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Pathogenesis of early neonatal hypocalcemia: Studies of serum calcitonin, gastrin, and plasma glucagon

  • Pankaja S. Venkararaman
  • , Reginald C. Tsang
  • , I. Wen Chen
  • , Mark A. Sperling

Research output: Contribution to journalArticlepeer-review

62 Scopus citations

Abstract

In 64 maternal-infant pairs, we tested the hypotheses that serum calcitonin, serum gastrin, and plasma glucagon concentrations are elevated in infants at risk for early neonatal hypocalcemia, and that elevated serum gastrin and plasma glucagon result in elevated serum calcitonin and low serum calcium values in neonates. Serum Ca declined significantly in neonates at 24 hours of age, and was inversely correlated with serum calcitonin. Cord serum calcitonin, gastrin, and plasma glucagon concentrations rose significantly at 24 hours of age. Cord calcitonin was significantly higher in preterm compored with term infants, and there was no significant difference between asphyxiated and nonasphyxiated preterm neonates; in term neonates cord calcitonin concentration was inversely correlated with Apgar scores at 1 and 5 minutes. Cord calcitonin was not correlated with cord gastrin or glucagon. Cord and 24-hour gastrin and glucagon values were not related to prematuritly; cord glucagon, but not gastrin, was related to birth asphyxia. We conclude that (1) serum calcitonin, gastrin, and plasma glucagon values rise postnatally; serum calcitonin. concentration does not correlate with the elevated serum gastrin and plasma glucagon values; and at 24 hours of age, decreased serum Ca is correlated with serum calcitonin, and hence calcitonin might play a role in the pathogenesis of early neonatal hypocalcemia.

Original languageEnglish
Pages (from-to)599-603
Number of pages5
JournalJournal of Pediatrics
Volume110
Issue number4
DOIs
StatePublished - Apr 1987
Externally publishedYes

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