Abstract
In addition to rickets arising from diets deficient in vitamin D or salts of calcium or phosphorus, bone dystrophy has been noted in various disturbances of mineral metabolism which lead to imperfect deposition of the mineral constituents of bone, or to their excessive mobilization. Because of the similarity of clinical picture and the mechanics of production, the term rickets may justifiably be applied to the whole of this diverse group of bone dystrophies. Those cases arising from deficient absorption of inorganic bone constituents should be considered of exogenous origin, whether the deficient absorption be due to inadequate intake of minerals or of vitamin D, to inadequate ultraviolet irradiation, or to other cause. Those instances in which the metabolic disturbance is not dependent upon inadequate absorption are secondary to some endogenous disturbance of metabolism.
Several patients with endogenous rickets have been studied intensively in this clinic, and while their bone lesions were very similar, the metabolic data indicate that their anomalies were not dependent upon a common metabolic defect. The nature of the metabolic data indicated that in one group of patients the condition was secondary to chronic acidosis, due in one instance to persistent ketosis, and in another to constant reabsorption of urine. In a second group the bone changes were dependent upon hyperparathyroidism. The remaining group must be termed idiopathic, until further studies serve to establish the etiology of their condition. This third group is very similar in some respects to infantile rickets of the usual, or exogenous, type; it is distinguished from it in its failure to respond satisfactorily to adequate calcium and phosphorus ingestion, to vitamin D in the form of cod liver oil or viosterol, or to ultraviolet irradiation.
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