Background: The onset and progression of Chronic Obstructive Pulmonary Disease (COPD) are influenced by both environmental and genetic factors. Persistent hypoxia at high altitudes is a major environmental stressor. Under hypoxic conditions, EPAS1 is stably expressed and activates its downstream target gene VEGFA; however, the underlying mechanisms remain unclear. Methods: We conducted a case-control study in Gansu Province: to evaluate the association between EPAS1 gene polymorphisms (rs4953354, rs6743991, rs7589861, rs13419896) and susceptibility to COPD in high-altitude populations, we enrolled 517 patients and 580 controls (no significant differences in ethnic distribution, no stratification was performed); To evaluate the association of VEGFA gene polymorphisms (rs10434, rs2010963, rs3025020, rs833070) in Tibetan and Han populations, we enrolled 397 patients (148 Tibetans, 249 Han) and 807 controls (251 Tibetans, 556 Han). Results: For EPAS1, rs4953354 A>G was associated with a decreased risk of COPD (AG vs. AA: OR = 0.680, 95% CI = 0.523-0.885; AG+GG vs. AA: OR = 0.708, 95% CI = 0.551-0.910). For VEGFA, in Han population, rs2010963 C>G (CG vs. CC: OR = 1.619, 95% CI = 1.070-2.449; GG vs. CC: OR = 1.751, 95% CI = 1.119-2.740; CG+GG vs. CC: OR = 1.670, 95% CI = 1.133-2.462) and rs3025020 C>T (TT vs. CC: OR = 2.290, 95% CI = 1.321-3.971; TT vs. CT+CC: OR = 2.151, 95% CI = 1.276-3.626) were associated with an increased risk of COPD. Conversely, in the Tibetan population, rs3025020 C>T was associated with a decreased risk of COPD (CT vs. CC: OR = 0.530, 95% CI = 0.329-0.853; CT+TT vs. CC: OR = 0.571, 95% CI = 0.365-0.893). No significant associations were observed for other loci. Conclusion: This study reveals that EPAS1 and VEGFA gene polymorphisms are associated with susceptibility to COPD in populations residing at high altitudes.

Chronic obstructive pulmonary disease (COPD) is an incompletely reversible heterogeneous lung disease with high morbidity and mortality. Progressive worsening of dyspnea is its core clinical manifestation, and patients often develop severe complications such as pulmonary hypertension during the advanced stages of the disease. The oxygen-sensitive gene endothelial PAS domain-containing protein 1 (EPAS1) is a core transcription factor activated under hypoxic conditions. EPAS1 acts as a key regulator of hypoxia-induced pulmonary vascular remodeling in COPD, although other hypoxia-responsive factors, including HIF-1α and NF-κB, also contribute to this complex process. This gene is involved in the pathological progression of COPD and is closely associated with pulmonary vascular remodeling. Pulmonary vascular remodeling, in turn, is a critical process in COPD pathogenesis, driven by chronic hypoxia, inflammatory responses, tobacco exposure, and cytokine dysregulation. These pathological changes can directly lead to the development of pulmonary hypertension and further exacerbate dyspnea symptoms. Under hypoxic conditions, aberrant expression of EPAS1 regulates the transcriptional activation of its target gene, vascular endothelial growth factor (VEGF), while also mediating the activation of the mitogen-activated protein kinase (MAPK) signaling pathway. These molecular events are closely related to the structural remodeling of pulmonary vasculature in COPD patients. Therefore, in-depth investigation into the molecular mechanisms by which EPAS1 regulates pulmonary vascular remodeling in the hypoxic microenvironment will not only help elucidate the pathogenesis of complications in advanced COPD but also provide potential molecular targets for clinical intervention, offering significant theoretical and clinical value for the precision treatment of COPD.

