Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Helicobacter”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed1990

Microbiological aspects of Helicobacter pylori (Campylobacter pylori).

The human gastric pathogen Campylobacter pylori has recently been reclassified as Helicobacter pylori, and a related spiral bacterium found in the stomach of ferrets has been designated Helicobacter mustelae. The general microbiological features of Helicobacter pylori are delineated here, with details of phenotypic differences between Helicobacter pylori and Helicobacter mustelae; comparisons are made with Wolinella succinogenes and Campylobacter jejuni. The Helicobacter organisms possess an external glycocalyx which can be visualised by electron microscopy, and which may be involved in bacterial adherence. The finding of soluble and cell-associated haemagglutinins of Helicobacter pylori is reported. Detection of Helicobacter pylori in clinical specimens, susceptibility of the organism to antibacterial agents, and other aspects of practical and clinical significance are briefly reviewed.

Animals↗
PubMed2002

Relationship between gastritis severity, Helicobacter pylori intensity and mast cell density in the antrum and corpus.

BACKGROUND/AIMS: The aim of this study was to investigate the relationship between mast cell density, Helicobacter pylori intensity and histopathological severity of gastritis in the corpus and antrum mucosa. METHODS: The study included 59 Helicobacter pylori-positive and 20 Helicobacter pylori-negative patients. All cases underwent endoscopy, and biopsies were obtained for the evaluation of Helicobacter pylori and histopathological examination. All biopsies were evaluated according to the Sydney system and mast cell density in both the corpus and antrum mucosa was analyzed by modified Giemsa stain. Spearman's correlation test was used to determine the relationship between mast cell density and other histopathological parameters. The comparision of mast cell density between H. pylori positive and negative groups was analysed by Mann Whitney U test. RESULTS: Both in the antrum and the corpus, mast cell density was significantly higher in the Helicobacter pylori-positive group than in the Helicobacter pylori-negative group (p<0.001). The higher mast cell distribution was correlated with increased inflammation, activity and Helicobacter pylori in the antrum and corpus (p<0.001). No relationship was found between mast cell distribution and intestinal metaplasia or atrophy. CONCLUSIONS: In the light of the results of our study, mast cells may play a role in the development of Helicobacter pylori gastritis.

Journal Article↗
PubMed1992

Serodiagnosis of Helicobacter pylori infections with an enzyme immunoassay using the chromatographically purified 120 kilodalton protein.

A membrane-associated 120 kDa protein of Helicobacter pylori with known species-specificity was isolated and used in an enzyme immunoassay (EIA) for the detection of Helicobacter pylori-specific IgG antibodies in patient sera. The EIA was compared with two other methods used for serodiagnosis of Helicobacter pylori infections: an EIA using sonicated whole Helicobacter pylori cell antigen and Western immunoblot. In a prospective study 127 unselected patients (76 patients with antrum gastritis, 51 patients without gastritis) who underwent gastroscopy were studied histologically and serologically. The EIA using the purified 120 kDa protein had the highest specificity (92%) compared with the EIA using a whole cell sonicate of a single Helicobacter pylori strain as antigen (60.7%) and the immunoblot (90.2%). The sensitivity was 96%, 100% and 92%, respectively. Sera of three control patients reacted strongly in all three methods, indicating possible Helicobacter pylori infection with negative histological findings. The EIA using the 120 kDa protein as antigen was shown to be a specific and sensitive technique for the serodiagnosis of Helicobacter pylori infections.

Adult↗
PubMed1995

Long-term prospective study of Helicobacter pylori in nonulcer dyspepsia.

