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.     

十二指肠胃化生与幽门螺杆菌感染

本文调查了155例十二指肠溃疡旁粘膜的组织病理学变化,并与对照组相比较。结果显示:溃疡旁组织炎症、胃化生和Hp检出率分别为69.7％、75.5％和24.5％,显著高于对照组的18.8％、10.4％和4.2％(P<0.01)。Hp在胃化生组织中的检出率为32.8％,81例不伴胃化生的粘膜中均未检出Hp(P<0.01)。透射电镜观察胃化生有其特征性改变。提示胃化生可能是溃疡形成的基础,Hp在化生区定植并非是产生溃疡的唯一直接因素,还可能通过其他复杂环节间接起作用。     

Prevalence of Helicobacter pylori infection in different ethnic groups in New Zealand children and adults

Background: Helicobacter pylori infection is a major risk factor for peptic ulcer disease and gastric cancer. A study of patients with dyspepsia attending for gastroscopy showed significant differences in H.pylori seropositivity between ethnic groups. Aims: To determine the prevalence of H.pylori in children and adults in the community in different ethnic groups and to identify risk factors for infection. Methods: Serum samples (324) were randomly selected from a cross-sectional survey of 11–12 year old school children with a high proportion of Maori and Pacific Island groups. Serum samples (579) were randomly selected from a cross-sectional workforce survey of 5677 participants aged 40–64 years. Serum samples were tested for H.pylori IgG. Results: The percentage seropositivity in 11–12 year old children was European 7%, Maori/part Maori 21%, all Pacific Island groups 48% and for the workforce survey 35.8%, 57.4% and 73.2% respectively. Compared with Europeans the increased relative risk of seropositivity for H.pylori in Maori and Pacific Island participants was significant after adjusting for age and socio-economic status (1.43 [1.13, 1.80] and 1.76 [1.43, 2.18]) respectively. The relative risk of H.pylori infection significantly increased with age, lower socio-economic status and lower household income, but was not significantly associated with gender, alcohol or cigarette use. Conclusions: The high seroprevalence of H.pylori in Maori and Pacific Island groups is consistent with the differences in incidence of gastric cancer. H.pylori continues to be a common infection in Maori and Pacific Island school children. Ethnicity appears to be a risk factor for H.pylori independent of socio-economic status.     

Prevalence of Intestinal Metaplasia in Helicobacter pylori Gastritis

Eidt S, Stolte M. Prevalence of intestinal metaplasia in Helicobacter pylori gastritis. Scand J Gastroenterol 1994;29:607-610

Background: The prevalence of intestinal metaplasia (IM) in underlying Helicobacter pylori gastritis was studied in 1446 patients.

Methods: Antral and body mucosa biopsy specimens (stains: hematoxylin and eosin, Warthin-Starry) were taken from five groups of patients: gastritis with no lesions, gastritis with duodenal, pyloric, or gastric ulcers or with chronic antral erosions.

Results: The prevalence of IM was higher in the antral than in the body mucosa (22.9% versus 2.8%; p < 0.001). Patients with IM had a higher mean age than those without IM in the overall group (p < 0.01). IM could be detected with the highest frequency in patients with gastric ulcers (p < 0.001).

Conclusions: The higher prevalence of IM in the antral mucosa–the preferred location of gastric carcinomas–further supports the postulated association of H. pylori and gastric carcinoma. The various prevalences of IM might contribute to explaining the different probabilities of gastric carcinoma developing in the groups investigated.     

