Baseline Serum Luteinizing Hormone Research Articles

Age and dual trigger were found to be significant predictors of live birth in POSEIDON group 3 and 4 women treated with the GnRH antagonist protocol: a retrospective cohort study.

Despite recent advancements in assisted reproductive technology (ART), the effective management of patients with poor ovarian response (POR) remains a formidable challenge. While various treatment strategies and predictors of live births have been documented to provide guidance to fertility specialists in managing poor responders, research efforts have predominantly encompassed all POSEIDON groups. In this study, our objective was to analyze the factors correlated with live births (LB) within a subset of the POSEIDON groups, with a particular focus on POSEIDON groups 3 and 4. Charts of 406 patients belonging to POSEIDON groups 3 and 4 who underwent ART treatment at a university-affiliated infertility clinic following a gonadotropin-releasing hormone (GnRH) antagonist cycle between January 2016 and December 2021 were analyzed. Clinically significant factors associated with live births were incorporated into a logistic regression model for multivariate analysis to ascertain independent predictors of LB. Additionally, a receiver operating characteristic (ROC) curve analysis was conducted to establish the optimal cut-off values. Live births were achieved in 48 cycles (8.7%). Female age (OR, 0.930; 95% CI: 0.874-0.991; p < 0.024), baseline serum luteinizing hormone (LH) levels (OR, 0.854; 95% CI: 0.741-0.984; p < 0.029), and dual triggers (OR, 4.004; 95% CI: 1.290-12.426; p < 0.016) were identified as independent factors associated with LB following multivariate logistic regression analysis. The optimal age cut-off was determined to be 33 years, with a sensitivity of 70.8% and specificity of 75%. Younger age, lower baseline serum LH levels, and dual-trigger administration appear to enhance the likelihood of live birth in POSEIDON groups 3 and 4 following treatments with the GnRH antagonist protocol.

The impact of baseline serum luteinizing hormone levels on follicular output rate and follicle-to-oocyte index in ovarian stimulation cycles with gonadotropin-releasing hormone antagonist protocol

The impact of baseline serum luteinizing hormone levels on follicular output rate and follicle-to-oocyte index in ovarian stimulation cycles with gonadotropin-releasing hormone antagonist protocol

Prediction of ovarian response in IVF/ICSI cycles.

Objective:Our study aims to evaluate the various correlations between demographic, biochemical, ultrasound, and ovarian stimulation parameters with the percentage of mature oocytes in conventional stimulation for IVF/ICSI cycles in order to develop a predictive model to improve our understanding of the oocyte maturation process.Methods:This is a retrospective cohort study; patients underwent conventional antagonist ovarian stimulation protocols for fresh IVF/ICSI cycles. A total of 256 IVF/ICSI cycles were included. Age, antral follicle count (AFC), baseline serum follicle-stimulating hormone (FSH) levels, baseline serum luteinizing hormone (LH) levels, baseline serum estradiol (E2) levels, peak estradiol, P4 on hCG day, the body mass index (BMI), and stimulation length were measured. The variables were tested for correlations with the number of retrieved oocytes (#RO) and the number of mature oocytes (#MO). A backward stepwise regression was performed to identify the variables that correlated more strongly with percentage of mature oocytes (%MO).Results:A predictive equation was obtained with the variables that were not excluded in the model. % MO = 72.700 - 0.910 (Age) + 0.979 (BMI) + 1.209 (Baseline serum LH) - 0.647 (Progesterone on human Chorionic Gonadotropin day).Conclusions:We concluded that age, the BMI, baseline serum LH, and progesterone level on hCG day may predict %MO. Prospective studies are required to validate this predictive equation.

Does basal luteinizing hormone help predict the fate of in vitro fertilization?

