The reasons why diabetic patients with microalbuminuria have marked endothelial damage (1,2) and an increased risk of atherosclerosis (3,4) are unclear. Infection with Helicobacter pylori , especially with strains carrying the cytotoxin-associated gene A (CagA), might represent a causal factor, since anti-CagA antibodies elicited by infection may cross-react with endothelial antigens (5), increasing the vascular damage associated with diabetes itself and consequent albumin leakage. Furthermore, infection might induce a persistent systemic inflammatory response, which is a recognized risk factor for atherosclerosis (6). In this study, we investigated the possible pathogenetic role of CagA-positive H. pylori strains in type 2 diabetic patients with microalbuminuria. Consecutive ambulatory patients with a known history of type 2 diabetes who were ≥40 years of age were considered. Data on age, sex, BMI, smoking habit, history of hypertension or hyperlipidemia, disease duration, previous myocardial infarction, previous stroke, and HbA1c (A1C) were collected. Serum level of C-reactive protein (CRP), a marker of systemic inflammation, was measured only in patients without obvious inflammatory conditions. Exclusion criteria were presence of renal failure (creatinine >133 μmol/l), previous H. pylori eradication, and evidence of connective tissue, neoplastic, or hematological disease. Since virtually all peptic ulcers are due to H. pylori (7), and most of them to CagA-positive strains (8), a history of …