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。     

根除Hp感染患者胃黏膜组织学变化及胃癌患病率的随访研究

目的研究幽门螺杆菌（Hp）阳性患者根除Hp后对胃黏膜炎症、萎缩和肠上皮化生（IM）及胃癌患病率的影响。方法采用随机、对照研究方法,对在我院行胃镜检查同时行Hp及胃黏膜组织学检查者236例进行随访观察,3a后复查胃镜和组织病理学,评定组织学变化。分析Hp阳性组和阴性组在胃黏膜炎症、萎缩及IM的变化。结果Hp阳性组中胃黏膜的炎症、腺体的萎缩和肠化的总人数明显高于Hp阴性组（P〈0．05）。结论根除Hp感染可减轻胃黏膜活动性炎症、萎缩和肠上皮化生以及胃癌的发病率。     

胃镜下射频治疗十二指肠球部良性隆起病变疗效观察

十二指肠球部良性隆起性病变在病理上主要为Brunner腺增生、胃上皮化生、炎性隆起、良性淋巴组织增殖等，目前其发病机制不十分清楚，尚无具体的治疗方案，多数仅随访观察，部分有幽门螺杆菌（Hp）感染者进行抑酸、根除Hp治疗，个别患者行手术或高频电圈套切除治疗，但根除Hp治疗对隆起病变的程度无改变，而后者的风险较大。为此我们探讨内镜下射频治疗十二指肠球部良性隆起病变的疗效。     

根除幽门螺杆菌对胃黏膜组织学变化及胃癌患病率的3年随访研究

目的幽门螺杆菌(Helicobacter pylori,Hp)是导致胃黏膜病变的重要因子,研究Hp阳性患者根除Hp后对胃黏膜炎症、萎缩和肠上皮化生(IM)及胃癌患病率的关系。方法采用随机、对照研究方法,2006年1月-2009年6月间在我院胃镜检查同时行Hp及胃黏膜组织学检查者236例进行随访观察,3年后复查胃镜和组织病理学,评定组织学变化。分析治疗组(Hp阴性)和对照组(Hp阳性)在胃黏膜炎症、萎缩及IM的变化。结果对照组中胃黏膜的炎症、腺体的萎缩和肠化及发生胃癌的总人数明显高于治疗组的总人数,差异有显著性(P0.05)。结论根除Hp感染可减轻胃黏膜活动性炎症、萎缩和肠上皮化生以及胃癌的发病率。     

根除幽门螺杆菌对胃黏膜炎症变化的人群随访研究

目的 观察胃癌高发区中幽门螺杆菌(Hp)阳性者根除Hp5年后胃黏膜组织的炎症变化,以探讨。Hp感染与胃黏膜组织炎症及胃癌的关系。方法 对胃癌高发区山东省烟台市成年人群随机抽样1006例,做内镜、快速尿素酶试验及胃窦、胃体部黏膜组织学检查,将Hp阳性者随机分为治疗组(奥美拉唑20mg、克拉霉素500mg、阿莫西林1000mg)及对照组,2组入选者分别于1年后、5年后进行内镜复检,本研究是将5年后复查胃镜及相同部位胃黏膜组织病理检查与5年前结果进行比较并做χ^2检验。结果 552例Hp阳性者随机分为治疗组及对照组各276例,5年后Hp持续阴性者161例,持续阳性者198例。2组结果统计显示：(1)入选前2组胃窦部炎症及活动度发生率与体部相比差异无显著性,P值分别为0．105及0．084,但萎缩及肠化生发生率明显高于体部,P值均为0．000;(2)根除Hp 5年后胃窦、胃体部炎症及活动度均明显减轻,P值均为0．000;(3)根除Hp5年后胃窦部肠化生减轻或未进展,而Hp持续阳性组肠化生发生率明显增加,P=0．032;(4)根除Hp 5年后窦、体部萎缩改善差异无显著性,两组比较P值分别为0．223及0．402。结论 根除Hp可使胃慢性炎症及活动度明显减轻,窦部肠化生得到显著控制,溃疡病发病明显减少;持续Hp感染可使萎缩及肠化生呈进行性加重。     

