幽门螺杆菌感染对冠心病患者血清生化水平及颈动脉硬化的影响

目的 探讨幽门螺杆菌感染对冠心病患者血清生化水平及颈动脉硬化的影响。方法 选取150例冠心病患者,所有患者均接受14C呼气试验检查,将呼气试验阳性患者分为观察组,阴性患者分为对照组。两组患者均检测甘油三酯（TG）、胆固醇（TC）、低密度脂蛋白（LDL-C）、血清同型半胱氨酸（HCY）和血清超敏C反应蛋白（hs-CRP）水平,并接受彩色多普勒超声检查颈动脉。观察并比较两组患者血清生化水平及颈动脉情况。结果 观察组患者血清TC、LDL-C、HCY和hs-CRP水平显著高于对照组（P0.05）。观察组患者内膜厚度显著大于对照组（P0.05）。结论 冠心病患者感染幽门螺杆菌会影响脂蛋白代谢,激活炎症反应,增加冠心病患者动脉硬化发生的风险,应早期积极干预治疗。     

幽门螺杆菌感染与急性心肌梗死患者血清炎症反应的关系

目的:探讨幽门螺杆菌(Hp)感染与急性心肌梗死(AMI)患者血清炎症反应的关系,为临床防治AMI提供参考。方法:选取2013年4月-2014年11月我院收治的74例AMI患者作为研究组,另选取同期在我院进行体检的74例健康人作为对照组。采用酶联免疫法检测和比较两组患者Hp免疫球蛋白G(Immunoglobulin G,IgG)浓度及血清IL-6、IL-8、IL-18、TNF-α和hs-CRP水平,分析Hp IgG阳性与血清炎症因子水平的相关性。结果:研究组患者的Hp IgG浓度为(60.92±45.15)KU/L,相比于对照组的(32.36±24.08)KU/L明显偏高(P0.05),且其阳性率为72.97%,明显高于对照组的51.35%(P0.05);Hp阳性患者IL-6、IL-8、IL-18、TNF-α、hs-CRP明显高于Hp阴性患者的(P0.05)。Pearson相关分析显示Hp IgG浓度与血清IL-6、IL-8、IL-18、TNF-α、hs-CRP水平均呈显著正相关,相关系数分别为0.735、0.644、0.798、0.674、0.616(P0.05)。结论:Hp感染与AMI患者血清炎症反应之间存在着密切的关系。     

急性上消化道出血严重程度与患者幽门螺杆菌感染和炎症因子及凝血功能的相关性

目的 探究急性上消化道出血（AUGIH）患者病情严重程度与幽门螺杆菌（H. pylori）感染和炎症因子及凝血功能的关系,为该类患者的治疗提供参考。方法 选取2020年1月至2022年3月太和县人民医院收治的186例AUGIH患者为研究对象,根据H. pylori感染情况分为HP感染组（102例）和HP未感染组（84例）;此外根据AUGIH的严重程度将患者分为轻度组（46例）、中度组（30例）、重度组（26例）。采用酶联免疫吸附法（ELISA）测定患者C-反应蛋白（CRP）、降钙素原（PCT）和白介素-6(IL-6)水平;采用全自动血凝仪检测血浆凝血酶原时间（PT）、纤维蛋白原（Fbg）、活化部分凝血活酶时间（aPTT）、D-二聚体（DD）的水平和国际正常化比值（INR）;采用Logistic回归分析AUGIH患者H. pylori感染的影响因素。结果 HP感染组患者血清CRP、PCT、IL-6的水平高于HP未感染组,重度组患者CRP、PCT、IL-6水平显著高于轻度组和中度组,同时中度组高于轻度组（均P<0.05）。HP感染组患者Fbg、aPTT水平显著低于HP未感染组,D-D...     

