183例儿童和青少年胃粘膜活检中幽门螺旋菌检出的研究

通过取自二个地区共183例儿童和青少年胃窦部及体部粘膜活检材料的组织学观察,结果表明:幽门螺旋菌检出率低于国内成人组,与慢性浅表性胃炎及地区性有明显关系,中、重度慢性浅表性胃炎中幽门螺旋茵的检出率明显增多,而与活检的取料部位无关。     

Helicobacter pylori Distribution in Human Gastric Mucosa with Chronic,Atrophic Gastritis

In animals a continuous administration of 0.02% NH₃ induced by Helicobacter pylori is well known to lead to glandular atrophy of the gastric mucosa and to induce active, chronic gastritis. In addition, this organism has been demonstrated to be closely related to chronic, active gastritis in man. In the present study, a phenol red dye spraying endoscopy was re-formed in 54 patients with chronic, atrophic gastritis to elucidate the distribution of this organism in the human gastric mucosa, and to clarify the relationship between its presence and chronic, atrophic gastritis. No red color reaction was found in 12 (92.3%) of 13 patients who had no glandular atrophy of the stomach. A diffuse and/or regional red color reaction was most prominent in those with slight degrees of glandular atrophy of the stomach, and was less striking in those with severe atrophy of the gastric mucosa associated with intestinal metaplasia. In addition, no red color reaction was visible in 14 (87.5%) of 16 patients showing a C₀ pattern in the fundic-pyloric border classification, whereas a diffuse and/or regional red color reaction was observed in over 75% of patients showing C₁ -O₂ patterns and less frequently in those with an O₃ Pattern. These data suggest a positive relationship between the presence of this organism and chronic, atrophic gastritis in man.     

幽门螺杆菌感染胃粘膜抗体产生细胞的研究

利用免疫组织化学方法对幽门螺杆菌(HP)感染胃粘膜内IgA,IgG和IgM产生细胞进行了研究.结果表明,HP感染引起了胃粘膜内局部抗体产生细胞的增加.其中以IgG和IgM产生细胞增加更着.提示:HP感染时局部体液免疫反应增强,进一步为HP是引起慢性活动性胃炎的病原提供了依据.     

“疗胃煎剂”胃粘膜保护作用的实验研究

目的研究“疗胃煎剂”对胃粘膜慢性损伤的防护作用。方法应用2级Wistar大鼠灌胃接种SSlHp菌株,灌胃3％水杨酸钠溶液,交替自由饮用5％乙醇与5mmol/L去氧胆酸钠溶液及饥饱失常的综合方法制备Hp相关CAG动物模型。模型制备成功后均先行根除Hp,进行“疗胃煎剂”治疗,并以三九胃泰作对照,12周疗程结束后,进行Hp感染,组织病理学检查及血清EGF及粘膜氨基己糖含量检测。结果“疗胃煎剂”中、高剂量组大鼠胃粘膜固有层、粘膜表面上皮层、PAS(＋)层厚度较模型自然恢复组明显增加(P＜0.01),其中粘膜固有层与表面上皮层厚度增加明显优于三九胃泰(分别(P＜0.05),已接近正常组水平(P＞0.05)。“疗胃煎剂”与三九胃泰组均有增加PAS(＋)层厚度的作用(P＜0.05)。“疗胃煎剂”中剂量组粘膜氨基己糖含量较模型自然恢复组明显增加(P＜0.05)。各治疗组血清EGF浓度均较模型自然恢复组明显下降。结论“疗胃煎剂可以增加氨基己糖含量及粘膜表面上皮层厚度,具有增强粘膜屏障功能的作用。     

