Gastric Helicobacter and upper gastrointestinal symptoms in chronic renal failure

We studied histologically antral biopsies from 89 consecutive patients with chronic renal failure for Helicobacter pylori (previously Campylobacter pylori). A dose-response gastric secretion test was also performed. The frequency of Helicobacter-positive subjects was low (15/89, 17%), corresponding to figures reported in the literature for young symptomless volunteers. Helicobacter-positive patients had significantly more frequently upper gastrointestinal symptoms than Helicobacter-negative individuals (P less than 0.05). Antral gastritis was more common in the Helicobacter-positive than in the Helicobacter-negative renal patients (P less than 0.01), but the incidence of body gastritis did not differ between them. The Helicobacter-positive patients had lower serum urea levels (P less than 0.01) and higher acid outputs (P less than 0.001) than Helicobacter-negative subjects. All patients had raised fasting serum gastrin levels, which possibly obscured the difference between Helicobacter-positive (283 pg/ml) and -negative (331 pg/ml) patients. We conclude that in chronic renal failure gastric colonization of Helicobacter pylori is not more frequent than usual. It correlates positively with antral gastritis, gastric acid output and upper gastrointestinal symptoms, but negatively with serum urea levels.     

幽门螺杆菌血清分型与上消化道疾病的关系

目的 探讨幽门螺杆菌(helicobacter pylori,Hp or H.pylori)分型与消化道不同疾病的关系。方法 入选198例Hp阳性的胃镜检查患者，采用免疫印迹法进行Hp的血清学分型，并取胃窦黏膜经HE染色观察胃窦黏膜病理组织学变化。结果 198例患者中检出HpI型菌株173例(87．4％)，Ⅱ型菌株25例(12．6％)。I型较II型Hp感染者胃镜下消化性溃疡、胃癌的比例更高，P=0.012；与胃炎组比较，十二指肠球部溃疡组、胃癌组的I型感染者更高（P值分别为0.026、0.048），而与胃溃疡组无显著差别(P=0.125)。病理组织学改变I型较II型Hp感染者的结果更为严重（P=0.038）。结论 临床上消化道疾病患者Hp感染以I型菌株最为多见。Hp感染的分型诊断有助于对胃、十二指肠疾病类型及病情的判断，I型菌株感染者需要更为积极的治疗。     

Helicobacter pylori associated antral gastritis in peptic ulcer disease patients and normal healthy population of kashmir, India

Aim: To study the association of Helicobacter pylori infection with chronic antral gastritis in peptic ulcer disease patients and healthy population of Kashmir.Methods: 50 peptic ulcer patients (duodenal ulcer = 46, gastric ulcer = 2 and combined duodenal and gastric ulcer = 2) and 30 asymptomatic healthy volunteers were included in this study. Peptic ulcer was diagnosed on endoscopic examination. 4-6 punch biopsies were taken from gastric antrum in all the individuals and in case of gastric ulcer an additional biopsy was taken from the edge of the ulcer to exclude its malignant nature. Helicobacter pylori (H. pylori) organism was diagnosed using three different test methods, viz. Histology (using Giemsa Stain), Microbiology (Gram Stain) and Biochemistry (using one minute Endoscopy Room Test). Histological diagnosis of H. pylori was taken as the "gold standard" for the presence of H. pylori organism. Histological diagnosis of gastritis was made using Hematoxylin and Eosin Stain and the gastritis was classified as active chronic gastritis and superficial chronic gastritis.Results: Out of 30 peptic ulcer disease patients with associated antral gastritis, 27 (90%) were positive for H. pylori on histological examination (13 superficial chronic gastritis and 14 active chronic gastritis) whereas out of 8 healthy volunteers with histological evidence of chronic antral gastritis, H. pylori was observed in 7 individuals (87.50%) (4 active chronic gastritis and 3 superficial chronic gastritis).Conclusion: A highly significant association between H. pylori infection with chronic antral gastritis both in peptic ulcer disease patients and healthy volunteers of Kashmir was found in this study. Association between H. pylori infection and chronic gastritis was 90% in peptic ulcer group and 87.50% in healthy population (P<0.005).     

