Rise In FSH Research Articles

The Possible Protective Role of N-acetylcysteine against Testicular Toxicity Induced by Paracetamol Overdose in Adult Male Rats

Many substances, even medicines with proven therapeutic benefits, can harm cells by metabolically activating them into extremely reactive substances. Paracetamol is one of the most widely used over-the-counter analgesics. This study examines the harmful effects of paracetamol on the lipid peroxidation process in testes homogenates as well as enzymatic and non-enzymatic antioxidant activities. Also, examine the effects on male hormones and sperm count. The study also assesses if N-acetylcysteine protects against testicular damage induced by paracetamol excess. Forty mature male albino rats were created. Group 1 as a control, Group 2 paracetamol (650 mg/kg), Group 3 NAC (150 mg/kg), and Group 4 both paracetamol and NAC. Samples of blood and testicles were taken after 15 days to measure sperm and testicular biochemistry. Testicular tissues had considerably higher amounts of MDA and H2O2. SOD, GSH, and CAT levels significantly decreased. FSH and LH rise. On the other hand, testosterone levels decrease following paracetamol exposure. The administration of NAC generated changes in testosterone levels, FSH, LH, and antioxidant enzymes. The sperm morphology showed an increase in abnormalities but a significant decrease in motility and count. NAC effectively lowers the toxicity of paracetamol to the testicles while restoring biomarkers associated with normal testicular function.

SAT-211 Gonadotrophin Rise Following Kisspeptin Analogue (MVT-602) Is Increased In Women With Hypothalamic Amenorrhoea Compared To Healthy Women

Background Hypothalamic amenorrhoea (HA) is a condition characterised by reduced GnRH pulsatility as a result of low body weight, excessive exercise, or psychological stress. HA leads to anovulatory infertility and osteoporosis. Kisspeptin is a neuropeptide that is known to be a key regulator of hypothalamic GnRH function. Hypothalamic kisspeptin expression is reduced, and kisspeptin receptor expression increased, in a rodent model of HA. We have previously demonstrated that a continuous infusion of the native form of kisspeptin (kisspeptin-54; KP54) can restore GnRH pulsatility in women with HA, but excessive doses cause tachyphylaxis. Kisspeptin analogue (MVT-602) is a modified form of kisspeptin with a longer half-life compared to native kisspeptin-54 (1.5-2.2h vs 0.5h). Importantly, the more prolonged gonadotrophin profile induced by MVT-602 could enable restoration of physiological hormonal secretion with less frequent administration than by KP54, and thus mitigate against the risk of tachyphylaxis. We therefore investigated the hormonal response to MVT-602 in women with HA to evaluate its potential future utility in the treatment of anovulatory infertility. Methods A previous dose-finding study during the follicular phase of healthy women determined that no further increase in gonadotrophin rise was observed at doses of MVT-602 higher than 0.03nmol/kg. We therefore compared the gonadotrophin rise following a subcutaneous bolus of MVT-602 at a dose of 0.03nmol/kg in 6 women with HA compared to 9 healthy women studied during the follicular phase of their menstrual cycle (day 1-4). Serum gonadotrophin and oestradiol levels were monitored every 30mins for 24hrs. Groups were compared by unpaired t test. Results The maximal rise in LH following MVT-602, was over two-fold greater in women with HA compared to healthy women in the follicular phase (mean±SD of maximal change in LH: HA 18.3±11.0iU/L, follicular phase 7.4±2.7iU/L; P=0.01). The time to peak LH was expedited in women with HA (time to first peak: HA 380±53mins, follicular phase 1067±415mins; P=0.002). Serum FSH rise was also augmented by over four-fold in women with HA (mean±SD of maximal change in FSH: HA 10.0±4.4iU/L, follicular phase 2.2±1.6iU/L; P=0.0003). Maximal rise in oestradiol was higher in women with HA (700pmol/L) when compared with healthy women (297pmol/L; P=0.03). Conclusion In women with HA, the rise in gonadotrophins following MVT-602 is more pronounced and occurs sooner than in healthy women during the follicular phase. The augmented and sustained rise in oestradiol highlights the potential for MVT-602 to be used as an ovulation induction agent in women with anovulatory HA. Therefore, further research is indicated to evaluate repeated administration of MVT-602 as a novel therapeutic approach to restore fertility in HA.

