| Summary: | In order to characterize and compare the pattern of
inhibin production in the follicular phase between patients of
the clomiphene citrate/human menopausal gonadotropin (hMG) and
Buserelin/hMG protocols in in-vitro fertilization, serum
inhibin levels from 20 patients in each protocol were
measured. The patients were matched for age and had tubal
diseases only. It was hypothesized that the serum inhibin
levels would be different in these two groups due to possible
local actions of clomiphene citrate and Buserelin (a GnRH
agonist) on the ovary. Serum inhibin levels were measured
using an immunoenzymatic assay kit, with the mean interassay
and intraassay coefficients of variation being 14.1% and 8.9%
respectively. This assay did not cross-react with folliclestimulating
hormone, luteinizing hormone, transforming growth
factor β, activin A, insulin-like growth factor-1, seminal
inhibin like peptide and human chorionic gonadotropin (hCG),
but it could detect free a subunits of inhibin in addition to
dimric inhibin. Apart from inhibin, serum estradiol-17/3
levels in patients from the two protocols were compiled from
patient records. Serum inhibin was found to correlate
significantly with serum estradiol-17/3 in the follicular phase
(r= 0.844; P< 0.0001). In the clomiphene citrate/HMG
protocol, on day 0 (day of ovulation trigger with hCG), day -1
(one day before hCG administration) and day -2 (two days
before hCG administration), the serum inhibins were 6.84 +/- 0.76, 5.11 +/- 0.61, and 3.55 +/- 0.31 U/ml respectively; the
serum estradiol-170 levels were 5141 +/- 353.6, 3332.7 +/-
192.6, and 2112.5 +/- 117.3 pmol/1 respectively. In the
Buserelin/HMG protocol, on days 0, -1, and -2, the serum
inhibin levels were 6.48 +/- 0.71, 5.47 +/- 0.49, and 4.0 +/-
0.35 U/ml respectively; the serum estradiol-17/3 levels were
4287.8 +/- 409.4, 2991.7 +/- 259.8, and 2093.5 +/- 151.3
pmol/1 respectively. Serum inhibin and estradiol-17/3 levels
in these two protocols were compared by the unpaired t-test.
No significant differences were found in serum inhibin and
estradiol-17/3 levels on days 0, -1 and -2 between these two
groups of patients (inhibin: P= 0.73, 0.639, and 0.37,
respectively; estradiol-17/3: P= 0.123, 0.298 and 0.93,
respectively).
With respect to follicular growth as assessed by
ultrasonography, the Buserelin/HMG protocol resulted in
significantly greater number of large follicles with diameter
greater than or equal to 17 mm on day 0 (2.45 +/- 0.28),
compared with that in the corresponding size category of the
clomiphene citrate/HMG protocol (1.50+/- 0.21) (P=0.0095).
Whereas, in the size category of 10 to 13mm in follicular
diameter on day 0, the number of follicles in the
Buserelin/HMG protocol (4.7 + /- 0.7) was significantly smaller
than that in the clomiphene citrate/HMG protocol (7.1 +/- 0.8)
(P= 0.0306). Nevertheless, no significant differences were
found in the number of oocytes retrieved, mature and total, between the two groups of patients. In summary, the
clomiphene citrate/HMG and "ultra-short" Buserelin/HMG
protocols resulted in similar ovarian responses as reflected
by serum inhibin and estradiol-17/3 levels. Therefore, the
data of the present study did not support the proposed
hypothesis, despite the observation that the Buserelin/HMG
protocol produced larger follicles.
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