Chronic gastritis: last decade's achievements and problems

Classifications of chronic gastritis and neoplastic gastric diseases, developed in recent years (1996 Houston update of 1990 Sidney classification system, 2002 New Orlean classification of atrophic gastritis according to recommendations of International Group for Atrophy Studies; 1998 Padova classification of gastric displasia, and 1998 Vienna classification of gastrointestinal neoplasia) allow to statandardize international research and perform more objective diagnostics of pathological changes in the gastric mucosa. Studies carried out in recent years have established that morphological manifestations of chronic gastritis caused by Helicobacter pylori infection can be reduced after its eradication. Longterm treatment with proton pump inhibitors have been demonstrated not to cause atrophic changes in the gastric mucosa when undertaken after successful eradicational therapy. It has been established that corporal gastritis intensifies in patients treated with proton pump inhibitors. The studies show that measurement of serum levels of Helicobacter pylori antibodies, gastrine, pepsinogen I and II can be used in non-invasive serologic diagnostics of atrophic gastritis. Achievements in diagnostics and treatment of chronic gastritis create the necessary prerequisites for the development of gastric cancer preventing measures.     

Potentialities of a serological method in diagnosis of atrophic gastritis

AIM: To analyse diagnostic potential of "serological gastrobiopsy" in patients with various gastroduodenal diseases. MATERIAL AND METHODS: A total of 244 patients with gastroduodenal pathology have been examined. The diagnoses made morphologically were compared with those made by the serological method. The diagnosis of duodenal ulcer, gastric ulcer, atrophic gastritis, nonatrophic gastritis was made in 155, 31, 43 and 15 patients, respectively. The type of chronic gastritis was diagnosed by the levels of gastrin-17, pepsinogen I, pepsinogen II and antibodies to Helicobacter pylori in blood serum. The diagnoses made serologically were compared with those made morphologically. RESULTS: The highest accuracy of a serological diagnosis of mucosal atrophy of the antral stomach was observed in gastric ulcer (80.6%) and duodenal ulcer (71.6%) in high sensitivity and low specificity. The accuracy of the diagnosis of gastric body mucosa atrophy in atrophic gastritis was 60.5%, in gastric ulcer--51.6%, in duodenal ulcer 58.7% in high specificity and low sensitivity. Serological diagnosis of gastric atrophy was accurate in 71.7%. In weak morphological picture of gastric body atrophy false negative serological diagnosis is possible. No false positive results occurred in diagnosis of gastric body mucosal atrophy (specificity 100%). A negative correlation was found between the severity of gastric body atrophy and pepsinogen I serum level (r = -0.380), pepsinogen I to pepsinogen II in blood serum (r = -0.392). No differences were revealed in gastrin-17 levels in the serum in different atrophy severity in the antral mucosa. CONCLUSION: "Serological gastrobiopsy"provides satisfactory accuracy of atrophic gastritis diagnosis in gastroduodenal diseases.     

老年人消化性溃疡与慢性萎缩性胃炎的相关性研究

目的研究老年人消化性溃疡与慢性萎缩性胃炎的相关性。方法对十二指肠溃疡（DU）、胃溃疡（GU）和复合性溃疡（CU）的老年患者胃窦、胃窦胃体交界处和胃体黏膜以及慢性胃炎（CG）患者胃窦黏膜活检标本进行组织学检查,统计各自胃黏膜的萎缩、肠化生、慢性炎症、活动性和幽门螺杆菌（Hp）感染的发生率。结果 DU患者胃窦、胃窦胃体交界处和胃体黏膜的萎缩发生率分别为54.0%、8.0%和16.0%,肠化生发生率分别为19.0%、6.0%和4.0%。其胃窦黏膜肠化生的发生率明显低于相应的GU、CU或CG者。3种消化性溃疡和CG患者均存在胃窦部慢性炎症,且老年消化性溃疡患者胃体部炎症的发生率较高,其胃炎活动性以胃窦部为主,且均较CG者高。结论老年人消化性溃疡均可有胃窦部灶性萎缩和肠化生发生,但DU胃窦黏膜肠化发生率最低,这可能是老年DU患者罹患胃癌危险性较低的原因之一。     

