EXCITING CAUSES.—Paroxysms of acute or subacute gouty inflammation of the joints, skin, or mucous membranes, as well as the neuroses of gouty origin, are excited by a variety of causes: errors in diet, both as to quantity and as to specific articles; excesses in the use of fermented liquors—even moderate indulgence, in persons with strong gouty tendencies—are perhaps the most common exciting causes. Sudden changes in temperature, and especially sudden changes in barometrical pressure, sometimes excite and often aggravate the sufferings of gouty persons. Blows, contusions, and mechanical strain frequently determine arthritic attacks; the large proportion of paroxysms affecting the metatarso-phalangeal joint of the great toe is explained by the fact that this joint is more exposed than any other to strain and injury. Finally, nervous exhaustion, from any cause, from overwork or sexual excesses, from grief, anger, or shock, may provoke any of the inflammatory or neurotic consequences of this disease.
PATHOLOGY.—It would be impossible in the limits of this article to review the many theories that have prevailed in regard to the pathology of gout, or even to discuss fully those that may be said to divide professional opinion at the present day. Since the discovery, by Garrod, of the salts of uric acid in the blood-serum of gouty patients, the humoral pathology of gout has certainly had the largest number of adherents.
The lithæmic pathology may be said to be based primarily upon the chemical theory of digestion or food-transformation. This theory proceeds upon the idea that every atom of albuminous or carbonaceous food that enters the body, whether it goes to the construction of tissue or is destined for the direct conversion of potential into active energy, is finally eliminated, for the most part, as urea, carbonic acid, and water. This transformation, of course, is supposed to be effected by a process of oxidation, but neither the exact mode of transformation nor the share which the different organs and tissues take in its accomplishment can be said to be certainly known. Recent investigations seem to indicate that the liver is chiefly concerned, not only in the metamorphosis of the carbohydrates, but also in the formation of urea, so that the arrest in the conversion of starches and sugars which results in glycosuria, and the check in the metabolism of the proteids which give rise to lithæmia, may both have their origin in hepatic derangement. The not infrequent association of glycosuria and lithæmia in the same patient, and the frequent alternation of gout and saccharine diabetes in gouty families, are significant facts in support of the common origin of these diseases.
The purely chemical theory of gout and diabetes, that they are diseases of suboxidation—a theory most ably advocated by Bence Jones2—has much to commend it from the valuable suggestions which it affords in the clinical management of these maladies; but it must be acknowledged that while a defective oxidation seems to be an essential factor in the production of gout and diabetes, it is impossible to reduce the process to the simplicity of a chemical equation. It cannot be claimed that the complex chain of transformations which organic chemistry has demonstrated in the destructive metamorphosis of albumen and starch in the laboratory is represented in the vital chemistry of the body. All that can be said in the present state of knowledge is, that the metabolism of food is in its nature a chemical analysis, modified and regulated by vital force, and resulting in the building up of tissues and in the conversion of potential into active energy. Imperfect blood-elaboration must depend upon much besides a disturbance of the balance between the amount of food ingested and the oxygen inhaled, though this must unquestionably be an important factor in its production. Heredity and the mysterious influence of the nervous system complicate the problem of the malnutrition which leads to gout, in such a way that while the general proposition may be maintained that gout is a disease in which suboxidation occurs, it is not possible to affirm whether suboxidation is the essence of the disease or only one of its phenomena.
2 Lectures on Some of the Applications of Chemistry and Mechanics to Pathology and Therapeutics, H. Bence Jones, London, 1867.
It is probable, however, that the pathogenesis of the gouty dyscrasia involves a much more complex process than the simple accumulation of uric acid salts in the blood. Uric acid, like urea, is one of the normal results of the metamorphosis of the albuminous foods and tissues. In birds and reptiles it takes the place of urea as the final issue of this metabolism. It has been supposed, as one atom of uric acid can be split by oxidation into two atoms of urea and one of mesoxalic acid, that uric acid was the penultimate of urea, the result of a lower degree of oxidation. It is by no means certain, however, that it is a necessary antecedent of urea. In birds, who consume by their rapid breathing an enormous proportion of oxygen, as well as in the slow-breathing reptilia, the nitrogenous excrements are in the form of urates; and under such divergent conditions it is impossible to explain the variations in the proteid metabolism by varying degrees of oxidation. The only reason that can be assigned for the elimination of the nitrogenous waste in some animals in the form of urea and in others in that of urates is the teleological one that the urea is destined for a fluid and the urates for a solid excretion.
