肝硬化患者幽门螺杆菌感染与血氨的关系

目的 :探讨幽门螺杆菌 (Hp)感染对肝硬化患者血氨浓度的影响。 方法 :35例肝硬化患者及 2 5例消化性溃疡患者分别测定Hp感染情况及空腹血氨浓度 ,对于Hp阳性病人口服质子泵抑制剂三联方案1周后测定空腹血氨。结果 :Hp阳性的肝硬化患者空腹血氨较Hp阴性的肝硬化患者空腹血氨显著升高(P <0 0 1)。根除Hp后 ,肝硬化患者空腹血氨浓度显著下降 (P <0 0 5 )。 结论 :Hp感染可引起肝硬化患者血氨浓度升高 ,对此类患者采用Hp根除治疗 ,可显著降低血氨浓度。抗Hp治疗可能有助于预防及治疗肝硬化患者的高氨血症及由此诱发的肝性脑病及亚临床肝性脑病。     

幽门螺杆菌感染对肝硬化患者高氨血症的影响

目的探讨幽门螺杆菌(Hp)感染对肝硬化患者血氨浓度的影响.方法 51例确诊为Hp阳性的肝硬化患者为阳性组,27例Hp阴性的肝硬化患者为阴性组,40例Hp阳性的消化性溃疡或胃炎患者为对照组.分别检验3组的血氨浓度并进行比较,应用三联法治疗1周,于4周后再测定3组的血氨并进行比较.结果阳性组与阴性组、对照组血氨浓度相比差异有显著性(P＜0.01).阴性组与对照组相比差异无显著性(P＞0.05),阳性组治疗前后血氨浓度变化差异有显著性(P＜0.01).阳性组不同肝功能分级组血氨浓度之间差异有显著性(P＜0.05);阴性组不同肝功能分级组血氨浓度之间差异无显著性(P＞0.05).结论幽门螺杆菌感染可导致肝硬化患者血氨的升高,根除Hp后可使血氨水平明显下降.     

幽门螺旋杆菌诱发肝硬化大鼠高氨血症的实验研究

目的：探讨幽门螺旋杆菌与肝硬化大鼠高氨血症的相关性。方法：选取32 只SD大鼠,将其随机分为正常组(n=8)、Hp 感染组 (n=8)、肝硬化组(n=8)、肝硬化合并Hp 感染组(n=8)。肝硬化组及肝硬化合并Hp 感染组给予50%四氯化碳橄榄油腹腔注射;正常 组与Hp 感染组给予同量的橄榄油腹腔注射。从建立模型的第9 周开始,Hp 感染组与肝硬化合并Hp 感染组每周感染2 次Hp,共 8 次。记录各组大鼠的一般状态,检测大鼠血氨水平及胃粘膜Hp数量。结果：与正常组比较,肝硬化组及肝硬化合并Hp感染组体 重较低(P＜0.05);与肝硬化组比较,肝硬化合并Hp 感染组体重较低(P＜0.05)。与正常组比较,其余各组胃粘膜Hp 数量较高(P＜ 0.05),与肝硬化组与Hp 感染组比较,肝硬化合并Hp 感染组胃粘膜Hp 数量高(P＜0.05)。与正常组比较,肝硬化组及肝硬化合并 Hp 感染组血氨水平高(P＜0.05),与肝硬化组比较,肝硬化合并Hp 感染组血氨水平高(P＜0.05)。结论：幽门螺旋杆菌能诱发肝硬 化大鼠高氨血症     

残胃的幽门螺杆菌感染及与胆汁反流关系探讨

目的 :探讨幽门螺杆菌 (Hp)感染与残胃及Hp与胆汁反流的关系。 方法 :用回顾性方法分析残胃患者 197例。结果 :Hp阳性检出患者中消化性溃疡术后与胃恶性肿瘤术后患者差异无显著性 (P >0 0 5 )。BillrothI式术后残胃炎组Hp阳性检出率为 75 4 % (4 9/ 6 5 ) ;而BillrothⅡ式术后残胃炎组Hp阳性检出率为 4 7 7% (6 3/ 132 ) ,二者差异有显著性 (P <0 0 1)。BillrothⅠ式术后组中伴有胆汁反流者 2 6 1%(17/ 6 5 ) ;BillrothⅡ式术后组中伴有胆汁反流者 5 9 8% (79/ 132 ) ,二者差异有显著性 (P <0 0 1)。胆汁反流组中Hp阳性检出率为 4 0 6 % (39/ 96 ) ;无胆汁反流组中Hp阳性检出率为 72 3% (73/ 10 1) ,二者差异有非常显著性 (P <0 0 1)结论 :残胃的Hp感染与胆汁反流有明显相关性。Hp感染可能是BillrothⅠ式术后残胃炎的主要病因 ;而胆汁反流可能是BillrothⅡ式术后残胃炎的主要病因 ,Hp感染为其另一因素。     