The Relationship Between Progesterone, Sleep, and LH and FSH Secretory Dynamics in Early Postmenarchal Girls.

During puberty, LH pulse frequency increases during sleep; in women, LH pulse frequency slows during sleep in the early/middle follicular phase (FP) of the menstrual cycle. The origin and significance of this developmental transition are unknown. To determine the relationship between progesterone (P4) exposure, sleep-related slowing of LH pulses in the FP, and the intercycle FSH rise, which promotes folliculogenesis, in early postmenarchal girls. 23 girls (gynecologic age 0.4 to 3.5 years) underwent hormone measurements and pelvic ultrasounds during two consecutive cycles and one frequent blood sampling study with concurrent polysomnography during the FP. Subjects demonstrated one of four patterns during cycle 1 that represent a continuum of P4 exposure: ovulatory cycles with normal or short luteal phase lengths or anovulatory cycles ± follicle luteinization. Peak serum P4 and urine pregnanediol (Pd) in cycle 1 were inversely correlated with LH pulse frequency during sleep in the FP of cycle 2 (r = -0.5; P = 0.02 for both). The intercycle FSH rise and folliculogenesis in cycle 2 were maintained after anovulatory cycles without P4 or Pd exposure or nocturnal slowing of LH pulse frequency in the FP. During late puberty, rising P4 levels from follicle luteinization and ovulation may promote a slower LH pulse frequency during sleep in the FP. However, a normal FSH rise and follicle growth can occur in the absence of P4-associated slowing. These studies therefore suggest that an immature LH secretory pattern during sleep is unlikely to contribute to menstrual irregularity in the early postmenarchal years.

The Impact of Laparoscopic Ovarian Cystectomy on Ovarian Reserve in Cases of Endometrioma

Background: An endometrioma is one of the most common manifestations of endometriosis. Laparoscopic cystectomy is the preferred approach to managing bengin ovarian cysts in adolescents and adults, but unfortunately it affects the ovarian reserve. Aim of the work: This study was aimed to evaluate the effects of laparoscopic cystectomy on ovarian reserve in patients with endometriomas. Patients and methods: This prospective study was conducted on 44 cases suffering from ovarian endometriomas and subjected to laparoscopic cystectomy. The patients in the study were selected from the Outpatient Clinic in Sayed Galal University Hospital and EL-Gala Maternity Teaching Hospital. This study was conducted between April 2017and March 2018. Serum anti-mullerian hormone (AMH), FSH and E2, as well as the antral follicle count (AFC) were measured preoperatively and 3 months postoperatively. Main outcome measures: Ovarian reserve based on the comparison of AMH alterations. The secondary end points are changes in FSH, E2 and AFC. Results: There was a statistically significant reduction in postoperative median, values of AFC, serum, AMH, serum E2 and serum E2: FSH ratio, and a statistically significant rise in postoperative median serum FSH, when compared to preoperative measurements in included women. Conclusion: The AMH level decreased and the FSH level increased after laparoscopic cystectomy for endometriomas, especially in older patients and those with bilateral cysts.

FSH, Bone Mass, Body Fat, and Biological Aging.

The Study of Women's Health Across the Nation has taught us that impending ovarian failure during late perimenopause is associated with a sharp rise in serum FSH, which coincides with the most rapid rate of bone loss and the onset of visceral adiposity. At this time in a woman's life, serum estrogen levels are largely unaltered, so the hypothesis that hypoestrogenemia is the sole cause of bone loss and visceral obesity does not offer a full explanation. An alternative explanation, arising from animal models and human data, is that both physiologic aberrations, obesity and osteoporosis, arise at least in part from rising FSH levels. Here, we discuss recent findings on the mechanism through which FSH exerts biological actions on bone and fat and review clinical data that support a role for FSH in causing osteoporosis and obesity. We will also provide a conceptual framework for using a single anti-FSH agent to prevent and treat both osteoporosis and obesity in women across the menopausal transition.