十二指肠粘膜胃上皮化生的诊断及临床意义

目的：探讨十二指肠粘膜胃上皮化生的诊断及临床意义。方法：对58例经胃镜检查确诊的十二指肠球部溃疡患者行十二指肠美蓝染色,于不染区或着色区取材作病理检查和快速尿素酶试验。结果：58例患者中,26例于溃疡附近出现斑片状粉红色不染区,13例出现白色不染区,19例着蓝色,三者的胃上皮化生检出率分别为80．8％（21／26）,15．4％（2／13）和10．5％（2／19）,粉红色不染区的胃上皮化生检出率明显高于着色区（P＜0．01）,25例检出胃上皮化生者中22例幽门螺杆菌（H.pylori)阳性（88．0％）,33例无胃上皮化生者中4例H.pylori阳性（12．1％）,前者的阳性率显著高于后者（P＜0．01）,结论：十二指肠美蓝染色用于辨别十二指肠胃上皮化生效果较好,对针对性取材及[观察十二指肠球部溃疡患者胃上皮化生的动态变化有指导意义。     

胃幽门螺杆菌感染与所致淋巴组织病变的相关性及其治疗评价

目的探讨胃幽门螺杆菌（Hp）感染与所致各级胃淋巴增殖症（GLH）病变的相关性及其有关影响因素,对各级患者的治疗结果进行对照评价。方法对Hp感染而有淋巴细胞性胃炎（LCG）和GLH病变的患者（n=77）,根据胃镜和组织学病理表现参照Isaacson组织学评分标准分为4组／级,所有患者均采用根除Hp方案治疗,治疗后2个月复查胃镜及黏膜活检标本,观察Hp与LCG、GLH、萎缩、肠化等病变之间的消涨关系。结果所有患者组织学病理均不同程度减轻或消失,Ⅰ～Ⅱ级病变疗效明显优于Ⅲ～Ⅳ级（P〈0．05）,Hp与LCG和GLH之间存在明确的消涨关系,抗Hp治疗可逆转病变。结论抗Hp治疗对LCG和GLH病变有积极作用,影响疗效的因素包括病程、淋巴细胞生发中心、上皮病变及黏膜萎缩和肠化等。     

幽门螺杆菌根除治疗前后快速尿素酶试验诊断的准确性

目的 评价快速尿素酶试验(RUT)在根除治疗前后诊断幽门螺杆菌(Hp)感染的准确性。方法 选择250例接受胃镜检查的患者，123例无Hp根除治疗史，127例为Hp根除治疗后复查患者。每例患者取胃窦和胃体活检标本各3块，分别用于RUT、细菌培养和病理组织学检查。以细菌培养及病理组织学检查结果作为“金标准”，即培养和(或)组织学检查结果阳性者为Hp阳性，而培养和组织学检查结果同时阴性者为HP阴性或HP根除。结果 末行Hp根除治疗的患者RUT正确的诊断了86例Hp阳性中的84例和37例Hp阴性中的34例，其敏感性和特异性分别为97．7％和91.9％。根除治疗后RUT敏感性和特异性分别为64.3％和99.0％。然而，根除治疗后6个月以上复查胃镜，RUT敏感性和特异性均达100％。结论 根除治疗前和根除治疗后6个月以上复查，RUT诊断Hp感染准确性高。     

十二指肠粘膜胃上皮化生的组织学及电镜观察

胃上皮化生是十二指肠球部溃疡病灶旁的一种常见病理改变,我们通过对十二指肠球部溃疡、炎症和慢性浅表性胃炎患者的十二指肠球部粘膜胃上皮化生的观察,探讨胃上皮化生在十二指肠球部溃疡发病中的作用。一、材料和方法十二指肠球部溃疡活动期（ＤＵ－Ａ）患者６１例,十二指肠球部溃疡瘢痕期（ＤＵ－Ｓ）４０例,十二指肠球炎（ＤＩ）１９例,慢性浅表性胃炎（ＣＳＧ）３０例。在常规胃镜检查时,每组病例均取胃窦和十二指肠球部粘膜标本各１块：各组胃窦粘膜标本均取自胃窦前壁２ｃｍ处,ＤＵ患者十二指肠球部粘膜标本取自溃疡旁或溃疡瘢…     

