Helicobacter pylori colonizes the human stomach and may affect the inflammatory response, hormone production related to energy regulation, and gastrointestinal microbiota composition. Previous studies have explored a potential association between H. pylori infection and pediatric obesity with varying results. Considering the immunomodulatory effects of early-life infection with H. pylori that can confer beneficial effects, we hypothesized that we would find an inverse relationship between H. pylori seropositivity and obesity among Danish children and adolescents.

We assessed H. pylori seroprevalence in 713 subjects from an obesity clinic cohort and 990 subjects from a population-based cohort, aged 6 to 19 years, and examined its association with obesity and other cardiometabolic risk factors.

No association was found between H. pylori and body mass index standard deviation score (BMI SDS). H. pylori seropositivity was, however, significantly associated with higher fasting plasma glucose levels and the prevalence of hyperglycemia.

While we did not find an association between H. pylori seropositivity and BMI SDS, we observed a significant association with higher fasting plasma glucose levels and increased prevalence of hyperglycemia, suggesting that H. pylori infection may contribute to impaired glucose regulation in Danish children and adolescents.

Background and Objectives: Type 1 diabetes mellitus (T1DM) is a chronic and serious condition that is characterized by inadequate pancreatic-β-cells' insulin production. The connection between T1DM and Helicobacter pylori infection remains uncertain. This study aimed to conduct a systematic meta-analysis to examine the association between H. pylori infection, hemoglobin A1c levels, and the development of T1DM. Materials and Methods: The initial search identified 451 articles on the association between H. pylori infection and T1DM. Among them, 12 articles had 2797 participants who met the inclusion criteria for an advanced meta-analysis. Results: A significant association was observed between H. pylori infection and T1DM (OR 1.77, 95% CI 1.47-2.12, p < 0.0001), with heterogeneity: Tau2 = 0.47; Chi2 = 57.07, df = 11 (p < 0.0001); I2 = 81%. Subgroup analysis showed that H. pylori infection was significantly associated with a longer duration of T1DM and higher hemoglobin A1c levels (p < 0.001 for both) but not with age at T1DM diagnosis (p = 0.306). Conclusions: These findings contribute to the understanding of the association between H. pylori infection and T1DM and highlight the potential role of H. pylori in influencing the duration and glycemic control of diabetes. Therefore, pediatric patients who have longstanding T1DM and poor glycemic control should be screened for H. pylori infection.

Data regarding Helicobacter pylori (Hp) infection frequency in concurrent celiac disease (CD) and type 1 diabetes mellitus (T1DM) (CD + T1DM) are anecdotal. This study aimed to evaluate the association between Hp and concomitant CD + T1DM in children.

In this 2-center, case-control study, children who underwent esophago-gastro-duodenoscopy (EGD) were studied. CD diagnosis was established by favorable histology and serology. Hp infection was confirmed by both histology and the rapid urease test. Patients were divided into 3 groups as CD only (CDo), CD + T1DM, and non-CD children who underwent endoscopy as controls.

Among the 1,431 EGDs performed, 783 cases were eligible. Overall, 215 cases had CDo (mean age: 9.12 ± 4.18 years, 58.1% girls), 63 cases had CD + T1DM (mean age: 9.29 ± 4.46 years, 50.8% girls), and 505 cases were controls (mean age: 9.69 ± 4.52 years, 56.6% girls). Hp infection rate was significantly lower in CD + T1DM group (controls: 49.7% vs. CDo: 32.1% vs. CD + T1DM: 20.6%, p < 0.01). After adjustment for age, gender, and socioeconomic status, the Hp infection rate was still significantly low (adjusted odds ratio [aOR]: 1.57, 95% confidence interval (CI): 1.35-1.83, p < 0.01). A difference in Hp infection rate between controls and CDo group (aOR: 1.43, 95% CI: 1.09-2.12, p < 0.05), and between CDo and CD + T1DM (aOR: 0.89, 95% CI: 0.65-1.54, p < 0.05) group was significant. The severity of duodenal lesions and the presence of Hp infection were not correlated in all celiac children (r: 0.113, p > 0.05).

