Role of Helicobacter pylori in cirrhotic patients with dyspepsia: a 13C-urea breath test study

The role ofHelicobacter pylori in dyspeptic, cirrhotic patients remains unclear. This prospective outpatient study, conducted to assess the relationship of gastroduodenal disease andH. pylori as determined by the (¹³C) urea breath test, enrolled 109 consecutive cirrhotic patients with dyspepsia. All patients underwent upper-gastrointestinal endoscopy, which revealed respective prevalences of peptic ulcer, gastric ulcer, and duodenal ulcer of 41.3%, 23.9%, and 22.9%;H. pylori infection was found in 52.3%. The rate of peptic ulcer disease in theH. pylori-positive (45.6%) and -negative (36.5%) groups was not significantly different; neither was the prevalence ofH. pylori in patients with or without portal hypertensive gastropathy and with or without esophageal varices. The relationship between peptic ulcer disease andH. pylori in dyspeptic patients with cirrhosis appears to be weak. Likewise, no significant relationship was evident betweenH. pylori and portal hypertensive gastropathy or esophageal varices. This organism may not be a major pathogenetic factor in gastroduodenal diseases in dyspeptic patients with cirrhosis.     

Geographical Pathology of Helicobacter pylori Infection: Is There More than One Gastritis?

Helicobacter pylori is the aetiological agent of chronic gastritis and a major causative factor in duodenal and gastric peptic ulcer disease; a strong association also exists with gastric cancer and primary gastric lymphoma. The prevalence of infection in adults ranges from less than 15% in developed countries to virtually 100% in less developed areas. If H. pylori infection alone was responsible for the development of gastritis, peptic ulcer disease, gastric carcinoma and primary gastric lymphoma, one would expect the frequency of all these conditions to parallel closely the prevalence of H. pylori infection. This is clearly not the case: therefore, genetic, environmental and cultural factors must act in concert with H. pylori to induce different outcomes of the infection.

This paper outlines the geographic approach to the study of disease and discusses the possible application of this methodology to the inquiry into the relationship between H. pylori, atrophic gastritis and gastric cancer. Preliminary results of a study showing great variation in the prevalence of intestinal metaplasia in duodenal ulcer patients from different geographic origin are presented and briefly discussed.     

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.     

Strategies for peptic ulcer healing after 1 week proton pump inhibitor-based triple Helicobacter pylori eradication therapy in Japanese patients: differences of gastric ulcers and duodenal ulcers

Helicobacter pylori (H. pylori) eradication therapy alone is insufficient to ensure healing of large ulcers with H. pylori-positive gastric ulcer (GU). The question of what is the optimum antiulcer treatment following H. pylori eradication therapy has not been fully elucidated. Furthermore, the ulcer healing effects of eradication therapy itself with H. pylori-positive duodenal ulcer (DU) have not been investigated. In GU study, the eradication therapy + proton pump inhibitor (PPI) group (group A) were administered eradication therapy followed by 7 weeks of a PPI, and the eradication therapy + gastroprotective drug (GP) group (group B) eradication therapy followed by 7 weeks of a GP. In DU study, the eradication therapy + PPI group (group C) were administered eradication therapy followed by 5 weeks of a PPI, and the eradication therapy only group (group D) was eradication therapy alone. In GU study, healing rates for ulcer of ≥15 mm in diameter were significant greater in the group A. In DU study, high healing rates were seen both the group C and D. In conclusion, a PPI could significantly heal GU than a GP after eradication therapy in GU. Meanwhile, the eradication alone is sufficient for DU.     

B超诊断消化性溃疡的临床价值

目的：评估Ｂ超诊断消化性溃疡的临床价值，提高Ｂ超诊断消化性溃疡的准确率。方法：将超声首诊的５３例消化性溃疡和５例疑诊为溃疡型癌的资料全部与胃镜、部分与手术病理检查作了对照分析。结果：Ｂ超诊断胃溃疡的符合率为８６％。诊断十二指肠球部溃疡的符合率为８８％。超声疑诊的５例溃疡型癌经病理证实３例为溃疡型癌，２例为慢性胃溃疡。结论：超声可以检出一定大小和深度的活动期溃疡。胃粘膜和粘膜下层回声向溃疡边缘集中是超声诊断胃溃疡的特征性表现，有别于胃癌。较大的胃溃疡需依赖胃镜和病理组织活检与胃癌鉴别。对于浅表性溃疡，超声诊断有困难     

Are tryptase and cathepsin D related toHelicobacter pylori infection and mucosal gastrin in peptic ulcer?

