Inhibin: a new circulating marker of hydatidiform mole?

Abstract

Objective-To define the concentrations ofinhibin in serum and tissue of patients with hydatidiform mole and assess their value as a clinical marker ofthe condition.Design-Prospective study of new patients with hydatidiform mole, comparison of paired observations, and case-control analysis.Setting-A university hospital, two large public hospitals, and a private women's clinic in Japan.Patients-Seven consecutive referred patients seen over four months with newly diagnosed complete hydatidiform mole, including one in whom the mole was accompanied by viable twin fetuses (case excluded from statistical analysis because of unique clinical features). All patients followed up for six months after evacuation of molar tissue.End point-Correlation of serum inhibin concentrations with trophoblastic disease.Measurements and main results-Serum concentrations of inhibin, human chorionic gonadotrophin, and follicle stimulating hormone were compared before and seven to 10 days after evacuation of the mole. Before evacuation the serum inhibin concentrations (median 8*3 U/ml; 95% confidence interval 2-4 to 34.5) were significantly greater than in 21 normal women at the same stage of pregnancy (2.8 U/ml; 2*1 to 3.6), and inhibin in molar tissue was also present in high concentrations (578 U/mI cytosol; 158 to 1162). Seven to 10 days after evacuation inhibin concentrations in serum samples from the same patients declined significantly to values (0 4 U/mI; 0-1 to 1-4) similar to those seen in the follicular phase of normal menstrual cycles. None of the four patients whose serum inhibin concentrations were 0 4 U/mI or less after evacuation developed persistent trophoblastic disease. Though serum human chorionic gonadotrophin concentrations declined after evacuation (6-6x 103 IU/l; 0-8x 103 to 32-6x 103), they remained far higher than in non-pregnant women. Serum follicle stimulating hormone concentrations remained suppressed.Conclusions-In this small study serum inhibin concentrations higher than those found in the early follicular phase one to two weeks after evacuation of a hydatidiform mole seemed to be specific for persistent trophoblastic disease. Further data are needed to confirm these promising results. IntroductionInhibin, a glycoprotein hormone produced by the testis and ovary, has the ability preferentially to suppress the secretion of follicle stimulating hormone by the pituitary. After its initial isolation from bovine follicular fluid' we showed that inhibin was also produced by the placenta2 and that concentrations rose during early pregnancy.3 Other studies using immunocytochemistry have localised inhibin to the cytotrophoblast of the placenta,4 which has been shown to contain messenger ribonucleic acid for the inhibin subunits.5 The production of inhibin by trophoblastic tissue and the availability of specific radioimmunoassays for inhibin prompted us to study the concentrations of inhibin in women with a gestational trophoblastic disease such as hydatidiform mole. This paper reports our results.

Second‐trimester maternal serum immunoreactive inhibin as a marker for fetal Down's syndrome

“…Inhibin may even have a role in embryogenesis, as a similar protein has been reported to play an important role in the embryogenesis of Drosophila (MacLachlan et al, 1987;Padgett et al, 1987). The inhibin levels in our study were slightly lower in comparison with other reports (Healy et al, 1990;Abe et a/., 1990;Yohkaichiya et a/., 1989;Tabei et a/., 1991). The differences between the reported values are probably due to the use of bioassays and immunoassays specific for different peptide chains.…”

Inhibins and activins: roles in clinical practice

“…Inhibin is markedly elevated in molar pregnancy 132 and in contrast to hCG the clearance rate of inhibin is high. It was therefore hoped that inhibin would prove useful in the follow up of treated moles, identifying persistent or recurrent disease more quickly than hCG.…”

Inhibins and activins: clinical advances in reproductive medicine

“…Unfortunately, the return of ovarian function leading to a rise in circulating inhibin A complicated the interpretation of surveillance inhibin A level, leaving hCG as the preferred marker (D'Antona et al, 1998a). Similarly, while an early report suggested that immunoreactive inhibin levels fell more rapidly than hCG following treatment of gestational trophoblastic disease (Yohkaichiya et al, 1989), offering the potential for inhibin to replace hCG in this setting, it became apparent subsequently that some cases of persistent or recurrent tumour detected by rising hCG may be missed by inhibin (Badonnel et al, 1994). Activin A has also been assessed as a marker of trophoblastic disease and similarly found wanting (Lambert-Messerlian et al, 1998).…”