Abstract
It has been recognized now for some time that the administration of salicylates and phenylcinchoninic acid (cinchophen) resulted in an increased excretion of uric acid in the urine. Quite recently it has been shown by Folin and Lyman, 1 and Fine and Chace, 2 in particular, that this action was accompanied by a marked drop in the uric acid content of the blood, and later the same was shown to be true of salicylates by Fine and Chace, 3 and Denis. 4 It has been assumed that these drugs induce an increased output of uric acid by endowing the renal cells with an increased power for eliminating uric acid. Fine and Chace 5 have pointed out that, in the last stages of interstitial nephritis cinchophen has little influence on the excretion of the uric acid, indicating that the renal cells can no longer be stimulated to increased activity.
We have been endeavoring to obtain further light on the mechanism of the action of these drugs by experiments upon both man and animals. Setting aside cases of advanced interstitial nephritis where the action of cinchophen is comparatively slight, we have been struck by the fact that this drug and its methyl derivative show quite different ability to lower the blood uric acid in different individuals, the action being very pronounced in some cases and comparatively slight in others.
In their experiments Folin and Lyman noted the interesting fact (in two cases) that cinchophen not only brings about a dimunition of the uric acid in the blood but also seems to lead to a dimunition of the nonprotein nitrogen and urea whenever these are present in the blood in unusual amounts. Unfortunately these two experiments were not followed by a control after period.
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