Helicobacter pylori is present in up to 87% of patients with nonulcer dyspepsia. This study assessed the effect of eradicating Helicobacter pylori infection on the symptoms of nonulcer dyspepsia at four weeks and one year after treatment. Dyspepsia was assessed on the frequency and severity of six symptoms [epigastric pain (night and day), nausea and vomiting, upper abdominal discomfort, and regurgitation] where each symptom was scored from 0 to 4. Helicobacter pylori status was assessed before treatment and four weeks after treatment with histology and microbiology, and at one year with a carbon-13 urea breath test. Eighty-three patients (23 males, 60 females; mean age 56.3 years; mean symptom duration 3.6 months) with nonulcer dyspepsia and Helicobacter pylori infection entered the study. Seventy-five were available at one year follow-up. Four weeks after treatment, the mean symptom score improved in those with eradication (6.95-2.3, P = 0.01, N = 41) or persistent infection (6.69-3.0, P = 0.015, N = 42). At one year, those with persistent Helicobacter pylori infection (N = 38, score 5.24) had a higher score than those remaining clear of infection (N = 24, score 1.4, P < 0.0001) and those with reinfection (N = 13, score 2.2, P < 0.0001). In addition, persistent Helicobacter pylori infection was associated with more additional treatments than those with eradication (34/38 versus 4/37, P < 0.001). These results suggest that Helicobacter pylori plays an important role in the symptoms of nonulcer dyspepsia.

Adult↗
PubMed1995

Ecological study of association between Helicobacter pylori infection and gastric cancer in Taiwan.

The association between Helicobacter pylori infection and gastric cancer remains controversial. A community-based serosurvey was carried out in Taiwan to investigate the association. Serum IgG antibodies against Helicobacter pylori were examined in 728 subjects randomly selected from three townships with different gastric cancer mortality rates. The overall seropositivity of Helicobacter pylori was 54.7% (398/728) with no gender difference (males: 54.5%; females: 54.8%). The seroprevalence of Helicobacter pylori progressively increased with age in all three study townships. The age-specific seropositivity of Helicobacter pylori correlated well with age-adjusted gastric cancer mortality in the three townships. The difference in seropositivity was more profound in younger age groups. The ecological study in Taiwan suggests an association between Helicobacter pylori infection and gastric cancer. Helicobacter pylori infection in early childhood may be a key issue; in addition, a long induction time appears to be required for gastric carcinogenesis.

Adolescent↗
PubMed1993

Interferon-gamma and tumour necrosis factor production in patients with Helicobacter pylori infection.

The production of the cytokines, interferon-gamma and tumour necrosis factor by human antral mucosa cells and stimulated peripheral blood mononuclear cells were determined by enzyme linked immunosorbent assay and L929 bioassay respectively. Tumour necrosis factor production by peripheral blood mononuclear cells in response to Helicobacter pylori stimulation was depressed in Helicobacter pylori positive individuals, compared to Helicobacter pylori negative individuals (P < 0.05). There was no difference in tumour necrosis factor production by peripheral blood mononuclear cells in response to purified protein derivative. However, tumour necrosis factor production by cells isolated from gastric mucosa during short term culture was significantly higher in Helicobacter pylori positive patients (P < 0.05) than negative patients, indicating a probable macrophage response. Levels of interferon-gamma did not differ significantly in the gastric explant culture from the two groups. The results show that Helicobacter pylori negative patients have a stronger peripheral cellular immune response to Helicobacter pylori infection. The higher levels of tumour necrosis factor production by antral mucosa cells in Helicobacter pylori positive patients may reflect the infiltration of T lymphocytes and macrophages within the local mucosa.

Adult↗
PubMed2004

Inhibitory effect of green tea catechins in combination with sucralfate on Helicobacter pylori infection in Mongolian gerbils.

BACKGROUND: The occurrence of antibiotic-resistant Helicobacter pylori has been reported. It is desirable to develop an effective method to prevent the occurrence of resistant strains of Helicobacter pylori. Green tea catechins (GTCs) have been reported to have an antibacterial effect. Therefore, the possibility of eradicating Helicobacter pylori by the oral administration of GTCs was investigated. METHODS: Solutions of GTCs and solutions of GTCs adsorbed to sucralfate (GTC-scf), at concentrations of 20 mg GTCs and/or 20 mg sucralfate/ml were prepared. Then 1 ml of the GTC-scf or the GTC solution was administered daily, for 10 days to Mongolian gerbils infected with Helicobacter pylori. Then the stomachs were extirpated and homogenized. The homogenate was spread on selective medium plates. After 5-day culture, colony-forming units (CFU) of Helicobacter pylori were counted. RESULTS: The CFU of Helicobacter pylori was significantly decreased by GTC-scf. CONCLUSIONS: GTC-scf may have a bactericidal effect on Helicobacter pylori infection.

