Van Steenbergen W, Matthijs G, Roskams T, Fevery J
Dienst Inwendige Geneeskunde, Afdeling Leverziekten, Universitair Ziekenhuis Gasthuisberg Katholieke Universiteit Leuven 3000 Leuven, België.
Acta Clin Belg. 2002 Mar-Apr;57(2):79-84. doi: 10.1179/acb.2002.018.
The discovery of the gene responsible for most cases of hereditary haemochromatosis has made it possible to evaluate the role of this gene in iron accumulation in other conditions. Previous observations in patients with various inherited anaemias are suggestive of a role of the haemochromatosis gene in the noniatrogenic form of iron overload that may occur in these conditions.
We studied two brothers with congenital dyserythropoietic anaemia type II, presenting with marked noniatrogenic iron overload. Young age, familial occurrence, concordance of iron overload, and histology were all suggestive of a genetic basis for the iron overload. A search for C282Y, H63D, S65C, and IVS3 + 1G?T mutations was performed by polymerase chain reaction after extraction of genomic DNA from whole blood.
A search for the C282Y, H63D, S65C, and IVS3 + 1G?T mutations in the HFE gene proved to be negative. Despite the existence of ineffective erythropoiesis with mild anaemia, both patients were treated with regular phlebotomies in order to prevent long-term complications of their iron-overload. This treatment was well tolerated.
导致大多数遗传性血色素沉着症病例的基因已被发现,这使得评估该基因在其他病症铁蓄积中的作用成为可能。先前对各种遗传性贫血患者的观察提示血色素沉着症基因在这些病症可能出现的非医源性铁过载形式中发挥作用。
我们研究了两名患有II型先天性红细胞生成异常性贫血的兄弟,他们表现出明显的非医源性铁过载。年轻、家族性发病、铁过载的一致性以及组织学均提示铁过载存在遗传基础。从全血中提取基因组DNA后,通过聚合酶链反应对C282Y、H63D、S65C和IVS3 + 1G?T突变进行检测。
对HFE基因中的C282Y、H63D、S65C和IVS3 + 1G?T突变检测结果为阴性。尽管存在无效红细胞生成并伴有轻度贫血,但为预防铁过载的长期并发症,两名患者均接受了定期放血治疗。这种治疗耐受性良好。