Dear Dvoryanchikovو Thanks for sharing discussion as a lot of controversy is raising as regards H. pylori pathogenicity and the the question of; is a commensal cause Adenocarcinoma and MALT lymphoma which is proved by WHO as 6 fold carcinogenic to guard against GERD?! Helicobacter pylori are gram-negative, microaerophilic spiral rod-shaped bacteria that live just beneath the antral

gastric mucous layer, on the surface of epithelial cells. Stomach infection with this organism causes inflammation of the gastric mucosa, which can lead to gastritis,

duodenal or gastric ulcer and even in rare cases to gastric carcinoma or Mucosa Associated Lymphoid Tissue (MALT) lymphoma (Covacci et al., 1999). Approximately 50% of the world's population is believed to be infected with H. pylori. Most infections are probably acquired in childhood (Czesnikiewicz-Guzik et al., 2004), but geographic locale, age, race, socioeconomic status, and hygiene seem to play roles in the prevalence of H. pylori. Most of the informations about H. pylori infection rates come from seroprevalence studies. Higher rates of

infection tend to occur at a younger age in developing countries compared to developed countries and in regions characterized by lower socioeconomic status and higher density living.1 Looking at racial differences in the US, it is found that whites of non-Hispanic origin have lower prevalence of infection compared to African- Americans or Hispanics (Brown, 2000). It has been speclated that dental plaque might harbor H. pylori and, therefore, might be a source of gastric infection

(Czesnikiewicz-Guzik et al., 2004). Aside from iatrogenic transmission of H. pylori via endoscopy, no definite modes of transmission for H. pylori have been identified.

However, association studies suggest that there are three other potential routes for the transmission of H. pylori: person-to-person transmission (example, oral-oral or

fecal-oral), waterborne transmission (example, contaminated water), zoonotic (example, cats and other pets and animals) or vector borne transmission (example, flies). Person-to-person transmission is considered to be the most likely route of transmission considering that isolation of H. pylori from non-human reservoirs has been inconsistent (Brown, 2000). Chronic urticaria (CU) and

concurrent angioedema are frustrating problems for both physicians and patients (Wedi et al., 1998). Based on a number of reports, a possible relationship of H. pylori infection to a variety of different dermatosis has been suggested, including urticaria, rosacea, acne-rosacea, atopic dermatitis, alopecia areata, Sjögren’s syndrome, Schönlein-Henoch purpura, and Sweet’s syndrome. Larger case-control studies, however, do not confirm this relationship. Therefore, H. pylori eradication therapy cannot be generally recommended in this dermatosis

(Boni et al., 2000). Pathogenic strains of H. pylori have been shown to activate the epidermal growth factor receptor (EGFR), a membrane protein with a tyrosine kinase domain. Activation of the EGFR by H. pylori is associated with altered signal transduction and gene expression in host epithelial cells that may contribute to pathogenesis (Tomb et al.,1997).

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Covacci A, Telford, JL, Del Gludice G, Parsonnet J, Rappuoli R

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immunological assays for the diagnosis of Helicobacter pylori

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of Helicobacter pylori-associated gastritis in chronic urticaria. Int.

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 Bashir, A.H.H. Clinico-epidemiological study in Sudanese patients, Prevalence and effect of eradicative triple therapy on extra digestive Helicobacter pylori skin manifestations, EdHpSm. Clinical Reviews and Opinions Vol. 3(2), pp. 14-19, February 2011.

When in doubt for what to write about, write about controversial topics.Thanks Dvoryanchikov,