Despite the advances of modern medicine, the problem of gastropathy of bacterial origin remains relevant, its destructive complications in particular. Peptic ulcer (PU) is one of the most common diseases among the working population and accounts for about 20-30% of all diseases of the gastrointestinal tract, which, in turn, take the third place on the prevalence of diseases in the world after cardiovascular diseases and cancer . In the understanding of the etiology of ulcer in the past few years there have been significant changes in connection with the discovery of Helicobacter pylori (HP) by Australian scientists B.Marshall and G.Warren in 1983: 60% of the total population is infected with HP since childhood; 90-96.3% of duodenal ulcer and more than 60% of peptic ulcer is associated with the persistence of HP. Existing methods for diagnosing HP are divided into two groups: invasive and noninvasive. Invasive methods include endoscopic examinations followed by taking biopsies and conducting rapid urease test, histomorphological and/or bacteriological research. Noninvasive techniques include various types of immunoassays detecting the presence of antibodies in serum, as well as urease breath test and stool test. The discovery of HP infection has changed the approach to therapeutic treatment, which basic formula “No acid – no ulcer” has been completed with “No HP infection – no ulcer”. It has led to the creation of new ways of treatment, as well as to the Maastricht Consensus Report, which recommends taking two antibiotics and a proton pump inhibitor (PPI). Recently, however, it has appeared more and more data about the low quality of the eradication while using these regimens. The reasons for failure are explainable in terms of the properties of HP infection. HP moves from the active to inactive (cocci) form in the presence of unfavourable conditions in the stomach: temperature change, a change in osmotic pressure, as well as the use of antibiotics and changes in pH, aided by modern treatment regimens, – and then, adapting to the new conditions, it penetrates parietal cells, making an “intracellular store”. When applying these treatment regimens, there is a rapid healing of erosive and ulcerative lesions, regardless of the acidity level, that impresses a lot of supporters of these regimens, but in this case in 91.1% of cases the basis for future exacerbations is being formed, because after stopping the treatment HP can leave “intracellular stores” and, with a favorable background in the stomach, rapidly achieve a high level of contamination in the mucosa that increases the risk of ulcer recurrence. Furthermore, 18% of the PPI application may result in atrophy of the mucosa, which is always regarded as a precancerous condition. In recent years, there have been a lot of criticisms of the serious side effects associated with the use of proton pump inhibitors: when the level of acidity is being reduced, the digestion of proteins is disturbed, the process of potentially immunogenic proteins denaturation is getting decreased, the process of iron, calcium and vitamin B12 absorption is disrupted, the process of inactivation of potentially pathogenic microorganisms entering per os is getting worse; taking PPI for extended period of time increases hip fractures by more than 30%; it increases the risk of the intestine Clostridium difficile 2 times as large, and also increases the risk of recurrence of the intestine Clostridium difficile by 42% (in elderly people – by 86%); in children using drugs of this group it increases the risk of acute infectious gastroenteritis more than 2 times; violation of the protective acid barrier when applying PPI is followed by bacterial overgrowth syndrome (ARIS) in the small intestine; frequent progression of pneumonia in patients receiving PPIs is observed both in adults and children; as well as inhibition of neutrophil function. Regarding the main issue – whether PPI in the long admission have carcinogenic potential due to the stimulation of hypergastrinemia, the opinions of scholars have been divided: some scientists argue that this potential is not clear, the other ones, on the contrary, claim that prolonged hypergastrinemia causes tumors that originate from the ECL-cells, as gastrin is a trophic hormone, and ECL-cells can give rise to gastric carcinomas of diffuse type, which incidence is persistently increasing. As can be seen from the above, the win over the ulcerative defect with the application of these treatment regimens can be achieved at a high cost. It makes using treatment regimens, based on De-Nol, more appropriate, because they don`t suppress the acidity which helps to avoid the negative consequences arising when using PPI, and not to break, but only to improve the beginning of a proteolytic cascade of digestion. The low level of releasing the cocci HP forms outside reduces the risk of the formation of fecal-oral transmission routes, and eliminating the “intracellular stores” under the influence of treatment with De-Nol removes the basis for further relapse.
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