Genetic Determinants and Clinico-Pathological Outcomes of Helicobacter Pylori Infection

Helicobacter pylori is a spiral Gram-negative bacterium with a relatively small genome and is known to be the most common human bacterial infection worldwide; infecting about half of the world's population. The bacterium represents one of the most successful human pathogens; inducing severe clinical symptoms only in a small subset of individuals; thus signifying a highly balanced degree of co-evolution of H. pylori and humans. The prevalence of Helicobacter pylori infection varies greatly among countries and among population groups within the same country; but is falling in most developed countries. The clinical course of H. pylori infection is highly variable and is influenced by both microbial and host factors including genetic susceptibility while the pattern and distribution of inflammation correlate strongly with the risk of clinical sequelae; namely duodenal or gastric ulcers; mucosal atrophy; gastric carcinoma; or gastric lymphoma. Cytokine gene polymorphisms directly influence inter-individual variation in the magnitude of cytokine response; and this clearly contributes to an individual's ultimate clinical outcome. Polymorphisms in genes coding for innate immune factors have also been incriminated in the pathogenesis of H. pylori related disease; while promoter hypermethylation of tumor suppressor genes is considered an important factor in carcinogenesis and known to be present in H. pylori associated gastric tumors. Functional genomics may fill many of the gaps in our understanding of the pathogenesis of H. pylori infection and accelerate the development of novel therapies; including H. pylori specific antimicrobial agents

Helicobacter pylori-associated chronic antral gastritis in Kuwait- A histopathological study

In order to study the causal relationship between Helicobacter pylori [HP] and various inflammatory reactions in gastric antral mucosa, we have reviewed 268 endoscopic gastric biopsies in the Department of Pathology of Mubarak Al-Kabeer Teaching Hospital in Kuwait. Of the 219 HP-positive biopsies, 95.4% showed chronic gastritis [CG], 59.8% active chronic gastritis [ACG] and 78.5% lymphoid hyperplasia [LH]. The prevalence of LH, CG or ACG, either alone or in combination, increased with increasing density [grade] of HP colonization, assuming statistical significance for LH and ACG [P<0.05], especially when these changes in Grade 1 HP cases were compared to those of Grades 2 and 3 combined. Moreover, the grade of LH by itself also showed statistically significant correlation [P<0.01] with the grade of inflammation. Our results confirm a causal relationship between HP colonization of gastric mucosa and the various forms of gastritis, and also provide evidence in support of induction of mucosa-associated lymphoid tissue [MALT] by HP, an observation which may have significance in the genesis of gastric MALTomas