Body weight and bone/calcium metabolism. FSH and obesity, osteoporosis.

It is well known that the rise of FSH is a hallmark of menopause associated with osteoporosis and visceral adiposity. Recent days, Zahidi's group reported that blocking FSH signals prevents bone loss in ovariectomized mice by inhibiting bone resorption and stimulating bone synthesis. The same research group also showed that blocking FSH action reduces body fat volume by promoting beige fat thermogenesis. These findings open new doors for novel and complementary treatments addressing post-menopausal osteoporosis and metabolic diseases.

Gonadotropin Surge-Attenuating Factor: A Nonsteroidal Ovarian Hormone Controlling GnRH-Induced LH Secretion in the Normal Menstrual Cycle.

Gonadotropin surge-attenuating factor (GnSAF) is a nonsteroidal ovarian substance, which attenuates the endogenous LH surge in superovulated women. Different molecular sequences have been found, but only one of them has shown substantial homology to a known substance of the human genome. A molecular mass of 12.5kDa showing identity to the carboxyl-terminal fragment of human serum albumin and expressing GnSAF bioactivity in vitro has been identified. It has been suggested that in the normal menstrual cycle the in vivo bioactivity of GnSAF increases under the influence of the intercycle rise of FSH. GnSAF is considered the "missing link" between the ovaries and the hypothalamo-pituitary system, maintaining the pituitary in a state of low responsiveness to GnRH in the early- to midfollicular phase of the cycle. A marked decline in GnSAF bioactivity in the late follicular phase facilitates the onset and the full expression of the midcycle LH surge.

Profil hormonal chez l’homme en cas d’infertilité au laboratoire de radio immunologie de l’institut des radioisotopes de Niamey

ObjectiveThe aim of this study was to determine the sociodemographic parameters and hormonal profile of infertile man. Patients and methodsWe included in our study, all patients presenting with infertility dating back at least two years, with abnormal semen analysis. These patients came to radio immunological laboratory assays for determination of FSH, LH, PRL and testosterone in the assessment of infertility. ResultsThe age of the patients ranged from 25 years to 64 years with an average age of 44.5 years. Employees are the most represented with a frequency of 63.93%, with 54.41% had consulted a primary infertility, followed by traders in 15.63% and 70% for primary infertility. The hormonal assessment was abnormal in 86% of cases (55/64). A rise in FSH was observed in 36% of patients, the LH was elevated in 31.25% of patients, 48.44% in PRL. 12 patients (18.75%) had low testosterone Among the endocrinopathies suspected, the hypogonadism hypergonadotrophic is the most represented with a frequency of 32.8%, testicular deficiencies are found in 12.5% of cases, hypogonadism hypogonadotrophic in 10.93% of cases, hyperprolactinemia isolated in 18.75% of cases and obstructive causes in 14 04% of cases. ConclusionThere are many endocrinopathies that can induce male infertility. They can be congenital or acquired and can concern several stages, hypothalamus, pituitary and testis. It's important to diagnose thoses endocrinopathies, because some of them are accessible to treatment.

Reversible downregulation of the hypothalamic-pituitary-gonadal axis in stallions with a novel GnRH antagonist

