GERD and H. pylori: is there a link?

The incidence of gastroesophageal reflux disease (GERD) and esophageal adenocarcinoma have increased in recent years as the incidence of peptic ulcer disease and distal gastric cancer have declined. Given the simultaneous decline in Helicobacter pylori infection, it is tempting to propose a relationship between H. pylori infection and these opposing time trends. Although H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from developing GERD and its complications. The most likely mechanism in which H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.     

The possible role of Helicobacter pylori in GERD

A variety of abnormalities contribute to the development of gastroesophageal reflux disease (GERD) including transient lower esophageal sphincter relaxation, low esophageal sphincter pressure, presence of a hiatal hernia, diminished esophageal clearance of refluxed gastric contents, and alterations in esophageal mucosal resistance. Helicobacter pylori infection clearly plays a role in the pathogenesis of peptic ulcer disease and mucosa associated lymphoma of the stomach and is a definite risk factor for distal gastric cancer. The role of H. pylori infection in GERD remains controversial and incompletely understood. Although H. pylori infection does not cause reflux disease, circumstantial evidence suggests that it may protect against the development of GERD and its complications in some patients. The most likely mechanism whereby H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.     

Helicobacter pylori and gastroesophageal reflux disease: friends or foes?

Gastroesophageal reflux disease (GERD) is responsible for a high proportion of digestive symptoms attributable to the upper gastrointestinal tract. Helicobacter pylori (H. pylori) is the main etiologic factor in chronic gastritis and gastroduodenal ulcer disease, but its relation with GERD has not yet been established. The aim of this paper is to review the relationship between H. pylori and GERD, trying to answer the question whether a nexus of "friendship" or "hate" exists between them. Although H. pylori may, in theory, represent a cause for GERD, available data suggest that the infection is not a risk factor for the development of GERD, and the microorganism could even represent a protective factor against this disease. The antisecretory effect of proton pump inhibitors (PPIs) seems to depend on the presence of the infection and H. pylori eradication has, therefore, negative consequences on the efficacy of antisecretory drugs (although its possible clinical relevance, precisely in patients with GERD, remains unknown). Moreover, H. pylori eradication in patients with duodenal ulcer disease is associated in some studies, but not in others, with a higher incidence of GERD, although the reported reflux esophagitis is usually mild. It can be concluded, from these data, that investigating or treating H. pylori infection is not recommended in patients with GERD (when these patients do not need PPI maintenance therapy). Finally, it has recently been recommended to eradicate H. pylori infection in those patients with GERD needing long-term treatment with omeprazole, as some studies have reported that this drug induces, in presence of the microorganism, an atrophic gastritis, with the consequent theoretic risk of gastric cancer. However, several arguments against this attitude can be postulated, and noteworthy are the following: many studies suffer important methodological defects, several authors report contrary results, and the possibility that H. pylori could play, as previously mentioned, a protective role against GERD. It may be concluded, therefore, that the indication of eradicating H. pylori in patients with GERD and maintenance therapy with PPIs, although supported by several arguments, cannot be considered as definitively established. In conclusion, H. pylori and GERD seem to have, in any case, a "friendly" relationship, although it may be transformed into one of "hate" when PPIs enter the scene.     

Should we test for Helicobacter pylori before treating gastroesophageal reflux disease?

Gastroesophageal reflux disease (GERD) is a common problem in childhood. The cause is uncertain but because the incidence of GERD is increasing in developed countries and the prevalence of Helicobacter pylori is decreasing, it has been suggested that this infection protects against GERD. Observational data from 95 children, however, suggest that H. pylori eradication does not have a deleterious effect on GERD and this is supported by randomized controlled trials in adults. H. pylori eradication may also reduce the efficacy of proton pump inhibitor therapy in infected patients. There are no data from children but inferences from randomized controlled trials in adults suggest this effect is likely to be modest and of uncertain clinical significance. H. pylori is an important risk factor for distal gastric adenocarcinoma. It is likely that treating the infection in childhood will prevent pre-malignant changes associated with H. pylori from developing in the future. A meta-analysis of four randomized controlled trials suggest that there is a statistically significant impact on healing of chronic gastritis after one year compared with placebo (RR of chronic gastritis: 0.27; 95% CI 0.23 to 0.32). H. pylori eradication is therefore recommended in children with GERD that are having an endoscopy. However, when the diagnosis of GERD is being made clinically or by pH monitoring, it is not necessary to screen for H. pylori.     