Antigastric autoantibodies inHelicobacter pylori infection: role in gastric mucosal inflammation

The aim of the study was to ascertain whether there is an association between the presence of serum parietal cell autoantibodies (PCA) and: (1) Helicobacter pylori infection; (2) the presence and degree of gastritis and intestinal metaplasia; and (3) the H. pylori infecting strain. Gastric mucosal biopsies were obtained from 49 consecutive patients in order to assess and grade gastritis, make a histological diagnosis, and culture and genotype H. pylori. H. pylori infection was present in 26 patients (group 1), had been present in 17 patients (group 2), and the remaining 6 (group 3) had never had the infection. The infecting strain was cagA positive in 21 of 26 group 1 patients. Positive PCA results were found in 84%, 76%, and 14% of patients in groups 1, 2, and 3, respectively. PCA results were correlated with anti-H. pylori antibody titers (P<0.05). In group 2 patients, PCA were associated with the degree of antral gastritis (Fisher's exact test P<0.05). cagA status was not associated with the presence of PCA (chi2=0.68, NS). The frequency of positive findings for PCA in group 2 was higher in patients with (90%) than in those without (50%) intestinal metaplasia. In conclusion: (1) H. pylori infection is associated with the production of PCA, which, after eradication of the infection, persist and might contribute to the persistent antral chronic gastritis and intestinal metaplasia; (2) the gastric lesions associated with infections sustained by the more-virulent H. pylori strains do not appear to be due to the induction of antigastric autoantibodies.     

血清抗幽门螺杆菌IgG抗体、胃蛋白酶原水平与胃癌发病的相关性分析

目的研究长春地区人群血清抗幽门螺杆菌(Helicobacter pylori,Hp)IgG抗体、胃蛋白酶原水平和胃癌发病的相关性,为胃癌的防治研究提供依据和流行病学资料。方法选择2008年10月至2011年2月吉林大学第一医院明确诊断的450例原发性胃癌患者作为病例组,选择同时期体检中心1072例健康体检者作为对照组。采用酶联免疫吸附(ELISA)法检测血清中Hp IgG抗体、胃蛋白酶原Ⅰ(PGI)和Ⅱ(PGII)的水平,确定Hp菌感染和萎缩性胃炎的发生状况。以PGI≤82.3μg/L,同时PGI/PGII≤6.05作为萎缩性胃炎的诊断标准。结果胃癌组与对照组相比,Hp感染阳性率明显增高(69.1%vs.52.4%,χ2=36.1,P<0.001)。胃癌组中血清PGI水平与对照组比较无显著差异(93.2vs.88.9μg/L,P<0.001),而PGII浓度显著升高(15.9vs.11.3μg/L,P<0.001),同时PGI/PGII比值明显降低(5.4vs.7.8,P<0.001)。胃癌组中患萎缩性胃炎的比例明显高于对照组(31.4%vs.10.4%,P<0.001)。多因素回归分析显示:在调整年龄和性别因素后,Hp感染和萎缩性胃炎均为胃癌发病的独立危险因素。结论本研究对象人群中Hp感染率,尤其是青年胃癌患者中Hp感染率仍然较高,Hp感染和萎缩性胃炎是胃癌发病的危险因素。与PGI相比,血清PGII浓度和PGI/PGII比值可能成为胃癌筛选的潜在血清学标志物。     

