Expression of mutant type-p53 products in H pylori-associated chronic gastritis

AIM:To investigate the mutation of p 53 immuno-histochemically in non-tumorous gastric mucosa with H pylori infection before and after H pylori eradication therapy.METHODS:53 subjects(36 male,17 female,mean age ± SEM,57.1 ± 12.1)undergoing endoscopic examination were included in this study.42 of 53 patients were H pylori-positive,and 11 were H pylori-negative.All H pylori-positive patients had successful eradication therapy.Biopsy specimens were taken from five points of the stomach,as recommended by the updated Sydney system.Immunohistochemical studies were performed by using primary antibodies against p53(DO-7 and PAb240).RESULTS:p53(DO-7 and PAb240)immunoreactivity was shown in the neck region of the gastric pits,however,quite a few cells were found to be immunopositive for p 53(PAb240)in the H pylori-infected gastric mucosa.The proportion of patients immunopositive for p 53(PAb240)was significantly reduced 6 mo after eradication [28/42(66.7%)to 6/42(14.3%)](P < 0.05),while the biopsies taken from H pylori-negative patients showed no immunoreactivity for p53(PAb240).p53(PAb240)-positive patients were divided into two groups by the number of positive cells detected:one with more than six positive cells per 10 gastric pits(group A,n = 12),and the other with less than five positive cells per 10 gastric pits(group B,n = 30).Atrophy scores in group A were significant higher than those in group B at the greater curvature of the antrum(group A:2.00 ± 0.14 vs group B:1.40 ± 0.15,P = 0.012),the lesser curvature of the corpus(group A:2.00 ± 0.21 vs group B:1.07 ± 0.23,P = 0.017),and the greater curvature of the corpus(group A:1.20 ± 0.30vs group B:0.47 ± 0.21,P = 0.031).Group A showed significant higher intestinal metaplasia scores than group B only at the lesser curvature of the antrum(group A:2.10 ± 0.41 vs group B:1.12 ± 0.29,P = 0.035).CONCLUSION:H pylori-associated chronic gastritis expressed the mutant-type p53,which was significantly associated with more severe atrophic and metaplastic changes.H pylori eradication led to a significant reduction in the expression of the mutant-type p53.It is considered that H pylori-infected chronic gastritis is associated with a genetic instability that leads to gastric carcinogenesis,and H pylori eradication may prevent gastric cancer.

Prevalence of H pylori associated 'high risk gastritis' for development of gastric cancer in patients with normal endoscopic findings

AIM: To investigate the prevalence of H pylori associated corpus-predominant gastritis (CPG) or pangastritis, severe atrophy, and intestinal metaplasia (IM) in patients without any signifi cant abnormal fi ndings during upper- GI endoscopy. METHODS: Gastric biopsies from 3548 patients were obtained during upper GI-endoscopy in a 4-year period. Two biopsies from antrum and corpus were histologically assessed according to the updated Sydney-System. Eight hundred and forty-fi ve patients (mean age 54.8 ± 2.8 years) with H pylori infection and no peptic ulcer or abnormal gross fi ndings in the stomach were identifi ed and analyzed according to gastritis phenotypes using different scoring systems. RESULTS: The prevalence of severe H pylori associated changes like pangastritis, CPG, IM, and severe atrophy increased with age, reaching a level of 20% in patients of the age group over 45 years. No differences in frequencies between genders were observed. The prevalence of IM had the highest increase, being 4-fold higher at the age of 65 years versus in individuals less than 45 years. CONCLUSION: The prevalence of gastritis featuring at risk for cancer development increases with age. These findings reinforce the necessity for the histological assessment, even in subjects with normal endoscopic appearance. The age-dependent increase in prevalence of severe histopathological changes in gastric mucosa, however, does not allow estimating the individual risk forgastric cancer development-only a proper follow-up can provide this information.

Direct measurement of gastric H^+/K^+-ATPase activities in patients with or without Helicobacter pylori-associated chronic gastritis

