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Calcium and phosphorus metabolism in the premature infant

P D Mayne1, I Z Kovar

  • 1Department of Chemical Pathology, Charing Cross and Westminster Medical School, Westminster Hospital, London, UK.

Annals of Clinical Biochemistry
|March 1, 1991
PubMed

Insights

Preterm infants may develop rickets due to insufficient calcium and phosphorus from breast milk. Early diagnosis and treatment are crucial for bone health in premature infants.

Area of Science:

  • Neonatology
  • Pediatric Endocrinology
  • Nutritional Science

Background:

  • Fetal development involves significant calcium and phosphorus accumulation in the third trimester.
  • Human breast milk may lack adequate minerals for preterm infants, hindering bone mineralization.
  • Rickets of prematurity can manifest clinically 6-12 weeks after birth.

Purpose of the Study:

  • To highlight the risk of rickets in preterm infants due to inadequate mineral intake.
  • To discuss the diagnostic criteria and biochemical markers for rickets of prematurity.
  • To outline the biochemical indicators of successful treatment.

Main Methods:

  • Clinical observation of preterm infants.
  • Biochemical testing including plasma and urinary mineral levels.
  • Assessment of 1-alpha hydroxylase activity and 1,25-dihydroxyvitamin D levels.

Main Results:

  • Inadequate phosphorus intake is a primary cause of rickets of prematurity.
  • Delayed maturation of 1-alpha hydroxylase can lead to low 1,25-dihydroxyvitamin D.
  • Treatment response is indicated by decreased alkaline phosphatase and increased phosphate levels.

Conclusions:

  • Rickets of prematurity is a significant concern in preterm infants.
  • Biochemical tests are vital for diagnosis and monitoring treatment.
  • Optimizing mineral and vitamin D supplementation is essential for bone health.

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