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Picolinic Acid in Patients with Chronic Hepatitis C Infection: A Preliminary Report

机译：尿素酸患者慢性丙型肝炎感染患者：初步报告

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Macrophage activation seems to be a feature of chronic liver diseases. Picolinic acid (PA) as a macrophage secondary signal causes the activation of interferon-gamma- (IFN-gamma-) prime macrophage and triggers cytokine-driven inflammatory reactions. The rationale for seeking increased PA formation in chronic viral hepatitis is based on the involvement of activated macrophages in chronic viral hepatitis-associated inflammation. The aim of this study was to determine serum PA levels in patients with chronic hepatitis C infection, taking into account the presence of diabetes. We assessed PA and high-sensitivity C-reactive protein (hsCRP) as a marker of inflammation in 51 patients with chronic hepatitis C infection (CHC), both with and without diabetes and 40 controls. Compared with the controls, the patients with CHC showed a significant increase in plasma concentrations of PA and hsCRP (P < 0.01 and P < 0.05, resp.). The values of PA and hsCRP were more elevated in patients with diabetes than without diabetes (both P < 0.01). The positive relationships were between PA and hsCRP levels (P < 0.05) and the presence of diabetes (P < 0.00,1). We documented that significant elevation in serum PA levels is associated with diabetes prevalence and increased inflammatory response reflected in hsCRP levels in CHC patients. Hepatitis C virus (HCV) infection has been associated with various extrahepatic manifestations, and diabetes mellitus is one of these. Diabetes in patients with chronic hepatitis C infection (CHC) has unique and complex pathogenesis, which distinguishes this metabolic disorder from type 2 diabetes mellitus. In this regard, a high prevalence of diabetes has been reported in HCV-infected patients in comparison with other liver diseases. Mehta et al. have reported that preexisting HCV infection may increase the risk of type 2 diabetes mellitus in patients with recognized diabetes risk factors. The mechanisms by which chronic hepatitis C infection induces increased insulin resistance and the. risk for development of diabetes have not been completely clarified. It has been observed that type 2 diabetes mellitus occurs in the early stages of liver disease.
机译：巨噬细胞活化似乎是慢性肝病的特征。作为巨噬细胞二级信号的鸟苷酸（PA）导致干扰素-γ-（IFN-Gamma-）巨噬细胞的激活，并触发细胞因子驱动的炎症反应。寻求慢性病毒性肝炎中PA形成增加的基础是基于活化巨噬细胞在慢性病毒性肝炎相关炎症中的参与。本研究的目的是确定慢性丙型肝炎感染患者的血清PA水平，考虑到糖尿病的存在。我们评估了PA和高敏感性C-反应性蛋白（HSCRP）作为51例慢性丙型肝炎感染（CHC）的炎症的标志物，无论是糖尿病和40个对照。与对照相比，CHC患者显示PA和HSCRP的血浆浓度显着增加（P <0.01和P <0.05，REAC。）。糖尿病患者的PA和HSCRP的值比没有糖尿病（P <0.01）患者更高。阳性关系在PA和HSCRP水平之间（P <0.05）和糖尿病的存在（P <0.00,1）。我们记录了血清PA水平的显着升高与糖尿病患病率和增加的炎症反应增加了CHC患者的HSCRP水平。丙型肝炎病毒（HCV）感染与各种脱毛表现有关，糖尿病是其中一种。慢性丙型肝炎感染患者（CHC）患有糖尿病具有独特且复杂的发病机制，其区分了来自2型糖尿病的这种代谢紊乱。在这方面，与其他肝脏疾病相比，HCV感染患者患有高患糖尿病患者。 Mehta等。据报道，预先存在的HCV感染可能会增加患有认可糖尿病患者患者的2型糖尿病的风险。慢性丙型肝炎感染诱导胰岛素抵抗力增加的机制。糖尿病发展风险尚未完全阐明。已经观察到，2型糖尿病发生在肝脏疾病的早期阶段。

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