高频电凝联合中西药治疗幽门螺杆菌阳性的成熟型疣状胃炎

目的:观察胃镜下高频电凝联合中西药治疗合并幽门螺杆菌(H pylon)感染的成熟型疣胃炎的临床疗效,以寻找安全有效的治疗方法.方法:212例疣状胃炎患者随机分为中西药组和西药组,每组106例,西药组胃镜下对合并H pylon感染的成熟型疣状病变行高频电凝治疗,术后予H pylori根除治疗,中西药组在此基础上序贯服用中药治疗.结果:治疗2 mo后,中西药组和西药组总有效率差异有统计学意义(95.28%vs98.30%,P＜0.01);中西药H pylori转阴95例,根除率达89.62%,西药组89例,根除率为83.94%,二组差异无统计学意义.结论:胃镜下高频电凝联合西药根除H pylori 和中药序贯疗法能够有效治疗Hpylori阳性的成熟型疣状胃炎,值得推广.     

疣状胃炎与幽门螺杆菌,胃泌素和表皮生长因子等相关的研究

疣状胃炎（verrucousgastritis，VG）是指胃粘膜上形成脐窝状凹陷的隆起性病变，主要分布在胃窦部。本文测定了VG患者的胃液甘胆酸（GA、表皮生长因子（EGF）、pH值和血液胃泌素（Gas）、生长抑素（SS）值及胃窦粘膜的Hp、病理炎症分级，以探讨其发病的相关同素。材料与方法一、研究对象与标本采集（－一研究对象：经胃镜检查证实的疣状胃炎60例（病变均在胃窦，直径4～smm，个数1～15个），其中男52例，女8例，年龄为23～60岁，平均50岁；对照组为慢性浅表性胃炎（CSG）25例，其中男22例，女3例，年龄为18～58岁，平均45岁，无明显…     

连蒲汤治疗幽门螺杆菌阳性胃炎51例

笔者自拟连蒲汤与辨证结合,经多年临床实践,治疗幽门螺杆菌(Hp)阳性胃炎51例,疗效尚好,现总结如下。 1 对象和方法 1.1 对象 本组病例男38例,女13例,年龄16-62岁,平均年龄39岁,以中青年男性为多;病程最短3个月,最长12年。平均2年。所有患者均经内镜和Hp检测确诊为胃炎并Hp感染。其中18例合并有十二指肠球部溃疡,11例胃溃疡,8例十二指肠球炎,2例胃息肉。其中胃部灼痛,口干便结、舌质红、苔薄黄、脉弦、属肝胃郁热型者24例;胃脘冷痛,喜暖喜按、纳差便溏、肢软无力、舌质淡红、舌苔薄白,脉细弱,属脾胃虚寒者12例;胃脘胀痛、牵引两胁、嗳气则舒、泛酸嘈杂、舌质淡红、脉弦、属肝胃气滞型者11例;胃部刺痛、     

幽门螺杆菌感染与疣状胃炎伴或不伴糜烂及慢性浅表性胃炎相关性的研究

疣状胃炎 (Verrucous gastritis)是一种特殊类型的胃炎,而慢性浅表性胃炎 (Chronic superficial gastritis)十分常见,幽门螺杆菌 (Hp)与这两型胃炎之间关系的对比研究国内少见报道,特别是疣状胃炎伴糜烂及不伴糜烂时, Hp阳性率的比较国内尚未见报道,我们在这方面做了一些尝试。 　　一、观察对象： 2000年 3月至 2000年 12月门诊及住院患者,根据胃镜结果随机选择疣状胃炎患者 33例,其中男 30例,女 3例,年龄 18～ 61岁,平均 33.48岁, 6例同时伴有活动性十二指肠球部溃疡。慢性浅表性胃炎 35例,其中男 28例,女 7例,年龄 17～ …     

367例疣状胃炎与幽门螺杆菌及病理关系的探索

疣状胃炎是一种内镜下具有特征性改变的胃黏膜病变，是慢性胃炎悉尼分类的一种，根据对本院9年来的资料分析，探索其病理及与幽门螺杆菌（Hp）的关系。     

吸烟合并幽门螺杆菌感染与患疣状胃炎的相关性分析

目的 探讨吸烟合并幽门螺杆菌感染与疣状胃炎的相关性.方法 选择2006-2011年在本院行电子胃镜检查和活检确诊为疣状胃炎的患者进行问卷调查.结果 (1)500例疣状胃炎患者中有94%以为上长期吸烟(或被动吸烟)合并幽门螺杆菌感染者,较无吸烟合并幽门螺杆菌感染者发病率高(P＜0.01).Logistic回归分析显示:吸烟(或被动吸烟)是患疣状胃炎的危险因素.结论 吸烟(或被动吸烟)合并幽门螺杆菌感染与患疣状胃炎密切相关,禁烟可减少疣状胃炎发病率.     