不同类型胃息肉与幽门螺杆菌感染、粘膜炎症相关性的研究

目的 探讨不同类型胃息肉与幽门螺杆菌（Hp）感染以及与胃粘膜炎症、萎缩和肠上皮化生的相关性。方法 对2203例胃粘膜活检发现的278例胃息肉（检出率12.6%）进行组织学分类,并对胃窦粘膜活检组织同时行Hp检测及粘膜炎症、萎缩和肠上皮化生的观察,比较不同类型胃息肉的Hp感染率及其与癌相关病变的关系。结果 278例息肉中,组织学分类以小凹上皮增生型息肉为多见,有130例,占息肉总数的46.8%,胃体腺型增生性息肉67例,占24.1%,炎性息肉和腺瘤性息肉较少见,分别为55例（19.8%）和26例（9.4%）。约53.9%的胃息肉患者存在Hp感染,其中以小凹上皮增生型息肉感染率最高,达73.1%。这型息肉常伴有胃粘膜的活动性炎症,且粘膜萎缩和肠上皮化生的发生率均近腺瘤性病变。胃体腺型增生性息肉,Hp感染率、活动性炎症及萎缩、肠上皮化生等发生率均较低,提示这两种息肉在组织发生和病理生物学形态上存在差异。结论 小凹上皮增生型息肉的发生可能与Hp感染有关,且常伴有明显的活动性炎症以及粘膜萎缩的肠上皮化生,因此可能与胃癌的发生有潜在的关系。     

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.     

Effect of Helicobacter pylori eradication on gastric metaplasia of the duodenum.

Helicobacter pylori associated duodenal ulcers occur in patches of gastric metaplasia. The pathogenesis of gastric metaplasia is unclear, but it has been produced in experimental animals by acute injury and has been shown to be present to a greater extent of H pylori positive subjects. This study aimed to discover if gastric metaplasia regressed with eradication of H pylori or healing of duodenal ulcers, or both. Thirty two duodenal ulcer patients with H pylori infection confirmed by biopsy urease test and by antral histological examination were studied. Patients were treated with triple therapy (deNol 240 mg twice daily, amoxycillin 500 mg three times daily, and metronidazole 400 mg three times daily) for two weeks after the first endoscopy and were subsequently re-endoscoped. Three duodenal bulb biopsy specimens were obtained per patient at each endoscopy. Biopsy sections were stained with haematoxylin and eosin to determine the severity of duodenitis, and with diastase periodic acid-Schiff/alcian blue to assess the extent of gastric metaplasia. Slides were assessed by two histopathologists unaware of treatment status. H pylori was eradicated in 63% of subjects and all ulcers were healed at follow up. The median extent of gastric metaplasia at the start of treatment and 6-18 months (median 10) after treatment was compared in the two groups. Gastric metaplasia declined in eradicators from 16% to 8% (p < 0.05) while in non-eradicators there was no significant change (25% initially and at follow up). A positive relation between extent of gastric metaplasia and duodenal inflammation score was present before treatment (r(s) = 0.74, p < 0.001) and was unchanged after treatment in the non-eradicator group (r(s) = 0.89, p < 0.001). In the eradicator group, however, the inflammation score had significantly declined (p < 0.02) and the close relation with gastric metaplasia was no longer present. These results suggest that H pylori itself is at least in part responsible for producing gastric metaplasia of the duodenum.     

