Effect of Helicobacter pylori eradication on gastroesophageal function

BACKGROUND: To elucidate the cause of possible occurrence of reflux esophagitis after Helicobacter pylori eradication, gastric and esophageal function among H. pylori infected Japanese patients were evaluated both before and after eradication therapy. METHODS: Nine H. pylori-positive patients were studied before and 6 months after successful H. pylori eradication. Studies included gastric emptying, esophageal manometry, gastric and esophageal pH monitoring as well as measuring serum levels of gastrin, pepsinogen I and pepsinogen II. RESULTS: Helicobacter pylori eradication was associated with a significant change in serum gastrin and pepsinogen levels, consistent with the improvement in mucosal inflammation. There was no significant change in gastric emptying, fasting or postprandial lower esophageal sphincter (LES) pressure, esophageal primary peristaltic contractions, frequency of transient LES relaxation, or gastroesophageal reflux, as assessed by 24 h pH monitoring. The percent time of the gastric pH>4 at night decreased significantly. A 41-year-old male developed erosive gastroesophageal reflux disease (GERD) (Los Angeles Classification Grade A) after eradication. Physiological studies showed he had abnormal esophageal motility prior to H. pylori eradication. CONCLUSIONS: With the exception of gastric pH at night, most patients did not experience a significant change in gastric or esophageal function after H. pylori eradication. Development of GERD post H. pylori eradication likely reflects an increase in the acidity of the refluxate superimposed on pre-existing abnormalities in gastroesophageal motility.     

Corpus gastritis and erosive esophagitis: a report from the Middle East.

OBJECTIVE: To assess whether corpus gastritis due to Helicobacter pylori protects against erosive esophagitis in an area with high prevalence of H. pylori infection. METHODS: Biopsies obtained from gastric corpus and antrum in 151 patients with symptoms of gastroesophageal reflux disease were studied for presence of H. pylori and endoscopic evidence of gastritis. Presence and grade of esophagitis at endoscopy was recorded. RESULTS: Fifty-four (36%) patients had endoscopic esophagitis. Patients with severe esophagitis (>or= grade II) less often had active gastritis (15/45 vs. 55/98; p=0.02) and had a lower density of H. pylori (p=0.0003) than those without esophagitis. CONCLUSION: Active corpus gastritis due to H. pylori infection may protect against erosive esophagitis in patients with gastroesophageal reflux disease in the Middle East.     

Motion--Helicobacter pylori causes or worsens GERD: arguments against the motion.

Data from large epidemiological studies show that Helicobacter pylori is less prevalent in patients with gastroesophageal reflux disease (GERD) than in control subjects. The more virulent cagA-positive strains of the organism are also less commonly seen in patients with erosive esophagitis and in those with Barrett's esophagus than in those with less severe forms of GERD. Although the relationship between H pylori and gastric physiology is complex, the organism has little effect on acid secretion in most North American or Western European subjects, and has a net suppressive effect, especially in elderly subjects, in other parts of the world. Thus, the organism has a potential protective effect against GERD, which is exacerbated by gastric acidity. H pylori has no proven effect on other gastric factors that might provoke reflux, including delayed gastric emptying or inappropriate relaxation of the gastric fundus. Two well-designed interventional studies have found that eradication of H pylori either provoked GERD or had no effect. A third smaller study, which seemed to demonstrate that persistent infection was associated with GERD, was flawed, in that the two treatment groups were not comparable. The evidence thus does not support the idea that H pylori infection provokes or aggravates GERD.     

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.     