The Distribution of Helicobacter pylori in Human Gastric Mucosa in vivo

Abstract: To estimate the distribution of Helicobacter pylori in human gastric mucosa in vivo, the phenol red dye spraying endoscopy lias been successfully developed and is performed after an oral and/or intravenous premedication of famotidine 20mg. This technique was conducted on 25 patients with chronic, atrophic gastritis, on 21 patients with a gastric ulcer and on 14 patients with duodenal ulcers. The red color changes which occurred on the gastric mucosa were classified into three types; the diffuse staining type, the regional staining type and the patchy staining type. In the chronic gastritis group, the diffuse staining type, the regional staining type and the patchy staining type occurred in 11 patients (44%), 7 patients (28%) and 2 patients (8%), respectively. The remainder of the patients' mucosa was unstained. In addition, the regional staining type occurred most frequently in the gastric ulcer group, while the diffuse staining type was dominant in the duodenal ulcer group. Notably, a recurrent and intractable ulcer was surrounded by regional staining fields in the stomach, and showed a diffuse staining at the antrum of the duodenum. These facts suggest that Helicobacter pylori prevented ulcer healing. This concurs with the results of our previous experimental study which found that the low concentration NH₃ solution, produced by Helicobacter pylori, prevented an acetic acid ulcer healing in rats and resulted from the suppression of the cell kinetics of the regenerative epithelial cells and the fibroblasts in the connective tissues at the ulcer margins.     

幽门螺杆菌感染对胃黏膜病理变化的影响

背景：幽门螺杆菌(H．pylori)感染已被公认为慢性胃炎和消化性溃疡的重要危险因素，根除H．pylori能加速消化性溃疡的愈合，但其对胃黏膜病理变化的影响尚有待进一步探索。目的：了解根除H．pylori对慢性胃炎胃黏膜病理变化和癌前状态的影响。方法：采用多中心随机对照临床试验和回顾性队列研究，样本选自胃癌高发区：上海郊区的金山区和奉贤区。共纳入360例经内镜检查证实有H．pylori感染的慢性胃炎伴或不伴十二指肠溃疡患者，随机分为两组。治疗组用三联疗法(质子泵抑制剂或Hz受体阻滞剂加两种抗生素)治疗，对照组单纯慢性胃炎患者予西沙必利、十二指肠溃疡患者予西米替丁治疗。在第1年和第4年末随访胃镜，根据H．pylori是否根除将患者分为两组：H．pylori阳性组和H．pylori阴性组。所有胃黏膜活检标本由两位病理科医师统一复读。结果：至第4年末，有120例患者完成全部随访，其中H．pylori持续根除组54例，阳转组5例；H．pylori持续未根除组45例，阴转组16例。持续根除组第1年随访时，活动性炎症比例减少(P＜O．05)；第4年随访时，慢性炎症和肠化程度以及活动性炎症比例减少(P＜O．05)。持续未根除组第1年随访时，慢性炎症程度增加(P＜O．05)；第4年随访时，慢性炎症和肠化程度以及活动性炎症比例增加(P＜O．05)，萎缩程度较第1年随访时增加(P＜O．05)。结论：根除H．pylori可以减轻慢性胃炎的炎症程度，防止肠化的发生和发展。     

胃粘膜肠化与幽门螺杆菌分布的关系

目的：探讨胃癌高发地区人群中胃粘膜肠化与幽门螺杆菌（Ｈ．ｐｙｌｏｒｉ）分布的关系。方法：对５３３例胃癌高发地区成年人行内镜及胃粘膜活检组织学检查,Ｗａｒｔｈｉｎ－Ｓｔａｒｒｙ染色阳性定为Ｈ．ｐｙｌｏｒｉ感染。结果：５３３例成年人的Ｈ．ｐｙｌｏｒｉ检出率为６４．５％。Ｈ．ｐｙｌｏｒｉ阳性组肠化检出率为５５．５％,阴性组肠化检出率为３１．８％（Ｐ〈０．０１）。Ｈ．ｐｙｌｏｒｉ阳性组无肠化和轻、中、重度     

