rspНаучно-практическая ревматологияRheumatology Science and Practice1995-44841995-4492IMA-PRESS, LLC10.14412/1995-4484-2017-560-565rsp-2440Research ArticleОБЗОРREVIEWИммунологические механизмы развития неалкогольной жировой болезни печени у больных подагрой и псевдоподагрой: обзор литературыIMMUNOLOGICAL MECHANISMS FOR THE DEVELOPMENT OF NONALCOHOLIC FATTY LIVER DISEASE IN PATIENTS WITH GOUT AND PSEUDOGOUT: A REVIEW OF LITERATUREНабиеваД. А.NabievaD. A.

100109 Республика Узбекистан, Ташкент, ул. Фараби, 2

2, Farabi St., Tashkent 100109, Uzbekistan

dil_nab@mail.ruТашкентская медицинская академияУзбекистанTashkent Medical AcademyUzbekistan201727102017555560565Copyright © Набиева Д.А., 20172017Набиева Д.А.Nabieva D.A.This work is licensed under a Creative Commons Attribution 4.0 License.https://rsp.mediar-press.net/rsp/article/view/2440

Современные представления о подагре включают в себя как традиционную метаболическую теорию нарушения пуринового обмена и внешнесредового воздействия, так и участие в патологическом процессе иммуновоспалительных факторов. Воспаление является отличительной чертой острой тканевой реакции на кристаллы моноурата натрия при подагре и пирофосфата кальция – при псевдоподагре. Кристаллы взаимодействуют с мембранами плазматических клеток, с активацией NLRP3, протеолитическим расщеплением проинтерлейкина 1β и секрецией зрелого интерлейкина 1β, который модулирует ряд событий, приводящих к активации эндотелиальных клеток и нейтрофилов, что также предшествует жировой дистрофии печени. В данном обзоре подробно рассмотрены последние данные по патогенетическим механизмам, служащим в качестве предикторов развития метаболических сдвигов и неалкогольной жировой болезни печени у больных подагрой.

The current ideas of gout include both the traditional metabolic theory of disorders of purine metabolism and environmental exposure and the involvement of immunoinflammatory factors in the pathological process. Inflammation is a hallmark of an acute tissue reaction to monosodium urate the crystals in gout and to calcium pyrophosphate crystals in pseudogout. The crystals interact with the membranes of plasma cells, with the activation of NLRP3, the proteolytic cleavage of pro-interleukin 1β, and the secretion of mature interleukin-1β that modulates a sequence of events leading to the activation of endothelial cells and neutrophils, which is also preceded by fatty degeneration of the liver. This review details recent data on the pathogenetic mechanisms that serve as predictors of metabolic changes and nonalcoholic fatty liver disease in patients with gout.

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