The pathogenesis of peptic ulcer is a complex phenomenon and several factors are thought to be involved in this process. Among others,Helicobacter pylori infection, hypergastrinaemia and some proteases seem to play an essential role in inducing peptic ulceration. We investigated whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (a lysosomal hydrolase which seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked toHelicobacter pylori infection and mucosal content of gastrin. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer and 11 with duodenitis. Tryptase and cathepsin D were measured in mucosal biopsy specimens (body and antrum of the stomach and duodenum) using IRMA methods. Gastrin was assayed in the antral mucosa by means of a RIA method.Helicobacter pylori infection was histologically evaluated (Giemsa). Tryptase and cathepsin D levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. The mucosal content of cathepsin D, but not that of tryptase, was associated withHelicobacter pylori infection. Tryptase, on the other hand, was related to gastrin content. No correlation was found between the two enzymes. It is concluded that tryptase and cathepsin D probably reflect different pathophysiological modifications in ulcer disease. Cathepsin D seems to be mainly related to the phlogistic reaction of the mucosa toHelicobacter pylori infection; tryptase may reflect and indirect link between the action of gastrin and the function of mast cells.     

Helicobacter pylori in Peptic Ulcer: Have Koch's Postulates Been Fulfilled?

This brief review considers whether or not Koch's postulates have been fulfilled for Helicobacter pylori and peptic ulceration. The histological features of peptic ulcer disease in man are active chronic gastritis with antral predominance, duodenal gastric metaplasia and active duodenitis. Other features are hyperpepsinogenaemia, relative postprandial hypergastrinaemia and basal acid hypersecretion. The macroscopic features are duodenal bulb ulceration or lesser curve and antral gastric ulceration.

At present, gastric colonization with H. pylori has been produced in small animal species (rats and mice), but the infection is difficult to establish in immunocompetent animals, and histological gastritis is unconvincing. In larger animals the germ-free pig has been the most reliable model but the gastritis tends to be chronic with little activity.

The best examples of acute infection are in three ‘self-administration’ experiments in humans. In these cases acute gastritis with hypochlorhydria developed which, when it converted to active chronic gastritis, tended to be asymptomatic. Either the circumstances were incompatible with ulceration, or the experiments were not continued for the many years necessary to develop peptic ulceration. It is concluded that only one of the many steps required for the development of peptic ulceration has so far been fulfilled, i.e. the ability of H. pylori to produce histological gastritis in a susceptible host.     

老年人消化性溃疡并大出血临床及病理特征分析

目的探讨老年人消化性溃疡出血的临床及病理特征。方法 116例消化性溃疡患者,根据年龄将患者分为老年组(≥60岁)和中青年组(<60岁),比较两组的消化性溃疡出血的临床及病理特征。结果老年组典型上腹痛、无症状、伴随发病率依次为11.8%、35.3%、30.9%;中青年组依次为43.8%、31.3%3、5.4%(P<0.05);老年组胃溃疡、十二指肠溃疡、巨大溃疡(直径>2 cm)发生率依次为52.9%、19.1%、20.6%;中青年组依次为10.4%、60.4%、8.4%(P<0.05)。老年组出血量1 000 mL以上分别为22.1%,中青年组为8.3%(P<0.05)。结论老年组典型上腹痛少、无症状伴随疾病多,胃溃疡及十二指肠溃疡多、异型增生多,大出血、中重度贫血多见,临床治疗难度大。     

慢性肺源性心脏病合并消化性溃疡的原因探讨

目的 探讨慢性肺源性心脏病合并消化性溃疡的原因,为早期防治提供依据.方法 回顾了1998年1月至2005年1月8年间共236例慢性肺源性心脏病患者的病历,对已经作了胃镜检查,提示有确切消化性溃疡病变的病人的病史、临床表现、用药、治疗措施以及其他辅助检查的结果进行了分析.结果 236例中有68例作了胃镜检查,36例提示有活动期消化性溃疡病变,其发病率为15.25%,检出率为52.94%.36例中胃溃疡22例,十二指肠溃疡14例,临床上均缺乏消化性溃疡的典型表现.结论 慢性肺心脏病容易合并消化性溃疡,且临床表现不典型,应该早期防范与处理.     

