172 PATHOLOGY OF PURIN METABOLISM 



assuming that the primary factor in the pathology of gout 

 is to be ascribed to cellular destruction. A uniform increase 

 of phosphorus elimination was not to be found in gout, 

 although necessarily this should be coincident with any in- 

 crease in the decomposition of nucleins. It cannot, of course, 

 be denied that in the course of gout, just as in many other 

 affections, there does at times take place an exaggerated de- 

 struction of tissue. This is brought out in the carefully 

 conducted studies of the protein metabolism in gout by 

 Magnus-Levy. We frequently refer to a * * toxogenic protein 

 decomposition" in acute gouty exacerbations, and often rec- 

 ognize in the paroxysms of gout that a period of nitrogen 

 retention succeeds this increased protein decomposition. In 

 gouty individuals it may often be observed that periods of 

 nitrogen retention and of nitrogen deficit are likely to occur 

 intermittently without any regularity ; and v. Noorden be- 

 lieves "that in a subject of gout even in the intervals there 

 exist (specific?) gout-substances, which exert now more, 

 now less harmful influence upon protein decomposition just 

 as in other chronic affections. " 4 However, the author is 

 unable to appreciate the least reason for forcing these points 

 into the foreground of the general problem. 5 



There is therefore no basis for seeking the cause of gout 

 in an increased formation of uric acid from oxidation pro- 

 cesses ; but there is actually less reason for assuming that 

 it is to be met in an increased synthetic formation of uric 

 acid, for we have seen that while this method plays an im- 

 portant role in birds and reptiles we have no right to assert 

 its existence in the mammalian economy. 



If the uric acid accumulation in the blood, character- 



4 Literature upon Protein Exchange in Gout : K. v. Noorden, v. Noorden's 

 Handb. d. Pathol. d. Stoffwechsels, 2d ed., 2, 139-143, 1907. 



'That, however, an increased cellular destruction, as induced experi- 

 mentally, for example, by exposure to Rontgen rays, is capable of raising the 

 haemic content of uric acid in a gouty subject and of precipitating a gouty 

 paroxysm, may be inferred from the observations of P. Linsen (Romberg's 

 Clinic) : Therap. d. Gegenw., 49, 159, 1908. 