胃炎保康方治疗幽门螺杆菌阳性慢性浅表性胃炎30例

本研究采用中药治疗幽门螺杆菌 ( Hp)阳性慢性浅表性胃炎 ,旨在寻找一种对该病疗效好、副作用小、依从性好的中药制剂。1　资料与方法1 .1　临床资料 :50例门诊患者 ,病程均在 3个月以上 ,有明显消化道症状和体征 ,经胃镜、病理、快速尿素酶试验、C13 - UBT及相关检查确诊为 Hp     

CagA^＋幽门螺杆菌与疣状胃炎的关系研究

目的 探讨细胞毒素相关蛋白(Cytotcxin Associated gene A，CagA)阳性株幽门螺杆菌感染在疣状胃炎中的意义。方法 分别观察50例疣状胃炎伴有、60例慢性浅表性胃炎伴有幽门螺杆菌感染的病人中CagA的阳性率。结果 疣状胃炎组CagA的阳性率为88％，慢性浅表性胃炎组CagA的阳性率为61．7％，两组比较有显著的差异(P＜0，01)。结论 CagA^ 的幽门螺杆菌在疣状胃炎的发病中起重要作用，需进行HP的根治。     

Treatment of Helicobacter pylori infection in atrophic gastritis

Helicobacter pylori(Hp) is a major human pathogen causing chronic, progressive gastric mucosal damage and is linked to gastric atrophy and cancer. Hp-positive individuals constitute the major reservoir for transmission of infection. There is no ideal treatment for Hp. Hp infection is not cured by a single antibiotic, and sometimes, a combined treatment with three or more antibiotics is ineffective. Atrophic gastritis(AG) is a chronic disease whose main features are atrophy and/or intestinal metaplasia of the gastric glands, which arise from long-standing Hp infection. AG is reportedly linked to an increased risk for gastric cancer, particularly when extensive intestinal metaplasia is present. Active or past Hp infection may be detected by conventional methods in about two-thirds of AG patients. By immunoblotting of sera against Hp whole-cell protein lysates, a previous exposure to Hp infection is detected in all AG patients. According to guidelines, AG patients with Hp positivity should receive eradication treatment. The goals of treatment are as follows:(1) Cure of infection, resolution of inflammation and normalization of gastric functions;(2) possible reversal of atrophic and metaplastic changes of the gastric mucosa; and(3) prevention of gastric cancer. An ideal antibiotic regimen for Hp should achieve eradication rates of approximately 90%, and complex multidrug regimens are required to reach this goal. Amongst the factors associated with treatment failure are high bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance. AG, when involving the corporal mucosa, is linked to reduced gastric acid secretion. At a non-acidic intra-gastric p H, the efficacy of the common treatment regimens combining proton pump inhibitors with one or more antibiotics may not be the same as that observed in patients with Hp gastritis in an acid-producing stomach. Although the efficacy of these therapeutic regimens has been thoroughly tested in subjects with Hp infection, there is a paucity of evidence in the subgroupof patients with AG. Bismuth-based therapy may be an attractive treatment in the specific setting of AG, and specific studies on the efficacy of bismuth-based therapies are needed in patients with AG.     

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

AIMS: To evaluate the effect of Helicobacter pylori infection and aging on atrophy and intestinal metaplasia of the gastric mucosa. METHODS: One hundred and sixty-three patients were divided into three age groups and underwent an upper gastrointestinal endoscopy where no esophagitis, peptic ulcers, or malignancies were detected. Two biopsy specimens were obtained from the anterior and posterior walls of the antrum and of the fundus. These were used to evaluate the grade of gastritis, bacterial culture and histologic evidence of H. pylori infection. RESULTS: Helicobacter pylori infection was found to be directly associated with an increased risk of gastritis grade (odds ratio (OR) = 90 (95% CI; 30-270)). An age of 60 years and older along with H. pylori infection was also strongly associated with an increased risk of atrophy (OR = 6.6, (95% CI; 2.9-15.2)); OR = 9.8, (95% CI; 2.7-35.4)), as was intestinal metaplasia of the gastric mucosa (OR = 5.5, (95% CI; 1.7-17.6)); OR = 7.9, (95% CI; 2.8-46.1)). The prevalence of atrophic gastritis increased with advancing age in H. pylori-infected patients, but no such phenomenon was observed in H. pylori-uninfected patients. The prevalence of intestinal metaplasia significantly increased with advancing age, irrespective of the presence of H. pylori infection. In addition, H. pylori uninfected female patients had a decreased risk of intestinal metaplasia. CONCLUSIONS: These results suggest that atrophic gastritis is not a normal aging process, but instead is likely to be the result of H. pylori infection, while intestinal metaplasia is caused by both the aging process and H. pylori infection. A decreased risk of intestinal metaplasia found in uninfected female subjects may partly explain the lower prevalence of gastric cancer in females than in males.     

