Abstract
Extract: Thirty-nine infants with simple vitamin D deficiency were studied; three stages of deficiency were recognized. Stage I comprised hypocalcemia, usually as the sole important biochemical finding, while convulsions were a common clinical sign. Stage II revealed normocalcemia with hyperaminoaciduria, hypophosphatemia, and hyperphosphaturia; rickets was also in evidence. Stage III was comparable to stage II, but with recurrence of hypocalcemia and convulsions, the rickets was more severe. Patients progressed spontaneously from the early to the later stages of the deficiency syndrome; administration of parathyroid extract appeared to accelerate the rate of progression. Calcium infusion and vitamin D therapy each initially raised the serum calcium level in hypocalcemic patients; thereafter, aminoaciduria and hyperphosphaturia were suppressed.
These diverse observations were interpreted in accordance with current knowledge of vitamin D and parathyroid hormone interrelations. The acquired excretory abnormality involving amino acid and phosphorus is the result of impaired tubular absorption; this defect is considered to be dependent on the development of endogenous reactive hyperparathyroidism, and not dependent on cellular deficiency of vitamin D per se. The stimulus for the hyperparathyroidism is hypocalcemia induced by deficiency of vitamin D. Normocalcemia is restored if sufficient vitamin D is present in cellular membranes to amplify the stimulative action of parathyroid hormone on intestinal transport of calcium and its release from bone. Severe deficiency of vitamin D blocks this regulatory effect upon calcium, but does not block the inhibitory effect of parathyroid hormone on renal tubular transport of amino acids and phosphorus.
Speculation: An excess of parathyroid hormone rather than a simple deficiency of vitamin D at the renal tubular epithelial cell appears to cause the disturbance of transport affecting the absorption phosphorus, amino acids and other solutes. This impairment of function is the price paid in renal cellular economy for the conservation of calcium. The cellular mechanisms underlying this coexistent inhibitory effect of parathyroid hormone constitutes an important and fascinating subject for further investigation.
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Fraser, D., Kooh, S. & Scriver, C. Hyperparathyroidism as the Cause of Hyperaminoaciduia and Phosphaturia in Human Vitamin D Deficiency. Pediatr Res 1, 425–435 (1967). https://doi.org/10.1203/00006450-196711000-00001
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DOI: https://doi.org/10.1203/00006450-196711000-00001
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