艾司奥美拉唑与泮托拉唑治疗幽门螺杆菌阳性慢性胃炎的临床价值

探讨分析在治疗幽梦螺杆菌阳性慢性胃炎的药物中艾司奥美拉唑与泮托拉唑的治疗效果差别和临床价值。方法 选取2022年1月到12月在张家口市经开区老鸦庄镇卫生院接诊的100例幽梦螺杆菌阳性慢性胃炎患者作为研究对象,随机分为两组,各50例。对照组采取泮托拉唑、阿莫西林、甲硝唑等药物进行治疗,观察组使用艾司奥美拉唑、甲硝唑、阿莫西林等药物进行治疗,观察使用药物后的情况改善,使用两组患者的临床症状情况进行反映。结果 经过治疗,两组患者临床症状得到明显改善,并且观察组效果优于对照组,同时观察组患者幽梦螺杆菌的检出率,。结论 使用艾司奥美拉唑的患者疗效更加,不良反应发生概率更小,具有重要的临床意义和价值。

序贯药物方案与四联疗法对Hp阳性慢性胃炎活动期患者Hp根除率及复发的影响

目的研究序贯药物方案与四联疗法对幽门螺旋杆菌(Hp)阳性慢性胃炎活动期患者Hp根除率及复发的影响。方法选择2018年8月—2019年11月本院收治的91例Hp阳性慢性胃炎活动期患者作为研究对象,采用双盲法分为A组(n=45)和B组(n=46)两组。A组给予四联疗法治疗,B组给予序贯药物方案治疗。对比两组患者的治疗14 d后的Hp根除率、症候积分、3个月和6个月复发率以及治疗期间不良反应。结果 A组Hp根除39例(84.78%),B组Hp根除42例(93.33%),B组根除率较A组高,差异无统计学意义(χ^(2)=0.939,P=0.192);治疗后症候积分比治疗前低,且B组低于A组,差异有统计学意义(P<0.05);随访3个月,B组复发率(4.44%)低于A组(10.87%),差异无统计学意义(P>0.05);随访6个月后,B组复发率(11.11%)低于A组(28.26%),差异有统计学意义(P<0.05);B组不良反应发生率(6.67%)较A组(17.39%)低,差异有统计学意义(P<0.05)。结论 Hp阳性慢性胃炎活动期患者经序贯药物方案治疗,可提高Hp根除率,改善临床症状,降低复发率,且安全性高。

Correlation between CD4, CD8 cell infiltration in gastric mucosa, Helicobacter pylori infection and symptoms in patients with chronic gastritis

AIM: To evaluate the correlation between CD4, CD8 cell infiltration in gastric mucosa, Helicobacter pylori(H pylori)infection and symptoms or the assemblage of symptoms in cases with chronic gastritis.METHODS: Biopsy samples at the gastric antrum were obtained from 62 patients with chronic gastritis. CD4 and CD8 cell infiltration was evaluated by immunohistochemical assays on frozen sections of the biopsy samples. Fifteen symptoms referring to digestion-related activity and nondigestion related activity were observed. The correlation between lymphocyte infiltration and each symptom or symptom assemblage was analyzed by logistic regression and K-mean cluster methods.RESULTS: CD4 cell infiltrations in gastric mucosa were much more in patients with H pylori infection, while CD8 cell infiltrations were similar in patients with or without H pylori infection. Logistic regression analysis showed that the symptoms including heavy feeling in head or body (t= 2.563), and thirst (t= 2.478) were significantly related with CD4 cell infiltration in gastric mucosa (P＜0.05), and cool limbs with aversion to cold were related with CD8cell infiltration (t = 2.872, P＜0.05). Further analysis showed that non-digestive related symptom assemblage could increase the predicted percentage of CD4 and CD8cell infiltration in gastric mucosa, including lower CD4infiltration by 12.5%, higher CD8 infiltration by 33.3%,and also non-H pylori infection by 23.6%.K-means cluster analysis of all symptoms and CD4 and CD8 cell infiltration in gastric mucosa showed a similar tendency to increase the predicted percentage of CD4, CD8 cell infiltration and H pylori infection.CONCLUSION: Based on correlation between the gastric mucosa lymphocyte infiltration, H pylori infection and clinical symptoms, symptoms or symptomatic assemblages play an important role in making further classification of chronic gastritis, which might help find a more specific therapy for chronic gastritis.

