<i>Helicobacter pylori</i> Persistence in Patients with Peptic Ulcer Disease and Chronic Gastritis in the Treatment with Antibiotics and Acid-Suppressive Agents

Background. Chronic gastritides still have no division into forms according to the data of the genotyping of Helicobacter pylori isolates. Monitoring the results of anti- Helicobacter pylori therapy cannot be limited to eradication, by taking into account the data on Helicobacter pylori detection in healthy individuals. Is increased acid production associated with the presence of virulent or nonvirulent strains? Objective. To search for the predominance of cagA or any allelic combination of vacA in the isolates from patients with mild and severe chronic gastritis and from those with peptic ulcer disease. To track the time course of changes in the disappearance and repeated gastric colonization with different Helicobacter pylori strains in patients with peptic ulcer disease immediately after anti- Helicobacter pylori therapy and 1.5–2 months later. To confirm or refute the fact that the increased acid production is associated with the presence of virulent Helicobacter pylori strains rather than with the persistence of nonvirulent strains. Methods. The Helicobacter pylori isolates from the gastric biopsy specimens taken from patients with chronic gastritis and peptic ulcer disease were genotyped for cagA and allelic combinations of vacA . The strains from patients who had received anti- Helicobacter pylori therapy were genotyped using the variable number tandem repeat (VNTR) method. Patients with an exacerbation of peptic ulcer disease and those wth an exacerbation of chronic pancreatitis with concomitant gastritis were compared from the level of acid production and from the belonging of Helicobacter pylori to virulent strains. Results. Patients with mild chronic gastritis were observed to have an abundance of nonvirulent allelic combination of vacAs2m2, which differed significantly from its frequency in both the patients with severe chronic gastritis and those with peptic ulcer disease. In the latter patients, the differences between the background bacteriological pattern and the pattern observed after 1.5–2 months had a high degree of significance; in these follow-up periods, in contrast to the control immediately after therapy, the number of eradications increased and the number of cagA-containing strains decreased due to the change of strains. Acid production was significantly higher in the patients with peptic ulcer disease than in those with chronic pancreatits and concomitant gastritis; the former patients show a statistically significant predominance of virulent strains; the latter patients had nonvirulent strains (at the same rate of Helicobacter pylori detection). Conclusion. Filling the blank spots in the study of helicobacteriosis remains relevant due to the progress of genetic methods in bacteriology and to the introduction of novel approaches to assessing the results of anti- Helicobacter pylori therapy.