舍曲林辅助治疗对抑郁症合并冠心病患者血清炎症因子水平及预后的影响

目的：探讨舍曲林辅助治疗对抑郁症合并冠心病患者血清炎症因子水平及预后的影响。方法：选择2009年8月-2011年8月我院收治的86例抑郁症合并冠心病患者,将其随机分入对照组与观察组,40例对照组患者接受冠心病常规治疗,46例观察组患者在常规治疗基础上给予舍曲林口服,每次504100mg,每日1次,疗程24周。比较两组治疗期间心血管事件发生率、治疗前后汉密尔顿抑郁量表（HAMD）评分及血清炎症因子超敏c-反应蛋白（hs—CRP）、肿瘤坏死因子-α（TNF—α）及白介素-6（IL-6）的变化．结果：观察组心血管不良事件发生率显著低于对照组（13．0％VS32．5％,P〈0．05）;观察组治疗后HAMD评分、血清hs—CRP、TNF一双及IL-6水平显著均显著低于对照组（P〈0．05）。结论：舍曲林辅助治疗可显著改善抑郁症合并冠心病患者的抑郁状态,降低炎症因子水平并改善其预后．     

舍曲林辅助治疗对抑郁症合并冠心病患者血清炎症 因子水平及预后的影响

目的：探讨舍曲林辅助治疗对抑郁症合并冠心病患者血清炎症因子水平及预后的影响。方法：选择2009 年8 月～2011 年8 月我院收治的86 例抑郁症合并冠心病患者,将其随机分入对照组与观察组,40 例对照组患者接受冠心病常规治疗,46 例观察组 患者在常规治疗基础上给予舍曲林口服,每次50～100 mg,每日1 次,疗程24 周。比较两组治疗期间心血管事件发生率、治疗前 后汉密尔顿抑郁量表(HAMD)评分及血清炎症因子超敏C- 反应蛋白（hs-CRP）、肿瘤坏死因子-alpha（TNF-alpha）及白介素-6（IL-6）的变 化。结果：观察组心血管不良事件发生率显著低于对照组(13.0 %vs 32.5%,P<0.05);观察组治疗后HAMD 评分、血清hs-CRP、 TNF-alpha及IL-6 水平显著均显著低于对照组(P<0.05)。结论：舍曲林辅助治疗可显著改善抑郁症合并冠心病患者的抑郁状态,降低 炎症因子水平并改善其预后。     

冠心病患者幽门螺杆菌感染与血清Ghrelin、同型半胱氨酸水平的相关性研究

目的探讨冠心病患者幽门螺杆菌(Helicobacter pylori,H.pylori)感染与血清Ghrelin、同型半胱氨酸(Hcy)水平的相关性。方法选择2013年1月至2014年12月行冠状动脉造影确诊冠心病患者136例作为冠心病组,另选择同期健康体检人员60例作为对照组。运用14 C尿素呼气试验方法测定H.pylori感染情况,观察组患者的冠状动脉病变程度进行Gensini评分,测定血清Ghrelin和Hcy水平,分析H.pylori感染与Ghrelin、Hcy水平及Gensini积分之间的关系。结果冠心病组血清Ghrelin水平明显低于对照组,差异有统计学意义(t=10.65,P0.05);冠心病组血清Hcy水平明显高于对照组,差异有统计学意义(t=6.08,P0.05)。冠心病患者中,H.pylori感染组血清Ghrelin明显低于H.pylori未感染组,差异有统计学意义(t=7.58,P0.05);H.pylori感染组组血清Hcy明显高于H.pylori未感染组,差异有统计学意义(t=5.63,P0.05)。随着冠心病H.pylori感染程度的加重,血清Ghrelin水平逐渐下降,血清Hcy水平、Gensini积分逐渐升高。H.pylori感染根治后血清Ghrelin水平较治疗前明显升高,而Hcy水平明显下降,差异均有统计学意义(t=14.84、6.25,P0.05)。结论 H.pylori感染能够影响冠心病患者血清Ghrelin、Hcy水平,H.pylori感染可能参与冠心病发生发展。H.pylori感染程度与冠心病患者冠状动脉病变程度相关。     

