Role Of Helicobacter Pylori Infection Research Articles

Secretory leukocyte protease inhibitor expression in various types of gastritis: a specific role of Helicobacter pylori infection

Secretory leukocyte protease inhibitor (SLPI) represents a multifunctional protein of the gastrointestinal mucosa exerting antimicrobial and anti-inflammatory effects. SLPI expression is generally induced during inflammation; however, Helicobacter pylori-mediated gastritis is associated with significantly decreased antral SLPI levels. The aim of the study was to investigate whether SLPI downregulation of gastric mucosa represents a specific phenomenon of H. pylori infection or is generally linked to gastric inflammation. SLPI expression was retrospectively analysed by immunohistochemistry in 85 paraffin-embedded samples: H. pylori-induced (n=13), non-steroidal anti-inflammatory drug (NSAID)-enhanced (n=18), autoimmune (n=11), lymphocytic gastritis (n=26) and H. pylori-negative controls (n=17). The intensity of the staining was semiquantitatively analysed using an immunoreactivity score. Statistical analysis of differences was performed using an analysis of variance test. In comparison with the control group, the SLPI expression of antral mucosa in H. pylori-mediated and lymphocytic gastritis was significantly lower (P<0.001), whereas epithelial SLPI expression was not affected in NSAID-enhanced and autoimmune gastritis either in the antrum or corpus, respectively. Both the H. pylori-mediated and lymphocytic gastritis revealed a significantly lower expression of SLPI in infiltrating immune cells (P<0.01), whereas immune cells infiltrating the corpus in autoimmune gastritis showed higher SLPI levels than the immune cells of other groups (P<0.03). The local downregulation of SLPI in antral mucosa is specifically linked to H. pylori infection and is not a general phenomenon of gastric inflammation.

Role of Helicobacter pylori infection and nonsteroidal anti-inflammatory drug use in bleeding peptic ulcers in Japan

Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) are well-known major causes of peptic ulcers. This study aimed to characterize the features of bleeding peptic ulcers in Japan. This prospective study evaluated 116 patients revealed to have bleeding peptic ulcers from January 2000 to December 2002. Eighty-eight of the 116 patients (75.9%) had H. pylori infection. Seventy (60.3%) patients were positive for H. pylori with no history of NSAID use (group A), and 18 (15.5%) were positive for H. pylori with a history of NSAID use (group B). Among the H. pylori-negative patients, 15 (12.9%) were associated with NSAID use (group C). Thirteen (11.2%) patients had no H. pylori infection or history of NSAID use (group D). Among the 33 patients with a history of NSAID use, 11 were on-demand NSAID users and 14 took daily low-dose aspirin. The patients in groups B and C were significantly older that those in groups A and D, and they more frequently had coexisting diseases compared with group A. In group D, 11 patients had atrophic changes revealed by endoscopic examination, suggesting a past H. pylori infection, and these atrophic changes remained at the time of bleeding. Many of the patients in group D had serious comorbidity. Compared with healthy control subjects, the concentrations of both phosphatidylcholine and phosphatidylethanolamine were significantly decreased in the antral gastric mucosa in all patient groups. NSAID use contributed to bleeding ulcers in 28.4% of patients; thus, low-dose aspirin or on-demand NSAID use may cause bleeding ulcers. There were only two (1.7%) confirmed cases of H. pylori-negative, non-NSAID ulcers.