Background: Chronic Obstructive Pulmonary Disease (COPD) is influenced by both genetic and environmental factors, with chronic hypoxia playing a pivotal role in its pathogenesis. Peroxisome proliferator-activated receptor alpha (PPARA), a core regulator of the hypoxia pathway, exhibits genetic differentiation in high-altitude populations. This study aimed to investigate the association between PPARA gene polymorphisms and COPD susceptibility in Tibetan and Han populations in Gansu Province. Methods: A case-control study design was employed. A total of 1276 participants (399 Tibetans and 877 Han Chinese) were recruited from Gansu province. Using Haploview software, four tag SNPs of the PPARA gene (rs135538, rs135539, rs135549, rs4253758) were selected. Genotyping was performed using the iMLDR (Improved Multiple Ligase Detection Reaction) multiplex SNP genotyping technique. Results: In the Tibetan population, the rs135539A>C polymorphism under a dominant model was associated with an increased risk of COPD (CC+CA vs. AA: OR = 1.779, 95% CI: 1.080-2.903, P=0.024). In the Han population, rs135549T>C under a dominant model was associated with a reduced COPD risk (CC+CT vs. TT: OR = 0.719, 95% CI: 0.547-0.944, P = 0.017). The rs4253758T>C SNP exhibited a dual effect in Han Chinese: under an additive model, both TC (OR = 1.722, 95% CI: 1.504-2.813, P = 0.030) and CC (OR = 1.778, 95% CI: 1.083-2.922, P = 0.023) genotypes increased risk compared to the TT genotype. However, under a recessive model, the CC genotype was protective compared to TT+TC (OR = 0.572, 95% CI: 0.356-0.918, P = 0.021). No significant associations were found for other SNPs. Conclusion: PPARA gene polymorphisms are associated with COPD susceptibility in a population-specific manner among Tibetan and Han populations in Gansu. The rs135539A>C variant increases COPD risk in Tibetans, whereas rs135549T>C and rs4253758T>C exert protective and dual effects, respectively, in the Han population.

Chronic obstructive pulmonary disease (COPD) ranks as the third leading cause of death globally, with persistently high prevalence and mortality. In developing countries, exposure to biomass fuel smoke accounts for 30% to 50% of the COPD burden, posing a significant public health challenge. Given its exceptionally large population exposed to biomass fuels, China faces immense public health challenges in disease prevention and control. This review summarized the recent domestic and international evidence on the epidemiological characteristics of COPD, the current status of biomass fuel exposure, and the major harmful components generated during biomass fuel combustion. It also examined the risk factors of biomass fuel smoke-associated COPD (BMF-COPD), compared its clinicopathological, pulmonary functional, and radiological characteristics with those of smoking-induced COPD, and discussed potential mechanisms centered on PM2.5-mediated oxidative stress and fungal microbiome dysbiosis. Current evidence suggests that BMF-COPD differs from smoking-induced COPD in exposed populations, clinical phenotypes, and pathogenic mechanisms, with prominent features of small airway disease and chronic bronchitis. Prevention and control strategies should prioritize primary prevention, including clean energy substitution and stove retrofitting, together with early screening among highly exposed populations. Future research should focus on regional heterogeneity, genetic susceptibility, and specific biomarkers to support precision prevention and targeted management of BMF-COPD.

Objective:Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. However, the effects of chronic hypobaric hypoxia on COPD in high-altitude areas remain controversial. This study aimed to evaluate the impact of chronic hypobaric hypoxia on COPD in high-altitude areas. Methods:C57BL/6J mice were randomized into the sham control (MOCK; intranasal PBS), cigarette smoke extract/lipopolysaccharide (CSE/LPS, CL; intranasal CSE five times/week and LPS twice/week), chronic hypobaric hypoxia (Hy; hypobaric hypoxia at simulated 4000 meters with intranasal PBS), and chronic hypobaric hypoxia plus CL (HyCL; CSE/LPS plus chronic hypobaric hypoxia) groups for 12 weeks. After 12 weeks, pulmonary function, bronchoalveolar lavage fluid cell counts, and pulmonary histopathology were assessed. To elucidate the effects of chronic hypobaric hypoxia on COPD, we performed RNA sequencing on lung tissues to profile molecular alterations and validated key targets using qPCR and Western blotting. Results:The results indicate that chronic hypobaric hypoxia promotes COPD progression, characterized by exacerbated pulmonary function decline, emphysema, as well as small airway remodeling. Transcriptome analysis reveals that "chemical carcinogenesis-reactive oxygen species" and "extracellular matrix-receptor interactions" are common transcriptomic characteristics of COPD both with and without chronic hypobaric hypoxia exposure, whereas inflammatory and immune responses are major transcriptomic signatures driven by chronic hypobaric hypoxia. Furthermore, our results identify Cstdc4 as a key differentially expressed gene (DEG) implicated in COPD progression under chronic hypobaric hypoxia. Conclusion:These results indicate that chronic hypobaric hypoxia in high-altitude areas promotes COPD progression and correlates with a transcriptomic signature marked predominantly by the activation of inflammatory and immune responses.

