PHYSIOLOGICAL HEMOLYSIS OF THE NEWBORN 537 



ments have been confirmed by other workers. Hellmeyer {1210,1212) 

 assumes that the spleen is a contributory factor in idiopathic hemolytic 

 anemia and that in acquired hemolytic anemias it causes the breakdown of 

 apparently normal erythrocytes.* 



6.3. Pernicious Anemia 



Since before the discovery of the antipernicious anemia principle in the 

 liver by Minot and Murphy and by Castle pernicious anemia had been 

 erroneously assumed to be caused by a hemolytic toxin, there has been a 

 tendency to disregard the evidence for increased hemoglobin breakdown in 

 this disease. Some workers went so far as to assume that the increased excre- 

 tion of urobilinogen in the feces (740,1209,2969) and the raised bilirubin 

 content of the plasma {1955) during relapse were due to the inability of the 

 bone marrow to use the "pyrrole body store" for hemoglobin synthesis, and 

 to the excretion of the bile pigments from this store. Whipple's later experi- 

 ments {cj. Chapter XIII), however, have forced him to abandon the assump- 

 tion of such a store. There is now no biochemical evidence for its existence, 

 for the assumed ability of the bone marrow to utilize bile pigment for hemo- 

 globin synthesis, or for an independent synthesis of bile pigment from 

 pyrrole precursors. The lifetime of the red cell is decreased in pernicious 

 anemia; in the untreated disease it is only 9-19 days and the erythrocytes 

 are destroyed by a random process {2082) . The erythrocytes are more sensi- 

 tive to small concentrations of saponin {2171; cf. also 2755). There can be 

 little doubt that pernicious anemia is due to faulty construction of the 

 erythrocyte stroma and membrane; see class (6) of our classification. f The 

 permeability of the membrane to glucose is greater than that of normal 

 cells {132a); erythrocyte respiration is abnormally low and no Michaelis- 

 Salomon effect {cf. Section 3.2.) is found {528). The increase of copropor- 

 phyrin I excretion indicates an increased, rather than a decreased, hemo- 

 poietic activity of the bone marrow {cf. Chapters XII and XIII). 



6.4. Physiological Hemolysis of the Newborn 



The explanation of the polycythemia of the newborn and the rapid decrease 

 of erythrocyte and hemoglobin contents of the blood after birth is still a 

 matter of controversy. It is accompanied by an increase of bilirubin in the 

 plasma (YUpo, 3150) which is evidently due to the increased hemoglobin 



* By studies of t^he life span of erythrocytes of patients transfused into normal 

 recipients, and of normal cells transfused into the patient's blood, Loutit and Mollison 

 {17Sla) have recently found that in familial hemolytic anemia the cells are abnormal 

 and undergo a rapid breakdown in the (normal) spleen, whereas in acquired hemolytic 

 anemia the cells are normal ajid are hemolyzed intravascularly by a hemolysin. 



fin a recent review of work on the life sp^n of the erythrocyte, Ashby {91a) states 

 that the erythrocytes have a normal life span in this disease. The data on which this 

 statement is based {'.)l,-i()0'>) refer, however, to the life span of normal cells in the 

 blood of patients suffering from pernicious anemia; thus they do not contradict the 

 view put forward here. Recent findings of London and co-workers {1777a) on the 

 appearance of N'^ in stercobilin after ingestion of glycine containing N'* may, how- 

 ever, necessitate a revision. 