幽门螺杆菌感染与十二指肠球部黏膜胃上皮化生的关系

目的 研究十二指肠球部黏膜幽门螺杆菌(Hp)感染与黏膜胃上皮化生的关系，探讨其在十二指肠球部炎症和溃疡发生中的作用。方法 2002年十二指肠球部黏膜活检的存档蜡块82例，作H-E、改良Giemsa和AB／PAS染色。内镜诊断为基本正常球部黏膜10例；十二指肠球炎47例(其中充血糜烂型16例；隆起型31例)和球部溃疡25例。结果 (1)内镜诊断基本正常的十二指肠球部黏膜，组织学60％有轻中度的炎症细胞浸润，但无胃上皮化生和Hp定植。(2)胃上皮化生是十二指肠球部黏膜最常见的病理变化(37／82，45％)。(3)Hp只有在胃上皮化生的黏膜中才能找到，检出率为76％(28／37)。十二指肠球部溃疡边缘黏膜胃上皮化生发生率(72％)明显高于球炎黏膜(40％)，差异有显著性(P=0．0078)。(4)虽然十二指肠球部溃疡边缘胃上皮化生黏膜的Hp检出率(89％，16／18)明显高于十二指肠球炎黏膜(63％，12／19)，但是两者差异无显著性(P=0．062)。不论何期溃疡Hp检出率均很高，本研究中溃疡活动期、愈合期和瘢痕期分别为15例、6例和4例，其溃疡边缘胃上皮化生中Hp检出率分别高达9／10、5／6和2／2例。结论 十二指肠球部溃疡周围黏膜高发胃上皮化生，使Hp更易于定植，推测如不根除Hp感染，可成为十二指肠球部溃疡复发的重要原因。     

Endoscopic duodenitis, gastric metaplasia and Helicobacter pylori

BACKGROUND AND AIMS: The purpose of this study was to investigate the relationship between gastric metaplasia and Helicobacter pylori in patients with endoscopic duodenitis. METHODS: The subjects were 57 patients with endoscopic duodentitis with or without H. pylori-associated gastritis. Biopsy specimens were obtained from the stomach and duodenal bulb to assess the histological findings and H. pylori infection. Gastric metaplasia was divided into three types: complete, intermediate and incomplete, according to the amount of mucus in the metaplastic cells. In 10 H. pylori-positive patients, endoscopic and histological findings of duodenitis were compared before and after eradication of the bacteria. RESULTS: There was no significant difference in the extent of gastric metaplasia or the appearance and severity of endoscopic duodenitis between H. pylori-positive and -negative groups. The complete type of gastric metaplasia was frequently detected in the H. pylori-negative group, whereas the incomplete type was frequently observed in the H. pylori-positive group. After eradication of H. pylori, the incomplete type changed to the complete type with a decrease of histological inflammation. CONCLUSIONS: The complete type of gastric metaplasia occurred frequently without H. pylori infection, whereas the incomplete type was frequently associated with H. pylori infection.     

幽门螺杆菌长期感染与胃黏膜炎症和肠上皮化生的关系

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71例5年前和78例10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5年前Hp阳性71例中,现在52例(73.2％)Hp仍呈阳性,19例(26.8％)转阴;10年前Hp阳性的78例中,现在59例(75.6％)Hp仍呈阳性,19例(24.4％)转阴。Hp长期阳性者5年前和现在及10年前和现在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的发生率分别为17.3％(9/52)与26.9％(14/52)(P>0.05)和11.9％(7/59)与39.0％(23/59)(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5年前和现在及10年前和现在慢性炎症严重程度积分分别为1.684±0.369与1.369±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％(6/19)和52.6％(10/19);IN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,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,而且能防止IM的发生。     

Helicobacterpylori infection and gastropathy： A comparison between Indonesian and Japanese patients

AIM: To compare the effects of Helicobacter pylori ( H pylori) infection on gastropathy between Indonesian and Japanese patients.METHODS: Biopsy specimens were obtained during upper gastrointestinal endoscopy from 167 subjects (125 Indonesians and 42 Japanese) with uninvestigated symptoms of dyspepsia. The specimens were analyzed for the presence of H pylori using urease analysis, histopathology, and cell culture. The grade and activity of gastritis was assessed using the updated Sydney system.RESULTS: The percentages of Indonesian and Japanese patients who were H pylori-positive at the antrum or body of the stomach were similar (68% and 59.5%, respectively; P = 0.316). Of those who were H pylori-positive, more Japanese patients than Indonesian patients had high levels of polymorphonuclear cells ( P = 0.001), mononuclear cells ( P = 0.013), glandular atrophy ( P = 0.000), and intestinal metaplasia ( P = 0.011) in both the antrum and body of the stomach.CONCLUSION: The grade of gastritis and prevalence of mucosal atrophy and intestinal metaplasia were higher in Japanese patients. The difference between Indonesian and Japanese patients was significant.     