HELICOBACTER PYLORI PREVALENCE IN A ROUTINE UPPER GASTROINTESTINAL ENDOSCOPY POPULATION

SUMMARY The presence of Helicobacter pylori (HP) in gastric biopsy specimens of 500 patients referred for routine upper gastrointestinal endoscopy for various abdominal complaints was investigated histologically and microbiologically. HP was detected in 429 of the 500 patients (86%). Antral biopsy specimens revealed gastritis in 457 out of 500 cases (91.4%). In the 43 patients who had normal histological findings, only 3 had HP infection (7%). The prevalence of HP in the patients with gastric and duodenal ulcers was 91%. In 95.6% of the ulcer patients, biopsy specimens showed gastritis. There was a statistically significant rise in the prevalence of HP with age. The correlation between histologic and microbiologic diagnostic methods was good. This study shows that HP positivity and gastritis are common in a routine endoscopy population and that there is a strong association between H. pylori, gastritis and peptic ulcer disease.     

胃癌患者血清巨噬细胞移动抑制因子水平的临床意义

目的：检测胃癌患者血清巨噬细胞移动抑制因子（MIF）的浓度水平,并评估其在胃癌诊断中的应用价值。方法用ELISA方法检测2007年2月至2010年4月在我院手术胃癌患者106例,其中男71例,女35例,平均年龄56.2岁（22～78岁）。所有病例均经病理学确认为原发性胃癌）、48例胃炎患者（接受胃镜检查诊断为慢性胃炎）及50例健康（健康体检者,排除一切肿瘤以及炎症性相关疾病）对照者血清MIF水平,同时测定癌胚抗原CEA。通过多因素Logistic回归分析,利用受试者工作特征（ROC）曲线分析MIF、CEA以及联合诊断对胃癌的诊断价值。结果胃癌患者血清中MIF平均浓度为4586 pg/ml,均高于单纯胃炎患者（1602.4 pg/ml）和健康对照（1105.6 pg/ml）,差异均有显著统计学意义（P均＜0.05）。胃癌患者血清MIF的水平与患者性别、年龄、病理类型不相关。但胃癌患者血清MIF水平随着肿瘤分期的升高而升高,差异有显著统计学意义（P＜0.05）。伴有淋巴结转移胃癌患者MIF水平显著高于未转移者（P＜0.05）。根据ROC曲线分析,MIF检测胃癌的临界值为3018 pg/ml时诊断效能最大,敏感度为79.4%,特异度为85.1%。MIF与CEA联合检测诊断价值高于单独诊断（P＜0.05）。结论胃癌患者血清中存在高水平的MIF,MIF可能为胃癌潜在的肿瘤标志物,MIF联合CEA可提高胃癌的诊断率,值得临床应用。     

胃黏膜癌前病变中bcl-2蛋白表达与幽门螺杆菌感染的关系

目的 观察幽门螺杆菌(HP)感染后胃黏膜癌前病变中bcl—2蛋白表达的特点，探讨服在胃癌发生发展过程中的作用。方法 应用免疫组织化学SP法及Warthin-Starry嗜银染色(WS染色)，对56例慢性胃炎、46例慢性胃炎伴肠化生、34例异型增生进行bcl—2蛋白表达及服检测的研究。结果 胃黏膜肠化生组及异型增生组的服感染率及bcl—2蛋白阳性表达率均明显高于慢性胃炎组(P＜0．05)；86例HP阳性者bcl-2蛋白表达39例，阳性率45．3％，50例HP阴性者bcl—2蛋白表达12例，阳性率24％，两者比较，差异显著(P＜0．05)。结论 在慢性胃炎、肠上皮化生、异型增生的进展过程中，bcl—2蛋白的表达水平在增高。HP感染在胃癌发生、发展过程中起一定作用。bcl—2蛋白的表达可能是服致癌的作用机制之一。     

Helicobacter pylori infection enhances mucosal interleukin-1β, interleukin-6, and the soluble receptor of interleukin-2

