In serum rich in soda salts the biurate crystals are more easily separated than usual; irrespective of the acid with which they are combined, the salts of lime and magnesia, of lithia and piperazin do not affect the rapidity and the degree of osition, whereas all salts of potash de lay the deposition of crystals of biurate from blood-serum.
The granular urate is always the pre cursor of the crystalline form, and in the body-fluids the uric acid circulates in the form of invisible granules of sodium urate.
Gouty deposits are only met with in non-vascular tissues, and, as acids and acid salts diffuse more rapidly and ily than alkalies and alkaline salts, we must suppose that the alkalinity of the non-vascular tissues is less than that of 3 the blood. Hence if a transudate almost saturated with urate enters such a less alkaline tissue, the solution becomes supersaturated and granular urate is precipitated in the tissue, the precipita tion being favored by such additional factors as lowered temperature or in creased concentration of the fluids of the tissue. The precipitation of the granular urate in the spaces of the interstitial tissue and in the lymph-channels is the cause of the various phenomena of gout. In the course of time the urate deposited converted into acicular crystals of sodium biurate, or, under favorable conditions, may be redissolved and dis appear, and with them disappear the lesions to which they gave rise. C. Mordhorst (Zeits. f. kiln. Med., p. 65, '97).
Gout defined as a constitutional di ease of nutrition, most often hereditary. characterized by a dyscrasia termed nriccemia, causing a series of manifesta tions called arthritic. and inflammations, of the joints especially, with the deposit of uric acid at the spots affected. It de pends upon some aberration of nutri tion. It is distinctly constitutional. affecting the entire body, yet shows he redity. occurring, as it does. in families. develops easily, followed by the deposition of tophi, especially near the joints. The symptoms are described in detail, with a brief review of the eti ology. It is noted both with arterial hypertension and hypotension. Bou lomni6 (Jour. des I'raticiens. ug. 23. 1902).
The researches of von Jaksch have shown that in various diseases the blood contains an abnormal quantity of uric acid, and different authors have proved this to be the constant result of an in creased disintegration of leucocytes. A
physiological leucocytosis has been ob served in the first days of life, amounting to the double or triple, followed in the fifth day by a sudden fall of the number of leucocytes almost to the normal; this is accompanied by an excessive formation and excretion of uric acid, giving rise 15 almost constantly to the excretion of uric-acid sand and frequently to the for mation of uric-acid infarctus in the kid neys (Gundobin, Flensburg). Bartels, Laache, Ebstein, and various other in vestigators found an extraordinary in crease of the daily excretion of uric acid in leukTmia; von Jaksch, Lltr, and Ewing observed a hyperproduction of uric acid and leucocytosis in pneumonia, and similar results have been found in the first stage of carcinomatous and all other diseases accompanied by leucocy tosis. In all these maladies the hyper production of uric acid is distinguished only by the increase of the excretion of this compound, but the existing uricfe mia is not conducive to gout or any of the symptoms of this complaint. The pathogenesis of gout is consequently not depending on uricaimia alone, and it is necessary to examine the special condi tions under which uricmmia may pro duce gout.
Various theories have been proposed to explain this. The best supported of them shall now be shortly discussed.
According to Garrod, gout depends on a temporary or continuous decrease in the ability of the kidneys to excrete uric acid, by which an overcharging of the blood with uric acid is caused. Gout, in his opinion, is never caused by hyper production of uric acid, but by retention of it, although the progress of the dis ease is accelerated by temporary hyper productions.
Garrod found a distinct diminution of the percentage of uric acid in the urine as well in chronic gout as in the acute cases, except during the attacks, when more uric acid than commonly was ex creted; he, therefore, regarded the gouty attack as a salutary process which tends to deliver the system of its surplus of uric acid. It is to be regretted that the analytical methods used by Garrod (Heintze's method and the thread method) are not reliable enough to give full evidence to the correctness of his statements.