Serum and Tissue Beta-2 Microglobulin Levels in Patients with Helicobacter pylori Infection

Background and aim Beta-2 microglobulin (β₂-m) is a minor plasma protein, secreted from the plasma membranes as a result of the continuous regeneration of membrane proteins in the cell surface of all nucleated cells. The relationship between Helicobacter pylori and β₂-m has not been adequately established in studies. In this study, we aimed to compare the levels of serum and tissue β₂-m in patients with and without H. pylori infection, and to examine the relationship between levels of serum and tissue β₂-m. Material and methods About 30 patients with H. pylori gastritis and 22 healthy persons were enrolled in this study. Gastric biopsies were histologically analyzed and compared according to tissue and serum β₂-m levels. Results Serum β₂-m levels were comparable in H. pylori and control groups. There was no significant link between tissue H. pylori grade and serum β₂-m levels. Subendothelial β₂-m was detected in 19 (63.3%) cases with H. pylori and none of the control group with immunohistochemical staining (P < 0.001). There was no correlation between serum and tissue levels of β₂-m. Conclusion β₂-m accumulates in the majority of gastric tissues of patients with active chronic gastritis who were H. pylori (+), whereas no accumulation was found in H. pylori (−) control subjects.     

Helicobacter pylori Seroprevalence in Patients with Coronary Artery Disease

Recent studies have suggested that chronic infections such as Helicobacter pylori may be a risk factor for coronary artery disease (CAD). The aim of thIS study was to investigate the seroprevalence of H. pylori in patients with CAD. We enrolled 151 patients with CAD (93 men and 58 women, aged 48.1 ± 17.3 years [mean ± SD]) and 149 control subjects matched by age and sex (90 men and 59 women, aged 51.4 ± 13.9 years). An enzyme-linked immunosorbent assay immunoglobulin (Ig) G test for H. pylori diagnosis was performed on all enrolled subjects (CAD patients and controls). Ninety-one of 151 patients with CAD (60.2%) and 86 of the 149 subjects in the control group (57.7%) were H. pylori positive (P > 0.05). H. pylori infection rates were similar in patients with CAD and control groups. The main conclusion of this study is that H. pylori infection is not a risk factor for developing CAD. Further studies should be undertaken to confirm our results.     

Infection by CagA-Positive Helicobacter pylori Strains in Patients with Ischemic Heart Disease: Prevalence and Association with Exercise-Induced Electrocardiographic Abnormalities

The role of H. pylori infection in increasing the risk of ischemic heart diseases (IHD) is still debated. We determined serologically the prevalence of overall H. pylori and CagA-positive H. pylori infection in 63 consecutive patients with IHD and 189 gender- and age-matched controls. We also determined in patients the influence of the infection and the CagA serological status on the results of an exercise ECG test and other parameters considered possible variables that may enhance the risk of IHD. The prevalence of H. pylori infection in patients and controls was 79.3% and 73.0%, respectively (P = 0.403) and that of CagA-positive H. pylori infection was 69.8% and 42.3%, respectively (P = 0.0002). The scores of the ECG S-T segment and T-wave abnormalities in the course of an exercise ECG in uninfected patients and in patients infected by CagA-negative and CagA-positive H. pylori strains were (mean ± sd): 1.59 ± 0.67, 1.92 ± 0.64, and 2.19 ± 0.70, respectively; (P = 0.011, 95% confidence limits of difference 0.15–1.07, CagA-positive infected vs uninfected patients). There was no intergroup difference in the levels of peripheral whiteblood cells, glucose, cholesterol, triglycerides, creatinine, and systolic and diastolic pressure. In conclusion, genetic heterogeneity of H. pylori could possibly explain some conflicting results concerning the association of H. pylori infection with IHD. Coronary vessels of IHD patients infected by CagA-positive H. pylori strains may be damaged more severely than those of uninfected patients.     