Causal role of Helicobacter pylori infection in gastric cancer: An Asian enigma

Helicobacter pylori (H pylori) has been etiologically linked to gastric cancer.H pylori infection is more frequent in less developed Asian countries like India, Bangladesh, Pakistan,and Thailand and is acquired at early age than in more developed Asian countries like Japan and China. Frequency of gastric cancer, however, is very low in India, Bangladesh, Pakistan and Thailand compared to that in Japan and China. Similar enigma has been reported from Africa as compared to the West. Seroprevalence of H pylori infection in adult populations of India, Bangladesh, Pakistan and Thailand varies from 55% to 92%. In contrast, seroprevalence of H pylori in Chinese and Japanese adults is 44% and 55%,respectively. Annual incidence rate of gastric cancer in India, Bangladesh, and Thailand is 10.6, 1.3, 7.1 per 100,000 populations, respectively; in contrast, that in China and Japan is 32-59 and 80-115 per 100,000 populations, respectively. Several studies from India failed to show higher frequency of H pylori infection in patients with gastric cancer than controls. Available evidences did not support difference in H pylori strains as an explanation for this enigma. Despite established etiological role of H pylori, situation is somewhat enigmatic in Asian countries because in countries with higher frequency of infection,there is lower rate of gastric cancer. Host's genetic make-up and dietary and environmental factors might explain this enigma. Studies are urgently needed to solve this issue.

An observational study of upper gastrointestinal bleeding in intensive care units: Is Helicobacter pylori the culprit?*

Upper gastrointestinal bleeding (UGIB) related to stress ulcers was formerly a fearsome complication of intensive care. The incidence of this event has decreased over the years. However, the morbidity, mortality, and causes of UGIB, particularly the etiologic role of Helicobacter pylori infection, are still controversial. Therefore, we prospectively assessed the incidence of UGIB in the intensive care unit (ICU) and evaluated the role of H. pylori infection. A prospective observational study followed by a case-control study. Seven ICUs in the Paris area, five of them located in teaching hospitals. All patients admitted consecutively to seven ICUs during a 1-year period were monitored for signs of clinically relevant UGIB. None. Only cases of endoscopically confirmed UGIB were analyzed. Patients whose hemorrhage originated from the stomach and/or duodenum were tested for H. pylori infection, by means of serology, histologic examination, and stool antigen detection. The possible association between H. pylori and UGIB was examined in a case-control study. Twenty-nine of the 4,341 patients admitted to the seven ICUs during the study period had clinically relevant, endoscopically confirmed UGIB (incidence, 0.67%; 95% confidence interval, 0.56%-0.77%). Ulcers were most frequently observed endoscopically. Patients who bled had a higher Simplified Acute Physiology Score (SAPS II) at admission (mean +/- sd, 47 +/- 14 vs. 36 +/- 28; p < .001). Despite a higher in-ICU mortality rate among patients who bled (73% vs. 16%; p < .001), death was never due to bleeding. H. pylori infection was more frequent in patients who bled than in matched controls (36% vs. 16%; p = .04). Clinically relevant, endoscopically confirmed UGIB is a rare event in the ICU setting and tends to occur in severely ill patients. H. pylori infection is more frequent in patients with gastroduodenal hemorrhage than in nonbleeding patients.

Helicobacter pylori Infection and Abdominal Symptoms Among Swedish School Children

The role of Helicobacter pylori infection in the etiology of abdominal symptoms remains unclear. Our aim was to investigate the association between type-specific H. pylori infection and gastrointestinal symptoms among school children in Stockholm, Sweden. In a community-based cross-sectional study, 695 children aged 10-12 years participated with a blood sample and a questionnaire on sociodemographic characteristics and gastrointestinal symptoms, including minor abdominal pain not necessitating medical consultation, during the preceding six months. Infection was investigated by an enzyme-linked immuno-sorbent assay and confirmed by immunoblot and urea breath test. Abdominal pain was reported by 440 (63%) children and recurrent abdominal pain (RAP) by 88 (13%). Of 112 (16%) infected children, 73% had antibodies to CagA and 59% to VacA. There was no positive association between H. pylori status and the occurrence of abdominal pain; in fact, the association with any abdominal pain report was inverse (odds ratio [OR] 0,5; 95% Confidence Interval [CI] 0.3-0.8), while RAP was unrelated to the infection (OR 1.0; 95% CI 0.5-2.1) when adjusted for gender, age and family background variables. The prevalence of RAP tended to be lower among children harboring CagA+/VacA+ infections than among the uninfected (adjusted OR 0.3; 95%CI 0.1-1.1). Furthermore, CagA+/VacA+ infected children reported less acid regurgitation (adjusted OR 0.2; 95% CI 0.1-0.5). Taking background factors into account, the presence of H. pylori is not accompanied by an increased occurrence of abdominal symptoms in Swedish 10-12-year-olds. However, unexpected differential associations with strain specific infections may indicate a so far overlooked complex relationship that needs to be further confirmed.

