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PubMedDate not supplied

Longitudinal follow-up of amenorrhea in eating disorders.

The authors recruited 229 treatment-seeking anorexic and bulimic women for a prospective, longitudinal study. Telephone interviews were arranged every 3 months for at least 1 year for 225 patients. At intake, 132 subjects were menstruating, 34 subjects were taking oral contraceptives, 5 subjects had an organic cause for amenorrhea (e.g., hysterectomy), and 58 subjects were amenorrheic. Each patient met Diagnostic and Statistical Manual of Mental Disorders, third edition, revised (DSM-III-R) criteria for anorexia nervosa (AN, N = 41), bulimia nervosa (BN, N = 98), or AN/BN (N = 90). All subjects were interviewed with the Schedule for Affective Disorders and Schizophrenia-Lifetime Version, which was modified to include a section for DSM-III-R eating disorders, the Longitudinal Interval Follow-Up Evaluation, and the Structured Interview for DSM-III Personality Disorders. It was found that body weight was associated with menstrual status: those with amenorrhea had a mean percent ideal body weight (IBW, Metropolitan Life criteria) of 74 +/- 1% compared with 102 +/- 19% for menstruating patients (p < .01). Affective illness was more prevalent among patients with amenorrhea than among menstruating patients (75% vs. 56%, p < .05). Menses were regained within 1 year by 33% of amenorrheic patients. These patients gained an average of 7.3% of their IBW. Longer duration of eating disorder (p < .03) and the presence of an anxiety disorder (p < .05) were associated with persistent amenorrhea. Menses were lost within 1 year by 8% of menstruating patients. These patients lost an average of 5.0% of their IBW.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1996

Nocturnal melatonin and luteinizing hormone rhythms in women with hyperprolactinemic amenorrhea.

To examine the role of melatonin in pathological hyperprolactinemia we compared untreated young females (N = 5) with hyperprolactinemic amenorrhea owing to pituitary microadenoma to healthy female controls (N = 6). Serum samples for melatonin, prolactin, and luteinizing hormone (LH) concentrations were obtained every 15 min from 1900 hr to 0700 hr in a controlled light-dark environment with simultaneous sleep recordings. The mean (+/- SD) light-time period, dark-time period, and the integrated nocturnal melatonin secretion values (area under the curve, or AUC) in patients (51 +/- 11 pmol/L, 157 +/- 33 pmol/L, and 102 +/- 19 pmol/min.L x 10(3), respectively) were similar to the values obtained in controls (79 +/- 39, 165 +/- 44, 111 +/- 31, respectively). The onset of the nocturnal melatonin rise, peak level, and peak time were similar in the two groups. A significant nocturnal prolactin rise was observed in patients (112 +/- 9 vs. 65 +/- 11 micrograms/L, P < 0.006) and controls (19 +/- 2 vs. 10 +/- 3 micrograms/L, P < 0.006). The time of prolactin peak was similar in patients and controls (0424 +/- 3:36 vs. 0350 +/- 2:21) and paralleled that of melatonin (0354 +/- 1:46 vs. 0337 +/- 1:30). The mean +/- SD light-time period, dark-time period, and the AUC values of LH were similar in patients and controls. The number of LH pulses in patients (7.2 +/- 1.9 per 12 hr) were not different from those in controls (7.7 +/- 2.1). The LH pulse interval was 100 +/- 22 min in patients compared with 94 +/- 23 min in controls. The mean (+/- SD) nocturnal estradiol (E2) levels were significantly lower in patients (84 +/- 15 pmol/L) than in controls (224 +/- 77) (P < 0.005). Analysis of LH and melatonin secretory profiles revealed significant pulses for both hormones. No significant relationship was observed between the LH and melatonin pulses. However, a negative correlation between LH pulse amplitude and the number of melatonin pulses (P < 0.04) and a positive correlation between LH amplitude and duration of melatonin pulses (P < 0.04) were observed. Taken together, these data suggest that the suppression of normal ovarian cycles in women with hyperprolactinemic amenorrhea owing to pituitary microadenoma may be mediated by blocking of gonadotropin action by prolactin at the ovarian level; yet it remains possible that chronically elevated prolactin might prevent the LH surge and thus lead to amenorrhea. Pulsatile melatonin secretion is unaltered in these patients, and frequent occurrence of amenorrhea in this population is not mediated by melatonin.