Prevalence of Non-Organ-Specific Autoantibodies in Patients Suffering from Duodenal Ulcer With and Without Helicobacter pylori Infection

Autoimmunity, a feature of chronic infection by Helicobacter pylori, is first directed against gastric cells but is also associated with extragastric diseases. The aim of the present work was to look for the influence of the infection on induction of non-organ-specific autoantibodies (NOSAs). We compared 49 patients (28 males and 21 females; age range, 36-72 years; mean, 61 +/- 4.6 years) suffering from duodenal ulcer and H. pylori infection (Group A) to 38 subjects (20 male, 18 female; age range, 40-78 years; mean, 63 +/- 3.8 years) affected by duodenal ulcer related to the assumption of nonsteroidal antiinflammatory drugs (Group B). H. pylori infection was diagnosed by histology, 13C-urea breath test, and serum IgG antibodies. Autoimmunitary pattern was demonstrated by the presence of NOSAs in serum. Antinuclear (ANA), anti-smooth muscle (SMA), and anti-liver/kidney microsomal-1 (LKM-1) antibodies were present in 5 of 49 (10.2%), 2 of 49 (4%), and 0 Group A patients, respectively. In Group B, ANA was present in 3 of 38 (7.9%), SMA in 3 of 38 (7.9%), and anti-LKM-1 in 0 patients. The difference was not statistically significant. In this population, H. pylori infection is not associated with an increased prevalence of NOSAs.     

Association Between Helicobacter pylori Infection and Cirrhosis in Patients with Chronic Hepatitis C Virus

We evaluated, employing a logistic regression model, the association between Helicobacter pylori infection and cirrhosis in a cohort of 106 patients (57 males; mean age, 52.9 years; range, 20–78 years) with chronic hepatitis C virus (HCV) from Rosario, Argentina. HCV was confirmed by ELISA and PCR. H. pylori status was determined by ELISA. Of the 106 patients evaluated, 47 (44.3%) had cirrhosis. A total of 70.2% (33/47) of cirrhotic patients and 47.5% (28/59) of noncirrhotic patients were H. pylori-positive. In univariate analyses, cirrhosis was associated with age (P = 0.016) and H. pylori-positive status (P = 0.019) but not with gender (P = 0.28) or length of infection (P = 0.35). In multivariate analysis, H. pylori infection (P = 0.037; OR = 2.42; 95% CI = 1.06–5.53) and age (P = 0.033; OR = 1.04; 95% CI = 1.00–1.07) of patients remained significant and independently associated with cirrhosis. In conclusion, our results demonstrate an association between H. pylori infection and cirrhosis in patients with hepatitis C virus.     

Helicobacter pylori Infection and Gender: A Meta-Analysis of Population-Based Prevalence Surveys

Although most of Helicobacter pylori–related diseases are associated with male gender, the role of gender as a risk factor for H. pylori infection is still debated. To assess the true association between H. pylori and gender, we conducted a meta-analysis of large, population-based studies where the measure of association had been adjusted at least for age and socioeconomic status, and obtained primary data from authors when information on gender associations were not presented. In 18 adult populations, the test of heterogeneity was not significant and male gender was significantly associated with H. pylori infection (summary odds ratio [OR] 1.16 [95% confidence interval (CI) 1.11, 1.22]). In 10 pediatric populations, the test of heterogeneity was of borderline significance, and the summary OR computed using a random effect model was close to 1 (summary OR 1.03 [95% CI 0.91, 1.17]). This study confirms the male predominance of H. pylori infection in adults as a global and homogeneous phenomenon; such predominance is not apparent in children. Differential antibiotic exposure or differential protective immunity between genders may explain the different results observed between children and adult studies.     

