Helicobacter pylori (HP) is a Gram-negative bacteria that infects approximately half of the world's population (1). These bacteria colonize the mucosa of the stomach antrum and cause chronic gastritis. Although the prevalence of this infection is high, most individuals remain asymptomatic. Factors that cause HP-associated disease are called virulence factors. CagA is one of the important virulence factors that trigger inflammation. CagA is associated with peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma (2).Coronary heart disease, iron-deficiency anemia, pernicious anemia, and idiopathic thrombocytopenic purpura have been linked to HP infection (3). These extragastric manifestations of HP infection are thought that they are derived from HP-triggered systemic inflammation.C-reactive protein (CRP) is an acute phase reactant that is sensitive to systemic inflammation. Because of its sensitivity, it is used as a clinical marker of infection and tissue damage. CRP is not only specific for infection, serum CRP levels usually increase to high levels after infections, myocardial infarction, stress, trauma, neoplastic proliferation, and surgery (4, 5). High-sensitivity CRP (hsCRP) assays allow measuring very low levels of circulating CRP. Levels of hsCRP are affected by diverse states other than systemic infection, including body mass index, alcohol, and tobacco consumption, and diseases such as diabetes mellitus and coronary heart disease (6). In the past few decades, hsCRP has emerged as a predictor of coronary heart disease (7).Procalcitonin (PCT) is a polypeptide precursor of calcitonin that is produced by thyroid gland (8). In the early 1990s, it was observed that PCT levels increase after bacterial infections. Because PCT does not increase during neoplastic and autoimmune processes, or viral infections, it is used as a marker for sepsis and severe bacterial and fungal infections (9). PCT levels are increased independently from calcitonin in bacterial infections. Its major production sites are not exactly known but, it has became apparent that hepatocytes, neutrophils, and mononuclear cells can produce PCT (10).CagA is an important virulence factor for HP infection. We hypothesized that CagA-positive HP infection would cause more serious systemic responses vs. CagA-negative HP infection. Thus we investigated the effect of CagA positivity to serum levels of CRP and PCT in patients with HP infection.