U-Shaped Relationship Between Serum Lactate Dehydrogenase with All-Cause Mortality in Patients with Chronic Obstructive Pulmonary Disease

• Published in: International journal of chronic obstructive pulmonary disease Vol. 18; pp. 305 - 316
• Main Authors: Huang, Lihua, Lu, Zhanpeng, Zhou, Xiaoqing, He, Liuliu, You, Xiaoyan, Chen, Chunmei, Zou, Chunsheng
• Format: Journal Article
• Language: English
• Published: New Zealand Dove Medical Press Limited 01.01.2023; Dove Medical Press Ltd; Dove; Dove Medical Press
• Subjects: Age; Analysis; Biomarkers; Blood pressure; Body mass index; Cancer; Cardiovascular disease; China; chronic obstructive; Chronic obstructive pulmonary disease; Data collection; Dehydrogenases; Development and progression; Diabetes; Ethnicity; Family income; Hispanic Americans; Humans; Hypertension; Inflammation; L-Lactate Dehydrogenase; lactate dehydrogenase; Lung diseases, Obstructive; Mortality; nonlinear; Nutrition Surveys; Original Research; Patient outcomes; pulmonary disease; Pulmonary Disease, Chronic Obstructive; Questionnaires; Regression analysis; Smoking; Spirometry; Stroke; Surveys; threshold; Variables; China; United States > US; lactate dehydrogenase; chronic obstructive; nutrition surveys; threshold; nonlinear; pulmonary disease
• ISSN: 1178-2005; 1176-9106; 1178-2005
• DOI: 10.2147/COPD.S386269

In the anaerobic metabolic pathway, lactate dehydrogenase (LDH) plays an important role in hypoxia, inflammation, and cell damage, making it a potential biomarker for the progression of chronic obstructive pulmonary disease (COPD). We aimed to examine the relationship between LDH levels and all-cause mortality in participants with COPD. Data of participants in the US National Health and Nutrition Examination Surveys (NHANES) 2007-2012 aged ≥20 years who underwent spirometry tests were examined, and follow-up mortality data were obtained. According to serum LDH levels, participants with COPD were divided into five groups (59-111, 112-123, 124-135, 136-150, and 151-344 U/L). To evaluate whether LDH levels were independently associated with COPD mortality, we used multivariate Cox regression analysis and smooth curve fitting. We included 1320 subjects, 64 with stage III or IV COPD and 541 with stage II COPD. Over a median follow-up of 9.7 years (IQR: 7.8, 11.2), 252 of the 1320 subjects died. The mean LDH level was 132.5 U/L (standard deviation [SD], 27.0). A U-shaped relationship was observed between LDH levels and all-cause mortality. Below and above the inflection point, which was approximately 110 U/L, we found different slopes for the correlation between LDH and all-cause mortality of patients with COPD. Below the threshold, per 1-standard deviation (1SD) increase in LDH resulted in a 68% reduced risk of all-cause mortality (hazard ratio [HR] 0.32, 95% confidence interval [CI] 0.13-0.81, P=0.016); conversely, above the threshold, per 1SD increase in LDH accelerated the risk of all-cause mortality (HR 1.23, 95% CI: 1.08-1.41, P= 0.002). Using the nationally representative NHANES data, we found a U-shaped association between LDH level and all-cause mortality in participants with COPD. An optimal LDH level of approximately 110 U/L was associated with the lowest risk of all-cause mortality.