Owen, Elizabeth J.; (1993) Growth hormone co-treatment in superovulation programmes. Doctoral thesis (M.D), UCL (University College London).

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Abstract

The role of insulin-like growth factor I (IGF-I) in modulating the granulosa cell response to gonadotrophins is now well established and recent work has suggested that growth hormone (GH) administration increases intraovarian IGF-I production. Following the successful use of GH administration in patients who had previously had a poor response to clomiphene citrate and human menopausal gonadotrophins (hMG) prior to in-vitro fertilisation and embryo transfer, twenty women were recruited into a prospective, double blind, placebo controlled trial of GH co-treatment. Women with PCO developed more follicles and had more oocytes collected but the women with normal ovaries showed no response. Circulating IGF-I concentrations rose during GH treatment but follicular fluid concentrations were significantly lower than serum. IGF-II concentrations did not alter with GH treatment. Gonadotrophin releasing-hormone analogues are associated with increased requirements for hMG and twenty eight women were subsequently recruited into a randomised, placebo controlled study using GH in combination with buserelin and hMG. Women who received GH and who had ultrasound diagnosed PCO had an improved outcome, however there was a substantial placebo effect. Women with normal ovaries did not demonstrate any effect of GH treatment. IGF-I concentrations rose with GH administration but not with hMG alone. Follicular fluid concentrations of IGF-I were lower than serum concentrations, suggesting that IGF-I is not synthesised in the ovary. As women with PCO formed the responsive group we wished to establish a biochemical marker for the condition. 11[beta]-hydroxyandrostenedione (11[beta]-OH-A4) concentrations had been suggested to be abnormal in PCO. We therefore developed an in-house method for determining the concentrations of 11[beta]-OH-A4 in serum and follicular fluid. We were, however, unable to define differences in concentrations between women with normal and polycystic ovaries and concluded that 11[beta]-OH-A4 was not a suitable marker for PCO.

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