Журнал «Медицина неотложных состояний» Том 22, №3, 2026
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Кишковий бар’єр як «файрвол» при гострому панкреатиті: дисбіоз і каскад ускладнень
Авторы: Чуклін С.М., Чуклін С.С.
Медичний центр Святої Параскеви, м. Львів, Україна
Рубрики: Медицина неотложных состояний
Разделы: Справочник специалиста
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Актуальність. Гострий панкреатит (ГП) є гетерогенним системним запальним синдромом, у якому рання недостатність кишкового бар’єра та дисбіоз сприяють ендотоксемії, транслокації мікробних продуктів і ескалації системних ускладнень. Мета: узагальнити сучасні докази ролі кишкового бар’єра та мікробіоти у формуванні ускладнень ГП, окреслити механістичні ланки каскаду та потенціал багатоомних біомаркерів для ранньої стратифікації ризику. Матеріали та методи. Наративний синтез із елементами систематизованого пошуку. Пошук у PubMed/Medline, Scopus, Google Scholar; включали клінічні та експериментальні роботи з оцінкою мікробіоти/метаболітів і кінцевих точок (органна недостатність, інфікований панкреонекроз, сепсис, ГРДС, летальність). Результати. Дані свідчать про раннє підвищення кишкової проникності при ГП, що корелює з тяжкістю перебігу та створює «вікно» для дисбіозу і транслокації, особливо при некротизуючому фенотипі. Найбільш відтворювані таксономічні зсуви включають зростання Enterococcus/Enterobacteriaceae/Escherichia — Shigella та зниження Bifidobacterium/Blautia, асоційовані з інтенсивною терапією, інфекційними ускладненнями й легеневими проявами. Інтегративні підходи (метагеноміка + метаболоміка) виявляють сигнатури, пов’язані з ризиком органної недостатності/ГРДС, а функціональний внесок мікробіоти опосередковується метаболітами (SCFA, жовчні кислоти, ароматичні токсини), що підвищують інформативність прогностичних моделей за інтеграції з клінічними параметрами. Висновки. Кишковий бар’єр і мікробіота є ключовими детермінантами каскаду ускладнень ГП; для впровадження мікробіомних біомаркерів потрібні стандартизація преаналітики/аналітики, максимально ранній забір зразків, контроль конфаундерів і зовнішня валідація моделей.
Background. Acute pancreatitis (AP) is a heterogeneous systemic inflammatory syndrome in which early failure of the intestinal barrier and gut dysbiosis promote endotoxemia, translocation of microbial products, and increased systemic complications. Objective: to synthesize current evidence on the role of the gut barrier and microbiota in AP complications, outline key mechanistic links, and highlight how multi-omics biomarkers may support early risk stratification. Materials and methods. Narrative synthesis with a structured search. PubMed/Medline, Scopus, and Google Scholar were searched. We included clinical and experimental studies assessing microbiota/metabolites and relevant outcomes (organ failure, infected pancreatic necrosis, sepsis, acute respiratory distress syndrome, mortality). Results. Evidence indicates an early rise in intestinal permeability in AP, associated with disease severity and enabling dysbiosis and microbial translocation, particularly in necrotizing phenotypes. The most reproducible taxonomic shifts include increases in Enterococcus/Enterobacteriaceae/Escherichia-Shigella and decreases in Bifidobacterium/Blautia, which in several cohorts correlate with intensive care need, infectious complications, and pulmonary involvement. Integrative approaches (metagenomics + metabolomics) reveal signatures linked to the risk of organ failure/acute respiratory distress syndrome, while microbiota-derived metabolites (short-chain fatty acids, bile acids, aromatic toxins) provide a functional layer that can improve prognostic models when combined with clinical variables. Conclusions. The gut barrier and microbiota are pivotal drivers of the AP complication cascade. Clinical translation of microbiome-based biomarkers requires standardized preanalytics/analytics, very early sampling, rigorous confounder control, and external validation on independent cohorts.
гострий панкреатит; кишковий бар’єр; мікробіота; дисбіоз; транслокація; ендотоксемія; багатоомні біомаркери
acute pancreatitis; intestinal barrier; microbiota; dysbiosis; translocation; endotoxemia; multi-omics biomarkers
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