Reflux esophagitis patients in Singapore have motor and acid exposure abnormalities similar to patients in the Western hemisphere

OBJECTIVE: Endoscopic esophagitis is less common in the East than in the West. The reason for this is unknown. This study examines prospectively the relationship between endoscopic esophagitis and lower esophageal sphincter pressure, distal esophageal contractility, esophageal peristaltic performance, esophageal acid exposure, gastric acid output, and Helicobacter pylori (H. pylori) status in a consecutive series of Asian patients. METHODS: Esophageal manometry and ambulatory pH monitoring were carried out in 48 patients with endoscopic esophagitis and 208 patients with symptoms suspicious of gastroesophageal reflux disease but without esophagitis. Gastric acid output and H. pylori serology were determined in 22 of the esophagitis group and 36 of the nonesophagitis group. RESULTS: Compared to the nonesophagitis patients, esophagitis patients had a higher prevalence of hypotensive lower esophageal sphincter (49% vs 24%, p < 0.001), impaired esophageal contractility (45% vs 22%, p < 0.005), poor peristaltic performance (23% vs 12%, p < 0.05), and pathological acid reflux (48% vs 27%, p < 0.005). However, there was no difference in the two groups with respect to gastric acid output and H. pylori positivity. CONCLUSIONS: Lower esophageal sphincter competence, esophageal peristaltic contractility, and esophageal acid exposure were important factors in the pathogenesis of reflux esophagitis--results identical to Western studies. Gastric acid output per se and H. pylori infection might not be responsible for susceptibility to esophagitis.     

Empirical treatment based on "typical" reflux symptoms is inappropriate in a population with a high prevalence of Helicobacter pylori infection

BACKGROUND: Empirical therapy or early endoscopy have been recommended as acceptable management options for GERD. The objective of this study was to determine whether diagnosis and empirical treatment based on reflux symptoms alone are appropriate as initial management for patients with gastroesophageal reflux. METHOD: Consecutive patients presenting with weekly reflux symptoms were evaluated with a structured questionnaire followed by endoscopy. Patients with dyspepsia as the predominant symptom, "alarm" symptoms (weight loss, dysphagia, or bleeding), history of peptic ulcer or gastric surgery, or recent nonsteroidal anti-inflammatory drugs intake were excluded. RESULTS: Four hundred sixty patients were studied: 82 (18%) were found to have peptic ulcer disease and 78 (95%) were infected with Helicobacter pylori. Concomitant erosive esophagitis was found in 26 (32%) of these patients with peptic ulcer disease. In the remaining 378 patients, 218 (58%) had erosive esophagitis and 1 had esophageal cancer. Among the 159 patients with no endoscopic lesion, 148 (93%) had relief of symptoms when treated with a proton pump inhibitor. Multivariate analysis showed that male gender (OR: 1.8, p = 0.03), age greater than 60 years (OR: 2.2, p = 0.01) and H pylori infection (OR: 3.6, p = 0.008) were significantly associated with a diagnosis of peptic ulcer disease. Coexisting dyspeptic symptom was not a predictor (p = 0.13) for peptic ulcer disease. CONCLUSIONS: In populations with a high prevalence of H pylori infection, a significant proportion of patients with GERD have concomitant peptic ulcer disease. Empirical treatment based on "typical" GERD symptoms alone may not be appropriate.     

Endoscopically demonstrable esophageal changes after Helicobacter pylori eradication in patients with gastric disease

BACKGROUND AND AIMS: An increased prevalence of reflux esophagitis has been reported following Helicobacter pylori (H. pylori) eradication in patients with duodenal ulcers in Western countries. However, it has remained unknown whether this might also appertain to individuals with other diseases. We therefore carried out this study to determine the effect of eradicating H. pylori infection in a series of Japanese patients. METHODS: Of a total of 203 H. pylori-positive patients successfully cured of infection, 82 cases (58 males, 24 females) with gastric disease, but not duodenal ulcers, were included in the present study; median age 56 years (range 18-80) and median follow up of 24 months (range 6-65). The patients were investigated clinically and endoscopically at regular intervals. RESULTS: Mild reflux esophagitis developed after eradication in three of 55 (5.5%) patients formerly without this condition, while it improved after eradication in five of 27 (18.5%) patients, with the disease endoscopically diagnosed prior to eradication. The estimated incidence of esophagitis within 3 years was 4.8% after cure of infection. Short segment Barrett's esophagus developed after eradication in six of 58 (10.3%) patients who did not have it prior to the therapy, while the condition did not improve in 24 patients affected before eradication. CONCLUSIONS: Endoscopic esophageal changes after H. pylori eradication in the present series of Japanese patients were relatively infrequent and mild. This therapeutic approach thus appears to be safe and unproblematic.     