Chronic obstructive pulmonary disease (COPD) is a complex respiratory disorder influenced by various factors and involving multiple genes. Respiratory dysfunction in COPD patients leads to hypoxia, resulting in limited oxygen uptake. Peroxisome proliferator-activated receptor alpha (PPARA) is a plateau-adapted gene that regulates respiratory function in populations adapted to high-altitude areas through multiple pathways. Interestingly, PPARA expression is higher in long-term inhabiting Tibetan populations that have adapted to the plateau environment. However, in patients with COPD, the expression of PPARA is downregulated, leading to dysregulation of the hypoxia-inducible factor pathway. Moreover, abnormal PPARA expression in lung epithelial cells triggers inflammatory responses, oxidative stress, and disrupted lipid metabolism, thereby exacerbating disease progression. Thus, this paper explored the mechanism underlying the role of plateau-adapted PPARA in COPD, providing essential theoretical insights into the treatment and prevention of COPD in high-altitude regions.

Background: Environmental and genetic factors are jointly involved in the development of chronic obstructive pulmonary disease (COPD). The EGLN1 gene is a major factor in upstream regulation of the hypoxia-inducible pathway. EGLN1 negatively regulates the hypoxia-inducible factors HIF-lα and HIF-2α by regulating the concentration of oxygen, mainly in a hypoxic environment. Hypoxia is a common physiologic condition during the progression of COPD, and several studies have identified genetic variants in EGLN1 as a key factor in the adaptation to hypoxic environments. However, it is still unclear whether there is an association between EGLN1 variants and the risk of developing COPD. Methods: A case-control study was conducted in the Gannan Tibetan Autonomous Prefecture, Gansu Province. A total of 292 COPD patients and 297 healthy controls were enrolled to assess the association of EGLN1 single nucleotide polymorphisms (SNPs) (rs41303095 A>G, rs480902 C>T, rs12097901 C>G, rs2153364 G>A) with COPD susceptibility. Results: The EGLN1 rs41303095 A>G, rs480902 C>T, rs12097901 C>G, and rs2153364 G>A polymorphisms were not associated with COPD susceptibility (p > 0.05). Conclusions: The EGLN1 rs41303095 A>G, rs480902 C>T, rs12097901 C>G and rs2153364 G>A polymorphisms were found in this study not to be associated with susceptibility to COPD in Gannan Tibetans.