AIM: The role of Helicobacter pylori (H pylori) infection in gastric acid secretion of patients with chronic gastritisremains controversial. This study was designed to elucidate the effect of H pylori on H+/K+-ATPase activities in gastric biopsy specimens.METHODS: Eighty-two patients with chronic gastritis who had undergone upper endoscopy were included in this study. H pylori infection was confirmed by rapid urease test and histology. Gastric H+/K+-ATPase activities and serum gastrin concentrations were measured by an enzymatic method and radioimmunoassay, respectively. For those patients who received triple therapy for eradicating H pylori, changes in the activity of gastric H+/K+-ATPase and serum gastrin levels were also measured. RESULTS: The mean gastric H+/K+-ATPase activity in H pyloripositive group (42 patients) was slightly higher than thatin H pylori-negative group (29 patients) (169.65±52.9 and eradication of H pylori, the gastric H+/K+-ATPase activities slightly decreased compared to prior therapy (165.03±59.50 The mean basal gastrin concentration was slightly higher in H pylori-positive patients than in H pylori-negative patients (87.92±39.65 pg/mL vs75.04± 42.57 pg/mL, P= 0.228). The gastrin levels fell significantly after the eradication of Hpylori. (Before treatment 87.00±30.78 pg/mL, aftertreatment 64.73±18.96 pg/mL, P = 0.015).CONCLUSION: Gastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronicgastritis.

Effects of Chaihu Guizhi Ganjiang Decoction Combined with Standard Triple Therapy on Reducing Serum CagA and Hp-NAP in Patients with H.pylori-Related Gastritis

OBJECTIVE: To explore the effects of Chaihu Guizhi Ganjiang Decoction combined with standard triple therapy on treating H.pylori-related gastritis. METHODS: Eighty-two patients with H. pylori-related gastritis treated in our hospital from January 2016 to December 2017 were selected according to the random number table method and divided into experimental group and control group, with 41 patients in each group. The control group was treated with standard triple therapy, while the experimental group was additionally treated with modified Chaihu Guizhi Ganjiang Decoction. The venous blood of one elbow was taken before and after treatment. The concentrations of serum CagA and Hp-NAP were detected by enzyme-linked immunosorbent assay(ELISA). The symptoms were evaluated according to the change of symptom scores before and after the intervention. The H.pylori eradication rate was calculated. RESULTS: There was no significant difference in CagA and Hp-NAP concentrations between the 2 groups before intervention(P > 0.05). After intervention, CagA and Hp-NAP concentrations in experimental group were(19.21±6.27) ng/L and(24.37±6.10) ng/L respectively which were lower than(25.81±7.14) ng/L and(32.09±5.73) ng/L of control group. The differences were statistically significant(P < 0.05). The total effective rate of major symptoms in experimental group was 39 cases(95.12%), which was significantly higher than that of the control group(31 cases, 75.61%). There was statistically significant difference between the 2 groups(P < 0.05). The eradication rate of H.pylori was 38 cases(92.68%) in the experimental group, which was significantly higher than 31 cases(75.61%) of the control group. The difference between the 2 groups was statistically significant(P < 0.05). CONCLUSION: Chaihu Guizhi Ganjiang Decoction combined with standard triple therapy can effectively reduce CagA, Hp-NAP of serum level in patients with H.pylori-related gastritis, improve efficacy of symptoms and eradication rate of H.pylori, and is worthy of clinical promotion.

兰索拉唑、阿莫西林二联疗法治疗幽门螺杆菌相关性慢性胃炎的疗效分析

目的 探讨对幽门螺杆菌(Hp)相关性慢性胃炎患者给予兰索拉唑、阿莫西林二联疗法治疗后获得的临床疗效。方法 120例Hp相关性慢性胃炎患者,以投掷硬币法分为参照组和研究组,每组60例。参照组患者施以兰索拉唑治疗,研究组患者施以兰索拉唑、阿莫西林二联疗法治疗。比较两组患者炎症因子水平[白细胞介素-8(IL-8)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)]、Hp清除率、复发率以及不良反应(口苦、胃肠道反应、皮肤反应以及头晕)发生率。结果 治疗后,研究组患者IL-8、IL-6、TNF-α水平分别为(7.63±1.32)ng/L、(16.39±3.22)ng/L、(1.21±0.42)μg/ml,显著低于参照组的(9.39±1.55)ng/L、(34.52±13.49)ng/L、(1.85±0.53)μg/ml(P<0.05)。研究组患者Hp清除率98.33%(59/60)高于参照组的81.67%(49/60),复发率1.67%(1/60)低于参照组的13.33%(8/60)(P<0.05)。研究组患者不良反应发生率5.00%与参照组的3.33%比较,未呈现出明显差异(P>0.05)。结论 临床对Hp相关性慢性胃炎患者在治疗期间应用兰索拉唑+阿莫西林二联疗法,可将患者的炎症因子水平显著改善,同时将Hp清除率提高,将复发率降低,并且不会导致口苦、胃肠道反应、皮肤反应以及头晕等不良反应增加,疗效显著。

