HEMOLYSIS l.\ DISKASE 225 



(Seo "Pisincntutioii," (hap. xviii.) Whoiicvcr (luring disca^; red 

 corpuscles arc more rapidly injured than they are under normal condi- 

 tions, these processes of normal hemolysis are exaggerated and we not 

 only find the phagocytic cells of the spleen and glands packed with 

 corpuscles, but endothelial cells elsewhere, and also leucocytes, take 

 on the hemolytic function. At the same tinie there results an exces- 

 sive production of bile-pigment from the destroyed red corpuscles, 

 which has an etiological relation to the so-called "hemato-hepatogen- 

 ous" jaundice. If hemolysis is very excessive, the blood pigment 

 accumulates in other organs than the liver and spleen. According to 

 Pearcc^^ and his associates, when the blood contains at one time more 

 than 0.06 gm. of free hemoglobin per kilo of body weight, it begins to 

 be excreted by the kidneys; smaller amounts are cared for chiefly 

 by the liver, and even when much larger amounts of hemoglobin are 

 present in the blood the liver takes care of most of it, only a rela- 

 tively small proportion, 17 to 36 per cent, being excreted in the urine. 

 Hence it is possible to have hemolytic jaundice without hemoglobin- 

 uria. Part of the pigment is converted into urobilin, and the amount 

 of this pigment in the stool is an index of the amount of hemolysis.-^ 

 In persons with hemolytic hemoglobinemia, intravenous injection of 

 hemoglobin will produce hemoglobinuria with smaller dosage than in 

 normal persons, who require at least 17 c.c. of laked corpuscles to pro- 

 duce hemoglobinuria.-^ 



It is possible that the globin, which is quite toxic when free,'^ may 

 play a part in the symptomatology of hemolytic poisons. The stroma 

 of the erythrocytes also seems to be toxic. ^^ 



The hemolj^sis of the acute febrile diseases is readily explained by the 

 demonstrable hemolytic property of the products of the organisms 

 that cause them, such as streptocolysin, staphylolysin, etc. Perhaps 

 at the same time products of altered metabolism may also play a 

 part, but it does not seem probable from experimental results that 

 the thermic condition per se has much effect. In malaria, although 

 the parasites enter and destroy the corpuscles in which they live, yet 

 this alone does not account for all the blood destruction of the disease, 

 for the amount of anemia is quite without relation to the number 

 of parasites to be found. There is good reason to believe that the 

 Plasmodia produce hemolytic substances that are chschargcd into the 

 serum. 



In the primary anemias hemolj^sis seems to be the essential process, 

 although the agents involved are at present unknown. Absorption 

 of hemolytic products of intestinal putrefaction or infection has 

 always come in for much suspicion, without ever becoming completely 



"Jour. Exp. Med., 1912 (16), several articles. 



" See Robertson, Arch. Int. Med., 1915 (15), 1072. 



" Sellards and Minot, .Jour. Med. Res., 1916 (34), 469. 



" Schittenhelin and Weichardt, Miinch. med. Woch., 1912 (59), 1089. 



-« Barratt and Yorke, Brit. Med. Jour., Jan. 31, 1914. 



