単純性V.D抵抗性佝僂病の発症病理に関する研究
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The pathogenesis of hypophosphatemic vitamin D refractory rickets of the simple type or "Phosphatdiabetes", which is the commonest type in vitamin D refractory rickets, was studied in eight children. The following results were obtained : (1) According to Howard Test 1 case out of 5 was normal, 2 cases were in hyper-parathyroid state and 2 other defied the judgment in deciding whether they were in hyper-parathyroidism or hypoparathyroidism. (2) Ellsworth and Howard Test was made in six cases. The responses of all the 6 cases tested were poor in comparison with those of normal children. Three out of 6 cases scarcely showed any response, while 3 others responded slightly. (3) Fraser Test was made in five cases. Three out of 5 showed a remarkable decrease in the amount of phosphate excretion in urine from 3 to 5 hrs. after the 1st injection of calcium salt into the vein, and they showed a marked increase in urinary phosphate excretion by injection of parathormone 7 to 8 hrs. after the 1st injection of calcium salt. One case showed a gradual increase in the quantity of phosphate excretion in urine after starting the injection of calcium salt and showed a slight decrease in urinary phosphate excretion 8 hrs. after the 1st injection of parathormone into the vein. Another case did not show any decrease even 10 hrs. after starting the injection of calcium salt, when the patient showed a slight increase in urinary phosphate excretion by the parathormone injection. (4) The balance study of calcium and phosphorus was made in five cases. Three cases opt of the 5 tested showed fecal calcium excretion above normal, whereas two gave normal values. These children showed a remarkable decrease in calcium excretion when large does of vitamin D or AT10 was administered. Fecal excretion of phosphorus was normal in all cases. On the basis of our observations, it is evident that the pathogenesis of this disease is divided at least 2 types which are produced and developed respectively through the distinct pathogenesis, namely the pathogenesis of causing secondary parathyroid hyperfunction owing to the lowering of serum calcium through the deficient absorption of calcium from the gastrointestinal tract and the pathogenesis of causing the defect in the renal tubular mechanism for the reabsorption of phosphate.
- 千葉大学の論文
- 1962-11-28
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