Effects of immunization with the β-subunit of ovine luteinizing hormone (oLHβ) on luteal function in rhesus monkeys

Thau, Rosemarie B.; Yamamoto, Yasutake; Sundaram, K.; Seidman, Linda S.

doi:10.1016/0165-0378(81)90124-8

Cited by 6 publications

(7 citation statements)

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“…1989. in humans were utilized in all the experiments described below. This criterion eliminated FCA, the most potent immune enhancer, [12][13][14] and thus other methods of inducing highly effective anti-LHRH antibodies in the shortest possible time were investigated. Although previous investigators used doses of immunogen from 2.2 ug/mousa'" to 5 mg/rabbit," no attempts had been made to conduct systematic dose-response studies.…”

Section: Introductionmentioning

confidence: 99%

Active Immunization Against LHRH: I. Effects of Conjugation Site and Dose

Ladd

Tsong

et al. 1990

American J Rep Immunol

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Section: Introductionmentioning

confidence: 99%

Active Immunization Against LHRH: I. Effects of Conjugation Site and Dose

Ladd

Tsong

et al. 1990

American J Rep Immunol

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“…Therefore, it could be documented that in clinical cases limited FSH stimulation during the course of folliculogenesis is seldom to occur, and, if occurs, it does not cause impairment of the corpus luteum function but anovulation, as seen in anorexia nervosa. It has been shown that aberrant LH secretion during the luteal phase causes LPD [6][7][8]. In the present study, it was noted that steroidogenesis, especially P production, was depressed in some LPD women, despite that their corpora lutea developed appropriately, as evidenced by decreased basal-FSH in MLP and by sufficient potential to produce P and E2.…”

Section: Analysis By Using the Modified Classification O F Lpdmentioning

confidence: 64%

“…Insufficient LH in the luteal phase could also be a culprit in LPD, since LH plays an important role in inhibin and progesterone secretion by the human corpus luteum [5]. Active immunization of monkeys with /3-subunit of ovine LH is shown to induce infertility as a result of LPD, being evidenced by decreased peripheral concentrations and production rates of P and shortened luteal phase length, which can be reversed by supplementation with medroxyprogesterone acetate [6,7]. In support of these findings, abnormal patterns of LH secretion is reported to be related to LPD [8].…”

mentioning

confidence: 99%

Endocrine Pathophysiology of Luteal Phase Deficiency as Assessed by GnRH/TRH Stimulation Tests Performed in the Early Follicular and Midluteal Phases of the Menstrual Cycle.

et al. 1993

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Abstract. To investigate endocrine pathophysiology of luteal phase deficiency (LPD), GnRH/TRH stimulation tests were performed in the early follicular (EFP) and midluteal phases (MLP) of the menstrual cycle in 52 infertile women with a history of short luteal phase, in whom pituitary responsiveness to GnRH/TRH and steroidogenic competency of the corpus luteum were analyzed. Twelve women with either elevated basal-LH or exaggerated PRL response to GnRH/TRH in EFP were eliminated, and the remaining 40 women were studied. Basal-FSH in EFP inversely correlated with steroidogenic parameters in MLP, indicating that compromised folliculogenesis causes LPD. In a fraction of LPD women, decreased basal-LH in MLP was associated with decreased basal-progesterone (p), in spite of normal steroidogenic potential of the corpus luteum, suggesting that aberrant LH secretion is another progenitor of LPD. The other group of LPD women showed shortening of high phase period and/or extravagant discrepancy in endometrial dating without apparent abnormal endocrine parameters, suggesting that unknown factors are involved in establishment of LPD. From the diagnostic point of view, they were discriminated into three groups, normal, incomplete LPD and complete LPD groups, with a modified classification of LPD; 1) shortening of high phase period <11 days, 2) delay in histological to chronological dating of the endometrium >2 days, and 3) decreased max-P in MLP < 10 ng/ml. Normal (n=14) and complete LPD (n=7) groups consisted of women having all the criteria of classification within and out of the cut-off values, respectively. The remainders were enrolled into incomplete LPD group (n=19). Complete LPD group mainly consisted of women having compromised folliculogenesis as a cause of LPD. In contrast, incomplete LPD group appeared a mixture of heterogenous populations as to the genesis of LPD. GnRH/TSH stimulation test, especially when performed in MLP, would unveil endocrine pathophysiology of LPD and provide an accurate standard for diagnosis of LPD.

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“…Active immunization of female rhesus monkeys with the β-subunit of ovine LH (β-oLH) led to inhibition of fertility, which was accompanied by reduced progesterone levels during luteal phase. 40 The anti-fertility effect mediated by active immunization with β-oLH could be reversed by administration of medroxyprogesterone acetate. 41 In addition to LH, the potential of LH-receptor has also been studied.…”

Section: Veterinary Applications Of Gnrh-based Contraceptive Vaccinementioning

confidence: 92%

Milestones in contraceptive vaccines development and hurdles in their application

Gupta

Shrestha

Minhas

2013

Human Vaccines & Immunotherapeutics

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Effects of immunization with the β-subunit of ovine luteinizing hormone (oLHβ) on luteal function in rhesus monkeys

Cited by 6 publications

References 0 publications

Active Immunization Against LHRH: I. Effects of Conjugation Site and Dose

Active Immunization Against LHRH: I. Effects of Conjugation Site and Dose

Endocrine Pathophysiology of Luteal Phase Deficiency as Assessed by GnRH/TRH Stimulation Tests Performed in the Early Follicular and Midluteal Phases of the Menstrual Cycle.

Milestones in contraceptive vaccines development and hurdles in their application

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