In this condition an excess of uric or lithic acid in the form of urate of sodium is present in the blood and fluids of the body, and is deposited in a solid (mostly crystalline) form in the articular cartilages and elsewhere. The primary fact is the excess of urates in the blood, a condition which has been called variously lithaemia and urataemia, and this excess may be very considerable. Whilst in normal blood traces of urates may be found by elaborate analysis, in gouty persons urates can be readily detected in the blood serum or blister fluid. This is done by acidulating the fluid, placing a few linen fibres in it, and leaving it in a warm place to evaporate, when crystak of uric acid will be found adherent to the threads.

The explanation of the excess of urates is not that of an accumulation from defective excretion as in the case of uraemia. The kidneys are indeed frequently involved, but this is often secondary, and there are many cases of gout without any disease of the kidneys. The excess seems due to a defective metabolism by which urates are produced in excess, and this again has mostly a constitutional origin. Inheritance plays a great part in the causation, and, consistently with the general facts of heredity, it is a defect in the finer adjustments of the bodily organization. Besides the hereditary predisposition, diet plays an important part in the causation, an excess of animal food, and of alcohol, more particularly in certain of its forms, being prominent factors. Lead poisoning is by many regarded as concerned in the causation, but it appears that it is so only when hereditary predisposition is pronounced (Roberts).

The excessive production of urates occurs in paroxysms, these being determined mostly by irregularities in diet. The paroxysm culminates in a deposition of solid urates, usually accompanied by great pain in certain joints. According to Roberts, the normal status of uric acid in the body, that is, in the blood, fluids, or urine, is that of a quadriurate. This form is readily soluble in presence of a soda salt, but it is a somewhat unstable compound. On the other hand, it is a biurate which is found in gouty deposits, and this is very insoluble in solutions containing soda. It is suggested by Roberts that, as the gouty paroxysm proceeds, the soluble quadriurate present in excess in the stagnant synovial fluid passes into the form of biurate, which is at first amorphous, and is finally deposited by the synovia in the crystalline form.

The urate is deposited in the superficial layers of the cartilage, but not on the surface, in the form of stellate crystals or needles (see Fig. 117). It is by their mechanical influence that they produce the local symptoms. The urates are deposited not only in the cartilages, but may be so in the synovial membranes and even apart from the joints altogether. Thus, the rim of the ear is a frequent seat of deposition, the tendons, the skin of the hands, feet and face, the dura mater, the pia mater, the sclerotic coat of the eye, and the fibrous sheaths of the nerve trunks. The kidneys are frequently the seat of deposit both in the cortical and pyramidal portions. The articular cartilages by their nature are exceedingly sensitive to interference in their texture, and the deposition in them gives rise to severe pain, whilst in other situations local symptoms may scarcely exist.

The question of the general effect of an excess of urates on the body is an important one. It cannot be said that urates are poisonous in the proper sense of the term, yet the ordinary premonitory signs of gout, consisting chiefly of digestive and nervous troubles, seem to indicate a certain general affection of the body. The local symptoms, other than the articular, such as various cardiac, pulmonary, or gastric troubles, seem also to point to auto-intoxication by the urates.


Garrod, Nature and Treatment of Gout, 1859; and Reynold's Syst. of Med., i., 1866; Gairdxer, On Gout, 1849; Ebstein, Nat. u. Behandl. d. Gicht, 1882; and Lehre v. d. harns. Diath., 1891; Pfeiffer, Das Wesen d. Gicht, 1891; Roberts in Allbutt's Syst. of Med., iii., 1897.