Background: Chronic obstructive pulmonary disease (COPD) is a chronic respiratory ailment influenced by a blend of genetic and environmental factors.Inflammatory response and an imbalance in oxidative-antioxidant mechanisms constitute the primary pathogenesis of COPD.Glutathione S-transferase P1(GSTP1) plays a pivotal role as an antioxidant enzyme in regulating oxidativeantioxidant responses in the pulmonary system.The activation of the NOD-like receptor thermal protein domain (NLRP3) inflammatory vesicle can trigger an inflammatory response.Several investigations have implicated GSTP1 and NLRP3 in the progression of COPD; nonetheless, there remains debate regarding this mechanism.Methods: Employing a case-control study design, 312 individuals diagnosed with COPD and 314 healthy controls were recruited from Gansu Province to evaluate the correlation between GSTP1 (rs4147581C>G and rs1695A>G) and NLRP3 (rs3806265T>C and rs10754558G>C) polymorphisms and the susceptibility to COPD.Results: The presence of the GSTP1 rs4147581G allele substantially elevated the susceptibility to COPD (CGvs.CC:OR=3.11,95%CI=1.961-4.935,P<0.001;GGvs.CC:OR=2.065,95%CI=1.273-3.350,P=0.003; CG+GGvs.CC:OR=2.594,95%CI=1.718-3.916,P<0.001).Similarly, the NLRP3rs3806265T allele significantly increased the susceptibility to COPD (TC:TT:OR=0.432,95%CI=0.296-0.630;TC+CCvs.TT:OR=2.132,95%CI=1.479-3.074,P<0.001).However, no statistically significant association was discerned between the rs1695A>G and rs10754558G>C polymorphisms and COPD susceptibility (P>0.05). Conclusion:In summary, this study ascertained that the GSTP1 rs4147581C>G polymorphism is associated with increased COPD susceptibility, with the G allele elevating the risk of COPD.Similarly, the NLRP3 rs3806265T>C polymorphism is linked to elevated COPD susceptibility, with the T allele heightening the risk of COPD.

Background: The occurrence and development of chronic obstructive pulmonary disease (COPD) are regulated by environmental and genetic factors. In hypoxia, Erythropoietin (EPO) satisfies the body's need for oxygen by promoting the production of red blood cells. Hypoxia was proven to be a common physiological condition in COPD progression and associated with many complications. Some studies have found that EPO is involved in the development of COPD. But the mechanism has not been fully proven. Methods: We conducted a case-control study enrolled 1095 COPD patients and 1144 healthy controls in Guangdong Province to evaluate the association between EPO polymorphisms (rs1617640 A>C, rs507392 A>G, rs564449 G>T) and COPD susceptibility. 872 participants from southern Gansu Province were recruited to verify the effect of EPO polymorphisms on lung function. Results: EPO rs1617640 C allele reduced COPD susceptibility in southern Chinese significantly (AC vs. AA: adjusted Odds ratio (OR) = 0.805, 95% CI = 0.669-0.969; AC+CC vs. AA: adjusted OR = 0.822, 95% CI = 0.689-0.980). However, there was no association between rs507392 A>G and rs564449 G>T polymorphisms and COPD susceptibility (p > 0.05). We further observed that the rs1617640 C allele was associated with higher FEV1 and FVC in Guangdong and Gansu populations significantly (both p < 0.05). In brief, the level of FEV1 and FVC increased with the C allele number. We modeled the relative risk for men and women, in which the population-attributable risks chances were 0.449 (0.258-0.641) and 0.262 (0.128-0.396) respectively. In this model, smoking status, coal as fuels, education level, and rs1617640 A>C were finally retained for males, while smoking status, biomass as fuels, and1617640 A>C were retained for females. In the end, using the method developed by Gail and Bruzzi, we fitted a 10-year absolute risk model for southern Chinese with different individual relative risks, which was presented as a table. Conclusions: In conclusion, this study found that EPO rs1617640 A>C polymorphism is associated with COPD susceptibility in southern Chinese, and the C allele was associated with better lung function. In addition, it could also be considered a genetic marker associated with environmental factors to predict the absolute 10-year risk of COPD in southern Chinese.

Chronic obstructive pulmonary disease (COPD) is a disease characterized by irreversible airflow restriction with a high incidence, and the inflammatory mechanism is currently recognized as the pathogenesis.Peroxisome proliferator-activated receptor alpha gene, PPARA gene, can make Tibetans′ hemoglobin concentration lower than other people in the plateau environment, which plays an important role in adapting to the hypoxia environment.Moreover, PPARA encoded by this gene is related to improving the utilization rate of oxygen, ensuring energy supply under hypoxia, and inhibiting inflammation.The occurrence of COPD is closely related to the inflammatory mechanism, and patients will suffer different degrees of hypoxia.Therefore, it is speculated that the inflammatory mechanism of COPD may be related to the PPARA gene.In this paper, the role of PPARA gene and PPARα in altitude adaptation was briefly described and the relationship between PPARA gene and the mechanism of COPD was explored, so as to find the genes related to the pathogenesis of COPD in the altitude hypoxia environment, finally to provide new ideas for the follow-up study of the pathogenesis of COPD.

