580 SAMUEL H. HURWITZ 



interest in these conditions, because of the well-established relationship 

 between the excessive destruction of body cells and the increased elimina- 

 tion of purin bodies, and more especially of uric acid, in the urine. 

 Since the amount of uric acid excreted is influenced by many fac- 

 tors, but more particularly by the methods used and the composition 

 of the food, only those studies of the endogenous uric acid metabolism are 

 of value in which the purin intake has been accurately controlled and the 

 determinations made by reliable methods. 



Experimental and Clinical Observations in the Anemias. The effect 

 of acute losses of blood on uric acid metabolism has been studied experi- 

 mentally by Haskins(a) and by Buell(fc), and in man by Strauss (e). Al- 

 though it has been supposed that, on account of the autolysis of tissue 

 protein caused by hemorrhage the uric acid output might show some 

 increase, neither Buell nor Strauss could find any appreciable change 

 in uric acid elimination after blood-letting. The increase noted by Has- 

 kins lasted only one day. In acute posthemorrhagic anemia following a 

 gastric hemorrhage, on the other hand, Strauss and also Mohr(e) demon- 

 strated high values for uric acid. In one instance, Strauss records a rise 

 in the uric acid nitrogen from a minimum of 0.136 gram on the second 

 day of the hemorrhage to an average output of 0.358 gram during the 

 following fourteen days. In Mohr's patient, the uric acid excreted on 

 the seventh day after the hemorrhage was about twice the normal figure. 

 Where the anemia resulted from repeated small hemorrhages Strauss ob- 

 served no changes in the uric acid output. It has been suggested that the 

 increased excretion of purins following large internal hemorrhages might 

 be due to the excessive decomposition and absorption of nucleoprotein re- 

 sulting from the destruction of red cells. 



Purin metabolism in the secondary anemia of Banti's disease has been 

 studied by Umber(&). The diet was purin-free and a fully controlled 

 metabolic study was made. Umber, in his studies, does not report uric 

 acid output, but groups his findings under total purins, of which he found, 

 in Banti's disease, a somewhat greater output before splenectomy than 

 after. 



The available studies of the nuclein metabolism on patients with 

 chlorosis are subject to the criticism that there was no control of the purin 

 intake in the food. Even though purins were ingested by the chlorotic 

 patients studied the quantities of uric acid excreted by them were found 

 only slightly higher than normal. Thus Von Noorden obtained 0.22 gram 

 of uric acid nitrogen per day in a patient with severe chlorosis, while von 

 Moraczewski(fr) found in eleven cases an average value of 0.26 gram, a 

 figure on the upper limits of normal. Similar results were obtained by 

 Vannini. 



In the hemotytic anemias wide fluctuations in uric acid elimination 

 have been observed, but the general view appears to prevail that during 



