Himoto Takashi, Hosomi Naoki, Nakai Seiji, Deguchi Akihiro, Kinekawa Fumihiko, Matsuki Michiko, Yachida Mikage, Masaki Tsutomu, Kurokochi Kazutaka, Watanabe Seishiro, Senda Shoichi, Kuriyama Shigeki
Department of Gastroenterology and Neurology, Kagawa University School of Medicine, Kagawa, Japan.
Scand J Gastroenterol. 2007 Sep;42(9):1078-87. doi: 10.1080/00365520701272409.
Zinc supplementation has been shown to contribute to inhibition of liver fibrosis and improvement in hepatic encephalopathy. However, little is known about the anti-inflammatory effect of zinc on hepatitis C virus (HCV)-related chronic liver disease (CLD). We therefore examined the effects of zinc administration on inflammatory activity and fibrosis in the liver of patients with HCV-related CLD.
Polaprezinc, a complex of zinc and l-carnosine, was administrated at 225 mg/day for 6 months to 14 patients with HCV-related CLD, in addition to their ongoing prescriptions. Peripheral blood cell counts, liver-related biochemical parameters, serological markers for liver fibrosis, HCV-RNA loads, and serum levels of zinc and ferritin were evaluated before and after zinc administration.
Serum zinc concentrations were positively correlated with hepatic reserve before zinc supplementation. A significant increase in serum zinc level was observed after zinc supplementation (64+/-15 versus 78+/-26 mg/dl, p=0.0156). Treatment with polaprezinc significantly decreased serum aminotransferase levels (aspartate aminotransferase (AST): 92+/-33 versus 63+/-23 IU/l, p=0.0004; alanine aminotransferase (ALT): 106+/-43 versus 65+/-32 IU/l, p=0.0002), whereas alkaline phosphatase levels were significantly increased (305+/-117 versus 337+/-118 U/l, p=0.0020). Serum ferritin levels were significantly decreased by treatment with polaprezinc (158+/-141 versus 101+/-80 ng/ml, p=0.0117). The reduction rate of ALT levels by polaprezinc was positively correlated with that of ferritin (r(2)=0.536, p=0.0389). There was a tendency toward a decrease in serum type IV collagen 7S levels after treatment with polaprezinc. However, administration of polaprezinc did not affect peripheral blood cell counts, other liver function tests, or HCV-RNA loads.
These findings suggest that polaprezinc exerts an anti-inflammatory effect on the liver in patients with HCV-related CLD by reducing iron overload.
已表明补充锌有助于抑制肝纤维化和改善肝性脑病。然而,关于锌对丙型肝炎病毒(HCV)相关慢性肝病(CLD)的抗炎作用知之甚少。因此,我们研究了锌给药对HCV相关CLD患者肝脏炎症活性和纤维化的影响。
除正在进行的处方治疗外,对14例HCV相关CLD患者给予聚普瑞锌(一种锌与L-肌肽的复合物),剂量为225mg/天,持续6个月。在锌给药前后评估外周血细胞计数、肝脏相关生化参数、肝纤维化血清标志物、HCV-RNA载量以及锌和铁蛋白的血清水平。
补充锌之前,血清锌浓度与肝脏储备呈正相关。补充锌后血清锌水平显著升高(64±15对78±26mg/dl,p=0.0156)。聚普瑞锌治疗显著降低血清转氨酶水平(天冬氨酸转氨酶(AST):92±33对63±23IU/l,p=0.0004;丙氨酸转氨酶(ALT):106±43对65±32IU/l,p=0.0002),而碱性磷酸酶水平显著升高(305±117对337±118U/l,p=0.0020)。聚普瑞锌治疗使血清铁蛋白水平显著降低(158±141对101±80ng/ml,p=0.0117)。聚普瑞锌使ALT水平的降低率与铁蛋白的降低率呈正相关(r²=0.536,p=0.0389)。聚普瑞锌治疗后血清IV型胶原7S水平有下降趋势。然而,聚普瑞锌给药不影响外周血细胞计数、其他肝功能检查或HCV-RNA载量。
这些发现表明,聚普瑞锌通过减少铁过载对HCV相关CLD患者的肝脏发挥抗炎作用。