But apart from these physiological objections to the theory that uric acid is necessarily the offending substance in gout, it is well known that uric acid salts accumulate in the blood in febrile diseases, in disorders of digestion, and in anæmia—notably in splenic anæmia—and do not produce either the symptoms or lesions of gout. Todd maintained that gout might occur without an excess of uric acid in the blood; and it is certain that in the atonic and irregular forms of the disease uric acid may not be found in excess in the blood or appear in excess in the urine. Another significant circumstance in the history of gouty persons tending to show that uric acid may be, after all, only an epiphenomenon in the disease, and not its exciting cause, is that the power of digesting farinaceous and saccharine foods in this disease is markedly diminished. To such a degree is this true that sufferers from the gouty dyscrasia are most promptly relieved of their symptoms of primary indigestion by restricting their diet very largely to albuminous foods; and not only does such a diet diminish the dyspeptic symptoms, but I am persuaded by a considerable experience that it is one of the surest prophylactics against the recurrence of gouty lesions. It is well known that the fermented preparations of alcohol are among the most frequent exciting causes of acute gout, and cases are by no means infrequent in which indulgence in sweet foods and in fruits will provoke many of the well-recognized local lesions of the disease.
The explanation of this anomaly in the uric acid pathology of gout may possibly be found in the suggestion of Garrod, that the deposition of the urates is caused by their insolubility, and, as this insolubility is increased by the diminished alkalinity of the serum, that the evolution of the acids in the digestion of the carbohydrates so diminishes the normal alkaline state of the blood that the uric acid salts are more readily precipitated. But even if we accept this explanation, the fact remains that as efficient factors in the production of the gouty diathesis the carbonaceous foods may play as large and perhaps a larger part than the albuminous foods. It would seem, therefore, in view of the conflicting evidence in regard to the theory of the uric acid origin of gout, that the chemical pathology of this dyscrasia is still involved in considerable obscurity.
The recent advances in neuropathology have revived of late years the views of Cullen on the pathology of gout. Dyce Duckworth3 has lately advocated the theory that gout is a trophoneurosis. This theory grows out of the recognition of the protean manifestations of this disease, and especially of the neurotic element which is so prominently developed in its evolution. The frequency of purely nervous symptoms in gouty persons is a fact which is daily brought to the notice of those who have much opportunity to study the disease. These symptoms may be said to affect all the functions of the nervous system; among these we may mention psychical disturbances, such as hypochondriasis and hysteria; derangements of sensation, such as neuralgias and dysæsthesias of every variety; and spasms of voluntary and involuntary muscles, such as cramps, grinding of the teeth, asthma, and vesical tenesmus. Another fact which arrests attention in the history of gouty persons is the frequency with which purely nervous influences determine attacks of gout; the effect of nervous exhaustion, whether provoked by overwork or mental anxiety, or the more explosive discharges of nerve-force in rage and great emotional excitement of any kind, is well recognized as a frequent precursor of gouty lesions. The influence of certain diseases of the nervous centres also, such as cerebro-spinal meningitis, Pott's disease, and tabes dorsalis, in determining arthropathies and lesions of the skin and mucous membranes, furnishes a striking analogical argument in favor of the possible nervous origin of the lesions in gout. The recognition of these facts, however, does not necessarily militate against the commonly accepted humoral pathology of gout. The healthy action of the nervous centres must depend primarily upon a normal nutrition, and a normal nutrition depends on healthy blood-elaboration. That perverted innervation may be an important factor in the development of malnutrition through the accident of inheritance is doubtless true, but in the acquired disease it seems more probable that the lithæmic condition is the primary source of disturbed innervation. It may be that gouty lesions are determined as reflex phenomena through the medium of the trophic centres—if such centres there be—rather than by the direct irritation of the affected tissues by the gouty blood; and it is not unreasonable to suppose that nervous exhaustion from any cause may produce in these centres greater reflex excitability.4
3 Brit. Med. Jour., March 26, 1881.