Assessment of the relation between Helicobacter Pylori infection and metabolic syndrome

Abstract

Helicobacter pylori infection is now recognizedas a worldwide problem. H. pylori infection is the most common cause of chronic gastritis, and has been strongly linked to peptic ulcer disease and gastric cancer. H. pylori is estimatedto infect one-half of the world’s population. In addition to morphologic characterization, the organism can be biochemically characterized as catalase, oxidase, and urease positive. Urease appears to be vital for its survival and colonization; it is produced in abundance, making up more than 5 percent of the organism's total protein weight. Bacterial urease activity is clinically important because it forms the basis for several invasive and noninvasive tests to diagnose infection. Among microbial virulence factors identified so far, the H-pylori cytotoxin-associated gene A (cagA), its related pathogenicity island (cagPAI), vacuolating toxin A (VacA), and factors involved in adherence of H pylori to gastric epithelial cells, have been linked to enhanced pathogenicity of the bacterium. The immunoreactive 120–145 kDa protein CagA is encoded by cagA, which is found in 60–70% of H pylori strains in the industrialized world.( Suerbaum et al., 2002) cagA maps to the cagPAI, a gene cluster of 29 genes spanning 37 kb of genomic DNA. Some of the genes in the cagPAI region encode a type IV bacterial secretion apparatus, which can translocate cagA into host target cells. Phosphorylation of cagA may activate host signalling-pathways and subsequently influence host cellular functions, including proliferation, apoptosis, cytokine release, and cell motility. (6) In addition, several other cagPAI genes, such as cagG, cagH, cagI, cagL, and cagM, seem to be associated with particular epithelial cell responses relevant to H pylori pathogenicity. Associations between H. pylori infection and a range of cardiovascular, respiratory, hepatobiliary, dermatological, neurological, autoimmune, allergic and haematological diseases, as well as growth and weight disorders and retardation, have been investigated. However, there is by no means consensus with regard to the findings of such studies, Mechanisms for an association of H. pylori with diabetes mellitus or insulin resistance or metabolic syndrome are unclear. Clinical diabetes might promote infection by lowering immunocompetence or altering gastric motility with autonomic neuropathy. Aim: We aim in this study to assess the correlation between helicobacter pyloriinfection and metabolic syndrome.