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Impaired Corpus Luteum Function in Ectopic Pregnancy Cannot be Explained by Altered Human Chorionic Gonadotropin

South African Medical Research Council, Preclinical Diagnostic Chemistry Research Unit, Department of Chemical Pathology, University of Natal Medical School Durban, Natal, Republic of South Africa

Address all correspondence and requests for reprints to: Prof. R. J. Norman, Department of Chemical Pathology, University of Natal Medical School, P.O. Box 17039, Congella 4013, Republic of South-Africa.

We studied the cause of the low serum progesterone, 17β-estradiol, and 17-hydroxyprogesterone levels that occur in women with an ectopic pregnancy. Only women who had been amenorrheic for less than 8 weeks were studied in order to assess corpus luteum rather than placental biosynthesis of these steroids; each woman with an ectopic pregnancy was matched to a woman with a normal intrauterine pregnancy on the basis of serum intact hCG levels within 10% of one another to obviate the influence of different levels of this luteotropic hormone. Every woman with an ectopic pregnancy had lower serum progesterone, estradiol, and 17-hydroxyprogesterone levels than her matched normal pregnant pairmate (median values: progesterone, 27.9 vs. 83.5 mmol/L; estradiol, 0.36 vs. 1.79 nmol/L; 17-hydroxyprogesterone, 4.95 vs. 22.1 nmol/L, respectively; all P < 0.002). The ratios of intact hCG, measured by immunoradiometric assay, to hCG, measured by a hCGβ-specific RIA, were similar in the two groups.

Serum hCG bioactivity was assayed by measuring the ability of serum to stimulate testosterone secretion from mouse Leydig cells. The mean biological to intact immunological hCG ratios were 2.06 ± 1.39 (±SD) for ectopic pregnancy and 1.91 ± 0.81 for normal pregnancy (P > 0.05). The biological hCG to immunoreactive hCGβ ratios were 1.98 ± 0.75 and 2.02 ± 0.82, respectively. Serum hCG from both groups of women stimulated cAMP generation by testicular cells similarly.

We conclude that the lower serum steroid levels in women with ectopic pregnancy cannot be explained by altered hCG bioactivity. The lower steroid levels may thus reflect a primary defect of the corpus luteum, absence of another stimulator of ovarian steroid biosynthesis, or more subtle alterations in hCG glycosylation which are important in vivo but not assessed by the in vitro bioassay.

Received September 28, 1987.

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