慢性胃炎粘膜内CD3+细胞,S-100+树突状细胞和nNOS表达与幽门螺旋杆菌感染的关系研究

目的　探讨幽门螺旋杆菌 (Hp)与慢性胃炎粘膜内CD3+ 细胞 ,S 10 0 + 树突状细胞和nNOS表达之间的关系。方法　用免疫细胞化学方法 ,检测Hp+ 和Hp 胃炎患者及正常人的胃窦部活检标本。结果　Hp+ 胃炎组胃窦粘膜内CD3+ 细胞和S 10 0 + 树突状细胞数量明显高于Hp-胃炎和正常组 ,且有显著性差异 (P <0 0 1和P <0 0 5 ) ,而nNOS呈高表达 ,与Hp-胃炎组相比有显著性差异 (P <0 0 1)。结论　Hp+ 胃炎患者胃窦粘膜内CD3+ 细胞和S 10 0 + 树突状细胞的增加是机体对Hp的免疫应答 ,而nNOS在Hp+ 胃炎组的高表达可能与Hp感染有密切关系。     

慢性多灶萎缩性胃炎患者胃酸分泌与Hp感染及血清胃泌素的关系

目的:探讨多灶萎缩性胃炎(BAG)患者胃酸分泌与幽门螺杆菌(HP)感染及血清胃泌素水平的关系。方法:根据病理结果将60例确诊的慢性BAG患者分为轻度、中度、重度BAG组,监测各组患者24小时胃内PH值的变化、血清胃泌素水平及HP感染情况。结果:随着萎缩程度的加重,HP阳性率、胃内中位PH值及算数均数p H值逐渐升高,血清胃泌素水平逐渐降低;轻度、中度、重度BAG组组间中位p H值、算数均数p H值及血清胃泌素水平比较有显著差异(均P0.05);重度BAG组HP感染与轻度组、中度组比较有统计学差异(均P0.05),而轻度组HP感染与中度组差异无统计学意义(P0.05)。结论:随着慢性BAG萎缩程度的加重,HP阳性率和p H值逐渐升高,血清胃泌素水平逐渐降低。HP感染、胃泌素水平及胃酸分泌水平三者相互影响,相互作用。     

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。     

输卵管妊娠时输卵管壁肥大细胞的研究

目的　探讨肥大细胞在输卵管妊娠中的数量变化及其与血清性激素的关系。方法 :取输卵管妊娠时的输卵管及月经周期的增生期、分泌期和正常宫内早孕时的输卵管 ,常规石蜡切片 ,用甲苯胺蓝染色法显示肥大细胞 ;用酶免疫分析法检测输卵管妊娠患者、正常育龄未孕妇女 (增生期和分泌期 )及正常宫内早孕妇女血清雌二醇和孕酮水平。结果 :输卵管妊娠患者血清雌二醇和孕酮水平均高于正常育龄未孕妇女 (增生期和分泌期 ) ,低于正常宫内早孕妇女 ,四组间两两比较差异均有显著性 (P <0 0 5 ) ;肥大细胞主要分布于输卵管肌层 ,其数量变化为 :输卵管妊娠组较增生期和分泌期这两组均少 ,差异均有显著性 (P <0 0 5 ) ,而增生期和分泌期这两组肥大细胞数量变化不明显 ,差异无显著性 (P >0 0 5 ) ;两例正常宫内早孕时的输卵管壁肥大细胞数量明显比输卵管妊娠组多 ,与增生期和分泌期这两组比较 ,肥大细胞数量变化不明显。结论 :1 人输卵管壁内肥大细胞的数量不受血清性激素水平的影响。 2 输卵管妊娠时肥大细胞数量减少     

