Pathogenesis of hypocalcemia in neonatal polycythemia

P. Merlob; J. Amir

doi:10.1016/0306-9877(89)90124-2

Pathogenesis of hypocalcemia in neonatal polycythemia

P. Merlob^*
, J. Amir

^*Corresponding author for this work

Rabin Medical Center Israel

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

Hypocalcemia (HC) is a frequent complication of neonatal polycythemia (NP): 9.93% in the present study. Its pathogenesis is not clear. We suggest that one of the main pathogenetic explanation of HC in NP is the high level of phosphate significantly different (p < 0.01) than serum phosphate of normal normocalcemic non-polycythemic newborns. The intense postnatal erythrocyte breakdown will increase the serum level of phosphate. This hyperphosphatemia will decrease calcium ion concentration by their combination and bone deposition, a process allowed by inadequate postnatal parathyroid gland response.

Original language	English
Pages (from-to)	49-50
Number of pages	2
Journal	Medical Hypotheses
Volume	30
Issue number	1
DOIs	https://doi.org/10.1016/0306-9877(89)90124-2
State	Published - Sep 1989
Externally published	Yes

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abstract = "Hypocalcemia (HC) is a frequent complication of neonatal polycythemia (NP): 9.93\% in the present study. Its pathogenesis is not clear. We suggest that one of the main pathogenetic explanation of HC in NP is the high level of phosphate significantly different (p < 0.01) than serum phosphate of normal normocalcemic non-polycythemic newborns. The intense postnatal erythrocyte breakdown will increase the serum level of phosphate. This hyperphosphatemia will decrease calcium ion concentration by their combination and bone deposition, a process allowed by inadequate postnatal parathyroid gland response.",

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AB - Hypocalcemia (HC) is a frequent complication of neonatal polycythemia (NP): 9.93% in the present study. Its pathogenesis is not clear. We suggest that one of the main pathogenetic explanation of HC in NP is the high level of phosphate significantly different (p < 0.01) than serum phosphate of normal normocalcemic non-polycythemic newborns. The intense postnatal erythrocyte breakdown will increase the serum level of phosphate. This hyperphosphatemia will decrease calcium ion concentration by their combination and bone deposition, a process allowed by inadequate postnatal parathyroid gland response.

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Pathogenesis of hypocalcemia in neonatal polycythemia

Abstract

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