The effect of Helicobacter pylori eradication on gastroesophageal reflux disease

BACKGROUND: The effect of Helicobacter pylori (H. pylori) eradication on gastroesophageal reflux disease is controversial. We aimed to investigate the effect of H. pylori eradication in this group of patients. MATERIALS AND METHODS: Thirty-four consecutive patients with H. pylori infection and reflux esophagitis (grade 1 or 2) were enrolled into the study. Twenty-four hour intra-esophageal pH recording and esophageal manometry were performed before and 3 months after eradication of H. pylori, which was achieved using lansoprazole 30 mg b.i.d., amoxycillin 1 g b.i.d., and clarithromycin 500 mg b.i.d. for 14 days. H. pylori was evaluated in biopsy specimens taken from the antrum and corpus by rapid urease test and by histopathologic examination before and 3 months after eradication. RESULTS: Eighteen patients (11 men and 7 women, median age 42 years) completed the study. Three months after the treatment, there was no significant change in any of the 24-hour esophageal pH recording parameters and mean lower esophageal sphincter resting pressure (P > 0.05). The percentage of total time esophageal pH <4 increased in 10 patients, and decreased in 8 patients. There was a significant decrease in the scores of heartburn and regurgitation (P < 0.01). Esophagitis persisted in 16 patients and disappeared in 2 patients. Esophagitis score decreased in 6 patients, and did not change in 12 patients (P < 0.05). CONCLUSION: H. pylori eradication does not have any effect on gastroesophageal acid reflux in patients with reflux esophagitis 3 months after eradication, but significant improvement is achieved in some reflux associated symptoms.     

Influence of Helicobacter pylori infection on the prevalence of reflux esophagitis in Japanese patients

BACKGROUND AND AIM: Reflux esophagitis is caused by esophageal motor dysfunction in patients with sufficient gastric acid secretion. Helicobacter pylori causes atrophic gastritis and influences gastric acid secretion. Hiatus hernia (HH) of the esophagus causes motor dysfunction in the lower esophagus. Therefore, this study aimed to test whether H. pylori infection, gastric mucosal atrophy and HH are predictive factors for reflux esophagitis. METHODS: Helicobacter pylori infection was examined in 781 patients by the measurement of serum immunoglobulin (Ig)G antibody, bacteriological culture and histological examination of biopsy specimens. The prevalence of HH, endoscopically identified gastric mucosal atrophy (closed- or open-type) and reflux esophagitis were investigated by reviewing endoscopic films. Investigated patients were divided into three age groups, under 49, 50-69, and over 70 years. The prevalence of esophagitis, H. pylori infection, gastric mucosal atrophy, and HH were compared to identify the possible predictive factors for reflux esophagitis by using logistic regression analysis. RESULTS: Sixty-nine patients with reflux esophagitis were found among the 781 investigated cases. The odds ratios of negative H. pylori infection, endoscopically identified closed-type gastric mucosal atrophy, and HH for the prevalence of reflux esophagitis were 1.342, 1.751 and 5.527, respectively. These results indicated that the presence of H. pylori infection was only a weak negative risk factor, and that HH was the most reliable endoscopic predictive factor for reflux esophagitis. CONCLUSION: Helicobacter pylori infection is a weak negative risk factor for the prevalence of reflux esophagitis, while HH is the most reliable predictive factor.     

