440 JOSEPH H. PKATT 



saturation point as a result of local changes. The experiments of Almagia 

 and Brugsch and Citron show that uric acid may be deposited in cartilage 

 placed in weak uric acid solutions. This is possibly due to the richness 

 of cartilage in sodium. If the more soluble lactam form of sodium urate 

 were changed in the tissues to the much less soluble lactim salt its de- 

 position would be favored. Histogenetic influence might interfere with the 

 formation of Schade's uric acid-colloid phase and thus favor the precipita- 

 tion of uric acid (Umber). But this subject is too hypothetical to deserve 

 further discussion. The injection of urates into the tissues produces in- 

 flammation and necrosis (Freudweiler(a) (&), His(&)(c)). 



The acute local symptoms in gout are most probably due to the deposi- 

 tion of crystalline urates which has been shown by Van Loghem to produce 

 an inflammatory reaction. 



The intramuscular injection of 0.5 gram uric acid dissolved in piper- 

 azin produced in a gouty subject much more severe reactions than have 

 been observed in healthy persons (Brugsch and Schittenhelm(gr)). Uric 

 acid introduced intravenously, however, does not produce symptoms either 

 in gouty or in healthy individuals. Nucleosids when injected subcu- 

 taneously have produced typical attacks (Thannhauser) and so has nucleic 

 acid when fed in the form of nucleoproteins. These recent observations 

 with nucleosids suggest that these precursors of uric acid rather than uric 

 acid itself are the toxic substances in gout. 



General Metabolism in Gout. The general metabolism in gout is not 

 altered ( Magnus-Levy (d), Wentworth and McClure). In attacks there is 

 an increase in the nitrogen metabolism due to toxic nitrogenous catabolism 

 ( Magnus-Levy (d), Brugsch (6)). Between the attacks the nitrogenous 

 metabolism which von Noorden thought subject to disturbances of toxic 

 origin has been definitely shown by Brugsch and Schittenhelm to be 

 normal. 



Glycocoll in Gout. The part that glycocoll might play in the origin 

 of gout has attracted considerable attention. Uric acid by hydrolysis 

 is converted into glycocoll and urea. Ignatowski(fr) found glycocoll 

 in the urine of seven gouty patients. This was confirmed by Lipstein 

 and Walker Hall (6). But the finding was apparently robbed of any sig- 

 nificance in gout by the discovery that it occurred in equal amounts in the 

 urine of normal persons (Abderhalden and Schittenhelm (c), Samuely 



(&)) 



Umber still asserts that the glycocoll found in normal urine is not pre- 

 formed, but is the result of the long continued action of alkalies on the 

 uric acid in the chemical analysis. It is claimed by Umber and his co- 

 workers, Hirschstein(a), Burger and Schweriner, that in gout an antagon- 

 ism exists between the excretion of uric acid and glycocoll. During the 

 period of uric acid retention the glycocoll excretion is high, while during 

 the period of "uric acid flood" in the attack it may entirely cease. Umber 