Administration, Oral↗
PubMedDate not supplied

Is Helicobacter pylori infection associated with chronic idiopathic urticaria?

BACKGROUND: Chronic idiopathic urticaria (CIU) is one of the most frequent skin diseases, however its causes remain unknown in the vast majority of cases. There is increasing evidence for systemic effects of gastric Helicobacter pylori infection, which may result in extra gastrointestinal disorders. Although CIU can result from several causes, a possible relationship between chronic urticaria and Helicobacter pylori has been recently suggested. OBJECTIVE: The aim of this study is to determine the prevalence of Helicobacter pylori infection in a series of patients with CIU, and measure the effectiveness of eradication therapy on the skin disease. METHOD: We assess Helicobacter pylori infection by 13C urea breath test (UBT) in 21 CIU patients. Amoxicillin, clarithromycin, and omeprazole were given to infected patients for seven days. The results of therapy were assessed by urea breath test one month after therapy. Urticaria and gastrointestinal symptoms were assessed on enrolment and for six months after eradication. RESULTS: Prevalence of Helicobacter pylori infection was of 71.4 % (15/21). There were no differences concerning age (31.83 vs. 33.82 years) and duration of symptoms (38.40 vs. 35.38 months) in patients with respectively positive and negative UBT. Helicobacter pylori eradication rate was of 80 % (12/14). Three patients had clinical improvement with total resolution of urticaria starting immediately after eradication therapy, being able to completely withdrawn antihistamine and corticosteroids therapy without complaints. In relation to the rest of the patients, these three had smaller duration of urticaria disease (14.3 vs. 43.7 months; p = 0.038) and greater titters in the UBT results (42.39 vs. 25.81; p = 0.073). DISCUSSION: Although some authors found convincing evidence of the involvement of Helicobacter pylori as one possible cause of chronic urticaria, our results have failed to confirm the existence of this etiological association. The most remarkable finding was that those patients who had clinical remission of disease were the ones with greater UBT titters suggesting a role for the amount of colonization by Hp in the pathogenesis of urticaria disease.

Adult↗
PubMed2000

Relationship between intestinal metaplasia of the gastro-oesophageal junction, Helicobacter pylori infection and gastro-oesophageal reflux disease: a prospective study.

BACKGROUND: The role of Helicobacter pylori infection and/or gastro-oesophageal reflux disease in pathogenesis of intestinal metaplasia in gastric cardia is still unclear. AIMS: To prospectively evaluate prevalence of inflammation and intestinal metaplasia of cardia in relationship to Helicobacter pylori infection in patients with gastro-oesophageal reflux disease and in healthy controls. PATIENTS: A total of 122 consecutive patients with gastro-oesophageal reflux disease and 49 control subjects were included. METHODS: During endoscopy, a total of six biopsies were taken from antrum, corpus and cardia. Helicobacter pylori infection was assessed by histology and rapid urease test. Degree of chronic gastritis, inflammatory activity and Helicobacter pylori colonization were scored from 0 to 3. RESULTS: No difference in prevalence was observed between gastro-oesophageal reflux disease patients and controls as far as concerns Helicobacter pylori (41% vs 38%), inflammation of cardia (59.5% vs 70%) and intestinal metaplasia of cardia (18% vs 19%). Inflammation of cardia was significantly (p<0.001) associated with Helicobacter pylori irrespective of gastro-oesophageal reflux disease symptoms. Cardial intestinal metaplasia was more frequently (p=0.03) found in infected subjects ((27%) than in uncolonized subjects (13%). No relationship was observed between gastro-oesophageal reflux disease and carditis and cardial intestinal metaplasia. Cardial intestinal metaplasia was more frequently detected in association with carditis (26% vs 6%, p=0.001). CONCLUSIONS: Inflammation and intestinal metaplasia of the gastric cardia are not markers of gastro-oesophageal reflux disease but are related to Helicobacter pylori.

Cardia↗
PubMed2003

Helicobacter pylori infection in subjects with acute ischaemic stroke.