It is thought thatHelicobacter pylori colonization of the gastric mucosa might stimulate the production of several cytokines, which might trigger and maintain the gastric inflammation associated withHelicobacter pylori infection. In the present study we evaluated interleukin-1β, interleukin-6, and the soluble receptor of interleukin-2 both in mucosal homogenates and in the sera ofHelicobacter pylori-infected (39 cases) and uninfected (40 cases) patients to investigate whether there was any relationship between variations in cytokines and (1) the severity ofHelicobacter pylori-associated gastritis or (2) CagA-positiveHelicobacter pylori strains. Mucosal, but not serum levels of interleukins-1 and-6 and interleukin-2 receptor were significantly higher in infected than uninfected patients, Serum levels ofHelicobacter pylori antibodies were significantly higher in infected than uninfected patients, These levels correlated with mucosal interleukin-1β. The degree of antral or body inflammatory grade was higher in infected than in uninfected patients; cytokines levels were higher in patients with high-grade gastritis, most of whom wereHelicobacter pylori positive. Patients infected with CagA-positive strains also had higher levels of interleukin-1β, but not of interleukin-2 receptor or interleukin-6. In conclusion,Helicobacter pylori infection results in a local increase in interleukins-1β and-6 and interleukin-2 receptor associated with high-grade mucosal inflammation. Interleukin-1β seems to favor anti-Helicobacter pylori antibody production, and mucosal levels are enhanced mainly in patients infected with cytotoxicHelicobacter pylori strains.     

胆汁反流和幽门螺杆菌感染在胆汁反流性胃炎和消化性溃疡发病中的作用

目的探讨胆汁反流和幽门螺杆菌感染在胆汁反流性胃炎和消化性溃疡发病中的作用。方法采用病理组织学检查和快速尿素酶试验对76例胆汁反流性胃炎及22例兼有胆汁反流性胃炎和消化性溃疡的患者行幽门螺杆菌检测,并与29例消化性溃疡患者作对照。结果胆汁反流性胃炎组幽门螺杆菌阳性率为31.6%(24/76例),兼有胆汁反流性胃炎和消化性溃疡组幽门螺杆菌阳性率为59.0%(13/22例),消化性溃疡组幽门螺杆菌阳性率为72.4%(21/29例),前二组比较,差异有显著意义(P<0.05),后二组比较,差异无显著意义(P>0.05)。结论胆汁反流在胆汁反流性胃炎的发病中起主要作用,幽门螺杆菌感染在消化性溃疡的发病中起主要作用。胆汁反流和幽门螺杆菌感染在胆汁反流性胃炎和消化性溃疡的共同发病中互不明显影响,幽门螺杆菌感染所起的作用可能更大一些。     

Differential diagnosis of upper gastrointestinal bleeding proximal to the ligament of Trietz

Upper gastrointestinal bleeding (UGIB) is an important medical problem for patients and the medical system. The causes of UGIB are varied and their accurate identification guides appropriate management. The major cause of UGIB is peptic ulcer disease, for which Helicobacter pylori and nonsteroidal antiinflammatory drug use are major risk factors. Lesser causes include Dieulafoy lesion, gastric antral vascular ectasia, hemobilia, aortoenteric fistulas, and upper gastrointestinal tumors. Awareness of causes and management of UGIB should allow physicians to treat their patients more effectively.     

Relationship of Helicobacter pylori CagA(+) status to gastric juice vitamin C levels

