Vatsalya Vatsalya, Agrawal Ruchita, Frimodig Jane, Srivastava Shweta, Schwandt Melanie L
Department of Medicine, University of Louisville, Louisville, KY, USA.
Robley Rex VA Medical Center, Louisville, KY, USA.
Adv Virol. 2020 Jun 9;2020:7835875. doi: 10.1155/2020/7835875. eCollection 2020.
Alcohol use disorder (AUD) patients comorbid with hepatitis C virus (HCV) infection (HCV + AUD) could have progressively severe clinical sequels of liver injury and inflammation. Serum zinc and several polyunsaturated fatty acids (PUFAs) get dysregulated in AUD as well as HCV. However, the extent of dysregulation of PUFAs and zinc deficiency and their interaction in HCV + AUD as a comorbid pathology has not been studied. We examined the role of dysregulation of FAs and low zinc in HCV + AUD patients. 138 male and female participants aged 21-67 years were grouped as HCV-only (Gr. 1; = 13), HCV + AUD (Gr. 2; = 25), AUD without liver injury (Gr. 3; = 37), AUD with liver injury (Gr. 4; = 51), and healthy volunteers (Gr. 5 or HV; = 12). Drinking history, individual demographic measures, fasting fatty acids, liver function, and zinc were measured and analyzed. HCV + AUD patients showed the highest ALT level compared to the rest of the groups. Serum zinc concentrations were the lowest, and the proinflammatory shift was the highest (characterized by 6 : 3 ratio) in the HCV + AUD patients. Total 3, eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA5,3) were the lowest in HCV + AUD patients. Total 3, -linoleic acid (-LA) along with covariable number of drinking days past 90 days (NDD90), eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA5,3) independently showed significant association with low zinc in the HCV + AUD patients. Heavy drinking pattern showed that NDD90 has a significant mediating role in the representation of the relationship between candidate 3 PUFAs and zinc uniquely in the HCV + AUD patients. Low serum zinc showed a distinctively stronger association with total and candidate 3s in the HCV + AUD patients compared to the patients with HCV or AUD alone, supporting dual mechanism involved in the exacerbation of the proinflammatory response in this comorbid cohort. This trial is registered with NCT#00001673.
酒精使用障碍(AUD)合并丙型肝炎病毒(HCV)感染(HCV+AUD)的患者可能会出现逐渐严重的肝损伤和炎症临床后果。在AUD以及HCV患者中,血清锌和几种多不饱和脂肪酸(PUFA)会出现失调。然而,PUFA失调的程度、锌缺乏及其在HCV+AUD作为一种共病病理中的相互作用尚未得到研究。我们研究了脂肪酸失调和低锌在HCV+AUD患者中的作用。138名年龄在21至67岁之间的男性和女性参与者被分为仅HCV组(第1组;n=13)、HCV+AUD组(第2组;n=25)、无肝损伤的AUD组(第3组;n=37)、有肝损伤的AUD组(第4组;n=51)和健康志愿者组(第5组或HV组;n=12)。测量并分析了饮酒史、个人人口统计学指标、空腹脂肪酸、肝功能和锌。与其他组相比,HCV+AUD患者的ALT水平最高。HCV+AUD患者的血清锌浓度最低,促炎转变最高(以6:3比例为特征)。HCV+AUD患者的总ω-3、二十碳五烯酸(EPA)和二十二碳五烯酸(DPA5,3)最低。总ω-3、γ-亚油酸(γ-LA)以及过去90天的饮酒天数变量(NDD90)、二十碳五烯酸(EPA)和二十二碳五烯酸(DPA5,3)在HCV+AUD患者中独立显示出与低锌有显著关联。重度饮酒模式表明,NDD90在HCV+AUD患者中独特地代表了候选ω-3多不饱和脂肪酸与锌之间关系的显著中介作用。与仅患有HCV或AUD的患者相比,低血清锌在HCV+AUD患者中与总ω-3和候选ω-3的关联明显更强,这支持了该共病队列中促炎反应加剧所涉及的双重机制。该试验已在NCT#00001673注册。