Objective: Positive associations between body mass index (BMI) and clinical outcomes have been found and are called "the obesity survival paradox." However, whether obesity has protective effects or if this paradox is because of confounding remains unclear. Herein, we analyzed the effects of weight on long-term mortality in a large cohort of patients with community-acquired pneumonia (CAP) and investigated whether the differential effects of obesity on inflammation pathways accounted for mortality differences.
Methods: For this secondary analysis, we followed prospectively for 6 y 763 CAP patients who were previously included in a multicenter trial (the ProHOSP Trial). To assess associations of BMI with mortality and with several inflammatory biomarker levels, we calculated three regression models adjusted for severity: the pneumonia severity index (PSI); fully adjusted for PSI, age, sex, metabolic factors, cardiovascular diseases, and other comorbidities; and fully adjusted including biomarker levels.
Results: Within the 763 patients studied, all-cause 6-y mortality was significantly lower in obese patients (BMI >30 kg/m2) compared with normal-weight patients (BMI 18.5-25 kg/m2), with a severity-adjusted hazard ratio of 0.641 (95% confidence interval 0.462-0.889) and robust results in fully adjusted and fully adjusted plus biomarker models. No associations of increased BMI and C-reactive protein, procalcitonin, or white blood cell count were found, but BMI > 30 kg/m2 was associated with higher proadrenomedullin levels.
Conclusions: Over a 6-y long-term follow-up, we found obesity to be associated with lower all-cause mortality in CAP patients, confirming the obesity paradox in this population. However, differences in inflammatory pathways did not explain these findings.
Keywords: Inflammation; Obesity paradox; Pneumonia.
Copyright © 2016 Elsevier Inc. All rights reserved.