Prevalence of Gastroduodenitis and Helicobacter pylori Infection in a General Population Sample

Some benign and malignant diseases develop on the background of chronic gastritis or duodenitis. The present study was performed in order to determine the magnitude of these background changes with relations to symptomatology and life style in the general population. Examinations were performed in 501 volunteers (age 35–85 years). Fifty percent had gastritis; this was associated with H. pylori in 87%. H. pylori-negative gastritis was associated with regular use of NSAIDs [odds ratio 3.8 (1.6–9.9)]. Duodenitis, observed in 32%, was associated with H. pylori infection [odds ratio 2.3 (1.3–4.6)], previous cholecystectomy [odds ratio 3.6 (1.1–16.1)], and regular use of NSAIDs [odds ratio 3.0 (1.4–7.1)]. Neither gastritis nor duodenitis was associated with smoking or alcohol consumption. The rate of digestive symptoms did not differ between subjects with and without uncomplicated gastritis or duodenitis. In conclusion, half of this adult population had gastritis strongly associated with H. pylori infection. Gastritis without H. pylori infection was frequently associated with regular NSAID intake. One third had duodenitis, which was associated with H. pylori infection as well as with regular use of NSAIDs and previous cholecystectomy. Digestive symptoms were not overrepresented in uncomplicated gastritis or duodenitis.     

The Effect of Helicobacter pylori on Insulin Resistance

Helicobacter pylori causes a lifelong infection in the stomach after exposure. H. pylorihas been shown to be associated with peptic ulcer and gastric cancer development. Moreover, it is held responsible for some other nongastric diseases. Among them, coronary heart disease attracts much debate. Many studies have demonstrated a close relationship between insulin resistance and atherosclerosis. Chronic inflammation and alterations in counter-regulatory hormones are deemed responsible for the etiology of insulin resistance. We aimed to examine the effect of H. pylori on insulin resistance. Sixty-three patients were enrolled in the study. Patients were divided into two groups according to H. pylori presence. HOMA-IR (homeostasis model assessment of insulin resistance) level was used to assess insülin resistance. Thirty-six patients were H. pylori positive and 27 were H. pylori negative. There was no difference between the two groups with regard to age, gender, or body mass index. HOMA-IR level was 1.73± 1.1 in the H. pylori-negative group, whereas it was 2.56 ± 1.54 in the H. pylori-positive group (P < 0.05). This study provides the first direct evidence for an association between chronic H. pylori infection and insulin resistance.     

Helicobacter pylori Infection Is Not Associated with Subclinical Hepatic Encephalopathy in Stable Cirrhotic Patients

The importance of ammonia-producing Helicobacter pylori infection as a cause of subclinical encephalopathy in cirrhosis was investigated. In addition, a single psychometric test that can reliably detect subclinical hepatic encephalopathy was sought. Out-patients with cirrhosis and no overt encephalopathy underwent [¹⁴C]urea breath testing once and psychometric testing on two separate occasions, with an intervening course of clarithromycin/omeprazole if they had subclinical encephalopathy (two of four psychometric tests abnormal). Subclinical encephalopathy was present in 27 of 69 patients (39%), and Helicobacter pylori infection in 14 of 69 (20%). There was no association between the two conditions (P = 0.769). Subclinical encephalopathy resolved in 75% of treated Helicobacter pylori-positive patients and 37.5% of treated Helicobacter pylori-negative patients (P = 0.285). Number connection test-B had high reproducibility among untreated patients (R = 0.655) and high correlation (P 0.01) with three surrogate gold standards. In stable cirrhotic patients, subclinical hepatic encephalopathy was found to: (1) have a high prevalence, (2) not be associated with Helicobacter pylori infection, and (3) be readily detected with the number connection test-B alone.     

