THE SCIENCE AND ART OF PROTEAL THERAPY 201 



which the white corpuscle has ingested. It will be recalled that, 

 according to Van't Hoff's theory, each individual molecule, what- 

 ever its size, presses with equal force in a liquid medium. If, 

 then, in a given case, a leucocyte has ingested a large quantity 

 of protein, the decompounding of this protein might produce a 

 sufficient number of molecules, at, let us say, the proteose stage 

 to exert a disruptive force on the leucocytic membrane ; whereas, 

 had the amount of protein originally ingested been smaller, 

 decompounding to the peptone stage might have been necessary 

 before an equivalent pressure was exerted. 



If this suggestion be accepted, it follows that, given a fixed 

 quantity of protein papulum in the blood, the larger the number 

 of leucocytes the smaller would be their average intake of protein, 

 and hence the more complete the average stage of decompound- 

 ing before disruption. In other words, the larger the number of 

 leucocytes, the more efficient their work as protein hydrolyzers. 

 Where a small number of leucocytes must have turned over their 

 product to the red corpuscles at the peptone stage, a larger num- 

 ber of leucocytes may reduce it all to the polypeptid stage, and 

 thus, seemingly, conserve the resources of the red corpuscles by 

 limiting the work put upon them. 



If such are indeed the relations of white and red corpuscles, 

 and the hypothesis just suggested be accepted as plausible, a high 

 leucocyte count such as that recorded in the case of the patient 

 above reported (57,000) must be accepted as a salutary attempt 

 on the part of the organism to compensate for the inadequacy 

 of the red corpuscles, indicated not only by their small number 

 (3,850,000) but also by their extreme defects of size and quality. 

 This was a case, seemingly, where chronic intestinal defects of 

 secretion of the digestive enzymes (pancreatic, biliary, or enteric) 

 persistently led to the introduction into the blood of protein 

 products not hydrolyzed to the normal polypeptid or amino-acid 

 stage. This put an incessant strain on the red corpuscles, which 

 probably (could the full history of the case be known) were for 

 a time increased in number, but which ultimately, owing to ex- 

 haustion of the blood-forming mechanism through long sub- 

 jection to the same toxin, . became decreased in number and 

 utterly dyscrasic in quality. 



Then came the increase of white corpuscles to endeavor to 

 compensate the defects of the red cells. The white cells would 

 accomplish this, according to hypothesis, by handling as effec- 

 tively as possible the larger protein molecules normally or 

 abnormally present in the blood. If, however, the intermediate 

 and later products of hydrolysis continue to intrude themselves 

 in excessive quantities, the strain on the blood corpuscles would 

 be cumulative, and even though the white corpuscles were pro- 



