Rise In Luteinizing Hormone Levels Research Articles

The effect of LH rise during artificial frozen-thawed embryo transfer (FET) cycles.

PurposeTo evaluate the association between a rise in serum luteinizing hormone (LH) levels during artificial frozen–thawed embryo transfer (FET) cycles and clinical pregnancy rate.MethodsA retrospective cohort study of women undergoing artificial FET cycles. We compared cycles in which LH double itself from the early follicular phase and further (group A) to cycles without a rise in LH (group B). Endometrium preparation was achieved by administration of 2 mg three times per day estradiol valerate tablets. Embryo transfer (ET) was conducted after achieving endometrial thickness > 7 mm and vaginal progesterone was added according to the embryo’s age. A beta-hCG was measured 13–14 days after ET. Clinical pregnancy was diagnosed on transvaginal ultrasound.ResultsData from 984-FET cycles were retrieved. LH, exogenous estradiol (E2), progesterone values, endometrial thickness, and pregnancy outcomes were available in all patients. From 984-FET cycles, 629 (63.9%) had a doubling, and 355 (36.07%) had no rise in LH. Patients mean age was 30 years, similar in both groups. A multivariable logistic regression analysis was calculated to assess the effect of LH rise and pregnancy outcomes, after adjusting for confounders including a rise in E2 level and endometrial thickness. In this model, there was no association between doubling LH values and pregnancy rates (adjusted odds ratio: 1.06, 95% CI: 0.75–1.5, P = 0.74).ConclusionLH rise during artificial FET cycles does not alter pregnancy rates. Apparently, hormonal monitoring of LH levels may not yield useful information in the artificial FET cycle and may be omitted.Lay summarySupplementation of estradiol, a hormone produced by the ovaries, starting at the beginning of the menstrual cycle of an artificially frozen embryo transfer (FET) can lead to a rise in luteinizing hormone (LH), the hormone that induces ovulation. Such a rise in LH may interfere with embryo implantation, the process where the embryo attaches to the inner lining of the uterus and, therefore, could affect the chances of pregnancy. The current study is the first to assess the effect of a dynamic rise in LH levels during FET cycles on pregnancy rates. This study found no difference in pregnancy rates between FET cycles where the LH doubled compared to cycles without such a rise in LH. Larger, prospective studies should be conducted to assess the impact of LH elevation on pregnancy outcomes.

Chronic Exposure to Low Levels of Oestradiol‐17β Affects Oestrous Cyclicity, Hypothalamic Norepinephrine and Serum Luteinising Hormone in Young Intact Rats

Chronic exposure to oestrogens is known to inhibit the secretion of luteinising hormone (LH) in rats, leading to anovulation. Hypothalamic catecholamines, norepinephrine and dopamine play an important role in LH regulation. However, the effects of chronic exposure to low levels of oestradiol on hypothalamic catecholamines have not been investigated thoroughly. In the present study, adult female Sprague-Dawley rats were either sham implanted or implanted with 17beta-oestradiol (E(2)) pellets (20 ng/day) for 30 (E-30), 60 (E-60) or 90 (E-90) days. E(2) exposure affected oestrous cyclicity and ovarian morphology in a duration-dependent manner. There was no change in oestrous cyclicity in E-30 rats; however, 75% of E-60 and 95% of E-90 rats were acyclic (P < 0.05). Cycling rats from E-30 or the control group were killed at different time points on the afternoon of pro-oestrous. E-30 rats in oestrous, constant oestrous rats in the E-60 and E-90 groups and a group of old constant oestrous (OCE) rats were killed at 12.00 h. LH was measured in the serum by radioimmunoassay. Individual hypothalamic nuclei that are involved in LH regulation were microdissected and analysed for norepinephrine and dopamine levels using high-performance liquid chromatography/electrochemical detection. Norepinephrine levels in the hypothalamic nuclei increased significantly in control and E-30 groups during the afternoon of pro-oestrous, which was accompanied by a rise in LH levels (P < 0.05). On the day of oestrous, norepinephrine concentrations in hypothalamic nuclei and serum LH were significantly lower in E-60, E-90 and OCE rats compared to E-30 and control rats. On the other hand, dopamine levels declined significantly in one hypothalamic nucleus. These results indicate that chronic E(2) exposure affects hypothalamic catecholamine and serum LH levels in a duration-dependent manner. This coincides well with the loss of cyclicity observed in these animals. These results suggest that repeated exposure to endogenous oestrogens could play a role in reproductive senescence.

