Keywords
pancreas divisum, ідіопатичний панкреатит, обструктивний панкреатит, причини, мутації, лікування.
How to Cite
Tsys, O. V. (2026). Divided pancreas (pancreas divisum) and other possible causes of obstructive chronic pancreatitis: when and how to treat them?. Herald of Pancreatic Club, 70(1), 4-13. https://doi.org/10.33149/vkp.2026.01.01
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Abstract
The article presents current literature data confirming that idiopathic pancreatitis remains a diagnosis of exclusion and can only be established after careful exclusion of all known aetiological factors of pancreatitis development: anatomical, metabolic, infectious, and genetic. With the development of imaging and molecular diagnostic methods, the proportion of truly idiopathic pancreatitis is steadily decreasing.
Particular attention is paid to the divided pancreas (pancreas divisum — PD) — a variant of the duct system structure that occurs in 5–10% of the population. Current research does not confirm that PD is an independent cause of acute or chronic pancreatitis. In most carriers of this anatomical variant, the disease does not develop, and the frequency of PD is the same in individuals with and without pancreatitis.
Particular emphasis is placed on the role of genetic factors in the pathogenesis of chronic pancreatitis. The significance of mutations in the CFTR, SPINK1, and PRSS1 genes, which increase susceptibility to inflammatory changes in the pancreas, is considered. Their detection in patients with PD and pancreatitis indicates that PD is not a causal factor, but rather a coincidental anatomical association.
It is noted that endoscopic or surgical “treatment” of PD has no proven efficacy and should be used exclusively in clinical trials. Optimal management of such patients requires a comprehensive, personalized approach that takes into account anatomical, functional and genetic characteristics.
References
1. Термін «ідіопатичний панкреатит» є діагнозом виключення і має використовуватися тільки після того, як аргументовано відкинуто всі відомі етіологічні фактори, включаючи генетичні, анатомічні та метаболічні. З розвитком інструментальної та молекулярної діагностики частка істинного ІП прогресивно зменшується.
2. PD являє собою анатомічний варіант будови протокової системи ПЗ, що відмічають у 5–10% популяції, і в більшості випадків не має клінічного значення. Сучасні дані не підтверджують прямий причинно-наслідковий зв’язок між PD та розвитком панкреатиту.
3. Генетичні фактори, зокрема мутації генів CFTR, SPINK1 та PRSS1, відіграють ключову роль у патогенезі ХП, включаючи випадки, що поєднуються з PD. Наявність PD у таких пацієнтів, ймовірно, відображає випадкове поєднання, а не патогенетичну залежність.
4. Ендоскопічне та хірургічне лікування при PD не є стандартом ведення пацієнтів з панкреатитом і має розглядатися винятково в рамках клінічних досліджень. Більшість інтервенційних підходів не демонструють достовірного терапевтичного ефекту та пов’язані з ризиком виникнення ускладнень.
5. Серед інших причин обструктивного ХП слід враховувати широкий спектр вроджених та набутих станів: холедохоцеле, кісти холедоха, дуплікаційні кісти, дивертикули фатерового сосочка, пухлинні та запальні ураження, а також ятрогенні зміни. Тактику лікування слід визначати індивідуально, з урахуванням анатомічних та функціональних особливостей.
6. Оптимальне ведення пацієнтів із ХП потребує комплексного персоналізованого підходу, що включає детальну візуалізаційну оцінку, функціональне тестування та обов’язкове генетичне обстеження у разі наявності підозри на спадкову схильність.
Таким чином, PD слід розглядати не як самостійну причину ХП, а як анатомічний варіант, який у поєднанні з певними генетичними та середовищними факторами може спричиняти розвиток захворювання. Перспективним напрямком залишається подальше вивчення взаємодії анатомічних та молекулярних механізмів у патогенезі ХП.
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2. PD являє собою анатомічний варіант будови протокової системи ПЗ, що відмічають у 5–10% популяції, і в більшості випадків не має клінічного значення. Сучасні дані не підтверджують прямий причинно-наслідковий зв’язок між PD та розвитком панкреатиту.
3. Генетичні фактори, зокрема мутації генів CFTR, SPINK1 та PRSS1, відіграють ключову роль у патогенезі ХП, включаючи випадки, що поєднуються з PD. Наявність PD у таких пацієнтів, ймовірно, відображає випадкове поєднання, а не патогенетичну залежність.
4. Ендоскопічне та хірургічне лікування при PD не є стандартом ведення пацієнтів з панкреатитом і має розглядатися винятково в рамках клінічних досліджень. Більшість інтервенційних підходів не демонструють достовірного терапевтичного ефекту та пов’язані з ризиком виникнення ускладнень.
5. Серед інших причин обструктивного ХП слід враховувати широкий спектр вроджених та набутих станів: холедохоцеле, кісти холедоха, дуплікаційні кісти, дивертикули фатерового сосочка, пухлинні та запальні ураження, а також ятрогенні зміни. Тактику лікування слід визначати індивідуально, з урахуванням анатомічних та функціональних особливостей.
6. Оптимальне ведення пацієнтів із ХП потребує комплексного персоналізованого підходу, що включає детальну візуалізаційну оцінку, функціональне тестування та обов’язкове генетичне обстеження у разі наявності підозри на спадкову схильність.
Таким чином, PD слід розглядати не як самостійну причину ХП, а як анатомічний варіант, який у поєднанні з певними генетичними та середовищними факторами може спричиняти розвиток захворювання. Перспективним напрямком залишається подальше вивчення взаємодії анатомічних та молекулярних механізмів у патогенезі ХП.
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