十二指肠球部多发隆起病变与幽门螺杆菌和胃上皮化生的关系

目的探讨内镜下十二指肠球部多发隆起病变与幽门螺杆菌（Hp）感染和胃上皮化生等组织学异常关系.方法连续调查86例经胃镜检查证实十二指肠球部多发隆起病变患者,并以40例球部基本正常患者作为对照.病变组Hp阳性患者接受三联根除治疗（奥美拉唑20mg、克拉霉素250mg、甲硝唑400mg,每天2次）,疗程7 d,停药后随访6个月后复查胃镜;病变组Hp阴性者接受奥美拉唑20 mg,每天1次治疗,疗程4～6个月,停药后2周复查胃镜.比较2次胃镜检查结果,包括胃镜下隆起病变程度及球部黏膜胃上皮化生等组织学异常,分析Hp感染与上述胃镜下表现及组织学异常关系.结果对照组患者组织学仅部分发现轻度慢性炎症,未发现球部Hp感染.病变组患者Hp检出率为58.1%,胃上皮化生检出率为57.0%.Hp阳性与Hp阴性患者胃镜下隆起病变程度差异无统计学意义（P＞0.05）,但胃上皮化生检出率更高,程度更严重（P＜0.05）.76例患者复查胃镜,根除Hp或奥美拉唑治疗对Hp阳性或阴性患者球部多发隆起病变无明显作用,但根除Hp后6个月,53.6%（15/28）患者胃上皮化生消失,61.0%（25/41）患者绒毛萎缩恢复正常,所有患者淋巴滤泡完全消失（26/26）,杯状细胞减少完全恢复（25/25）,同时炎症和活动性显著减轻（P值均＜0.01）.奥美拉唑疗效不显著.结论十二指肠球部多发隆起病变患者半数以上有Hp感染.Hp感染与隆起病变伴随组织学炎症密切相关,而与其内镜下表现及严重程度无关.根除Hp可使炎症显著减轻,胃上皮化生范围缩小或消退.     

Relevance of high virulence Helicobacter pylori strains and futility of CDX2 expression for predicting intestinal metaplasia after eradication of infection

Abstract

Objective. Different Helicobacter pylori genotypes are associated with distinct inflammatory responses and consequent development of pre-neoplastic lesions, namely intestinal metaplasia (IM), which is dependent on the expression of CDX2. We aimed to evaluate IM progression/regression in the context of H. pylori eradication, bringing into play the effect of the virulence of infecting H. pylori strains and the hypothesis that CDX2 expression might be a marker for later development of IM. Material and methods. Sixty-five male volunteers were evaluated by endoscopy before H. pylori eradication and after a median six-year follow-up. Histological diagnosis was performed at baseline and follow-up, and baseline H. pylori genotypes and CDX2 expression in non-metaplastic foci were also assessed. Results. Fifty-one individuals remained free from infection at follow-up. Six out of 27 who had no metaplastic lesions at baseline developed IM. CDX2 nuclear expression was observed in 15 of the 21 cases (71.4%) showing no progression to IM, and in three out of six cases (50%) with progression to IM (p = 0.367). Six of the 24 cases with IM at baseline showed regression to less severe outcomes, which was less frequent in those infected with high-virulence strains (7.7% vs. 50%, p = 0.047). In the latter there is a significant persistence of lymphoid follicles. Conclusions. Our results support that under infection with high virulence H. pylori strains, IM is a point of difficult return in the gastric carcinogenic pathway. The appearance of CDX-expressing cells in non-metaplastic foci was not associated with the development of IM during the six-year follow-up.     

