Smillie D
Histocompatibility Laboratory, National Blood Service (Trent Centre), Sheffield, UK.
Mol Pathol. 1998 Aug;51(4):232-3. doi: 10.1136/mp.51.4.232.
Hereditary haemochromatosis is an autosomal recessive disease in which there is defective regulation of iron absorption, causing gradual accumulation of excessive amounts of iron in certain organs. Recently, a candidate gene for hereditary haemochromatosis has been identified, located on the short arm of chromosome 6, telomeric to the major histocompatibility complex (MHC) and showing sequence homology to the human leucocyte antigen (HLA) class I genes. Two mutations have been found in this gene that are potential markers for haemochromatosis. The first, a cysteine to tyrosine substitution (Cys282Tyr) is strongly associated with the disease, whereas the second mutation, a histidine to aspartic acid substitution (His63Asp) shows a less obvious relation. To examine the importance of this second mutation in hereditary haemochromatosis it is important to study the links between this genotype and abnormalities of iron metabolism. A polymerase chain reaction method using sequence specific primers is described which might be useful for identifying those individuals carrying the mutation that encodes the His63Asp substitution, who might be at risk from a milder form of haemochromatosis.
遗传性血色素沉着症是一种常染色体隐性疾病,其铁吸收调节存在缺陷,导致特定器官中过量铁逐渐积累。最近,已确定遗传性血色素沉着症的一个候选基因,位于6号染色体短臂上,在主要组织相容性复合体(MHC)的端粒位置,并且与人类白细胞抗原(HLA)I类基因具有序列同源性。在该基因中发现了两个突变,它们是血色素沉着症的潜在标志物。第一个突变是半胱氨酸到酪氨酸的替换(Cys282Tyr),与该疾病密切相关,而第二个突变是组氨酸到天冬氨酸的替换(His63Asp),其关联不太明显。为了研究这第二个突变在遗传性血色素沉着症中的重要性,研究该基因型与铁代谢异常之间的联系很重要。本文描述了一种使用序列特异性引物的聚合酶链反应方法,该方法可能有助于识别携带编码His63Asp替换突变的个体,这些个体可能面临症状较轻的血色素沉着症风险。