幽门螺杆菌感染对冠心病患者冠状动脉病变程度与血清Ghrelin/obestatin比值的影响

目的探讨幽门螺杆菌(Helicobacter pylori,H.pylori)感染与冠心病患者冠状动脉病变程度和血清Ghrelin/obestatin比值之间的关系。方法选取2013年1月至2014年10月行冠状动脉造影确诊冠心病患者116例作为冠心病组,选取同期健康体检人员80例作为对照组。对所有患者的冠状动脉病变程度进行Gensini评分,运用14 C尿素呼气试验方法测定H.pylori感染情况,测定血清Ghrelin和obestatin水平,分析H.pylori感染与冠状动脉病变程度、血清Ghrelin/obestatin比值之间的关系。结果冠心病组H.pylori感染阳性率明显高于对照组,差异有统计学意义(P0.05)。H.pylori感染阳性组Gensini积分明显高于H.pylori感染阴性组,差异有统计学意义(P0.05);H.pylori感染阳性组Ghrelin/obestatin比值明显低于H.pylori感染阴性组,差异有统计学意义(P0.05)。结论 H.pylori感染能够加重冠心病患者冠状动脉病变程度,引起Ghrelin/obestatin比值异常升降低。H.pylori感染与冠心病发生发展密切相关。     

幽门螺杆菌感染与血清抗体及滴度的相关性研究

为了解幽门螺杆菌（ＨｅｌｉｃｏｂａｃｔｅｒＰｙｌｏｒｉ,ＨＰ）感染时机体的免疫状况,我们对１３４例上消化道疾病患者的血清免疫球蛋白进行了检测。结果表明,细菌培养阳性患者的三种血清抗体滴度显著高于细菌培养阴性患者。血清ＩｇＧ、ＩｇＡ、ＩｇＭ阳性与细菌培养阳性的符合率分别为７９．１％,７４．６％和４３．２％。活动性胃炎和非活动性胃炎的细菌培养阳性率分别为６６％和４２％。证实ＨＰ菌感染与活动性胃炎的发生密切相关,而与胃炎的严重程度无显著性差异。并证实了抗ＨＰ菌ＩｇＧ、ＩｇＡ检测具有较高的诊断ＨＰ菌感染的敏感性和特异性。     

幽门螺杆菌感染激活NF-κB信号通路促进胃癌SGC-7901细胞炎症因子释放

为了探讨幽门螺杆菌对胃癌SGC-7901细胞炎症因子释放的影响,本研究将幽门螺杆菌感染SGC-7901细胞后,采用细胞计数盒(CCK-8)检测SGC-7901细胞活力,酶联免疫吸附实验(ELISA)检测炎症因子TNF-α、IL-1β以及IL-8的水平,Real-time PCR检测细胞TNF-α、IL-1β以及IL-8 m RNA的表达,蛋白免疫印迹法(Western blotting)检测NF-κB信号通路相关蛋白NF-κB p65蛋白表达以及IκBα磷酸化水平。研究结果表明,幽门螺杆菌感染后,SGC-7901细胞活力显著增加;幽门螺杆菌感染明显上调SGC-7901细胞TNF-α、IL-1β以及IL-8 mRNA的表达;本研究还进一步发现幽门螺杆菌感染显著增加SGC-7901细胞TNF-α、IL-1β以及IL-8的水平;此外,幽门螺杆菌处理的SGC-7901细胞,其NF-κB p65的蛋白表达以及IκBα磷酸化水平均显著上调。本研究的结论初步表明,幽门螺杆菌感染促进胃癌SGC-7901细胞炎症因子的释放,其机制可能涉及激活NF-κB信号通路。     

幽门螺杆菌感染与冠心病

幽门螺杆菌感染与慢性胃炎、消化性溃疡的发病密切相关。近年来的研究还发现,幽门螺杆菌感染可能与冠心病发病也有关系,但其机制仍不清楚,可能与炎症免疫反应、高半胱氨酸血症、脂质代谢紊乱、促凝物质增加等因素有关。进一步探讨其作用机制将为冠心病的防治提供一条新的途径。     