The GnRH antagonist, acyline, has not yet been investigated in the stallion. Our study aimed to: (1) evaluate the downregulation of the stallion hypothalamic-pituitary-gonadal axis by acyline through assessment of seminal parameters, testicular volume, and sexual behavior; (2) assess hormonal response of acyline-treated stallions to GnRH stimulation; and (3) verify reversibility after treatment. Stallions were assessed pretreatment and subsequently treated (every five days) for 50 days: acyline (n = 4; 330 μg/kg acyline) or control (n = 4, vehicle). The stallions were then monitored for 62 days after the last day of treatment. Treatment-induced declines (P < 0.05) in FSH, LH, testosterone, and estrone sulfate. Gonadotropins and testosterone returned to control values within 9 days, and estrone sulfate by 14 days, after discontinuation of treatment. Acyline-treated stallions failed to respond with a rise in FSH, LH, and testosterone after exogenous GnRH stimulation (gonadorelin) at Day 46 of treatment compared to pretreatment stimulation and control stallions. Decreases (P < 0.05) were observed in total sperm numbers and motility (week 2) in acyline-treated stallions, as well as total seminal plasma protein (week 2) and testicular volume (week 5). Over the course of the study, the time to erection, time to ejaculation, and number of mounts increased (P < 0.0001) across both groups of stallions; however, there was no effect of treatment or treatment by time interactions on these parameters. Testicular volume, and most seminal parameters regained normal levels within 62 days after treatment ended; on follow-up, sperm output of acyline-treated stallions was regained within 7 months after the end of experiment. In conclusion, acyline reversibly suppresses the stallion hypothalamic-pituitary-gonadal axis.

Evaluating the Impact of Anti-Estrogenic Medications on Gonadotropins Levels and Oocyte Yield During Controlled Ovarian Hyperstimulation (COH) in Breast Cancer Patients

Fertility is a primary concern among female cancer survivors. Women desiring biological children may undergo oocyte or embryo cryopreservation prior to cancer treatment. However, rising serum estrogens during COH have caused concern in estrogen-sensitive cancer populations. Thus, it has become standard to use anti-estrogenic medications such as tamoxifen or letrozole as adjuncts during COH in these women pursuing oocyte or embryo cryopreservation. With the use of anti-estrogenic medications a rise in endogenous FSH is expected, which could enhance COH.

Parturition to resumption of ovarian cyclicity: comparative aspects of beef and dairy cows

There is a variable anoestrous period following parturition in the cow. Follicular growth generally resumes within 7 to 10 days in the majority of cows associated with a transient FSH rise that occurs within 3 to 5 days of parturition. Dairy cows that are not nutritionally stressed generally ovulate their first postpartum dominant follicle (~15 days), whereas beef suckler cows in good body condition normally have a mean of 3.2±0.2 dominant follicles (~30 days) to first ovulation; moreover, beef cows in poor body condition have a mean of 10.6±1.2 dominant follicles (~70 to 100 days) to first ovulation. The lack of ovulation of dominant follicles during the postpartum period is associated with infrequent LH pulses, with both maternal–offspring bonding and low body condition score (BCS) at calving being implicated as the predominant causes of delayed resumption of cyclicity in nursed beef cows. In dairy cows, the normal pattern of early resumption of ovulation may be delayed in high-yielding Holstein type cows generally owing to the effects of severe negative energy balance, dystocia, retained placental membranes and uterine infections. First ovulation, in both dairy and beef cows, is generally silent (i.e., no behavioural oestrus) and followed by a short inter-ovulatory interval (>70%). The key to optimizing the resumption of ovulation in both beef and dairy cows is appropriate pre-calving nutrition and management so that cows calve down in optimal body condition (BCS; 2.75 to 3.0) with postpartum body condition loss restricted to <0.5 BCS units.

Comparison between two clomiphene citrate protocols for induction of ovulation in clomiphene resistant polycystic ovary syndrome