下丘脑腹内侧核Orexin-1及其受体对大鼠胃酸分泌的影响及其机制

目的:探讨下丘脑腹内侧核Orexin-1及其受体对大鼠胃酸分泌的影响及其机制。方法:大鼠麻醉后侧脑室及VMH置管,大鼠分组后分别VMH注射orexin-A、[Pro~(34)]-酪酪肽、[c PP1-7、NPY~(19-23)、Ala~(31)、Aib~(32)、Gln~(34)]胰多肽;腹腔注射SB-334867;皮下注射阿托品;侧脑室微量注射GR-231118、CGP-71683。给药结束后使用幽门结扎模型检测大鼠的胃酸分泌。结果:OXA能够促进胃酸分泌,且呈量效依赖关系。腹腔注射SB-334867能够抑制胃酸分泌,且呈量效依赖关系;SB-334867能够抑制orexin-A对胃酸分泌的促进作用;阿托品不但能够抑制胃酸分泌并且还能够完全阻断OXA的促胃酸分泌作用。侧脑室微量注射GR-231118或CGP-71683胃酸及胃液量减少,呈量效依赖关系,并且能够完全阻断OXA的促胃酸分泌作用。VMH内微量注射[cPP~(1-7),NPY~(19-23),Ala~(31),Aib~(32),Gln~(34)]胰多肽胃酸分泌增多,且呈量效依赖关系。结论:Orexin-A能够作用于下丘脑VMH促进胃酸分泌,orexin受体、Y1和Y5受体以及迷走神经系统均参与该过程。     

幽门螺杆菌感染对慢性胃炎胃窦部EC细胞和CgA细胞的影响

目的探讨幽门螺杆菌（Helicobacter pylori Hp）感染与慢性胃炎（CG）患者胃窦粘膜内肠嗜铬细胞（Enterochromaffin,EC细胞）、嗜铬粒素A细胞（CgA细胞）变化的关系。方法采用免疫细胞化学方法,检测Hp相关性慢性胃炎胃窦部粘膜内EC细胞、CgA细胞的分布。结果1．Hp^＋组CgA^＋细胞数低,与Hp^＋组和正常组比较差异显著（P〈0．01）;2.EC细胞数随病理类型加重呈下降趋势,三组间的差异性极显著（P〈0．01）,慢性萎缩性胃炎组（CAG）CgA^＋细胞数与慢性非萎缩性胃炎（CNAG）组和正常组比较,差异极显著（P〈0．01）。结论Hp感染和慢性胃炎胃窦部EC细胞和CgA细胞之间存在密切关系。     

奥美拉唑与呋喃唑酮及阿莫西林联用治疗幽门螺杆菌阳性十二指肠肠溃疡的疗效观察

目的：观察奥美拉联用呋喃唑酮及阿莫西林治疗幽门螺杆菌(Hp)阳性十二指肠溃疡的临床疗效。方法：对45例经胃镜活检证实的Hp阳性十二指肠溃疡应用奥美拉唑20mg Bid 呋喃唑酮0．2g Bid 阿莫西林1．0g Bid,疗程1w。结果：45例病例中,42例愈合,40例根除,7d疼痛缓解率为87％。结论：呋喃唑酮三联疗法能有效地根除Hp,且不良反应少,疗效高,病人依从性好,价格适中,是较理想的方案,值得进一步尝试。     

Gastric Helicobacter pylori infection is associated with adverse metabolic traits in severely obese subjects

Objective:

Asian studies have reported on an association of Helicobacter pylori (Hp) infection with insulin resistance (IR) in normal‐weight subjects. Whether such an association likewise exists in European subjects with severe obesity was questioned.

Design and Methods:

To address this question, 370 severely obese patients from our database were identified, who had undergone a gastroscopy with a histological examination of gastric mucosal biopsies and a concurrent assessment metabolic blood parameters as a standard examination before bariatric surgery.

Results:

Seventy‐five (20.3%) of the subjects displayed a histologically proven Hp infection (Hp+). Sex distribution, age, and body mass index of Hp+ subjects did not differ from that of the subjects with no Hp infection (Hp–; all P > 0.293), but Hp+ subjects were significantly smaller (P = 0.006). Fasting glucose, insulin, high‐sensitive C reactive protein, and alanine aminotransferase levels as well as calculated indices of IR (i.e., HOMA‐IR, QUICKI) did not differ between Hp+ and Hp– subjects (all P > 0.42). However, Hp+ subjects showed significantly higher triglyceride levels and a higher total chloesterol‐to‐HDL ratio but lower sex‐hormone binding globulin (SHGB) levels than Hp– subjects (all P ≤ 0.05).

