3 on admission correlates with mortality.

Article and Author Information

  • From the University of Southern California School of Medicine, Los Angeles, California. For current author addresses, see end of text.

  • Grant Support: The research was supported in part by NIH grants DK11727 and DK31431 and the General Clinical Research Centers Program RR43.

  • Requests for Reprints: Jonathan S. LoPresti, MD, PhD, Department of Medicine, University of Southern California School of Medicine, 2025 Zonal Avenue, Los Angeles, CA 90033.

  • Current Author Addresses: Drs. LoPresti, Spencer, and Nicoloff: Department of Medicine, University of Southern California School of Medicine, Los Angeles, CA 90033.

    Dr. Fried: 601 E. Arrellaga Street, Santa Barbara, CA 93103.

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