幽门螺杆菌与胃食管反流病

幽门螺杆菌（Helicobacter pylori，H．pylori）与胃食管反流病（gastroesophageal reflux disease，GERD）的关系各研究结果不尽一致，流行病学研究表明，在GERD中不仅Mpylori感染率较低，而且cagA的检出率也低，二者都与食管疾病严重程度呈负相关。亦有文献报告H．pylori感染与GERD发生无明显关系。H．pylori对食管保护作用机制可能与其能提高LES压力、降低胃内酸度和影响食管对酸的敏感性有关。有研究表明，H．pylori可以提高质子泵抑制剂的抑酸效果，亦有人认为H．pylori并不影响GERD疗效。因此H．pylori与GERD的关系仍需进一步的临床和基础研究来评价。     

Helicobacter pylori infection, pattern of gastritis, and symptoms in erosive and nonerosive gastroesophageal reflux disease.

BACKGROUND: The aim of this study was to evaluate the prevalence of Helicobacter pylori infection and the characteristics of gastritis and symptoms of patients with erosive and nonerosive gastroesophageal reflux disease (GERD). METHODS: We studied 202 consecutive patients with a diagnosis of GERD (symptoms score and endoscopy): group A (n = 110), erosive GERD; group B (n = 92), nonerosive GERD; 200 patients with upper abdominal complaints without abnormalities at endoscopy (functional dyspepsia, group C); and 200 asymptomatic controls tested for H. pylori serum antibody (group D). Antral and body biopsy specimens were taken for histology and the rapid urease test in groups A, B, and C. RESULTS: The prevalence of H. pylori infection was higher in groups B and C (62% and 55%, respectively) than in A and D (36% and 40%) (P < 0.05). In positive patients H. pylori colonization and gastritis grade scores in the gastric body were higher in nonerosive than in erosive GERD and functional dyspepsia (P < 0.05). No differences in H. pylori colonization or gastritis grades were found in the antrum. Fifty-nine patients with nonerosive GERD (64%) and 42 with erosive GERD (38%) showed other dyspeptic symptoms associated with reflux symptoms (P < 0.05). CONCLUSIONS: H. pylori prevalence is higher in patients with nonerosive GERD than in normal subjects and in patients with erosive GERD and similar to that of patients with dyspepsia. Patients with nonerosive GERD often show dyspeptic symptoms and higher H. pylori colonization and inflammation grades in the proximal stomach. Our data support the hypothesis that in GERD H. pylori gastritis may, on the one hand, protect against the development of esophageal erosions and, on the other, contribute to the esophageal hypersensitivity to acid which is a feature of GERD.     

Motion--Helicobacter pylori worsens GERD: arguments for the motion.

There are several reasons for eradicating Helicobacter pylori in patients with chronic gastroesophageal reflux disease (GERD). Perhaps the most compelling is the evidence that chronic acid suppression therapy can lead to the development of atrophic gastritis, a premalignant condition, in patients with H pylori infection. Epidemiological data that suggest that H pylori is less prevalent in GERD patients than in control subjects may be susceptible to publication bias, and confounding social and environmental factors may also be involved. Although it has been thought that eradication of the organism might lead to increased esophageal acid exposure, this has not been demonstrated in practice. Studies that appeared to show that GERD could be provoked by antimicrobial therapy of duodenal ulcers also have methodological weaknesses. Underlying GERD symptoms might be unmasked after withdrawal of acid-suppression therapy, for reasons that are unrelated to H pylori. In fact, eradication of the organism has been shown to decrease heartburn in patients with peptic ulcer disease. When H pylori is successfully eradicated in patients with GERD, relapse rates are not increased, and the disease-free interval seems to be prolonged. Eradication of the organism is a wise policy in patients who face long term acid-suppression therapy for GERD.     

