Volume 1

The haemolytic anaemias, congenital and acquired / by J.V. Dacie.

  • Dacie, John V. (John Vivian), Sir.
Date:
1960-1967
Catalogue details

Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

Credit: The haemolytic anaemias, congenital and acquired / by J.V. Dacie. Source: Wellcome Collection.

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    According to Crosby (1952), William Hunter, of London, was the first to coin and to use the term “haemolytic.” In his book Pernicious Ancemia, published in 1901, Hunter referred to the presence of yellow 1 spherical microcytes (Eichhorst’s corpuscles) in pernicious anaemia. He wrote (p. 67): “My experiments shew that similar bodies can be produced artificially by action of destructive agents; that they mark the anaemia as due to excessive destruction of blood and not to deficient formation, that they denote the anaemia to be hcemolytic, not haemogenic, in its origin” [my italics]. Glassification. The classification of the haemolytic anaemias presents a number of difficulties, and no new or elaborate system will be presented in this work. A clinical classification into acute or chronic cases, primary or secondary cases, or into cases with or without haemoglobinuria, is of limited usefulness. Classifications according to aetiology or pathogenesis are also unsatisfactory, because often one or both are unknown or incompletely known. The classification adhered to in this book, in which a distinction is drawn between congenital and acquired cases, is orthodox: separation of the congenital haemolytic anaemias from the rest is based not only on the concept of a genetic cause but also on a distinct type of pathogenesis, the congenital haemolytic anaemias being the result of various intrinsic abnormalities of the erythrocyte, or of its haemoglobin, or are secondary to a definite genetically-controlled disorder of haemopoiesis. The acquired haemolytic anaemias are an even more mixed collection of anaemias of varied, and often unknown, causation. Some of them may have an as yet undetermined genetic basis, as has recently been established in certain drug-induced “acquired” haemolytic anaemias (see Chapter 15). Most of them, nevertheless, certainly depend upon pathological processes which affect normal erythrocytes as well as the patient’s corpuscles (extrinsic mechanism of haemolysis). Paroxysmal nocturnal haemoglobinuria appears to be unique in that there is no clear evidence for a genetic basis, yet the abnormality is one which seems to be intrinsic to the patient’s erythrocytes. This fascinating disease is dealt with in the penultimate chapter; it is followed by haemolytic disease of the newborn which is unique in a different way, being congenital and “acquired” (from the mother), yet not hereditary. The separation of the haemolytic anaemias into two main groups—those due to intrinsic defects of the erythrocyte and those due to mechanisms extrinsic to the cell—has been widely adopted, 1 1 As viewed unstained.