gastro-jРоссийский журнал гастроэнтерологии, гепатологии, колопроктологииRussian Journal of Gastroenterology, Hepatology, Coloproctology1382-43762658-6673«Gastro» LLC10.22416/1382-4376-2017-27-3-45-56gastro-j-157Research ArticleГЕПАТОЛОГИЯHEPATOLOGYРоль синдрома избыточного бактериального роста и системного воспаления в патогенезе гемодинамических изменений у больных циррозом печениSmall intestinal bacterial overgrowth syndrome and systemic inflammation in pathogenesis of hemodynamic changes at liver cirrhosisМасленниковР. В.MaslennikovR. V.mmmm00@yandex.ruДригаА. А.DrigaA. A.noemail@neicon.ruИвашкинК. В.IvashkinK. V.noemail@neicon.ruЖарковаМ. С.ZharkovaM. S.noemail@neicon.ruМаевскаяМ. В.MayevskayaM. V.noemail@neicon.ruПавловЧ. С.PavlovCh. S.noemail@neicon.ruАрсланянМ. Г.ArslanyanM. G.noemail@neicon.ruМусинаН. Б.MusinaN. B.noemail@neicon.ruБерезинаЕ. Н.BerezinaYe. N.noemail@neicon.ruИвашкинВ. Т.IvashkinV. T.noemail@neicon.ruФГАОУ ВО «Первый Московский государственный медицинский университет им. И. М. Сеченова»РоссияFederal State Autonomous Educational Institution of Higher Education «I.M. Sechenov First Moscow State Medical University»Russian Federation2017120820182734556Copyright © Масленников Р.В., Дрига А.А., Ивашкин К.В., Жаркова М.С., Маевская М.В., Павлов Ч.С., Арсланян М.Г., Мусина Н.Б., Березина Е.Н., Ивашкин В.Т., 20182018Масленников Р.В., Дрига А.А., Ивашкин К.В., Жаркова М.С., Маевская М.В., Павлов Ч.С., Арсланян М.Г., Мусина Н.Б., Березина Е.Н., Ивашкин В.Т.Maslennikov R.V., Driga A.A., Ivashkin K.V., Zharkova M.S., Mayevskaya M.V., Pavlov C.S., Arslanyan M.G., Musina N.B., Berezina Y.N., Ivashkin V.T.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.gastro-j.ru/jour/article/view/157

Цель исследования. Оценить роль синдрома избыточного бактериального роста (СИБР) в тонкой кишке в развитии гемодинамических изменений при циррозе печени (ЦП). Материал и методы. В исследование были включены 50 больных ЦП и 15 клинически здоровых лиц, составивших контрольную группу. У всех обследованных проведены диагностика СИБР с использованием водородного дыхательного теста с лактулозой, определение уровня С-реактивного белка (СРБ) в плазме крови и эхокардиографическое исследование с одновременным определением артериального давления (АД) и частоты сердечных сокращений, рассчитаны основные гемодинамические показатели: среднее АД, сердечный выброс (СВ), общее периферическое сосудистое сопротивление (ОПСС). Результаты. У больных ЦП с СИБР по сравнению с больными ЦП без СИБР были ниже среднее АД (82,7±9,0 мм рт. ст. vs 92,0±14,0 мм рт. ст.) и ОПСС (16,4±4,4 мм рт. ст.× мин/л vs 21,3±5,3 мм рт. ст. мин/л), а также выше СВ (5,38±1,41 л/мин vs 4,52±1,03 л/мин) и концентрация СРБ в плазме крови (1,2÷10,5÷16,5 мг/л vs 0,6÷2,8÷9,1 мг/л). СИБР приводил к подобным изменениям только у больных декомпенсированным ЦП. При этом значимые гемодинамические нарушения практически не выявляли у больных декомпенсированным ЦП без СИБР и компенсированным ЦП независимо от наличия СИБР. У больных ЦП выявлена значимая корреляция концентрации СРБ в плазме крови с ОПСС (r= -0,367; p=0,009) и СВ (r=0,313; p=0,027), но не со средним АД (r= -0,227; p=0,113). Заключение. СИБР при ЦП играет важную роль в развитии вазодилатации, артериальной гипотензии и гипердинамического кровообращения. Поскольку эти гемодинамические нарушения усугубляют течение портальной гипертензии, терапия, проводимая с целью устранения СИБР, может уменьшить ее выраженность.

Aim of investigation. To estimate the impact of small intestinal bacterial overgrowth (SIBO) to development of hemodynamic disorders at liver cirrhosis (LC). Material and methods. Original study included 50 LC patients and 15 generally healthy controls. Lactulose hydrogen breath test, serum level of C-reactive protein and cardiac ultrasound with simultaneous blood pressure (BP) and heart rate measurement, estimation of basic hemodynamic scores: mean blood pressure (MBP), cardiac output (CO), total peripheral vascular resistance (TPVR) were investigated in all patients. Results. LC patients with SIBO as compared to LC patients without SIBO had lower mean blood pressure (82.7±9.0 mm Hg vs 92.0±14.0 mm Hg) and TPVR (16.4±4.4 mm Hg × min/l vs 21.3±5.3 mm Hg • min/l), higher CO (5.38±1.41 l/min vs 4.52±1.03 l/ min) and serum C-rp (SIBO - 1.2÷10.5÷16.5 mg/l vs 0.6÷2.8÷9.1 mg/l). The presence of SIBO led to similar changes only at decompensated LC. At the same time no significant hemodynamic disorders were revealed at decompensated LC without SIBO and compensated LC irrespective of SIBO. At LC significant correlation of serum C-rp to TPVR (r=-0.367; p=0.009) and CO (r=0.313; p=0.027) was found, but not to mean BP (r=-0.227; p=0.113). Conclusion. SIBO at LC plays important role in vasodilation, arterial hypotension and hyperdynamic circulation. As these hemodynamic disorders aggravate the course of portal hypertension, the treatment of SIBO may reduce severity of the latter.

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The authors declare that there are no conflicts of interest present.