Objective: COPD is the most common chronic respiratory disease with complex environmental and genetic etiologies. It was reported that EPAS1 might participate in the occurrence and development of respiratory diseases. However, the association between EPAS1 and COPD was unclear.Methods: First, a case-control study enrolling 1130 COPD patients and 1115 healthy controls in Guangzhou was conducted to clarify the association between EPAS1 polymorphisms and COPD susceptibility. Secondly, a prevalence study recruited 882 participants in Gansu to verify the effect of positive polymorphisms on lung function. Finally, the 10-year absolute risk considering environmental factors and genetic variations was calculated by the method of Gail and Bruzzi. Results: EPAS1 rs13419896 AA genotype reduced COPD risk in southern Chinese (AA vs. GG: adjusted OR = 0.689, 95% CI = 0.498-0.955; AA vs. GG/GA: adjusted OR = 0.701, 95% CI = 0.511-0.962). Further, the rs13419896 A allele was significantly associated with higher preFEV1/pre-FVC in both the Guangzhou and Gansu populations (P < 0.05). Smoking status, coal as fuels, education level, and rs13419896 G > A were finally retained to develop a relative risk model for males. Smoking status, biomass as fuels, and rs13419896 G > A were retained in the female model. The population-attributable risk of the male or female model was 0.457 (0.283-0.632) and 0.421 (0.227-0.616), respectively.Conclusions: This study first revealed that EPAS1 rs13419896 G > A decreased COPD susceptibility and could be a genetic marker to predict the 10-year absolute risk for COPD.

Objective:To analyze the interaction between obesity and diabetes, obesity and central obesity, central obesity and diabetes on hypertension.Methods:A questionnaire survey on 7 622 residents of Han Chinese ethnicity, aged 35-75 years, of Liangzhou district of Wuwei city were performed using multi-stage random sampling method in September to December 2018. Relative excess risk due to interaction, attributable proportion, synergy index, and 95% CI of the three were used to evaluate the additive interaction. Logistic regression analysis was used to analyze the multiplicative interaction. Results:Among the 7 622 residents, hypertension was detected in 3 212 residents, with a crude prevalence rate of 42.14% and a standardized incidence of 33.81%. There was a significant difference in incidence of hypertension between residents of different sexes, between residents at different ages, between obese residents and normal weight residents, between residents who had central obesity and those who had no central obesity, between residents who smoked and those who did not, between residents of different family economic situations, between residents who had different occupations, and between residents who had diabetes and those who had no diabetes (all P < 0.05). Getting primary, middle, and high school education was a protective factor against hypertension, while obesity, central obesity, diabetes, male gender, age greater than 45 years were the risk factors for hypertension. Multivariate logistic regression analysis showed that there was no additive interaction between obesity and diabetes, obesity and central obesity, central obesity and diabetes on hypertension. There was a multiplicative interaction between obesity and central obesity on hypertension ( P = 0.031, 95% CI: 0.53-0.97) and the interaction was antagonistic, but there were no multiplicative interaction between obesity and diabetes, central obesity and diabetes on hypertension. Conclusion:There was a negative multiplicative interaction between obesity and central obesity on hypertension.