Helicobacter pylori Infection and Oncogene Expressions in Gastric Carcinoma and Its Precursor Lesions

Although it is fairly well accepted that Helicobacter pylori infection plays a significant role in causing gastric cancer, the exact mechanisms involved in its pathogenesis are unclear. We have examined the relationship between H. pylori infection and oncogene expression in different stages of disease progression from precursor lesions to gastric carcinoma. We used Diff-Quik stain to diagnose H. pylori infection and immunohistochemical stains against c-erbB-2, p53, ras, c-myc, and bcl-2 to determine expression of oncogenes. H. pylori infection was found in all cases of chronic gastritis, atrophic gastritis, intestinal metaplasia, and early gastric carcinoma, and in 16 of 30 (53%) cases of advanced gastric carcinoma. Overexpression of c-erbB-2 was found in 2 (7%) cases of advanced gastric carcinoma, which were H. pylori negative. Suppressor gene, p53, was overexpressed in 3 (30%) cases of intestinal metaplasia, 2 (33%) cases of early gastric carcinoma, and 18 (60%) cases of advanced gastric carcinoma. Of these 18 p53-positive advanced gastric cancer cases, 11 (61%) were H. pylori positive. Expression of ras p21 was found in 4 (40%) cases of H. pylori-negative normal mucosa, 10 (100%) cases of chronic gastritis, 1 (10%) case of atrophic mucosa, 6 (60%) cases of intestinal metaplasia, 2 (33%) cases of nonneoplastic mucosa adjacent to early gastric carcinoma, and 7 (23%) nonneoplastic mucosa adjacent to advanced gastric carcinoma, all of which showed H. pylori. No evidence of expression of either c-myc or bcl-2 was detected in any of the above-mentioned samples. The data suggest that H. pylori infection may increase expression of ras p21 proteins and induce p53 suppressor gene mutation early in the process of gastric carcinogenesis.     

High Eradication Rates of Helicobacter pylori Infection with First- and Second-Line Combination of Esomeprazole, Tetracycline, and Metronidazole in Patients Allergic to Penicillin

H. pylori eradication is a challenge in patients allergic to penicillin, both first-line and failures of prior therapy. We aimed to assess the eradication rate of H. pylori in patients allergic to penicillin, first-line and failures of prior therapy, the efficacy of healing of active duodenal ulcer disease (DUD) and erosive gastritis, and the safety and tolerability of the combination. Twenty patients with documented allergy to penicillin, DUD, and H. pylori infection, 17 (85%) for first-line treatment and 3 (15%) prior therapy failures, were given a 10-day regimen of esomeprazole, 40 mg qid, tetracycline, 500 mg qid, and metronidazole, 500 mg qid. Baseline and follow-up panendoscopy 30 days after end of treatment was performed for rapid urease test (Clotest), and four site biopsies for H. pylori, and to document endoscopic peptic ulcer disease. All adverse events during treatment were documented. Eradication rates by intention to treat (ITT) were 85% for first-line treatment and 100% for failures. Seventy percent of all cases had a normal endoscopy at follow-up, and 85 and 100% of patients had healed erosive gastritis and DUD, respectively, from baseline. There were histological improvements in most patients. A high eradication rate was obtained even in patients who had a shorter duration of treatment. The combination was well tolerated. A combination of esomeprazole, tetracycline, and metronidazole is effective for eradication of H. pylori in patients allergic to penicillin, for both first-line treatment and failures of prior treatment.This research was supported by a grant from the Investigator Sponsored Studies Program of Astra Zeneca.     

Helicobacter pylori Prevalence in Diabetes Mellitus Patients with Dyspeptic Symptoms and its Relationship to Glycemic Control and Late Complications