Evaluate the role of baseline serum luteinizing hormone (LH) in predicting the success of in-vitro fertilization (IVF) in terms of clinical pregnancy and live birth rate. Women who underwent IVF and/or intracytoplasmic sperm injection (ICSI), following either the agonist or the antagonist protocol, were retrospectively evaluated over a period of two years at the All India Institute of Medical Sciences, New Delhi. We investigated the correlation of serum LH levels in the follicular phase with pregnancy outcomes. A P-value lower than 0.05 was considered as statistically significant. The individuals (351) were divided into four groups based on LH and FSH baseline values, and the levels were correlated with clinical pregnancy and live births. The highest clinical pregnancy rate (25%) was achieved in women with low LH (< 2IU/l); whereas the miscarriage rate was almost similar in all the groups. The pregnancy rate was the lowest (16%) in women with high LH levels (> 8IU/L). Pregnancy rates were intermediate (20%) if LH was intermediate (2-8IU/L). However, none of the results had statistical significance. Early follicular serum LH levels before an IVF/ICSI treatment cycle did not have any clear relationship with clinical pregnancy or live birth rates.

Gonadotropin-releasing hormone agonist as a probe for the pathogenesis and diagnosis of ovarian hyperandrogenism.

We have found that women with typical polycystic ovary syndrome have supranormal plasma 17-hydroxyprogesterone responses to a 100-micrograms test dose of the gonadotropin-releasing hormone agonist nafarelin without evidence of hindered estrogen secretion. To understand the basis of this response, we computed the apparent efficiency of the steps in steroid biosynthesis from the pattern of plasma steroids in response to nafarelin. The proximate cause appears to be excessive 17 alpha-hydroxylase activity and high, yet partially down-regulated, 17,20-lyase activity in the delta 4-pathway. These results suggest that this pattern of steroid secretion results from abnormal regulation (dysregulation) of these activities, possibly involving the enzyme cytochrome P450c17. To determine the usefulness of nafarelin testing for the diagnosis of ovarian hyperandrogenism, we then prospectively studied 40 hyperandrogenic women. The plasma 17-PROG response to nafarelin was supranormal in 58% of the women. The responses of 17-PROG to nafarelin and free testosterone to dexamethasone correlated well and were concordant in approximately 85% of cases. Baseline serum luteinizing hormone concentration was elevated in only 48% of cases. To understand ovarian structure-function relationships, we studied another 20 consecutive hyperandrogenic women. Among seven women with polycystic ovaries, five had an elevated LH level, and four of these five (80%) had an elevated 17-PROG response to nafarelin. Conversely, about half of patients with the PCOS-like disorder of ovarian function did not have polycystic ovaries. Ovarian stromal area, but not LH levels, correlated significantly (r = 0.45) with the 17-PROG response to nafarelin. Thus, both stromal hyperplasia and dysregulation of steroidogenesis seem to be manifestations of abnormal intraovarian regulation of cell growth and function. We conclude that a PCOS-like disorder of ovarian function in response to nafarelin testing is found in approximately half of hyperandrogenic women. The pathogenetic implication of our results is that abnormal intraovarian modulation of LH action seems to be a major factor in ovarian hyperandrogenism. The diagnostic implication of our data is that ovarian androgen excess will often be missed by use of common diagnostic criteria for PCOS.

Detection of functional ovarian hyperandrogenism in women with androgen excess.

Distinguishing between ovarian and adrenal causes of androgen excess may be difficult. We have found that women with the polycystic ovary syndrome have supranormal plasma 17-hydroxyprogesterone responses to the gonadotropin-releasing hormone agonist nafarelin. We determined the usefulness of testing with nafarelin to distinguish ovarian causes of hyperandrogenism in women. We studied 40 consecutive women with hyperandrogenism who had oligomenorrhea, hirsutism, or acne. All 40 underwent testing with nafarelin, dexamethasone, and corticotropin with measurement of circulating concentrations of gonadotropins and steroid hormones, and 19 underwent ovarian ultrasonography. The plasma 17-hydroxyprogesterone response to nafarelin was supranormal in 23 of the 40 women (58 percent), and the plasma androgen response to corticotropin was elevated in 23; 13 women had both abnormalities. Only one woman had conclusive evidence of a steroidogenic block; she had nonclassic adrenal 21-hydroxylase deficiency. Of the 23 women with abnormal responses to nafarelin, only 11 (48 percent) had elevated base-line serum luteinizing hormone concentrations. Of the 13 women with abnormal responses to nafarelin who underwent ultrasonography, 7 (54 percent) had polycystic ovaries. Peak plasma 17-hydroxyprogesterone concentrations after nafarelin administration correlated closely with plasma free testosterone concentrations after dexamethasone administration (r = 0.75, P less than 0.001). Approximately half of women with oligomenorrhea, hirsutism, or acne have an abnormal response to the gonadotropin-releasing hormone agonist nafarelin, suggesting an ovarian cause of their androgen excess.