Occurrence and risk factors for benign epithelial gastric polyps in atrophic body gastritis on diagnosis and follow‐up

Benign epithelial gastric polyps have been reported to be more common in atrophic body gastritis. The role of Helicobacter pylori infection in the induction of gastric atrophy is well-known. The development of hyperplastic polyps may be in relation to H. pylori infection. To investigate occurrence of benign epithelial gastric polyps in atrophic body gastritis patients at diagnosis and follow-up, and the role of H. pylori and other risk factors for the development of benign epithelial gastric polyps. A total of 259 consecutive atrophic body gastritis patients included in a follow-up programme, of whom 202 were followed up for median period of 4 years (range: 2-11). At baseline and follow-up gastroscopies, the presence of benign epithelial gastric polyps was evaluated. Biopsies for histology were obtained from all detected benign epithelial gastric polyps. Frequency of benign epithelial gastric polyps in atrophic body gastritis patients were 4.6% at baseline and 5.9% at follow-up. About 91.7% were hyperplastic polyps. H. pylori infection was detected in 79.2% atrophic body gastritis patients with benign epithelial gastric polyps, and in 70.8% without benign epithelial gastric polyps. Smoking was more frequent among patients with benign epithelial gastric polyps [42% vs. 20%, OR 2.8 (95% CI: 1.2-6.9)]. Benign epithelial gastric polyps occur in about 5% of atrophic body gastritis patients, and the vast majority are hyperplastic polyps. Smoking habit, but not H. pylori infection, increases the risk for benign epithelial gastric polyps in atrophic body gastritis patients.

Role of Helicobacter pylori infection in iron deficiency during pregnancy

We investigated the possible role of Helicobacter pylori infection in iron deficiency during pregnancy in a large group of mothers in Germany after the birth of their baby under special consideration of iron supplementation. All women who were delivered of their baby between November 2000 and November 2001 at the Department of Gynecology and Obstetrics at the University of Ulm, Germany, were recruited for the study. Hemoglobin levels at various points of time during pregnancy were obtained from the mothers' health charts. Current H pylori infection was determined by 13 C-urea breath test. We used multiple linear regression analyses to assess the impact of infection status on hemoglobin level at the beginning of pregnancy and on hemoglobin change during pregnancy. Twenty-three percent of the 898 mothers had a H pylori infection, and 20% of the mothers had a hemoglobin level below 12 g/dL at the beginning of pregnancy. Compared with uninfected mothers, mothers with H pylori infection had a lower mean hemoglobin level at the beginning of pregnancy (-0.25 g/dL; 95% CI, -0.49, -0.003) and a more unfavorable change in hemoglobin level during pregnancy (-0.14 g/dL; 95% CI, -0.38, 0.10). This study supports a possible moderate, but still relevant, independent role of H pylori infection in iron deficiency during pregnancy.

