METABOLISM IN GOUT <):i7 



Tlu'ir deductions arc as follows: Cases of gout as a Kciicral rule 

 show some increase in the uric acid content of the blood, though some 

 of the chronic cases were within normal limits from this standpoint. 

 The increase is more marked in the acute type of the disease. The 

 uric acid content of the hlood in cases of gout is abnormally high with- 

 out a corresponding increase in the nonprotein nitrogen products of 

 the blood ; but the majority of cases show a slight but constant increase 

 in the nonprotein nitrogen and creatinin. An increase of uric acid in 

 the blood, with the patient on a purin-free diet, may be a symptom, 

 but is not diagnostic, of gout. 



McClure and Pratt^** found more than 3 mg. per 100 c.c. in their 

 cases when on purin-free diet, and also recognize that this uricaemia 

 is not diagnostic of gout. The former reports that in gout there is 

 evidence of impaired renal function. ^^ If abundant purines are fed to 

 gouty patients they may be found to have less than normal capacity 

 to excrete the excess/" also explainable on the ground of renal ineffici- 

 ency. 



In the intervals between the attacks of acute gout the elimination 

 of uric acid is said to remain within the normal limits; however, for a 

 period of one to three da3's before each acute attack the amount of uric 

 acid is usually decreased considerably. With the onset of the attack 

 the amount of uric acid excreted becomes increased, and for a few 

 days remains above the average, then subsides to about the normal. 

 Of these two features, the increased output of uric acid during the 

 attack seems to be more constant than the reduced output preceding 

 it, but cases occur in which the uric acid excretion shows no variation 

 from that of normal persons. In certain cases of rheumatoid arth- 

 ritis the behavior of the purine metabolism resembles that of gout.'*^ 



As yet we have no definite information either as to the cause of 

 this behavior of the uric acid during the paroxyms of acute gout, 

 or as to its part in causing the paroxysm. However, in view of the 

 fact that monosodium urate is found in the joints during the attacks, 

 it seems most probable that for some as yet unknown reason there 

 occurs a precipitation or anchoring of the urates in the tissues, which 

 is associated with the attacks of pain and swelling. We do not know, 

 however, that it is the deposition of urates that causes the attacks. 

 Indeed, the fact that uric-acid retention precedes the attack, rather 

 than accompanies it, seems to suggest that it is the absorption of the 

 urate rather than its deposition in the joints that is responsible for the 

 local disturbances. It is also possible that during the period of re- 

 tention the uric acid is held in the blood in some form that cannot 

 be eliminated by the kidnej^ and that its deposition in the joints in 



S8 Arch. Int. Med., 1917 (20), 481— bibliography. 

 39 Ibid., 1917 (20), 641. 



« Rosenbloom, Jour. Amer. Med. Assoc, 1918 (70) 285. 



« W. J. Mallorj', Jour. Path, and Bact., 1910 (15), 207; Ljungdahl. Zeit, klin. 

 Med., 1914 (49), 177. 



