Diabetic patients are at high risk for NAFLD to develop LF and LC. LFE and FTs showed a comparably high accuracy in the diagnosis of LC in patients with DM and these may be used for screening. With allowance made for the existing risk factors of LF and LC, it is necessary to identify groups of patients with DM for further examination and follow-up. Patients who are diagnosed with stage F4 should be examined carefully to evaluate concurrent diseases and to make liver biopsy.
Цель обзора: обобщить текущие знания об этиопатогенезе и клинические особенности первичного билиарного холангита (ПБХ), осветить актуальные вопросы диагностики, лечения и стратификации рисков у пациентов с ПБХ. Основные положения. ПБХ (ранее -первичный билиарный цирроз) -хроническое воспалительное аутоиммунное заболевание, при котором первоначально поражаются холангиоциты междольковых желчных протоков. ПБХ наблюдается в первую очередь у женщин среднего возраста. Без лечения ПБХ обычно прогрессирует до цирроза печени и печеночной недостаточности. Инициация и прогрессирование ПБХ -многофакторный процесс с влиянием на генетический, эпигенетический, иммунологический статус пациента различных факторов окружающей среды. Ранняя диагностика ПБХ значительно улучшилась благодаря выявлению классических серологических маркеров -антимитохондриальных антител. В 1980-х годах ПБХ был ведущим показанием для трансплантации печени. Урсодезоксихолевая кислота (УДХК) в настоящее время является препаратом первой линии, большинство пациентов с ПБХ на фоне терапии имеют нормальную продолжительность жизни. Однако 1 из 3 пациентов не отвечает на лечение УДХК, поэтому клинически важна оценка биохимического ответа через год от начала терапии. Заключение. Ранняя диагностика и стратификация пациентов с ПБХ низкого и высокого риска резистентности к терапии УДХК имеют большое клиническое значение для индивидуального подхода к лечению и определения необходимости дополнительной медикаментозной терапии. Ключевые слова: первичный билиарный холангит, первичный билиарный цирроз, антимитохондриальные антитела, биопсия печени, урсодезоксихолевая кислота.
Aim. To evaluate the frequency of liver fibrosis progression to stage 34 among patients with non-alcoholic fatty liver disease (NAFLD), type 2 diabetes and obesity, to identify predictors of severe liver fibrosis, to propose an algorithm for diagnosing fibrosis in this category of patients. Materials and methods. 160 patients with NAFLD, type 2 diabetes mellitus (DM) and obesity and 50 patients with NAFLD without diabetes were comprehensively examined. Patients underwent laboratory examination (clinical blood test, biochemical analysis, immunoglobulins G, M, autoantibody assay, coagulogram), liver ultrasound. All patients underwent determination of the liver fibrosis stage by two methods: the serological test FibroMax and indirect ultrasound elastometry of the liver; 40 patients underwent a liver biopsy. Statistical data processing was performed using the programming language and statistical calculations R: we used correlation analysis, multiple logistic regression method, one-way analysis of variance, multi-factor analysis, the Kruskal-Wallis method, and comparison of the number of patients using the Fisher test. Results. DM is a risk factor for the liver fibrosis progression in patients with NAFLD. Significant markers of severe fibrosis in this category of patients are increased levels of GGTP, haptoglobin and alpha-2-macroglobulin, lower platelet and prothrombin levels. Obesity and isolated steatosis without steatohepatitis are not markers of severe liver fibrosis at present, but obesity can be considered a risk factor for the progression of fibrosis in the future. Conclusion. All patients with NAFLD in combination with diabetes need screening to detect advanced liver fibrosis: it is advisable to determine the levels of GGTP, haptoglobin and alpha-2-macroglobulin.
Non-alcoholic fatty liver disease (NAFLD) is the first most common liver disease worldwide. In fact, NAFLD is associated with metabolic syndrome (MS) and is a certain phenotype that has developed as a result of the combined action of complex heterogeneous etiological factors. A feature of this disease is its extreme heterogeneity, which raises the demand for classification, which would help to distinguish between the supposedly metabolically favorable and the unfavorable subtypes. The task of the international consortium of the expert group was to integrate modern ideas about the heterogeneity of patients denoted by the abbreviation NAFLD, and to create a new definition that will more accurately account for the pathogenesis and can help in patients’ stratification for their further treatment. Experts reached consensus that the abbreviation NAFLD no longer reflects the essence of this disease and as a more appropriate and comprehensive concept which also integrates metabolic changes associated with fatty liver disease, the term ῾metabolically associated fatty liver disease’ (MAFLD) was proposed. This approach opens up opportunities for the scientific and medical community to update the nomenclature, highlight individual sub-phenotypes for the development of a new targeted therapy.
Introduction: Viral infections, especially with hepatotropic viruses, may trigger autoimmune liver diseases (AILDs) and deteriorate their course. However, association of previous hepatitis B virus (HBV) infection (presence of anti-HBc with or without anti-HBs or HBV DNA in serum) with AILDs is poorly studied so far. The aim of the study was to assess the prevalence of previous hepatitis B virus infection markers and its clinical significance in patients with autoimmune liver diseases. Methods: The study was based on the data obtained from 234 consecutive HBsAg-negative patients with AILDs [81 with autoimmune hepatitis (AIH), 122 with primary biliary cholangitis (PBC) and 31 with primary sclerosing cholangitis (PSC)] and 131 subjects of the control group without liver diseases. Blood samples of the enrolled patients were tested for anti-HBc and HBV DNA. Samples of liver tissue were examined by standard morphologic protocol and, in anti-HBc positive subjects, for HBV DNA. We assessed estimated risks of AILDs according to anti-HBc positivity and association of anti-HBc positivity with stage of liver fibrosis. Results: Anti-HBc was detected in 14.5% participants in the control group vs 26.1% (p = 0.016) in patients with AILDs (including 27.1% subjects with PBC (p = 0.021 vs control group), in 29% of PSC and 23.5% in AIH. HBV DNA was detected in three patients with PBC and in one with AIH. Positive anti-HBc test result was associated with higher risk of AILDsodds ratio (OR) = 2.078 [95% confidence interval (CI) 1.179-3.665], especially in PBC: OR (95% CI) 2.186 (1.165-4.101). Odds of advanced stage of liver fibrosis (F3-F4 by METAVIR) in anti-HBc-positive subjects with
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