The frequency of Hp infection was significantly lower in CD + T1DM children, compared to the CDo group and the controls.

There are several studies with varied and mixed results about the possible relationship between H. pylori and diabetes. Therefore, this current meta-analysis performed to determine the association between H. pylori infection and the risk of diabetes mellitus.

A systematic literature searches of international databases, including Medline (PubMed), Web of Sciences, Scopus, EMBASE, and CINHAL (January 1990-March 2019) was conducted to identify studies investigating the relationship between H. pylori infection and diabetes mellitus. Only case-control studies were analyzed using odds ratio (OR) with 95% confidence intervals (CIs). Stratified and subgroup analyses were performed to explore heterogeneity between studies and assess effects of study quality. Logarithm and standard error logarithm odds ratio (OR) were also used for meta-analysis.

A total of 41 studies involving 9559 individuals (case; 4327 and control; 5232) were analyzed. The pooled estimate of the association between H. pylori infection with diabetes was OR = 1.27 (95% CI 1.11 to 1.45, P = 0.0001, I2 = 86.6%). The effect of H. pylori infection on diabetes mellitus (both types), type 1 and type 2 diabetes was 1.17 (95% CI 0.94 to 1.45), 1.19 (95% CI 0.98 to 1.45), and 1.43 (95% CI 1.11 to 1.85) respectively. Subgroup analysis by the geographical regions showed in Asian population risk of the effect of H. pylori infection on diabetes was slightly higher than other population, CONCLUSION: In overall a positive association between H. pylori infection and diabetes mellitus was found.

This study aimed to investigate the association between Helicobacter pylori infection with diabetes mellitus type one and the effect of infected Helicobacter pylori on glycemic control.

This case control study was conducted on children with and without type 1 diabetes mellitus (T1DM). Demographic data and gastrointestinal symptoms in both groups and glycemic control status and duration of diabetes were recorded in patients with T1DM. Stool test was done on all children to detect Helicobacter pylori antigen.

Sixty three children with T1DM with a mean of 10.88 ± 2.84 years and 105 control children with an average age 10.17 ± 2.55 years (P = 0/09) were involved in this study. The frequency of Helicobacter pylori infection in patients with T1DM was 17/63 (27%) and 25/105 (23.8%) in control group, (P = 0/64). The frequency of bloating, epigastric pain and nausea was not significantly different between the two groups. The frequency of epigastric pain in children with diabetes with helicobacter infection was significantly higher than non-infected children with diabetes (29.4% vs. 2.2%) (P = 0.004).The mean duration of diabetes (P = 0.53), age diagnosis of diabetes (P = 0.09), fasting blood glucose (P = 0.18), glycosylated hemoglobin (P = 0.08) and the daily insulin dose (P = 0.18) in patients with T1DM with and without helicobacter pylori infection had not significantly different.

There was no significant association between Helicobacter pylori infection and diabetes in children 5-15 years old, and glycemic control status was not difference in patients with T1DM with and without Helicobacter pylori infection.

The association between Helicobacter pylori infection and glycated hemoglobin A has been confirmed in many studies, but these conclusions are still contradictory and controversial. Therefore, we conducted a meta-analysis to resolve the problem of inconsistent results in diabetes.

A comprehensive search was conducted on related researches published in PubMed, Embase, and China Academic Journal Full-text Database (CNKI) from the inception of each database to April 2019. Fixed or random effects model was used to pool the weighted mean difference with 95% confidence interval from individual studies. Subgroup and sensitivity analyses were also performed. Publication bias was estimated by funnel plot, Egger's test, and fail-safe numbers.

