Imbalance of Endogenous Hydrogen Sulfide and Homocysteine in Chronic Obstructive Pulmonary Disease Combined with Cardiovascular Disease

Abstract

Background: Considerable studies showed associations between chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD), we evaluated the role of endogenous hydrogen sulfide (H2S)/homocysteine (Hcy) in patients with COPD combined with CVD.Methods: Fifty one stable patients with COPD were enrolled (25 COPD, 26 COPD + CVD). Lung function, sputum, peripheral blood samples, serum H2S, Hcy, high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-α (TNF-α) levels were measured. Dyspnea, symptoms and quality of life were quantified by modified Medical Research Council dyspnea scale (mMRC), COPD assessment test (CAT) and St. George’s Respiratory Questionnaire (SGRQ).Results: Compared with COPD group, waist circumference and body mass index (BMI) were higher in COPD + CVD group, mMRC, CAT and activity scores were also higher, high density lipoprotein cholesterol (HDL-C) was lower, total cells, neutrophils (%) in sputum and serum hs-CRP level were higher, whereas macrophages (% ) in sputum was lower. H2S and Hcy levels from COPD + CVD group were higher than those from COPD group, but H2S/Hcy ratio was lower. With increasing COPD severity, H2S level was decreased, however, Hcy level was increased. H2S level was positively correlated with FEV1/FVC, FEV1% predicted, lymphocytes (%) and macrophages (%) in sputum, but negatively correlated with smoking pack-years and neutrophils (%) in sputum. Hcy level was positively correlated with BMI and total cells in sputum. The ratio of H2S/Hcy was also positively correlated with FEV1/FVC, but negatively correlated with total cells in sputum.Conclusion: The imbalance of H2S/Hcy may be involved in the pathogenesis of COPD combined with CVD and provide novel targets for therapy.

Estradiol‐17β inhibits homocysteine mediated damage by promoting H2S production via upregulating CBS and CSE expression in human umbilical vein endothelial cells

“…13 Reduced production of endogenous H 2 S during hyperhomocysteinemia has emerged as one of the causes of hypertension and vascular disease. 31 Our research also found that high concentrations of Hcy reduced endogenous H 2 S levels in vascular endothelial cells by reducing the expression of CBS and CSE. At the same time, lower expression CBS and CSE also cause Hcy metabolic disorders, which are accumulated in the body and damage the vascular endothelium.…”

Hyperhomocysteinemia and Cardiovascular Disease: Is the Adenosinergic System the Missing Link?

“…Accumulating evidence supports the inhibitory effect of HCy on H 2 S generation [ 83 , 84 , 85 ], but there were also reports of elevated H 2 S levels in HHCy [ 86 , 87 ]. The evidence of defective and enhanced H 2 S production under HHCy conditions and the metabolic imbalance of HCy and H 2 S in cardiovascular pathologies suggests that changes in the H 2 S/HCy ratio may be more valuable than changes in the absolute concentrations of H 2 S and HCy in depicting the role of these metabolites in disease pathogenesis [ 88 , 89 , 90 ]. There are growing controversies on the physiologically significant concentrations of H 2 S and its biological effects [ 91 , 92 ].…”

The diagnostic value of homocysteine for the occurrence and acute progression of chronic obstructive pulmonary disease

“…It has been reported that increased expression of Hcy can accelerate the development of the disease by causing damage to vascular endothelial cells [6]. More and more evidences have shown that elevated plasma Hcy levels may also contribute to poor prognosis of COPD patients [7][8][9]. In addition, studies have indicated that other methods of reducing total Hcy level may yield different results on serum inflammatory markers [3].…”