幽门螺杆菌相关慢性胃炎的胃微生态特征分析

目的探讨幽门螺杆菌(H.pylori)相关慢性非萎缩性胃炎和慢性萎缩性胃炎的胃菌群特征及差异。方法采用前瞻性研究设计,将24例H.pylori感染的慢性胃炎患者分为慢性非萎缩性胃炎组(n=18)和慢性萎缩性胃炎组(n=6)。测定2组的胃黏膜菌群特征,并进行Alpha和Beta多样性分析及物种相关性分析。结果2组胃菌群均主要包括变形菌门、拟杆菌门、厚壁菌门、放线菌门和梭杆菌门。2组胃菌群的物种多样性和丰度差异具有统计学意义(ANOSIM分析,P=0.046)。慢性萎缩性胃炎组的梭杆菌属(P=0.023)、纤毛菌属(P=0.047)、普雷沃菌属(P=0.016)、月形单胞菌属(P=0.042)和密螺旋体属(P=0.006)显著富集,H.pylori呈下降趋势(P=0.218)。胃黏膜菌群的部分菌属与H.pylori呈负相关性,且慢性萎缩性胃炎的胃黏膜菌群中与H.pylori负相关的菌属种类明显减少。结论慢性萎缩性胃炎的胃黏膜中梭杆菌属、纤毛菌属、普雷沃菌属、月形单胞菌属和密螺旋体属显著富集,与慢性胃炎进展相关。

SD大鼠H.pylori感染胃炎模型的建立

目的尝试在SPF级SD大鼠胃内定植H.pylori,以建立大鼠H.pylori感染胃炎模型。方法选用SD大鼠30只,随机分为5组,即对照组及4个模型组,模型组分别予NaHCO3溶液、56%酒精、消炎痛溶液、NaHCO3+消炎痛溶液联合H.pylori菌液灌胃造模,灌胃隔天1次,连续5次,并于最后一次灌胃结束后第2、4、6周处死大鼠,取胃黏膜组织分别记录损伤指数、进行快速尿素酶试验、胃黏膜涂片及病理切片。结果每组大鼠数、快速尿素酶试验及革兰染色阳性数:NaHCO3溶液+H.pylori组分别为6、4、4,56%酒精+H.pylori组分别为6、6、1,消炎痛溶液+H.pylori组分别为5、4、4,NaHCO3+消炎痛溶液+H.pylori组分别为4、4、4。损伤指数及病理切片:对照组胃黏膜形态正常,无损伤,各模型组胃黏膜肉眼观察均有不同程度的损伤,病理切片观察第2周有少量淋巴细胞浸润,第4周大量淋巴细胞及中性粒细胞浸润,腺体破坏,为活动性胃炎,第6周有大量淋巴细胞及中性粒细胞浸润,但损伤无进行性加重。结论 4种造模方式均可使H.pylori在SPF级大鼠胃内定植,定植时间至少长达6周,并能导致胃黏膜炎性损伤,损伤在第4周时最为严重,但以NaHCO3+消炎痛溶液+H.pylori造模最为成功,值得推广。

茯苓酸调节PI3K/AKT/NF-κB信号通路对大鼠幽门螺旋杆菌相关性胃炎的治疗作用

目的 探讨茯苓酸(PA)对大鼠幽门螺旋杆菌(Hp)相关性胃炎的治疗效果及作用机制。方法 建立Hp相关性胃炎大鼠模型;所有大鼠分为对照组(CT组)、模型组(M组)、PA低剂量组(PA L组)和PA高剂量组(PA H组)、PA H+磷脂酰肌醇3-激酶(PI3K)激活剂(740 Y-P)组;评估各组大鼠胃黏膜损伤指数(UI),透射电子显微镜观察胃黏膜细胞形态学,HE染色评价胃黏膜病理学特征,ELISA检测胃组织白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、IL-10、诱导型一氧化氮合酶(iNOS)、超氧化物歧化酶(SOD)的水平,Western blot法检测PI3K、磷酸化-PI3K(p-PI3K)、蛋白激酶B(AKT)、p-AKT、核因子(NF)-κB p65、p-NF-κB p65蛋白表达。结果 与CT组比较,M组大鼠胃黏膜糜烂,上皮水肿、充血、溃疡严重,上皮细胞固缩,炎性细胞浸润,UI、IL-6、TNF-α、iNOS以及p-PI3K/PI3K、p-AKT/AKT、p-NF-κB p65/NF-κB p65蛋白表达水平升高,IL-10和SOD水平降低(P<0.05);与M组比较,PA L组、PA H组大鼠胃黏膜损伤改善,炎性细胞浸润减少,UI、IL-6、TNF-α、iNOS以及p-PI3K/PI3K、p-AKT/AKT、p-NF-κB p65/NF-κB p65蛋白表达水平降低,IL-10和SOD水平升高(P<0.05);与PA H组比较,PA H+740 Y-P组大鼠胃黏膜病理损伤加重,上皮细胞固缩,UI、IL-6、TNF-α、iNOS以及p-PI3K/PI3K、p-AKT/AKT、p-NF-κB p65/NF-κB p65蛋白表达水平升高,IL-10和SOD水平降低(P<0.05)。结论 PA可能通过抑制PI3K/AKT/NF-κB信号通路发挥对大鼠Hp相关性胃炎的治疗作用。