Erosive esophagitis and nonerosive reflux disease (NERD): comparison of epidemiologic, physiologic, and therapeutic characteristics

Nonerosive reflux disease (NERD) and erosive esophagitis are the main presentations of gastroesophageal reflux disease. However, NERD is the most common presentation of gastroesophageal reflux disease in community-based patients. Patients with NERD differ in demographic characteristics from patients with erosive esophagitis, primarily in sex distribution, weight/body mass index, and prevalence of hiatal hernia. Physiologically, patients with NERD tend to have normal lower esophageal sphincter resting pressure, minimal esophageal body motility abnormalities, low esophageal acid exposure profile and minimal nighttime esophageal acid exposure. Patients with NERD have a lower symptom response rate to proton pump inhibitor once daily than patients with erosive esophagitis. Additionally, NERD patients demonstrate a longer lag-time for symptom resolution and lack of difference in symptom response rate between half to full dose proton pump inhibitor as compared with patients with erosive esophagitis.     

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.     

Gastroesophageal reflux disease in chronic renal failure patients with upper GI symptoms: multivariate analysis of pathogenetic factors

OBJECTIVE: The association between gastroesophageal reflux disease and end-stage renal disease remains unclear. We aimed to assess the prevalence of gastroesophageal reflux disease and also to identify possible pathogenetic factors in the development of reflux in symptomatic end-stage renal disease patients. METHODS: The study involved 42 end-stage renal disease patients with upper GI symptoms (group I) and 46 age- and sex-matched controls who did not have renal disease but had the same symptoms (group II). Endoscopy, endoscopic biopsies, and 24-h esophageal pH studies were used to diagnose gastroesophageal reflux disease. Subjects were also investigated for Helicobacter pylori gastritis and GI amyloidosis. RESULTS: The prevalences of gastroesophageal reflux disease in the two groups were similar (81% vs 84.8%, p = 0.423). The prevalence of H. pylori infection was significantly lower in group I than in group II (38.1% vs 67.4%, p = 0.01). There were II cases of GI amyloidosis in group I. Multivariate logistic regression analysis in group I showed that GI amyloidosis (OR = 7.28, 95% CI = 1.13-46.93), chronic ambulatory peritoneal dialysis treatment (OR = 5.54, 95% CI = 1.01-30.43), and absence of H. pylori infection (OR = 3.75, 95% CI = 1.01-13.9) were significantly associated with reflux esophagitis. CONCLUSIONS: Upper GI symptoms are important in predicting gastroesophageal reflux disease in end-stage renal disease patients. Chronic ambulatory peritoneal dialysis, GI amyloidosis, and absence of H. pylori infection seem to be risk factors for the development of gastroesophageal reflux disease in end-stage renal disease patients.     

The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with Barrett's esophagus in Japan

