• Lung · Dec 2017

    Multicenter Study Observational Study

    Asymmetric Dimethylarginine Predicts Long-Term Outcome in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

    • Alaadin Vögeli, Manuel Ottiger, Marc A Meier, Christian Steuer, Luca Bernasconi, Andreas Huber, Mirjam Christ-Crain, Christoph Henzen, Claus Hoess, Robert Thomann, Werner Zimmerli, Beat Mueller, and Philipp Schuetz.
    • University Department of Internal Medicine, Kantonsspital Aarau, Tellstrasse, Aarau, CH-5001, Switzerland.
    • Lung. 2017 Dec 1; 195 (6): 717-727.

    IntroductionIn chronic obstructive pulmonary disease (COPD), there is an activation of the L-arginine nitric oxide pathway. Pulmonary obstruction causes to elevated nitric oxide (NO) levels, which lead to higher production of the NO-inhibiting metabolites asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA).MethodsWe investigated the association of L-arginine, ADMA, and SDMA with clinical outcomes in a well-defined observational cohort of 150 patients with acute exacerbation of COPD. We measured L-arginine, ADMA, and SDMA by mass spectrometry in patients with pneumonic or non-pneumonic exacerbation of COPD included in a Swiss multicenter trial. We used Cox regression models to investigate the associations between blood marker levels and disease severity as well as all-cause mortality over a follow-up of 6.1 years.ResultsSix-year all-cause mortality was 54%. Admission levels of ADMA and SDMA (μmol L-1) were increased in 6-year non-survivors compared to survivors' median (0.60 vs. 0.46, p = 0.004; and 1.05 vs. 0.85, p = 0.012). In a multivariate Cox regression analysis, ADMA was associated with long-term mortality resulting in an age- and comorbidity-adjusted hazard ratio (HR) of 4.55 (95% confidence interval 1.02-20.43, p = 0.048). SDMA was only associated in univariate models and no association of L-arginine with outcome was found.ConclusionADMA was found to be an independent risk factor for long-term all-cause mortality in patients with acute exacerbation of COPD. Whether therapeutic modification of the L-arginine-nitric oxide pathway has the potential to improve outcome should be evaluated in future interventional trials.

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