根除幽门螺杆菌与胃食管反流病的关系研究

目的探讨根除幽门螺杆菌（H．pylori）与胃食管反流病（GERD）的关系。方法本研究采用食管内24hpH监测的方法，定量观察H．pylori阳性GERD患者根除H．pylori和单用兰索拉唑治疗3月后食管酸暴露的变化，以及H．pylori阳性慢性浅表性胃炎（CSG）根除H．pylori和姑息治疗3月后食管酸暴露的变化。RE组：反流性食管炎（RE）表现患者60例，按就诊门诊号随机分为治疗组和对照组。治疗组采用丽珠唯三联＋兰索拉唑方案，对照组单用兰索拉唑。CSG组：慢性浅表性胃炎（CSG）患者60例，按就诊门诊号随机分为治疗组和对照组。治疗组均采用丽珠唯三联方案，对照组不采用药物治疗。以上两组待H．pylori根除后，对比研究H．pylori根除组和对照组3月后食管24hpH监测参数。结果RE组：H．pylori根除和单用兰索拉唑治疗3月后两组24h食管pH监测主要观察5项指标均无显著性差异（P〉0．05）。CSG组：H．pylori根除和姑息治疗3月两组24h食管pH监测主要观察5项指标均无显著性差异（P〉0．05）。结论GERD患者根除幽门螺杆菌后食管酸暴露无明显改变，CSG患者根除幽门螺杆菌后食管酸暴露无明显改变，H．pylori感染可能与GERD的转归和发生无关。     

Gastric mucosal morphological consequences of acid suppression: a balanced view

In the chapter, an analysis of the literature on the relationship between Helicobacter pylori, the use of proton pump inhibitors and the development of atrophic gastritis is presented, and the difficulties of classifying gastritis and the new possibilities of quantifying chronic inflammation by morphometric analysis are discussed. The issue surrounding the necessity of eradicating H. pylori in H. pylori-positive patients has still not been solved. Most studies have now accepted that proton pump inhibitors indeed accelerate the onset of atrophic gastritis in H. pylori-positive patients, but evidence against such an association was published in one recent (Scandinavian) study; conclusions from this study have, however, been challenged by several groups. Some data are available on the efficacy of H. pylori eradication with regard to the prevention of atrophy. The limited significance of the development of parietal cell protrusions and fundic gland cysts is better understood, but much less is known of the development and long-term consequence of H. pylori-induced autoimmune gastritis. Finally, recent studies in H. pylori-positive patients indicate that treatment with proton pump inhibitors may promote bacterial N-nitrosation formation. These data taken together suggest that the eradication of H. pylori may be based not only on morphological arguments, but also on bacterial alterations in the gastric milieu.     

Prevalence and distribution of Helicobacter pylori in gastroesophageal reflux disease: a study from the East

OBJECTIVES: The relationship between Helicobacter pylori infection and gastroesophageal reflux (H. pylori) disease (GERD) is controversial. In Asian populations, the prevalence of H. pylori infection is high and GERD is relatively uncommon. The aim of this study was 1) to test the hypothesis that H. pylori protects the esophagus against GERD, and 2) to study the pattern of H. pylori colonization and gastritis in GERD. METHODS: We conducted a prospective case-control study in which patients with GERD and asymptomatic controls were compared for the prevalence of H. pylori infection. Diagnosis of GERD was based on symptoms of heartburn that improved with acid-suppressive therapy and/or endoscopic evidence of erosive esophagitis. H. pylori status was determined by serology and, when endoscopy was indicated, was confirmed by rapid urease test and histology. Gastric biopsies were examined under hematoxylin and eosin and Giemsa stains. Density of H. pylori colonization and activity of gastritis at different parts of stomach were graded and compared according to Updated Sydney system. RESULTS: A total of 106 patients with GERD and 120 age- and sex-matched, asymptomatic controls were enrolled. The prevalence of H. pylori infection was significantly lower in GERD patients (31%) compared with controls (61%, p < 0.001, odds ratio 0.229, 95% confidence interval 0.13-0.41). H. pylori-infected GERD patients showed significantly more severe gastritis in the antrum than in other parts of stomach (mean inflammatory scores: antrum; 3.3 +/- 1.63*, body; 1.85 +/- 1.31; fundus; 1.65 +/- 0.58; cardia, 1.65 +/- 1.39; *p < 0.005). H. pylori colonization was found less commonly and at lower density at the cardia compared with other parts of the stomach. CONCLUSIONS: H. pylori infection protects against the development of GERD, and carditis is unlikely to play an important role.     

