Cytokine-driven inflammatory response is associated with the hypermetabolism of AIDS patients with opportunistic infections

Background: To assess a possible role of systemic inflammation in the resti ng metabolic response in AIDS patients with active secondary infections. Me thods: Fifty-two patients with AIDS-defined criteria and concomitant active infections and 19 healthy subjects were studied. Measurements were as foll ows: body composition assessed by bioelectrical impedance; resting energy e xpenditure (REE) by 30-minute indirect calorimetry; cytokine concentrations (IL-6, IFN alpha, TNF alpha, sTNF-R1) by ELISA; C-reactive protein (CRP), erythrocyte sedimentation rate, fibrinogen, and nutritional parameters by s tandard techniques. Results: REE adjusted for fat-free mass (REEFFM) was si gnificantly increased in AIDS patients despite 39% of them not being hyperm etabolic. The patients were undernourished and were found to have increased levels of acute-phase proteins and increased concentrations of IL-6 and sT NF-R1 relative to controls. REE parameters were positively related to CRP, ESR, ferritin, IL-6, and sTNF-R1 and negatively related to albumin, prealbu min, and transferrin. CRP was an independent predictor of REEFFM in AIDS pa tients and explained 25% of its variability. Patients with severe inflammat ion (CRP greater than or equal to 37 mg/dL) were significantly hypermetabol ic with respect to patients without inflammation (CRP < 6 mg/dL) and had hi gher levels of IL-6 and sTNF-R1 and lower levels of albumin and prealbumin. Although no significant differences were observed with respect to the infe ction type, patients with tuberculosis and Pneumocystis carinii infections had higher resting metabolic and inflammatory responses, whereas patients w ith recurrent bacterial pneumonia were normometabolic and had lower levels of inflammatory markers. Conclusions: Resting hypermetabolism observed in A IDS patients with concurrent active infections is related to the presence a nd severity of systemic cytokine-driven inflammatory response, which could reflect the type of secondary infection.