This section is from the book "Part 8. Gout. Clinical Treatises On the Pathology and Therapy of Disorders of Metabolism and Nutrition", by Dr. H. Strauss. Also available from Amazon: Clinical treatises on the pathology and therapy of disorders of metabolism and nutrition. v.8:no.1.
While we should not venture so far as to ascribe to uric acid retention the origin of every case of gout, we are not prepared to deny the possibility of such a process for many cases. At the same time a deficient destruction of uric acid may lead to its increase in the blood. If we have dwelt somewhat at length upon diminished excretion as a factor in the increase of uric acid in the blood, it is because we consider it much more important in a large number of cases than others seem willing to concede. The fact that even in this connection we lay stress upon the importance of the uricolytic function of the kidneys, to which Brugsch and Schittenhelm particularly refer, seems to us necessary for the following reason : Even though we attribute much importance to the retention phenomena in many cases, the question always arises why in these cases the organism should not be capable of compensating for the deficient secretion in some way or other. However, the organism is still in a condition to contend with a surplus of retained uric acid. This is shown, not only in the fact mentioned that the administration of a large amount of uric acid caused no toxic symptoms, and also that while in leukemia there is a great overproduction of uric acid, a certain amount present in the blood is never exceeded. Also Weintraud saw an increase of only 5 mg. in 100 cc. of blood after feeding thymus, and we have observed approximately the same value in the cases of gout which we have had the opportunity to study. That other factors than the retention are also responsible for the increase of uric acid in the blood of gouty patients is suggested by the fact that gout is closely related to a whole sequence of metabolism diseases, especially to obesity and diabetes, maladies which we can perhaps assign to an insufficiency of the katabolic powers of the organism. During the course of the so-called metabolism diseases, changes are many times found in the liver, which is concerned with sugar metabolism (in connection with diabetes, these changes are not so far reaching as was earlier believed), and, on the other hand, as we have seen, also shares in uric acid metabolism. These hepatic changes, according to Ebstein, appear most often in the form of hypertrophic cirrhosis. In this connection may be mentioned a case that we had under our observation several years ago, a patient, who suffered simultaneously from obesity, gout, hypertrophic cirrhosis, and bronzed diabetes. The clinical history of the patient in so far as it deals with his residence in the third medical clinic has already been given briefly in the article published by Raphael at our suggestion (Researches on alimentary glycosuria, Zeitschr. f. klin. Med. Bd. 37). As the patient was seen many times in the ensuing three years, the history of the further course of the disease is now possible. The case also possesses especial interest because it belongs to the slow and relatively mild form of bronzed diabetes, to which special attention has recently been called by Murri. The patient suffered from no in herited disease. He was sixty years of age, a master tailor. Ten years ago he repeatedly had typical attacks of gout, and at present still complains of acute pain in his left shoulder. He was a man of average size, strongly built, with well-developed muscles and fairly thick panniculus. The skin showed a decidedly brown coloration, which had not been present in early life and which persisted during the three years of observation. The body was well rounded, the subcutaneous fat being normal. The liver was markedly enlarged, smooth, and blunt edged; the spleen was likewise considerably enlarged and hardened. The stools were bile colored. In amount the urine varied from two to three liters per day; it was clear and, considering the quantity, had a slight excess of urobilin. There was no albumen present. In the course of the three years repeated urine examinations showed at times a total absence of sugar, but it was usually present in small amounts, which scarcely ever exceeded a total of from 10 to 40 grams per day. Since the patient complained of itching of the skin, polydipsia and polyuria, and also at times became greatly emaciated, there remained scarcely a doubt that we had to deal with a case of true diabetes in a gouty subject, accompanying hypertrophic cirrhosis of the liver, and brown pigmentation of the skin.
 
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