Abstract Objective To compare two protocols of CC therapy for induction of ovulation in a group CC resistant PCOS women. Study design Double blind randomized controlled trial. Subjects and methods 260 nulliparous CC resistant PCOS women randomized between two groups; In the first group each patient received 200 mg/day for 5 days while the second group received 100 mg/day for 10 days, both starting on day 3 of progestin induced withdrawal bleeding. Main outcome measures Ovulation defined as at least one follicle reaching ⩾14 mm diameter, and confirmed by timed serum progesterone. Secondary outcome measures included; number of dominant follicles, endometrial thickness, clinical pregnancy rate, and live birth rate. Results The extended protocol resulted in significantly higher ovulation, pregnancy, and live-birth rates than the high dose protocol ( p 0.001). Serum FSH levels on day 6 of treatment were comparable between the two groups while the level on day 11 was significantly higher in the second group ( p 0.02). Serum LH levels were comparable both on days 6 and 11. Patients on longer protocol (group II) required a longer time to ovulate (18 ± 4.4 versus 14 ± 3.6 days) but had a significantly higher endometrial thickness at the time of ovulation. ( p 0.02) FSH and LH levels were comparable between responders and non-responders in both groups. Conclusions The current study reports significantly higher ovulation and pregnancy rates with the longer lower dose protocol probably because of prolonged FSH rise. Study web address: ACTRN12611000639921.

Changes in Bone Resorption Across the Menopause Transition: Effects of Reproductive Hormones, Body Size, and Ethnicity

Our objective was to characterize changes in bone resorption in relation to the final menstrual period (FMP), reproductive hormones, body mass index (BMI), and ethnicity. Urinary type I collagen N-telopeptide (NTX), estradiol, and FSH levels were measured annually for up to 8 years spanning the menopause transition in 918 African American, Chinese, Japanese, or Caucasian women. Urinary NTX began to increase sharply about 2 years before the FMP, reaching its peak level about 1 to 1.5 years after the FMP. NTX levels declined modestly from 2 to 6 years after the FMP but remained about 20% higher than before the menopause transition. The sharp rise in FSH occurred in conjunction with a sharp decline in estradiol and shortly after FSH levels began increasing rapidly. The mean increase in urinary NTX across the menopause transition was greatest in women with BMI <25 kg/m² and smallest in women with BMI >30 kg/m². Increases in NTX were greatest in Japanese women and smallest in African Americans. These differences were attenuated, but not eliminated, when analyses were adjusted for covariates, particularly BMI. During the menopause transition, a decline in ovarian function beginning about 2 years before the FMP is followed by an increase in bone resorption and subsequently by bone loss. The magnitude of the increase in bone resorption is inversely associated with BMI. Ethnic differences in changes in bone resorption are attenuated, but not eliminated, by adjustment for BMI. Ethnic differences in BMI, and corresponding ethnic differences in bone resorption, appear to account for much of the ethnic variation in perimenopausal bone loss.

GnRH Increases c-Fos Half-Life Contributing to Higher FSHβ Induction

GnRH is a potent hypothalamic regulator of gonadotropin hormones, LH and FSH, which are both expressed within the pituitary gonadotrope and are necessary for the stimulation of gametogenesis and steroidogenesis in the gonads. Differential regulation of LH and FSH, which is essential for reproductive fitness, is achieved, in part, through the varying of GnRH pulse frequency. However, the mechanism controlling the increase in FSH during the periods of low GnRH has not been elucidated. Here, we uncover another level of regulation by GnRH that contributes to differential expression of the gonadotropins and may play an important role for the generation of the secondary rise of FSH that stimulates folliculogenesis. GnRH stimulates LHβ and FSHβ subunit transcription via induction of the immediate early genes, Egr1 and c-Fos, respectively. Here, we determined that GnRH induces rapidly both Egr1 and c-Fos, but specifically decreases the rate of c-Fos degradation. In particular, GnRH modulates the rate of c-Fos protein turnover by inducing c-Fos phosphorylation through the ERK1/2 pathway. This extends the half-life of c-Fos, which is normally rapidly degraded. Confirming the role of phosphorylation in promoting increased protein activity, we show that a c-Fos mutant that cannot be phosphorylated by GnRH induces lower expression of the FHSβ promoter than wild-type c-Fos. Our studies expand upon the role of GnRH in the regulation of gonadotropin gene expression by highlighting the role of c-Fos posttranslational modification that may cause higher levels of FSH during the time of low GnRH pulse frequency to stimulate follicular growth.

