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Related Experiment Videos

Plasma lactoferrin content in pregnancy.

R D Baynes1, R D Lamparelli, W R Bezwoda

  • 1Department of Chemical Pathology, South African Institute for Medical Research, Johannesburg.

South African Medical Journal = Suid-Afrikaanse Tydskrif Vir Geneeskunde
|November 18, 1989
PubMed
Summary
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Pregnancy is linked to lower lactoferrin release from white blood cells, despite increased lactoferrin levels. This suggests an acquired defect in leucocyte degranulation during gestation.

Area of Science:

  • Obstetrics and Gynecology
  • Hematology
  • Immunology

Background:

  • Iron status and inflammatory markers change significantly during pregnancy.
  • Lactoferrin, an iron-binding protein, is primarily released by leucocytes (white blood cells).
  • Pregnancy involves complex physiological adaptations affecting maternal blood parameters.

Purpose of the Study:

  • To investigate changes in plasma lactoferrin and leucocyte count during pregnancy.
  • To assess the relationship between lactoferrin, leucocytes, and prolactin levels.
  • To explore potential defects in lactoferrin release by leucocytes in pregnant women.

Main Methods:

  • Cross-sectional study of 313 pregnant women at various gestational stages.
  • Measurement of plasma lactoferrin, leucocyte count, serum prolactin, and iron status parameters (serum iron, transferrin saturation, ferritin, TIBC).

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  • Statistical analysis to determine trends and correlations with advancing gestation.

    • Main Results:

    • Serum iron, transferrin saturation, and ferritin decreased with advancing pregnancy.
    • Total iron-binding capacity increased significantly during gestation.
    • Plasma lactoferrin increased mildly, but the lactoferrin:leucocyte ratio decreased significantly, suggesting impaired leucocyte release.

    Conclusions:

    • Pregnancy is associated with an acquired abnormality in leucocyte degranulation.
    • The reduced lactoferrin:leucocyte ratio is likely due to a defect in lactoferrin release by leucocytes.
    • Prolactin is unlikely to be the primary cause of this defect.