Background Chronic Obstructive Pulmonary Disease (COPD) is a common and harmful disease that requires an effective tool to early screen high-risk individuals. Gansu has unique environments and customs, leading to the different prevalence and etiology of COPD from other regions. The association between altitude and COPD once attracted epidemiologists' attention. However, the prevalence in Gansu and the role of altitude are still unclarified. Methods In Gansu, a multistage stratified cluster sampling procedure was utilized to select a representative sample aged 40 years or older. The questionnaire and spirometry examination were implemented to collect participants' information. The diagnosis and assessment of COPD were identified by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criterion, while post-bronchodilator FEV1/FVC < LLN was for sensitivity analysis. Furthermore, the effect of high altitude on COPD was evaluated by the logistic regression model after propensity score matching (PSM). Finally, the participants were randomly divided into training and validation sets. The training set was used to screen the relative factors and construct a nomogram which was further assessed by the receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA) in the two sets. Results There were 2,486 eligible participants in the final analysis, of which 1,584 lived in low altitudes and 902 lived in high altitudes. Based on the GOLD criterion, the crude and standardized prevalences in Gansu were 20.4% (18.7–22.0) and 19.7% (17.9–21.6). After PSM, the logistic regression model indicated that high altitude increased COPD risk [PSM OR: 1.516 (1.162–1.978)]. Altitude, age, sex, history of tuberculosis, coal as fuel, and smoking status were reserved for developing a nomogram that demonstrated excellent discrimination, calibration, and clinical benefit in the two sets. Conclusions COPD has become a serious public health problem in Gansu. High altitude is a risk factor for COPD. The nomogram has satisfactory efficiency in screening high-risk individuals.

慢性阻塞性肺疾病(COPD)是一种常见的进行性呼吸系统疾病,其主要特点是气流受阻和肺泡壁严重破坏,导致患者呼吸困难、咳嗽以及咳痰.COPD 难以治愈,且病程长,患者的恢复受到多种因素的影响,包括患者呼吸功能恢复水平、自身营养状况,很难达到理想的恢复水平.因此,临床干预COPD患者的早期恢复至关重要.在呼吸功能锻炼基础上开展饮食干预具有更高的临床价值.

目的 分析肥胖和中心性肥胖对高血压患病影响的交互作用,为制定高血压防控措施提供依据.方法 于2018年9-12月,采用多阶段随机抽样方法抽取甘肃省白银市白银区35～75岁居民进行问卷调查和体格检查;采用logistic回归模型分析肥胖与中心性肥胖对高血压影响的交互作用,采用ANDERSSON等编制的Excel表计算交互作用指数(SI)、相对超额危险度比(RERI)和归因比(AP)等交互作用指标.结果 发放调查问卷6 246份,回收有效问卷6 169份,回收有效率为98.77％.调查男性3 038人,占49.25％;女性3 131人,占50.75％.年龄为(52.05±8.78)岁.检出肥胖832例,占13.49％;中心性肥胖2 278例,占36.93％.高血压粗患病率为35.89％,标化患病率为33.05％.多因素logistic回归分析结果显示,肥胖(OR=2.020,95％CI:1.705～2.393)和中心性肥胖(OR=1.622,95％CI:1.433～1.836)与高血压患病均有统计学关联;肥胖和中心性肥胖对高血压患病的影响不存在相乘交互作用(OR=1.011,95％CI:0.655～1.560),也不存在相加交互作用(SI=1.405,95％CI:0.815～2.424;RERI=0.658,95％CI:-0.298～1.614;AP=0.201,95％CI:-0.075～0.476).结论 肥胖和中心性肥胖增加高血压患病风险,但未发现两者存在交互作用.

Chronic obstructive pulmonary disease (COPD) is a pulmonary disease characterized by airflow restriction, with high morbidity and mortality and complex pathogenic factors, mainly the combined action of genetic factors and environmental factors.The pathogenesis is mainly based on three hypotheses: inflammatory mechanism, protease-antiprotease imbalance, and oxidation-antioxidation imbalance.GSTP1, as an antioxidant enzyme, plays an important role in lung oxidation.However, due to the polymorphism of GSTP1 gene, the antioxidant capacity of GSTP1 is significantly reduced, leading to the imbalance between oxidation and antioxidant in vivo.Therefore, GSTP1 gene polymorphism is considered one of the risk factors of COPD.NLRP3, as an inflammasome component, is confirmed to be involved in the inflammatory response of COPD, and its gene polymorphism may alter the structure of NLRP3, which may affect the occurrence of COPD.This paper reviews the correlation of GSTP1 and NLRP3 gene polymorphism and COPD, so as to, through relevant experimental evidence, provide new approaches and noval ideas for COPD intervention and targeted therapy.

