Critical review : polycythaemia, erythrocytosis and erythraemia.

  • Weber, Frederick Parkes, 1863-1962.
Date:
1908
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Licence: In copyright

Credit: Critical review : polycythaemia, erythrocytosis and erythraemia. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    a long bone (‘biopsy’ method). The results of this excessive erythroblastic activity of the bone-marrow may be compared to what would be the consequences of persistent slow transfusion of blood into the veins of an animal. Experimental sudden transfusion of blood in animals (von Lesser, Worm-Muller) leads to temporary plethora followed quickly by polycythaemia, and it is reasonable to suppose that a slow transfusion of blood, lasting not for a few minutes only but for months and years (were it possible from the experimental point of view), wrould give rise to a condition of persistent absolute polycythaemia associated with true plethora, such as is met with in cases of erythraemia (see Part I, sections on the Cause of Absolute Polycythaemia and on the Blood-Yolume in Absolute Polycythaemia). Dilatation of capillaries and venules would necessarily follow, and probably in most cases, for a time at least, there would be increased arterial blood-pressure. Ultimately degenerative changes in the vascular system would be likely to occur, leading to true passive congestion, cyanosis, bleeding from the gums, thrombosis in various organs, and local circulatory disorders. The excess of the total erythroblastic activity in cases of erythraemia may be supposed to be the primary change giving rise to the clinical symptoms. It may be regarded as analogous to the increased leucoblastic activity in leukaemia, or as a return of the marrow to the condition of foetal activity. In a few cases it appears as if the bone-marrow had never lost its foetal characteristics, and as if the polycythaemia was the result of this ‘infantile’ (or rather ‘foetal’) condition of the blood-forming organ (see Blumenthal’s case and other cases of polycythaemia commencing in early life—in Appendix A and Appendix B). That increased leucoblastic activity nearly always accompanies the increased erythroblastic activity in the bone-marrow is evidenced during life by the usually large number of white corpuscles, especially polymorphonuclears, and by the occasional presence of myelocytes, in the circulating blood. At necropsies the examination of the marrow of the shafts of long bones has shown that a decided increase of leucoblastic tissue (see Appendix A, Nos. 12, 22) does accompany the increase of erythroblastic tissue, and probably in most cases the leucoblastic elements occupy more space in the bone-marrow than the erythroblastic elements do. This feature of the bone-marrow seems to have been exaggerated in Blumenthal’s case (Appendix A, 15), in which during life 36 per cent, of the white cells of the blood were found to be myelocytes; after death the leuco- blastic elements of the bone-marrow were found very greatly to exceed the erythroblastic elements. In fact, Blumenthal’s case appears almost to represent a link in a chain, which future observations may discover, connecting erythraemia with myelocytic (myeloid) leukaemia. We fully expect in the future to read of cases showing conditions of the blood and bone-marrow more or less similar to those in Blumenthal’s case described as examples of ‘ Blumenthal’s disease’. It is not quite clear why in erythraemia more of the bone-marrow should consist of leucoblastic than of erythroblastic elements. I think the most probable explanation is that in the marrow of these patients (and probably also in that of healthy individuals) the red cells are much more rapidly produced than are the