P3 Imbalance of endogenous hydrogen sulfide and homocysteine pathway in chronic obstructive pulmonary disease combined with cardiovascular disease

Abstract

Background Chronic obstructive pulmonary disease (COPD) is a multi-system disease. The pathogenesis of COPD combined with cardiovascular disease (CVD) is not fully identified. Endogenous hydrogen sulfide (H2S) is a third gaseous transmitter playing an important role in the pathophysiology of COPD. Homocysteine (Hcy) is an important substrate for the endogenous H2S production. Studies showed that hyperhomocysteinemia is a risk factor in the pathogenesis of CVD. The present study is to explore the imbalance of endogenous H2S and Hcy metabolic pathway in patients with COPD combined with CVD. Methods 51 patients with stable COPD with (n = 15) and without CVD (n = 36) were prospectively enrolled in the study. We collected demographics, clinical variables including modified Medical Research Council (MMRC) dyspnea score, St. George Respiratory Questionnaire (SGRQ) score, COPD assessment test (CAT) score, pulmonary function, sputum cell differential counts. Serum H2S and Hcy were measured by sulfide sensitive electrode and ELISA, respectively. We also measured other inflammatory mediators such as serum C-reactive protein (CRP) and tumor necrosis factor-a (TNF-a). Results Patients had similar age, gender distribution and smoking history in COPD + CVD group and COPD group. BMI was higher in COPD + CVD group than COPD group (24.7 ± 2.1 vs. 22.3 ± 3.2 kg/m2, p Conclusion Imbalance of endogenous H2S and Hcy pathway may be involved in the pathogenesis in COPD combined with CVD. Supported by National Natural Science Foundation of China (Nos. 30871127 and 81170012).