Prognostic value of the early serum estradiol response to leuprolide acetate in in vitro fertilization

One hundred in vitro fertilization (IVF)-stimulated cycles were analyzed to evaluate the prognostic value of the early follicle-stimulating hormone (FSH), luteinizing hormone (LH), and estradiol (E2) response to the agonist action of leuprolide acetate. Four distinct early E2 response patterns were found. Pattern A (n = 41) showed a prompt elevation of E2, followed by a fall by cycle day 4. Pattern B (n = 16) showed a delayed elevation of E2, followed by a fall by cycle day 6. Pattern C (n = 19) showed a persistent elevation of E2. Pattern D (n = 18) lacked the early E2 response. The clinical pregnancy rates per cycle for patterns A, B, C, and D were 46%, 38%, 16%, and 6%, respectively. A baseline serum FSH level greater than 20 mIU/mL was associated with a lower clinical pregnancy rate, although not statistically significant. Baseline serum LH levels and stimulated FSH and LH levels did not predict IVF outcome. We conclude that the early E2 response pattern to leuprolide acetate is the best early prognostic indicator of IVF outcome.

Neuroendocrine aspects of primary endogenous depression VIII. Pituitary-gonadal axis activity in male patients and matched control subjects

To determine the extent of hypothalamo-pituitary-gonadal (HPG) axis dysfunction in endogenous depressed men, we measured nocturnal and diurnal serum luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone (T), and estradiol (E 2) concentrations, and their responses to gonadotropin releasing hormone (LHRH) and dexamethasone administration, in 16 Research Diagnostic Criteria primary, definite endogenous male depressives and 16 individually matched male normal controls. Compared to their controls, the patients showed no differences in basal nocturnal or diurnal gonadotropin or gonadal steroid hormone concentrations, and no differences in hormone concentrations either post-LHRH or post-dexamethasone. Age was negatively correlated with baseline serum T in the patients but not in the controls, and it was modestly positively correlated with baseline serum LH in both groups of subjects. In the patients, the presence of DSM-III melancholia was modestly negatively correlated with baseline and post-LHRH concentrations of both LH and FSH and was positively correlated with baseline serum T, but it bore no relation to serum E 2. None of the other subject characteristics or specific dimensions of depressive symptomatology were significantly related to the HPG axis measures. The HPG axis measures also were unrelated to pre- and post-dexamethasone cortisol concentrations in both groups of subjects. The results of this study suggest that, in contrast to the hypothalamo-pituitary-adrenal cortical and thyroid axis abnormalities frequently found in endogenous depressives, HPG axis function in male depressives is relatively normal.

Prolactin response after gonadotropin-releasing hormone in the polycystic ovary syndrome

The administration of gonadotropin-releasing hormone (GnRH) has been shown to stimulate prolactin (PRL) release under certain conditions. The authors compared PRL responses after GnRH in normoprolactinemic patients with the polycystic ovary syndrome (PCO) with those of normal ovulatory women in the follicular phase. Seven of 15 patients had a significant increase in PRL after GnRH, whereas none of the control subjects had a positive response. After 1 week of oral L-dopa, the responders no longer exhibited this positive response. Baseline PRL levels in responding patients with PCO were similar to levels in control subjects, whereas nonresponding patients with PCO had higher PRL levels. Baseline follicle-stimulating hormone (FSH)/luteinizing hormone (LH) ratios were higher in patients with a positive response. The positive PRL response after GnRH was not correlated with baseline serum LH, the LH/FSH ratio, delta maximum LH responses, serum testosterone (T), unbound T, or baseline PRL. The positive response correlated positively with serum levels of unbound estradiol (P less than 0.05) and serum unbound estradiol/unbound T ratios (P less than 0.01). These data suggest that under certain conditions a subgroup of patients with PCO may demonstrate a positive PRL response after GnRH. Dopamine, gonadotropins, and estrogen may play a role in this interaction.

