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e remarked, is still far from full, we may assume that lymphatic and myelogenous leukaemia have quite a different aetiology. The recent discovery of Loewit should be decisive on this point, for he demonstrated in myelogenic leukaemia the presence of forms like plasmodia within the white blood corpuscles, but was unable to find them in lymphatic leukaemia. The necessity of separating lymphatic from myelogenic leukaemia is further shewn by the fundamental clinical differences between them. ~Lymphatic leukaemia~ falls clinically into two readily distinguishable forms. In the first place acute lymphatic leukaemia, characterised by its rapid course, the small splenic tumour, the tendency to petechiae and to the general haemorrhagic diathesis. By its startling course this disease has given all observers the impression of an acute infectious process. The second form of lymphatic leukaemia is marked off from the preceding by its chronic, and often very protracted course. The spleen shews its participation in the disease, as a rule by very considerable enlargement. We have at present no investigations adequate to decide whether chronic lymphatic leukaemia represents a single disease, or should be etiologically subdivided. Haematologically, all lymphatic leukaemias are characterised by a great preponderance of lymph cells, in particular of the larger varieties. It should here be expressly mentioned, that richness of the blood in large lymph cells, is by no means characteristic of the acute form of leukaemia, for chronic, very slowly progressing cases shew the same condition. Thus in a case of this kind under observation in Gerhardt's wards, all observers (Grawitz, v. Noorden, Ehrlich) found the large cells during its whole course. In agreement with our remarks elsewhere (see p. 104), we assume with regard to the origin of lymphatic leukaemia, =that the increase of the lymph cells is brought about by a passive inflow into the blood; and not by an active emigration from chemical stimuli=. ~Myelogenic leukaemia~ presents a picture that is different in every particular. In former years the distinction between myelogenic leukaemia and simple leucocytosis offered great difficulties. These conditions were regarded as different stages of one and the same pathological process, and when the proportion of white to red corpuscles exceeded a certain limit (1:50) it was said that leucocytosis ceased, and leukaemia began. By the aid of t
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