Cdx2蛋白在不同亚型肠上皮化生中的表达及其与H.pylori感染的关系

目的探讨胃黏膜肠上皮化生（intestinal地metaplasia,IM）中尾型同源异型盒基因2（caudal type homeobox genes2,Cdx2）蛋白的表达及其与幽门螺杆菌（helicobacter pylori,H.pylori）感染的关系。方法选取内镜下活检的18例正常胃黏膜和53例IM胃黏膜。采用高铁二铵-爱先蓝-过碘酸雪夫反应（HID-AB-PAS）将胃黏膜IM分为Ⅰ、Ⅱ、Ⅲ型,然后用Cdx2单克隆抗体进行免疫组织化学染色,检测Cdx2在正常胃黏膜及不同亚型IM中的表达。采用一分钟快速尿素酶实验及甲苯胺蓝染色检测H．pylori感染。结果Cdx2蛋白在正常胃黏膜中不表达,IM中Cdx2阳性表达率为83．02％（44／53）,其中Ⅰ型IM阳性率为95．45％（21／22）。Ⅱ型为83．33％（15／18）,Ⅲ型为61．53％（8／13）,三者间Cdx2蛋白表达有显著性差异（P=0．036）。IM中H．pylori感染阳性率为47．17％（25／53）,其中Ⅰ型IM中H．pylori感染阳性率为27．27％（6／22）,Ⅱ型为55．56％（10／18）,Ⅲ型为69．23％（9／13）,三者间Mpylori感染率亦有显著性差异（P=0．038）。Cdx2蛋白表达主要集中于H．pylori感染阴性者,但H．pylori感染阳性者和阴性者Cdx2表达无统计学差异（P〉0．05）。结论Cdx2蛋白异常表达可能参与了胃黏膜IM向胃癌的转变,检测其表达有助于预测胃黏膜IM向胃癌转变的可能性。     

Effects of Helicobacter pylori infection on mucin expression in gastric carcinoma and pericancerous tissues

BACKGROUND: Helicobacter pylori infection is one of the major causes of human gastric carcinoma and can disturb the gastric mucosa barrier. Mucins have not only lubricating and protecting functions, but are also related to signal transduction, turnover of gastric epithelium and carcinogenesis of gastric mucosa. The aim of this study was to investigate the relationship between H. pylori infection and aberrant mucin expression in patients with gastric carcinoma. METHODS: H. pylori infection was diagnosed by the Warthin-Starry staining method. Different kinds of mucins were detected using an immunohistochemical method. RESULTS: Of 46 patients with gastric carcinoma, there were 26 patients who had H. pylori infection (56.5%). Of 21 pericancerous mucosas from the H. pylori-positive patients, 14 had MUC2 expression (66.7%), seven had strong MUC1 expression (+ + +) (33.7%), seven had strong MUC6 expression (+ + +) (33.3%), and five had strong MUC5AC expression (+ + +) (23.8%). In contrast, only six of 18 H. pylori-negative pericancerous mucosas had MUC2 expression (33.3%) (P < 0.05 compared with H. pylori-positive pericancerous mucosas), 12 had strong MUC1 expression (+ + +) in 16 H. pylori-negative pericancerous mucosas (75%) (P < 0.05), 11 had strong MUC6 expression (+ + +) in 16 H. pylori-negative pericancerous mucosas (68.8%) (P < 0.05), and 10 had strong MUC5AC expression (+ + +) in 14 H. pylori-negative pericancerous mucosas (71.4%) (P < 0.01). Of the H. pylori-positive cancerous tissues, 50% (13/26) had MUC1 expression and 38.5% (10/26) had MUC6 expression. In comparison, of the H. pylori-negative cancerous tissues, 80% (16/20) had MUC1 expression (P < 0.05) and 80% (16/20) had MUC6 expression (P < 0.01). CONCLUSIONS: The results indicate that H. pylori infection can alter the expression of some mucin genes in pericancerous mucosa and cancerous tissues of gastric carcinoma, then destroy the gastric mucosa barrier.     