Adenoma↗
PubMed1981

Depression hostility and anxiety in hyperprolactinemic amenorrhea.

In order to evaluate the relationship of psychological distress to hyperprolactinemia, 20 patients with secondary amenorrhea were evaluated by a semi-structured research interview and administered the Kellner Symptom Questionnaire. Group A (10 patients with amenorrhea and hyperprolactinemia) reported significantly more symptoms of depression, hostility and anxiety than group B (10 patients with amenorrhea and normal basal levels of plasma prolactin). Both groups were significantly more anxious, depressed and reported more somatic symptoms than a normal control group (n = 10). 6 of the 10 patients in group A reported decrease in libido, while this was found only in 1 of the 10 patients of group B. The findings suggest that the syndrome of depression, hostility and anxiety in a woman complaining of amenorrhea, especially if associated with decreased libido and galactorrhea, can be a manifestation of hyperprolactinemia.

Adolescent↗
PubMed1995

Hormone testing in women with adult-onset amenorrhea.

To assess the clinical utility of routine endocrine testing in women with adult-onset amenorrhea, charts were identified from 127 women diagnosed with adult-onset amenorrhea who had a thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), and prolactin (PRL) level performed. Women who were pregnant or previously diagnosed with thyroid disease were subsequently excluded and 120 subjects remained. Of the 120 women screened, 12 (0.100) had abnormal FSH levels, 9 (0.075) had abnormal PRL levels, and 5 (0.042) had abnormal TSH levels. The incidence of an abnormal FSH level (95% CI 0.053, 0.168; p < 0.001) and PRL level (95% CI 0.035, 0.138; P = 0.007) was significantly elevated as compared to the reference laboratory normal values. However, the incidence of an abnormal TSH level in the study population was not statistically different from that of the reference laboratory normal values (95% CI 0.014, 0.095, p = 0.88). The evaluation of 120 women with adult-onset amenorrhea demonstrated abnormal concentrations of FSH, PRL and TSH in 10, 7.5 and 4.2% of patients, respectively. A rank ordering of these endocrine tests may be useful when evaluating women with adult-onset amenorrhea.

Adolescent↗
PubMed1982

Metergoline in the management of hyperprolactinemic amenorrhea and anovulation.

84 patients with elevated serum PRL levels, ranging from 25 to 253 ng/ml, were treated with an antiserotonin agent, metergoline, at the dose of 12 mg/day for 90 days. The clinical complaint was of amenorrhea in 70 cases (plus galactorrhea in 44 cases) and of anovulation in 14 cases (plus galactorrhea in 6 cases). Hyperprolactinemia was due to a pituitary adenoma in 18 cases; in 53 cases it was of unknown origin, while in 7 cases it followed treatment with neuroleptics or with oral contraceptives and in 6 cases it followed a puerperium. In patients with amenorrhea, metergoline induced the appearance of menses in 61 cases (94%), and of ovulation in 46 cases (82%). In 13 of the 14 patients with anovulation, ovulation was restored. Galactorrhea disappeared in 40 out of 50 patients. Metergoline normalized serum PRL levels (less than 20 ng/ml) in 46 cases and significantly reduced serum PRL levels in all but 3 of the remaining patients. In spite of suggested nonhormonal contraceptive measures, 14 patients became pregnant; 2 had abortions and the remaining 12 patients completed by vaginal delivery, uneventful pregnancies. These results indicate metergoline as a safe and effective drug in the management of hyperprolactinemic amenorrhea and anovulation. 49 patients were followed for 2 additional months, receiving no treatment (24 cases) or metergoline at a reduced daily dosage (8 mg/day, 25 cases). Within 60 days, 60% of the first group had relapse of the clinical condition and a rebound elevation of serum PRL levels while only 20% of the second group experienced relapse of amenorrhea and rebound elevation of serum PRL levels (p less than 0.01).

Amenorrhea↗
PubMedDate not supplied

Chemotherapy-induced amenorrhea and fertility in women undergoing adjuvant treatment for breast cancer.