A concept on the role of Helicobacter pylori infection in autoimmune pancreatitis

Autoimmune pancreatitis, an inflammatory process of the pancreas due to an autoimmune mechanism establishing etiology of chronic pancreatitis, is characterized by the presence of autoantibodies, hypergammaglobulinemia, pancreatic enlargement, pancreatic duct strictures, and pathologic features of fibrotic changes with intense, mainly lymphocytic infiltrations, which may contribute to tissue destruction probably by apoptosis. In almost 60% of the cases, this type of pancreatitis coexists with other autoimmune diseases such as Sjogren's syndrome, sclerosing extrahepatic cholangitis, primary biliary cirrhosis, autoimmune hepatitis, or other extrapancreatic disorders, and recently with gastric peptic ulceration. The diversity of extrapancreatic lesions with similar histopathologic findings suggests general involvement of the digestive system in this disease, although the presence of such involvement has not been fully elucidated. Similarly, Helicobacter pylori (H. pylori) infection, a well known cause of gastric ulcer, has been associated, via molecular mimicry of host structures by its constituents with the same autoimmune conditions, also characterized by fibrotic changes and/or lymphoplasmacytic inflammations, accompanied by aberrations of T cell apoptosis that contribute to hepatobiliary- or extrahepatic-tissue destruction. Considering that H. pylori is involved in the pathogenesis and pathophysiology of these autoimmune disorders, we propose that this organism might trigger autoimmune pancreatitis through induction of autoimmunity and apoptosis.

Helicobacter pylori infection and the prevention of peptic ulcer with proton pump inhibitors in elderly subjects taking low-dose aspirin

Introduction. The role of Helicobacter pylori infection on the risk of low-dose aspirin-related gastroduodenal damage and on the efficacy of the prevention therapy in elderly chronic users of low-dose aspirin is still controversial. Aim. To evaluate in symptomatic elderly chronic users of low-dose aspirin: (1) the association between H. pylori infection and the prevalence of upper gastrointestinal lesions; and (2) the effect of H. pylori infection on the efficacy of proton pump inhibitors in the prevention of aspirin-related gastroduodenal lesions. Patients and methods. Two hundred and forty-five symptomatic elderly who were taking aspirin 75–300 mg daily, at least during the last 3 months, were evaluated by endoscopy. A structured interview was carried out to evaluate gastrointestinal symptoms and the use of proton pump inhibitors. H. pylori infection was diagnosed according to histology and the rapid urease test on gastric biopsies. Results. One hundred and twelve patients were H. pylori-positive and 133 patients were H. pylori-negative. A significantly higher prevalence of peptic ulcers was observed in H. pylori-positive than in H. pylori-negative subjects (36.6% versus 15.8%, P = 0.0002). The use of proton pump inhibitors was associated with a significant decreased risk of peptic ulcer both in H. pylori-positive (absolute risk reduction, ARR = −36.2, 95% confidence interval: −51.2 to −21.3, P < 0.001) and H. pylori-negative patients (ARR = −12.6, 95% confidence interval: −23.9 to −1.2, P = 0.03). However, the number of patients who needed to be treated in order to gain a reduction of one peptic ulcer (number needed to treat, NnT) was lower in H. pylori-positive than in H. pylori-negative patients (NnT = 3 versus 8). Conclusions. In symptomatic elderly chronic users of low-dose aspirin, H. pylori infection may influence the prevalence of peptic ulcers and the cost-effectiveness of the proton pump inhibitor prevention therapy.

The role of cagA Helicobacter pylori strains in gastro-oesophageal reflux disease.

The role of Helicobacter pylori infection in gastro-oesophageal reflux disease is controversial. The aim of this study was to evaluate the prevalence of colonization by cagA-positive and cagA-negative H. pylori strains in the spectrum of gastro-oesophageal reflux disease. A total of 108 patients (50 male/58 female; mean age, 50.3 years) with dyspepsia and peptic ulcer or erosive gastritis/duodenitis were categorized into patients without reflux and patients with reflux oesophagitis graded from I to IV. All patients underwent upper endoscopy with biopsies of the antrum. H. pylori was detected by histology, urease test and polymerase chain reaction. The cagA status was diagnosed in the gastric biopsy by polymerase chain reaction. The overall prevalence of H. pylori colonization in patients with reflux was 68.6% and was 70.2% in those without oesophageal disease (P = 0.862). Colonization by cagA-positive strains was also not statistically different between the two groups (31.4% versus 40.4%, P = 0.332). However, patients with grades II-IV reflux oesophagitis were less colonized by the bacterium (36.4%) than patients with grade I oesophagitis (77.5%) (P = 0.009). H. pylori cagA-positive strains were also less likely to colonize the stomach of patients with grades II-IV oesophagitis (0%), than grade I reflux oesophagitis (40%) patients and controls (40.4%). Infection of the stomach by H. pylori and especially by H. pylori cagA strains may play a protective role against the development of the most severe forms of gastro-oesophageal reflux disease.