甘草甜素对大鼠幽门螺杆菌相关性胃炎的改善作用及机制

目的探讨甘草甜素(GL)对大鼠幽门螺杆菌(HP)相关性胃炎的改善作用及机制。方法以接种1×10^(9) cfu/mL HP建立HP相关性胃炎大鼠模型,将造模成功大鼠随机分为模型组、阳性对照组(HP标准四联方案)和GL低、中、高剂量组(5、20、50mg/kg),每组12只;另取12只正常大鼠作为正常对照组。除正常对照组和模型组大鼠灌胃等体积生理盐水外,其他各组大鼠灌胃相应药物,每天1次,连续30 d。给药结束后大鼠行13C尿素呼气试验,记录超基准值(DOB);观察大鼠胃黏膜组织病理变化和细胞形态学变化,并进行病理评分;检测大鼠胃黏膜组织中白细胞介素8(IL-8)、IL-1β、肿瘤坏死因子α(TNF-α)、活性氧(ROS)、丙二醛(MDA)水平,高迁移率族蛋白B1(HMGB1)、核因子κB(NF-κB)m RNA相对表达量,一氧化氮合酶(iNOS)、HMGB1蛋白相对表达量以及NF-κB p65磷酸化水平。结果与正常对照组比较,模型组大鼠DOB值,胃黏膜组织病理评分,IL-8、IL-1β、TNF-α、ROS、MDA水平,HMGB1、NF-κB mRNA相对表达量,iNOS、HMGB1蛋白相对表达量和NF-κB p65磷酸化水平均显著升高(P<0.05);大鼠胃黏膜上皮细胞结构不完整且数量减少,细胞碎片及空泡增多,细胞固缩明显。与模型组比较,GL各剂量组和阳性对照组上述指标变化均显著逆转(P<0.05),且GL高剂量组上述指标变化均较GL低、中剂量组更显著(P<0.05);大鼠胃黏膜细胞病理变化均改善。结论GL可能通过抑制HMGB1/NF-κB信号通路的激活,抑制炎症和氧化应激反应,从而减轻HP引起的胃黏膜损伤。

Influence of H pylori on plasma ghrelin in patients without atrophic gastritis

AIM:To determine the association between H pylori infection and serum ghrelin levels in patients without atrophic gastritis.METHODS:Fifty consecutive patients(24 males and 26 females)with either H pylori-positive gastritis(n = 34)or H pylori-negative gastritis(n = 16)with normal gastric acid secretion determined by 24-h pHmetry and without atrophic gastritis in histopathology were enrolled in this study.Thirty-four H pylori-infected patients were treated with triple therapy consisting of a daily regimen of 30 mg lansoprazole bid,1 g amoxicillin bid and 500 mg clarithromycin bid for 14 d,followed by an additional 4 wk of 30 mg lansoprazol treatment.H pylori infection was eradicated in 23 of 34(67.6%)patients.H pylori-positive patients were given eradication therapy.Gastric acidity was determined via intragastric pH catethers.Serum ghrelin was measured by radioimmunoassay(RIA).RESULTS:There was no signifficant difference in plasma ghrelin levels between H pylori-positive and H pylori-negative groups(81.10 ± 162.66 ng/L vs 76.51 ± 122.94 ng/L).In addition,there was no significant difference in plasma ghrelin levels and gastric acidity levels measured before and 3 mo after the eradication therapy.CONCLUSION:H pylori infection does not influence ghrelin secretion in patients with chronic gastritis without atrophic gastritis.

