I. Definition Of Gout

In the case of gout one is confronted with difficulties in attempting to formulate any exact definition of the disease. We know that in this disorder the fate of uric acid differs from the normal, in so far as deposits of urates occur in the body, and certain disturbances in the excretion of uric acid make their appearance. We know, further, that in the vicinity of urate deposits inflammatory processes are apt to develop that run either a chronic or an acute febrile course; furthermore that the tissues that have become permeated with urates (especially cartilage) very readily undergo degeneration and necrosis, in this way causing serious interference with the function of the affected joints. Beyond this we know very little that is positive in regard to the significance of uric acid in the production of gouty processes. We do not even know whether the formation and destruction of uric acid deviates quantitatively from the normal. It is clear that the visible outward evidences of gout (urate deposits and articular inflammations) are merely the consequences of gouty disease, and an individual is afflicted with gout long before such visible evidence of gout appears. There are no doubt many cases in which metabolic perversions characteristic of gout are present and in which numerous consequences of these perversions appear, without the occurrence at the same time of specific gouty deposits. Unfortunately we know so little in regard to these stages of gout that precede the period of visible manifestations that we can hardly diagnose them with certainty. Only within recent times have certain endeavors been made to secure a solid basis for this diagnosis. Unfortunately numerous vague symptoms of varying character, as fleeting pains in the extremities, in the body, the head, attacks of migraine, gastrointestinal disturbances are often christened with the name "Gout" simply because no other diagnosis can be made. As a rule, this diagnosis is merely the result of ignorance and it can rarely tolerate the light of scientific criticism.

In the course of this lecture I will also have occasion to speak of the internal treatment of nephrolithiasis uric a, because the treatment of this disease corresponds in many respects with the treatment of gout. At the same time it is questionable whether the deposit of urate concretions in the renal pelvis really has anything to do with the gouty process. We are probably dealing with two diseases that are fundamentally different in the following respects, namely, that in gout the retention of uric acid in the organism plays an important rôle, whereas in nephrolithiasis urica uric acid is excreted in normal (perhaps even supra-normal) quantities but is subsequently deposited in a crystalline form outside of the body tissues proper on account of an unfavorable composition of the liquids that are expected to hold it in solution. In studying the nature of the two diseases one encounters more points of difference than of correspondence; nevertheless, in both disorders the same cause may increase or decrease the morbid process and this justifies the joint discussion of the two disorders, at least from a therapeutic standpoint; for in both cases anything that leads to an increase in the formation of uric acid must be considered detrimental.

Unfortunately, the definition of the term "gout" is exceedingly confused and uncertain. I have already mentioned the fact that numerous diseases associated with pain are unreservedly declared to be gout, among them nenralgia, myalgia, diseases of the tendon sheaths, of the periosteum, of the bones. If in such cases an analysis of the urine reveals high absolute or (as is usually the case) only high percentic values for uric acid, then the diagnosis of gout (see below) is often made. Very serious diagnostic errors in this direction are of common occurrence. The great majority of symptoms that are grouped under the name of gout are really due to rheumatic disease. They are attributable to masked forms of acute articular rheumatism and like the latter can be cured in a short time by the prompt administration of sufficiently large doses of salicylic acid and antipyrin. Frequently luetic disorders of the muscles and periosteum lead to confusion. Even unquestionably rheumatic neuralgias and myaglias may be diagnosed as gout. If no further error were committed than a wrong diagnosis, the patients would not be particularly injured, but unfortunately the diagnosis of gout immediately conjures up an army of dietetic restrictions and other far-reaching measures that are by no means indifferent in their effect upon the general strength of the patient, while at the same time the best period for proper treatment is sacrificed. A rheumatic neuralgia that could have been cured within a week by the daily administration of from 5 to 6 g. of sodium salicylate may drag along for weeks and even months, if these patients are treated by an anti-gouty diet, by exhausting baths and diet, by massage that is apt to increase rather than decrease inflammatory disorders. Frequently one is told that a neuralgia must have been gouty as salicyclic acid did not help. As soon as a more careful inquiry is made, however, it will be found that only from 1 to 3 g. of aspirin or of some similar preparation were given, and that merely for a few days. Such small doses never suffice to cure acute inflammatory rheumatism. I see each month several cases of luetic myositis or periostitis that have been mistreated for months by weakening baths, mineral water cures, restriction of the food and a weakening diet, simply because the disease was considered to be gout. One could elaborate almost indefinitely on this subject.

It is equally deplorable that the nature of certain articular lesions is very frequently misinterpreted. Acute inflammatory rheumatism is relatively rarely diagnosed as gout, although here the possibility of error is greatest. Mistakes are more frequently made in the opposite direction, in so far as genuine gouty disorders are often misinterpreted as acute rheumatic polyarthritis. A. Magnus-Levy some time ago called attention to the fact that acute polyarthritis occurring for the first time in an individual over 50 years old is always very suspicious of gout. With this statement I fully agree. This suspicion is strengthened if only a single joint or merely two or three joints are affected and when the characteristic jumping from joint to joint so often seen in acute rheumatism is absent.

Still more frequently chronic articular disorders are falsely considered to be gout. Here the monoarticular and oligoarticular forms of true articular rheumatism that run a slow course from the beginning and that are by no means rare must be considered (especially when affecting the knee joints), also tabetic and less frequently tuberculous joint lesions. The latter, if the disease runs an atypical course (and this is more common in older individuals than in young people) may so closely simulate the symptom complex of genuine gouty articular lesions that the correct diagnosis may be exceedingly difficult and can frequently not be arrived at until an operation is performed. Even X-ray pictures occasionally fail to settle the question. Particularly important in this respect are the atrophic degenerative joint lesions that are usually included under the name of arthritis deformans. To this group belong malum coxae senile and corresponding changes about the shoulder joints and the vertebra. These are often falsely called gouty. This error is still more frequently committed in the case of deformities that develop about the phalanges of the fingers. Occasionally the changes are limited to thickening of the joint capsule edges producing the well-known protuberances known under the name of "Heberden's Nodes" ; in other cases there develop advanced wear and destruction of the whole joint capsule and of the head of the phalanx. These degenerative processes are originally not of an inflammatory character, the lesions should therefore more appropriately be designated "Arthrosis'' rather than "Arthritis." Secondarily, however, inflammatory changes may appear in the adjacent soft parts causing considerable pain. All of these diseases have nothing to do with arthritis urica, for the diseased joints are completely free from uric acid. It may, of course, occur that an individual suffering from one of these forms of degenerative arthrosis becomes at the same time affected with genuine gout; and in such a case the gouty process is easily engrafted upon joints that are already diseased. If, therefore, in isolated cases urate concretions have been found in such joints, this merely proves that gout complicated the original disorder without indicating that the primary process was in itself gouty. To consider Heberden's disease as evidence of the existence of uric acid diathesis is exceedingly careless diagnostic work.

Genuine gout is common in some regions and rare in others. In Austria-Hungary the disease is very rare. During the 2 1/2 years that I have been working in Vienna I have seen only 25 cases of genuine arthritis urica, notwithstanding the fact that I am justified in assuming that gouty patients are somewhat concentrated in my particular practice. Of these 25 gouty cases 20 were foreigners. In Frankfort during the same period of time I saw twice as many gouty cases recruited from the region of middle Rhine, the Palatine, and the Mosel region. The frequency with which the diagnosis "gout" is made in Austria is in marked contrast to the actual frequency of genuine arthritis urica. This is attributable to the fact that Heberden's disease, which is very common, is always christened with the name of gout.