抗胆汁反流治疗对胃内幽门螺杆菌感染的影响

体外研究发现胆汁可抑制幽门螺杆菌（H.pylori)的生长，但人体内胆汁反流对H.pylori的作用尚不清楚。目的：探讨抗胆汁反流治疗对胃内H.pylori感染的影响。方法：50例经胃镜检查确诊有胆汁反流的慢性胃炎患者纳入本研究。取胃窦黏膜活检标本行组织病理学检查和快速尿素酶试验（RUT），用改良Giemsa染色、RUT或血清H.pylori-IgG检测H.pylori感染情况。患者接受铝碳酸镁治疗（1000mg.tid,4周），治疗结束后复查胃镜和H.pylori感染情况。结果：治疗前患者的H.pylori感染率为66．0％，H.pylori感染者在I、Ⅱ、Ⅲ级胆汁反流性胃炎中的分布无显著差异。治疗后共有48例患者接受胃镜复查，结果显示胃内胆汗反流程度较治疗前明显减轻，H.pylori感染率为64．6％，与治疗前相比无显著差异。合并H.pylori感染者的胃黏膜炎症细胞浸润较非H.pylori感染者为重，且肠化发生率（39．4％）与非H.pylori感染者（11．8％）相比有显著差异（P＜0．05）。结论：合并H.pylori感染胆汁反流患者的胃炎和肠化均较单纯胆汁反流者为重。抗胆汁反流治疗可有效缓解胆汁反流性胃炎，但未能改善胃黏膜的H.pylori感染情况。     

胃黏膜炎症和肠上皮化生与幽门螺杆菌长期感染分析

目的 探讨幽门螺杆菌(Hp)长期感染及根除与胃黏膜炎症和肠上皮化生(IM)的关系.方法 随访142例4年前和156例7年前Hp感染者,分析对比其前后Hp感染情况、胃黏膜炎症和IM的变化.结果 4年前Hp阳性142例中,现在104例(73.2%)Hp仍呈阳性,38例(26.8%)转阴.7年前Hp阳性的156例中,现在118例(75.6%)Hp仍呈阳性,38例(24.4%)转阴.Hp长期阳性者4年前和现在及7年前和现在的慢性炎症严重程度积分分别为1.635±0.376与1.808±0.301(P＞0.05)和1.661±0.398与2.232±0.335(P＜0.01);IM发生率分别为17.3%(18/104)与26.9%(28/104)(P＞0.05)和11.9%(14/118)与39.0%(46/118)(P＜0.01);IM严重程度积分分别为1.444±0.527与1.667±0.442(P＞0.05)和1.571±0.534与2.286±0.488(P＜0.05).Hp转阴者4年前和现在及7年前和现在的慢性炎症严重程度积分分别为1.684±0.369与1.367±0.426(P＜0.05)和1.647±0.389与1.182±0.396(P＜0.01);IM的发生率为31.6%(12/38)和52.6%(20/38);IM严重程度积分分别为1.333±0.516与1.167±0.775(P＞0.05)和1.600±0.516与1.100±0.316(P＜0.05).结论 Hp感染持续时间越长,胃黏膜炎症越严重,可能IM程度亦越严重,且发生率高;根除Hp不仅能减轻胃黏膜的炎症程度和IM程度,也可能防止IM的发生.     

幽门螺杆菌感染对胃上皮细胞凋亡的影响

本文采用切口末端标记方法前瞻性观察了16例正常胃牯膜标本和31例幽门螺杆菌阳性胃炎患者抗幽门螺杆菌治疗前后胃窦部上皮细胞凋亡的变化。结果表明,幽门螺杆菌感染者的凋亡指数(0.7044)明显高于正常对照者(P<0.005);幽门螺杆菌根除后凋亡指数由0.7624降至0.1159(P<0.005),而持续阳性者则无明显降低;凋亡指数与胃炎程度无关。提示幽门螺杆菌能促进胃上皮细胞凋亡,这可能是幽门螺杆菌引起胃癌和溃疡的重要机理。     

Disappearance of Gastritis after Eradication of Helicobacter pylori: A Morphometric Study