BACKGROUND: To date it is not known whether gastric juice vitamin C levels are influenced by Helicobacter pylori CagA(+) strains. The aim of the present study, therefore, was to study the impact of H. pylori CagA status on gastric juice vitamin C levels. MATERIALS AND METHODS: We studied 30 H. pylori(+) patients, and the results were compared with 10 endoscopically and histologically normal H. pylori(-) subjects (control group) who were similar to the H. pylori(+) group in terms of age and sex. In all patients, gastric juice vitamin C levels were determined and the severity of gastritis was graded on a scale of 0 (absent) to 3 (severe). CagA was determined by immunoblotting the sera from patients against H. pylori antigens. RESULTS: Among 30 H. pylori(+) patients, 20 were CagA(+) and 10 CagA(-). In the entire group of H. pylori(+) patients, the median gastric juice vitamin C levels (mg L-1) were 16.35 (range 3.5-33.6) and were significantly lower (P < 0.001) than in the control group of H. pylori(-) patients [35.5 (23.1-50.2)]. In addition, in the entire group of H. pylori(+) patients there was a highly significant (P < 0.0001) inverse correlation between the gastritis activity score and the gastric juice vitamin C levels. In the group of H. pylori CagA(+) patients, the median levels of gastric juice vitamin C were 13.8 (3.5-31.2) and were significantly lower than the corresponding levels in both the H. pylori CagA(-) group [24.8 (22-33.6), P < 0.01] and the H. pylori(-) control group [35.5 (23.1-50.2), P < 0.001], the last groups being similar. Furthermore, the gastritis activity median score in the H. pylori CagA(+) group [2 (1-3)] was significantly higher (P < 0.05) than in the H. pylori CagA(-) group [1 (1-2)]. CONCLUSION: These data indicate that infection with CagA(+) H. pylori strains significantly lowers the gastric juice vitamin C levels in comparison with CagA(-) H. pylori strains, which might have a significant impact on gastric carcinogenesis.     

幽门螺杆菌相关性胃溃疡与内皮素、降钙素相关基因肽的变化及临床意义

目的 为了探讨内皮素（ET）、降钙素相关基因肽（CGRP）在幽门螺杆菌（H．pylori）相关性胃溃疡发病中的作用。方法选择幽门螺杆菌感染（H．pylori）阳性胃溃疡患者50例，阴性组50例，健康人50例，用放射免疫法测定其血清降钙素相关基因肽（CGRP）内皮素（ET）水平。结果幽门螺杆菌阳性胃溃疡患者血清CGRP水平分别明显低于和ET高于阴性组和健康者，差异均有显著性（P〈0．01）．抗Hp治疗后血清CGRP上升，ET下降。结论提示血清CGRP水平下降，ET上升可能与幽门螺杆菌感染所致疡的发病有关.     

Real-time detection of Helicobacter Pylori infection and atrophic gastritis: comparison between conventional methods and a novel device for gastric juice analysis during endoscopy

BACKGROUND AND STUDY AIMS: Gastric juice may represent a valuable source of clinicopathological information if properly analyzed. We evaluated the reliability and clinical validity of data obtained using an innovative device (the "Mt 21-42") that analyzes gastric juice, thus allowing the identification of Helicobacter pylori infection and atrophic gastritis of the oxyntic mucosa during endoscopy. METHODS: Validation studies were carried out to evaluate the measuring performance of the device. In addition, the H. pylori status and the presence of atrophic gastritis were assessed in 150 patients undergoing upper gastrointestinal endoscopy. In all these patients the Mt 21-42 device was used to assist endoscopy. Conventional tests (involving histology, urease testing, urea breath testing, anti- H. pylori IgG, serum gastrin, pepsinogen, intrinsic factor and parietal cells autoantibodies, vitamin B12, and folate) were also performed for comparison with the Mt 21-42 results. RESULTS: The measuring performance of the Mt 21-42 was good; for pH, the relative percent error and the coefficient of variation were 1.9 % +/- 4.2 and 1.3 %, respectively, and for ammonium they were 0.1 % +/- 0.2 % and 2.1 %. For the detection of H. pylori infection, the sensitivity and specificity of the device (96.7 % and 94.3 %) were similar to those of the urea breath test (90.5 % and 93.3 %) and serology (87.1 % and 88.8 %), and higher than those of the urease test (78.6 % and 98.7 %; P < 0.01) and routine histology (94.3 % and 76.3 %; P < 0.05). When compared with the currently available standard methods, use of the Mt 21-42 was found to be the most sensitive technique for the detection of atrophy (94.7 % vs. 5.3 % - 47.4 %; P < 0.001); the device failed to detect the disease in only one case (5 %), whereas failure rates of 53 % - 95 % were reported with the conventional methods. CONCLUSION: Atrophic gastritis of the oxyntic mucosa is a risky condition that often goes undetected in current clinical practice. The Mt 21-42 is an effective, useful, and desirable tool that may help to overcome this diagnostic limitation; it produces time and cost savings and also allows the detection of H. pylori infection.     