Amenorrhea in anorexia nervosa neuroendocrine control of hypothalamic dysfunction

Amenorrhea is one of the cardinal features of anorexia nervosa and is associated with hypothalamic dysfunction. Earlier theories of weight loss, decreased body fat, or exercise do not fully explain the etiology of amenorrhea in anorexia nervosa. Disturbances in central dopaminergic and opioid activity have been described in anorexia nervosa and both these substances are known to modulate gonadotropin-releasing hormone (GnRH)-mediated luteinizing hormone (LH) release. Serum LH, follicle-stimulating hormone (FSH), estradiol, and prolactin levels were measured at baseline and after administration of metoclopramide (a central D-2 dopamine receptor blocker) in 10 newly diagnosed women with anorexia nervosa and in 10 healthy age-matched controls. Basal prolactin levels and the prolactin response to metoclopramide were significantly impaired in the group with anorexia nervosa. Metoclopramide did not induce a significant rise in LH levels in either the anorexic or the control groups. Neurotransmitter abnormalities may influence hypothalamic dysfunction in anorexia nervosa but the exact mechanism remains to be determined.

The effects of a dopamine antagonist on luteinizing hormone and prolactin release in women with anorexia nervosa and in normal controls

To evaluate the possible role of central dopaminergic suppression of gonadotropin secretion in the genesis of amenorrhea associated with anorexia nervosa (A.N.), a central D-2 dopamine receptor blocker was administered to 10 women with A.N. and 10 regularly menstruating age-matched controls. Serum prolactin and luteinizing hormone (LH) levels were measured at − 15, 0, 30, 60, 120, and 180 min after administration of metoclopramide (10 mg orally). Mean basal prolactin ( p < 0.001) and estradiol levels ( p < 0.02) were significantly lower in women with A.N. The prolactin response to metoclopramide was significantly impaired in women with anorexia nervosa. No correlation was found between the prolactin response and percentage ideal body weight. Basal and post-stimulation prolactin levels were correlated with estradiol levels. After adjusting for the effects of estradiol, significant differences between patients with A.N. and controls remained in prolactin levels at baseline ( p < 0.01), 120 min ( p < 0.02) and 180 min ( p < 0.05). Metoclopramide did not induce a significant rise in LH levels in either the A.N. or control groups. These data are consistent with central dopaminergic inhibition of prolactin secretion in anorexia nervosa but do not support the hypothesis that central dopaminergic inhibition is related to diminished LH release in this state.

Endocrine profile in breast cancer patients receiving chemotherapy.

Cyclophosphamide and other alkylating agents suppress ovarian function in pre-menopausal women. However, endocrine details remain unknown regarding the influence of patients' age and obesity on CMF-induced hormonal changes. We studied changes in endocrine profile due to chemotherapy (CMF) in 70 pre-menopausal patients with axillary node positive, stage II and/or III breast carcinoma. Plasma levels of estrone (E1), estradiol (E2), androstenedione (A2), luteinizing hormone (LH), and prolactin (PRL) were determined on day 1 and 8 of each chemocycle for 12 cycles. After receiving therapy, 23% of the women continued to have regular menstrual cycles (non-amenorrheic group). In the remaining 77%, ovarian function was suppressed, as evidenced by the onset of amenorrhea within 0-11 months (amenorrheic group). The mean time to amenorrhea was 2.83 +/- 0.33 months (SE). The time required to develop amenorrhea inversely correlated to the patient's age. Both incidence of amenorrhea and time to amenorrhea remained unaffected by either patient's obesity or the timing of chemotherapy initiation in relation to menstrual cycle phase (progestational, follicular). Plasma hormone levels fluctuated widely in both groups during the first three chemocycles. During chemocycle months 4 to 10, in the amenorrheic group, plasma E1, E2, and P declined to their baseline levels with a concomitant rise in LH levels. At this time, E1, E2, and P levels were significantly lower in amenorrheics, despite menstrual cycle associated fluctuations in the non-amenorrheic group. Estrogens (E1 and E2) gradually declined further following the onset of amenorrhea in subsequent months. Further data analysis suggests that host age or obesity did not influence CMF-induced changes in the plasma endocrine profile.