Low activities of disaccharidases associated with inflamed duodenal bulb mucosa

In order to establish whether an enzymatic method (a "functional" test) could be used instead of the histological picture as an indicator of damage to enterocytes of duodenal mucosa, biopsies were taken from 39 patients with upper gastrointestinal symptoms suggestive of peptic ulcer disease, but without active ulcers at endoscopy. Eleven patients with a normal appearance of the duodenal bulb mucosa and twenty-eight patients with various degrees of endoscopic inflammation ("bulbitis") were evaluated. The histological degree of duodenitis was assessed, and the activities of maltase, invertase, trehalase and lactase in the biopsy specimens were measured. Disaccharidase activities were inversely proportional to severity in both endoscopic and histological scoring of degree of inflammation. Low disaccharidase activities were also present in patients with endoscopic inflammation of the duodenal bulb, but without histological duodenitis. Focal and especially widespread gastric metaplasia was, in itself, significantly associated with low disaccharidase activities. The correlation between endoscopic and histologic scoring of inflammation of duodenal mucosa was not significant as assessed by kappa statistics. A previous history of peptic ulcer disease was significantly more common in patients with, than in those without, endoscopic inflammation of the duodenal bulb.     

Prevalence of Helicobacter pylori infection and related gastroduodenal lesions in spouses of Helicobacter pylori positive patients with duodenal ulcer.

BACKGROUND: To date, very few studies have evaluated the risk of infection among spouses of Helicobacter pylori positive patients and their results are conflicting. AIM: To assess the seroprevalence of H pylori infection in spouse of H pylori positive patients with duodenal ulcer as compared with age and sex matched volunteer blood donors, as well as the frequency of endoscopic gastroduodenal lesions in these spouses, according to the presence or absence of gastrointestinal complaints. METHODS: Some 124 spouses (48% males) of patients with duodenal ulcer consecutively seen over a 10 month period were studied. They were all screened for serum IgG anti-H pylori antibodies and asked to complete a questionnaire with particular reference to the presence of chronic or recurrent dyspepsia. Upper gastrointestinal tract endoscopy with antral and corpus biopsy specimens taken for histological examination and urease rapid test was offered to all seropositive spouses. Volunteer blood donors (248), living in Milan and matched for age, sex, north-south origins, and socioeconomic status to the cases, were used as controls. RESULTS: Spouses of patients with duodenal ulcer had a significantly higher seroprevalence of H pylori infection than controls (71% v 58%, p < 0.05); 30 of 88 (34%) H pylori positive spouses complained of dyspeptic symptoms compared with only four of 34 (12%) seronegative spouses (p < 0.02). At endoscopy, H pylori infection was confirmed in 48 of 49 (98%) seropositive spouses. The endoscopic findings in those spouses showed active duodenal ulcer in eight (17%), duodenal scar and cap deformity in two (4%), active gastric ulcer in two (4%), erosive duodenitis in three (6%), antral erosions in two (4%), antral erosions plus duodenitis in one, and peptic oesophagitis in another patient. The prevalence of major endoscopic lesions was significantly higher in symptomatic spouses than in those who had never been symptomatic. CONCLUSIONS: These findings show that being the spouse of an H pylori positive patient with duodenal ulcer may increase the risk of H pylori colonisation and perhaps of peptic ulcer disease, and raises questions as to whether serological screening of cohabiting partners of H pylori positive patients with duodenal ulcer may be indicated.     

