Diabetes mellitus (DM) and Helicobacter pylori infection (HPI) pose increasing public health challenges in aging societies, sharing common pathophysiological mechanisms, and linked to significant health risks. Our study examines their respective impacts on all-cause and cardiovascular mortalities in a comprehensive longitudinal population-based analysis.

The study analyzed data from the National Health and Nutrition Examination Survey (NHANES) database conducted between 1999 and 2019, which included information on Diabetes mellitus status and Helicobacter pylori infection status. Mortality data were obtained from the same database mentioned above.

Among the 2719 participants, 1362 (50.1%) were free of both diabetes mellitus (DM) and Helicobacter pylori infection (HP) (DM -/HP -), 140 (5.1%) had DM alone (DM +/HP -), 1011 (37.2%) had HP alone (DM -/HP +), and 206 (7.6%) had both DM and HP (DM +/HP +). Compared to the DM -/HP - group, the DM +/HP - and DM + /HP + groups demonstrated increased all-cause mortality with adjusted hazard ratios (HRs) of 1.40 (95% [CI] 1.07-1.78) and 1.46 (95% CI 1.15-1.84), respectively. For diabetic mortality, DM +/HP- group and DM + /HP + group showed increased HR of 6.30 (95% CI 1.30-30.43) and 8.56 (95% CI 1.98-36.94), respectively. For cardiovascular mortality, the DM + /HP- group and DM + /HP + group exhibited increased HR of 1.75 (95% CI 1.14-2.69) and 1.98 (95% CI 1.40-2.79), respectively. The DM + /HP + cohort displayed the highest risk of overall mortality (p for trend = 0.003), diabetic mortality (p for trend < 0.0001), an6d cardiovascular mortality (p for trend < 0.0001).

The concurrent presence of DM and Helicobacter pylori infection significantly amplifies the risk of all-cause, cardiovascular, and diabetic mortality. Individuals with either condition may necessitate heightened management to prevent the onset of the other ailment and reduce mortality rates.

To investigate whether Helicobacter pylori (H. pylori) infection is associated with glycemic control and whether hyperglycemia is modified by eradication therapy.

The databases of PubMed, Cochrane Library, Chinese BioMedicine Web Base and Chinese Science and Technology Journals were searched from inception to June 2014. Studies examining the association between H. pylori infection and glycemic control and/or the effect of eradication treatment on glycemic control in diabetic humans were eligible for inclusion. Meta-analyses were conducted using the Review Manager software version 5.2. The outcome measures are presented as weighed mean differences (WMDs) with 95% confidence intervals (CIs). Statistical heterogeneity was assessed by the Cochran Q test and the I(2) statistic.

A total of 21 relevant publications were identified. A meta-analysis of 11 studies with 513 patients with diabetes mellitus (DM) showed significantly lower glycosylated hemoglobin (HbA1c) levels in the H. pylori-negative than H. pylori-positive DM participants (WMD = 0.43, 95%CI: 0.07-0.79; P = 0.02). In children and adolescents with type 1 DM (T1DM), there was a positive association between H. pylori infection and HbA1c level (WMD = 0.35, 95%CI: 0.05-0.64; P = 0.02), but there was no difference in those with type 2 DM (T2DM, WMD = 0.51, 95%CI: -0.63-1.65; P = 0.38). A meta-analysis of six studies with 325 T2DM participants showed a significant difference in the fasting plasma glucose levels between H. pylori-positive and H. pylori-negative participants (WMD = 1.20, 95%CI: 0.17-2.23; P = 0.02). Eradication of H. pylori did not improve glycemic control in the T2DM participants in a three-month follow-up period (HbA1c decrease: WMD = -0.03, 95%CI = -0.14-0.08; P = 0.57; fasting plasma glucose decrease: WMD = -0.06, 95%CI: -0.36-0.23; P = 0.68). Glycemic control was significantly better in T1DM participants who were not reinfected than in those who were reinfected (HbA1c: WMD = 0.72, 95%CI: 0.32-1.13: P = 0.00).

H. pylori infection is associated with poorer glycemic control in T1DM patients, but eradication may not improve glycemic control in DM in a short-term follow-up period.

