de Almeida Jorge P Sales, Liberatti Lucas Silva, Barros Fernanda Esteves Nascimento, Kallaur Ana Paula, Lozovoy Marcell A Batisti, Scavuzzi Bruna Miglioranza, Panis Carolina, Reiche Edna Maria V, Dichi Isaias, Simão Andréa Name Colado
Department of Pathology, Clinical Analysis and Toxicology, Health Sciences Center, University of Londrina, Paraná, Brazil.
Department of Infectology, Health Sciences Center, University of Londrina, Londrina, Brazil.
Nutrition. 2016 Mar;32(3):362-7. doi: 10.1016/j.nut.2015.09.016. Epub 2015 Nov 12.
Although vitamin D deficiency can change liver injury progression in patients with hepatitis C virus (HCV), the main molecular mechanisms involved are largely unknown. The first aim of this study was to evaluate the association between oxidative stress and hypovitaminosis D in patients with HCV. The second aim was to verify whether oxidative stress is involved in the molecular mechanisms related to liver injury.
The study included 147 participants: 89 controls and 58 patients with HCV (vitamin D < 30, n = 32; vitamin D > 30, n = 26).
Patients with HCV and hypovitaminosis D presented significantly higher aminotransferase-to-platelet ratio index (APRI; P = 0.0464) and viral load (P = 0.0426) levels than patients with HCV without hypovitaminosis D. Regarding oxidative stress, HCV patients with hypovitaminosis D had higher advanced oxidation protein products (P = 0.0409), nitric oxide metabolites (P = 0.0206) levels, and oxidative stress index (P = 0.0196), whereas total radical-trapping antioxidant parameter (P = 0.0446) levels were significantly lower than HCV patients without hypovitaminosis D. Vitamin D in patients with HCV showed inverse correlations with levels of iron (r = -0.407, P = 0.0285), ferritin (r = -0.383, P = 0.0444), APRI (r = -0.453, P = 0.0154) and plasma lipid hydroperoxides levels (r = -0.426, P = 0.0189).
Vitamin D insufficiency contributes to the inflammatory process and oxidative stress imbalance in patients with HCV. The profile of oxidative stress markers in these patients depends on vitamin D levels, which probably change intracellular signalling pathways and increase inflammation and liver injury.
尽管维生素D缺乏可改变丙型肝炎病毒(HCV)患者的肝损伤进程,但其中主要的分子机制仍大多未知。本研究的首要目的是评估HCV患者氧化应激与维生素D缺乏之间的关联。第二个目的是验证氧化应激是否参与了与肝损伤相关的分子机制。
本研究纳入了147名参与者:89名对照者和58名HCV患者(维生素D<30,n = 32;维生素D>30,n = 26)。
与无维生素D缺乏的HCV患者相比,HCV合并维生素D缺乏的患者转氨酶与血小板比值指数(APRI;P = 0.0464)和病毒载量(P = 0.0426)水平显著更高。关于氧化应激,HCV合并维生素D缺乏的患者具有更高的晚期氧化蛋白产物(P = 0.0409)、一氧化氮代谢产物(P = 0.0206)水平和氧化应激指数(P = 0.0196),而总自由基捕获抗氧化参数(P = 0.0446)水平显著低于无维生素D缺乏的HCV患者。HCV患者体内的维生素D水平与铁(r = -0.407,P = 0.0285)、铁蛋白(r = -0.383,P = 0.0444)、APRI(r = -0.453,P = 0.0154)和血浆脂质氢过氧化物水平(r = -0.426,P = 0.0189)呈负相关。
维生素D不足会导致HCV患者的炎症过程和氧化应激失衡。这些患者氧化应激标志物的情况取决于维生素D水平,这可能会改变细胞内信号通路并加重炎症和肝损伤。