Anemie emolitiche da anomalie ereditarie dell'Hb.

Abstract

SUMMARYNew researches have made it evident that besides the two normal Hb, the adult one (a) and the phoetal (f), there are other pathologic Hb:c, e, s, d, g, h, i.These Hb, excepting theh, are present in the hetherozygote on every healthy person and in the homozygote, excepting thegHb, determine chronic hemolitic anemia.ThefHb, or a very similar Hb, is present in the Thalassemia minor and major, in some homozygote cases of abnormal Hb, in the interreaction between two different genes of these Hb, or between one of these genes with the one of Thalassemia.We may retain that the genesa, c, s, d, e, g, i, form an allelomorphic series. The geneThis not a part of this series.Since in the homozygotesss, cc(in absence of the genea) the quantity of abnormal Hb does not always reach the same percentage, we may logically retain that the different quantity of abnormal Hb possessed by thesandchetherozygotes depends from the different synthetic capacity of the genes of the two abnormal Hb. The appareance offHb may be the expression of a phenomenon of physiopatological compensation, which occurs when Hbaformation is prevented.