Effects of environment and lifestyle on gastroesophageal reflux disease

BACKGROUND: Gastroesophageal reflux disease (GERD) is comprised of a spectrum of related disorders, including hiatal hernia, reflux disease with its associated symptoms, erosive esophagitis, peptic stricture, Barrett's esophagus, and esophageal adenocarcinoma. Besides multiple pathophysiological associations among these disorders, they are also characterized by their comorbid occurrence in identical patients and by their similar epidemiologic behavior. The occurrence of GERD is shaped by marked temporal and geographic variations, suggesting the influence of environmental risk factors in the etiology of these diseases. VARIATIONS BY TIME, GEOGRAPHY, AND RACE: Between 1975 and 2005, the incidence of GERD and esophageal adenocarcinoma increased fivefold in most Western countries. The incidence of GERD also appears to be rising in the most developed countries of Asia. All severe forms of GERD, such as erosive esophagitis, peptic stricture, Barrett's metaplasia, and esophageal adenocarcinoma, are more common among whites than other ethnic groups. AFFLUENCE AND OBESITY AS RISK FACTORS: Barrett's esophagus and esophageal adenocarcinoma tend to occur slightly more often in subjects with higher income. Overweight and obesity contribute to the development of hiatal hernia, increase intra-abdominal pressure, and promote gastroesophageal reflux. Weight gain increases reflux symptoms, whereas weight loss decreases such symptoms. Other risk factors, such as smoking, alcohol, dietary fat, or drugs, play only a minor role in shaping the epidemiologic patterns of GERD. PROTECTION THROUGH HELICOBACTER PYLORI: On a population level, a high prevalence of H. pylori infection is likely to reduce levels of acid secretion and protect some carriers of the infection against reflux disease and its associated complications. Several studies have confirmed a lesser prevalence of H. pylori among subjects with than without GERD. Until recently, populations in Africa and Asia may have been protected against the development of GERD and esophageal adenocarcinoma by their higher prevalence of H. pylori infection. CONCLUSION: The study of environmental risk factors may provide an opportunity to better understand GERD and develop a means of its prevention.     

Gastroesophageal reflux disease and Helicobacter pylori infection

The prevalence of Helicobacter pylori infection has been decreasing while the prevalence of gastroesophageal reflux disease and esophageal adenocarcinoma has been increasing in developed countries since the 1930s. This has raised concerns that H. pylori infection may protect against esophageal disease and that the disappearance of H. pylori from the population might lead to a further increase in gastroesophageal reflux disease. Some studies have suggested that eradication of H. pylori in patients with duodenal ulcer disease results in an increase in the incidence of erosive esophagitis, whereas other studies have shown no such increase. Studies on gastric acid secretion have demonstrated that proton pump inhibitors are more effective in controlling gastric pH in individuals who are infected with H. pylori. Studies on the impact of therapy in patients with erosive esophagitis have been conflicting. This article reviews each of the issues in the debate separately and concludes that there is little evidence to suggest a major effect of H. pylori eradication on the outcome of gastroesophageal reflux disease.     

The changing epidemiology of GERD: geography and Helicobacter pylori

BACKGROUND: Issues have arisen regarding H. pylori infection and GERD that have caused unnecessary confusion among practicing physicians. In the last century GERD became increasingly recognized in the West and it has become evident that the prevalence of GERD is now occurring in many previously underdeveloped countries. METHODS: This review article fosters understanding of the issues by focusing on the esophageal acid load and the factors that control it. In particular, we discuss the effects of the change in the patterns of gastritis that have occurred naturally as well as after H. pylori eradication and correlate those changes with their effects on the esophageal acid load. We show how it is possible to separate gastroesophageal reflux from gastroesophageal reflux disease based on differences in esophageal acid load. We also describe how the practice of assessing gastroesophageal reflux based on the time the intraesophageal pH is less than 4 resulted in investigators systematically discarding data critical to understanding of the effect of their interventions on esophageal acid load. Testable hypotheses are presented to explain the interactions between H. pylori and GERD and between H. pylori and the changing epidemiology of GERD. CONCLUSIONS: We propose that the confusion regarding H. pylori and the changing epidemiology of GERD is based on the failure to critically examine the historical evidence in relation to the other H. pylori-related diseases as well as reliance on techniques that are either unable to measure, or systematically discard data critical for understanding effects of various interventions on the esophageal acid load. This has resulted in propagation of erroneous concepts regarding H. pylori and adenocarcinoma of the esophagus and has resulted in some patients being denied appropriate therapy.     