Tumour necrosis factor alpha stimulates gastrin release from canine and human antral G cells: possible mechanism of the Helicobacter pylori–gastrin link

There is evidence that gastric Helicobacter pylori ( Hp ) infection promotes duodenal ulceration by releasing gastrin. We therefore asked how Hp releases gastrin. Tumour necrosis factor alpha (TNF-α) is up-regulated in Hp gastritis and stimulates hormone release from pituitary cells, so we tested its effect on primary cultures of canine antral G cells and human antral fragments. TNF-α pretreatment (100ngmL^–1) of canine G cells significantly increased both basal (by 89%: P <0.01) and bombesin-stimulated (by 39% P <0.05) gastrin release. A similar pattern of increase was seen following TNF-α (20ngmL⁻¹) pretreatment of human antral fragments: basal gastrin release was increased by 38% ( P  < 0.05) and bombesin-stimulated by 26% ( P  < 0.05). This effect persisted during immunoblockade with anti-somatostatin antibody S6. We propose that TNF-α provides the link between Hp infection and gastrin release and thus contributes to duodenal ulceration.     

Reduced amoxicillin uptake into human gastric mucosa when gastric juice pH is high.

Amoxicillin when administered with gastric acid suppressors has been shown to be effective in eradication of Helicobacter pylori in 50 to 80% of subjects. The aim of this investigator-blind crossover study was to determine if gastric mucosal amoxicillin uptake was affected by increasing gastric juice pH. Fifteen male subjects (7 H. pylori positive and 8 H. pylori negative) were randomized to receive 150 mg of ranitidine twice a day, 300 mg of ranitidine twice a day, or no drug for 2 days prior to upper endoscopy. The last dose of ranitidine was given 60 min prior to upper endoscopy, and amoxicillin (500 mg) was given 30 min prior to upper endoscopy. The amoxicillin concentrations in mucosal biopsy samples, gastric juice, and serum were determined by a standard microbiological bioassay technique. Mean amoxicillin levels were greater in samples of antrum, fundus, and duodenum for volunteers who received no ranitidine than in those receiving 300 mg of ranitidine (P < 0.05) and those receiving 150 mg of ranitidine (P < 0.05 except for fundus). Amoxicillin levels in the antrum, fundus, and duodenum were negatively correlated with gastric juice pH (P < 0.005 for antrum; P < 0.001 for fundus and duodenum). There was no correlation between gastric juice pH and amoxicillin levels in either gastric juice or serum. The amoxicillin concentration in gastric juice was significantly higher with 300 mg of ranitidine than with no ranitidine (P < 0.05). Thus, lower gastric juice pH is associated with a higher rate of mucosal uptake of amoxicillin.     

Campylobacter pylori in chronic gastritis

Altogether 301 patients with duodenal, gastric and prepyloric ulcers and non-ulcer controls were examined to study whether the Campylobacter pylori is related to ulcer itself or to coexisting chronic gastritis. Histological sections from antral and body mucosa were stained according to Warthin-Starry, Giemsa and with hematoxylin-eosin. The Campylobacter pylori was strongly associated with chronic superficial gastritis in both ulcer and non-ulcer patients and in both antral and body mucosa. No differences were found in the frequency of Campylobacter-positive cases between ulcer patients and non-ulcer controls when the comparison was made within this category of chronic gastritis (p greater than 0.05). The gastric ulcer patients have more often than non-ulcer controls the Campylobacter pylori in atrophic body gastritis (p less than 0.001). The bacteria were only occasionally seen in normal mucosa.