Human obesity and thinness, hyperlipidemia, hyperglycemia, and insulin resistance associated with HIV1 protease inhibitors. Prevention by alternating several antiproteases in short sequences [editorial]

Important note: Information in this article was accurate in 2000. The state of the art may have changed since the publication date.

Biomed Pharmacother. 1999 Dec;53(10):449-51. Unique Identifier : AIDSLINE MED/20128721
Mathe G

Abstract: In 1997, and mainly in 1998 and 1999, a lipodystrophic syndrome with central obesity, peripheral fat loss, hyperlipidemia, hyperglycemia and insulin-resistant-diabetes II, was described as the most frequent manifestation of toxicity of HIV1 virostatic therapy, associated with protease inhibitors (PI) in 83% of the patients who used them for 10 months. Almost similar syndromes had been published before the latter, due, for example, to graft vs host reaction, or autoimmunity against insulin receptors, or to caloric excess in the presence of androgens (the mediator being hyperinsulinemia). Carr and Cooper have presented an original pathophysiological mechanism for the PI-associated syndrome, residing in 63% homology between HIV1-protease and the 3-low-density-lipoprotein-receptor-related protein (LRP), and in 53% homology between this virus enzyme and retinoid-binding-protein type 1 (CRAB1). The treatment should be more subtle than those of common obesity and/or type II diabetes. This HIV1-protease inhibitor toxicity can be prevented by alternating several antiproteases in short sequences of the different ones.

Keywords: EDITORIAL REVIEW REVIEW, TUTORIAL JOURNAL ARTICLE Acquired Immunodeficiency Syndrome/DRUG THERAPY Diabetes Mellitus, Non-Insulin-Dependent/*CHEMICALLY INDUCED Drug Administration Schedule Human Hyperglycemia/*CHEMICALLY INDUCED Hyperlipidemia/*CHEMICALLY INDUCED HIV Infections/*DRUG THERAPY HIV Protease Inhibitors/ADMINISTRATION & DOSAGE/*ADVERSE EFFECTS *Insulin Resistance Obesity/*CHEMICALLY INDUCED Thinness/*CHEMICALLY INDUCED
000530
A0052215

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