It may be observed that the attacks of _sub-acute arthritis_ that ensued in rheumatoid subjects followed the administration of _hypoxanthine_, as shown in Ackroyd’s series. That this reaction to exogenous purin is suggestive of a relationship between rheumatoid arthritis and gout derives colour from the fact that it has been repeatedly induced in _gouty_ subjects by the same means. Thus, Brugsch and Mallory (1910), after giving 0·5 gram of hypoxanthine to a gouty patient, noted a typical outbreak of gout. Again, Brugsch and Schittenhelm, in the same year, reported attacks of arthritis following the administration of _nucleinic_ acid to gouty subjects. Another feature worthy of note is that, in the cases of _rheumatoid arthritis_ investigated by Ackroyd and Mallory, the percentage of exogenous purin nitrogen excreted as uric acid nitrogen largely exceeds that observed in any case of _gout_ available for comparison by these authors. Mallory’s final conclusions were that “there seemed to be sufficient data to show that, in certain cases of so-called rheumatoid arthritis, the purin metabolism is not normal. Whether these cases are real gout, or only resemble that disease in certain features, must be determined by further studies.” PURIN METABOLISM IN CHRONIC ALCOHOLISM AND PLUMBISM Quoting from Mallory’s contribution, we note that Pollak investigated the purin metabolism in a series of cases of _chronic alcoholism_. In five of the examples a marked derangement of _purin metabolism_ was noted and manifested, “partly in retention, and partly in delayed excretion, or a combination of the two.” Having observed these variations in cases of what he considered were _non-gouty_ alcoholics, Pollak felt justified in attaching but limited diagnostic import to the results of the examination of uric acid metabolism in gout, this though he realises the importance of alcoholic excess as a cause of disturbed purin metabolism. Mallory’s observations, too, on uric acid excretion in gout complicated by _lead poisoning_ are highly interesting. In two cases of this nature he noted that the percentage of uric acid nitrogen excreted was relatively small—in this respect in full accord with previous observations of Brugsch and Schittenhelm on a gouty patient with a history of plumbism, with this reservation, that in the latter observers’ example there were indications of early _renal_ disease, while in Mallory’s two cases such was absent, the urine being normal, and likewise the blood pressure. Again, Pollak in a case of _lead gout_ noted an extremely _low endogenous average_, viz., a daily average endogenous excretion of 0·06 gram uric acid in a period of five days. Eschemburg, quoted by Pollak, has recorded an instance of gout with plumbism in which the excretion fell as low as 0·02-0·04 grams. It may be noted that Pollak’s was the victim also of incipient _renal_ disease.