Low prevalence of Helicobacter pylori but high prevalence of cytomegalovirus‐associated peptic ulcer disease in AIDS patients: Comparative study of symptomatic subjects evaluated by endoscopy and CD4 counts

The role of Helicobacter pylori infection in gastroduodenal lesions might be different between the general population and AIDS patients. The aim of the present study was to compare the prevalence of H. pylori and cytomegalovirus (CMV) infection in AIDS patients and HIV-negative controls. The impact of CD4 lymphocyte counts on H. pylori and CMV infection in the same subjects was also assessed. One hundred and fifty-six patients (52 HIV-positive, 104 HIV-negative) with gastrointestinal symptoms were evaluated with upper gastrointestinal endoscopy and biopsy. Comparison of the prevalence of H. pylori and CMV infection was made by dividing AIDS patients into two groups: those with CD4 counts >100/mm3 and those with CD4 counts <100/mm3, and ulcer and non-ulcer patients. In comparison with HIV-negative controls, AIDS patients had a lower prevalence of H. pylori infection (P < 0.0001) but a higher prevalence of CMV infection (P < 0.0001). Cytomegalovirus infection was frequently found in AIDS patients with CD4 count <100/mm3, in comparison with those with a CD4 count >100/mm3. In AIDS patients, CMV was more frequently detected in subjects with peptic ulcers (P = 0.0125). Conversely, the prevalence of H. pylori infection in AIDS patients was not different between those with and without peptic ulcers. The low prevalence of H. pylori infection and peptic ulcer in AIDS patients suggests a different role of H. pylori infection in peptic ulcer or even a different mechanism of peptic ulcerogenesis in HIV-positive subjects. Cytomegalovirus, rather than H. pylori, may be the main causative pathogen of peptic ulcers in AIDS patients.

S38.5: Role of Helicobacter pylori infection in iron deficiency during pregnancy.

Biometrical JournalVolume 46, Issue S1 p. 83-83 Oral Sessions Abstracts S38.5: Role of Helicobacter pylori infection in iron deficiency during pregnancy. Maria Weyermann, Maria Weyermann weyermanndzfa@aol.com Search for more papers by this authorDietrich Rothenbacher, Dietrich RothenbacherSearch for more papers by this authorLydia Gayer, Lydia GayerSearch for more papers by this authorGünter Bode, Günter BodeSearch for more papers by this authorGuido Adler, Guido AdlerSearch for more papers by this authorDieter Grab, Dieter GrabSearch for more papers by this authorFelix Flock, Felix FlockSearch for more papers by this authorHermann Brenner, Hermann BrennerSearch for more papers by this author Maria Weyermann, Maria Weyermann weyermanndzfa@aol.com Search for more papers by this authorDietrich Rothenbacher, Dietrich RothenbacherSearch for more papers by this authorLydia Gayer, Lydia GayerSearch for more papers by this authorGünter Bode, Günter BodeSearch for more papers by this authorGuido Adler, Guido AdlerSearch for more papers by this authorDieter Grab, Dieter GrabSearch for more papers by this authorFelix Flock, Felix FlockSearch for more papers by this authorHermann Brenner, Hermann BrennerSearch for more papers by this author First published: 17 March 2004 https://doi.org/10.1002/bimj.200490137AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume46, IssueS1Supplement: Abstracts of the Joint Meeting of the IBS‐DR and the DAEMarch 2004Pages 83-83 RelatedInformation

Active peptic ulcer disease in patients with hepatitis C virus-related cirrhosis: the role of Helicobacter pylori infection and portal hypertensive gastropathy.