Conclusion:

While our results obtained in European severely obese patients do not provide evidence for an enhanced IR state associated with gastric Hp infection, they suggest that the presence of the bacterium in gastric biopsies is associated with an adverse lipid profile and reduced SHGB levels.     

Vacuolating cytotoxin A is associated with increased thrombin generation in gastric mucosa

BACKGROUND: Activation of the coagulation system is a critical response for both the repair of tissue injury and the host defense against microbial pathogens. Activation of the coagulation cascade culminates with the generation of thrombin. In vitro studies have shown that thrombin protects gastric epithelial cells from injury. The present study was undertaken to assess in vivo the relationship between gastric intramucosal generation of thrombin and Helicobacter pylori infection. MATERIALS AND METHODS: This study comprised 59 patients with gastroduodenal disorders. There were 27 patients with H. pylori infection (Hp+), 14 without it (Hp-), and 18 patients with cured H. pylori infection (Hp c). The gastric intramucosal concentrations of thrombin-antithrombin complex (TAT), epidermal growth factor (EGF), prostaglandin E2 (PGE2), and vacuolating cytotoxin A (VacA) were measured by specific immunoassays. RESULTS: The level of TAT was significantly increased in patients with Hp+ compared to Hp- and Hp c. The levels of TAT, EGF and PGE2 were higher in VacA (+) patients than in those with VacA (-). VacA induced significant expression of tissue factor in gastric epithelial cells in vitro. The gastric intramucosal level of VacA antigen was proportionally and significantly correlated with TAT, EGF and PGE2 in Hp+ patients. The level of TAT was proportionally and significantly correlated with EGF in Hp+ patients but not in Hp- and HP c patients. CONCLUSIONS: These results showed that VacA produced by H. pylori is associated with increased thrombin generation, and that thrombin may play a protective role in H. pylori-associated gastroduodenal disorders.     

The role of the host versus the environment in duodenal ulcer disease.

Gastric functions can be understood only in the context of a network including the brain gut axis, neuro-endocrine and paracrine mechanisms and growth factors. These host factors including parietal cell sensitivity (PCS) may well interact with an important environmental factor, Helicobacter pylori (Hp), and help to explain its actions. The aim of this study was to investigate PCS related to Hp status and duodenal ulcer (DU). PCS was assessed by constructing dose-response curves after pentagastrin and calculating the D50. Five groups of patients were studied: I) active DU, Hp pos. (8); II) history of DU, Hp pos. (8); III) asymptomatic Hp pos. (8); IV) asymptomatic Hp neg. (10); V) DU on maintenance H2 blocker therapy, Hp pos. (20). PCS was repeated after Hp eradication. PCS was lowest in group IV, and in Hp pos. groups, was significantly higher, with insignificant differences among them, irrespective of DU. PCS declined significantly after Hp eradication. Group V showed an insignificant decline in PCS during treatment, not preventing recurrence. A higher PCS in Hp infection irrespective of DU, declining after eradication, suggests that this may be a reversible epiphenomena related to Hp infection. This may offer an explanation as to why DU develops only in some subjects with Hp, suggesting the importance of the host in the pathogenesis of DU.     

Genetic factors in the development of gastric precancerous lesions--a role of Helicobacter pylori ?

