Serum lactate dehydrogenase and its isoenzymes as predictors of clinical outcomes in acute exacerbation of chronic obstructive pulmonary disease: a retrospective analysis of a hospitalized cohort.

We aimed to test the association between serum lactate dehydrogenase (LDH) and its isoenzymes and treatment outcomes during hospitalization for acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Thirty-eight AECOPD patients were recruited from a tertiary hospital from December 2017 to June 2018. Serum LDH and LDH isoenzymes were measured on venous blood collected at admission. Treatment outcomes included duration of hospital stay, initiation of non-invasive (NIV) or mechanical ventilation, initiation of antipseudomonal antibiotics, change in empirical antibiotic treatment, need for intravenous corticosteroids or methylxanthines, and percentage of change in C-reactive protein from admission to the third day. Multivariate linear and binary logistic regression analyses were used to test the study's objectives. We found that, after adjusting for age, gender, comorbidities, COPD severity, level of hypoxemia, and inflammation markers, each 10 U/L increase in serum LDH was associated with prolongation of the hospital stay by 0.25 (0.03, 0.46) days, 42% higher odds (odds ratio [OR] 1.42 [1.00, 2.03]) for need of NIV, and 25% higher odds (OR 1.25 [1.04, 1.49]) for initiation of antipseudomonal treatment. LDH1 and LDH2 were the LDH isoenzymes that mainly drove these relationships. LDH release in the context of an AECOPD could originate from lung, muscle, or heart tissue damage due to airway inflammation, respiratory muscle recruitment, and myocardial stress. Myocardial injury and aerobic adaptation in respiratory muscles may explain the predominance of LDH1 and LDH2 isoenzymes in these associations.