Department of Clinical Laboratory, The Second Affiliated Hospital of Gannan Medical University, Ganzhou, People's Republic of China.
Department of Critical Care,The Eighth Affiliated Hospital of Sun Yat sen University, Shenzhen, People's Republic of China.
Int J Chron Obstruct Pulmon Dis. 2023 Mar 15;18:305-316. doi: 10.2147/COPD.S386269. eCollection 2023.
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.
在无氧代谢途径中，乳酸脱氢酶（LDH）在缺氧、炎症和细胞损伤中起着重要作用，使其成为慢性阻塞性肺疾病（COPD）进展的潜在生物标志物。我们旨在研究 LDH 水平与 COPD 患者全因死亡率之间的关系。
检查了美国国家健康和营养检查调查（NHANES）2007-2012 年期间年龄≥20 岁接受肺功能检查的参与者的数据，并获得了随访死亡率数据。根据血清 LDH 水平，将 COPD 患者分为五组（59-111、112-123、124-135、136-150 和 151-344U/L）。为了评估 LDH 水平是否与 COPD 死亡率独立相关，我们使用多变量 Cox 回归分析和光滑曲线拟合。
我们纳入了 1320 名受试者，其中 64 名患有 III 或 IV 期 COPD，541 名患有 II 期 COPD。在中位随访 9.7 年（IQR：7.8，11.2）期间，1320 名受试者中有 252 人死亡。平均 LDH 水平为 132.5U/L（标准差 [SD]，27.0）。观察到 LDH 水平与全因死亡率之间呈 U 形关系。在拐点以下和以上，即大约 110U/L，我们发现 COPD 患者 LDH 与全因死亡率之间的相关性有不同的斜率。在阈值以下，LDH 每增加 1 个标准差（1SD），全因死亡率的风险降低 68%（风险比 [HR]0.32，95%置信区间 [CI]0.13-0.81，P=0.016）；相反，在阈值以上，LDH 每增加 1SD 会加速全因死亡率的风险（HR 1.23，95%CI：1.08-1.41，P=0.002）。
使用具有全国代表性的 NHANES 数据，我们发现 COPD 患者 LDH 水平与全因死亡率之间呈 U 形关联。大约 110U/L 的最佳 LDH 水平与全因死亡率的最低风险相关。
