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replication in acute hepatitis with typical and atypical clinical course. J Med Virol 2003;71:1-6.
11. Kim HW, Yu MH, Lee JH, Chang JW, Yang WS, Kim SB, Lee SK, Park JS, Park SK: Experiences with acute kidney injury complicating non-fulminant hepatitis A. Nephrology (Carlton) 2008;13:451-458.
12. Rezende G, Roque-Afonso AM, Samuel D, Gigou M, Nicand E, Ferre V, Dussaix E, Bismuth H, Feray C: Viral and clinical factors associated with the fulminant course of hepatitis A infection. Hepatology 2003;38:613- 618.
13. Fujiwara K, Yokosuka O, Ehata T, Saisho H, Saotome N, Suzuki K, Okita K, Kiyosawa K, Omata M: Association between severity of type A hepatitis and nucleotide variations in the 5 non-translated region of
hepatitis a virus RNA: strains from fulminant hepatitis have fewer nucleotide substitutions. Gut 2002;51:82-88.
14. Hussain Z, Husain SA, Pasha ST, Anand R, Chand A, Polipalli SK, Rehman S, Kar P: Does mutation of hepatitis A virus exist 6in North India Dig Dis Sci 2008;53:506-510.
15. Lee D, Cho YA, Park Y, Hwang JH, Kim JW, Kim NY, Lee DH, Lee W, Jeong SH: Hepatitis A in Korea: epidemiological shift and call for vaccine strategy. Intervirology 2008;51:70- 74.
16. Kim JM, Lee YS, Lee JH, Kim W, Lim KS: Clinical outcomes and predictive factors of spontaneous survival in patients with fulminant hepatitis A (article in Korean). Korean J Hepatol 2008;14:474-482.
Honcharuk L.,
PhD in Medical Sciences, Associate Professor Bukovinian State Medical University Kushnir L.D.,
PhD in Medical Sciences, Associate Professor Bukovinian State Medical University Piddubna A.,
PhD in Medical Sciences, Associate Professor Bukovinian State Medical University
Andrushchak M.
PhD in Medical Sciences, assistant Bukovinian State Medical University DOI: 10.24412/2520-6990-2023-6165-13-14 THE ROLE OF HELICOBACTER PYLORI IN HUMAN PATHOLOGY
Abstract.
The article presents data on the features of the gastrointestinal tract in people infected with Helicobacter pylori. The role ofHelicobacter pylori in the development of diseases of the gastrointestinal tract has been reliably proven. Twenty years of research has established a link between this bacterium and the development of gastric mucosal disease. The disease develops as a result of a close interaction between environmental factors, bacteria and the host's organism. Interest in chronic Helicobacter pylori-associated gastritis is due not only to the widespread and widespread distribution of this bacterium, but also to the high oncogenic potential of some variants of this disease.
Keywords: Helicobacter pylori, pathogenesis, diagnosis
Until 1970, it was believed that inflammatory processes of the mucous membrane of the gastrointestinal tract and stomach ulcers were caused by stress factors and dietary disorders. To prove what Helicobacter pylori infection leads to, its researcher Australian scientist B. Marshall drank a concentrate of this culture. During the examination, it was established that after a few days he developed gastritis. Barry Marshall and his team were awarded the Nobel Prize in 2005 for their work.
Helicobacter pylori is a microaerophilic gramnegative bacterium, has an S-shaped or spiral shape, 2.5-3.5 microns in length, 0.5-1.0 microns in width, and approximately 0.5 microns in diameter. During cultivation on artificial nutrient media, it takes the form of a stick, and during long-term cultivation - a coccoid form. The most favorable conditions of existence for Helicobacter pylori are a temperature of 37-42oC and a pH of 6-8. At lower pH levels, the bacterium retains its viability, but stops growing and multiplying. It has 4-6 flagella, with the help of which it can move very quickly even in thick slime or agar. More than 2/3 of
the world's population is infected with it, but many people do not have clinical symptoms [1]. Despite the advances in modern medicine, Helicobacter pylori continues to be a serious health problem worldwide, causing significant morbidity and mortality due to peptic ulcer disease and gastric cancer. The literature reports that Helicobacter pylori is associated with the development of gastritis, duodenitis, gastric and duodenal ulcer (SPD), as well as gastric adenocarcinoma [2]. Statistics show that 95% of gastric ulcers and 70% of gastric ulcers are associated with Helicobacter pylori [3].