The relationship between Helicobacter pylori infection and peptic ulcer disease in cirrhosis remains controversial. The purpose of the present study was to investigate the role of H pylori infection and portal hypertension gastropathy in the prevalence of active peptic ulcer among dyspeptic patients with compensated hepatitis C virus (HCV)-related cirrhosis. Patients undergoing upper endoscopy with compensated HCV-related cirrhosis were enrolled. Child-Pugh's score was determined at the entry. Variceal size was measured endoscopically and the severity of portal hypertensive gastropathy was graded. H pylori infection status was determined by urea breath testing and/or histology. A total of 178 patients positive for HCV (A and B Child-Pugh's score) were prospectively included. The prevalence of H pylori infection was 43%. An active peptic ulcer was found in 14 patients (8%) and was significantly more common among those with H pylori infection (16% versus 2% in H pylori uninfected patients, odds ratio: 8.0). No association was observed between H pylori infection and variceal size, or hypertensive gastropathy. Patients with compensated cirrhosis and H pylori infection showed higher risk of developing a peptic ulcer. Clinical relevance of this result would be that dyspeptic patients with HCV-related cirrhosis may benefit from preventive screening and eradication of H pylori, especially those with features of insufficient hemostasis.

Clinical significance of cytotoxin-associated gene A status of Helicobacter pylori among non-steroidal anti-inflammatory drug users with peptic ulcer bleeding: a multicenter case-control study

Background: The role of Helicobacter pylori infection and especially of the cytotoxin-associated gene A (CagA) product strain in peptic ulcer bleeding among non-steroidal anti-inflammatory drugs (NSAIDs) users remains controversial. Methods: A case-control study was carried out including 191 consecutive chronic NSAIDs users admitted to hospital because of peptic ulcer bleeding. Peptic ulcer was verified by endoscopy. Controls comprised 196 chronic NSAIDs users without signs of bleeding of similar age and gender to cases. Multivariate regression analysis was performed for further evaluation of the relationship between H. pylori, CagA status and other risk factors. Results:H. pylori infection was present in 121 (63.4%) cases compared with 119 (60.7%) controls (odds ratio (OR) = 1.14, 95% CI, 0.76-1.72). CagA-positive strains were found to be significantly more frequent in cases than in controls (65/106 versus 41/99 P = 0.008). Current smoking (OR = 2.65; 95% CI, 1.14-6.15; P = 0.02), CagA status (OR = 2.28; 95% CI, 1.24-4.19; P = 0.008), dyspepsia (OR = 6.89; 95% CI, 1.84-25.76; P = 0.004) and past history of peptic ulcer disease (OR = 3.15; 95% CI, 1.43-6.92; P = 0.004) were associated significantly with increased risk of bleeding peptic ulcer. Conclusions: The results suggest that CagA-positive H. pylori infection is associated with a more than 2-fold increased risk of bleeding peptic ulcer among chronic NSAIDs users.