Modulation of luteinizing hormone secretion by estrogens in patients with Reifenstein’s syndrome

The role of estrogens on gonadotropin secretion was assessed in two siblings with incomplete virilization syndrome type I due to partial androgen insensitivity (Reinfenstein's syndrome). Serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured before and after 100 micrograms LH-releasing hormone (RH) intravenous (IV) stimulation, as well as during long-term clomiphene citrate (CC) administration. Serum testosterone (T) and estrogens were determined before and during daily administration of human chronic gonadotropin (hCG) and also during the CC treatment. Basal levels of LH were elevated in both patients: 12.5 +/- 1.1 mIU in patient A and 19.8 +/- 1.8 mIU/ml in patient B. Conversely, FSH levels were within normal limits. Administration of LH-RH in both subjects induced a rise in LH levels, while FSH concentration showed no increase. The CC administration resulted in a significant (P less than 0.005) increment in serum LH levels without changes in FSH concentration. An important increase of serum T and estradiol (E2) levels was noted during CC administration; thus, in patient A those levels augmented from 20 to 48 ng/ml for T and from 78 to 220 pg/ml for E2; and patient B showed an increment from 20 to 35 ng/ml for T, and from 55 to 180 pg/ml for E2. The daily administration of hCG was followed by an increment in both T and E2 levels, which was of lesser degree for estrone concentration. These results suggest that endogenous estrogens, particularly E2, modulate LH secretion in patients with partial androgen insensitivity; however, it appears that estrogens had no physiologic effect on FSH secretion.

Gonadotropin deficiency in Tourette's syndrome: a preliminary communication.

Plasma baseline levels of gonadotropins and sex steroids were measured in 17 patients with Tourette's Syndrome (TS). In addition, a Gonadotropin Stimulation test, using a synthetic Gonadotropin releasing factor analogue (GnRH, 100 micrograms, i.v.), was performed in 7 patients. Plasma levels of Luteinizing Hormone (LH) were uniformly low in all patients, while those of Follicle Stimulating hormone (FSH) and sex steroids were less depressed in some patients and in the normal range in others. In all patients, stimulation with GnRH analogue produced a marked rise in LH levels, but the FSH responses were much less dramatic and did not significantly exceed that of normal controls. Our findings indicate reduced gonadotropin release in patients with TS, and support the hypothesis of hypothalamic involvement in the disease.

SUSTAINED SUPPRESSION OF TESTOSTERONE PRODUCTION BY THE LUTEINISING-HORMONE RELEASING-HORMONE AGONIST BUSERELIN IN PATIENTS WITH ADVANCED PROSTATE CARCINOMA: A New Therapeutic Approach?

Nine patients with advanced carcinoma of the prostate were treated with the luteinising-hormone-releasing-hormone agonist buserelin (2 mg/day subcutaneously for 3 days then 0·4-1·2 mg/day intranasally for up to 24 weeks). There was a rise in luteinising-hormone levels during the first few days of treatment, but levels fell after 3 weeks and remained lower than normal after 24 weeks' treatment. In patients receiving 0·6-1·2 mg buserelin per day testosterone levels fell to less than 1 ng/ml within 3 weeks and were still as low as those found in surgically castrated men after 24 weeks. Histology showed regressive changes in some tumours after 3-6 months' buserelin treatment similar to those seen in surgically castrated men. Buserelin treatment may be an alternative to surgery in patients with advanced carcinoma of the prostate.

Testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) in plasma of rabbit from birth to adulthood. Correlation with sexual and behavioural development.

Plasma testosterone, LH and FSH levels were determined and correlated with reproductive organs growth, testicular differentiation, fighting and mounting behaviour in maturing rabbit. An infantile phase of development extends from birth to 40 days, characterized by low testosterone and FSH levels, decreasing LH levels (until 20 days) and by a slow growth of testis and seminal vesicle. The peripubertal phase starts abruptly around day 40. It is marked by simultaneous events: the appearance of mature Leydig cells in the testis, a striking increase in testosterone and FSH levels, a small rise in LH levels and an acceleration of testicular growth. The phase of rapid growth of seminal vesicle and the first meiotic divisions start around day 70, in presence of high circulating levels of FSH and testosterone. Fighting (3 months) and mounting behaviour (146 +/- 13 days) occur lately after a long period of high circulating testosterone levels.

