fact that fragility of the bones, of the ribs and of the long bones, was often associated with pellagra. These various clinical similarities should not be construed as evidence in favor of the "avitamine" nature of pellagra. They indicate, rather, that in nutritional disorders, whatever may be their underlying cause, the vessels, the bones, and other tissues may suffer and lead to similar--but not identical--clinical pictures.[58] [58] There is no adequate reason for placing in this group "coeliac disease," a nutritional disorder of children recently described by Still, and suggested by McCarrison as belonging to the category of the vitamine deficiency diseases. A case of this kind has come to our attention which resembled pellagra in many respects. It showed the bright red, denuded tongue, the intestinal symptoms, the occasional edema, marked loss in weight, and evanescent erythema--all symptoms of markedly disturbed nutrition but not distinctive of a lack of vitamines. The relation between scurvy and rickets is a subject which was discussed by Glisson. With the renewed interest in infantile scurvy which followed Barlow's work toward the end of the last century, children's specialists ranged themselves into opposing camps on the question of the interrelationship and interdependency of these two diseases. Some accepted Barlow's dictum that infantile scurvy is an absolutely distinct and separate entity; others, for example, Hirschsprung, declared that the so-called scurvy was merely a form of rickets; whereas a third group considered it a combination of rickets and scurvy. This last viewpoint was actively maintained by Cheadle on the clinical side, and later by Schoedel and Nauwerk on the pathologic side--the latter declaring that rickets is "an inseparable component of infantile scurvy," and that the entire disease should be regarded merely as "an episode in the course of rickets." Even Barlow, in a paper published in 1894, wrote: "Rhachitic changes already present may act as a physiological determinant of the sites in which scurvy becomes manifest" and "rickets as a basis plus inadequate food gives the simplest explanation of the typical case" (of scurvy). We had an exceptional opportunity to test this thesis in 1914, in an institution where scurvy broke out among infants who were on a diet of pasteurized milk. All these infants were receiving cod liver oil daily, as prophylactic treatment against rickets. Many infants have been seen since that time, who in spite of receiving cod liver oil developed scurvy, and others in whom large doses of this oil failed to mitigate the scurvy, although it prevented rickets. The same failure has been encountered in the treatment of scurvy in guinea-pigs. This experience has been without exception, both from a prophylactic and a curative standpoint.