Definition And Causes

Gout is a well-defined disease described clearly by characteristic symptoms. Goutiness is a condition which predisposes to gout and often manifests itself by variable symptoms. It is frequently also called 'gouty diathesis' or a 'lithemic state.' Gout as a constitutional disease is due to a fault of nutrition.

Its exact cause and the physiological perversions or changes which constitute gout and the gouty state are unknown. The symptoms of the disease are well known as are many of its complications. It is known that in this disease uric acid compounds exist in the blood in larger quantities than is normal and that often certain of these are deposited in the tissues of joints, of the kidneys, of the ear and other structures. But it has been demonstrated also that uric acid will not cause the phenomena of gout or goutiness and that it may exist for long periods of time in large quantities in the blood in other diseases, for instance, leukemia, without producing symptoms which even suggest gout. The excess of uric acid in the blood may be due to overproduction, to imperfect elimination or imperfect destruction and conversion into substances more easily eliminated. There is not adequate evidence that too much uric acid is formed. It is probable that there is imperfect elimination and conversion of uric acid into compounds which are readily eliminable. However, the latter is still a matter of controversy. That purin bodies occur in different tissues in different forms and in different relative proportions is well established. Furthermore it is established that various cell-ferments have the power of modifying the various purin bodies and transforming them into simpler ones and that uric acid itself can be converted by oxidase in the liver and in other tissues into urea. It may be that a ferment of this kind is no longer formed or becomes inactive in gout, thus causing an excess of uric acid to accumulate in the blood. However, this is theory with few facts to support it. It is known, nevertheless, that alcohol given with a definite quantity of purin bodies or nuclein will cause greater elimination of uric acid by the kidneys than occurs when no alcohol is given or when alcohol and a smaller quantity of purin bodies are given. It therefore seems probable that alcohol inhibits the transformation of uric acid into urea by oxidase.

Uric acid is derived from the nucleins of foods and hypoxan-thin of muscle used as food and from the same substances in the living body set free by the disintegration of nuclei and by the activity or wear of muscles. It has therefore an exogenous and endogenous origin. It is not known certainly whether in gout it is derived more from food or from the tissues of the gouty.

Why urates are deposited in certain tissues in gout is not known. It is not because urates exist in the blood in excessive quantities. There is doubtless a change in the tissues involved which leads to their deposition in them. Various theories have been propounded to account for this phenomenon but no one can be regarded as an established explanation.

Some believe that uric acid in excess in the blood of the gouty causes arteriosclerosis and interstitial nephritis. However as it does not do so when injected into the blood in large quantities nor in other diseases in which it exists in the blood in excess this belief is not tenable. It is more probable that the blood vessels, the heart and the kidneys are effected as a part of the disease and not by uric acid which is in a sense a by-product of the disease very much as sugar is in diabetes.

These explanations make it evident that as yet enough is not known to establish diatetic or other treatment upon a scientific basis. Treatment must still be empiric or guided by theories.

An attack of gout is recognized by painful swelling of certain, sometimes numerous, joints. The first attacks of gout are usually limited to the larger joint of the great toe. The joint which is affected becomes swollen, extremely painful, slightly reddened, and often exquisitely tender. If a joint is repeatedly attacked, or the disease becomes subacute or chronic, it is often permanently injured by the deposition of sodium urate in the tissues. Such deposits also occur quite frequently along the sheaths of tendons and in other places where fibrous tissue is abundant. Lack of appetite and disturbed digestion are in most instances associated with these local symptoms.

Goutiness often shows itself by disturbances of the nervous system. Mental depression is a noticeable feature in some instances; in others, periodical headaches. In a third group the symptoms usually described as those of biliousness are characteristic of an attack. In still other cases the anatomic changes and symptoms of arteriosclerosis are indicative of the uric acid diathesis. Contracted kidney is often developed in these cases.

Some patients in the lithemic state tend to develop obesity early in life, which frequently leads to fatty infiltration of the heart and causes a fatal weakness of that organ. In other cases the liver becomes enlarged and degenerated. Not infrequently, and especially in women who are inclined to a gouty condition, Heberden's nodes develop about the finger-joints.

Those who are hereditarily inclined to goutiness are often plagued with skin eruptions in early life; as, for instance, successive attacks of eczema. During youth, early manhood and womanhood, periodical attacks of migraine frequently take the place of the skin eruptions of the earlier years of life, and, later still, renal and hepatic colics become common in these patients. In a few a rebellious bronchitis develops which responds best to treatment for gout.

While there is no doubt the disease is generally an inherited one, it is equally certain that it may be acquired. The same systemic conditions that are most frequently the immediate cause of outbreaks of acute gout in those who have inherited a tendency to it are the causes of its acquisition by others. Long-continued use of food in too large quantities or too rich in quality is a common cause of the ailment. Prolonged constipation, and the indigestion and torpidity of the liver associated with it, are common causes. A sedentary life and too little exercise are particularly apt to produce the constipation and the indigestion which predispose to it. Long-continued or intense mental depression also may bring on acute attacks. While oftenest too rich and too much food and too little exercise provoke gout, occasionally acute attacks of the disease develop in those who are prone to it because they eat too little food or take an excessive amount of exercise.