AIMS: To determine whether infection with Helicobacter pylori is a significant risk factor for stroke. SUBJECTS: A total 467 in-patients with clinical evidence of acute ischaemic stroke and 388 healthy controls with no evidence of cerebrovascular disease. METHODS: This was a case control study. The prevalence of Helicobacter pylori was measured by enzyme-linked immunosorbent assay in stroke patients and controls. A positive titre was defined as >15 U/ml and relationship with circulating plasma fibrinogen and social depravation was expressed using the Townsend Index. RESULTS: There were significantly more Helicobacter pylori positive individuals (274/398 (69%)) in the cases compared to the controls (206/352 (58.5%)). Fibrinogen levels were also significantly higher in Helicobacter pylori positive (mean 4.14, standard deviation 1.33) than negative individuals (mean 3.78, standard deviation 1.28). The association between Helicobacter pylori and stroke was lost in a logistic model controlling for socio-economic status. Furthermore, fibrinogen levels were not associated with Helicobacter pylori status in a linear regression model controlling for socio-economic status. CONCLUSIONS: Infection with Helicobacter pylori is associated with an increased risk of stroke and increased fibrinogen levels but these findings can be attributed to a confounding effect of socio-economic status.

Aged↗
PubMed2002

Detection of Helicobacter pylori specific DNA in human atheromatous coronary arteries and its association to prior myocardial infarction and unstable angina.

BACKGROUND: Chronic infections have been proposed to play a role in the aetiology or progression of atherosclerotic plaques. Increased risk of coronary artery disease has been suggested in patients seropositive for Helicobacter pylori. AIM: To analyse coronary specimens in patients with severe (coronary artery disease) for Helicobacter pylori specific DNA. PATIENTS AND METHODS: Atherosclerotic plaques were obtained in 46 consecutive patients (9 female, 37 male, mean age 62.7+/-9.17 years) during coronary bypass procedures. Serum was analysed for IgG -/cagA-antibodies specific for Helicobacter pylori. Polymerase chain reaction and sequence analysis were used to identify bacterial DNA. Coronary artery biopsies from 19 autopsies without coronary artery disease were examined as a control group. RESULTS: Of the 46 coronary artery disease patients, 32 (69.6%) were Helicobacter pylori seropositive. Positive results for Helicobacter pylori DNA showed 18 seropositive and 4 seronegative (with anamnesis of eradication therapy). A total of 22 patients (47.8%) of the coronary artery disease group but none of controls revealed positive DNA. In the coronary artery disease group, a correlation between DNA presence and prior myocardial infarction (p=0.008) and unstable angina (p<0.001) was found. CONCLUSION: Identification of DNA in atherosclerotic plaques of patients with severe coronary artery disease supports the hypothesis that Helicobacter pylori infection may influence the development of atherosclerosis. Our results may indicate an direct involvement of Helicobacter pylori in the progression and instability of plaques in these patients.

Aged↗
PubMed2002

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease.

BACKGROUND: It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS: To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS: . Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS: Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). CONCLUSIONS: . The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.

Adult↗
PubMed1998

Prevalence of upper gastrointestinal lesions and Helicobacter pylori infection in Crohn's disease.

Crohn's disease can affect the upper gut with reported variable frequency, although concurrent Helicobacter pylori infection has been reported to be low. We prospectively investigated the prevalence of esophageal, gastric, and duodenal lesions and Helicobacter pylori infection in 67 Crohn's disease, 41 ulcerative colitis patients, and 43 controls. Symptoms, esophagogastroduodenoscopy, and multiple biopsies were performed on all patients consecutively. Endoscopic lesions were found in 63% of Crohn's disease patients, with a Helicobacter pylori prevalence of 28%. Granulomas were found in three patients. Twenty-two percent of the ulcerative colitis patients had lesions, with a 29% prevalence of Helicobacter pylori infection. Half of the controls had pathological endoscopy, and Helicobacter pylori was positive in 40% of the cases. Subjective symptoms did not predict the presence of endoscopic lesions or Helicobacter pylori infection in inflammatory bowel disease patients. Chronic gastritis and duodenitis are common in Crohn's disease patients, and the majority are not associated with Helicobacter pylori infection.

Adult↗
PubMedDate not supplied

Detection, eradication, and research implications of Helicobacter infections in laboratory rodents.