OBJECTIVES: The acidity of the refluxate into the esophagus is a key factor for the pathogenesis of gastroesophageal reflux disease. Helicobacter pylori (H. pylori) infection can influence gastric acid secretion. We have reported that H. pylori infection prevents reflux esophagitis by decreasing gastric acid secretion in Japanese patients, but the role of this organism in Barrett's esophagus is unclear. The aim of this study was to investigate the prevalence of H. pylori infection and gastric acid secretion in Japanese patients with reflux esophagitis with or without Barrett's esophagus. METHODS: We enrolled 112 reflux esophagitis patients who were examined for the status of H. pylori and acid secretion in this study. They were divided into three groups, according to the presence or absence of Barrett's esophagus as follows: reflux esophagitis group without Barrett's esophagus (reflux esophagitis alone) (80 patients); short-segment Barrett's esophagus group (16 patients); and long-segment Barrett's esophagus group (LSBE) (16 patients). Age- and sex-matched control subjects were also assigned to the 80 patients with reflux esophagitis alone. The prevalence of H. pylori infection was determined by histology, rapid urease tests, and serum IgG antibodies. Gastric acid secretion was evaluated by the endoscopic gastrin test (EGT). RESULTS: The overall prevalence of H. pylori infection in the reflux esophagitis patient group (24.1%) was significantly lower than the control group (71.2%) (odds ratio 0.13, 95% confidence interval 0.07-0.24; p < 0.0001). The prevalence of H. pylori infection in the patients with Barrett's esophagus tended to be lower than that in the patients with reflux esophagitis alone (reflux esophagitis alone; 30.0%, SSBE; 18.7%, LSBE; 0%), especially in the patients with LSBE compared with the reflux esophagitis alone group (p < 0.01). The EGT value of the respective reflux esophagitis patient group was significantly higher than the control group. The EGT value in the patients with Barrett's esophagus tended to be higher than that in the patients with reflux esophagitis alone, but the difference was not statistically significant. When examined in H. pylori-negative subjects, no difference was found in the EGT value between the control subjects and the patients with reflux esophagitis alone, but it was significantly higher in patients with Barrett's esophagus than the control subjects (p < 0.05). On the other hand, when examined in the H. pylori-positive subjects, the EGT value was significantly higher in the patients with reflux esophagitis alone than in the control subjects (p < 0.01). CONCLUSIONS: H. pylori infection may play a protective role in the development of Barrett's esophagus, especially in the development of LSBE in Japan. Gastric acid hypersecretion may be concerned with the development of Barrett's esophagus in addition to the absence of H. pylori infection.     

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。     

Gastroesophageal reflux disease: An Asian perspective

The prevalence of gastroesophageal reflux disease (GERD) ranges from 2.5% to 7.1% in most population‐based studies in Asia. There is evidence that GERD and its complications are rising, coinciding with a decline in Helicobacter pylori (H. pylori) infection. Asian GERD patients share similar risk factors and pathophysiological mechanisms with their Western counterparts. Possible causes for the lower prevalence of GERD include less obesity and hiatus hernia, a lesser degree of esophageal dysmotility, a high prevalence of virulent strains of H. pylori, and low awareness. Owing to the lack of precise translation for ‘heartburn’ in most Asian languages, reflux symptoms are often overlooked or misinterpreted as dyspepsia or chest pain. Furthermore, a symptom‐based diagnosis with a therapeutic trial of the proton pump inhibitor (PPI) may be hampered by the high prevalence of H. pylori‐related disease. The risk stratification for prompt endoscopy, use of a locally‐validated, diagnostic symptom questionnaire, and response to H. pylori‘test and treat’ help improve the accuracy of the PPI test for diagnoses. PPI remain the gold standard treatment, and ‘on‐demand’ PPI have been shown to be a cost‐effective, long‐term treatment. The clinical course of GERD is benign in most patients in Asia. The risk of progression from non‐erosive reflux disease to erosive esophagitis is low, and treatment response to a conventional dose of PPI is generally higher. Although H. pylori eradication may lead to more resilient GERD in a subset of patients, the benefits of H. pylori eradication outweigh the risks, especially in Asian populations with a high incidence of gastric cancer.     

Role of gastric acid secretion in the pathogenesis of Barrett’s esophageal cancer in a Japanese population

The acidity of the refluxate into the esophagus is an important factor not only for reflux esophagitis, but also for Barrett’s esophagus and the development of Barrett’s esophageal cancer. On the other hand, H. pylori infection is thought to prevent reflux esophagitis and Barrett’s esophagus by causing atrophic gastritis, which in turn decreases gastric acid secretion. Moreover, the preservation of gastric acid secretion may be important for the development of gastroesophageal junction cancer, including Barrett’s esophageal cancer, irrespective of the H. pylori infection status. An increase in gastric acid secretion in Japanese populations has been predicted based on a decreasing rate of H. pylori infection and the westernization of eating habits in Japan; this, in turn, may lead to an increase in the prevalence of Barrett’s esophageal cancer in Japan in the future.     