Background There are contradictory reports on Helicobacter pylori prevalence and its relationship to late complications of diabetes mellitus (DM). The aim of this study was to determine the prevalence of H. pylori infection in type 2 DM patients and to evaluate the relationship between H. pylori infection and the glycemic control, late complications. Material and Method A total of 141 type 2 DM patients and 142 nondiabetic subjects with upper gastrointestinal symptoms were enrolled in the study. All patients underwent upper gastrointestinal endoscopy with biopsy specimens obtained from gastric antrum and corpus. H. pylori status was evaluated in each patient by both the rapid urease test and histopathological examination. Plasma glucose, HbA1c, microalbuminuria in 24 h collected urine, electroneuromyography, and fundoscopic examinations were performed in all subjects. Results The prevalence of H. pylori infection was 61.7% and 58.5%, respectively, among type 2 diabetic patients and nondiabetic controls and was not statistically significant (P = 0.577). The duration of diabetes, fasting blood glucose and haemoglobin A1c levels, nephropathy and retinopathy prevalence did not differ significantly between the two groups (diabetics versus nondiabetics). There was no late complication in 60.3% of the type 2 diabetic patients as compared to at least one late complication in the remainders. A statistically significant correlation was found between H. pylori infection and the presence of neuropathy (P = 0.021). Conclusions The prevalence of H. pylori infection did not differ significantly between the diabetic patients and nondiabetic controls. Interestingly, diabetics with H. pylori infection had a higher incidence of neuropathy, although there was no association between the duration and regulation of diabetes, retinopathy, nephropathy and H. pylori status.     

Helicobacter pylori Seroprevalence in Patients with Autoimmune Hepatitis

Autoimmune hepatitis is characterized by a continuing hepatocyte necrosis that usually progresses to liver cirrhosis. Autoimmunity is also a feature of chronic infection by Helicobacter pylori, a gram-negative bacterium involved in the pathogenesis of peptic ulcer and upper gastrointestinal bleeding, with both events frequently occurring in patients with chronic liver disease. A newly described pathogenetic mechanism for chronic hepatitis and hepatocellular carcinoma in the mouse is linked to Helicobacter spp. infection. A high prevalence of H. pylori infection was demonstrated in patients with viral-related cirrhosis but never studied in cases of autoimmune hepatitis. In a case-control study, we examined 31 consecutive patients (25 women and 6 men, age range 20–66, mean age 46 ± 4.3 years) suffering from autoimmune hepatitis and 62 sex- and age-matched blood donors (50 women, 12 men, age range 20–65, mean age 46 ± 5.4 years) resident in the same area. Antibodies to H. pylori were present in 20 of 31 (64.5%) autoimmune patients compared to 33 of 62 (53.2%) controls (P = 0.3, odds ratio 1.60, 95% CI 0.60–4.28). The difference was not statistically significant either in female or male patients. In conclusion, the prevalence of H. pylori infection in patients and controls was similar in our study of patients with chronic autoimmune hepatitis.     

Helicobacter pylori Recurrence and Infection Rate in Israeli Adults

Introduction In developing countries the recurrence rate of Helicobacter pylori after successful eradication therapy is as high as 42%, while in developed countries it is estimated to be less than 3%. Such figures are very important in terms of determining clinical strategy and outcome. Aim To estimate the recurrence rate of H. pylori in Israel using the database of the "Central H. Pylori Laboratory of Clalit Health Services". Methods The database was searched for patients who had undergone the [¹³C]-urea breath test ([¹³C]-UBT) for validation of the successful eradication of H. pylori or for evaluation of dyspepsia 7 years previously and for whom the result had been negative. These patients were invited to participate in the trial, fill a symptom questionnaire and undergo another [¹³C]-UBT. Results A In total, 65 patients participated; of these, 26 patients had tested negative in the first ¹³CUBT, indicating the successful eradication of H. pylori (Group A), and 39 had been tested for dyspepsia (Group B). One patient in each group had a positive [¹³C]-UBT – 3.84% in Group A and 2.56% in Group B (non-significant difference, NS). The mean annual H. pylori recurrence rate was calculated to be 0.55% and 0.37% in Group A and Group B patients, respectively (NS). Conclusion Our results shown a very low re-infection or new infection rates in Israeli adults and are in line with other trials in developed countries; they do not support the a retesting program for patients after a successful eradication therapy.     