Management of patients with hyperprolactinemia and normal or abnormal tomograms

Forty women with hyperprolactinemia with and without radiologic evidence of prolactin-secreting pituitary adenoma were prospectively treated with bromocriptine. On the basis of tomographic studies, the patients were divided into either a microadenoma group (N = 19) or no adenoma group (N = 21). Both groups had similar distributions as to obstetric history, menstrual abnormalities, levels of baseline serum luteinizing hormone, follicle-stimulating hormone, and thyrotropin. Patients in the adenoma group had significantly higher (p < 0.001) baseline serum prolactin levels (173 ± 4.4 ng/ml) than those of patients without adenoma (61.1 ± 4.5 ng/ml). Patients without an adenoma required significantly less bromocriptine (5 to 7.5 mg) (p < 0.005) to normalize serum prolactin or establish a pregnancy than did those who had an adenoma (5 to 20 mg). Similarly, patients with adenoma resumed ovulatory cycles (8.7 ± 1.2 versus 5.7 ± 0.06 weeks), had their galactorrhea disappear (11.3 ± 2.1 versus 5.6 ± 1.1 weeks), and become pregnant (16.2 ± 2.5 versus 9.8 ± 1.5 weeks) in a significantly longer time (p < 0.01) than did those who had no adenomas. There was no significant difference in the pregnancy rate between the groups, and the overall rate was 86% of 28 patients desiring pregnancy. No complications were observed during pregnancy. The conclusion is that both patients with and those without radiologic evidence of a prolactin-secreting pituitary adenoma can be safely treated with bromocriptine. In addition, the resumption of ovulatory cycles is more important than the absolute normalization of serum prolactin.

The Treatment of Metastatic Prostatic Cancer With A Potent Luteinizing Hormone Releasing Hormone Analogue

Metastatic prostatic cancer generally is treated by either castration or the administration of exogenous estrogens, both of which have significant clinical disadvantages. Luteinizing hormone releasing hormone analogues have been shown to suppress gonadal steroidogenesis in animals and humans. To assess the effect of the administration of a potent luteinizing hormone releasing hormone analogue, (D-Leu-6)luteinizing hormone releasing hormone (1-9) nonapeptide ethylamide, 9 patients with previously untreated stage D2 prostatic cancer were treated with this agent for 3 to 8 months. By 3 months of treatment all patients demonstrated a significant decrease in serum testosterone and a decreased peak serum luteinizing hormone and testosterone response to the acute administration of the analogue, with no change in baseline serum luteinizing hormone or prolactin. These data suggest that this analogue acts by decreasing the pituitary release of luteinizing hormone. No major adverse effects were noted with this treatment modality, and all patients were symptomatically improved and demonstrated a decrease or stabilization in tumor activity as measured by prostatic computerized tomography or ultrasound scan, prostatic acid phosphatase and bone scan. A representative case is presented.Luteinizing hormone releasing hormone analogues may prove to be valuable new agents in the treatment of advanced prostatic cancer.

Abnormalities of the Hypothalamic—Pituitary—Leydig Cell Axis in Young Adult Rats with Vitamin A Deficiency

