Zinc in liver disease

K. Grüngreiff
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引用次数: 20

Abstract

The essentiality of zinc for humans was first documented by Prasad in the 1960s. During the past 35 years, zinc deficiency in humans a result of nutritional factors and several disease states has been recognized. Many of the clinical features of liver cirrhosis have been linked to zinc deficiency, including loss of body hair, testicular atrophy, poor appetite, immune dysfunction, altered taste and smell, reduced vitamin A and thyroid hormone metabolism, altered protein metabolism, delayed wound healing, and diminished drug elimination capacity. One of the most interesting and novel aspects concerning the presumable role of zinc deficiency in producing clinical features of liver cirrhosis is the possible relationship between zinc and hepatic encephalopathy (HE). Long-term zinc supplementation in patients with HE improves neurological symptoms and metabolic parameters. In Wilson's disease, an inherited defect of hepatic copper, zinc is used for maintenance as well as treating presymptomatic, pregnant, and pediatric patients. Zinc may be involved in the pathogenesis of chronic hepatitis C. This work is an attempt to review the information available in this field to understand the important role that zinc plays in the pathogenesis and therapy of several liver diseases. J. Trace Elem. Exp. Med. 15:67–78, 2002. © 2002 Wiley-Liss, Inc.
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肝病中的锌
普拉萨德在20世纪60年代首次记录了锌对人类的重要性。在过去的35年里,人们已经认识到,人类缺锌是营养因素和几种疾病状态的结果。肝硬化的许多临床特征与缺锌有关,包括体毛脱落、睾丸萎缩、食欲不佳、免疫功能障碍、味觉和嗅觉改变、维生素A和甲状腺激素代谢降低、蛋白质代谢改变、伤口愈合延迟和药物消除能力下降。关于锌缺乏在肝硬化临床特征产生中的可能作用,最有趣和最新颖的方面之一是锌与肝性脑病(HE)之间的可能关系。HE患者长期补充锌可改善神经系统症状和代谢参数。Wilson病是一种遗传性肝脏铜缺陷,锌用于维持和治疗症状前、孕妇和儿童患者。锌可能参与慢性丙型肝炎的发病机制。这项工作试图综述该领域的现有信息,以了解锌在几种肝病的发病机制和治疗中的重要作用。J.Trace Elem。Exp.Med.15:67-782002。©2002 Wiley-Liss,股份有限公司。
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International Society For Trace Element Research In Humans (ISTERH) Seventh International Conference, Bangkok, Thailand, November 7–12, 2004 Response† Erratum Fluoride: A toxic or therapeutic agent in the treatment of osteoporosis? Interleukin-1α, tumor necrosis factor-α, and interleukin-12 secreted by zinc-induced murine macrophages in vivo and in vitro
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