Helicobacter Pylori Infection and Vascular Complications in Patients with Type 2 Diabetes Mellitus

The present work was designed to study H. pylori infection in type 2 DM, its relation to some clinical; metabolic and radiological markers of atherosclerosis and vascular complications in type 2 DM. The study included sixty type 2 diabetic patients and fifteen healthy controls matched with age and sex. Both patients and controls were subjected to full history taking, clinical examination, estimation of BMI, resting ECG. laboratory tests including HbA1C, FBG, Serum creatinine; Lipid profile; fibrinogen assay, ESR; CRP; TNF α; IL-6; IL-1B; H. pylori IgG. 24 hours and urine collection for urinary albumin excretion. Radiological investigations include aabdominal ultrasound. Ultrasound on the carotid arteries used in measuring the intima-medial thickness (IMT). The present study found non significant increase in prevalence of H. pylori infection in type 2 diabetic patients in relation to controls. H. pylori infection had no relation to sex, age of the patients, duration of diabetes, BMI, type of therapy or the degree of diabetic retinopathy. H. pylori infection did not affect levels of FBG, HbA1c and microalbuminuria and caused a significant increase in the level of triglycerides, TNFα, IL-1B, CRP and fibrinogen, decrease in the level of HDL and non significant effect on WBCs count, the levels of total cholesterol, LDL, ESR and IL-6 in type 2 diabetic patients. H. pylori infection does not affect IMT of both Right and Left common carotid arteries. No significant increase of the prevalence of H. pylori infection among diabetic patients with diabetic vascular complications. There is no significant increase in prevalence of H. pylori infection among type 2 diabetic patients. H. pylori infection is not related to patient age, degree of glycaemic control, IMT or diabetic vascular complications among type 2 diabetic patients. However, H. pylori infection could affect atherosclerotic process through its effects on lipid profile (increase in TG and decrease HDL levels), increase levels of inflammatory cytokines (TNF-alpha and IL-1B) and acute phase reactants (CRP and Fibrinogen).