Effects of bile reflux on gastric mucosal lesions in patients with dyspepsia or chronic gastritis

AIM: To investigate the influences of bile reflux on profiles of gastric mucosal lesions in patients with dyspepsia or chronic gastritis.METHODS: A total of 49 patients diagnosed with dyspepsia and chronic gastritis underwent 24-h ambulatory andsimultaneous monitoring of intragastric bilirubin absorbance and pH values, and then they were divided into bile refluxpositive group and bile reflux negative group. Severity of pathological changes in gastric mucosa including activeinflammation, chronic inflammation, intestinal metaplasia, atrophy and dysplasia as well as Helicobacter pylori (H pylori) infection at the corpus, incisura and antrum were determined respectively according to update Sydney system criteria. The profiles of gastric mucosal lesions in the two groups were compared, and correlations between time-percentage of gastric bilirubin absorbance ＞0.14 and severity of gastric mucosal lesions as well as time-percentage of gastric pH ＞4 were analyzed respectively. RESULTS: Thirty-eight patients (21 men and 17 women, mean age 44.2 years, range 25-61 years) were found existing with bile reflux (gastric bilirubin absorbance ＞0.14) and 11 patients (7 men and 4 women, mean age 46.2 years,range 29-54 years) were bile reflux negative. In dyspepsia patients with bile reflux, the mucosal lesions such as active inflammation, chronic inflammation, intestinal metaplasia, atrophy or H pylori infection in the whole stomach, especially in the corpus and incisura, were significantly more severe than those in dyspepsia patients without bile reflux. Moreover, the bile reflux time was well correlated with the severity of pathological changes of gastric mucosa as well as H pylori colonization in the near-end stomach, especially in the corpus region. No relevance was found between the time of bile reflux and pH ＞4 in gastric cavity. CONCLUSION: Bile reflux contributes a lot to mucosal lesions in the whole stomach, may facilitate H pylori colonization in the corpus region, and has no influence on acid-exposing status of gastric mucosa in patients with dyspepsia or chronic gastritis.

Relationship between the cytotoxin-associated gene-A status of H pylori strains and cerebral infarction in European Caucasians and Chinese Han: A meta-analysis

AIM:To study the relationship between the cytotoxin-associated gene-A (CagA) status of H pylori strains and cerebral infarction among European Caucasians and Chinese Han by conducting a meta-analysis. METHODS:Ten case-control studies, with data on a total of 907 cases and 966 controls, were retrieved and considered;disqualified studies were excluded. The included studies were then tested for heterogeneity, and a meta-analysis was performed. RESULTS:The combined data revealed CagA-bearing strains of H pylori which cause chronic infection are associated with an increased risk of cerebral infarction (OR = 2.66, 95% CI:2.17-3.26), but no such relationship was found with CagA-negative strains (OR = 0.74, 95% CI:0.49-1.10) in the overall population. We performed subgroup analyses, dividing the overall population into European Caucasians and Chinese Han subgroups, and analyzed the studies according to their subgroup classification. Through the subgroup analysis, an association between cerebral infarction and CagA-bearing strains was found in both subgroups (OR = 2.60, 95% CI:1.93-3.49 in Chinese Han;OR = 2.71, 95% CI:2.05-3.59 in European Caucasians), but no significant association was found between cerebral infarction and CagA-negative strains (OR = 0.81, 95% CI:0.45-1.48 in Chinese Han;OR = 0.64, 95% CI:0.37-1.09 in European Caucasians).CONCLUSION:These results suggest CagA-bearing strains of H pylori are significantly associated with susceptibility to cerebral infarction in Chinese Han and European Caucasians, but that CagA-negative strains are not a definite predisposing factor in either subgroup. The magnitude of this association with cerebral infarction needs to be confirmed by prospective studies and combined studies of H pylori eradication.

Red wine and green tea reduce H pylori- or VacA-induced gastritis in a mouse model

AIM: To investigate whether red wine and green tea could exert anti-H pylori or anti-VacA activity in vivo in a mouse model of experimental infection.METHODS: Ethanol-free red wine and green tea concentrates were administered orally as a mixture of the two beverages to H pylori infected mice, or separately to VacA-treated mice. Gastric colonization and gastric in? ammation were quantifi ed by microbiological, histopathological, and immunohistochemical analyses. RESULTS: In H pylori -infected mice, the red wine and green tea mixture significantly prevented gastritis and limited the localization of bacteria and VacA to the surface of the gastric epithelium. Similarly, both beverages significantly prevented gastric epithelium damage in VacA-treated mice; green tea, but not red wine, also altered the VacA localization in the gastric epithelium. CONCLUSION: Red wine and green tea are able to prevent H pylori -induced gastric epithelium damage, possibly involving VacA inhibition. This observation supports the possible relevance of diet on the pathological outcome of H pylori infection.