Helicobacter pylori is believed to predispose to gastric cancer by inducing gastric precancerous alterations. There is a well known predisposition to gastric cancer and the risk of developing it is greater in relatives of patients with familial cases of this malignancy. The aim of this study was to determine the prevalence of gastric precancerous lesions (atrophy and intestinal metaplasia) and their association with Hp infection in first-degree relatives in patients with noncardia gastric cancer. METHODS: Hp status and gastric histology assessed by upper gastrointestinal endoscopy, biopsies from the antral and body region, the rapid urease test and staining for Hp, inflammation, activity, atrophy and intestinal metaplasia (prevalence and grading) were studied in 108 first-degree relatives of patients with noncardia gastric cancer and compared with 73 controls with mild non-ulcer dyspepsia who had no cancer relatives and were examined in the same way. RESULTS: subjects with and without cancer relatives had a similar prevalence of Hp infection (49 vs. 47%). Endoscopy revealed a few asymptomatic duodenal ulcers and small hiatus hernias in Hp positive subjects of both groups. Hp positive relatives of gastric cancer had a markedly higher prevalence of atrophy than those with Hp negativity without cancer relatives (29 vs. 9%) and those with Hp negativity and cancer relatives (29 vs. 3%. Prevalence of intestinal metaplasia was also higher in those with Hp positivity and cancer relatives than in those without cancer relatives (15 vs. 5% and was not present in Hp negative subjects with cancer relatives. Inflammation and activity showed similar scores in subjects with and without cancer relatives with higher scores in both Hp positive groups. The prevalence of precancerous lesions in the relatives of gastric cancer was nearly always confined to those with Hp positivity. One year after eradication the prevalence of atrophy in cancer relatives decreased from 29 to 14%; prevalence of intestinal metaplasia remained without substantial changes. Scores for inflammation and activity were also lower after eradication. CONCLUSIONS: First-degree relatives of patients with gastric cancer have an increased prevalence of gastric precancerous abnormalities which are strongly confined to those with Hp infection. Eradication of Hp in these subjects with cancer relatives reduces the prevalence of precancerous lesions (atrophy) and grades of inflammation and activity. In view of these results, eradication of Hp should be offered to such subjects.     

Triple eradication therapy counteracts functional impairment associated with Helicobacter pylori infection in Mongolian gerbils.

Gastric Helicobacter pylori (Hp) infection in Mongolian gerbils is an established experimental model of gastric carcinogenesis resulting from the long-term Hp infection but functional aspects accompanying this Hp-induced progression from gastritis to the cancer, especially changes in gastric acid secretion, gastric blood flow (GBF) and gastrin-somatostatin link have been little studied. It is unclear whether Hp eradication therapy alters the functional and the histopathological changes in this animal model of Hp-infection. We examined the effects of intragastric (i.g.) inoculation of Mongolian gerbils with Hp strain (cagA+ vacA+, 5 x 10(6) CFU/ml) that had been isolated from a patient with gastric ulcer as compared to those induced by vehicle (saline) in gerbils with or without gastric fistula (GF) at 1.2, 4, 6, 9, 12 and 30 wks upon gastric inoculation with this bacteria. An attempt was made to evaluate the influence of anti-Hp triple therapy with omeprazole, amoxicillin and tinidazol on gastric Hp-infection and Hp-induced functional impairment of the gastric mucosa. Gastric mucosal biopsy specimens were taken for the assessment of the morphological changes and the presence of Hp infection using rapid urease test (CLO-test) and the density of Hp-colonization were assessed by counting of the number of bacterial colonies per plate. Gastric blood flow (GBF) was measured by H2-gas clearance technique and the venous blood and the gastric content were collected for the measurement of plasma gastrin levels and the gastric luminal somatostatin level by radioimmunoassay (RIA). The Hp in gastric mucosa was detected in all animals by culture and rapid urease test at various periods upon Hp inoculation. Basal gastric acid in non-infected conscious gerbils with GF reached the level of about 28 +/- 4 micromol/h and this was reduced by over 50% immediately upon the Hp-inoculation and persisted for time intervals tested up to 30 wk. Early lesions were seen 4 wks after the Hp-inoculation and consisted of chronic gastritis with thickened gastric mucosal foldings and elongated interfoveolar ridges. Edema and congestion as well as significant mucosal inflammatory infiltration with lymphoid infiltrate in lamina propria of the mucosa occurred in all infected gerbils. Adenomatous hyperplasia with cellular atypia was observed at 12 wk upon Hp-inoculation together with increased mitotic activity and numerous apoptotic bodies formation, while lamina propria was reduced leaving dilated atypical gastric gland situated "back-to-back". This glandular atypia failed to show lamina propria or submucosa infiltration corresponding to gastric intraepithelial neoplasia. The GBF in Hp-infected gerbils was significantly lower, and a 6-7 fold increase in plasma gastrin levels combined with a significant fall in gastric luminal somatostatin contents observed at all tested periods as compared to vehicle-controls and these effects were counteracted by anti-Hp triple therapy. We conclude that: 1). Hp-infection in Mongolian gerbils in early stages before adenocarcinoma formation results in the development of typical functional and pathological changes such as suppression of gastric secretion and impairment of both, gastric mucosal microcirculation and gastrin-somatostatin link, and 2). this deleterious influence of Hp on gastric morphology and gastric functions is greatly attenuated in gerbils treated with Hp-eradication therapy.     