35 studies with 4,401 participants with diabetes were included in the meta-analysis. Glycated hemoglobin A levels were elevated in patients with Helicobacter pylori infection compared with patients without Helicobacter pylori infection (WMD = 0.50, 95% CI: 0.28-0.72, p < 0.001). In subgroup analysis by the subtype of diabetes, there was a correlation between Helicobacter pylori infection and elevated glycated hemoglobin A in type 1 diabetes (I ² = 74%, p < 0.001, WMD = 0.46, 95% CI: 0.12-0.80), and in type 2 diabetes (I ² = 90%, p < 0.001, WMD = 0.59, 95% CI: 0.28-0.90, p < 0.001). In subgroup analysis by the study design, there was a correlation in cross-sectional study (I ² = 89%, p < 0.001, WMD = 0.42, 95% CI: 0.16-0.69, p ≤ 0.003) and in case-control study (I ² = 83%, p < 0.001, WMD = 0.39, 95% CI: 0.14-0.64, p ≤ 0.003). By different methods for detecting Helicobacter pylori, there was a correlation in the biopsy group (I ² = 83%, p < 0.001, WMD = 0.6, 95% CI: 0.11-1.09, p ≤ 0.03) and in other groups of test methods (I ² = 87%, p < 0.001, WMD = 0.37, 95% CI: 0.17-0.56, p < 0.001). Sensitivity analysis showed that our results were reliable, and no evidence of substantial publication bias was detected.

The meta-analysis might indicate a correlation between Helicobacter pylori infection and glycated hemoglobin A levels in diabetes.

Extragastric manifestations of Helicobacter pylori (H. pylori) infection have been reported in many diseases. However, there are still controversies about whether H. pylori infection is associated with diabetes mellitus (DM). This study was aimed at answering the question.

A systematic search of the literature from January 1996 to January 2016 was conducted in PubMed, Embase databases, Cochrane Library, Google Scholar, Wanfang Data, China national knowledge database, and SinoMed. Published studies reporting H. pylori infection in both DM and non-DM individuals were recruited.

79 studies with 57,397 individuals were included in this meta-analysis. The prevalence of H. pylori infection in DM group (54.9%) was significantly higher than that (47.5%) in non-DM group (OR = 1.69, P < 0.001). The difference was significant in comparison between type 2 DM group and non-DM group (OR = 2.05), but not in that between type 1 DM group and non-DM group (OR = 1.23, 95% CI: 0.77-1.96, P = 0.38).

Our meta-analysis suggested that there is significantly higher prevalence of H. pylori infection in DM patients as compared to non-DM individuals. And the difference is associated with type 2 DM but not type 1 DM.

We performed to reveal the association between the Helicobacter pylori infection and body weight among children.

Out retrospective study included patients who underwent the H. pylori immunoglobulin G testing at Konyang University Hospital between March 2011 and June 2014. These patients were classified as seropositive (28 boys, 27 girls; mean age: 9.89±3.28 years) or seronegative (55 boys, 54 girls; mean age: 9.84±3.02 years). Next, we compared various characteristics between the seropositive and negative groups, as well as between obese children (body weight ≥90th percentile) and non-obese children (body weight <90th percentile). Furthermore, we compared the change in body weight after 2 months of treatment with amoxicillin, clarithromycin and omeprazole among the 55 seropositive children (14 treated children and 41 non-treated children).

There were no differences in the weights and laboratory data for the 55 seropositive children and 109 seronegative children (weight; 40.96±18.11 kg vs. 36.85±13.72 kg, respectively; p=0.14). And, there was no difference in the prevalence of H. pylori infection among the 29 obese and 135 non-obese children (p=0.581). However, after 2 months of eradication, the 14 treated patients exhibited a significant weight gain (+0.91±0.52 kg), compared to the 41 non-treated patients (-0.29±1.16 kg, p=0.025).

Our findings present that obesity was not associated with the H. pylori infection, although H. pylori eradication led to significant increase in body weight.