BACKGROUND: The majority of women diagnosed with early-stage breast cancer have an excellent long-term prognosis, but many will undergo temporary or permanent chemotherapy-induced amenorrhea. METHODS: While breast cancer is more common in older women, about 1 in 200 women under the age of 40 is at risk to develop breast cancer. Many of these women benefit from chemotherapy but are afraid to risk the opportunity to bear children. The authors review the current studies on the impact of adjuvant chemotherapy on amenorrhea and fertility in women with breast cancer. RESULTS: The likelihood of amenorrhea is based on the specific adjuvant chemotherapy regimen administered and the age of the patient. Future childbirth is a viable option for women treated for breast cancer at an early stage. While the use of tamoxifen as a hormonal therapy in premenopausal breast cancer is now the standard of care, no conclusive data confirm the benefit of GnRH agonists in adjuvant therapy after treatment with chemotherapy followed by tamoxifen. CONCLUSIONS: As more women over the age of 35 consider pregnancy, fertility issues are becoming important areas of investigation for the adjuvant treatment of breast cancer. Whether chemotherapy-induced amenorrhea has a prognostic effect remains unclear, and further studies are warranted.

Adult↗
PubMed1976

Impaired LH release following exogenous estrogen administration in patients with amenorrhea-galactorrhea syndrome.

Serum gonadotropin levels were determined in 10 patients with the amenorrhea-galactorrhea syndrome before and following acute iv administration of synthetic LH-releasing hormone (LHRH) or conjugated estrogens, in order to clarify the hypothalamic derangements in the gonadotropin secretion in patients with hyperprolactinemia. The basal prolactin (PRL) levels were elevated in all the patients, and blunted responses to 500 mug of iv synthetic thyrotropin-releasing hormone (TRH) injection were found in 9 out of the 10 patients. The basal levels of LH and FSH were subnormal in 2 and 3 patients, respectively, while those in the remaining patients were normal or slightly elevated. Normal or excessive responses of gonadotropins to 100 mug of iv LHRH were observed in most patients, 9 for LH and 10 for FSH out of 10 patients. In 10 normal cyclic women at the mid-follicular phase (D7-9) and 10 hypothalamic amenorrhea patients without galactorrhea, LH release was found 48 to 72 h after the iv injection of 20 mg conjugated estrogens (Premarin). This LH release following Premarin injection was completely abolished in the patients with amenorrhea-galactorrhea. These data seem to indicate that in patients with hyperprolactinemia, tonic secretion of gonadotropin is maintained fairly well, while of the positive feedback effect of Premarin on the release of LH is impaired. It is suggested that impaired LH release may be partly responsible for anovulation and amenorrhea in patients with hyperprolactinemia.

Abortion, Spontaneous↗
PubMed1977

Effect of triiodothyronine treatment on prolactin secretion in patients with amenorrhea-galactorrhea.

In order to determine the role of thyroid hormone in prolactin (PRL) secretion in patients with amenorrhea-galactorrhae, PRL response to 500 mug of iv thyrotropin-releasing hormone (TRH) was studied before and after the administration of triiodothyronine (T3) in 10 patients with amenorrhea-galactorrhea. Seven of these patients were euthyroid and the other 3 had hypothyroidism. The patients in the euthyroid group received 50 mug of T3 daily for 7 days and 75 mug q.d. for the ensuing 14 days. The hypothyroid patients received T3 at progressively increasing doses from 10 mug q.d. to 75 mug q.d. during 34 to 68 days. In the initial test, the elevated basal levels of PRL, 61.9 +/- 9.8 ng/ml (Mean +/- SE) exhibited a slight but insignificant net increase (7.7 +/- 2.1 ng/ml) after TRH injection in the euthyroid group. However, a marked response to TRH with a net increase of 147.2 +/- 26.3 ng/ml from the basal level of 47.3 +/- 11.2 ng/ml was observed in the hypothyroid patients. After treatment with T3, both the basal level (56.9 +/- 8.3 ng/ml) and the net increase (9.9 +/- 3.6 ng/ml) of PRL following TRH stimulation remained virtually unchanged in the euthyroid group. The hypothyroid group, in contrast, displayed a significant depression of both the basal level (26.1 +/- 13.0 ng/ml) and the net increase (33.8 +/- 6.5 ng/ml) of PRL to TRH stimulation. The diminution of the basal levels and responses of thyroid-stimulating hormone (TSH) to TRH stimulation was observed in all cases of both groups. These results suggest that the level of thyroid hormone has little pathogenic role in PRL secretion in euthyroid patients with amenorrhea-galactorrhea, in contrast to its marked effect in hypothyroid patients with amenorrhea-galactorrhea.