H pylori infection and other risk factors associated with peptic ulcers in Turkish patients: A retrospective study

AIM: To identify and evaluate the relative impact of H pylori infection and other risk factors on the occurrence of gastric ulcer (GU), duodenal ulcer (DU) and gastritis in Turkish patients. METHODS: A total of 4471 patients (48.3% female) out of 4863 attended the Samatya hospital in Istanbul (June 1999 - October 2003) were included. The records of H pylori status (CLO-test), endoscopic f indings of GU, DU and gastritis, personal habits (smoking, alcohol intake) and medication [non-steroidal anti-inflammatory drugs (NSAIDs), aspirin intake] were analyzed using multi-way frequency analysis. RESULTS: We have found that GU in the presence of H pylori had significant association with aspirin (P = 0.0001), alcohol (P = 0.0090) and NSAIDs (P = 0.0372). DU on the other hand had significant association with aspirin/ smoking/NSAIDs (P = 0.0259), aspirin/alcohol (P = 0.0002) and aspirin/smoking (P = 0.0233), also in the presence of H pylori. In the absence of H pylori GU had significant association with alcohol/NSAIDs (P = 0.0431), and NSAIDs (P = 0.0436). While DU in the absence of H pylori had significant association with smoking/alcohol/ NSAIDs (P = 0.0013), aspirin/NSAIDs (P = 0.0334), aspirin/alcohol (P = 0.0360). CONCLUSION: In the presence of H pylori, aspirin, alcohol and NSAIDs intake act as an independent risk factors that had an augmenting impact on the occurrence of GU and only together on the occurrence of DU in Turkish patients.

Furazolidone-based triple therapy for H pylori gastritis in children

AIM: To evaluate the furazolidone-based triple therapy in children with symptomatic H pylori gastritis.METHODS: A prospective and consecutive open trial was carried out. The study included 38 patients with upper digestive symptoms suffi ciently severe to warrant endoscopic investigation. H pylori status was defined based both on histology and on positive 13C-urea breath test. Drug regimen was a seven-day course of omeprazole, clarithromycin and furazolidone (100 mg, 200 mg if over 30 kg) twice daily. Eradication of H pylori was assessed two months after treatment by histology and 13C-urea breath test. Further clinical evaluation was performed 7 d, 2 and 6 mo after the treatment. RESULTS: Thirty-eight patients (24 females, 14 males) were included. Their age ranged from 4 to 17.8 (mean 10.9 ± 3.7) years. On intent-to-treat analysis (n = 38), the eradication rate of H pylori was 73.7% (95% CI, 65.2%-82%) whereas in per-protocol analysis (n = 33) it was 84.8% (95% CI, 78.5%-91%). All the patients with duodenal ulcer (n = 7) were successfully treated (100% vs 56.2% with antral nodularity). Side effects were reported in 26 patients (68.4%), mainly vomiting (14/26) and abdominal pain (n = 13). Successfully treated dyspeptic patients showed improvement in 78.9% of H pylori-negative patients after six months and in 50% of H pylori-positive patients after six months of treatment.CONCLUSION: Triple therapy with furazolidone achieves moderate effi cacy in H pylori treatment. The eradicationrate seems to be higher in patients with duodenal ulcer.