H pylori infection causes chronic pancreatitis in Mongolian gerbils

AIM： To investigate whether chronic H pylori infection has the potential to induce pancreatitis in the Mongolian gerbil model, and whether it is dependent on an intact type Ⅳ secretion system. METHODS： Mongolian gerbils were infected with wild type （WT） H pylori type Ⅰ strain B128 or its isogenic mutant B128 △cag γ （defective type Ⅳ secretion）. After seven months of infection, H pylori was reisolated from antrum and corpus and Hpylori DNA was analyzed by seminested polymerase chain reaction （PCR）. Inflammation and histological changes were documented in the gastric antrum, corpus, and pancreas by immunohistochemistry. Cytokine mRNA, gastric pH, plasma gastrin, amylase, lipase, and glucose levels were determined. RESULTS： The H pylori infection rate was 95%. Eight infected animals, but none of the uninfected group, developed transmural inflammation and chronic pancreatitis. Extensive interstitial fibrosis and inflammation of the pancreatic lobe adjacent to the antrum was confirmed by trichrome stain, and immuno-histochemically. Pro-inflammatory cytokine mRNA was significantly increased in the antral mucosa of all infected gerbils. In the corpus, only cytokine levels of WT-infected animals andthose developing transmural inflammation and pancreatitis were significantly increased. Levels of lipase, but not glucose or amylase levels, were significantly reduced in the pancreatitis group. H pylori DNA was detected in infected antral and corpus tissue,but not in the pancreas CONCLUSION： H pylori infection is able to induce chronic pancreatitis in Mongolian gerbils independently of the type Ⅳ secretion system, probably by an indirect mechanism associated with a penetrating ulcer.

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

AIM： To investigate the mutation of p53 immunohistochemically in non-tumorous gastric mucosa with H pylori infection before and aEer 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 pylorinegative. 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 p53 （PAb240）in the Hpylori-infected gastric mucosa. The proportion of patients immunopositive for p53 （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 ± 0.30 vs 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. Hpylori 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.

Helicobacter pylori-negative Russell body gastritis:Case report

Russell body gastritis is an unusual form of chronic gastritis characterized by the permeation of lamina propria by numerous plasma cells with eosinophilic cytoplasmic inclusions.Very few cases have been reported in the literature;the majority of which have shown Helicobacter Pylori(H.pylori)infection,thus suggesting a correlation between plasma cell presence and antigenic stimulation by H.pylori.We present a case of Russell body gastritis in a 78-year-old woman who was undergoing esophagogastroduodenoscopy for epigastric pain.Gastric biopsy of the gastroesophageal junction showed the presence of cells with periodic acid-Schiff-positive hyaline pink bodies.Giemsa staining for H.pylori infection was nega-tive,as well as immunohistochemical detection.The cells with eosinophilic inclusions stained positive for CD138,CD79a,andκand lambda light chains,which confirmed plasma cell origin.In particular,κand lambda light chains showed a polyclonal origin and the patient was negative for immunological dyscrasia.The histological observations were confirmed by ultrastructural examination.The cases reported in the literature associated with H.pylori infection have shown regression of plasma cells after eradication of H.pylori.Nothing is known about the progression of H.pylori-negative cases.The unusual morphological appearance of this type of chronic gastritis should not be misinterpreted during routine examination,and it should be distinguished from other common forms of chronic gastritis.It is mandatory to exclude neoplastic diseases such as gastric carcinoma, lymphoma and plasmocytoma by immunohistochemistry and electron microscopy,which can help with differential diagnosis.The long-term effects of plasma cells hyperactivation are still unknown,because cases of gastric tumor that originated in patients affected by Russell body gastritis have not been described in the literature.We are of the opinion that these patients should be scheduled for endoscopic surveillance.

