Pomacu Mihnea Marian, Trașcă Diana Maria, Pădureanu Vlad, Stănciulescu Elena Camelia, Busuioc Cristina Jana, Pisoschi Cătălina Gabriela, Bugă Ana Maria
PhD Doctoral School, University of Medicine and Pharmacy of Craiova.
4thDepartment of Medical Specialties, University of Medicine and Pharmacy of Craiova.
Curr Health Sci J. 2023 Jan-Mar;49(1):54-66. doi: 10.12865/CHSJ.49.01.54. Epub 2023 Mar 31.
In this study we investigated the relationship between vitamin D and markers of oxidative stress and apoptosis in patients with liver cirrhosis stratified according serum GGT activity. Forty-eight patients with liver cirrhosis of various aetiology were selected, among which 58% cases (n=28) diagnosed with alcoholic liver cirrhosis and 42% (n=20) with cirrhosis after hepatitis virus infection. Each group was divided into three quartiles according GGT activity. 25-hydroxyvitamin D [25-(HO) vit D], markers of oxidative stress (catalase, superoxide dismutase) and apoptosis (M30) were compared. Higher levels of GGT were correlated with elevated AST, ALT and ALP values in both groups. A statistically significant difference was observed when comparing 25-(OH) vit D levels of patients suffering from ethanol-induced liver cirrhosis versus control group for all the quartiles as well as for those from the first quartile of viral-induced liver cirrhosis. For SOD, statistically significant differences were noticed between all cirrhosis subgroups and the control group. CAT values in all cirrhosis subgroups were lower than in control, but significant differences were only between Q2.2 and Q1.3 quartiles and Q2.2 and control. Correlation of 25-(OH) vit D versus SOD yields statistically significant results in ethanol-induced cirrhosis patients. M30 activity was increased in patients with alcoholic cirrhosis compared to controls and those with virus-induced cirrhosis, being correlated with the degree of GGT activity. Our results emphasized that vitamin D deficiency is associated with enhanced liver dysfunction regardless of the trigger responsible for disease onset. Furthermore, vitamin D deficiency augments liver injury by promoting oxidative stress which influence the survival mechanisms of parenchymal liver cells.
在本研究中,我们调查了根据血清γ-谷氨酰转移酶(GGT)活性分层的肝硬化患者中维生素D与氧化应激和细胞凋亡标志物之间的关系。选取了48例不同病因的肝硬化患者,其中58%(n = 28)为酒精性肝硬化,42%(n = 20)为肝炎病毒感染后肝硬化。根据GGT活性将每组分为三个四分位数。比较了25-羟维生素D [25-(OH) vit D]、氧化应激标志物(过氧化氢酶、超氧化物歧化酶)和细胞凋亡标志物(M30)。两组中较高的GGT水平均与AST、ALT和ALP值升高相关。在比较乙醇性肝硬化患者与对照组所有四分位数以及病毒诱导性肝硬化第一四分位数患者的25-(OH) vit D水平时,观察到统计学上的显著差异。对于超氧化物歧化酶(SOD),所有肝硬化亚组与对照组之间均存在统计学上的显著差异。所有肝硬化亚组的过氧化氢酶(CAT)值均低于对照组,但仅在第二四分位数的2.2与第一四分位数的1.3以及第二四分位数的2.2与对照组之间存在显著差异。在乙醇诱导的肝硬化患者中,25-(OH) vit D与SOD的相关性产生了统计学上的显著结果。与对照组和病毒诱导性肝硬化患者相比,酒精性肝硬化患者的M30活性增加,且与GGT活性程度相关。我们的结果强调,无论导致疾病发生的触发因素如何,维生素D缺乏都与肝功能障碍的加重有关。此外,维生素D缺乏通过促进氧化应激加重肝损伤,而氧化应激会影响肝实质细胞的存活机制。