THE SCIENCE AND ART OF PROTEAL THERAPY 215 



urates occur here, with the gradual development of the char- 

 acteristic malformations of chronic arthritis. 



There is nothing in these end-product deposits to give new 

 stimulus to the mother-cells of the leucocyte. The case is differ- 

 ent, however, with an individual, who, with the same aetiological 

 conditions, as to protein invasion, has an hereditary predisposi- 

 tion to hyperplasia of cells under stimulus of a local irritation 

 which may lead to the development of a malignant neoplasm. 



I have elsewhere developed the thesis (see the Monograph) 

 that the essential characteristic of malignancy in a neoplasm 

 is that its cells are more or less subject to proteolysis by the 

 corpuscular enzymes. According to this view, the cancer cells, 

 in thus undergoing hydrolysis, stimulate the blood-forming mech- 

 anisms and lead thus to leucocytosis, and in particular to large 

 monocytosis. Whether the sequel will show complete hydrolysis 

 and elimination of the cancer cells or not depends upon the per- 

 sistence of the local irritative stimulus, the degree of develop- 

 ment of the cancer cells themselves, the responsiveness of the 

 blood-forming mechanism, and other factors that do not here 

 concern us. What is here significant is that one does, in point 

 of fact, find a leucocytosis, and a relative monocytosis, as the 

 almost constant accompaniment of a cancerous invasion; and 

 that the stimulus given by the disintegrating cancer cells them- 

 selves may be supposed adequately to explain the condition, in 

 contrast with the leucopcenia of the arthritic patient who lacks 

 this stimulus. But I repeat that, could we have seen the arthritic 

 patient at an earlier stage, we should probably have found that 

 the protein invasion (usually from the intestines) had produced 

 a leucocytosis that long persisted before exhaustion of the cyto- 

 genic mechanism came about. In substantiation of this view, we 

 not infrequently find a leucocytosis, and in particular a notable 

 large monocytosis, present in young individuals suffering from 

 intestinal toxaemia, in whom the cytogenic apparatus is still re- 

 sponsive. Moreover, such an increase has been observed in cases 

 of intestinal toxaemia that have not undergone proteal treatment ; 

 although in other cases of this type (as above noted) the large 

 monocyte count is low. 



Here, for example, is a man of 26, who has suffered all his 

 life from intestinal toxaemia. So poor is his assimilation that, 

 even when in best condition, he is almost skeletal, carrying no 

 excess avoirdupois whatever. His stomach is his perpetual en- 

 emy. His differential count shows 50 per cent, polynuclears, 

 34.3 per cent, small lymphocytes, 22 per cent, large mononuclears, 

 and 0.6 per cent, eosinophiles. It is observed that the small 

 lymphocytes are mostly relatively large and with abundant cyto- 

 plasm, so that one is constantly tempted to classify them as large 



