THE METABOLISM IN GOUT 433 



After injecting 0.5 gram of uric acid with 1 gram of piperazin intra- 

 venously McClure and Pratt found in four gouty patients that uric acid 

 was increased from 0.5 to 1.8 mg. four hours later. In three patients 

 the increase persisted for forty-eight hours or longer. In four out of 

 five non-gouty subjects there was a similar increase, but it disappeared in 

 all of these within twenty-four hours. Retention of uric acid in the blood 

 either when injected intravenously or when large amounts of nucleo- 

 proteins are fed, would seem to be a characteristic feature of the disturbed 

 metabolism in gout. 



A marked increase of uric acid in the blood has been repeatedly found 

 in different types of chronic arthritis by different observers, but the hyper- 

 uricemia in my experience is not persistent as in gout. Folin and 

 Denis (h ) hold that in chronic non-gouty arthritis the other waste products 

 represented in the non-protein nitrogen of the blood are not infrequently 

 abnormally high, while in gout they are usually within normal limits. 



In early chronic interstitial nephritis the uric acid is frequently as 

 high as in gout while the urea nitrogen is slightly if at all increased (Myers 

 and Fine(c)). Baumann found the uric acid increased in the blood in 74 

 out of 100 cases of renal involvement. In this group the maximum amount 

 of Uric acid found in cases with slight impairment of renal function was 

 6.4 mg., in cases with moderate disturbance of the kidneys 7.3 mg. 



Much larger amounts of uric acid have been obtained in the terminal 

 stages of chronic interstitial nephritis than are ever found in gout. The 

 largest amount ever reported was 27 mg. in a case of uremia shortly be- 

 fore death (Myers and Fine(fo)). In several cases of nephritis amounts as 

 high as 15 mg. were observed by these investigators. High values do not 

 occur in chronic parenchymatous nephritis (Myers). Uric acid in the 

 blood is also increased in leukemia, but the large amount found in a case 

 by Magnus-Levy (t) was probably in excess of the true value as the method 

 used was inaccurate. It is also increased in lead poisoning and acute in- 

 fections, especially lobar pneumonia and according to Gudzent, Wille and 

 Keeser in many cases of old lues, tabes, paralysis, and tuberculosis studied 

 by them. 



The exact state in which uric acid circulates in the blood in gout is 

 not known. Whether in normal blood uric acid occurs in the form of 

 sodium monourate is undecided although that is the opinion of most author- 

 ities. Gudzent (&) holds that uric acid occurs in the blood as the easily 

 soluble labile lactam urate which readily changes into the stable but poorly 

 soluble lactim urate. It is possible that in gout the uric acid is chiefly in 

 the latter state which would favor its deposition in the tissues. The col- 

 loidal properties of uric acid may have some relation to the pathology of 

 gout. Uric acid and the urates tend to form supersaturated solutions. Be- 

 fore the uric acid changes from the clear solution to the solid crystalline 

 form it passes according to Schade and Boden(&) through a colloid stage 



