medsovetМедицинский СоветMeditsinskiy sovet = Medical Council2079-701X2658-5790REMEDIUM GROUP Ltd.10.21518/ms2025-399medsovet-9460Research ArticleЗАБОЛЕВАНИЯ ПИЩЕВОДА И ЖЕЛУДКАESOPHAGEAL AND GASTRIC DISEASESАутоиммунный гастрит и инфекция Helicobacter pylori: молекулярные механизмы взаимосвязиAutoimmune gastritis and Helicobacter pylori infection: Molecular mechanisms of relationshiphttps://orcid.org/0000-0001-7200-7082МозговойС. И.MozgovoiS. I.

Мозговой Сергей Игоревич - д.м.н., доцент, профессор кафедры патологической анатомии.

644099, Омск, ул. Ленина, д. 12

Sergei I. Mozgovoi - Dr. Sci. (Med.), Professor of the Department of Pathological Anatomy, Omsk State Medical University.

12, Lenin St., Omsk, 644099

simozgovoy@yandex.comhttps://orcid.org/0000-0001-9370-4768ГаусО. В.GausO. V.

Гаус Ольга Владимировна - д.м.н., профессор кафедры факультетской терапии и гастроэнтерологии.

644099, Омск, ул. Ленина, д. 12

Olga V. Gaus - Dr. Sci. (Med.), Associate Professor, Professor of the Department of Faculty Therapy and Gastroenterology, Omsk State Medical University.

12, Lenin St., Omsk, 644099

gaus_olga@bk.ruhttps://orcid.org/0000-0002-6581-7017ЛивзанМ. А.LivzanM. A.

Ливзан Мария Анатольевна - чл.- корр. РАН, д.м.н., профессор, ректор, заведующая кафедрой факультетской терапии и гастроэнтерологии.

644099, Омск, ул. Ленина, д. 12

Maria A. Livzan - Corr. Member RAS, Dr. Sci. (Med.), Professor, Rector, Head of the Department of Faculty Therapy and Gastroenterology, Omsk State Medical University.

12, Lenin St., Omsk, 644099

mlivzan@yandex.ruhttps://orcid.org/0000-0003-2815-3992БординД. С.BordinD. S.

Бордин Дмитрий Станиславович - д.м.н., заведующий отделом патологии поджелудочной железы, желчных путей и верхних отделов пищеварительного тракта, МКНЦ им. А.С. Логинова; профессор кафедры пропедевтики внутренних болезней и гастроэнтерологии, РосУниМед; профессор кафедры общей врачебной практики и семейной медицины, ТверьГМУ.

111123, Москва, ул. Новогиреевская, д. 1, корп. 1г; 127006, Москва, ул. Долгоруковская, д. 4г; 170100, Тверь, ул. Советская, д. 4

Dmitry S. Bordin - Dr. Sci. (Med.), Head of the Department of Pancreatic, Bile and Upper Gastrointestinal Pathology, Loginov Moscow Clinical Scientific Center; Professor of Department of Propaedeutic of Internal Diseases and Gastroenterology, Russian University of Medicine (ROSUNIMED); Professor of Department of General Medical Practice and Family Medicine, Tver State Medical University.

1, Bldg. 1, Novogireevskaya St., Moscow, 111123; 4g, Dolgorukovskaya St., Moscow, 127006; 4, Sovetskaya St., Tver, 170100

dbordin@mail.ruhttps://orcid.org/0000-0003-1834-3629РубцовВ. А.RubtsovV. A.

Рубцов Вячеслав Александрович - к.м.н., доцент кафедры патологической анатомии.

644099, Омск, ул. Ленина, д. 12

Vyacheslav A. Rubtsov - Сand. Sci. (Med.), Associate Professor of Department of Pathological Anatomy, Omsk State Medical University.

12, Lenin St., Omsk, 644099

rubtsov.omgmu@mail.ruhttps://orcid.org/0009-0009-1007-8382РыльскаяИ. А.RylskaiaI. A.

Рыльская Ирина Алексеевна - студент педиатрического факультета.

