Hepatocyte growth factor, epidermal growth factor, and placenta growth factor concentrations in peripheral blood of pregnant women with alcohol abuse
P Vuorela, T Sarkola, H Alfthan… - Alcoholism: Clinical …, 2002 - Wiley Online Library
P Vuorela, T Sarkola, H Alfthan, E Halmesmäki
Alcoholism: Clinical and Experimental Research, 2002•Wiley Online LibraryBackground: Alcohol abuse during pregnancy compromises fetal development not only
directly but also by abnormal placental function. Therefore, hepatocyte growth factor (HGF),
epidermal growth factor (EGF), and placenta growth factor (PlGF), expressed in the placenta,
may play a role in alcohol‐induced placental dysfunction. Methods: Peripheral venous blood
samples were collected from 40 pregnant alcohol‐abusing women and 42 abstinent
pregnant women from gestational weeks 4 to 41. Plasma HGF and serum PlGF were …
directly but also by abnormal placental function. Therefore, hepatocyte growth factor (HGF),
epidermal growth factor (EGF), and placenta growth factor (PlGF), expressed in the placenta,
may play a role in alcohol‐induced placental dysfunction. Methods: Peripheral venous blood
samples were collected from 40 pregnant alcohol‐abusing women and 42 abstinent
pregnant women from gestational weeks 4 to 41. Plasma HGF and serum PlGF were …
Background: Alcohol abuse during pregnancy compromises fetal development not only directly but also by abnormal placental function. Therefore, hepatocyte growth factor (HGF), epidermal growth factor (EGF), and placenta growth factor (PlGF), expressed in the placenta, may play a role in alcohol‐induced placental dysfunction.
Methods: Peripheral venous blood samples were collected from 40 pregnant alcohol‐abusing women and 42 abstinent pregnant women from gestational weeks 4 to 41. Plasma HGF and serum PlGF were assessed by enzyme‐linked immunosorbent assays and serum EGF by an immunofluorometric assay.
Results: Plasma HGF concentrations were similar in alcohol‐abusing and abstinent mothers, although in the latter women these concentrations increased with advancing pregnancy. Serum EGF concentrations were consistently higher in alcohol‐abusing than in abstinent mothers. In the latter, these concentrations decreased with advancing pregnancy. Serum PlGF concentrations increased with advancing pregnancy in both groups and were higher in alcohol‐abusing mothers during the second and third trimesters but not during the first.
Conclusions: Alcohol abuse during pregnancy is associated with changes in maternal circulating EGF and PlGF but not HGF concentrations. The observed changes may be caused by alcohol per se or may be secondary to possible alcohol‐induced changes in placental physiology.