The Utility of Menstrual Cycle Length as an Indicator of Cumulative Hormonal Exposure

Associations between menstrual cycle length and chronic diseases are hypothesized to be due to differences in underlying hormonal patterns. The aim of the study was to evaluate the association between menstrual cycle length and the hormonal profile and anovulation. We conducted a prospective cohort study at the University at Buffalo from 2005 to 2007. We recruited 259 healthy, regularly menstruating women aged 18-44 yr. Cycle length was observed for up to two cycles. Serum estradiol, progesterone, LH, and FSH were measured up to eight times per cycle for up to two cycles. Women with short cycles (<26 d) had higher FSH concentrations during menses and in the late luteal phase, higher follicular estradiol concentrations, and lower LH concentrations across the cycle. Among women with longer cycles (>35 d), estradiol and LH peaks occurred on average about 3 d later, and FSH peaks about 1 d later compared to women with normal-length cycles. Both short and long cycles, compared with normal-length cycles, had an increased probability of anovulation. In general, per-cycle exposure to hormones was less in short cycles based on the area under the curve, although over time the cumulative exposure to estradiol would be greater for women with short cycles. Short ovulatory cycles were associated with higher follicular phase estradiol, an earlier rise in FSH, and an increased risk of anovulation. These results suggest that menstrual cycle length may be a relevant indicator of estradiol exposure and risk of anovulation among regularly cycling women.

Effect of purified llama ovulation-inducing factor (OIF) on ovarian function in cattle

Two experiments were designed to determine the effect of purified ovulation inducing factor (OIF) on ovarian function in cattle. In Experiment 1, prepubertal heifers (n = 11 per group) were treated on Day 5 (Day 0 = day of follicular wave emergence) of the follicular wave with an intramuscular dose of saline (1 mL), GnRH (100 μg), or purified OIF (1 mg/100 kg body weight). Ovulation occurred in 9/11 heifers treated with GnRH, and 1/11 heifers in each of the OIF- and saline-treated groups (P < 0.05). Compared to saline-treated controls, OIF treatment was associated with a smaller dominant follicle diameter (P < 0.01), a rise in plasma FSH concentration (P < 0.1), and earlier emergence of the next follicular wave (P < 0.05). In Experiment 2, sexually mature heifers were given either GnRH or purified OIF on Days 3, 6 or 9 of the first follicular wave (i.e., early growing, early static, or late static phase of the dominant follicle; n = 5 per group per day), or were untreated (n = 10). In heifers treated with OIF on Day 6, the dominant follicle diameter profile tended to be smaller than in controls, and was associated with a rise (P < 0.05) in plasma FSH concentrations. A similar rise in FSH was detected after OIF treatment on Day 9. Compared to untreated controls, treatment with OIF and GnRH was associated with a larger CL diameter (Days 3 and 6 groups; P < 0.05) and a greater concentration of plasma progesterone (Days 6 and 9 groups; P < 0.05). Treatment with purified OIF did not induce ovulation in heifers, but hastened new follicular wave emergence in prepubertal heifers, influenced follicular dynamics in a phase-specific manner in mature heifers, and was luteotrophic.

Arcuate kisspeptin/neurokinin B/dynorphin (KNDy) neurons mediate the estrogen suppression of gonadotropin secretion and body weight.