Isolation of Helicobacter pylori from the intestinal mucosa of patients with Crohn's disease

BACKGROUND: Helicobacter species are associated with inflammatory bowel disease in rodents and in nonhuman primates. Therefore, we prospectively investigated the presence of Helicobacter species in the intestinal mucosa of patients with and without Crohn's disease by culture and polymerase chain reaction (PCR) assays. MATERIALS AND METHODS: Mucosal fragments were obtained from the ileum, different colon regions, and rectum of 43 patients with Crohn's disease and of 74 patients without inflammatory bowel disease. RESULTS: Helicobacter pylori strains, identified by 16S rRNA gene sequencing, were more frequently isolated and PCR-detected in the intestinal mucosa of patients with ulcerative colitis-like Crohn's disease than in intestinal mucosa of the control group. Otherwise, anti-H. pylori immunoglobulin G levels were significantly lower in fibrostenosing and fistulating Crohn's disease subgroups. No other Helicobacter species were found in the intestinal mucosa of the patients. CONCLUSIONS: Although our results suggest an association between the presence of H. pylori in the intestine and ulcerative colitis-like phenotype of Crohn's disease, H. pylori infection in the actual causality of Crohn's disease is still to be determined.     

Quantitative assessment of IgG antibodies to Helicobacter pylori and outcome of ischaemic heart disease

Criticisms of serological studies on Helicobacter pylori and ischaemic heart disease (IHD) include: undiagnosed heart disease in live controls; no assessment of severity or outcome of IHD; and qualitative not quantitative measurements of IgG to the bacteria. The aim was to assess quantitatively IgG levels specific for H. pylori (ng ml(-1)) among patients who survived a myocardial infarction (MI) with those who died of IHD. Sera were from four groups: (1) men who survived one MI; (2) men matched for age and socioeconomic background to group 1; (3) individuals who died suddenly of IHD; (4) accidental deaths matched for age and sex to group 3. Levels of IgG to H. pylori increased with age (P<0.005) but were not associated with smoking or socioeconomic groups. There was a correlation between IgG to the bacteria and decreasing socioeconomic levels only among group 1 (P<0.01). IgG levels were higher for subjects who died of heart disease (median=151 ng ml(-1)) compared with survivors (median=88 ng ml(-1)) (P=0.034) and higher for survivors compared with their controls (median=58 ng ml(-1)) (P=0.039). Future serological studies of H. pylori in relation to IHD should be quantitative and severity of disease considered in analyses.     

Lower prevalence of Helicobacter pylori infection in patients with inflammatory bowel disease but not with chronic obstructive pulmonary disease - antibiotic use in the history does not play a significant role

BACKGROUND: Patients with inflammatory bowel disease have lower prevalence of Helicobacter pylori infection, but the exact reason for this is not yet clear. AIM: To examine whether the antibiotics frequently used in inflammatory bowel disease are responsible for the lower prevalence of H. pylori infection. Patients with chronic obstructive pulmonary disease on prolonged previous antibiotic therapy were used for comparison. METHODS: Presence/absence of H. pylori infection was detected by a (13)C-urea breath test in 133 patients with inflammatory bowel disease (82 ulcerative colitis, and 51 Crohn's disease) and compared with that of 135 patients with chronic obstructive pulmonary disease and with two age-matched control groups (200 patients each). Primary disease location, duration of disease and detailed analysis of previous and current medication (dose and duration of antibiotics, steroids, 5-aminosalicylic acid) were analysed in each cases. RESULTS: Seventeen of the 133 patients with inflammatory bowel disease [12.2% (10/82) of ulcerative colitis and 13.7% (7/51) of Crohn's disease] and 90/135 patients with chronic obstructive pulmonary disease (66.7%) were positive for H. pylori. A total of 78/200 (39%) for the inflammatory-bowel-disease-group-matched controls and 110/210 (55%) for the chronic-obstructive-pulmonary-disease-matched controls were positive for H. pylori. The history of any antibiotic or steroid therapy had no influence on H. pylori status of patients with inflammatory bowel disease. CONCLUSION: The prevalence of H. pylori compared to the age-matched controls is significantly lower in patients with inflammatory bowel disease but not in those with chronic obstructive pulmonary disease. Antibiotic use is not responsible for the lower prevalence of H. pylori infection in patients with inflammatory bowel disease.     

