Alkaptonuria is a hereditary disease in which there is a defect in the metabolism of tyrosine, with the result that patients with this disorder excrete varying amounts of homogentisic acid, an intermediary product of tyrosine breakdown. The recent evidence of Ravdin and Crandall1 suggests that this defect may be caused by the absence of some factor in an enzyme system required to break down homogentisic acid. This metabolic defect resulting in alkaptonuria is associated in many patients with ochronosis, a disease process in which pigment deposits occur in various body structures, especially cartilage. In patients so afflicted early and severe arthritis often develops, which resembles osteoarthritis on radiographic examination. Any method that can possibly interrupt this course of events seems worthy of trial.
Galdston and his co-workers2 recently reported their attempts to facilitate or replace this disordered enzyme system by the administration of many different vitamins, brewer's yeast,