Estrogen withdrawal increases gonadotropin secretion and body weight, but the critical cell populations mediating these effects are not well understood. Recent studies have focused on a subpopulation of hypothalamic arcuate neurons that coexpress estrogen receptor α, neurokinin 3 receptor (NK(3)R), kisspeptin, neurokinin B, and dynorphin for the regulation of reproduction. To investigate the function of kisspeptin/neurokinin B/dynorphin (KNDy) neurons, a novel method was developed to ablate these cells using a selective NK(3)R agonist conjugated to the ribosome-inactivating toxin, saporin (NK(3)-SAP). Stereotaxic injections of NK(3)-SAP in the arcuate nucleus ablated KNDy neurons, as demonstrated by the near-complete loss of NK(3)R, NKB, and kisspeptin-immunoreactive (ir) neurons and depletion of the majority of arcuate dynorphin-ir neurons. Selectivity was demonstrated by the preservation of proopiomelanocortin, neuropeptide Y, and GnRH-ir elements in the arcuate nucleus and median eminence. In control rats, ovariectomy (OVX) markedly increased serum LH, FSH, and body weight, and these parameters were subsequently decreased by treatment with 17β-estradiol. KNDy neuron ablation prevented the rise in serum LH after OVX and attenuated the rise in serum FSH. KNDy neuron ablation did not completely block the suppressive effects of E(2) on gonadotropin secretion, a finding consistent with redundant pathways for estrogen negative feedback. However, regardless of estrogen status, KNDy-ablated rats had lower levels of serum gonadotropins compared with controls. Surprisingly, KNDy neuron ablation prevented the dramatic effects of OVX and 17β-estradiol (E(2)) replacement on body weight and abdominal girth. These data provide evidence that arcuate KNDy neurons are essential for tonic gonadotropin secretion, the rise in LH after removal of E(2), and the E(2) modulation of body weight.

4H syndrome, dento-leukoencephalopathy or a new syndrome?

Background Leukoencephalopathies in children can pose a diagnostic problem. New conditions with associated non neurological features have been described such as 4H syndrome (hypomyelination, hypodontia and hypogonadotropic hypogonadism) and Dento-leukoencephalopathy...

Characterisation of transient benign hCG elevations in women following chemotherapy for GTT

The occurrence of post-chemotherapy transient low level hCG elevations has been observed in a number of women treated for gestational trophoblastic tumours (GTT). The authors reviewed the records of patients treated at Charing Cross Hospital over the last 10 years and identified those with a benign rise in hCG. Stored serum samples were assayed for hCG, LH, FSH and oestradiol at varying points during patient management. The endocrine profile in patients experiencing benign hCG elevation is comparable with that seen in post-menopausal women, with low oestradiol, combined with greatly elevated LH and FSH levels. In contrast, women with genuine disease relapse as the cause of their post-chemotherapy hCG elevation had normal or only minor elevations of LH and FSH. These findings support the observation that a major rise in LH and FSH can be used as an indicator for benign pituitary hCG production in patients experiencing a low level rise in hCG levels following chemotherapy for GTT.

Change in Follicle-Stimulating Hormone and Estradiol Across the Menopausal Transition: Effect of Age at the Final Menstrual Period

To determine whether patterns of change in serum estradiol (E2) and FSH across the menopausal transition were associated with age at the final menstrual period (FMP). The Study of Women's Health Across the Nation (SWAN) is a seven-site, multiethnic, longitudinal study of the menopausal transition being conducted in 3302 menstruating women who were aged 42-52 yr at the 1996 study baseline. Annually collected serum was assayed for E2 and FSH levels. Patterns of hormone change were evaluated in the 1215 women with a documented natural FMP by follow-up visit 9 (2006) using semiparametric stochastic and piecewise linear mixed modeling. The FSH pattern across the menopausal transition began with an increase 6.10 yr before the FMP, an acceleration 2.05 yr before the FMP, deceleration beginning 0.20 yr before the FMP, and attainment of stable levels 2.00 yr after the FMP, independent of age at the FMP, race/ethnicity, or smoking status. Obesity attenuated the FSH rise and delayed the initial increase to 5.45 yr before the FMP. The mean E2 concentration did not change until 2.03 yr before the FMP when it began decreasing, achieving maximal rate of change at the FMP, then decelerating to achieve stability 2.17 yr after the FMP. Obesity, smoking behavior, and being Chinese or Japanese were associated with some variation in E2 levels but not the pattern of E2 change. Time spans and overall patterns of change in serum FSH and E2 across the menopausal transition were not related to age at FMP or smoking, whereas time spans but not overall patterns were related to obesity and race/ethnicity.