644099, Омск, ул. Ленина, д. 12

Irina A. Rylskaia - Student of Paediatric Faculty, Omsk State Medical University.

12, Lenin St., Omsk, 644099

rylskaai329@gmail.comОмский государственный медицинский университетРоссияOmsk State Medical UniversityRussian FederationМосковский клинический научный центр имени А.С. Логинова; Российский университет медицины (РосУниМед); Тверской государственный медицинский университетРоссияLoginov Moscow Clinical Scientific Center; Russian University of Medicine (ROSUNIMED); Tver State Medical UniversityRussian Federation2025171020250151626Copyright © Мозговой С.И., Гаус О.В., Ливзан М.А., Бордин Д.С., Рубцов В.А., Рыльская И.А., 20252025Мозговой С.И., Гаус О.В., Ливзан М.А., Бордин Д.С., Рубцов В.А., Рыльская И.А.Mozgovoi S.I., Gaus O.V., Livzan M.A., Bordin D.S., Rubtsov V.A., Rylskaia I.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.med-sovet.pro/jour/article/view/9460

Инфекция Helicobacter pylori (H. pylori) и аутоиммунное воспаление слизистой оболочки желудка признаны ведущими этиологическими факторами хронического атрофического гастрита. При этом механизмы формирования и прогрессирования атрофии слизистой оболочки с риском развития рака желудка при данных типах гастритов очень гетерогенны, требуют более глубокого изучения данного вопроса для разработки последующего персонифицированного подхода к ведению больных. Так, в последние годы появились данные, свидетельствующие о том, что аутоиммунный гастрит (АИГ) без сопутствующей инфекции H. pylori и без признаков значительного воспаления другой этиологии характеризуется относительно доброкачественным течением и низкой вероятностью неопластической трансформации слизистой оболочки желудка в рак желудка. Однако появление данных о возможности инфекции H. pylori индуцировать аутоиммунный процесс в отношении собственных париетальных клеток с развитием атрофии слизистой оболочки тела желудка делает актуальным проблему ведения и определения рисков канцерогенеза у больных хроническим гастритом смешанной этиологии. Целью данного научного обзора является систематизация имеющихся данных в отношении АИГ, механизмов развития атрофии и ассоциированных с ней рисков канцерогенеза как при изолированном аутоиммунном воспалении, так и в условиях персистирующей или предшествующей инфекции H. pylori («чистый» АИГ), персистирующей инфекции H. pylori или в период после эрадикационной терапии. Особое внимание уделено феномену молекулярной мимикрии между антигенами H. pylori и эпитопами собственных париетальных клеток желудка при развитии гастрита смешанной этиологии.

Helicobacter pylori (H. pylori) infection and autoimmune inflammation of the gastric mucosa are recognized as the leading etiologic factors of chronic atrophic gastritis. At the same time, the mechanisms of the development and progression of gastric mucosal atrophy associated with a risk of gastric cancer in these types of gastritis are highly heterogeneous, and need a more detailed study of this issue to work out a follow-up personalized approach to the management of patients. In recent years, there have been reports confirming that autoimmune gastritis (AIG) without concurrent H. pylori infection and without signs of significant inflammation of other etiologies has a relatively benign course and a low risk of neoplastic transformation of the gastric mucosa into gastric cancer. However, the emergence of reports that H. pylori infection may elicit autoimmunity toward parietal cells, which results in the atrophy of the gastric body mucosa makes the issue of management and identification of carcinogenesis risks in patients with chronic gastritis of mixed etiology more urgent. This scientific review aims to systematize the available data on AIG, the mechanisms of development of atrophy and atrophy-associated risks of carcinogenesis, both in isolated autoimmune inflammation and in persistent or previous H. pylori (“pure” AIG), persistent H. pylori infection, or in the post-eradication therapy period. Special attention is paid to the phenomenon of molecular mimicry between H. pylori antigens and epitopes of gastric parietal cells during the development of gastritis of mixed-etiology.

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The authors declare that there are no conflicts of interest present.