头花蓼调控H.pylori相关性胃炎信号通路的作用机制

目的 NF-κB信号通路的激活在幽门螺杆菌相关性胃炎的发生发展中起到重要作用。文中旨在研究头花蓼在治疗HAG中NF-κB信号通路的作用,并观察其是否通过沉默信息调节因子1(SIRT1)调控NF-κB的乙酰化影响HAG的治疗效果。方法培养人永生化胃黏膜上皮细胞(GES-1),将H.pylori标准菌株ATCC700392按100∶1复制HAG细胞模型,随机分为模型组和头花蓼组,头花蓼组以80μg/m L的头花蓼进行处理,模型组以H.pylori与GES-1细胞共培养,未做任何处理的GES-1细胞设为对照组;Real time PCR检测SIRT1、NF-κB/p65和肿瘤坏死因子α(TNF-α)mRNA水平;Western blot检测总蛋白中SIRT1、NF-κB/p65及其乙酰化蛋白表达水平,细胞质、细胞核蛋白中SIRT1和NF-κB/p65的表达水平。结果 H.pylori感染GES-1细胞12 h后,培养上清液中TNF-α水平较对照组升高[(2.02±0.60)vs(1.02±0.42),P<0.05]。与对照组相比,模型组SIRT1表达含量下降[(1.637±0.085)vs(1.000±0.127),P<0.05],NF-κB/p65表达增加[(0.488±0.258)vs(1.000±0.044),P<0.05],TNF-αmRNA表达增加[(0.356±0.019)vs(1.011±0.019),P<0.05];头花蓼组SIRT1mRNA水平(3.474±0.349)上调,TNF-α表达(0.532±0.008)下调(P<0.05)。与模型组相比,头花蓼组SIRT1mRNA表达升高,NF-κB/p65及TNF-α表达下降(P<0.05)。与对照组比,模型组SIRT1蛋白表达水平下降,NF-κB/p65、Acetyl-NF-κB p65(Lys310)和TNF-α蛋白表达升高(P<0.05);头花蓼组SIRT1表达升高(P<0.05)。与模型组进行比较,头花蓼组SIRT1表达升高,而NF-κB/p65、AcetylNF-κB p6(Lys310)和TNF-α蛋白表达下降(P<0.05)。与对照组相比,模型组SIRT1在细胞质中表达下降(P<0.05),而在细胞核表达明显升高(P<0.05);头花蓼组SIRT1细胞质中表达下降,细胞核中表达明显升高(P<0.05),NF-κB/p65细胞质中表达上调(P<0.05)。与模型组相比,头花蓼组SIRT1在细胞质无明显变化,在细胞核明显表达上调(P<0.05);NF-κB/p65细胞质中表达升高,细胞核中则表达下调(P<0.05)。结论头花蓼能够活化胞核中的SIRT1,使胞核中活化的NF-κB/p65进行去乙酰化修饰来拮抗H.pylori诱导引发的细胞损伤。

Expression of mucosal addressin cell adhesion molecule 1 on vascular endothelium of gastric mucosa in patients with nodular gastritis

AIM: The interaction of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) with integrin α4β7 mediates lymphocyte recruitment into mucosa-associated lymphoid tissue (MALT). Nodular gastritis is characterized by a unique military pattern on endoscopy representing increased numbers of lymphoid follicles with germinal center, strongly associated with H pylori infection. The purpose of this study was to address the implication of the MAdCAM-1/integrin β7 pathway in NG.METHODS: We studied 17 patients with NG and H pylori infection and 19 H pylori-positive and 14 H pylori-negative controls. A biopsy sample was taken from the antrum and snap-frozen for immunohistochemical analysis of MAdCAM1 and integrin β7. In simultaneous viewing of serial sections,the percentage of MAdCAM-1-positive to von Willebrand factor-positive vessels was calculated. We also performed immunostaining with anti-CD20, CD4, CD8 and CD68 antibodies to determine the lymphocyte subsets coexpressing integrin β7.RESULTS: Vascular endothelial MAdCAM-1 expression was more enhanced in gastric mucosa with than without H pylori infection. Of note, the percentages of MAdCAM-1-positive vessels were significantly higher in the lamina propria of NG patients than in H pylori-positive controls. Strong expression of MAdCAM-1 was identified adjacent to lymphoid follicles and dense lymphoid aggregates. Integrin β7-expressing mononuclear cells, mainly composed of CD20 and CD4 lymphocytes, were associated with vessels lined with MAdCAM-1-expressing endothelium.CONCLUSION: Our results suggest that the MAdCAM-1/integrin α4β7 homing system may participate in gastric inflammation in response to H pylori-infection and contributes to MALT formation, typically leading to the development of NG.

Gastritis: Sociodemographic, Clinical, Endoscopic and Histological Aspects, about 593 Cases at the Digestive Endoscopy Unit of the General Hospital Idrissa Pouye

