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Growth hormone binding protein in normal and aneuploid pregnancy: a paradoxical decrease in trisomy 18
Author(s) -
Wallace Euan M.,
D'Antona Donato,
VeverisLowe Tara,
Crossley Jennifer A.,
Barnard Ross
Publication year - 2001
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.2001.00179.x
Subject(s) - trisomy , aneuploidy , gestation , intrauterine growth restriction , pregnancy , biology , endocrinology , fetus , gestational age , hormone , medicine , andrology , chromosome , genetics , gene
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 (0.51–0.84) 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.