This article reviews the epidemiological evidence linking diabetes and gastric cancer and discusses some of the potential mechanisms, confounders and biases in the evaluation of such an association. Findings from four meta-analyses published from 2011 to 2013 suggest a positive link, which may be more remarkable in females and in the Asian populations. Putative mechanisms may involve shared risk factors, hyperglycemia, Helicobacter pylori (H. pylori) infection, high salt intake, medications and comorbidities. Diabetes may increase the risk of gastric cancer through shared risk factors including obesity, insulin resistance, hyperinsulinemia and smoking. Hyperglycemia, even before the clinical diagnosis of diabetes, may predict gastric cancer in some epidemiological studies, which is supported by in vitro, and in vivo studies. Patients with diabetes may also have a higher risk of gastric cancer through the higher infection rate, lower eradication rate and higher reinfection rate of H. pylori. High salt intake can act synergistically with H. pylori infection in the induction of gastric cancer. Whether a higher risk of gastric cancer in patients with diabetes may be ascribed to a higher intake of salt due to the loss of taste sensation awaits further investigation. The use of medications such as insulin, metformin, sulfonylureas, aspirin, statins and antibiotics may also influence the risk of gastric cancer, but most of them have not been extensively studied. Comorbidities may affect the development of gastric cancer through the use of medications and changes in lifestyle, dietary intake, and the metabolism of drugs. Finally, a potential detection bias related to gastrointestinal symptoms more commonly seen in patients with diabetes and with multiple comorbidities should be pointed out. Taking into account the inconsistent findings and the potential confounders and detection bias in previous epidemiological studies, it is expected that there are still more to be explored for the clarification of the association between diabetes and gastric cancer.

Although the association between chronic Helicobacter pylori infection and type 2 diabetes has been suggested, findings have been inconsistent. This study evaluated the association between chronic H. pylori infection and glucose regulation.

We evaluated H. pylori infection status of participants recruited from the gastroenterology clinic at our hospital. At baseline, we performed blood tests including fasting plasma glucose, insulin, glycated haemoglobin A1c (HbA1c) and other biochemical measurements. Insulin resistance and beta-cell function were assessed by homoeostasis model assessment (HOMA-IR and HOMA-B, respectively).

A total of 2070 participants were recruited. Those who had H. pylori infections had higher serum HbA1c levels and lower HOMA-B than those who did not (5.78% vs. 5.69%, P = 0.01 and 53.85 + 38.43 vs. 60.64 + 43.40, P = 0.009, respectively). They also had a significantly higher prevalence of type 2 diabetes (8.97% vs. 5.57%, P= 0.02). Chronic H. pylori infection was significantly associated with high levels of HbA1c and type 2 diabetes in participants above 65 years old (P = 0.001) and decreased insulin secretion and sensitivity in those under 45 years (P = 0.05).

Long-term H. pylori infection is significantly associated with high levels of HbA1c and decreased insulin secretion in this Chinese population. Proper screening for H. pylori infection combined with regular monitoring of blood glucose and HbA1c levels might be effective for the early detection of glucose dysregulation and prevention of type 2 diabetes.

Diabetic patients may have a higher risk of gastric cancer. However, whether they have a higher incidence of Helicobacter pylori (HP) eradication is not known. Furthermore, whether insulin use in patients with type 2 diabetes may be associated with a higher incidence of HP eradication has not been investigated.

This is a retrospective cohort study. The reimbursement databases from 1996 to 2005 of 1 million insurants of the National Health Insurance in Taiwan were retrieved. After excluding those aged <25 years, cases of gastric cancer, cases receiving HP eradication before 2005, patients with type 1 diabetes mellitus and those with unknown living region, the reimbursement data of a total of 601,441 insurants were analyzed. Diabetes status and insulin use in patients with type 2 diabetes before 2005 were the main exposures of interest and the first event of HP eradication in 2005 was the main outcome evaluated. HP eradication was defined as a combination use of proton pump inhibitor or H2 receptor blockers, plus clarithromycin or metronidazole, plus amoxicillin or tetracycline, with or without bismuth, in the same prescription for 7-14 days. The association between type 2 diabetes/insulin use and HP eradication was evaluated by logistic regression, considering the confounding effect of diabetes duration, comorbidities, medications and panendoscopic examination.