Adult↗
PubMed1983

Amenorrhea with cryptic hyperandrogenemia.

It is current practice to assume that when menstrual disturbances are associated with androgen excess there will be additional clinical evidence of this. We have recently seen three women with secondary amenorrhea who did not have any other clinical features of androgen excess, i.e. hirsutism, acne, etc., but who had elevated plasma testosterone and androstenedione levels in addition to increased estrone values. Correction of hypertestosteronemia and elevated estrone levels was followed by ovulation, regular menstruation, and pregnancy. Variable tissue sensitivity to androgens probably accounts for these observations. If measurement of androgen levels is omitted in the evaluation of patients with amenorrhea without hirsutism, cryptic hyperandrogenemia will remain undetected. Plasma testosterone levels should be measured in all patients with amenorrhea of unknown etiology, and only if these are normal should a diagnosis of functional amenorrhea be assigned.

Adolescent↗
PubMed1985

Pulsatile luteinizing hormone patterns in the follicular phase of the menstrual cycle, polycystic ovarian disease (PCOD) and non-PCOD secondary amenorrhea.

To characterize the oscillations of plasma LH in normally cycling and amenorrheic women, three groups of women were studied: I, normal women during the follicular phase of the cycle (n = 9); II, women with polycystic ovarian disease (PCOD; n = 11); and III, women with non-PCOD secondary amenorrhea (n = 12). Blood samples were obtained at 10-min intervals for 6 h on 2 separate days. A pulse was defined as an increase in LH at least 20% over the preceding lowest value (nadir). Since LHRH release immediately follows the nadir of the LH levels, the nadir interval (NI) was used for analysis. For analysis, the results from 1 day were selected at random from each subject, and from each day, the same number of NIs also were randomly selected. When two NIs from each patient were selected, the median NI was 75 min in group I, 45 min in group II, and 45 min in group III. When three or four NIs were chosen, the median NI was 60 min in group I, 50 min in group II, and 40 min in group III. The differences between the groups were statistically significant. When three NIs were selected, the mean of the corresponding LH amplitudes was 2.8 U/liter in group I, 6.0 U/liter in group II, and 1.5 U/liter in group III. The differences between these groups were statistically significant. Thus, the NI in PCOD patients was shorter than that during the follicular phase of the cycle, but this short NI is not unique for PCOD, since the NI in non-PCOD secondary amenorrhea patients was even smaller. The LH amplitude was higher in PCOD and lower in non-PCOD secondary amenorrhea compared to that during the follicular phase of the cycle. The decrease in NI in PCOD and/or non-PCOD secondary amenorrhea vs. the NI of the follicular phase could be explained by either a higher frequency of LHRH pulses from the hypothalamus or an increased sensitivity of the pituitary leading to a greater response of the pituitary to LHRH pulses.

Adolescent↗
PubMed1989

Circadian variation of basal plasma prolactin, prolactin response to suckling, and length of amenorrhea in nursing women.

The circadian pattern of plasma PRL levels and the PRL response to suckling were examined at various times during the first postpartum year and related to the length of lactational amenorrhea. Ten healthy women whose infants were breast-fed exclusively and who were amenorrheic 3 months postpartum were studied 3, 6, and 9-11 months postpartum. The women and their babies were admitted to a metabolic unit for 48 h. On the second day, blood samples were drawn at 2-h intervals for 26 h starting at 0800 h and also 10 and 30 min after the initiation of six of the nursing episodes. During the three postpartum periods, there was a circadian rhythm of basal plasma PRL concentrations; the peak concentrations occurred between 2400-0600 h. Suckling induced a significant rise in plasma PRL levels at all hours except 0800 h. There was a positive correlation between the duration of the nursing episode and the suckling-induced PRL increase at 30 min. Both the basal plasma PRL levels and the PRL responses to suckling diminished with time after delivery. This trend was less evident at 0400 h and was not fully explained by changes in the nursing pattern. The five women in whom menstrual cycles resumed before day 180 postpartum had lower basal and suckling-induced plasma PRL levels than the women who had amenorrhea for a longer period. This difference was present in the third month, when all women were amenorrheic and fully nursing and when the frequency and duration of nursing episodes and infant growth rates were similar. The results indicate that comparable nursing patterns may be associated with different plasma PRL levels, which are associated with different lengths of lactational amenorrhea. An early difference in the sensitivity of the breast-hypothalamus-pituitary system to suckling may explain the differences in the duration of lactational amenorrhea, which are not dependant on the breastfeeding pattern. The magnitude of the PRL response to suckling may predict the likelihood of recovering ovarian function during lactation.

