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Measurement of Plasma Free Luteinizing Hormone ß-Subunit in Women

Service d’Endocrinologie et des Maladies de la Reproduction (B.C., P.C., J.Y., G.S.), Laboratoire de Biochimie Hormonale (S.B.), Hopital Bicêtre, 94275 Kremlin Bicêtre, France; Département de Biologie Clinique (J.P., J.M.B.), Institut Gustave-Roussy, 94805 Villejuif, France; and Department of Physiology, University of Turku (I.T.H.), Turku, 20520 Finland

Address all correspondence and requests for reprints to: Dr. Gilbert Schaison, Service d’Endocrinologie et des Maladies de la Reproduction, Hopital Bicêtre, 94275 Le Kremlin Bicêtre Cedex, France. E-mail: gilbert.schaison{at}bct.ap-hop-paris.fr

Little is known about the physiological secretion of the free ß- subunit of LH (LHß). The aim of this study was to compare in women the secretion of LHß, using sensitive and specific two-site immunoassays, with dimeric LH and the free common -subunit (FAS). The LHß assay does not recognize the dimeric LH and cross-reacts only with free hCG ß-subunit (CGß). Thus, all of the plasma samples were also tested with a highly specific immunoradiometric assay for free CGß. Molar concentrations (i.e. picomoles per L) were used to compare the plasma levels of LH and its free subunits. Plasma LH, LHß, FAS, and CGß levels were measured in five normally cycling women during the early follicular phase and the ovulatory peak of LH. The pulsatile profiles of LH, LHß, FAS, and CGß were studied in five postmenopausal women before and 21 days after injection of a depot preparation of the GnRH agonist D-Trp⁶ (3.75 mg, im) and in five women with functional hypothalamic amenorrhea (FHA), i.e. low plasma LH levels, during pulsatile GnRH administration (20 µg/pulse, 90 min, sc). Afterward, one of the patients with FHA received a single sc injection of 1350 U recombinant human LH, and plasma LH, LHß, FAS, and CGß levels were measured and compared with the high plasma levels of one postmenopausal woman.

In cycling women, basal plasma LHß and CGß levels were below the detection limit of the assays (1.34 and 0.65 pmol/L, respectively), and plasma FAS levels were 13.60 ± 0.13 pmol/L. During the LH surge, there was a parallel increase in LH, LHß, and FAS. Plasma CGß levels remained undetectable. In normal postmenopausal women, basal plasma dimeric LH, LHß, and FAS levels were increased in parallel, and their pulsatile profiles were similar, without measurable plasma CGß levels. After D-Trp⁶ administration, plasma LH and LHß levels were completely suppressed, whereas plasma FAS levels increased, and plasma CGß remained below 0.65 pmol/L. In FHA women, basal plasma levels of LH and FAS were low, without detectable LHß and CGß levels. During pulsatile GnRH administration, LHß became detectable, and pulses were synchronous with those of LH and FAS. The secretion of LH and LHß was almost equimolar. Plasma CGß levels remained undetectable. In the patient with FHA, administration of recombinant human LH increased only plasma LH levels, whereas plasma LHß and FAS levels remained very low.

In conclusion, when the production of dimeric LH increases, a concomitant, parallel, and almost equimolar hypersecretion of uncombined and biologically inactive LHß occurs. Like the -subunit, LHß may be secreted in the dissociated free form. This can lead to pitfalls during clinical investigations if assays of free CGß display some cross-reaction with free LHß.