In 2005, there were 10,051 incident cases receiving HP eradication. HP eradication was significantly increased with age, male sex, diabetes status, insulin use, use of calcium channel blocker, panendoscopic examination, hypertension, dyslipidemia, chronic obstructive pulmonary disease, stroke, nephropathy, ischemic heart disease and peripheral arterial disease. Significant differences were also seen for occupation and living region. Medications including statin, fibrate, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker and oral anti-diabetic agents were not associated with HP eradication. The adjusted odds ratios for diabetes, insulin use and use of calcium channel blocker was 1.133 (1.074, 1.195), 1.414 (1.228, 1.629) and 1.147 (1.074, 1.225), respectively.

Type 2 diabetes and insulin use in the diabetic patients are significantly associated with a higher incidence of HP eradication. Additionally, use of calcium channel blocker also shows a significant association with HP eradication.

The pathogenesis, incidence, complication rates, response to acid suppression and Helicobacter pylori (H. pylori) eradication therapy in peptic ulcer associated with chronic disease such as liver cirrhosis, chronic renal failure, diabetes mellitus, and critically ill conditions are different from those with general population, so that the management strategies also should be differentiated. The eradication of H. pylori are not so effective for preventing recurrence of peptic ulcer in liver cirrhosis patients as shown in general population, and conservative managements such as preventing deterioration of hepatic function and decrease in portal pressure are mandatory to reduce the risk of ulcer recurrence. The standard triple therapy for H. pylori eradication are as effective in chronic renal failure patients as in normal population, but the frequency of side effects of amoxicillin is higher in the patients not receiving dialysis therapy. Delay in eradication therapy until beginning of dialysis therapy or modification of eradication regimen should be considered in such cases. High prevalence of asymptomatic peptic ulcers and increased mortality in complicated peptic ulcer disease warrant regular endoscopic surveillance in diabetic patients, especially with angiopathy. The prolongation of duration of eradication therapy also should be considered in diabetic patients with angiopathic complication because of lower eradication rate with standard triple regimens as compared to normal population. Prophylactic acid suppressive therapy is highly recommended in critically ill patients with multiple risk factors. Herein, we propose evidence-based treatment guidelines for the management of peptic ulcer disease in special conditions based on literature review and experts opinion.

Antimicrobial resistance in Helicobacter pylori infection is an important factor leading to failure of therapy. The aim of this study was to determine the eradication rate of H pylori in type 2 diabetes mellitus and to assess the effect of clarithromycin resistance on H pylori eradication.

Fifty-six consecutive patients with type 2 diabetes mellitus and 58 age- and sex-matched control patients were included in the study. H pylori infection was assessed by a rapid urease test and histopathological examination of biopsy specimens. Biopsies were also taken for antibiotic susceptibility testing. All enrolled patients were treated with triple therapy consisting of clarithromycin, amoxicillin, and pantoprazole for 14 days. C-13 urea breath test was performed 6 weeks after completing the triple therapy to assess eradication and associated point mutations using real-time polymerase chain reaction (PCR).

H pylori was eradicated in 42.9% of diabetic patients and 79.3% of control patients, (P < 0.05). In type 2 diabetes mellitus patients, clarithromycin resistance was 64.3% (36/56), while in the control group, clarithromycin resistance was 35.7% (20/58) (P < 0.05). H pylori was eradicated in 14 (70%) of the 20 clarithromycin-susceptible diabetic patients and in only 10 (27.8%) of the 36 clarithromycin-resistant diabetic patients.

The H pylori eradication rate was significantly lower and clarithromycin resistance was significantly higher in type 2 diabetics. Alternative and new treatment protocols and antibiotic susceptibility testing are needed to achieve successful eradication rates.

Today there is evidence that Helicobacter pylori has a critical role in different extragastric diseases. The discovery of a number of other novel Helicobacter species has stimulated the research in different extragastric diseases, in which an infectious hypothesis is plausible. Enterohepatic Helicobacter species have been hypothesized to play a role in different disorders, including hepatocellular carcinoma, gallstones formation and cholangiocellular carcinoma, as well as enteric diseases and inflammatory bowel diseases. Concerning the extragastric manifestations of H. pylori infection, idiopathic thrombocytopenic purpura, and sideropenic anemia represent, based on the current data, the diseases in which the pathogenic link appears to be strongest. There is also an increasing evidence for a possible association of H. pylori with cardiovascular disease.