Serum IL-8 as a possible marker for determining the status of<Emphasis Type="Italic">Helicobacter pylori</Emphasis> infection in patients with untreated and treated peptic ulcer

Failure to eradicateHelicobacter pylori can lead to peptic ulcer recurrence and gastric malignancy. Therefore, the objective of this study was to develop a noninvasive method for determining whetherH pylori infection was eradicated with antibiotic-based triple therapy. A total of 17 patients with duodenal ulcer (DU) and 17 with gastric ulcer (GU) were evaluated both before and after treatment. Outcomes included serum levels of interleukin-8 (IL-8), pepsinogen I, and gastrin, and the Wilcoxon signed rank test was used to test significance. Changes in these parameters were also correlated with disease status. In those patients where both GU and DU healing occurred as a result of treatment, most showed an increase in serum IL-8 and a decrease in serum pepsinogen. Serum gastrin levels were not significantly changed in either group. Posttreatment increases in serum IL-8 were seen in 15 of 17 (88%) recovered DU patients and 14 of 17 (82%) recovered GU patients (P < .05 for each). Posttreatment decreases in pepsinogen I were found in 15 of 17 DU and 15 of 17 GU patients (P < .05 for each). These preliminary findings suggest that an increase in serum IL-8 and possibly a decrease in pepsinogen I may be useful in identifying the successful eradication ofH pylori infection in patients with peptic ulcer treated with antibiotics. A more systematic analysis of these putative diagnostic markers is now warranted.     

Helicobacter pylori infection in Finland

Helicobacter pylori causes chronic gastritis worldwide and it is the most important single factor in peptic ulcer disease. Up to half of H. pylori infected individuals develop atrophic gastritis over years and decades. H. pylori infection has also been classified as a class I carcinogen in human gastric cancer. Most infections are obtained in childhood, in Finland mainly before the age of 7 years but the exact transmission routes are not known. The infection shows an age‐dependent pattern, the infection being rare among children but gradually becoming more prevalent among older age groups. As new infections are few in adults and the infection only rarely disappears without effective antimicrobial therapy, the occurrence of the infection in the old actually reflects the prevalence of the infection in their childhood. In developed countries, such as Finland, a rapid decline of H. pylori prevalence rate has been demonstrated. In order to speed up this natural decline of the infection, a unique population based ‘screen and treat’ project was started in Vammala, a semiurban south‐western community in Finland. In this survey, young inhabitants were offered diagnosis and treatment for H. pylori.     

Phosphorylation of<Emphasis Type="Italic">Helicobacter pylori CagA</Emphasis> in patients with gastric ulcer and gastritis

The effects ofHelicobacter pylori infection are strongly associated with chronic gastritis, gastric and duodenal ulcer, gastric cancer, and MALT lymphoma. The microorganism has been classified as a type I carcinogen by the World Health Organization. Varying clinical results fromH. pylori infection are believed due, in part, to differences in virulence among species. Thecag pathogenicity island is a complex of virulent genes and a coding region for the type IV phosphorylated secretion system. Through this system, many virulent gene products or proteins are phosphorylated into the host cells. This study demonstrated the positiveCagA- phosphorylation effect ofH. pylori in patients with chronic gastritis and benign gastric ulcer and revealed significantly different rates ofCagA phosphorylation between these two diseases (P < .05).     

High prevalence of virulent Helicobacter pylori strains in symptomatic Bulgarian patients

