Review of Gout, 1939-1946.

The main contributions to the subject of gout during the period under review have not unnaturally come from American workers. In spite of outstanding research by Talbott and Coombs (1938), Bauer and Klemperer (1942), and others into the metabolic and clinical aspects of the disease, the essential problem remains unsolved. Gout used not to be regarded very seriously by American physicians, and it is only during the last decade that it has been recognized as a not infrequent cause of arthritis. Incidence Hench's claim (1935) that patients with gouty arthritis constitute at least 5% of all patients seen at the Mayo Clinic suffering from joint disease was supported by Kahlmeter (1938), by Kinell and Haden (1940) in their review of 62 cases of gout, and recently by Wright (1945) in Canada. Experience of work in two rheumatic hospitals in this country leaves an impression that this proportion is certainly not too high, especially considering the number of cases of acute gout which never reach hospital but are treated privately, and also the atypical forms which, even with long experience and the full resources of the laboratory and x-ray department , are difficult to recognize. Whatever be the incidence, sufficient evidence is now available to prove that gout is not a rare disease, and if it is diagnosed less frequently in this country and in Europe nowadays than heretofore, this merely reflects more accurate diagnostic criteria. Heredity Recent work has strengthened the impression that gout is a hereditary disease, and has confirmed the statement of Futcher (1914) that a woman can transmit the diathesis to her offspring without herself developing the disease. The medico-sociological studies of Talbott and of Coombs (1938 and 1940) are very interesting. An exhaustive examination was made of 136 blood relatives of 27 patients with well established gout, none of whom had ever had an attack. A plasma uric acid of over 6 mg. per 100 c.cm. was found in 25%, and of this number 80% were males. No alternative cause, renal or otherwise , could be found to account for the findings. These workers, therefore, conclude that the gouty constitution is a hereditary predisposition based on hyper-uricaemia, and they relegate social factors, environmental influences, and dietetic indiscretions to a position of secondary importance. A lifelong follow-up would be necessary before it can be known what proportion of such affected relatives will later develop clinical gout. It …