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THE MATERNAL OVARY IS NOT THE SOURCE OF CIRCULATING INHIBIN LEVELS DURING HUMAN PREGNANCY
Author(s) -
McLACHLAN R. I.,
HEALY D. L.,
LUTJEN P. J.,
FINDLAY J. K.,
KRETSER D. M.,
BURGER H. G.
Publication year - 1987
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1987.tb02949.x
Subject(s) - gestation , endocrinology , pregnancy , medicine , ovary , in vitro fertilisation , gonadotropin , trophoblast , oocyte , biology , embryo transfer , embryo , fetus , placenta , hormone , microbiology and biotechnology , genetics
SUMMARY The concentration of immunoreactive inhibin in serum was measured in three pregnant women with premature ovarian failure involved in a donor oocyte in‐vitro fertilization programme. Inhibin was not detectable in peripheral serum prior to conception but rose within 2‐4 weeks of embryo transfer, whereafter levels rose gradually during pregnancy (< 20 weeks 1‐22 U/ml (0.85‐1.76) versus >20 weeks 2.28 U/ml (1.42‐3.67), P < 0.01; geometric mean ± 67% confidence interval) and were similar to those observed in 24 normal pregnant women. hCG rose in parallel with inhibin during early gestation, but declined after 3 months. FSH levels were elevated before conception and were suppressed during pregnancy. In conclusion (i) immunoreactive inhibin is detectable from early gestation in women with no endogenous ovarian function indicating that the maternal ovary does not contribute significantly to inhibin secretion during pregnancy; (ii) the trophoblast is the likely source of inhibin during pregnancy; (iii) the regulation of hCG and inhibin secretion differs throughout gestation; and (iv) inhibin may have a role in FSH regulation during pregnancy and/or a local role within the feto‐placental unit.