Congenital and Acquired Thrombocytopenia

The diagnosis and management of thrombocytopenia is a growing component in the practice of hematology. The frequency with which hematologists are called in consultation for thrombocytopenia continues to increase with the advent of routine automated platelet determinations and the introduction of new medications. For most patients, such as those with inherited and auto-immune thrombocytopenia, emphasis is focused on efforts to treat or forestall bleeding without excess drug-induced toxicity or burden to the patient. However, in disorders such as heparin-induced thrombocytopenia (HIT), avoidance of thrombotic complications is the key to management. In this chapter, we provide the pediatric and adult hematologist with new insights into the pathogenesis and recognition of congenital inherited thrombocytopenias (CTP), a hitherto difficult to comprehend constellation of clinical entities. We also highlight new approaches to the diagnosis and treatment of two of the more common thrombocytopenic conditions encountered in practice, autoimmune or idiopathic thrombocytopenic purpura (ITP) and HIT. In Section I, Dr. James Bussel discusses CTPs and their distinction from childhood ITP. He emphasizes the clinical features that enable the pediatrician and hematologist to suspect the diagnosis of CTP and those that are of use to subcategorize the various entities, where possible. He also emphasizes newer molecular markers that afford definitive diagnosis in some cases and provide insight into platelet production. This section highlights the characteristic associated findings and differences in the natural history and approaches to management of the various entities. In Section II, Dr. Robert McMillan discusses adult chronic ITP. He revisits the utility of platelet antibody determination in diagnosis and review new insights into pathogenesis. The role of Helicobacter pylori infection and the timing of splenectomy in the management of acute and emergent ITP are examined. New insights into the natural history of ITP post-splenectomy and management strategies for patients with severe, chronic, refractory ITP are discussed. In Section III, Dr. James Zehnder updates us on HIT. He emphasizes new insights into the clinical presentation and pathogenesis of this condition. He critically reviews the utility of laboratory testing for heparin-dependent antibodies. Recent studies on the use of direct thrombin inhibitors are examined and the management of cardiopulmonary bypass surgery in patients with HIT is discussed.

Changes in Helicobacter pylori status in patients with rheumatoid arthritis under non‐steroidal anti‐inflammatory drugs

Background: The role of Helicobacter pylori infection in rheumatoid arthritis (RA) patients during treatment with non‐steroidal anti‐inflammatory drugs (NSAID) is still unclear. Methods: By means of endoscopy and biopsy, gastroduodenal lesions and H. pylori status were repeatedly examined in 88 RA patients at intervals ranging from 26 to 49 months. Histology and culture were applied to determine H. pylori status. Serial changes in gastroduodenal lesions and histologic score for mucosal atrophy were compared among groups classified by initial and second H. pylori status. Results: There were 28 patients with continuously positive H. pylori infection (CP group), 33 patients with continuously negative H. pylori infection (CN group), 7 patients in whom H. pylori status became negative (PN group), and 20 patients in whom H. pylori status could not be determined (UD group). Age, duration and species of NSAID, disease activity of RA, gastroprotective drugs applied and the prevalence of gastroduodenal mucosal lesions were not different among the groups at either the initial or the second examination. In the PN group, the score for mucosal atrophy at the second examination was significantly lower than at the initial examination, whereas no difference was found for the CP, CN and UD groups. Overall, histologic score for mucosal atrophy was higher in H. pylori‐positive patients than in H. pylori‐negative patients at both initial and second examination. Conclusions: In RA patients using NSAIDs, H. pylori infection may not affect the course of gastroduodenal lesions and activity of RA, but the infection contributes to mucosal atrophy.

Prognostic significance of antrum‐predominant gastritis in functional dyspepsia

Background: The role of Helicobacter pylori infection in functional dyspepsia is still controversial, and subgroups of patients with functional dyspepsia who may benefit from H. pylori eradication should be identified. Patients with functional dyspepsia and antrum‐predominant H. pylori‐positive chronic gastritis, it has been argued, have fewer symptoms after eradication therapy. In the present study, we analysed the clinical significance of antrum‐predominant gastritis on the long‐term prognosis of functional dyspepsia. Methods: Consecutive unselected dyspeptic patients were investigated in primary care and the patients with functional dyspepsia were enrolled in this long‐term follow‐up study. Altogether 182 patients were recruited: 65 with normal histology of the stomach, 36 with antrum‐predominant gastritis, 21 with corpus‐predominant gastritis and 60 with pangastritis. Patients' medical histories were reviewed after 6 to 7 years, with total number and outcome of repeated investigations analysed. At the end of follow‐up, all patients were invited for voluntary gastroscopy. Results: At the end of follow‐up, the proportion of asymptomatic patients ranged from 21% (normal histology) to 26% (antrum‐predominant gastritis). No statistically significant differences between groups appeared in regard to re‐visits or to proportion of patients examined by sigmoideo‐ or colonoscopy during follow‐up. Patients with antrum‐predominant gastritis less often underwent upper endoscopy. Peptic ulcer was more frequent (P = 0.05) in patients with antrum gastritis than in other groups, but no other differences existed among any organic gastrointestinal findings. No significant differences between subgroups appeared among the 30% of patients using drugs for upper abdominal complaints during the previous year. Conclusions: Functional dyspepsia has an excellent long‐term prognosis. Antrum‐predominant gastritis in functional dyspepsia seems to carry an increased risk for peptic ulcer, and for this group in particular, H. pylori eradication should be considered. This finding requires confirmation in future studies performed in primary care.