The hypothalamic concentration of gonadotrophin releasing hormone (GnRH), the in vivo pituitary responses to GnRH, and the in vivo Leydig cell responses to bovine luteinizing hormone (LH) and to endogenous LH were determined in young adult male rats who had been on a vitamin‐A‐deficient (VAD) diet for 64 days and in age‐matched controls. Hypothalamic GnRH content was 3.06 ± 0.25 ng/hypothalamus in VAD (mean ± SEM) and 3.26 ± 0.25 ng/hypothalamus in controls. Baseline serum LH concentrations were 24.6 ± 4.7 ng/ml in VAD and 11.3 ± 2.3 ng/ml in controls (P &lt; 0.02). Baseline serum follicle stimulating hormone (FSH) levels were 373 ± 61 ng/ml in VAD and 329 ± 16 ng/ml in controls. Fifteen minutes after administration of GnRH serum LH was 215 ± 16.3 ng/ml in VAD vs. 148 ± 18.3 ng/ml in controls (P &lt;0.02). Serum FSH levels 15 minutes after administration of GnRH were 866 ± 67 ng/ml in VAD vs. 566 ± 58 ng/ml in controls (P &lt; 0.01). Baseline serum testosterone (T) concentratio̊nswere 1.0 ± 0.2 ng/ml vs. 1.7 ± 0.3 ng/ml in controls (n.s.). Sixty minutes after exogenous LH administration, serum T concentrations were 21.7 ± 1.0 ng/ml in VAD vs. 17.8 ± 1.0 ng/ml in controls (P &lt;0.05). Sixty minutes after administration of GnRH, which elevated endogenous LH serum concentrations, serum T concentrations were similar in both groups (7.8 ± 0.9 ng/ml for VAD vs. 9.7 ± 0.5 ng/ml for controls). The elevated serum LH concentrations, together with the increased pituitary responses to GnRH, are compatible with an appropriate hypothalamic‐pituitary response to a direct impairment in testicular function secondary to the VAD. However, the increased in vivo Leydig cell responses to exogenous LH stimulation in these young adult males with VAD remains unexplained.

Gonadotropin profiles in fed and fasted obese women

Five obese women were studied before and at the end of a prolonged fast to determine the effect on luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and on the response to luteinizing hormone-releasing factor (LRF). Although baseline serum LH values declined from a mean value of 9.1 to 6.5 m.I.U. per milliliter measured at the end of the fast, these changes in mean serum level were not statistically significant. However the integrated LH secretion did decline when measured at the end of the fasts (p < 0.05). FSH secretion did not change. LRF-stimulated LH and FSH values showed augmented stimulation at the end of the fast. Pulsatile gonadotropin secretion patterns remained normal. Prolonged fasting appears to alter the baseline LH secretion and the pituitary response to exogenous LRF.

Regulation of gonadal function in uremia

Gonadal function and its neuroendocrine control were studied in seven uremic men on chronic hemodialysis. Testosterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were measured in plasma or serum by established radioimmunoassay techniques. The metabolic clearance rate (MCR) of testosterone was also determined by constant infusion of 3H testosterone, and blood production rates were then estimated from the AM plasma level and the metabolic clearance rates. Predialysis, plasma testosterone in these uremic men were subnormal, measuring only 289 ng 100 ml ± 60 SE (normal male values are 660 ± 70). The blood production rate of testosterone was also subnormal, averaging 2.7 mg/day in the two individuals studied, since the metabolic clearance rates were normal. However, after dialysis testosterone levels rose to 408 ± 49 ng 100 ml ( p < 0.01), the MCR to 1570 liters/day, and the calculated mean production rate increased to a normal level of 6.9 mg/day. Base-line serum LH was increased in the uremic state to 22.7 ± 1.8 mlU/ml (normal 5.9 ± 2), while FSH levels were normal at 7.7 mlU/ml ± 1.2 SE. Dialysis did not significantly alter serum immunoassayable gonadotropin levels. Gonadal stimulation by chorionic gonadotropin (4000 IU/day) initially did not increase testosterone levels, but continued stimulation-caused a two- to threefold rise by the fourth day. Clomiphene citrate (200 mg daily for 7 days) produced variable changes in testosterone and LH; two subjects did not respond, while two had a rise in both testosterone and gonadotropin. Luteinizing releasing hormone (LRH-Guillemin 150 μg intravenously) caused a two- to threefold rise in serum LH in both subjects studied. This work indicates that uremic men have subnormal testosterone production which is rapidly reversible with hemodialysis. The subnormal testosterone production appears to be primarily that of Leydig cell dysfunction, since there is elevated serum immunoassayable LH and a blunted initial response to exogenous gonadotropin.