Symptomatic benefit 1-3 years after H. pylori eradication in ulcer patients: impact of gastroesophageal reflux disease

OBJECTIVES: Eradication of Helicobacter pylori (H. pylori) infection markedly reduces the recurrence of duodenal and gastric ulcers. However, there is little information regarding its efficacy in resolving dyspeptic symptoms in ulcer patients. The primary aim of this study was to assess the effect of eradicating H. pylori infection on dyspeptic symptoms in ulcer patients. The secondary aim was to identify predictors of symptomatic response to H. pylori eradication. METHODS: A total of 97 dyspeptic patients with active duodenal and/or gastric ulceration associated with H. pylori infection and unrelated to NSAID use had the severity and character of their dyspeptic symptoms measured before and again 1-3 yr after H. pylori eradication therapy. RESULTS: Pretreatment, the median dyspepsia score was 12 (4-16). Posttreatment, 55% of those eradicated of H. pylori had resolution of dyspepsia (score <2) compared with 18% of those not eradicated of the infection (95% CI for difference, 11-62%). Of the ulcer patients 31% had symptoms and/or endoscopic evidence of coexisting gastroesophageal reflux disease (GERD) at initial presentation and this influenced the symptomatic response to eradication of H. pylori. Of the 22 patients with heartburn or acid reflux as the predominant presenting symptom, but no endoscopic esophagitis, only 27% experienced resolution of dyspepsia after H. pylori eradication, compared with 68% of the 59 without those as predominant symptoms (95% CI for difference, 18-63%). Only one of the five patients with coexisting endoscopic esophagitis at initial presentation experienced resolution of dyspepsia after H. pylori eradication. Symptomatic benefit was unrelated to time lapsed since the infection was eradicated. Only three of 50 subjects developed de novo GERD symptoms after eradication of H. pylori, whereas 21 of 36 subjects experienced resolution of GERD symptoms after eradication of the infection. CONCLUSIONS: A substantial proportion of ulcer patients have symptoms and/or signs of coexisting GERD at initial presentation and this reduces the symptomatic benefit from H. pylori eradication. However, we have found no evidence that eradicating H. pylori induces de novo GERD symptoms in ulcer patients.     

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.     

Impact of Helicobacter pylori infection on histological changes in non-erosive reflux disease

AIM: The evidence for an association between Helicobacter pylori (H pylori) and gastroesophageal reflux disease, either in non- erosive (NERD) or erosive esophagitis (ERD) remains uncertain. The available data on the histological changes in NERD and the effect on H pylori infection on them are elusive. The aim of this study therefore was to prospectively evaluate the histological findings and the impact of H pylori infection on a group of symptomatic patients with NERD. METHODS: Fifty consecutive patients were prospectively evaluated for symptoms compatible with GORD. In all cases, routine endoscopy and lugol directed biopsies were performed and assessed histologically in a blinded manner. RESULTS: The overall prevalence of H pylori infection was 70%. Twenty-nine patients out of 50 (58%) were NERD patients. No statistical significance was observed between the H pylori status and NERD. The remaining 21 (42%) were diagnosed as follows: 13 (26%), 6 (12%), 2(4%) with esophagitis grade A, B and C respectively. A statistically significant correlation was observed between the H pylori+ and esophagitis grade A, as well as between H pylori- and grade B. Biopsies from 2 patients were not included because of insufficient materials. Histologically, a basal zone hyperplasia was found in 47 (97.91%) patients, alterations of glycogen content in 47 (97.91%), papillae elongation in 33 (68.75%), blood vessels dilatation in 35(72.91%), chronic inflammation in 21 (43.75%), infiltration with eosinophils, neutophils and T-lymphocytes in 4 (8.33%), 6 (12.5%) and 39 (81.25%) respectively. No correlation was observed between the H pylori status and the histological parameters studied either in NERD or GERD. CONCLUSION: Histological assessment can not differentiate symptomatic patients with erosive versus non-erosive reflux disease. Moreover, H pylori infection may not act as an important factor in patients with NERD.