目的 通过对武威市凉州区城乡居民的基本信息、健康状况、生活方式等进行分析,为当地居民慢性病的预防提供科学依据及干预措施.方法 采用国家重点研发计划“精准医学研究”重点专项调查问卷,通过面对面调查收集信息,研究共纳入武威市凉州区35 ～75岁城乡常住居民7993人.调查内容包括:基本信息(性别、年龄、职业、婚姻状况、学历)、健康状况(疾病史、自我健康认知、肥胖状况、精神状况等)、生活方式(吸烟、饮酒、运动、膳食、睡眠等).结果 调查人群中男3293人,女4700人,居民自我健康认知状况良好;男性平均体质量指数(BMI)为(24.9±3.43) kg/m2,女性为(24.7±3.32) kg/m2,当地居民肥胖率为16.4％,居民BMI在65岁之前随年龄增长呈上升趋势,在65岁之后随年龄增长呈下降趋势;当地居民所患慢性病主要以糖尿病、高血压病、胆石症为主;当地居民食盐摄入量较高,不规律饮食情况较少;吸烟、饮酒现象严重,二手烟吸入情况较为严重;业余时间参加锻炼的居民较少;1年中经历重大事件、精神状态不良者较少;当地居民睡眠状况较好.结论 武威市凉州区城乡居民存在高盐饮食、缺乏锻炼、吸烟、饮酒等影响健康的不良生活方式,当地卫生部门应针对健康生活、健康饮食等对居民展开健康知识教育.

Background: Hypertension (HTN), dyslipidemia and hyperhomocysteinemia (HHcy) are risk factors for cardiovascular disease (CVD). Methods: Hypertensive Chinese subjects (n = 228) were enrolled. MTHFR C667T, MTHFR A1298C, MTR A2756G, and MTRR A66G genotypes were determined. Unconditional logistic regression was performed to determine the associations of serum Hcy status and genotypes with HTN and dyslipidemia. Results: The mean age of hypertensive adults was 65.53 ± 9.94 years, including 88 (38.6%) men and 140 (61.4%) women. Patients with MTHFR 667TT and MTRR GG carriers showed higher serum Hcy levels (P = 0.019 and 0.018, respectively), which is associated with higher serum triacylglycerols (TAG) and total cholesterol (TC) levels (P = 0.014 and 0.044, respectively) and a higher risk for hypertriglyceridemia (OR = 1.889, 95% CI: 1.105–3.229, P = 0.020). Compared with low Hcy and MTRR 66AA, those with high Hcy and 66AA or 66AG+GG showed higher odd\s of hypertriglyceridemia (MTRR 66AA+ high Hcy: OR: 2.692, 95% CI: 1.189–6.096, Pcombined = 0.018; MTRR 66AG/GG+ high Hcy: OR: 3.433, 95% CI: 1.517–7.772, Pcombined = 0.003, respectively). Patients with high Hcy and MTHFR 667CC, as well as those with low Hcy and 667CT+TT, showed lower odds of uncontrolled SBP (MTHFR 667CC+ high Hcy: OR: 0.338, 95% CI: 0.115–0.996, Pcombined = 0.049; MTHFR 667CT/TT+ low Hcy: OR: 0.421, 95% CI: 0.193–0.921, Pcombined = 0.030) compared to patients with low Hcy and MTHFR 667CC. Conclusions: Serum Hcy status and Hcy metabolism gene polymorphisms (MTHFR C667T and MTRR A66G) may have synergistic effects on the prevalence of HTN and dyslipidemia.

近年来,我国胆石病的发病率呈明显上升趋势,给患病人群和社会带来一定的疾病和经济负担.但由于胆石病是受多种因素影响的慢性非传染性疾病,国内外不同地区和人群的患病情况和影响因素存在一定的差异.因此,本文通过对胆石病相关危险因素的梳理,从流行病学角度详述影响我国胆石病的危险因素,为普通人群早期展开社区预防和高危人群加强相关因素控制提供理论依据.