Galanello R, Pirastu M, Melis M A, Paglietti E, Moi P, Cao A
J Med Genet. 1983 Dec;20(6):425-9. doi: 10.1136/jmg.20.6.425.
In this study we used restriction endonuclease mapping to characterise the molecular defect responsible for haemoglobin H disease in 14 Sardinian children. The resulting genotypes were then correlated with the respective clinical and haematological phenotypes. We found that patients with the combination of non-deletion alpha(+)-thalassaemia [(alpha alpha)th] and deletion alpha(0)-thalassaemia (-Med) have a more severe phenotype than that resulting from the interaction of deletion alpha(0)-thalassaemia (-Med) and alpha(+)-thalassaemia (-alpha) determinants. Clinically, presentation was earlier and with moderate anaemia or haemolytic crisis, enlargement of the liver and spleen, and thalassaemic bone changes. Haematologically, the anaemia was more severe and there were higher bilirubin levels, reticulocyte counts, Hb H levels, and percentage of red blood cells with inclusion bodies. These results suggest that in those Hb H disease patients with the non-deletion [(alpha alpha)th] determinant, two alpha globin genes produce fewer alpha globin chains than a single alpha globin locus.
在本研究中,我们使用限制性内切酶图谱分析来鉴定14名撒丁岛儿童中导致血红蛋白H病的分子缺陷。然后将所得基因型与各自的临床和血液学表型进行关联。我们发现,非缺失型α(+) -地中海贫血[(αα)th]与缺失型α(0) -地中海贫血(-Med)组合的患者,其表型比缺失型α(0) -地中海贫血(-Med)与α(+) -地中海贫血(-α)决定簇相互作用产生的表型更严重。临床上,发病更早,伴有中度贫血或溶血危象、肝脾肿大以及地中海贫血性骨改变。血液学方面,贫血更严重,胆红素水平、网织红细胞计数、Hb H水平以及有包涵体的红细胞百分比更高。这些结果表明,在那些具有非缺失[(αα)th]决定簇的血红蛋白H病患者中,两个α珠蛋白基因产生的α珠蛋白链比单个α珠蛋白基因座产生的要少。