The aim of the study was to evaluate the prevalence of main virulence genes in Helicobacter pylori strains from 116 patients with peptic ulcers (41 cases) and nonulcer diseases (75) by polymerase chain reaction (PCR) with pure cultures and to compare the results with those by multiplex PCR in 39 H. pylori-positive gastric biopsies in another center in Sofia, Bulgaria. Strain susceptibility to amoxicillin, metronidazole, and clarithromycin was determined by agar dilution method. By PCR with pure cultures, coinfections with multiple H. pylori strains were found in 8 (6.9%) patients who were excluded from the statistical analysis. Prevalence of toxigenic type vacA s1 was higher (91.7%) than that usually reported in Europe. cagA-positive genotype was detected in most (81.5%) strains, and almost all of them harbored vacA s1 genotype. Strains with cagA+/vacA s1a genotype were more common (80.6%) than the other genotypes (19.4%, P = 0.0001). The ulcer patients had more often virulent strains than the other patients (92.3% versus 75.4% for cagA+, 100.0% versus 87.0% for vacA s1, 100% versus 84.0% for vacA s1a, and 92.3% versus 73.9% for cagA+/vacA s1a, respectively). The prevalence of H. pylori virulence-associated genes was not associated with patients' sex and age or with the antibacterial resistance of strains. The most common H. pylori genotype was cagA+/vacA s1a. Similar prevalence of cagA-positive (82.1%), vacA s1 (97.4%), and cagA+/vacA s1 strains (79.5%) was found by multiplex PCR in gastric biopsies in the 2nd center. In conclusion, H. pylori strains with virulent genotypes are widespread in symptomatic Bulgarian patients.     

消化性溃疡幽门螺杆菌(Hp)清除前后血Hp抗体、PG、GAS 变化的研究

幽门螺杆菌(Helicobacter pylori,Hp)阳性消化性溃疡患者在Hp清除前后血清抗Hp-IgG,抗Hp-IgM,胃蛋白酶原(Pep-sinogen,PG)和胃泌素(Gastrin,GAS)水平如何?奥美拉唑,硫糖铝,罗红霉素治疗Hp感染的消化性溃疡的效果如何?本课题对上述问题进行了研究。1材料与方法1.1一般资料病例选     

Helicobacter pylori infection and peptic ulcer disease in cirrhotic patients: An updated meta-analysis

BACKGROUNDPeptic ulcer (PU) is more prevalent in patients with liver cirrhosis. The role of Helicobacter pylori (H. pylori) infection in the pathogenesis of PU in patients with cirrhosis is still not elucidated. AIMTo perform a meta-analysis on the prevalence of H. pylori infection and PU and their association in liver cirrhosis patients.METHODSWe searched PubMed, EMBASE, Web of Science, Cochrane, CNKI, Wangfang, and CQVIP databases from inception to July 10, 2020. Odds ratio (OR) and 95% confidence interval (CI) were pooled using a random-effects model. The statistical heterogeneity among studies (I²-index), subgroup analyses, regression analysis, sensitivity analysis, and the possibility of publication bias were assessed.RESULTSA total of 14 studies (13 cross-sectional studies; 1 cohort study) involving 2775 individuals (611 cases with PU and 2164 controls) were included in our meta-analysis. The prevalence of PU in patients with cirrhosis was 22%. The prevalence of H. pylori infection was 65.6% in cirrhotic patients with PU, and 52.5% in those without. The pooled overall OR was 1.73 (95%CI: 1.16-2.56, I² = 66.2%, P < 0.001, Z = 2.7, P_z < 0.05). We did not find the cause of heterogeneity in the subgroup analyses and meta-regression analysis except for one study. Funnel plot did not show significant publication bias. The results of Begg’s test and Egger’s test indicated no evidence of substantial publication bias (P_Begg = 0.732, P_Egger = 0.557).CONCLUSIONThere is a weakly positive association between H. pylori infection and PU in patients with liver cirrhosis. It is suggested that H. pylori infection may play a role in the pathogenesis of PU in liver cirrhotic patients.     

Coadaptation of Helicobacter pylori and humans: ancient history,modern implications

