Bacon B R, Fried M W, DiBisceglie A M
Department of Internal Medicine, St. Louis University School of Medicine, MO 63110-0250.
Semin Liver Dis. 1993 Feb;13(1):101-5. doi: 10.1055/s-2007-1007342.
The patient described is a heterozygote for hemochromatosis, and he has chronic hepatitis C. We have hypothesized that, because of chronic viral hepatitis, he could either have an increase in circulating NTBI or he could have up-regulation of hepatocyte TfR expression, perhaps caused by a viral effect on the IRE of TfR mRNA, or a combination of both. Either could result in an increase of his hepatocellular iron uptake, resulting in a redistribution of his total body iron burden (which is in the range seen for HHC heterozygotes) and, in effect, "concentrating" the iron in his liver, thus simulating homozygous HHC. It is likely that there are interrelationships between hepatic iron concentration, hepatocellular iron metabolism, and chronic viral hepatitis. Understanding of these interrelationships may be important in the understanding of some of the fundamental mechanisms of viral growth and replication and hepatocellular injury. A clearer understanding of these interactions is necessary to diagnose the cause of liver disease accurately in patients such as this one.
所述患者是血色素沉着症的杂合子，且患有慢性丙型肝炎。我们推测，由于慢性病毒性肝炎，他可能循环中非转铁蛋白结合铁（NTBI）增加，或者肝细胞转铁蛋白受体（TfR）表达上调，这可能是病毒对TfR mRNA的铁反应元件（IRE）产生影响所致，也可能是两者共同作用的结果。任何一种情况都可能导致其肝细胞铁摄取增加，从而使他全身铁负荷重新分布（处于血色素沉着症杂合子所见范围内），实际上是将铁“集中”在肝脏中，进而模拟纯合子血色素沉着症（HHC）。肝铁浓度、肝细胞铁代谢和慢性病毒性肝炎之间可能存在相互关系。了解这些相互关系对于理解病毒生长复制和肝细胞损伤的一些基本机制可能很重要。更清楚地了解这些相互作用对于准确诊断此类患者的肝病病因是必要的。
