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PubMed1984

Evaluation of commercially available radioimmunoassays for the determination of luteinizing hormone in serum and urine. Application for the detection of endogenous rise of luteinizing hormone in a in vitro fertilization program.

Three commercially available RIA kits for serum and urinary LH were assessed for their usefulness to detect endogenous LH rise in patients receiving ovarian stimulation as part of an in vitro fertilization treatment for infertility. Prerequisites included a turn-around time of 5 hours for an assay of 100 tubes. The following parameters were evaluated: reproducibility of standard curve, sensitivity, precision profile, within- and between-assay precision, analytical drift, recovery and linearity. The Amerlex LH RIA kit was selected because of superior precision profiles, higher precision and better recovery tests.

Clomiphene↗
PubMed1988

Effects of [D-Arg6, Trp7, Leu8, Pro9NEt]-luteinizing hormone-releasing hormone (sGnRH-A) and [D-Ala6, Pro9NEt]-luteinizing hormone-releasing hormone (LHRH-A), in combination with pimozide or domperidone, on gonadotropin release and ovulation in the Chinese loach and common carp.

The effects of LHRH-A and sGnRH-A alone and in combination with the dopamine receptor antagonists pimozide (PIM) and domperidone (DOM) on stimulation of gonadotropin (GtH) secretion and ovulation in Chinese loach (Paramisgurnus dabryanus) and common carp (Cyprinus carpio) were studied. When tested in the absence of a dopamine receptor antagonist, sGnRH-A was about 10-fold more potent than LHRH-A in stimulating GtH secretion in loach, whereas these peptides were of similar effectiveness in common carp. Both peptides were effective alone in inducing ovulation in loach, but were ineffective in common carp. PIM and DOM stimulate a small but significant increase in serum GtH, and greatly potentiate the effects of LHRH-A and sGnRH-A on GtH secretion and ovulation in both species. DOM was of equal or somewhat greater potency than PIM in potentiating the action of releasing hormone agonists in loach; however, DOM had markedly greater effectiveness in common carp. sGnRH-A in the presence of DOM was more effective than LHRH-A in stimulating GtH secretion and ovulation in common carp. The present studies suggest that there are marked differences in the relative contribution of GnRH and dopamine in the control of GtH secretion in loach and common carp, and indicate in particular that the more intense dopaminergic inhibitory control of GtH release in common carp modifies the responsiveness of the pituitary to GnRH peptides.

Animals↗
PubMed1985

Human anti-luteinizing hormone-releasing hormone antibodies in patients treated with synthetic luteinizing hormone-releasing hormone.

One hundred sixty-three patients who were given synthetic LH-RH therapeutically underwent monitoring of serum IgG anti-LH-RH antibodies. Five of the patients showed specific binding to antibodies. Development of anti-LH-RH antibodies was not limited to those patients with a congenital deficiency of LH-RH. Urticarial responses occurred in four patients, only one of whom had IgG antibodies. Patients who had IgG antibodies or an urticarial response underwent monitoring of their serum IgE anti-LH-RH antibodies, but none had a positive binding response. The refractory state which has been reported in patients in whom similar antibodies to LH-RH develop was not invariably observed among these patients.

Adult↗
PubMed1998

The unique exon 10 of the human luteinizing hormone receptor is necessary for expression of the receptor protein at the plasma membrane in the human luteinizing hormone receptor, but deleterious when inserted into the human follicle-stimulating hormone receptor.

The LH receptor (LHR) is a member of the family of G protein-coupled seven-times plasma membrane transversing receptors. Its gene consists of 11 exons, the last one encoding the transmembrane and intracellular domains of the receptor. The FSHR, and its gene, resemble structurally those of the LHR, with the exception that the sequences corresponding to exon 10 in LHR are missing in FSHR, which is thus encoded by a total of ten exons. Our recent studies on the marmoset monkey testis LHR cDNA indicated that an 81 bp nucleotide sequence, encoding the complete exon 10 of the LHR gene in other mammalian species, is absent in this species without affecting the LHR function. To study further the role of the exon 10 encoded sequences of the LHR in the gonadotropin receptor function, a deletion of exon 10 from the human LHR (hLHdeltaexon10R), and a chimeric hFSHR with exon 10 from hLHR inserted (hFSHLHexon10R), were constructed in expression vectors. The results presented here demonstrate that 293 cells transfected with the hLHdeltaexon10R display a decrease in the proportion of the receptor binding at the cell surface, compared with cells transfected with wild-type hLHR. However, the cells expressing hLHdeltaexon10R showed similar high affinity binding of [125I]iodo-hCG as those transfected with wild-type hLHR, in either intact cells or their detergent extracts. In addition, cells expressing the hLHdeltaexon10R and wild-type hLHR displayed similar dose-response of cAMP production to hCG stimulation. Cells transfected with chimeric hFSHLHexon10R showed barely detectable [125I]iodo-FSH binding in intact cells compared with those transfected with wild-type hFSHR. The FSH binding detected in cellular detergent extracts displayed 10-fold lower binding activity than wild-type receptors, in spite of similar level of immunoreactive FSHR protein expression in the transfected cells. The hFSHLHexon10R had a modest 5-fold lower binding affinity for FSH as compared with wild-type hFSHR. In conclusion, the present study indicates that the sequences encoding exon 10 of the hLHR are essential for the LHR expression at the plasma membrane, but deleterious for function if inserted into the hFSHR.

Animals↗
PubMed1991

National Cancer Institute study of luteinizing hormone-releasing hormone plus flutamide versus luteinizing hormone-releasing hormone plus placebo.

A randomized, double-blind trial in patients with disseminated, previously untreated prostate cancer (stage D2) was designed to test the hypothesis that maximal androgen blockade improves the effectiveness of the treatment of prostatic cancer. Six hundred three men received leuprolide in combination with either placebo or flutamide, and were followed for a minimum of 5 years. The 303 patients randomly assigned to receive leuprolide and flutamide had a longer progression-free survival and an increase in the median length of survival compared with the 300 patients receiving leuprolide plus placebo. Differences between the treatments were particularly evident for men with minimal disease and good performance status.

Antineoplastic Combined Chemotherapy Protocols↗