Метаболически ассоциированная жировая болезнь печени и желчнокаменная болезнь – удручающая коморбидность в XXI веке

Ахмедов В.А. Метаболически ассоциированная жировая болезнь печени и желчнокаменная болезнь – удручающая коморбидность в XXI веке. Consilium Medicum. 2025;27(12):732–738. DOI: 10.26442/20751753.2025.12.203509

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Akhmedov VA. Metabolically associated fatty liver disease and cholelithiasis – depressing comorbidity in XXI century: A review. Consilium Medicum. 2025;27(12):732–738. DOI: 10.26442/20751753.2025.12.203509

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Аннотация

Метаболически ассоциированная жировая болезнь печени (МАЖБП) – одно из наиболее распространенных заболеваний печени, встречающееся у 25–30% взрослого населения. Аналогичным образом желчнокаменная болезнь (ЖКБ) является одной из наиболее частых патологий желчевыводящих путей во всем мире, которую диагностируют у 10–20% взрослого населения. Холестериновые конкременты – частые компоненты ЖКБ, на патогенез которых в значительной степени влияют метаболические факторы, такие как дислипидемия, ожирение, инсулинорезистентность и быстрая потеря массы тела. В представленном литературном обзоре освещаются вопросы механизмов формирования конкрементов у пациентов с МАЖБП в аспекте влияния различных компонентов метаболического синдрома на нарушение моторики желчного пузыря и литогенность желчи. Отмечаются аспекты прогрессирования билиарной патологии от дисфункции сфинктера Одди до формирования хронического бескаменного холецистита, сладж-синдрома и далее до ЖКБ и постхолецистэктомического синдрома, что получило название «билиарный континуум». Перечисляются механизмы формирования конкрементов, связанные с печенью, кишечной микробиотой, гиперинсулинемией и инсулинорезистентностью. Показываются неспецифичность и системность холиноблокирующего эффекта нейротропных спазмолитиков, вследствие чего констатируется их ограниченное применение в гастроэнтерологии. Приводится мнение экспертов о более предпочтительной стратегии назначения спазмолитиков с минимально выраженными системными эффектами, в частности селективного миотропного спазмолитика мебеверина гидрохлорида (200 мг 2 раза в день внутрь). Результаты исследования демонстрируют эффективность Дюспаталина в купировании боли, связанной с дисфункцией желчного пузыря и сфинктера Одди, в том числе после холецистэктомии, у больных с физико-химической и клинически выраженной стадиями ЖКБ, а также при билиарном сладже. Особое внимание уделяется вопросам лечения коморбидного течения МАЖБП и ЖКБ. Показывается, что у пациентов с МАЖБП и билиарной коморбидностью (со сладж-синдромом, сформированными конкрементами в желчном пузыре) представляется крайне рациональным подход комплексной терапии адеметионином (оригинальным препаратом Гептрал^®) и мебеверином (оригинальным препаратом Дюспаталин^®). Применение данной стратегии вследствие взаимодополняющих клинических эффектов способствует улучшению функции печени изнутри, оттоку желчных кислот в желчевыводящие пути, желчи, снятию спазма и боли.

Ключевые слова: метаболически ассоциированная жировая болезнь печени, коморбидность, желчнокаменная болезнь, билиарный континуум, лечение, адеметионин, мебеверин

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Metabolically associated fatty liver disease (MAFLD) is one of the most common liver diseases found in 25–30% of the adult population. Similarly, cholelithiasis is one of the most common pathologies of the biliary tract worldwide, which is diagnosed in 10–20% of the adult population. Cholesterol concretions are common components of the gastrointestinal tract, the pathogenesis of which is significantly influenced by metabolic factors such as dyslipidemia, obesity, insulin resistance and rapid weight loss. The review highlights the mechanisms of concretion formation in patients with MAFLD in terms of the effect of various components of the metabolic syndrome on impaired gallbladder motility and bile lithogenicity. Aspects of the progression of biliary pathology from Oddi sphincter dysfunction to the formation of chronic stone-free cholecystitis, sludge syndrome, and further to gallstone disease and postcholecystectomy syndrome, called biliary continuum, are noted. The mechanisms of concretion formation associated with the liver, intestinal microbiota, hyperinsulinemia, and insulin resistance are described. The nonspecific and systemic nature of the holinoblocking effect of neurotropic antispasmodics is noted, as a result of which their limited use in gastroenterology is noted. The opinion of experts is given on a more preferable strategy for prescribing antispasmodics with minimal systemic effects, in particular, the selective myotropic antispasmodic mebeverine hydrochloride (200 mg 2 times a day orally). The results demonstrating the effectiveness of Duspatalin in relieving pain associated with gallbladder and Oddi sphincter dysfunction, including after cholecystectomy, in patients with physico-chemical and clinically pronounced stages of cholelithiasis, as well as with biliary sludge, are presented. Special attention is paid to the treatment of the comorbid course of MAFLD and cholelithiasis. It is shown that in patients with MAFLD and biliary comorbidity (with sludge syndrome, formed concretions in the gallbladder), the approach of complex therapy with ademetionine (the original drug Heptral^®) and mebeverine (the original drug Duspatalin^®) seems extremely rational. Due to the complementary clinical effects, the use of this strategy improves liver function from the inside, the outflow of bile acids into the biliary tract, the outflow of bile, and the relief of cramps and pain.

