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BackgroundNutritional status, weight loss and cachexia have important prognostic implications in patients with chronic obstructive pulmonary disease (COPD). Body mass index (BMI) has been implicated in COPD risk assessment, but information is mostly limited to composite scores or to patients with stable disease. We aimed to analyse the association between BMI and mortality in acute exacerbation of COPD.MethodsThis retrospective survey included 968 patients hospitalized due to acute exacerbation of COPD at the University Clinic Golnik from February 2002 to June 2007. Vital status was ascertained with Central Population Registry, and database was censored on November 1, 2008.ResultsMedian BMI was 25.08 kg/m2 (interquartile range, 21.55–29.05 kg/m2) and 210 patients (22%) had BMI < 21 kg/m2. During median follow-up of 3.26 years (1.79–4.76 years), 430 patients (44%) died. Lowest mortality was found for BMI 25.09–29.05 kg/m2. When divided per BMI decile, mortality was lowest for BMI 25.09–26.56 kg/m2 (33%). In univariate analysis, BMI per quartile and BMI per unit increase were predictive for all-cause mortality. In an adjusted model, BMI per 1 kg/m2 unit increase was associated with 5% less chance of death (hazard ratio 0.95, 95% confidence interval 0.93–0.97).ConclusionsLow BMI < 21 kg/m2 is frequent in patients hospitalized due to acute exacerbation of COPD. Higher BMI was independently predictive of better long-term survival. A better outcome in obese patients compared to normal weight is in contrast to primary prevention data but concurs with observations of an obesity paradox in other cardiovascular diseases.

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Studies of animal models have shown that the activation of the complement system could have a role in chronic obstructive pulmonary disease (COPD) and asthma by promoting inflammation and enhancing airway hyperresponsiveness. We sought to determine whether the levels of complement factors C3a, C4a, and C5a are elevated at the site of inflammation in patients with COPD and patients with asthma. We analyzed the induced sputum of seven patients with COPD, ten patients with asthma, and twelve healthy nonsmokers. The concentrations of anaphylatoxins in the induced sputum were measured by cytometric bead array. We found significantly increased C5a/C5a desArg concentrations in supernatants of the induced sputum of patients with COPD (P = 0.007) and those with asthma (P = 0.002) compared with the control group. In patients with COPD the C5a/C5a desArg concentrations were significantly negatively correlated with lung diffusion coefficient (r = -0.71, P = 0.035). There was no significant difference in C3a/C3a desArg or C4a/C4a desArg measurements between the three groups of subjects. These in vivo results propose the involvement of complement factor C5a in the pathogenesis of COPD and asthma.

This study provided evidence in a small sample of patients on the discontinuity of drug therapy at patient discharge in a hospital in Slovenia and its implications for patient care. To ensure continuity and safety of patient care, medication reconciliation should be implemented throughout a patient's hospital stay.