Current understandings of Helicobacter pylori, peptic ulcer and gastroesophageal reflux disease

H. pylori infection is a major pathogen inducing gastric mucosal inflammation and causing dysregulation of normal acid inhibitory regulatory mechanisms. The overall effect on gastric acid secretion is dependent on the location and severity of inflammation. Eradication results in healing of gastric mucosal inflammation, healing of peptic ulcers, prevention of new peptic ulcers, prevention or reduction in gastric cancer risk and in transmission of the infection. Neither H. pylori infection nor H. pylori eradication causes gastroesophageal reflux disease (GERD). H. pylori eradication also does not impede anti-secretory drug therapy of GERD. Misunderstandings of the negative association between H. pylori infection and GERD and/or Barrett's esophagus and misuse of the epidemiologic concept of 'protection' led to considerable confusion and likely resulted in some patients receiving poor care. Current evidence is consistent with the notion that H. pylori should be eliminated whenever the organism is found. However, H. pylori infection has become increasing difficult to cure in part due to the emergence of antimicrobial resistance. In Western countries, triple therapy consisting of a proton pump inhibitor, amoxicillin and clarithromycin no longer achieves adequate eradication rates and will soon need to be abandoned. When used, legacy triple therapy should be given for 14 days. Fluorquinolones may temporarily be useful: 10-14 day duration is superior to 7 days. However, worldwide resistance is rapidly increasing. Other potential replacement therapies and strategies are discussed including sequential therapies, high-dose proton pump inhibitor plus amoxicillin, and new quadruple therapies.     

Helicobacter pylori and gastroesophageal reflux disease

The nature of the relationship between Helicobacter pylori (Hp) infection and gastroesophageal reflux disease (GERD) remains unclear. This article reviews the current body of knowledge regarding the association between these two common entities. The authors examine the potential interactions of Hp and GERD from epidemiologic and pathophysiologic viewpoints and summarize and critique the prevalence and eradication studies that have been performed to date. Special consideration is given to the possible effects that long-term use of proton pump inhibitors may have on Hp gastritis.     

Positive serum antibody and negative tissue staining for Helicobacter pylori in subjects with atrophic body gastritis

Helicobacter pylori is rarely found in gastric biopsy specimens from individuals with atrophic gastritis of the body mucosa. To determine if subjects with atrophic body gastritis have evidence of previous infection with H. pylori, immunoglobulin G antibody to H. pylori was measured by enzyme-linked immunosorbent assay in sera of 399 Finnish subjects. In 124 subjects, multiple biopsy specimens from body and antrum had been evaluated for the presence of H. pylori by Giemsa staining. Antibody correlated well with H. pylori staining except in the subgroup with atrophic body gastritis, in whom the prevalence of seropositivity (86%) was significantly greater than the prevalence of positive staining (33%) (P less than 0.001). Twenty-five subjects had positive antibody and negative staining. This group had a significantly higher prevalence of atrophic body gastritis (80%), lower maximal acid output, lower serum pepsinogen I levels, and higher serum gastrin concentrations than did seropositive subjects with H. pylori. These data suggest that most patients with atrophic body gastritis, despite having a low incidence of current overt infection, have been infected with H. pylori at some point in their lives.     

Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett's esophagus, Barrett's dysplasia, and Barrett's adenocarcinoma

OBJECTIVE: This study was undertaken to prospectively determine the prevalence of gastric H. pylori infection in Barrett's esophagus and Barrett's complicated by dysplasia or adenocarcinoma. METHODS: The prevalence of H. pylori was determined in Barrett's esophagus patients compared to a control population of patients with gastroesophageal reflux disease (GERD) only. All patients had a minimum of 10 gastric surveillance biopsies obtained. H. pylori colonization was determined upon the basis of hematoxylin and eosin and use of a modified Giemsa and or Steiner's silver stain of all gastric biopsy specimens. RESULTS: Two hundred and eighty-nine Barrett's patients and 217 GERD control patients were included in the study. H. pylori was found in 95/289 (32.9%) of the Barrett's patients, compared with 96/217 (44.2%) of the GERD controls (NS). Forty-seven of the Barrett's patients had low-grade dysplasia/indefinite dysplasia, 14 high-grade dysplasia, and 20 Barrett's adenocarcinoma. When Barrett's was subgrouped according to absence of dysplasia, and presence of low-grade dysplasia, high-grade dysplasia, or adenocarcinoma, H. pylori prevalence was found to be significantly less for patients with Barrett's high-grade dysplasia (14.3%) and adenocarcinoma (15.0%) versus patients with GERD alone (44.2%), Barrett's alone (35.1%), or Barrett's with low-grade dysplasia (36.2%) (p = 0.016). This difference could not be explained by differences between Barrett's esophagus patients infected with H. pylori and those who were not with respect to gender, smoking history, alcohol consumption, use of proton pump inhibitor, or length of Barrett's mucosa. CONCLUSIONS: Barrett's high-grade dysplasia and adenocarcinoma are significantly more prevalent in patients who are not infected with H. pylori. H. pylori appears to have a protective effect against the development of Barrett's adenocarcinoma.     

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM： To compare the prevalence of H pylori infection, peptic ulcer, cytomegalovirus （CNV） infection and Candida esophagitis in human immunodeficiency virus （HIV）- positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.
METHODS： A total of 151 patients （122 HIV-positive and 29 HIV-negative） with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of Hpylori infection, CMV, candida esophagitis and histologic chronic gastritis.
RESULTS： The prevalence of Hpylori was less common in HIV-positive patients （22.1%） than in HIV-negative controls （44.8%; P 〈 0.05）, and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer （20.7% vs 4.1%; P 〈 0.01）, but a higher prevalence of chronic atrophy gastritis （6.9% vs 24.6%; P 〈 0.05）, Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis （P 〈 0.05）. In HIV-positive patients, chronic active gastritis was not significantly different between those with Hpylori infection and those without.
CONCLUSION： The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to Hpylori infection.     

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM: To compare the prevalence of H pylori infection,peptic ulcer,cytomegalovirus (CMV) infection and Candida esophagitis in human immunodeficiency virus (HIV)-positive and HIV-negative patients,and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections. METHODS: A total of 151 patients (122 HIV-positive and 29 HIV-negative) with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of H pylori infection,CMV,candida esophagitis and histologic chronic gastritis. RESULTS: The prevalence of H pylori was less common in HIV-positive patients (22.1%) than in HIV-negative controls (44.8%; P < 0.05),and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group,HIV-positive patients had a lower incidence of peptic ulcer (20.7% vs 4.1%; P < 0.01),but a higher prevalence of chronic atrophy gastritis (6.9% vs 24.6%; P < 0.05),Candida esophagitis and CMV infection. Unlike HIV-negative group,H pylori infection had a close relationship to chronic active gastritis (P < 0.05). In HIV-positive patients,chronic active gastritis was not significantly different between those with H pylori infection and those without. CONCLUSION: The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to H pylori infection.     

A low prevalence of H pylori and endoscopic findings in HTV-positive Chinese patients with gastrointestinal symptoms

AIM: To compare the prevalence of H pylori infection,peptic ulcer, cytomegalovirus (CMV) infection and Candida esophagitis in human immunodeficiency virus (HIV)-positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.METHODS: A total of 151 patients (122 HIV-positive and 29 HIV-negative) with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of H pylori infection,CMV, candida esophagitis and histologic chronic gastritis.RESULTS: The prevalence of H pylori was less common in HIV-positive patients (22.1%) than in HIV-negative controls (44.8%; P ＜ 0.05), and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer (20.7% vs 4.1%; P ＜ 0.01), but a higher prevalence of chronic atrophy gastritis (6.9% vs 24.6%; P ＜ 0.05), Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis (P＜0.05). In HIV-positive patients, chronic active gastritis was not significantly different between those with H pylori infection and those without.CONCLUSION: The lower prevalence of H pylori infection and peptic ulcer in HTV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer.The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to H pylori infection.