Introduction: Gastritis is a very common and widely distributed condition worldwide. It represents one of the most common pathological entities in gastroenterology and digestive endoscopy. Our objective was to determine the sociodemographic, clinical, endoscopic, and histological aspects of gastritis in the digestive endoscopy unit of the General Hospital Idrissa Pouye (GHIP). Materials and Method: This was a retrospective study over a period of 4 years (from 1 January 2014 to 31 December 2017) at the digestive endoscopy unit of GHIP. We had collated oesogastroduodenal endoscopy (EGDE) reports with gastritis appearance with gastric biopsies and reports with normal stomach appearance with gastric biopsies and their histological reports. We collected and analyzed data on age, gender, indications for endoscopy, endoscopic findings and histological results. Results: The reports of 593 patients were analyzed. The mean age was 45 years old (range 8 - 88 years old) and the sex ratio was 0.63 (230 men). The indications for endoscopy were epigastralgia in (91%) of cases, dyspepsia in (22%) of cases, pyrosis in (12%) of cases. The endoscopic appearance was normal in 229 patients (39%). The endoscopic location of the gastritis was antral in 76%, fundic in 22% and pangastric in 2%. The gastritis was erythematous in 327 patients (90%), erosive in 126 patients (35%), congestive in 53 patients (15%), pseudonodular in 14 patients (4%) and atrophic in 10 patients (3%). Histology was normal in 8 patients (1.3%) and showed gastritis in 585 patients (98.7%). Gastritis was chronic in 575 patients (98.2%), acute in 10 patients (1.7%). Gastritis activity was moderate in (52.7%) and mild in (42.9%). Atrophy was absent in 521 patients (88.6%) and mild in 46 patients (8.2%). Intestinal metaplasia was found in 66 patients (11%). Dysplasia was present in 1.7% of cases. This dysplasia was intermediate grade (60%) in 6 patients, low grade (20%) in 2 patients and severe grade (20%). H. pylori was present in 404 patients (68%). Conclusion: Gastritis is usually found in the digestive endoscopy unit of the GHIP. The indications for endoscopy are dominated by epigastralgia and histology is necessary for its diagnosis.

乳铁蛋白胶囊联合铋剂四联疗法治疗小儿幽门螺杆菌相关性胃炎的疗效

目的 探讨乳铁蛋白胶囊联合铋剂四联疗法治疗小儿幽门螺杆菌(Hp)相关性胃炎的疗效。方法前瞻性选取94例小儿Hp相关性胃炎的临床资料,按照随机数字表法分为对照组和研究组。对照组采取铋剂四联疗法(n=47),研究组采取乳铁蛋白胶囊联合铋剂四联疗法(n=47)。比较2组患儿的治疗效果、Hp清除率、治疗前后临床症状改善情况、营养指标[白蛋白(ALB)、血红蛋白(Hb)、铁蛋白(SF)]、免疫指标[T淋巴细胞亚群(CD3^(+)、CD4^(+)、CD8^(+)、CD4^(+)/CD8^(+))]、炎症反应指标[肿瘤坏死因子-α(TNF-α)、超敏C反应蛋白(hs-CRP)、白细胞介素-6(IL-6)]及不良反应发生率。结果 研究组的总有效率、Hp清除率高于对照组(P=0.025,0.016)。治疗4周后2组患儿的上腹部疼痛、反酸、上腹部胀气、嗳气评分及症状总评分较治疗前降低,研究组低于对照组,差别均有统计学意义(P<0.01);血清ALB、Hb、SF、CD3^(+)、CD4^(+)、CD4^(+)/CD8^(+)水平高于治疗前,研究组高于对照组,差别均有统计学意义(P<0.01);CD8^(+)低于治疗前,研究组低于对照组,差别均有统计学意义(P<0.01);血清TNF-α、hs-CRP和IL-6水平低于治疗前,研究组低于对照组,差别均有统计学意义(P<0.01);2组患儿不良反应发生率比较,差别无统计学意义(P>0.05)。结论 乳铁蛋白胶囊联合铋剂四联疗法治疗小儿Hp相关性胃炎能提高疗效,加速Hp清除,缓解临床症状,改善营养-免疫状态,减轻炎症反应,不增加药物不良反应。

邱健行治疗幽门螺旋杆菌感染胃炎经验

幽门螺杆菌感染相关胃炎临床较为常见,由于抗生素耐药率升高,其治疗效果不容乐观,加之西药抗幽门螺旋杆菌存在腹痛、便秘、口腔金属味等不良反应,越来越多人在初次根除失败后,开始求助中医药治疗。国家名老中医邱健行教授,辛勤杏林耕耘60载,对于本病的中医药辨治积累了丰富的临床经验。他认为HP感染相关胃炎在中医中属于“胃脘痛”“痞满”的范畴,主要病因为饮食不节、情志失调、感受外邪、素体虚弱等;病机为脾胃虚弱,外感湿热邪毒,导致其发病,多兼夹瘀血、痰湿等病理产物;病位在胃,与肝脾相关,涉及胆肾;病性属于虚实夹杂。本文将从病因病机、治法治则(健脾和胃、清热化湿、活血通络、疏肝理脾)介绍邱老对于本病的认识,并附验案一则。