Persistent presence of ATP4A autoantibodies (ATP4AA) directed towards parietal cells is typical for atrophic body gastritis (ABG), an autoimmune disease associated with type 1 diabetes. We assessed whether Helicobacter pylori (Hp) infection might be associated with positivity for ATP4AA in children with type 1 diabetes. Sera were collected from 70 (38♀) type 1 diabetes children [aged 13·2 ± 4·5 years, age at diagnosis 8·8 ± 4·3 years, diabetes duration 4·5 ± 3·8 years, mean HbA1c 7·8 ± 1·6% (62 ± 17·5 mmol/mol)] seen at the regional diabetes clinic in Katowice, Poland. Patients were tested concurrently for Hp infection by means of a 13C urea breath test. ATP4AA were measured using a novel radioimmunoprecipitation assay developed at the Barbara Davies Center for Childhood Diabetes, University of Colorado. ATP4AA were present in 21 [30%, 95% confidence interval (CI) = 19-41%] and Hp infection was detected in 23 (33%, 95% CI = 22-44%) children. There was no statistically significant association between ATP4AA presence and Hp status. ATP4AA presence was not associated with current age, age at type 1 diabetes diagnosis, diabetes duration or current HbA1c. ATP4AA were more prevalent in females [42% (26-58%)] than males [16% (3-28%)], P = 0·016. ATP4A are found in nearly one-third of children with type 1 diabetes and more common among females. In this cross-sectional analysis, Hp infection was not associated with autoimmunity against parietal cells.

Helicobacter pylori (H. pylori) infection has been associated with increased levels of inflammatory cytokines and subsequent insulin resistance and epidemiologically linked to type 2 diabetes.

To study the prevalence rate of H. pylori infection in type 2 diabetes and its relation with HbA1C levels.

In this cross-sectional case-control study, 80 patients (≥18 years) who met the Americans with Disabilities Act (ADA) criteria for diabetes were recruited. Similarly, 60 age, sex, and education matched healthy controls were taken. They were tested for H. pylori infection by rapid urease test, histological examination of antral endoscopic biopsy specimens and serology. The relationship between H. pylori infection and levels of plasma glucose and HbA1C was assessed.

Out of the 80 patients of type 2 diabetes, H. pylori infection was found in 62 (77.5%) while it was present in only 35 (58.3%) of 60 controls, which was found to be significant (Chi-square test: 5.919, df = 1, P value = 0.015). Mean HbA1C among diabetics with H. pylori infection was 8.19 ± 1.16% and without H. pylori infection was 6.9 ± 0.84% (t = 4.3872, P value = 0.0001).

Prevalence of H. pylori infection was significantly higher in diabetes as compared to controls. Presence of H. pylori infection significantly correlated with the level of HbA1C.

Helicobacter pylori (H. pylori) is a highly prevalent, serious and chronic infection that has been associated causally with a diverse spectrum of extragastric disorders including iron deficiency anemia, chronic idiopathic thrombocytopenic purpura, growth retardation, and diabetes mellitus. The inverse relation of H. pylori prevalence and the increase in allergies, as reported from epidemiological studies, has stimulated research for elucidating potential underlying pathophysiological mechanisms. Although H. pylori is most frequently acquired during childhood in both developed and developing countries, clinicians are less familiar with the pediatric literature in the field. A better understanding of the H. pylori disease spectrum in childhood should lead to clearer recommendations about testing for and treating H. pylori infection in children who are more likely to develop clinical sequelae. A further clinical challenge is whether the progressive decrease of H. pylori in the last decades, abetted by modern clinical practices, may have other health consequences.

OBJECTIVE. To assess the association between Helicobacter pylori (HP) infection and glycemic control in patients with diabetes through a meta-analytic approach. RESEARCH DESIGN AND METHODS. Electronic literature searches were conducted for cross-sectional studies that examined the hemoglobin A1c (A1C) level by whether patients with diabetes were or were not carriers of HP. Mean differences in A1C between groups with and without HP infection were pooled with a random-effects model. RESULTS. Thirteen eligible studies were included in this meta-analysis. Overall, the HP carriers did not have significantly higher A1C levels compared with HP noncarriers (mean difference (95% CI), 0.19% (-0.18 to 0.46), P = 0.16). When the analysis was limited to studies targeting patients with type 1 diabetes, there was also no significant difference in A1C (0.69% (-0.31 to 1.68), P = 0.18). CONCLUSIONS. There was insufficient evidence that HP infection worsened glycemic control in patients with diabetes.