Humans have been colonized by Helicobacter pylori for at least 50,000 years and probably throughout their evolution. H. pylori has adapted to humans, colonizing children and persisting throughout life. Most strains possess factors that subtly modulate the host environment, increasing the risk of peptic ulceration, gastric adenocarcinoma, and possibly other diseases. H. pylori genes encoding these and other factors rapidly evolve through mutation and recombination, changing the bacteria-host interaction. Although immune and physiologic responses to H. pylori also contribute to pathogenesis, humans have evolved in concert with the bacterium, and its recent absence throughout the life of many individuals has led to new human physiological changes. These may have contributed to recent increases in esophageal adenocarcinoma and, more speculatively, other modern diseases. Helicobacter pylori, Gram-negative bacilli that colonize the human stomach, are the main cause of peptic ulceration, gastric lymphoma, and gastric adenocarcinoma, the second leading cause of death from cancer worldwide. They also may contribute to other conditions, including iron and vitamin B12 deficiencies, idiopathic thrombocytopenic purpura (ITP), and growth retardation in children. H. pylori colonization occurs in childhood and persists throughout life, causing disease mainly in adults (1, 2). However, despite the fact that about half the world’s population carries H. pylori, only a small proportion develop ulcers or gastric cancer. This raises a number of questions, including how has H. pylori adapted to persistently colonize humans? and why (and how) does it cause disease in only a minority of those colonized? The other side of this coin is that although humans have been colonized for millennia by H. pylori, it is now disappearing (2, 3). During the time period over which H. pylori has gradually disappeared from some populations, including much of the USA and western Europe, other diseases have become more prevalent. For example, there is an increased incidence of gastroesophageal reflux disease (GERD) and its complications; obesity and its associated diseases, including type 2 diabetes; and atopic and allergic diseases, including asthma. These observations also raise a number of questions, including how have we adapted to H. pylori colonization over millennia? and does the absence of H. pylori cause any physiologic or immunologic imbalances that contribute to diseases of modern life? As we discuss in this Review, recent extensive genomic and molecular analyses have shed some light on these issues.     

General and local humoral immunity in patients with peptic ulcer

Systemic and local humoral immunity and nonspecific defense factors were investigated in 88 patients with duodenal peptic ulcers and 18 patients with gastric ulcers. In acute conditions, nonspecific defence was depressed and blood IgG level was increased in peptic ulcer patients. An increase in complement titre, C3 and lysozyme, and a decrease in IgG were recorded after treatment, although normal levels were never attained. Salivary, gastric-juice and duodenal-content secretory IgA levels were characteristically increased during acute phases of peptic ulcer; salivary IgA declined after treatment. The disturbance of nonspecific defence, systemic and local humoral immunity, demonstrated in patients with peptic ulcers, may be regarded as a possible ulcerogenic mechanism.     

食管上段胃黏膜异位内镜下合并症的研究

目的 研究食管上段胃黏膜异位(HGMUE)的内镜检出率、内镜下表现和合并症.方法 回顾性研究2019年1月-2020年6月该院消化内镜中心经电子食管胃镜检查且诊断为HGMUE的患者资料.分析HGMUE的检出率、内镜下表现和合并症.结果 51326例接受胃镜检查的患者中,375例诊断为HGMUE,检出率为0.73％.内镜...     

Effect of centrally administered prolactin on gastric and duodenal ulcers in rats

The effect of centrally administered prolactin on gastric acid secretion and experimentally-induced gastric and duodenal ulcers was studied. The acute gastric ulcer models used were pylorus ligation, indomethacin-induced and ethanol-induced gastric ulcers. Chronic gastric ulcers were induced using acetic acid and duodenal ulcers by cysteamine hydrochloride. In pylorus ligated rats, prolactin (1 microg/kg icv) produced 45% increase in gastric content volume, significant increase in free acidity (P < 0.001), total acidity (P < 0.001) and ulcer index (P < 0.001). It did not show any significant effect on ethanol-induced and indomethacin-induced gastric ulcers. Prolactin increased the ulcer index (P < 0.001) and ulcer score (P < 0.05) in acetic acid-induced chronic gastric ulcers. It also increased ulcer area (P < 0.05) in cysteamine-induced duodenal ulcers. Therefore, the proulcerogenic activity of prolactin was due to its gastric hypersecretory effect.     

老年人消化性溃疡166例胃镜分析

目的了解我院老年人消化性溃疡（Pu）发病特点。方法分析166例老年人消化性溃疡胃镜报告结果。结果老年人PU的检出率为10.78％,男女之比为4.35：1;胃溃疡（GU）占62.65％,十二指肠溃疡（DU）占30.72％,GU与Du之比为2.08：1,复合性溃疡占6.62％,多发性溃疡占24.1％。结论老年人PU的患者男性多于女性,Gu多于DU,GU的好发部位是胃窦和胃角,DU的好发部位是十二指肠球前壁;PU的幽门螺杆菌（Hp）感染率为81.93％。