The metabolism of healing in cœliac rickets.

As long ago as 1908 it was reported' that in intestinal infantilism there was serious derangement of the mineral metabolism. A number of investigations of the calcium anid phosphorus metabolism of patients with fatty diarrhoea, both adults and children, have been made at intervals since that time. It has been consistently found that the serum calcium tended to be low, and the serum inorganic phosphorus either normal or subnormal. Thus, the blood presents the picture of low calcium rickets2. Balance studies have shown that the urinary calcium excretion is much reduced, phosphorus excretion diminished, and the faecal calcium and phosphorus much increased, both relatively and absolutely3-8. The data in the literature thus suggest that the bone deformities are due to processes similar to those producing infantile rickets. Parsons2 in 1927 stated that the bone deformities of cceliac infantilism are rachitic in nature, and that although the blood phosphorus is low, the rickets is of the low calcium type. These conclusions were based on the clinical picture, blood analysis, radiography, and the results of treatment by ultra-violet light or vitamin D. Gerstenberger and his co-workers', on the other hand, suggested that their conception of the production of primary ' low calcium rickets ' does not fit in with the low calcium or combined low calcium low phosphorus types seen in association with coeliac disease. Parsonsl', however, in a later review maintained his former contention, stating that he could see no reason why there should be any distinction between the pathogenesis of the ordinary rickets of infancy and that of coeliac rickets. In view of this hesitancy to accept cceliac rickets.'and the ordinary rickets of young children as the same disease in different circumstances, it seemed worth while to record the metabolic observations in the active and healing stages of celiac rickets, and to compare the results with the changes known to occur in the healing of the infantile type of the disease. Two patients, girls of six and eight years respectively, presenting the history and clinical characteristics typical of cceliac disease, were found to have active rickets. This was decided on the radiological appearances. In each case the mineral metabolism was studied during this ' active ' period. One child (Case 1) was then given radiostol, one tablet, thrice daily; the other (Case 2) adexolin, one capsule, thrice daily; and the metabolic observa-