Metabolic syndrome is one of the most prevalent global health problems that predisposes to Type 2 diabetes. It is strongly linked to insulin resistance, which results in hyperglycemia. Over the past few years, lot of studies have been carried out on Helicobacter pylori infection and found a possible causal relationship through releasing some of the interleukins factors, which result in endothelial dysfunction. However, some studies attributed that due to coincidence were not able to establish any causal relationship. In this review, the literature has been reviewed to check this possible association.

Helicobacter pylori (Hp) is a chronic stomach infection common throughout the world. The pediatric diabetes literature on the relation between Hp and HbA1c is sparse and controversial. This study aimed to investigate this relation.

The study included 100 youth with type 1 diabetes and seropositive for Hp (European Caucasians: n=49; Moghrabin Caucasians: n=51). Mean socioeconomic status was lower among the latter. Hp infection was demonstrated by the (13)C-urea breath test and a gastric biopsy for antibiotic susceptibility testing. HbA1c levels were measured for a year (mean: 6 measurements; upper normal limit: 6.2%) before and after Hp eradication, which was proved by the (13)C-urea breath test.

Of 100 Hp-seropositive patients, 49 had active Hp infections and were treated. Mean age+/-SD was 14.2+/-2.8 years, and duration of diabetes at Hp diagnosis was 6.2 +/-2.3 years. Hp infection was eradicated in 38/49 subjects (78%). Eleven (22%) remained infected and required a second treatment. The two subgroups did not differ for age, duration of diabetes or pretreatment HbA1c levels (7.3+/-1.5% versus 7.8+/-0.8%; p=0.16). Mean HbA1c levels in the 49 infected subjects did not differ significantly in the year before and after eradication (7.4+/-1.3% versus 7.9+/-1.1%; p=0.08). Prevalence of infection was higher among youth of North African than European ancestry (47% versus 22%; p<0.001). Their HbA1c levels, however, did not differ (7.3+/-1.5% versus 7.7+/-0.9%; p=0.31), nor did age or duration of diabetes. Among the 100 Hp-seropositive patients, vague abdominal pain was reported by 45 of them; only 24 had active Hp infections.

Before treatment, patients seropositive for Hp did not differ in HbA1c levels or abdominal complaints according to whether they had active Hp infection. Hp infection was twice as frequent in Moghrabin Caucasians than in European Caucasians, perhaps associated with their lower socioeconomic status. HbA1c levels were similar in patients with and without Hp eradication after one treatment. After a one-year follow-up, Hp eradication had no significant effect on HbA1c levels.

The role of Helicobacter pylori infection in metabolic control and gastrointestinal symptoms in type 1 diabetes mellitus (DM1) patients has been debated. The aim of this study was to investigate the prevalence of H pylori, of the more cytotoxic Cag-A-positive strains, and the effects of infection on gastrointestinal symptoms and metabolic control in young DM1 patients. Research Design and Methods. H pylori infection was investigated by using the 13C-urea breath test in 121 DM1 patients (65 males, 56 females; mean age: 15 +/- 6 years) and 147 matched controls. In positive patients, an assay for specific immunoglobulin G against Cag-A was performed. Glycosylated hemoglobin A, daily insulin requirement, and duration of illness were established; a questionnaire concerning the presence of dyspeptic symptoms was administered.

No difference in H pylori infection rate between patients and controls was observed. Thirty-four (28.1%) of 121 patients and 43 (29.25%) of 147 controls were infected. Twenty-one patients and 24 controls were positive for Cag-A. Glycosylated hemoglobin A, daily insulin requirement, and duration of illness were not affected by infection nor by Cag-A status. Among gastrointestinal symptoms, only halitosis was related to H pylori infection, but this association disappeared after correction for age. Positive patients with halitosis showed a worse glycemic control than uninfected patients with halitosis.

H pylori infection and Cag-A-positive strains do not affect metabolic control in DM1 patients. With regard to gastrointestinal symptoms studied, H pylori infection, when present in participants with halitosis, seems to predict a worse metabolic control than in H pylori-negative patients with halitosis.