Studies on the pattern of circulating steroids in the normal menstrual cycle. 4. Periovulatory changes in relation to the LH surge.

ABSTRACT By the use of a non-thrombogenic pump, blood was withdrawn continuously at a rate of 4.0 ml/h over a period of 48 h from 10 normally menstruating women during various phases of the peri-ovulatory period and the integrated levels of oestradiol, oestrone, 17-hydroxyprogesterone, progesterone, 20α-dihydroprogesterone and biologically active luteinizing hormone (LH) were estimated in 3-hourly plasma collections. The first significant change detected two days prior to the LH surge (day LH-2) in one subject studied during this period was a continuous parallel rise in oestradiol and oestrone levels, which occurred in the absence of any simultaneous change in LH and 17-hydroxyprogesterone levels. Marked fluctuations followed by a sudden drop in oestradiol levels were observed in another woman during the day preceding the LH peak (day LH-1). These changes were not associated with similar alterations in oestrone levels. The marked drop in oestradiol coincided with the beginning of a simultaneous major rise in LH and 17-hydroxyprogesterone levels followed some 6 to 9 h later by a small but significant increase in progesterone levels. The period of the LH surge (day LH) was studied in 3 women. This period was characterised by a constant decline in oestradiol levels in the presence of unchanged oestrone values. The decrease in oestradiol levels preceded the LH peak by at least 12 h. The LH peak was biphasic in all subjects; both the ascending and descending limbs of it were significantly correlated to similarly changing levels of 17-hydroxyprogesterone. The increase in these two hormones preceded that in progesterone levels, which occurred later, at the time of the steepest rise in LH levels. The findings of the subsequent day (day LH+1) were characterised in two subjects by a parallel decrease in plasma oestradiol, LH and 17-hydroxyprogesterone levels, until a plateau was reached. This plateau coincided with a new rise in progesterone and 20α-dihydroprogesterone levels. The hormonal profile observed two days following the LH surge (day LH + 2) in 3 women was similar to that of the preceding day, with the exception of a beginning new rise in 17-hydroxyprogesterone levels by the end of day LH + 2. This second rise in 17-hydroxyprogesterone paralleled that in progesterone and 20α-dihydroprogesterone levels and occurred in the presence of decreasing levels of LH. The data reported strongly suggest that different control mechanisms are involved in the regulation of ovarian steroid secretion during the various phases of the peri-ovulatory period.

The effects of clomiphene citrate on the hypothalamic–pituitary–gonadal axis in anorexia nervosa

Serum luteinizing hormone (LH) responses to a course of clomiphene citrate were studied in eleven patients with anorexia nervosa at different stages of the illness. In malnourished patients basal levels of LH were invariably low. With the resumption of a normal weight a small but definite rise in LH levels was observed but this spontaneous response to weight gain was variable in that many patients continued to exhibit abnormally low LH levels. The response to clomiphene in terms of a rise in basal LH levels after administration of the drug, followed by a second peak of LH and subsequent menstrual bleeding, was clearly dependent in part on the patient's nutritional state. In the malnourished state the response to clomiphene was usually either absent or incomplete. After the resumption of a more normal weight, the patients invariably showed an initial rise in LH after the clomiphene, but the second LH peak and subsequent menstruation were frequently not demonstrated. Six patients maintained a normal body weight for at least six months after a course of clomiphene, but only three of them resumed cyclical menstrual bleeding. It was concluded that factors additional to the nutritional state contribute to the prolonged amenorrhoea in anorexia nervosa and that clomiphene appears to have only a limited role in the treatment and management of patients with the disorder. Some aspects of current knowledge of the endocrine mechanisms that regulate normal menstruation and of the mode of action of clomiphene are outlined. The results of the present study are discussed against this background in an attempt to elucidate further the hypothalamic disorder underlying the amenorrhoea in anorexia nervosa.