胃粘膜肠化中幽门螺杆菌感染与PCNA,c-erbB-2的表达

目的研究肠化胃粘膜幽门螺杆菌（Ｈｐ）阳性率与ＰＣＮＡ,ｃｅｒｂＢ２表达率之间关系,以探讨Ｈｐ感染在胃肠化发生、发展中作用．方法经病理检查证实的慢性胃炎伴肠化１１６例,对照组非溃疡性消化不良．应用改良ＷａｒｔｈｉｎＳｔａｒｙ法检测Ｈｐ,免疫酶组化ＳＰ法检测ＰＣＮＡ,ｃｅｒｂＢ２的表达,比较Ｈｐ阳性组和阴性组间ＰＣＮＡ,ｃｅｒｂＢ２的阳性表达率．结果胃粘膜肠化者Ｈｐ感染率增高（５８６％ｖｓ１８８％,χ２＝１０７９,Ｐ＜００１）,肠化胃上皮内少见Ｈｐ粘附,Ｈｐ阳性组ＰＣＮＡ,ｃｅｒｂＢ２表达高于阴性组（４８／６８ｖｓ１２／４８,χ２＝９０５,Ｐ＜００５;３６／７４ｖｓ２／４２,χ２＝１３２８,Ｐ＜００１）．结论Ｈｐ感染促进胃粘膜肠化,并使肠化胃粘膜细胞增殖迅速而启动恶性变,故Ｈｐ感染可能促进胃癌的形成．     

幽门螺杆菌感染与胃癌的相关性研究

目的：为了研究幽门螺杆菌（Hp）感染与胃癌及肠化类型的关系。方法：对胃癌高发区1333例普查人群的胃活检组织和30例胃癌手术标本病理切片做Warthin－starry染色，对慢性萎缩胃炎伴肠化生、慢性浅表胃炎伴肠化生、癌旁肠化生用粘液组化方法染色分型。结果：Hp感染与十二指肠球部溃疡高度相关，与胃溃疡、慢性浅表活动性胃炎、早期胃癌显著相关，与单纯萎缩性胃炎、萎缩胃炎伴肠化生、胃增生性息肉亦相关（P均＜0．05）；进展期胃癌的Hp感染率与慢性非活动性胃炎相比较，差异无显著性（P＞0．05）；各型胃癌中以腺癌Hp检出率高（75．4％），与粘液细胞癌Hp检出率（30％）相比较，差异有非常显著性（P＜0．01）。各型肠化生之间的Hp检出率比较，差异无显著性（P均＞0．05）。结论：Hp感染与胃癌有相关性。     

根除幽门螺杆菌对胃黏膜肠化的影响

目的　幽门螺杆菌 (Hp)感染可导致慢性活动性胃炎进一步发展为慢性萎缩性胃炎、胃黏膜肠化、最终发展成肠型胃癌。通过 5年随访 ,探讨根除Hp是否对胃黏膜肠化逆转、发生及发展有影响。方法　将 1996年快速尿素酶试验及组织学方法检测Hp均为阳性的 398例病人随机分为治疗组和对照组。治疗组 2 0 1例 ,进行根除Hp治疗 ;对照组 197例 ,给予安慰剂 ;服药前及 5年后分别从胃窦部及胃体部取材检测胃炎、胃炎活动性及肠化。结果　 5年后治疗组中 15 1/2 0 1例Hp为阴性 ,对照组中 16 1/197例Hp为阳性 ;治疗组中Hp被根除的病人胃炎活动性的检出率明显减少 ,与对照组持续Hp感染者比较 ,差异有显著性 (P <0 .0 0 0 1) ;对照组中持续Hp感染者 5年后肠化检出率与自身 5年前、治疗组成功根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (P均 <0 .0 0 1) ,治疗组根除Hp的病人 5年前后比较差异无显著性 ;对照组中持续Hp感染者胃窦部 5年后肠化检出率与自身 5年前、治疗组根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (分别为P <0 .0 0 1,P <0 .0 0 1和P<0 .0 1) ,治疗组根除Hp感染的病人 5年前后比较差异无显著性 ;对照组持续Hp感染的病人与治疗组根除Hp感染的病人胃窦部肠化新增及新减情况比较无差异。 结论　 5年     