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM： To compare the prevalence of H pylori infection, peptic ulcer, cytomegalovirus （CNV） infection and Candida esophagitis in human immunodeficiency virus （HIV）- positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections. METHODS： A total of 151 patients （122 HIV-positive and 29 HIV-negative） with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of Hpylori infection, CMV, candida esophagitis and histologic chronic gastritis. RESULTS： The prevalence of Hpylori was less common in HIV-positive patients （22.1%） than in HIV-negative controls （44.8%; P 〈 0.05）, and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer （20.7% vs 4.1%; P 〈 0.01）, but a higher prevalence of chronic atrophy gastritis （6.9% vs 24.6%; P 〈 0.05）, Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis （P 〈 0.05）. In HIV-positive patients, chronic active gastritis was not significantly different between those with Hpylori infection and those without. CONCLUSION： The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to Hpylori infection.

Effect of Hewei-Decoction on chronic atrophic gastritis and eradication of Helicobacter pylori

AIM: To demonstrate the effect of Hewei-Decoction (Decoction for regulating the stomach) on chronic atrophic gastritis (CAG) and eradication of Helicobacter pylori. METHODS: Ninety patients with CAG entering the investigation were divided into six differentiation syndromes, based on their major symptoms and signs. Hewei-Decoction was taken by all the patients orally for 4 or 8 wk. The efficacy was assessed by both the composite accumulation of reduced scores of major symptoms and the eradication of H pylori.X2 test was used to compare the efficacy between H pylori-positive and negative cases, and to disclose the relationship between efficacy and eradication of H pylori. RESULTS: In patients with six different syndrome types, the efficacy of Hewei-Decoction was 91.67% (11/12), 92.86% (13/14), 97.22% (35/36), 87.50% (14/16), 75.00% (6/8), 75.00% (3/4) respectively. The rate of highly efficacious was 58.33% (7/12), 50.00% (7/14), 77.78% (28/36), 62.50% (10/16), 12.50% (1/8) and 25.00% (1/4), respectively. The total efficacy was 91.11% (82/90), and the rate of highly efficacious was 60.00% (54/90). The eradication rate of H pylori was 67.86% (38/56). The therapeutic effect of Hewei-Decoction was better in H pylori positive cases than that in H pylori-negative cases with the total effect of 96.43% vs 82.35% (P<0.05). In 56 H pylori positive cases, the therapeutic effect was better in H pylori eradicated cases than that in H pylori-existent cases with the total effect of 97.37% vs 72.22% (P<0.01). CONCLUSION: Hewei-Decoction is effective in most cases of all the syndrome types. The results indicate that eradication of H pylori is one of the important mechanisms for alleviation of symptoms and signs. Also, the decoction is efficacious in H pylori-negative cases.

Gastric carcinoid in a patient infected with Helicobacter pylori:A new entity?

There are four types of gastric carcinoid tumors, classified according to their histology and malignant potential. Only a few cases of carcinoid tumors in patients infected with Helicobacter pylori （H. pylor/） have been reported so far. We report a patient infected with H. pylori presenting with a small solitary gastric carcinoid tumor with very low proliferative rate and normal gas- trin levels. The tumor was endoscopically removed and the patient received an eradication therapy against H. pylori. No signs of metastatic disease have been found so far during more than 3 year of follow-up. Infection with H. pylori may cause chronic gastritis with normal or elevated gastrin levels, leading to the develop- ment of gastric carcinoids by mechanisms unrelated to gastrin. Enterochromaffin-like cell tumors related to a chronic H. pylori infection may be considered as a distinct type of gastric carcinoid tumors.