Soluble receptors for tumor necrosis factor are markers for clinical course but not for major metabolic changes in human immunodeficiency virus infection☆

Abstract 

Tumor necrosis factor alpha (TNF) is a potential mediator of the metabolic changes in human immunodeficiency virus type 1 (HIV) infection. Soluble TNF receptor types I and II (sTNFR-I and -II) presumably reflect TNF activity. To examine the relationship between sTNFRs and host metabolism, resting energy expenditure (REE), body composition, and transferrin, albumin, triglyceride, retinol-binding protein, and sTNFR concentrations were measured in 12 asymptomatic and 18 symptomatic HIV-infected male subjects and 15 male control subjects, sTNFRs were increased in parallel with disease severity. REE was elevated approximately 8% in HIV-infected subjects (P = .005). REE correlated positively with fat free mass (FFM) and the presence of HIV infection, but not with sTNFRs. Inverse correlations existed between sTNFR-I or -II and albumin concentration (r = −.48, P = .007, and r = −.49, P = .006, respectively), between sTNFR-II and transferrin concentration (r = =.53, P = .003 and between In(sTNFR-II) and percent body fat (r = −.37, P < .05), but not between sTNFRs and triglyceride or retinol-binding protein. Thus, sTNFRs are markers for clinical course but not for major metabolic changes in HIV infection.

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