630 URIC-ACID METABOLISM AyD (JOIT 



gen retention and nitrogen loss are quite eonstant features. The 

 cause of this variability, and the form in which the nitrogen is re- 

 tained, are quite unknown, although there is some evidence that the 

 retained nitrogen is in the form of purine bodies (Vogt). Most of 

 the excessive loss occurs during the acute attacks,^'' and the retention 

 of nitrogen between attacks may be partly to repair the loss; against 

 this, however, is the fact that there is not sufficient gain in weight 

 to account for all of the nitrogen retention. Associated M'ith the de- 

 layed excretion of ingested purines is also a delayed excretion of the 

 other nitrogenous products of i)rotein food.-" The proportion of 

 purine bases to uric acid is not altered in gouty urine. -^ The state- 

 ments in regard to phosphoric acid elimination, which depends largely 

 on decomposition of nucleins, are contradictory, but it seems probable 

 that it shows no characteristic alterations in gout. Amino acids, espe- 

 cially glycocoll, are said to be excreted in excess.-^^ 



It may be seen from the foregoing discussion that we neither under- 

 stand fully the intricacies of metabolism in gout, nor know whether 

 uric acid is responsible for either the acute painful attacks or for 

 the anatomical alterations in the kidneys, heart, and bloodvessels. 

 Indeed, Daniels and McCrudden -^^ have shown that it is possible for 

 gouty patients to have a persistently low content of uric acid in the 

 blood, below the average normal quantity, and to have typical acute 

 attacks without change in either the uric acid content of the blood or 

 its excretion ; attacks were even observed to occur when the blood uric 

 acid was at a subnormal figure from administration of atophan, which 

 increases its elimination. Furthermore, Bass and Herzberg -^"^ found 

 that uric acid can be injected into the blood of gouty subjects until the 

 blood contains as much as 10 mg. per 100 c.c. without causing any 

 joint symptoms. 



It is very possible that some entirely difiPerent product of metabo- 

 lism than uric acid is responsible for most of the changes and symp- 

 toms of gout -- — indeed, this would seem to be the case were it not for 

 the great frequency of the deposition of monosodium urate in the 

 joints and cartilages, both during the acute attacks and in chronic 

 gout. This indicates that there is surely something abnormal in the 

 conditions of uric-acid solution and circulation. Why the urate is 

 precipitated in these definite places is another of the many unsolved 

 problems of gout. The local nature of the deposition indicates that it 

 must depend upon local changes; but the hypothesis that there occur 



in r{ruf,'scli, Zcit. cxp. Patli. u. Tlicr., 1000 (2), filO. 

 ^" I.ovcno and Kristeller, .Tour. Kxp. Mod., 1012 (Ki), 'MVA. 

 ai llcfrtor, DiMit. Arcl). klin. Mod., 1!>1;{ (109), :522. 

 2i;i IJiirtrcr and Scliwcririor, Arcli. oxp. Tatli.. lOi:! (74). :?5;?. 

 21b Arcli. Int. Med., 1!)].') (l.'-i), 1040. 

 •■:i<Deut. Arch. klin. .Med., 1010 (110), 482. 



-- In swine a "<,nianinc gout" oceuris; .see Schittonlioini and Hendix, /fit. i)liv.-;iol. 

 Ciioin., 1000 (48), 140. 



