Печінка при ендокринних захворюваннях. Огляд
DOI:
https://doi.org/10.30978/MG-2024-4-87Ключові слова:
гіпоталамо‑гіпофізарна вісь, печінка при гіпотиреозі та гіпертиреозі, статеві гормони й печінка, глюкокортикоїди та захворювання печінки, гіперальдостеронізм і печінкаАнотація
Патологія ендокринних органів може призводити до печінкової дисфункції та, навпаки, захворювання печінки можуть спричинити порушення ендокринної функції. В останні десятиліття відбулося стрімке зростання поширеності метаболічно асоційованої стеатотичної хвороби печінки (МАСХП) та ускладнень, пов’язаних із прогресуванням цього захворювання. Ліпідний обмін у печінці та синтез холестерину залежать від функції ендокринної системи й механізмів зворотного зв’язку. Саме тому необхідно оцінювати вплив ендокринної патології в пацієнтів із МАСХП, а лікування цих станів має бути включене до комплексу традиційної терапії. Функція печінки залежить від адекватної продукції гормонів щитоподібної залози, тому наявність патології печінки також може несприятливо впливати на вироблення гормонів щитоподібної залози внаслідок неадекватної конверсії тироксину. Клінічні наслідки гіпотиреозу різні та можуть призвести до підвищення рівня трансаміназ, а також зміни печінкового метаболізму. Порушення функції печінки можуть виявлятися у вигляді холестазу. Підвищення рівня трансаміназ відзначають у третини пацієнтів із гіпертиреозом. Імовірна первинна причина — підвищені метаболічні потреби, що призводять до гіпоперфузії та легкої ішемії печінки.
Глікогенова гепатопатія є рідкісним ускладненням цукрового діабету 1 типу, що погано контролюється. Вона характеризується гепатомегалією, підвищенням рівня печінкових ферментів і накопиченням глікогену в печінці. Цю гепатопатію часто помилково діагностують як МАСХП. Правильний діагноз залежить від результатів біопсії печінки з PAS‑реакцією. Естрогени можуть спричинити внутрішньопечінковий холестаз у пременопаузі в жінок, які використовують оральні контрацептиви, у жінок у постменопаузі, які приймають гормональну замісну терапію, а також у чоловіків, які отримують естрогени з приводу раку передміхурової залози. Підвищення рівня глюкокортикоїдів при синдромі Кушинга залучене в патогенез інсулінорезистентності, ожиріння, метаболічного синдрому та МАСХП. Пацієнти з первинним гіперальдостеронізмом мають підвищений ризик розвитку метаболічного синдрому, порушення метаболізму глюкози, резистентності до інсуліну та МАСХП.
У пацієнтів з ураженнями печінки, що прогресують, необхідно проводити моніторинг функції ендокринних органів, особливо при декомпенсованому цирозі печінки та гострій печінковій недостатності.
Посилання
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