Helicobacter pylori CagA status associated with gastric cancer incidence rate variability in Costa Rican regions

Background We evaluated several risk factors for gastric cancer in Costa Rican regions having contrasting gastric cancer incidence rates, despite the small dimensions of the country. Methods A total of 180 dyspeptic patients were classified into two groups according to the gastric cancer incidence (GCI) rate in their Costa Rican region: group A, with a high GCI rate (n = 91) and group B, with a low GCI rate (n = 89). Helicobacter pylori infection was detected by rapid urease test, Gram staining, and histological observation. Antral and corpus specimens were obtained to assess the grade of inflammation, topography of gastritis, gastric atrophy, and intestinal metaplasia by histological examination. Serum CagA antibody was measured by an antigen-specific enzyme-linked immunosorbent assay. Results There was no significant difference in H. pylori prevalence between groups A (73%) and B (63%); however, serum CagA antibody was more frequently detected in group A (79%) than in group B (54%) [P = 0.02; odds ratio (OR), 2.68]. Among patients under 60 years of age, serum CagA antibody was even more frequently detected in group A (81%) than in group B (49%) (P < 0.01; OR, 4.50). The prevalence of corpus-predominant gastritis, atrophic gastritis, and moderate/severe grades of neutrophilic infiltration was higher in serum CagA antibody-positive patients than in CagA antibody-negative patients (P = 0.003, 0.04, and 0.002, respectively). Conclusions Infection with H. pylori possessing the cagA gene is associated with the development of severe gastric damage such as gastric atrophy, leading to gastric cancer, and probably influences the differences in GCI between Costa Rican regions.     

An Inverse Relationship between the Expression of the Gastric Tumor Suppressor RUNX3 and Infection with Helicobacter pylori in Gastric Epithelial Dysplasia

Background/Aims

This study was performed to determine the association between RUNX3 expression and Helicobacter pylori infection in premalignant gastric lesions.

Methods

We examined 107 patients with gastric epithelial dysplasia who had undergone endoscopic mucosal resection or submucosal dissection. All tissue samples were evaluated by RUNX3 staining and subclassified by immunophenotype. H. pylori infection in dysplastic lesions and the normal surrounding tissue was examined by silver staining, and cagA status was assessed by polymerase chain reaction.

Results

The loss of RUNX3 expression was observed in 62 cases (57.9%), and an association with H. pylori infection was found in 54 cases (50.5%). The infection rate with the cagA-positive H. pylori strain was 63.0%. In RUNX3-negative lesions, the rate of H. pylori infection (p=0.03) and the frequency of category 4 lesions (according to the revised Vienna classification) were high (p=0.02). In addition, the gastric mucin phenotype was predominant. In RUNX3-negative category 4 lesions, the rate of cagA-positive H. pylori infection rate was high but not significantly increased (p=0.08).

Conclusions

Infection with H. pylori is associated with inactivation of RUNX3 in early gastric carcinogenesis. This mechanism was prominent in gastric cancer with a gastric mucin phenotype.     

Treatment of Helicobacter pylori Infection in Clinical Practice in the United States

Our objectives were to define treatment success, compliance, and side effects for treatment of Helicobacter pylori in clinical practice. In all, 224 consecutive patients received Helicobacter pylori treatment: 97 received two weeks of bismuth subsalicylate, metronidazole, tetracycline four times a day with a H₂-receptor antagonist twice a day (BMT); 89 received one week of metronidazole, lansoprazole, and clarithromycin twice a day (MLC); and 38 received one week of BMT with lansoprazole twice a day (BMT-PPI). Cure rates were: BMT 81% (95% CI 74–89%), MLC 90% (95% CI 84–96%) BMT-PPI 87% (95% CI 81–92%). More patients prescribed a bismuth-based regimen discontinued medications due to side effects compared to MLC (P = 0.049). Nausea was more common for BMT compared to MLC (P = 0.04). In conclusion, treatment of Helicobacter pylori infection with a one-week course of MLC achieves a high rate of cure in clinical practice. Significantly fewer patients prescribed PPI-based therapy discontinue medications due to side effects as compared to bismuth-based triple therapy.     