结节型十二指肠炎的内镜表现及其临床病理学特征

目的 探讨结节型十二指肠炎内镜下表现与其组织学特征的关系及其发病机制。方法 观察内镜下136例结节型十二指肠炎的表现，对其活检标本均行H-E染色，观察病理改变，Giemsa染色及快速尿素酶试验诊断幽门螺杆菌感染，十二指肠黏膜兼作AB／PAS染色，观察十二指肠胃上皮化生。结果 136例结节型十二指肠炎内镜下表现为直径0．2～1．0cm大小不等的结节，伴有不同程度的充血、水肿，其中伴糜烂21例，出血点及（或）瘀斑30例。检出率占同期15820例内镜检查的0．9％，十二指肠炎的3．8％。病理诊断为十二指肠炎107例，其中慢性十二指肠炎53例，表现为间质内可见慢性炎性细胞浸润，肠绒毛缩短或萎缩、变平．肠腺不同程度减少；活动性十二指肠炎54例，除慢性炎性细胞外，黏膜层及固有层内还有不同程度的中性粒细胞浸润，伴Brunner腺增生51例，胃型上皮化生59例。136例中检出胃黏膜异位增生7例以及血吸虫虫卵所致的炎性病变4例，107例结节型十二指肠炎中，幽门螺杆阳性（Hp^＋）者为45．8％（49／107）。其中，53例慢性十二指肠炎患者中HP^＋者为32．1％（17／53），54例活动性十二指肠炎中Hp^＋检出率为59．3％（32／54），后者的Hp^＋检出率显著高于前者（P〈0．01）。结论 结节型十二指肠炎是一类特殊的非特异性十二指肠炎，内镜下表现与组织学改变存在不一致性。其发生可能与Hp感染及胃上皮化生、Brunner腺增生有关。     

Endoscopic Kyoto classification of Helicobacter pylori infection and gastric cancer risk diagnosis

Recent advances in endoscopic technology allow detailed observation of the gastric mucosa.Today,endoscopy is used in the diagnosis of gastritis to determine the presence/absence of Helicobacter pylori(H.pylori)infection and evaluate gastric cancer risk.In 2013,the Japan Gastroenterological Endoscopy Society advocated the Kyoto classification,a new grading system for endoscopic gastritis.The Kyoto classification organized endoscopic findings related to H.pylori infection.The Kyoto classification score is the sum of scores for five endoscopic findings(atrophy,intestinal metaplasia,enlarged folds,nodularity,and diffuse redness with or without regular arrangement of collecting venules)and ranges from 0 to 8.Atrophy,intestinal metaplasia,enlarged folds,and nodularity contribute to gastric cancer risk.Diffuse redness and regular arrangement of collecting venules are related to H.pylori infection status.In subjects without a history of H.pylori eradication,the infection rates in those with Kyoto scores of 0,1,and≥2 were 1.5%,45%,and 82%,respectively.A Kyoto classification score of 0 indicates no H.pylori infection.A Kyoto classification score of 2 or more indicates H.pylori infection.Kyoto classification scores of patients with and without gastric cancer were 4.8 and 3.8,respectively.A Kyoto classification score of 4 or more might indicate gastric cancer risk.     

Gastric metaplasia and Helicobacter pylori infection.

Duodenal and antral mucosal biopsy specimens were obtained from 139 patients with dyspeptic complaints to study the prevalence and extent of gastric metaplasia in the duodenal bulb in relation to Helicobacter pylori (H pylori) infection and duodenal ulcer disease. On logistic regression, the presence and extent of gastric metaplasia was not significantly associated with H pylori infection. The prevalence of gastric metaplasia, however, was found to be higher in patients with current or past evidence of duodenal ulcer disease in comparison with subjects with functional dyspepsia (p = 0.01). A follow up study on 22 patients before and at least one year after eradication of H pylori showed that the mean extent of gastric metaplasia did not change significantly after eradication and did not differ when compared with 21 patients with persisting infection. It is concluded that the unchanged gastric acid output after eradication of H pylori is a more important factor in the development of gastric metaplasia than the H pylori related inflammatory process.     

Deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer： A correlated study

AIM: To investigate the correlation among the presence and degree of gastric metaplasia of duodenal regenerating mucosa, the deformity of bulb and the recurrence of duodenal ulcer. METHODS: A total of 99 patients with duodenal ulcer were treated with H2-antagonist with or without antimicrobial therapy. All patients received follow-up endoscopic examinations 6 wk after treatment. When the ulcer(s) were noted to be healed, two biopsies were taken from the ulcer scar for histological study of gastric metaplasia, and 4 biopsies were taken from antrum for Helicobacter pylori (H pylori) study. Out of these cases, 44 received further follow-up endoscopic examinations after 3,6 and 12 mo respectively for studying the recurrence rate of duodenal ulcers. The correlation among ulcer recurrence, degree of gastric metaplasia of regenerating mucosa, bulbar deformity, and colonization of H pylori in the stomach was then studied. RESULTS: The results showed that there was a strong correlation between the deformity of duodenal bulb and the degree of gastric metaplasia of regenerating duodenal mucosa. The recurrence rate of duodenal ulcer had a significant difference between patients with and without H pylori colonization in the stomach (P<0.001). The greater the degree of gastric metaplasia of duodenal regenerating mucosa, the higher the recurrence rate of duodenal ulcer (P= 0.021). The more deformed the duodenal bulb, the higher the incidence of recurrence of duodenal ulcer (P = 0.03). CONCLUSION: There is a correlation among deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer. A more severely deformed duodenal bulb is closely related to a greater extent of gastric metaplasia. Both factors contribute to the recurrence of duodenal ulcer.     

Short-segment Barrett��s esophagus and cardia intestinal metaplasia: A comparative analysis

AIM:To investigate the endoscopy and histology of short-segment Barrett’s esophagus (SSBE) and cardia intestinal metaplasia (CIM),and their correlation with Helicobacter pylori (H. pylori) gastritis and gastroesophageal reflux disease (GERD). METHODS:Biopsy specimens were taken from 32 SSBE patients and 41 CIM patients with normal appearance of the esophagogastric junction. Eight biopsy specimens from the lower esophagus,cardia,and gastric antrum were stained with hematoxylin/eosin,Alcian blue/periodic acid-Schiff,Alcian blue/high iron diamine and Gimenez dye. Results were graded independently by one pathologist. RESULTS:The SSBE patients were younger than the CIM patients (P < 0.01). The incidence of dysplasia and incomplete intestinal metaplasia subtype was higher in SSBE patients than in CIM patients (P < 0.01). H. pylori infection was correlated with antral intestinal metaplasia (P < 0.05),but not with reflux symptomatic,endoscopic,or histological markers of GERD in CIM patients. SSBE was correlated with reflux symptomatic and endoscopic esophagitis (P < 0.01),but not with H. pylori infection and antral intestinal metaplasia. CONCLUSION:Dysplasia risk is significantly greater in SSBE patients than in CIM patients. CIM is a manifestation of H. pylori-associated and multifocal atrophic gastritis,whereas SSBE may result from GERD.     

The clinical relevance of endoscopic and histologic inflammation of gastroduodenal mucosa in dyspepsia of unknown origin

Two hundred and ten patients were defined as having dyspepsia of unknown origin. At endoscopy 11% had body gastritis, 46% antral gastritis, and 19% bulbitis (two thirds combined with antral gastritis). Histologically, 22% had chronic corpus gastritis (79% superficial, 21% atrophic), which was combined with chronic antral gastritis in 84%, 33% had chronic antral gastritis (82% superficial, 18% atrophic); and 14% had duodenitis, which was combined with antral gastritis in 65%. Polymorphonuclear leukocytes were found in specimens from the body mucosa in 6%, from the antral mucosa in 13%, and from the duodenal cap in 4%. The endoscopic findings correlated significantly with the histologic findings in the duodenal bulb (kappa = 0.33) but not in the stomach. The frequency of endoscopic antral gastritis and the frequency of histologic chronic body and antral gastritis increased with age. Endoscopic bulbitis and histologic duodenitis and gastric metaplasia were commoner in men than in women. Peak acid output was higher in patients with than in those without endoscopic bulbitis and higher in smokers than in non-smokers when the significant sex differences in peak acid output were taken into account. Gastric metaplasia of the bulb was predominantly correlated to higher peak acid output and to some extent also to sex and smoking. Episodic pain was correlated to histologic duodenitis. Other dyspeptic symptoms and the intragastric bile acid concentration were not associated with any endoscopic or histologic findings. Of the 210 patients, 172 were reexamined after a double-blind 6-week treatment period with cimetidine, antacid, or placebo. The symptomatic outcome of these treatments was not associated with any significant change in endoscopic or histologic findings.