Аутоиммунный гастрит и инфекция Helicobacter pylori: молекулярные механизмы взаимосвязи

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.

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