As the results of a study by Italian scientists show, eradicating H. pylori can lead to an improvement in the evolution of autoimmune thrombocytopenic purpura in the form of an increase stable and significant number of platelets in this category of patients infected with H. pylori, although the efficacy of this treatment after a sufficiently long period remains uncertain.

During the study, examination and subsequent eradication of H. pylori in 75 adult patients with autoimmune thrombocytopenic purpura. Lymphocyte subpopulations have also been determined and the genotyping of H. pylori in biopsies of the gastric mucosa in 10 H. pylori -infected with thrombocytopenic purpura and 19 H. pylori -infected without thrombocytopenic purpura, but suffering from chronic gastritis.

An active form of Helicobacter pylori infection was detected in 38 patients (51%), 14 of whom suffered from severe thrombocytopenic purpura. The efficacy of the eradication treatment was observed in 34 patients (89%). After the follow-up period, which lasted an average of 60 months, a persistent platelet response was observed in 23 treated patients (68%) and a relapse of thrombocytopenic purpura was recorded. Differences between the T and B lymphocyte subpopulations in the gastric mucosa in 10 H. pylori -infected with thrombocytopenic purpura and 19 H. pylori -infected without thrombocytopenic purpura with chronic gastritis was not detected. In patients with thrombocytopenic purpura, the frequency of detection of the gene cagA H. pylori and strains H. pylori with the genotype cagA, vacA and ice A1 was higher than in the control group.

Thus, eradication H. pylori is a simple, safe, effective and affordable approach to treat thrombocytopenic purpura in a very large number of patients. Screening to identify H. pylori, and subsequent eradication with a positive test result, should be performed before or in combination with main treatment for thrombocytopenic purpura. The presence of specific genotypes of H. pylori in patients with thrombocytopenic purpura indicates a possible etiological role of bacterial factors in the pathogenesis of this autoimmune disease.