Helicobacter pylori stool antigen levels and serological biomarkers of gastric inflammation are associated with cardio-metabolic risk factors in type 2 diabetic patients
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© 2015 Korean Endocrine Society. Background: Helicobacter pylori infection and subsequent gastric inflammation have been proposed as risk factors for the development of insulin resistance and cardiovascular disease. In this study we assessed the possible association of H. pylori bacterial load, and serum biomarker of gastric inflammation with cardiometabolic risk factors in diabetic patients. Methods: In this cross-sectional study, 84 H. pylori-infected type 2 diabetic patients were assessed for anthropometrics, biochemical and clinical measurements. Pearson correlation test, linear, and logarithmic regression curve estimation models were used to assess the association of H. pylori stool antigen (HpSAg) levels, and pepsinogen I (PGI) to pepsinogen II (PGII) ratio with fasting serum glucose, insulin, serum lipid and lipoprotein parameters, malondialdehyde, high-sensitive C-reactive protein (hs-CRP), systolic and diastolic blood pressure, body weight, waist circumference and lipid accumulation product (LAP) index. Results: The mean age of participants was 54±10 years, and 44% were men. Mean HpSAg levels and PGI/PGII ratio were 0.24±0.23 μg/mL and 9.9±9.0, respectively. Higher HpSAg as well as lower PGI/PGII was correlated with higher anthropometric measures and LAP. A significant negative correlation between PGI/PGII ratio and blood pressure (r=-0.21 and r=-0.22, systolic and diastolic, respectively, P < 0.05), serum insulin (r=-0.17, P=0.05), and hs-CRP (r=-0.17, P=0.05) was observed. A significant linear association between PGI/PGII ratio with serum triglycerides (β=-0.24, P < 0.05), serum high density lipoprotein cholesterol (HDL-C; β=0.43, P < 0.01), and triglycerides/HDL-C ratio (β=-0.28, P < 0.05) were observed. Conclusion: Higher H. pylori bacterial load and lower PGI/PGII ratio was associated with higher levels of cardiometabolic risk factors in H. pylori infected type 2 diabetic patients.