Terapevticheskii arkhivTerapevticheskii arkhivТерапевтический архив0040-36602309-5342LLC Obyedinennaya Redaktsiya6189210.26442/00403660.2021.01.200595ReviewsОбзорыReview ArticleInflammatory diseases of the pancreas: what new do we know about the mechanisms of their development in the 21st century?Воспалительные заболевания поджелудочной железы: что нового мы знаем о механизмах их развития в XXI веке?https://orcid.org/0000-0002-7603-8481AkhmedovVadim A.АхмедовВадим Адильевич
Russian Federation

д.м.н., проф., зав. каф. медицинской реабилитации дополнительного профессионального образования

v_akhmedov@mail.ruhttps://orcid.org/0000-0001-9370-4768GausOlga V.ГаусОльга Владимировна
Russian Federation

к.м.н., доц. каф. факультетской терапии, профессиональных болезней

v_akhmedov@mail.ruOmsk State Medical University, Omsk, RussiaФГБОУ ВО «Омский государственный медицинский университет» Минздрава РоссииOmsk State Medical UniversityФГБОУ ВО «Омский государственный медицинский университет» Минздрава России1001202193166702502202125022021Copyright ©; 2021, Consilium MedicumCopyright ©; 2021, ООО "Консилиум Медикум"2021Consilium MedicumООО "Консилиум Медикум"https://creativecommons.org/licenses/by-nc-sa/4.0https://ter-arkhiv.ru/0040-3660/article/view/61892

Inflammatory diseases of the pancreas can range from acute to acute recurrent and chronic pancreatitis. With the improvement of laboratory diagnostics in the 21st century, the mechanisms of the pro-inflammatory and anti-inflammatory role of tight junctions, in particular the transmembrane proteins occludin, claudine and JAMs, cytoplasmic Zo-proteins, and adherens junctions, in particular α-catenin, β-catenin, E-cadherin, selectins and ICAMs in the pathogenesis of acute and chronic pancreatitis have become more clear. The study of genetic factors in the development of acute and chronic pancreatitis showed the role of mutations in the genes SPINK1 N34S, PRSS1, CEL-HYB in the progression of the disease.

Воспалительные заболевания поджелудочной железы могут варьировать от острого до острого рецидивирующего и хронического панкреатита. С совершенствованием лабораторной диагностики в XXI в. стали более понятны механизмы провоспалительной и противовоспалительной роли плотных соединений, в частности трансмембранных белков окклюдина, клаудина и JAMs, цитоплазматических Zo-белков, а также адгезивных соединений, в частности α-катенина, β-катенина, Е-кадгерина, селектинов и ICAMs, в патогенезе острого и хронического панкреатита. Изучение генетических факторов развития острого и хронического панкреатита показало роль мутаций генов SPINK1 N34S, PRSS1, CEL-HYB в прогрессировании заболевания.

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