Keywords: metabolically associated fatty liver disease, comorbidity, cholelithiasis, biliary tract, treatment, ademetionine, mebeverine

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1. Khan RTY, Akbar N, Ismail H, et al. Factors Predictive of Non-Alcoholic Fatty Liver Disease in Non-Obese Pakistani Population. JHRR. 2024;4(2):1122-218. DOI:10.61919/jhrr.v4i2.826
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4. Xue Y, Xu J, Li M, Gao Y. Potential screening indicators for early diagnosis of NAFLD/MAFLD and liver fibrosis: Triglyceride glucose index-related parameters. Front Endocrinol (Lausanne). 2022;13:951689. DOI:10.3389/fendo.2022.951689
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8. Guzik TJ, Nosalski R, Maffia P, Drummond GR. Immune and inflammatory mechanisms in hypertension. Nat Rev Cardiol. 2024;21(6):396-416. DOI:10.1038/s41569-023-00964-1
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13. Dang Y, Wang Y, Wei J, et al. 25-Hydroxycholesterol inhibits Hantavirus infection by reprogramming cholesterol metabolism. Free Radic Biol Med. 2024;224:232-45. DOI:10.1016/j.freeradbiomed.2024.08.029
14. Dorvash MR, Khoshnood MJ, Saber H, et al. Metformin treatment prevents gallstone formation but mimics porcelain gallbladder in C57Bl/6 mice. Eur J Pharmacol. 2018;833:165-72. DOI:10.1016/j.ejphar.2018.06.002
15. Hu X, Binxu Q, Shao GZ, et al. Gut microbiota, circulating metabolites, and gallstone disease: a Mendelian randomization study. Front Microbiol. 2024;15:1336673. DOI:10.3389/fmicb.2024.1336673
16. Dong Q, Wang Z, Hu N, et al. Total Iridoid Glycosides from Swertia mussotii Franch. Alleviate Cholestasis Induced by α-Naphthyl Isothiocyanate through Activating the Farnesoid X Receptor and Inhibiting Oxidative Stress. Int J Mol Sci. 2024;25(19):10607. DOI:10.3390/ijms251910607
17. Simbrunner B, Hofer BS, Schwabl P, et al. FXR-FGF19 signaling in the gut-liver axis is dysregulated in patients with cirrhosis and correlates with impaired intestinal defence. Hepatol Int. 2024;18(3):929-42. DOI:10.1007/s12072-023-10636-4
18. Song KH, Li T, Owsley E, et al. Bile acids activate fibroblast growth factor 19 signaling in human hepatocytes to inhibit cholesterol 7alpha-hydroxylase gene expression. Hepatology. 2009;49(1):297-305. DOI:10.1002/hep.22627
19. Liu J, Hu Z, Bo D, et al. Predictive role of insulin resistance surrogates in gallstone disease. Medicine. 2025;104(14):e41478. DOI:10.1097/md.0000000000041478
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Авторы

В.А. Ахмедов*
¹ФГБОУ ВО «Омский государственный медицинский университет» Минздрава России, Омск, Российская Федерация
²БУЗОО «Клинический диагностический центр», Омск, Российская Федерация
*v_akhmedov@mail.ru

________________________________________________

Vadim A. Akhmedov*

¹Omsk State Medical University, Omsk, Russian Federation
²Clinical Diagnostic Center, Omsk, Russian Federation
*v_akhmedov@mail.ru

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