Objective: To explore whether abnormalities in growth hormone binding protein (GHBP) may underlie the growth restriction associated with fetal aneuploidy.
Design: A retrospective casecontrol study.
Setting: Monash Medical Centre. Clayton, Victoria, Australia.
Population: Twenty-one trisomy 18, and 30 trisomy 21 pregnancies, and 170 chromosomally normal pregnancies at 15-18 weeks of gestation representing three to five controls per case matched for source, gestation and duration of storage.
Methods: GHBP was measured using a ligand immunofunctional assay
Results: In the chromosomally normal pregnancies GHBP levels decreased slightly but significantly across the narrow gestational window studied. Compared with controls, levels of GHBP, expressed as median (95% CI) multiples of the median (MoM). in the trisomy 21 pregnancies were similar, 1.0 (0.92-1.39) MoM and 1.27 (1.04-1.50) MoM, respectively; P = 0.061 (Mann-Whitney U test) but were significantly reduced in the trisomy 18 pregnancies, 0.68 (0.5 1-0.84) MoM: P = 0.0014 (Mann-Whitney U test).
Conclusions: These data suggest that decreased levels of maternal growth hormone binding protein, and by implication growth hormone receptor complement, may underlie the early severe growth restriction that is characteristic of trisomy 18.
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