Abstract
It is known that Helicobacter pylori to be a key factor in the etiology of various gastrointestinal diseases, ranging from chronic gastritis without clinical symptoms to peptic ulcer, autoimmune gastritis, adenocarcinoma and gastric MALT lymphoma. However, current research suggests that Helicobacter pylori may be associated with numerous extra-gastric diseases that lead to chronic local or systemic inflammation and the initiation of autoimmune reactions, including hematological ones. The article describes the role of Helicobacter pylori CagA in the pathogenesis of iron deficiency anemia, immune thrombocytopenic purpura and MALT lymphoma. Studies of the iron-deficiency anemia pathogenesis in infected H. pylori patients have shown a connection between the CagA oncoprotein and iron homeostasis. It was established that transferrin endocytosis is mediated and iron absorption increases. In the development of immune thrombocytopenic purpura, CagA leads to a systemic host immune response through mechanisms of molecular mimicry. In pathogenesis of MALT lymphoma, it is considered significant that after the transfer of CagA to B-cell lymphocytes, through the type 4 secretory system (T4SS), a phosphorylated CagA-SHP2 complex is formed by affecting endoplasmic reticulum kinases 1 and 2 (ERK1, ERK2), p38MAPK, BCL2 and NF -κB, as well as through inhibition of p53 accumulation or inhibition of the JAK-STAT signaling pathway, ultimately promoting lymphogenesis and immortalization of B-cell lymphocytes. So, it was established that the presence of CagA protein in the Helicobacter pylori strain is key to the development of inflammation and tumor transformation. The disclosure of these mechanisms is necessary for a more accurate understanding of some pathological processes caused by this bacterium, both in the stomach and outside it. This will help improve diagnosis, guide treatment and predict clinical prognosis. Keywords: hypomagnesaemia, blood pressure, diabetes mellitus.
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