13C-Urea breath test is superior in sensitivity to detect Helicobacter pylori infection than either antral histology or rapid urease test.

There is no single technique which fulfils the criterion for a reference method to detect Helicobacter pylori (Hp) infection. The aim was to compare the results of antral histology (H), rapid urease test (U) and urea breath test (UBT) from antral biopsy samples in patients having gastric or duodenal lesions during upper GI endoscopy. We used the following methods: 1) biopsy specimens for histology (Warthin-Starry staining); 2) rapid urease test; and 3) 13C-urea breath test with infrared spectrometry. The total number of patients was 166 examined by H, U, and UBT. H, U and UBT were negative (-) in 64 patients and positive (+) in 51. The true positivity and false negativity (%, number of patients in parentheses) of each method based upon the positivity of the other two tests were: H+, U+ (54): UBT+, 94.4% (51) and UBT-, 5.6% (3); H+, UBT+ (57): U+, 89.5% (51) and U-, 10.5% (6); U+, UBT+ (65): H+, 78.5% (51) and H-, 21.5% (14). If Hp infection is considered to be positive when at least two tests detect the presence of Hp, UBT shows the highest sensitivity in comparison to histology of biopsy specimens and urease test. UBT is highly recommended as a screening test for Hp infection in patients presenting upper GI endoscopic alterations.     

幽门螺杆菌在慢性阻塞性肺疾病发生及 发展过程中的作用

目的研究幽门螺杆菌(Helicobacter pylori,H.pylori)在慢性阻塞性肺疾病(COPD)发生及发展过程中的作用。方法对85例COPD患者(COPD组)和85例体检健康者(对照组)进行血清抗H.pylori抗体(抗Hp-IgG)检测,比较两组的抗Hp-IgG水平及H.pylori阳性率。全部COPD患者均行肺功能和免疫功能检查,分析抗Hp-IgG水平与COPD严重程度的相关性,比较合并H.pylori感染与无H.pylori感染COPD患者之间,以及合并H.pylori感染COPD患者根除H.pylori前后免疫功能的差异。结果 COPD组血清抗Hp-IgG水平和H.pylori阳性率均明显高于对照组(P0.05),FEV1%预计值与血清抗Hp-IgG水平呈负相关(P0.05)。与无H.pylori感染的COPD患者相比,合并H.pylori感染的COPD患者外周血CD_3~+和CD_4~+T细胞含量、CD_4~+/CD_8~+比值、血清免疫球蛋白(IgA、IgG、IgM)水平均明显较低(P0.05),经H.pylori根除治疗后各指标水平明显升高(P0.05)。结论 H.pylori感染可导致宿主免疫功能紊乱,可能因此促进了COPD的发生和发展。根除H.pylori可明显改善合并H.pylori感染COPD患者的免疫功能,有利于患者恢复。     

嗜酸乳杆菌(乐托尔)治疗幽门螺杆菌感染疗效

目的 :观察嗜酸乳杆菌 (乐托尔 )对人胃内幽门螺杆菌的治疗作用。方法 :经证实 Hp感染阳性的胃、十二指肠溃疡病人 ,分别给予嗜酸乳杆菌治疗组与胃三联的对照组 ,给药后观察临床症状恢复情况 ,溃疡愈合情况 ,胃粘膜 Hp感染情况 ;结果 :(1)总的临床症状改善率治疗组总有效率为 89.8% (35 / 37) ,对照组为 92 .9% (34/ 36 ) ,两组比较差异无显著性。 (2 )溃疡愈合率 :两组病人愈合治疗组与对照组分别是85 .9% (5 5 / 6 4 )和 92 .1% (71/ 77) ,两组χ2 检验比较差异无显著性 (P<0 .0 5 )。 (3) Hp转阴率 :两组在 4周末分别是治疗组 6 7.3% (33/ 4 9)和 84 .5 % (49/ 5 8) ,两组比较差异无显著性 (P>0 .0 5 )。结论 :嗜酸乳杆菌在抑制 Hp感染作用与抗菌素相仿 ,值得临床上应用 ,是临床上抗 Hp感染治疗极的前途的药物之一。