Duodenal gastric metaplasia and Helicobacter pylori infection in high and low duodenal ulcer-prevalent areas in India

Background: Previous reports, based on surgery, showed duodenal ulcer (DU) to be more common in the rice‐eating areas of southern India than in the northern wheat‐eating areas. Aims: Does this difference persist? Can it be explained by risk factors other than diet? Methods: A total of 20 053 records from patients undergoing endoscopy for dyspepsia, and 590 endoscopy patients from two northern and two southern centers in India were studied prospectively. Records were scrutinized to determine the relative incidence of DU and non‐ulcer dyspepsia in wheat‐ and rice‐eating areas. Age, sex, length of history, smoking and medication were recorded. Three antral biopsies and one from each duodenal quadrant were taken. A rapid urease test was carried out on one of the antral biopsies; the others were examined for Helicobacter pylori, gastritis, duodenitis and duodenal gastric metaplasia. Results: The difference in diet‐associated prevalence persisted. No differences in smoking, Helicobacter pylori infection or duodenal gastric metaplasia were found between the two regions, but all three were more common in DU than in non‐ulcer dyspeptic patients from both dietary areas. Conclusions: The dietary differences between the regions remain the only factor to account for the differences in DU prevalence. A strong interrelationship between duodenal gastric metaplasia and cigarette smoking is demonstrated.     

Long‐term infection with Helicobacter pylori in Mongolian gerbils

Objective: To investigate pathological changes occurring in the stomach of the Mongolian gerbil during long‐term Helicobacter pylori infection. Methods: Four‐week‐old male Mongolian gerbils were used, which were free from specific pathogens. Eighty Mongolian gerbils were inoculated orally with a suspension of H. pylori NCTC 11637 (0.5 mL, 2 × 10¹⁰ CFU/L) in a Brucella broth. To act as controls, a further 30 gerbils were fed with a Brucella broth only. Infected gerbils were killed 10, 25, 45, 55 and 65 weeks after infection. Control gerbils were killed at 10, 45 and 65 weeks. The stomach of each gerbil was removed and opened. Stomach samples for histological examination were fixed in neutral buffered formalin, embedded in paraffin, sectioned and stained with hematoxylin and eosin for analyzing histological changes, Giemsa stain for detecting H. pylori and Alcian blue (AB)/periodic acid?Schiff stain for examining intestinal metaplasia. Results: The Mongolian gerbil model for studying long‐term H. pylori infection was successfully established. Helicobacter pylori induced a progression from normal gastric mucosa to chronic gastritis, glandular atrophy, intestinal metaplasia and dysplasia, although no adenocarcinomas were found in the experimental animals. Conclusions: Helicobacter pylori NCTC 11637 is able to easily colonize the glandular stomach mucosa of the Mongolian gerbil. This model is stable, and the histological changes observed in the stomach are similar to those that occur in humans with H. pylori infection.     

Synchronously Multiple Gastric Adenocarcinomas with Intestinal Mucin Phenotype in a Patient not Infected with Helicobacter pylori,Showing a Gastritis-like Appearance

Helicobacter pylori (H. pylori)-negative gastric cancer (HPNGC) usually shows a gastric mucin phenotype, but there are a few case reports of HPNGC with an intestinal mucin phenotype. We herein report a case of multiple HPNGC with an intestinal mucin phenotype showing a gastritis-like appearance. A 68-year-old H. pylori-uninfected man was suspected of having antral gastritis on endoscopy, but a histologic examination revealed multiple well-differentiated adenocarcinomas with positive-CDX2/MUC2/CD10 and negative-MUC5AC/MUC6. P53 was overexpressed, and intestinal metaplasia was sporadically detected in the non-atrophic mucosal background, thus indicating H. pylori-unrelated multistage carcinogenesis. The neoplastic surfaces were covered by a non-neoplastic epithelium, which caused a gastritis-like appearance. This report suggested the possibility of overlooking this neoplasm.