Background: Patients with intestinal disease are at risk of developing selenium deficiency due to impaired intestinal absorption. The aim of the present study was to evaluate selenium status and to identify predictive factors of selenium depletion in patients with gastrointestinal disease. Methods: The concentration of selenium and the activity of glutathione peroxidase in plasma and erythrocytes were measured by fluorometry and by spectrophotometry. Eighty-six patients with Crohn's disease, 40 patients with ulcerative colitis, and 39 patients with various other gastrointestinal diseases were studied. Twenty-seven patients (16%) received home parenteral nutrition. Stool mass, faecal fat, and vitamin B₁₂ absorption were analysed in 100 patients. Results: The plasma selenium concentration was decreased in 85% of the patients receiving supplementary parenteral nutrition and in 20% of the patients receiving oral nutrition, among them in 26% of the patients with Crohn's disease. Almost all patients with ulcerative colitis had normal selenium levels. A statistically significant correlation was found between plasma selenium and vitamin B₁₂ absorption, stool mass, faecal fat excretion, body mass index, P-albumin, P-zinc, and the length of the remaining small bowel. Stepwise regression analyses showed that the strongest predictors of selenium deficiency were stool mass, vitamin B₁₂ absorption, and the length of the small-bowel resection. _Conclusion: Selenium deficiency is common in patients with severe gastrointestinal disorders. The deficiency is mainly related to malabsorption, and a low selenium level was almost invariably present in patients who needed parenteral supplementation due to gut failure.     

灭幽门螺杆菌胶囊结合低剂量标准三联法治疗慢性胃炎作用的研究

为进一步研究对幽门螺杆菌（HP）具有较高根治率且对胃粘膜病变具有治疗作用的药物疗法，将87例HP阳性慢性胃炎患者随机分为3组，分别以灭HP胶囊、灭HP胶囊结合低剂量三联和低剂量三联疗法治疗。结果，灭HP胶囊HP根治率为80．0％，与低剂量三联组（83．3％）相当；而灭HP胶囊结合低剂量三联组为97．4％（P＜0．05），且对胃粘膜活动性炎症有明显治疗作用（P＜0．01），对伴肠上皮化生的慢性萎缩性病变也具有一定作用（P＜0．05）。     

幽门螺杆菌感染能促进胃粘膜上皮细胞的增殖

用免疫组织化学染色方法,对30例幽门螺杆菌(Hp)相关性慢性胃炎和15例Hp阴性胃粘膜基本正常者胃粘膜中增殖细胞核抗原(PCNA)标记指数(LI％)和表皮生长因子受体(EGF-R)的表达进行了检测。结果表明,Hp阳性患者PCNA LI％为13.94±1.64,Hp阴性对照组为7.71±O.92.有显著差异(P0.05)。提示,Hp感染能引起胃粘膜上皮细胞过度增殖。这为阐明Hp感染在胃癌发病中作用的机理提供了线索。     

Helicobacter pylori and gastric cancer

Abstract This review focuses on the similarities between the epidemiology of gastric cancer and the epidemiology of Helicobacter pylori. Their demographic patterns and the results of studies regarding familial and environmental risk factors are described. The association of gastric cancer and H. pylori infection with both gastric ulcer and chronic atrophic gastritis is also characterized and the possibility that a H. pylori infection could lead to gastric cancer is discussed.     

早期胃癌和进展期胃癌患者幽门螺杆菌感染与胃黏膜组织学特点的关系

背景幽门螺杆菌(H.pylori)感染已被确认为慢性胃炎的主要病因,由慢性非萎缩性胃炎、慢性萎缩性胃炎至肠化生,经过数十年最终可能导致胃癌发生。目的评价H.pylori感染与胃镜检查正常者、慢性胃炎、早期胃癌和进展期胃癌患者胃黏膜组织学特点的关系。方法在受检者胃窦大弯侧、胃体大弯侧和胃角处各取一块黏膜活检标本,以Giemsa染色和免疫组化染色检测H.pylori感染情况;以HE染色评价胃黏膜炎症、活动性、萎缩和肠化生情况。结果慢性胃炎、早期胃癌和进展期胃癌患者的总体H.pylori感染率均显著高于胃镜检查正常者(52.4%、52.4%和81.2%对44.9%,P<0.05),慢性胃炎与早期胃癌患者的感染率无显著差异,但均显著低于进展期胃癌患者(P<0.05)。胃镜检查正常和慢性胃炎组H.pylori感染者的胃黏膜炎症、活动性、萎缩和肠化生检出率均显著高于无感染者(P<0.05);早期胃癌和进展期胃癌组H.pylori感染者的炎症活动性检出率显著高于无感染者(P<0.05),而炎症、萎缩和肠化生检出率与无感染者无显著差异。结论由H.pylori感染引起的胃黏膜慢性炎症、萎缩和肠化生可能在胃癌的发生、发展过程中起直接或间接作用。     

