Increased levels of TC and LDL-C were found in patients infected with H. pylori, and updated Sydney System score showed a positive correlation with LDL-C and TC levels. These findings may explain why H. pylori infection is associated with increased risk of atherosclerosis.

H. pylori is related to various gastrointestinal diseases. β 2 Microglobulin (β 2M) is an intrinsic element of major histocompatibility complex (MHC I). Serum β 2M level may increase in inflammatory states. The aim of current study is to evaluate the relationship between β 2M and H. pylori bearing CagA strains. Methods. H. pylori status was determined by histopathology of samples taken from stomach. CagA status and β 2M level were measured from blood samples of patients. Eradication therapy was administered to the patients with H. pylori infection. β 2 Microglobulin levels were measured before and after treatment. Results. 35 (29.2%) H. pylori(−) patients and 85 (70.8%) H. pylori (+) patients were included in the study. There were 52 (43.3%) patients with CagA negative and 33 (27.5%) patients with CagA positive H. pylori infection. The mean serum β 2M level was 1.83 mg/L in H. pylori (−) group, 1.76 mg/L in H. pylori (+) CagA (−) group, and 1.93 mg/L in H. pylori and CagA (+) group (P > 0.05). Serum β 2M levels (1.82 versus 1.64 mg/L P < 0.05) were decreased after eradication. Conclusion. H. pylori and CagA status did not affect β 2M level. Relationship between low grade systematic inflammation and H. pylori should be investigated to find out new predictors for diseases associated with inflammation.

Helicobacter pylori is one of the common infection of humans. It is associated with chronic gastritis, peptic ulcer, mucosa related tissue lymphoma and gastric cancer. Whether H. pylori gastritis is a local inflammation or contributes to systemic inflammation remains unclear. Mean platelet volume is an indicator of systemic inflammation that can be determined from routine hemogram analyses. The present study was aimed to evaluate the relationship between mean platelet volume and H. pylori gastritis. Two hundred and eighty three (283) patients admitted with dyspeptic symptoms, and to whom endoscopy was performed, were enrolled in the study. Mean platelet volume levels of patients with and without H. pylori gastritis were compared and also, mean platelet volume levels according to parameters of Sydney Score System were compared. There was no significant difference between patients with and without H. pylori gastritis in the mean of mean platelet volume (p>0.05). Also, mean platelet volume levels did not differ between groups with regards to H. pylori intensity (p>0.05). There was also no significant association between mean platelet volume levels and H. pylori gastritis intensity. Chronic and acute infection, atrophy and intestinal metaplasia also did not have relationship with mean platelet volume. It can be concluded therefore, that mean platelet volume cannot be used as an indicator of systemic inflammation for H. pylori gastritis.

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.