Elevated homocysteine levels in patients with slow coronary flow: relationship with Helicobacter pylori infection

BACKGROUND AND OBJECTIVE: Elevation of plasma homocysteine (Hcy) level has been implicated in the pathogenesis of slow coronary flow (SCF) as it can severely disturb vascular endothelial function. Helicobacter pylori chronically infect the human stomach and causes malabsorption of vitamin B(12) and folate in food, leading ultimately to an increase in circulating Hcy levels. METHODS: Forty-three patients with angiographically proven SCF (group I) were enrolled in this study; 43 cases with normal coronary flow pattern (group II) served as controls. Fasting plasma levels of Hcy, vitamin B(12), and folate were measured in all subjects. Presence of H. pylori infection was defined as positive 14 C urea breath test. Coronary flow patterns for each major epicardial coronary artery were determined with the Thrombolysis in Myocardial Infarction (TIMI) frame count method. RESULTS: Mean TIMI frame count was 46.3 +/- 8.7 in group I and 24.3 +/- 2.9 in Group II (p = .0001). Vitamin B(12) levels were similar, whereas folate levels were dramatically reduced in group I compared to group II (13.2 +/- 4.3 vs. 17.1 +/- 5.2, p = .0001). Plasma Hcy levels were significantly higher in group I compared to group II (13.4 +/- 5.6 vs. 7.9 +/- 2.5, p = .0001) as was the prevalence of H. pylori infection (90.7% in group I vs. 58.1% in group II, p = .001). Hcy levels were elevated (11.7 +/- 5.3 vs. 7.5 +/- 2.7, p = .0001) and folate levels were reduced (13.9 +/- 4.7 vs. 18.6 +/- 4.9, p = .0001) in patients with H. pylori infection, while vitamin B(12) levels were similar in patients with and without H. pylori infection. Correlation analysis revealed a significant negative correlation between plasma folate and Hcy levels and also between folate levels and mean TIMI frame counts (r = -.33, p = .002 vs. r = -.33, p = .003). Moreover, there was a significant positive correlation between plasma Hcy levels and mean TIMI frame counts (r = .66, p = .0001). In addition, the folate level was the only significant determinant of the variance of Hcy in multiple regression analysis (r = -.21, p = .03). CONCLUSION: Our data showed that plasma folate levels were decreased and plasma Hcy levels were increased in patients with SCF compared to controls. Also, the prevalence of H. pylori infection was increased in patients with SCF. These findings suggest that elevated levels of plasma Hcy, possibly caused by H. pylori infection, and/or a possible disturbance in its metabolism may play a role in the pathogenesis of SCF.     

Cardiovascular risk factors in subjects with Helicobacter pylori infection

Background. It has been proposed that Helicobacter pylori infection is related to cardiovascular disease, although this has not been fully investigated. The aim of this study was to investigate whether H. pylori in‐fection is associated with cardiovascular risk factors. Subjects and Methods. One thousand six hundred and fifty people undergoing annual medical checks at Shimane Institute of Health Science between September 1998 and August 1999 were enrolled. Gender, age, body mass index, habitual smoking and drinking, systolic and diastolic blood pressure, serum level of total cholesterol, triglyceride, high‐density lipoprotein cholesterol (HDLC), blood glucose, leukocyte count and hemoglobin were compared between H. pylori seropositive and seronegative cases. Results. In H. pylori seropositive individuals, HDLC was significantly lower than that in seronegative individuals. After adjustment for possible confounding factors (gender, age, BMI, smoking and drinking habits), mean HDLC in H. pylori‐seropositive and seronegative individuals were 56.1 and 58.2 mg/dl, respectively (p < .005). The percentage of the elderly (over 50 years old) individuals with HDLC < 35 mg/dl in H. pylori seropositive and seronegative groups were 7.4% and 4.7%, respectively (p < .001). In addition, the lower HDLC level was accompanied by an increased leukocyte count. Conclusion. Long‐term infection with H. pylori may have an important role in decreasing the serum HDLC concentration.     