Serologic Screening before Endoscopy: The Value of Helicobacter pylori Serology,Serum Recognition of the CagA and VacA Proteins,and Serum Pepsinogen I

Background: We wanted to assess the diagnostic value of pre-endoscopy screening by Helicobacter pylori serology, serum recognition of the CagA and VacA proteins, and serum pepsinogen I levels (sPGI) in patients up to 55 years of age with uncomplicated simple dyspepsia. Methods: Consecutive dyspeptic patients referred for open-access endoscopy, excluding patients with alarm symptoms, recent intake of acid suppressants, or ingestion of non-steroidal anti-inflammatory drugs. H. pylori status was determined by histology and urease testing. H. pylori serologic status was determined with the enzyme-linked immunosorbent assay (ELISA) and Western blotting, serum recognition of CagA and VacA with Western blot, and sPGI levels by radioimmunoassay. Results: One hundred and fifteen patients were studied (mean age, 40 years; range, 20-55 years), of whom 58 were H. pylori-positive in biopsy-based tests. Twenty-one patients (18%) had significant gastroduodenal lesions (erosions, ulcers, or cancer). The sensitivity (specificity) of the ELISA (optimized) and Western blot in determining H. pylori status was 94.8% (89.5%) and 100% (96.4%), respectively. Screening strategies based on the ELISA or Western blot for determining H. pylori serologic status would have detected 95% or 100% of significant lesions, respectively, and each 'saved' 47% of endoscopies for simple dyspepsia. Serum recognition of the CagA protein would have detected 95% of significant lesions and 'saved' 55% of endoscopies, whereas recognition of the VacA protein would have detected only 81% of the lesions. Screening by H. pylori serology plus a 'low' (&lt;55 ng/ml) or 'high' sPGI (&gt;125 ng/ml) would detect only 57% of significant lesions, although the only case of cancer was included in the hypopepsinogenaemic subgroup of just 11 patients. Conclusions: In patients with uncomplicated, simple dyspepsia up to 55 years of age, screening by H. pylori serology identified 95%-100% of patients with significant gastroduodenal lesions while potentially saving 46.9% of endoscopies. Serum recognition of the CagA protein identified 95% of lesions and would have saved an additional number of endoscopies (7.9%) compared with basic serology. Measurement of sPGI was of limited diagnostic value.     

幽门螺杆菌感染对胃黏膜基质金属蛋白酶表达的影响及其与胃癌的关系

基质金属蛋白酶（MMPs）是一组锌依赖性内肽酶，可降解细胞外基质蛋白，有助于肿瘤细胞浸润和转移。已证实幽门螺杆菌（H．pylori）胃癌的发生有关，但其对胃癌浸润和转移的作用尚未明确。近年有研究显示H．pylori感染可使胃黏膜上皮MMPs表达增高，推测H．pylori感染可能通过MMPs而促进胃癌浸润和转移。本文就H．pylori感染对胃黏膜MMPs表达的影响及其与胃癌的关系作一综述，并对金属蛋白酶组织抑制剂（TIMPs）治疗胃癌的前景作一展望．     

A Case of Giant Gastric Folds with Hypoalbuminemia Healed by Helicobacter pylori Eradication

A 66-year-old man with hypoalbuminemia was found to have diffuse giant mucosal folds in the body of the stomach. Helicobacter pylori (H pylori) status was evaluated by several examinations, all of which showed positive results. To eradicate H pylori, he was treated with clarithromycin (200mg b. i. d.), lansoprazole (30mg q. d.) and plaunotol (80mg t. i. d.). By two weeks, the serum albumin concentration had risen to 3.4g per dl. Four weeks after finishing clarithromycin therapy, endoscopy was repeated and H pylori status was evaluated as before. All examinations showed negative results and the giant mucosal folds had improved markedly. Before treatment, histological specimens showed irregular elongation of pits with inflammatory infiltrates. After treatment, the architecture of pits returned to its normal form with decreased inflammatory infiltrates. In this case, giant gastric folds and hypoalbuminemia were improved by H pylori eradication, suggesting that H pylori infection may play a role in the giant gastric folds associated with hypoalbuminemia.