piyee. Duckworth ("A Treatise on Gout," London, '90) and various other authors believe the cause of gout to be a functional disorder of a definite tract of the nervous system; this is, however, only a supposition, and, even if his state ment be accepted, it only removes the question to another field as long as the origin of the nervous derangement is not elucidated.
Ebstein ("Natur u. Behandlung d. Grebt") agrees with Garrod in the belief that in gout the blood is overcharged with uric acid, but he does not think that this arises from an affection of the kidneys. According to Ebstein, a pri mary gouty affection of the kidneys is a very rare occurrence; most frequently the kidneys remain for a long time healthy, and are only affected in the course of the disease in the same way as the articulations, etc. Ebstein's theory is that in gout uric acid is formed in excess in the body and that the hyper production also takes place in regions which ordinarily do not produce uric acid—as, for example, the bone-marrow, the cartilage, etc. When the blood and the lymph are overcharged with uric acid, it may act as a chemical poison, causing morbid processes in the tissues and giving rise even to necrobiotic changes; when these have reached a cer tain degree the biurate is deposited in the necrotic parts of the structures, whereas such deposition is never found elsewhere.
The theory of Ebstein must now be abandoned, as various authors,—such as Roberts, Cornil„and Riehl,—have found the crystals of biurate in comparatively healthy tissue, and have demonstrated that, after redissolution of the crystal needles, it was in many cases impossible to discover traces of necrobiosis in the structures in which the crystals had been imbedded. Moreover, experiments conducted by Ebstein and Nicolaier have demonstrated that it is impossible to inject large quantities of dissolved uric acid in the veins of animals or in their peritoneal cavity without causing serious damage; the kidneys, which are obliged to excrete such excessive quantities of uric acid, are alone irritated mechanically by the crystalline uric acid precipitated in them.
Pfeiffer (Berliner klin. Woch., '92; "Handbuch der specieler Therapie," B. 1) believes that the precipitation of urates in gout and of uric acid in the kidneys in gravel are caused by a com mon uric-acid diathesis in which uric acid is produced in the body in a modi fied, almost insoluble form. In gout the uric acid is deposited as biurate without causing any morbid symptoms, but when from any cause—as, for example, by the ingestion of alkaline drugs—the alka linity of the blood becomes so great that the blood redissolves the urates, they give rise to irritation and inflammation. The experiments of Pfeiffer, as well as his conclusions, have been contradicted by Roberts and many other observers.
The urine of gouty patients is not al ways more liable to precipitation of uric acid than normal urine, and, as Freud berg states, the alkalinity of the blood varies but little and cannot be modified by the commonly used doses of alkalies or acids.
Von Noorden ("Pathologic des Stoff wechsels," Berlin, '93) has proposed a new theory without trying to prove it. In his opinion gout is an inflammation of nervous structures caused by an un known irritant; by this inflammation a fermentation is set up, giving rise to a local formation of uric acid in the dis eased tissues.
Another theory is proposed by Kolisch (Wiener med. Woeh., '95). This author admits that the uric acid cannot be regarded as an irritating poison causing inflammation and nccrobiosis, but he points to the fact that, when uric acid is formed by the disintegration of nu clein, it is always combined with a series of basic products,—the alloxur bases (xantliin, hypoxanthin, adenin. guanin), —which, by injection in the veins of ani mals, manifest violent toxic effects. In Kolisch's opinion, the alloxur bases are changed into uric acid by the healthy kidney and excreted as such; in the uric-aeid diathesis the alloxur bases are formed in excess in the body, the kidney is overcharged and cannot convert them into uric acid; the alloxur bases are excreted in abnormal quantity and set up irritation of the kidneys as well as of the various structures of the body, and only when this inflammation has taken place the deposit of biurate occurs as a secondary symptom. This ingenious theory has already been abandoned, many observers having found that the chemical method (Kruger-Wulff) by which Kolisch demonstrated the excess ive excretion of alloxur bases in gout was not reliable, and that, moreover, the excreted quantity of alloxur bases varies so much as well in health as in disease that no conclusion can be drawn from their quantitive estimation. F. LEvi sox.] The phenomena of gout cannot be ex plained by a mere crystallization of urate from the blood or by the production of necrotic changes due to its presence in the circulation, seeing that in other con ditions in which uric acid is present in excess in the blood—such as leucocy thnmia and chronic nephritis—neither uratic deposits nor necrosis of cartilage are met with. Some unknown sub stances produce in gouty persons inflam mation and necrotic changes in various tissues, and the necrosed tissues possess the power of attracting to themselves the excess of uric acid in the blood, while the chemical affinity of the necrosed parts for uric acid prevents the deposits from being redissolved by the blood. G. Klemperer (Deutsche nied. Woch., xxi, p. 655, '95).