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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