Researchers first isolated and characterized Helicobacter hepaticus in 1994 as a cause of hepatitis that progressed to hepatocellular carcinoma in A/JCr mice. During the past decade, isolation and characterization of additional novel helicobacters from rodents has continued. In addition to causing overt disease, rodent helicobacter infections are important because intercurrent disease in select models will confound research data. Emerging evidence suggests that inflammatory responses to enterohepatic helicobacter infections may alter host responses to other experimental stimuli in unanticipated ways. Additionally, scientists have experimentally infected a variety of inbred mouse strains and genetically engineered mice with a variety of Helicobacter spp. isolated from rodents, birds, and higher mammals (including humans) to develop animal models of gastrointestinal diseases as well as idiopathic human disease syndromes. This review highlights current information about helicobacter infections in laboratory rodents and provides recommendations for the detection and eradication of these infections. The authors discuss the impact of subclinical and clinical disease and offer recommendations for managing helicobacter-free rodent colonies.

Animals↗
PubMed1997

Association of antral mucosal levels of interleukin 8 and reactive oxygen radicals in patients infected with Helicobacter pylori.

1. Helicobacter pylori infection is characterized by an infiltration of neutrophils in the gastric mucosa. Neutrophil activation is an important source of reactive oxygen radicals, which cause tissue damage. Studies have shown that in Helicobacter pylori-infected patients there is increased mucosal production of interleukin 8. However, the role of interleukin 8 in the Helicobacter pylori-related inflammatory process and its relationship with reactive oxygen radicals remains to be clarified. The aims of this study were to investigate if there is any association between antral mucosal levels of interleukin 8 and reactive oxygen radicals and their relationship to gastric antral inflammation. 2. Fifty-two patients referred for endoscopy were recruited into the study. Gastric antral biopsies were taken for histology, culture and measurement of interleukin 8 and chemiluminescence (measuring reactive oxygen radicals). Interleukin 8 was measured by ELISA and the result expressed as pg/mg biopsy. Luminol-enhanced chemiluminescence was measured as mV min-1 mg-1 biopsy. Antral inflammation was assessed by a pathologist in a blinded fashion. 3. Antral mucosal levels of interleukin 8 and reactive oxygen radicals were significantly higher in Helicobacter pylori-colonized mucosa than in Helicobacter pylori-negative mucosa. After the eradication of Helicobacter pylori in patients with duodenal ulcer the median values (ranges) of interleukin 8 and reactive oxygen radicals fell from 1.21 (0.10-2.40) to 0.65 (0.00-1.60) and from 110.0 (10.0-959.0) to 14.5 (0.0-85.0) respectively. There was a positive correlation between interleukin 8 concentration and chemiluminescence response in the antral mucosa (r = 0.72). A higher interleukin 8 concentration was associated with greater neutrophil infiltration (r = 0.72) and mononuclear cell infiltration (r = 0.55); the magnitude of the chemiluminescence response was also positively associated with neutrophil (r = 0.77) and mononuclear cell infiltration (r = 0.59). 4. Interleukin 8 concentration is associated with an infiltration of neutrophils and mononuclear cells and is correlated with the production of reactive oxygen radicals in antral gastric mucosa infected with Helicobacter pylori. These findings suggest that interleukin 8 may be important in attracting and activating phagocytes to release reactive oxygen radicals, thereby causing mucosal damage.

Duodenal Ulcer↗
PubMed2002

Helicobacter pylori masks differences in homocysteine plasma levels between controls and type 2 diabetic patients.