Postcoital Luteinizing Hormone Release in Male and Female Rabbits as Determined by Radioimmunoassay

We have developed a homologous radioimmunoassay for rabbit luteinizing hormone (LH), which was used to measure LH levels in sera of male and female rabbits before and after copulation. The results demonstrated the following: (1) LH concentrations in male and estrogen-primed female rabbits are similar prior to coitus; (2) following coitus, LH levels rise within 3 minutes in both sexes and reach a peak or plateau within 15 minutes; (3) elevated LH concentrations are maintained at a plateau for at least 1 hour in females and then fall toward base line values; (4) an increase in serum LH to 300 ng/ml (10- to 11-fold) or greater is sufficient to cause ovulation and the formation of corpora lutea; and (5) the postcoital rise in LH levels is greater in estrogen-primed females than in nontreated males.

Episodic release of luteinizing hormone in the domestic fowl.

Plasma luteinizing hormone (LH) levels were measured by radioimmunoassay in serial samples taken from intact adult cockerels, gonadectomized fowl of both sexes and laying hens. By sampling at 30 and 10 min intervals, it was shown that in cockerels LH is released episodically. Each secretory episode lasted 90-120 min and was characterized by a 100-200% rise in LH levels over a period of 10-15 min followed by a more gradual, exponential decline. Mean plasma LH levels were found to be depressed in cockerels as a result of the handling associated with taking blood samples; in cases where LH levels were most depressed, an episodic pattern of secretion could not be demonstrated. In the gonadectomized fowl, an episodic pattern of LH secretion was shown when blood samples were taken at 10 or 5 min intervals. During each secretory episode, which lasted 20-45 min, LH levels rose by 20-60%. It is suggested that the increase in mean plasma LH levels in gonadectomized fowl (30-77 ng/ml) over those in cockerels (7-16 ng/ml) is related to an increase in the frequency of the episodic release of the hormone. Episodic discharges of LH could not be demonstrated in laying hens. In these birds the mean LH levels are low (1-5--2-4 ng/ml) and consequently may be maintained by secretory episodes which are of too low an amplitude to be detectable.

Pituitary-gonadal relations in male children and adolescents.

Extract: Data are provided on levels of circulating follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone in healthy male children and adolescents, and these levels are correlated with the stage of sexual maturation, bone maturation, whole body 40K content, and the 24-hr excretion of creatinine, estrogens, 17-hydroxy-corticosteroids, total 17-ketosteroids, and fractionated ll-deoxy-17-ketosteroids (see Tables I and II). Before age 6 there was no significant change with age in testis size or hormone concentrations. From age 6–10 years there was a gradual rise in testis size (Fig. 1), serum FSH (Fig. 4) and serum LH (Fig. 3), but no change in plasma testosterone (Fig. 2), which remained below 40 ng/100 ml. From age 11–17 years there was a doubling of mean testis length, continued rise in serum FSH, and a steeper rise in LH; these changes were accompanied by a 20-fold increase in plasma testosterone concentration, the appearance of male secondary sexual characteristics (Figure 5), more rapid bone maturation and whole body 40K accretion, and enhanced excretion of estrogens and ll-deoxy-17-ketosteroids. Mean levels of FSH in the adult range (> 10 μUg/100 ml) were achieved by age 8, and levels reached a plateau by age 15 (Fig. 6). Adult LH levels (> 2.5 μUg/100 ml) were reached by age 13 and a plateau was observed after 17 years. Plasma testosterone also ceased to rise after age 17. The data suggest that the testis may undergo progressive gonadotropin-mediated maturation in late childhood. Testosterone secretion by the Leydig cells at puberty may result from a further rise in LH levels. Speculation: Pituitary secretion of gonadotropins, particularly FSH, in male children is a gradual phenomenon, antedeating by several years the release of testosterone by the testis. This gradual rise may represent a progressive reduction in hypothalamic sensitivity to feedback by testicular steroids other than testosterone. In late childhood, rising FSH and LH levels may induce increased activity of the enzymes responsible for both synthesis and catabolism of tesoterone. At puberty, an LH-mediated reduction in reductase activity might then result in testosterone accumulation and secretion.