以蛇胸蚴病侵袭为背景的自身免疫性肝病的实验室特征

E. S. Kosarenko, T. V. Zuevskaya, M. D. Orlov, S. I. Eremeev, S. S. Romanchenko
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摘要

目的-确定在阿片胸片病侵袭背景下发生的自身免疫性肝病的实验室特征,评估阿片胸片病对自身免疫性肝病病程的影响。材料与方法本研究对自身免疫性肝病及自身免疫性和寄生性肝损害合并患者的调查结果进行前瞻性分析。研究的方法论基础是一般科学方法、一般逻辑方法和特殊方法。结果。比较分析自身免疫性肝病伴和不伴蛇胸蚴病侵袭的实验室参数。结果发现,合并症患者的尿素(p=0.001)、葡萄糖(p=0.014)和总胆固醇(p= 0.012)水平均有统计学意义。结论。我们确定,在与蛇胸腺病相关的自身免疫性肝病中,没有特定的病理特征实验室体征,这在进行鉴别诊断时是重要的考虑因素。因此,所有患有opisthorchiasis的患者,无论先前的诊断如何,如果存在肝脾肿大、持续的细胞溶解和/或胆汁淤积,根据目前的诊断算法,需要额外检查自身免疫性肝损伤,特别是如果他们合并贫血和其他细胞减少、自身免疫性疾病、自身免疫性病理遗传加重或γ-球蛋白(IgG)急剧增加。
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Laboratory features of autoimmune liver diseases against the background of opisthorchiasis invasion
The purpose — to determine the laboratory features of autoimmune liver diseases occurring against the background of opisthorchiasis invasion, to assess the effect of opisthorchiasis on the course of autoimmune liver diseases. Material and methods The study is a prospective analysis of the survey results of patients with autoimmune liver diseases and combined autoimmune and parasitic liver damage. The methodological basis of the study was general scientific, general logical and special methods. Results. A comparative analysis of laboratory parameters in autoimmune liver diseases with and without opisthorchiasis invasion was carried out. It was found that patients with comorbidity had statistically significantly higher levels of urea (p=0.001), glucose (p=0.014) and total cholesterol (p = 0.012). Conclusion. It was determined that in autoimmune liver diseases associated with opisthorchiasis, there are no specific pathognomonic laboratory signs, which is important to consider when conducting differential diagnosis. Therefore, all patients suffering from opisthorchiasis, regardless of the previously established diagnosis, in the presence of hepatosplenomegaly, persistent cytolysis and/or cholestasis, require an additional examination for autoimmune liver damage, according to the current diagnostic algorithms, especially if they are combined with anemia and other cytopenias, autoimmune diseases, aggravated heredity for autoimmune pathology, or a sharp increase in γ-globulins (IgG).
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