Histological analysis of gastritis and Helicobacter pylori infection in patients with early gastric cancer: a case-control study

BACKGROUND AND AIMS: Infection with Helicobacter pylori is associated with an increased risk of gastric adenocarcinoma. However, most patients with H. pylori infection will not develop gastric cancer. The aims of the present study were to examine which histological features, including H. pylori infection, would increase the risk of gastric cancer using a case-control study. METHODS: Three gastric biopsy specimens were taken from 72 patients with early gastric cancer and 72 age- and sex-matched control subjects. The grade of gastritis was examined according to the updated Sydney System. The presence of H. pylori infection was determined by serology and histology. Odds ratio (OR) of developing gastric cancer was calculated for H. pylori positivity and histological features using conditional logistic regression. For patients with H. pylori infection, histological features in cancer patients and control subjects were compared. RESULTS: The OR of the presence of mononuclear cell infiltration in the corpus and intestinal metaplasia in the angulus were significantly elevated. The grade of mononuclear cell infiltration in the corpus and antrum was significantly higher in both types of cancer patients than controls. Glandular atrophy and intestinal metaplasia were increased in patients with intestinal-type cancer in the angulus and antrum. Bacterial density in the corpus and polymorphonuclear cell infiltration in the antrum were increased in patients with diffuse-type cancer. CONCLUSIONS: Severe chronic gastritis induced by H. pylori infection seems to be associated with diffuse-type gastric cancer. Glandular atrophy and intestinal metaplasia, which occur in gastric mucosa with chronic inflammation, are significantly associated with intestinal-type cancer.     

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...     

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...     

Helicobacter pylori infection and gastric function in patients with fundic atrophic gastritis

In the present study we evaluated the relation among histology, H. pylori, IgG to H. pylori, gastric emptying, and acid secretion in 43 patients with fundic atrophic gastritis. On the basis of gastric acid secretion, patients were divided into three subgroups: patients with preserved acid secretion (Group 1), patients with hypochlorhydria (Group 2), and patients with achlorhydria (Group 3). Fundic glandular atrophy was more severe in hypoachlorhydric patients than in those with preserved acid secretion (P < 0.05 vs Group 2, P < 0.005 vs Group 3). H. pylori colonization was found in 94% of patients in Group 1, in 61% of patients in Group 2, and in only 8% of patients in Group 3 (P < 0.001 vs Group 1, P < 0.05 vs Group 2). Conversely, serological positivity to H. pylori was high in all three subgroups of patients (100% in Group 1, 77% in Group 2, 92% in Group 3). Gastric emptying was delayed in atrophic patients, particularly in those with hypoachlorhydria. Our data suggest that fundic atrophic gastritis represents a possible end stage of H. pylori infection, characterized by a progressive disappearance of the bacterium and a progressive deterioration of gastric functions.     

慢性胃炎结节状改变与幽门螺杆菌感染的关系研究

目的　探讨慢性胃炎结节状改变与幽门螺杆菌 (Hp)感染的关系。方法　对 2 0 0 1～2 0 0 2年中胃镜检查发现的慢性胃炎结节状改变患者进行Hp检测 ,对Hp阳性患者 ,进行Hp根除治疗 ,随访 6个月 ,观察其胃镜下的改变。结果　 4 939例胃镜检查患者中共发现 1 3例慢性胃炎结节状改变 ,占检查总人数的 0 2 6 %。平均年龄 2 9岁 ,均为女性患者。主要症状均为上腹部疼痛。所有患者均有Hp感染。Hp根除成功后 ,症状和胃镜下结节状表现消失 ,病理证实胃黏膜下淋巴滤泡也随之消失。结论　慢性胃炎结节状改变可作为Hp阳性胃炎的内镜下的表现之一。     