Helicobacter pylori and extragastric diseases -- other helicobacters.

The role of Helicobacter pylori infection is explored in more and more extragastric diseases without definite proof in most of the studies, except possibly some hematologic diseases. In cardiovascular diseases, including stroke, the presence of CagA positive strains may be involved. The possible role of helicobacters in hepatobiliary diseases goes beyond that of H. pylori to involve enterohepatic helicobacters. New Helicobacter species are regularly described and molecular methods are developed to improve their detection. Helicobacter felis remains the major species to be used in animal models of Helicobacter infection.

Efficacy of Helicobacter pylori eradication on platelet recovery in children with chronic idiopathic thrombocytopenic purpura

Aim: Little is known about the influence of environmental factors on the epidemiology of idiopathic thrombocytopenic purpura (ITP). The role of Helicobacter pylori infection in relation to the development and/or persistence of ITP in infected patients remains controversial. Therapy used for eradicating H. pylori has led to a rise in platelet counts in a significant number of adult patients, but few paediatric studies have been undertaken to evaluate such treatment. The aim of this prospective study was to determine the prevalence of H. pylori and to evaluate whether H. pylori eradication can induce chronic ITP regression in children. Methods: To investigate new, non‐invasive techniques for diagnosis of H. pylori infection, an enzyme immunoassay for H. pylori antigens in faeces (HpSA) was evaluated. Patient eligibility criteria included isolated thrombocytopenia (±50 ± 109 L−1) for more than 6 months without any identifiable cause and either normal or increased marrow megakaryocytes. H. pylori status was monitored before eradication and 4, 12, and 24 mo, after the end of treatment using Premier Platinum HpSA. Results: In this study we evaluated 22 chronic ITP patients, 9 of whom were infected with H. pylori. Using repeated HpSA testing, we demonstrated for eradication of H. pylori after treatment in all infected patients. Five of the nine patients had increased platelet counts that persisted throughout the follow‐up period. Conclusion: These results should stimulate additional research into the involvement of H. pylori infection in chronic ITP in childhood. This approach may offer an accepted algorithm at least for some of these patients.

A role of Helicobacter pylori infection in the development of duodenal ulcer after adult living-related liver transplantation.

Gastrointestinal bleeding caused by peptic ulcer disease is one of the serious complications of living-related liver transplantation (LRLT). The aim of this study was to clarify the factors involved in peptic ulcer formation in adult LRLT recipients. Forty consecutive adult LRLT recipients without a history of peptic ulcer disease were studied. Twenty-five patients (62.5%) tested positive for Helicobacter pylori. After LRLT, duodenal ulcer (DU) developed in six patients, and all of them tested positive for H. pylori. In contrast, none of the H. pylori-negative patients developed DU. Preoperative serum gastrin levels in patients with DU were significantly higher than in those without DU, irrespective of H. pylori infection. Preoperative pepsinogen I levels in patients with DU were significantly higher than in those without DU with H. pylori infection. These data suggest involvement of H. pylori infection in the development of DU after LRLT. Eradication of H. pylori may prevent the development of DU after LRLT particularly in patients with hypergastrinemia and high serum pepsinogen I.