When studying the pathogenesis of Helicobacter pylori in recent years, it was established that the degree of risk of the disease is determined by the specific interaction between the pathogen itself and the carrier organism. This interaction, in turn, directly depends on strain-specific bacterial factors and effectors directly induced in the carrier. The main factors of the pathogenicity of Helicobacter pylori include both the properties of the bacterium itself (colonization of the gastric
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mucosa, adhesiveness to the gastric epithelium, intracellular penetration, cytotoxins, pathogenicity islands, a specific response to stress), and the corresponding response of the macroorganism to infection (immune response, apoptosis and proliferation in the mucous membrane of the gastroduodenal zone, changes in the motor function of the stomach). The uniqueness of this bacterium lies in its ability to live in one of the most aggressive environments of the body - in the acidic environment of the stomach, where any other microorganisms cannot survive. Colonization of the gastric mucosa by Helicobacter pylori is ensured by their production of urease, which splits urea and, due to ammonia, neutralizes H-ions, protects bacteria from the action of hydrochloric acid in the gastric contents. Unlike other bacteria that also produce urease (for example, Escherichia coli, Protea, Klebsiella), in Helicobacter pylori, urease is found not only in the cytoplasm, but also on the cell surface. Urease produced by Helicobacter pylori is a nickel-containing hexadimer. In the urease gene cluster of H.pylori seven genes were identified: ureA, ureB (encodes the structural subunits of urease), ureE, ureF, ureG, ureH (encode additional proteins necessary for the collection and inclusion of Ni2+ ions), urel (encodes the urease channel for H+ and is, in fact, a transport system to move urea into the bacterial cytoplasm [4]. The ureA/B genes form a membrane complex with urel. Being a strong antigen, urease, which is produced by Helicobacter pylori, binds antibodies potentially harmful to bacteria that are removed from the surface of bacterial cells in in the form of an antigen-antibody complex Recently, a potentially new function of urease was discovered - the dependence of the regulation of inducible hydrogen oxide synthase and the release of hydrogen oxide on the expression of ureA, which allowed us to hypothesize that urease is not only a necessary component for ammonia production, but also participates in the regulation of inflammation [5,6].
Helicobacter pylori belongs to anaerobes - that is, microbes that die in air. It is transmitted from person to person through saliva and mucus. Infection with Heli-cobacter pylori occurs more often within the family or other groups with close communication, because Heli-cobacter pylori spreads when using the same dishes, not observing the rules of hygiene, when living in crowded places. Helicobacter pylori is often transmitted from mother to child (through saliva that got on a nipple, spoon and other objects). You can get Helicobacter pylori infection even by kissing. Once in the human body, Helicobacter pylori descends into the stomach and further penetrates the mucous membrane of the stomach, disrupting the structure of its tissues and their functions.
Diagnosis of Helicobacter pylori remains an urgent problem in terms of developing the most convenient, simple and, at the same time, informative methods [7]. Bacteria detection methods are divided into two large groups: invasive and non-invasive.
Invasive diagnostic methods:
1. The histological method is the most reliable method of diagnosis.
2. Rapid urease test (estimation of urease activity) to detect Helicobacter pylori in a biopsy.
3. Cultural (bacteriological method) - consists in the isolation of a pure culture of bacteria from a biopsy of the mucous membrane by the bacteriological method
- sowing on artificial nutrient media and cultivating the culture.
Non-invasive diagnostic methods:
1. Breath test with urea
2. Determination of Helicobacter pylori antigen in stool "stool test".
3. Determination of antibodies (serological tests).
4. Molecular diagnostic methods
All methods have their pros and cons, but one thing is clear - many people with exacerbations of gastritis and ulcers did not manage to achieve full recovery while this bacterium was present in their body. Helico-bacter pylori treatment is complex. Eradication of Hel-icobacter pylori is an important task for general practitioners, therapists, gastroenterologists and even oncologists, because the level of infection of the world population with this pathogen is extremely high. Accordingly, timely diagnosis of Helicobacter pylori-associated diseases can reduce the incidence of chronic gastritis, peptic ulcer disease, and stomach cancer, as well as prevent their serious complications.
Referenses.
1. Shkytyn V.A. Rol helicobacter pylori v patolohyy cheloveka / Shkytyn V.A., Shpyrna A.Y., Storovoitov H.N. // Klynycheskaia mykrobyolohyia y antymykrobnaia khymyoterapyia. - 2002. -T2., Tom4.
- s. 128-145.
2. Koeppel M., Garcia-Alcalde F., Glowinski F. et al. (2015) Helicobacter pylori infection causes characteristic DNA damage patterns in human cells. Cell. Rep., Jun 10 [Epub ahead of print].
3. Ford A.C., Gurusamy K.S., Delaney B. et al. (2016) Eradication therapy for peptic ulcer disease in Helicobacter pyloripositive people. Cochrane Database of Systematic Reviews, Iss. 4. Art. No.: CD003840. DOI: 10.1002/14651858.CD003840.pub5.
4. Vara D. Perforated gastric ulcer in the child: a rare complication, a case report /D. Vara, I. Missotte, C. Menager // Archives de pediatrie: organe officiel de la Societefrancaise de pediatrie. - 2003. - 10(1):31-3. -P. 325-329.
5. Voland P. Interactions among the seven Helicobacter pylori proteins encoded by thecluster / P. Voland, D.L. Weeks, E.A. Marcus et al. // Am. J. Physiol. Gastrointest. LiverPhysiol. - 2003. - Vol.284. - P.96-106.
6. Smiian O.I. Rol Helicobacter pylori v pato-henezi vyrazkovoikhvoroby u ditei / O.I. Smiian, V.A. Plakhuta, O.M. Emets, Ya.O. Lata // Visnyk SumDU. Seriia «Medytsyna». - 2011. - №1,Tom 2. - s. 108-115.
7. Fedieienko H.D. Metody diahnostyky Helicobacter pylori: sovremennye vozmozhnosty v 2020 hodu // H.D. Fadieienko, Ya.V. Nykyforova // Hastroenter-olohiia. - 2010.- №1. - s.8-10.