Possible relationship between Helicobacter pylori infection and cap polyposis of the colon

BACKGROUND: Cap polyposis is a rarely encountered disease characterized by multiple distinctive inflammatory colonic polyps located from the rectum to the distal colon. The etiology of this disease is still unknown, and no specific treatment has been established. AIM: We report three cases of cap polyposis that were cured following eradication therapy for Helicobacter pylori infection. METHODS AND RESULTS: Three women were referred to Shinshu University Hospital because of mucoid and/or bloody diarrhea. Laboratory data showed hypoproteinemia in all cases; markers of inflammation such as C-reactive protein were negative. Colonoscopy revealed multiple sessile polyps with mucus adherent on the apices of the mucosal folds in the rectum and/or the sigmoid colon. The intervening mucosa was normal. Microscopic examinations of biopsy specimens taken from sessile polyps revealed inflamed mucosa with elongated tortuous crypts attenuated towards the mucosal surface. A granulation tissue 'cap' was observed on the surface of the mucosa. Various treatments were unsuccessful, including administration of metronidazole or prednisolone, avoidance of straining at defecation, and surgical or endoscopic resection. All were diagnosed with H. pylori infection in the stomach. Helicobacter pylori was not detected in the biopsy specimens from the colonic inflammatory polyps by immunohistochemical study using polyclonal anti-H. pylori antibody. After successful eradication therapy the clinical symptoms improved. Disappearance of cap polyposis was confirmed by colonoscopy in all three cases. CONCLUSION: We speculate that H. pylori infection might play a role in the pathogenesis of cap polyposis.     

Organ-specific autoantibodies in children with Helicobacter pylori infection

BACKGROUND: We compared the prevalence of organ-specific autoantibodies in a group of Helicobacter pylori infected children and a group of uninfected children and investigated the relationship between the presence of relevant autoantibodies and the status of the target organs. PATIENTS AND METHODS: One hundred and twenty-four children with dyspepsia (54 boys, 70 girls; mean age 10.5 years; range 4-19) underwent gastroscopy: 56 had H. pylori infection (31 girls, 25 boys), while 68 (37 girls and 31 boys), were H. pylori-negative. All sera were tested for the presence of: parietal cell autoantibodies (PCA), intrinsic factor autoantibodies (IFA), microsomial autoantibodies, thyroglobulin autoantibodies, islet cell autoantibodies, glutamic acid decarboxylase autoantibodies, adrenal cortex autoantibodies, steroid-producing cell autoantibodies; gastrin, pepsinogen A, pepsinogen C and anti-H. pylori antibodies. The histological features and the ureA and cagA genes were also considered. RESULTS: The frequency of organ-specific autoantibodies was higher in patients with H. pylori infection than in uninfected patients (chi2-test p < .0001). Specifically gastric autoantibodies were significantly higher: seven of the 56 H. pylori-positive children were PCA-positive and one was IFA-positive (chi2-test p = .0004). The presence of autoantibodies was not associated with any clinical or biohumoral signs of disease. CONCLUSIONS: Our study detected a relationship between H. pylori infection in childhood and the presence of organ-specific autoantibodies unassociated with any clinical or biohumoral signs of disease. Helicobacter pylori infection in childhood could trigger the onset of clinical autoimmune gastritis, and/or other clinical autoimmune diseases.