THE PATHOGENESIS OF GOUT 127 



prime importance, the use of alcohol. In the main, the periodic variations 

 which have been reported as to the frequency of gout may be referred to this. 



(c) There are acute and chronic intoxications as well as infections, which, 

 in combination with the uric acid diathesis, favor the development of gout, 

 and in which bacterial toxins also may play a part. I shall first mention the 

 relations of gout to rheumatism, to syphilis, and to lead intoxication. Influ- 

 enza, also, appears to predispose to gout. 



(d) Contagion, as was first asserted by no less an authority than Boer- 

 haave, does not seem to play any part in gout. 



(e) Climatic conditions apparently have no influence upon the develop- 

 ment of gout. 



4. The poison which causes gout, the actual materia peccans, appears to 

 be uric acid. Whether, besides this, other products of metabolism of the group 

 of alloxur and nuclein bases are operative, or, as some authors assume, a 

 poison the nature of which is unknown, is still an open question. It is likely 

 that only the endogenous nuclein substances of the human body, and not the 

 uric acid originating from the nucleins of the food, have a direct influence 

 upon the pathogenesis of gout. Whether an increased formation of uric acid 

 occurs in gout has not been proven with certainty, nor do I believe this proof 

 to be absolutely necessary. Nevertheless, I consider such increase to be prob- 

 able. That an increased production of uric acid (which we assume from an 

 increased excretion) does not alone give rise to gout is taught by the study 

 of leukemia. In some cases of this disease, as is well known, more uric acid 

 is excreted than in any cases of gout. 



5. Uric acid is a chemical, but not a septic, poison. Its action is not uni- 

 form in all species of animals, at different ages in the same animal, nor in 

 their different organs. Uric acid produces inflammation and necrotic changes 

 in the affected tissues, and finally causes complete death of the tissue (necro- 

 sis). Only after the tissue is wholly necrotic does a deposit of crystalline 

 uric acid take place in the form of acid sodium urate (monosodium urate, 

 Tollens, sodium biurate, Eoberts). According to Tollens, uric acid also circu- 

 lates in the blood and in the alkaline juices of the tissue in the same alkaline 

 combination, and not, as Eoberts has assumed, as sodium-quadriurate, a com- 

 bination which Tollens more technically designates as hemisodium-urate. It 

 is admitted at once that monosodium- urate, Tollens (sodium-biurate, Eoberts), 

 under otherwise similar conditions may also be deposited as crystals in tissues, 

 where not uric acid itself but another poison has caused necrosis. 



6. To understand the pathogenesis of the different symptoms of gout, we 

 must distinguish between (a) primary arthritic gout and (&) primary renal 

 gout. The first is by far the more frequent, and the sufferers from this often 

 reach extreme old age. Primary arthritic gout first develops under the infiu- 

 ence of a localized uric acid stasis, i. e., it is limited to one or more parts of 

 the human body. In primary renal gout we have from the onset a generalized 

 uric acid stasis, which, therefore, affects all parts of the body, and is invariably 

 due to a primary and severe disease of the kidney. 



It is evident from the Transactions of the Section of Internal Medicine 

 of the Xlllth International Medical Congress, that the opinions of the two 