BACKGROUND: Data in the literature have not clarified whether type 2 diabetes mellitus affects homocysteine plasma levels. Different variables able to influence homocysteine could be the cause of these controversial findings. An important but neglected confounding factor is Helicobacter pylori, which has been demonstrated to be a cause of elevated levels of homocysteine and which is prevalent in the Caucasian population, ranging from 30 to 40% incidence. Starting from these findings we wanted to verify whether differences in homocysteine levels exist between a type 2 diabetic population and a control group, taking into account the presence/absence of Helicobacter pylori. DESIGN: The study was carried out on a group of uncomplicated and normotensive type 2 diabetic patients (n = 30, 55.7 +/- 9.7 years) and on a control group (n = 43, 51.2 +/- 11.3 years). On these subjects we evaluated: main parameters of glyco- and lipo-metabolic balance, presence of Helicobacter pylori by 13C Urea Breath Test, plasma homocysteine, vitamin B12, folate and genetic polymorphism of methylenetetrahydrofolate reductase. RESULTS: Evaluating the two groups as a whole, significant differences in homocysteine were found when considering Helicobacter pylori presence/absence (14.0 +/- 6.5 vs. 10.6 +/- 4.7 micromol L-1, respectively, P < 0.01) without differences of vitamins and the genetic polymorphism of methylenetetrahydrofolate reductase. The positive interaction found among Helicobacter pylori, diabetes and homocysteine (P = 0.03) taking into account all the other evaluated confounding factors, demonstrates that a significant difference in homocysteine plasma levels exists between diabetics and controls (Helicobacter pylori-negative: diabetics 12.5 +/- 5.6 micromol L-1, controls 9.4 +/- 3.8 micromol L-1; Helicobacter pylori-positive: diabetics 13.6 +/- 5.8 micromol L-1, controls 14.3 +/- 7.0 micromol L-1). CONCLUSIONS: Type 2 diabetes seems to induce per se higher levels of homocysteine, which appears to be one of the factors responsible for the increased risk of vascular damage.

Adult↗
PubMed2006

Age-specific incidence of Helicobacter pylori.

BACKGROUND & AIMS: Helicobacter pylori is most likely acquired in childhood, but the incidence of infection has not been determined prospectively by using an appropriate noninvasive test. The aim of this study was to determine the age-specific incidence of Helicobacter pylori infection in children and the risk factors for infection. METHODS: Three hundred twenty-seven healthy index children between 24 and 48 months of age were enrolled over 15 months. At baseline, the Helicobacter pylori infection status of each index child and his or her older siblings and parents was assessed by using the carbon 13-urea breath test. All noninfected index children were then followed up with an annual carbon 13-urea breath test for 4 years to determine whether they became infected with Helicobacter pylori and, if so, the age at first infection. Information on potential risk factors was collected at baseline and each subsequent visit. RESULTS: At baseline assessment, 28 of 327 (8.6%) index children were infected with Helicobacter pylori. The mean age of the 28 infected children was 32.78 months (SD, 5.14 months). Over the next 4 years, 279 index children not infected at baseline contributed 970 person-years of follow-up to the study. During this time, 20 children became infected with Helicobacter pylori. The rate of infection per 100 person-years of follow-up was highest in the 2-3-year age group (5.05 per 100 person-years of follow-up (95% confidence interval, 1.64-11.78) and declined progressively as children aged. Only 1 child became infected after 5 years of age. Having an infected mother, an infected older sibling, and delayed weaning from a feeding bottle (ie, after 24 months of age) were all risk factors for infection. CONCLUSIONS: Children who become infected with Helicobacter pylori are infected at a very young age, and the risk of infection declines rapidly after 5 years of age. These findings have important implications for studies on the mode of transmission of infection.

Age of Onset↗
PubMed2004

Preferential placental transfer of Helicobacter pylori specific IgG.

OBJECTIVE: To evaluate the placental transfer of Helicobacter pylori-specific IgG in Iranian mothers. METHOD: The antibodies were measured in sera of 156 mother/newborn pairs using a commercially available indirect Enzyme Linked Immunosorbent Assay (ELISA). The study population was among healthy pregnant women who attended to the Zeinabieh hospital of Shiraz University of Medical Sciences in 1999. RESULTS: In total 74.7% of mothers were seropositive and more than 82% of seropositive mothers transferred Helicobacter pylori-specific IgG antibodies to their fetuses. The mean maternal Helicobacter pylori-specific IgG was significantly higher than that of the newborns (104.01 vs. 68.30 IU/ml, p < 0.001), however, there was a good correlation between maternal and neonatal antibodies. The level of maternal Helicobacter pylori-specific IgG was significantly lower in carriers of blood group B + compared to carriers of blood groups A + and O + . However, the cord/maternal ratio of Helicobacter pylori-specific IgG was significantly higher in blood group B + phenotype compared to blood group phenotypes A + and O + . CONCLUSION: The high rate of seropositivity among mothers highlights the risk of acquisition of Helicobacter pylori infection in early infancy for Iranian children. Our results also suggest that mothers having blood group B + are more likely to transfer Helicobacter pylori-specific IgG to their neonates.

ABO Blood-Group System↗