452 JOSEPH H. PEATT 



action has been accepted by Folin and Lyman and by American investi- 

 gators generally. The drop in the blood uric acid offers strong support 

 for this view. 



The increased output of uric acid is certainly not due to increased purin 

 metabolism for the following reasons: (1) The allantoin excretion in 

 mammals is not augmented by atophan ( Starkenstein, Pohl(e)) ; (2) the 

 uric acid in the blood would be higher not lower if more uric acid were 

 formed in man; (3) the phosphorus metabolism is not increased. 



Atophan not only stimulates the kidneys to secrete more uric acid, but 

 it seems also to "mobilize" uric acid, that is, it facilitates the transport of 

 uric acid from the tissue juices to the blood. It is, however, possible that 

 the removal of uric acid which is the end product of purin metabolism 

 in man from the blood by the kidney is the cause of an increased passage 

 of uric acid from the organs and tissues to the blood. Rosenberg in per- 

 fusion experiments with the dog's liver found that the addition of atophan 

 to the blood passed through the liver caused an increased discharge of uric 

 acid from that organ, and this work certainly supports Brugsch's mobiliza- 

 tion theory. Griesbach's recent observations suggest that atophan tends 

 to check the storage of uric acid in the tissues. In addition Starkenstein's 

 careful studies indicate that the drug has an inhibiting action on the 

 whole purin metabolism. This shows itself in the normal man in the di- 

 minished output of uric acid that occurs after the administration of atophan 

 is stopped and during its use when continued for more than a few days. 



Atophan has then a fourfold action. It increases the excretion, sets 

 free stored uric acid, prevents further storage, and inhibits purin metabo- 

 lism. "The action of the drug presents many analogies with that of phlor- 

 *idzin, and one may look on the process in the light of a temporary renal 

 uric acid diabetes" (Hopkins and Wolf). 



Tophi have been seen to diminish under the long-continued action of 

 atophan. Weintraud referred to such a case in his first paper, and Llewel- 

 lyn, a physician with large experience at Bath, England, says, that he 

 has been much impressed with the manner in which it produces softening 

 and diminution in the size of tophaceous deposits. 



Atophan has been found useful in acute attacks as well as in chronic 

 gout. It quickly lessens the pain. Brugsch would not give the drug dur- 

 ing the attack, but in acute cases only immediately before or immediately 

 after the attack. His reason for so doing is that the uric acid output is 

 high during the height of the attack and that atophan at that time will only 

 raise the output but slightly. Before and after the attack the excretion 

 is usually low, and then atophan causes a great increase in the excretion. 

 The usual amount is 3 grams daily, in divided doses of 0.5 gram each. It 

 is a good plan to give the patient a supply of atophan with instructions to 

 take it as soon as premonitory symptoms appear. In this way possibly 

 a severe attack may be prevented. 



