This section is from the book "Part 9. Technique Of Reduction Cures And Gout - On the Pathology and Therapy of Disorders of Metabolism and Nutrition", by Prof. Dr. Carl von Noorden. Also available from Amazon: Clinical Treatises On the Pathology and Therapy of Disorders of Metabolism and Nutrition, Part 9.
Our positive knowledge in regard to the metabolism of uric acid in gout is very scanty. I will not enter into a detailed discussion of this subject but will limit myself to a statement of the most important established facts.
1. The value for the endogenous uric acid excretion is, as a rule, reduced or remains near the lower level of the normal. Between the attacks from 0.28 to 0.4 g. of uric acid are found.
2. The uric acid of the blood is increased and it is very difficult to rid the blood of uric acid even though a purin-free diet is administered for a long period of time. The average amount of uric acid found in a liter of blood taken from a gouty subject was 70 mg.; normally only traces being found.
3. Urate deposits in joints and tendons as well as muscular and cutaneous tophi are often found. The tophi are not of constant size. They may grow larger and smaller. The reduction in the size of tophi is essentially due to phagocytosis inasmuch as the urate needles are devoured by the cells. In the joints (cartilage, epiphysis, ligaments, etc.) the disappearance of urate deposits seems to be much more difficult and to proceed much more slowly than in the skin and in the muscles.
4. The excretion of exogenous uric acid is insufficient and retarded. Frequently only one-half, one-third, or still less of the uric acid that one would ex pect to be eliminated according to the diet reappears in the urine.
5. The acute attack of gout is spontaneously accompanied by a greatly increased excretion of uric acid, in other words, the organism becomes purified of uric acid during the attack.
All in all, therefore, one finds in a gouty subject a chronic retention of uric acid, interrupted by an occasional critical elimination associated closely with more or less violent local inflammatory phenomena and general toxic symptoms.
I will refrain from discussing the theoretical conclusions that may be drawn from these fully established facts and from a series of other less positive and less constant observations of a different kind. I refer for an elucidation of this subject to my Handbook on the Pathology of Metabolism (1907).
The material that is positive renders it possible.
1. To strengthen the diagnosis of gout:
2. To determine the tolerance of gouty subjects for purin bodies and to regulate the treatment accordingly.
 
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