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Updated: Aug 10, 2026

Isolation of Leukocytes from the Human Maternal-fetal Interface
Published on: May 21, 2015
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.
Plasma lactoferrin concentration, leucocyte count, serum prolactin concentration and storage iron status were studied in 313 women at various stages of pregnancy. The mean serum iron value, percentage saturation of transferrin and geometric mean serum ferritin concentrations decreased as pregnancy progressed. In contrast, the total iron-binding capacity showed a highly significant increase with advancing gestation. Plasma lactoferrin concentration showed a mild progressive increase during pregnancy (peaking 29-32 weeks). The increase in lactoferrin concentration was, however, disproportionately small when compared with the concomitant pregnancy-related elevation in leucocyte count. The ratio of plasma lactoferrin concentration to leucocyte count therefore appeared to be abnormally low during pregnancy suggesting an acquired defect of lactoferrin release by leucocytes of pregnant women. It is unlikely that prolactin was the factor responsible for the reduced leucocyte release of lactoferrin. The lactoferrin:leucocyte ratio was already significantly reduced early in pregnancy at a time when prolactin concentration was relatively low. Furthermore, the correlation between prolactin concentration and both lactoferrin concentration and lactoferrin:leucocyte ratio was positive. Pregnancy appears to be associated with an acquired abnormality of leucocyte degranulation, the cause of which is not clear at present.
Plasma lactoferrin concentration, leucocyte count, serum prolactin concentration and storage iron status were studied in 313 women at various stages of pregnancy. The mean serum iron value, percentage saturation of transferrin and geometric mean serum ferritin concentrations decreased as pregnancy progressed. In contrast, the total iron-binding capacity showed a highly significant increase with advancing gestation. Plasma lactoferrin concentration showed a mild progressive increase during pregnancy (peaking 29-32 weeks). The increase in lactoferrin concentration was, however, disproportionately small when compared with the concomitant pregnancy-related elevation in leucocyte count. The ratio of plasma lactoferrin concentration to leucocyte count therefore appeared to be abnormally low during pregnancy suggesting an acquired defect of lactoferrin release by leucocytes of pregnant women. It is unlikely that prolactin was the factor responsible for the reduced leucocyte release of lactoferrin. The lactoferrin:leucocyte ratio was already significantly reduced early in pregnancy at a time when prolactin concentration was relatively low. Furthermore, the correlation between prolactin concentration and both lactoferrin concentration and lactoferrin:leucocyte ratio was positive. Pregnancy appears to be associated with an acquired abnormality of leucocyte degranulation, the cause of which is not clear at present.
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