基于京都胃炎评分判断胃镜下幽门螺杆菌感染状态的研究

目的　探讨京都胃炎评分判断国人幽门螺杆菌（Helicobacter pylori,HP）感染状态的价值。方法　回顾性收集2020年1—12月在武汉大学人民医院消化内镜中心同时间段行13C呼气试验和胃镜检查的902例受检者资料,其中HP阳性患者345例,HP阴性患者557例。分析HP阳性及HP阴性受检者的黏膜表现及京都胃炎评分差异,并绘制京都胃炎评分预测HP感染的受试者工作特征曲线。结果　与HP阴性患者相比,结节［8.1%（28/345）比0.2%（1/557）,χ2=86.29,P<0.001］、弥漫性发红［47.8%（165/345）比6.6%（37/557）,χ2=413.63,P<0.001］、萎缩［27.8%（96/345）比13.8%（77/557）,χ2=52.90,P<0.001］和皱襞肿大［69.0%（238/345）比36.6%（204/557）,χ2=175.38,P<0.001］在HP阳性患者中发生率高。对预测HP感染,结节表现出最高的特异度［99.8%（556/557）］和阳性预测值［96.6%（28/29）］;弥漫性发红表现出最高的受试者工作特征曲线下面积（area under the curve ,AUC）（0.707）;皱襞肿大表现出最高的灵敏度［69.0%（238/345）］和阴性预测值［76.7%（353/460）］。HP阳性患者的京都胃炎评分高于HP阴性患者［2（1,2）比0（0,1）,Z=20.82,P<0.001］。此外,在最佳阈值为2时,京都胃炎评分预测HP感染的AUC为0.779。结论　结节、弥漫性发红、萎缩及皱襞肿大对预测HP阳性均具有一定的提示作用,且京都胃炎评分≥2分时,有助于判断HP阳性,从而为临床工作者判断HP感染状态提供参考依据。     

Autoimmune gastritis: relationships with anemia and Helicobacter pylori status

Background: Autoimmune gastritis (AIG) is a gastric pathologic condition affecting the mucosa of the fundus and the body and eventually leading to hypo-achlorhydria.

Aims: We report our clinical and pathological experience with AIG.

Methods: Data from patients with a diagnosis of AIG seen in the period January 2002–December 2012 were retrieved. Only patients with complete sets of biopsies were analyzed.

Results: Data from 138 patients were available for analysis. Pernicious anemia was present in 25% of patients, iron deficiency anemia was found in 29.7% of patients, hypothyroidism in 23% of patients, type 1 diabetes in 7.9% of patients, and vitiligo in 2.8% of patients. Parietal cell antibodies were positive in 65% of patients, and no patient had serology positive for celiac disease. All gastric biopsies showed glandular atrophy associated with enterochromaffin-like (ECL)-cells hyperplasia, features limited to the mucosa of the fundus and body, and focal glandular intestinal metaplasia. Helicobacter pylori was negative in all cases.

Conclusions: AIG was strongly associated with anemia; atrophy, intestinal metaplasia and ECL hyperplasia in the gastric fundus and body are hallmarks of this condition.     

Helicobacter pylori infection in children

Helicobacter pylori was sought prospectively by culture of antral biopsy, histology and serology (IgG and IgA) in 440 consecutive endoscopies on children to determine the prevalence, clinical presentation and histological features of H. pylori infection in our population. Twenty-eight patients had H. pylori (8% overall). The mean age of infected patients was significantly higher than that of non-infected patients (P less than 0.0001). No patient under 5 years of age had H. pylori isolated. Overall, there was no significant difference in clinical presentation between those with and those without H. pylori infection, but 23% of patients 5 and 26 years of age who presented with abdominal pain as the indication for their endoscopy had H. pylori isolated. Macroscopic changes ranged from no abnormality to frank ulceration, but the typical antral mamilliform changes were 100% predictive of infection. Fifty-eight per cent of patients with duodenal ulcers, but only 17% with gastric ulcers had H. pylori infection. Histological gastritis was present in 144 patients (including all H. pylori positive patients). None of the patients with another definable cause for gastritis had H. pylori isolated. In conclusion, H. pylori is an important cause of primary gastritis in our population, occurring in children over 5 years of age. Culture of an antral biopsy should be performed in children over this age undergoing endoscopy for the investigation of abdominal pain and, more particularly, in those with peptic ulceration.