Efficacy of Triple Therapy Plus Cetraxate for the Helicobacter pylori Eradication in Partial Gastrectomy Patients

In the present study, we aimed to establish an additional standardized protocol with a higher H. pylori eradication rate in the remnant stomach. Fifty-five H. pylori–positive patients were randomly allocated to one of three regimens: LAC—lansoprazole, amoxicillin, and clarithromycin b.i.d. for 7 days (n = 17); LAC+CET—LAC b.i.d. plus cetraxate q.i.d. for 7 days (n = 20); and LEFT—LAC for 7 days in a horizontal body position on the left side for 30 min (n = 18). Patient compliance and side effects were checked via interviews. H. pylori eradication was successful in 75, 72, and 41% in LAC+CET, LEFT, and LAC, respectively. The eradication rate was significantly higher in LAC+CET than in LAC (P = 0.024) but not in LEFT (P = 0.058). Adverse events that occurred in each group were almost all mild ones. Cetraxate plus LAC for 1 week is a safe and effective regime for the eradication of H. pylori in patients after partial gastrectomy.     

Association Between Helicobacter pylori Infection in Mothers and Birth Weight

Helicobacter pylori infection may cause intrauterine growth restriction (IUGR). However, it is unknown whether the growth of children from H. pylori-infected mothers is also affected or whether transmission of infection from mother to child occurs. This study aimed to determine if maternal H. pylori infection was associated with IUGR and low birth weight in a mouse model, and whether transmission of infection from mother to infant occurs. Female C57BL/6 mice were inoculated with H. pylori (n = 18) or water (control; n = 18) via gavage. Mice were mated at 6 weeks postinfection, with half of the mice sacrificed after 2 weeks of gestation. The remaining mice gave birth and a third of the litter was weighed and sacrificed at birth, during milk feeding (1.5 weeks), and during solid feeding (4 weeks). Stomachs of all mice and whole foetuses were cultured for the presence of H. pylori. There were no differences in litter size or foetus weight between control and H. pylori-infected mice. Pups from infected mothers had a lower weight during milk feeding (control, 5.91 ± 0.23 g; H. pylori, 4.59 ± 0.16 g; p < 0.05) and solid feeding (control, 12.73 ± 0.58 g; H. pylori, 10.01 ± 1.02 g; p < 0.05). H. pylori was not detected by culture in the pups at any age. H. pylori infection in mothers was associated with a decrease in infant weight during milk feeding and after weaning. Transmission of infection from mother to infant was not detected by culture, suggesting that decreased baby weight may be due to decreased milk supply or altered nutrition from the mother.     

Association Between Gastric Atrophy and Helicobacter pylori Infection in Japanese Children: A Retrospective Multicenter Study

The purpose of this study was to determine whether Helicobacter pylori infection and mucosal inflammation result in gastric atrophy in Japanese children. A total of 196 patients ages 1–16 years were retrospectively studied: 131 patients were infected with H. pylori and 65 patients were uninfected. Antral (n = 196) and corpus biopsy specimens (n = 70) were investigated based on the Updated Sydney system. In both the antrum and corpus, H. pylori-infected patients showed significantly higher degrees of inflammation and activity of gastritis, compared with noninfected patients. The prevalence of grade 2 or 3 atrophy in the antrum was 10.7% in H. pylori-infected patients and 0% in the noninfected patients (P < .01) and in corpus 4.3% and 0%, respectively (P = .20). The frequency of intestinal metaplasia in the 2 study groups was 4.6% and 4.6% in the antrum and 0% and 4.2% in the corpus, respectively. Among H. pylori-infected patients, the antrum showed significantly higher degrees of H. pylori density, inflammation and activity of gastritis, and atrophy than the corpus. In the antrum, atrophy was significantly correlated with activity, whereas in the corpus, atrophy correlated with H. pylori density, inflammation, and activity. H. pylori-induced gastric inflammation can cause atrophy in Japanese children, predominantly in the antrum. It remains to be determined whether H. pylori-infected children with gastric atrophy are at increased risk for gastric cancer.