Thus he writes: “I consider a toxin to be the cause of this disease. If so, such toxin must be formed in the intestine. As the symptoms of gout are constant, it must be a definite toxin, the product of a definite bacillus acting upon the intestinal secretion. As gout is capable of being caused in any subject, it must be one of the bacilli normally found in the intestinal canal.”
Nor did Gore lack supporters in his suggestion that the alimentary tract was the primary source of the changes in the metabolism of gout. For in the same year Minkowski, Le Gendre, and in this country Watson, hazarded the view that intestinal derangements, through the medium of their resultant toxins, initiate disturbances in the liver, and these in turn determine those obliquities of metabolism typical of gout.
At the same time their contentions derive colour from the researches of Grübe, who, despite traditional views, maintained that in gout the hydrochloric acid of the gastric juice, far from being increased, was in most cases diminished or wholly lacking, while, on the other hand, lactic acid was present in some instances.
In 1903 Woods-Hutchinson ably contended that “gout and lithæmia are mere symptom names for a miscellaneous group of chronic toxæmic processes of widely varied origin, characterised by the production of uric acid and the urates.” He held that the uric acid in gout as well as the associated phosphoric acid are merely a criterion of the measure to which the nucleins of the body cells (chiefly probably of leucocytes) have undergone destruction in consequence of their invasion by a toxin or toxins of organic or inorganic nature. He furthermore contended that the rôle of the liver in gout was purely negative, consisting in its inability “to absorb or transform into harmless excretory substances the excess of toxins brought to it by the portal vein.”
In 1904 Falkenstein furnished collateral evidence that the starting point of gout lay in a diseased condition of the gastric glands, those responsible for the secretion of hydrochloric acid. The supply of hydrochloric acid being deficient in the gouty, their digestive capacity is distinctly lowered. Abnormal fermentation ensues with insufficient oxidation, and “the substances containing quantities of nuclein are partly prevented from being further split up, and partly favour the synthetic formation of uric acid.” He would thus refer the excessive formation of this latter directly to the diseased glands. He further observes that, despite the deficiency of hydrochloric acid, the gastric juice is often hyperacid, this being due to the presence therein of organic acids, such as butyric, lactic, and acetic acids.
In the same year Chalmers Watson, as the outcome of investigations into gout as it occurs in the fowl, held that:—
(a) There is ample evidence to prove that the uric acid in the blood is not the primary factor in gout, and
(b) Uric acid can be deposited in cartilages and other tissues, even in considerable amount, without the association of any inflammatory phenomena.
He concludes that the last-mentioned point clearly proves that:—
(c) Uric acid is not the factor which causes the inflammatory phenomena characteristic of the acute attack.