Adult↗
PubMed1991

Early difference in the endocrine profile of long and short lactational amenorrhea.

The endocrine profiles associated with long and short lactational amenorrhea were assessed in a longitudinal study in which morning blood samples were drawn in 48 women from the first postpartum month until the recovery of ovulation and in a cross-sectional study in which the samples were drawn throughout 24 h at the end of the third postpartum month in 10 fully nursing and amenorrheic women. PRL, LH, FSH, estradiol (E2), progesterone, cortisol, and dehydroepiandrosterone sulfate were measured. In both studies we detected a smaller PRL increase in response to suckling (P less than 0.001) and higher E2 levels (P less than 0.001) in nursing women who ovulated within 6 months postpartum compared to those in women who did not. Such differences were observed early after delivery when all women were fully nursing and amenorrheic. These results suggest some probable sources of variability in the duration of lactational amenorrhea in our population. The greater PRL response to suckling associated with longer amenorrhea may be due to higher sensitivity of the breast-hypothalamus-pituitary system or a stronger suckling stimulus in this group. Differences in plasma E2 levels between longer and shorter periods of amenorrhea may reflect dissimilar endogenous production, intake, or clearance of estrogens.

Adult↗
PubMed1992

Progressive trabecular osteopenia in women with hyperprolactinemic amenorrhea.

Reductions in cortical and trabecular bone mass have been documented in young women with hyperprolactinemic amenorrhea. It is unknown whether trabecular osteopenia is progressive or reversible with treatment of hyperprolactinemia. In addition, it is not known whether clinical or hormonal variables can predict trabecular bone density (BD) changes. Therefore, we investigated prospectively trabecular BD by computed tomography in 52 hyperprolactinemic women and 41 controls. The mean follow-up interval was 1.8 +/- 0.1 (SEM) yr. Patient groups were defined as follows: group 1, amenorrhea during the entire study; group 2, restoration of menses during the study by treatment of hyperprolactinemia; group 3, regular menses despite hyperprolactinemia, with no history of prior amenorrhea; group 4, history of prior amenorrhea, but menses restored with treatment of hyperprolactinemia before study entry; and group 5, oligomenorrhea. Groups 1, 2, and 4 had significant (P = 0.0006) initial spinal osteopenia [mean BD 141 +/- 7 (SEM), 144 +/- 9, and 151 +/- 5 mg/cc K2HPO4, respectively] compared with controls or with group 3 (170 +/- 4 and 173 +/- 8 mg/cc K2HPO4, respectively). Group 5 had an initial mean BD which was midway between that of the amenorrheic and eumenorrheic women (156 +/- 13 mg/cc K2HPO4). Group 1 had a significant (P = 0.04) decrease in mean BD to 132 +/- 8 mg/cc K2HPO4 over 1.7 +/- 0.2 yr, with BD in 42% of the group more than 2 SD below the control mean at the final study point. The mean BD in group 2 increased to 155 +/- 9 mg/cc K2HPO4, approaching significance (P = 0.07) when compared with the initial BD. Five of the nine patients in this group (56%) had an increase in BD greater than the variation expected for the computed tomography technique. However, 44% of the group 2 patients had a spinal BD which remained more than 1 SD below the normal mean. There was no change in BD in the other groups.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

[Study on galactorrhea-amenorrhea syndrome (GAS) with special reference to normoprolactinemic GAS].

In order to clarify the mechanism(s) which causes galactorrhea and amenorrhea in patients with Galactorrhea-Amenorrhea Syndrome (GAS) (Group A, n = 20), composed of Chiari-Frommel Syndrome (CFS) (Subgroup I, n = 3), Argonz-del Castillo Syndrome (ADCS) (Subgroup II, n = 5) and Drug-induced Galactorrhea-Amenorrhea (DIG) (Subgroup III, n = 12), we analysed basal plasma prolactin (PRL) and gonadotropin levels and their responsiveness to TRH and LH-RH, respectively in GAS patients. In addition, another group of galactorrhea patients without amenorrhea (Group B, n = 29) was selected, and further divided into three subgroups; subgroup I (n = 7) with persisting postpartum lactation, subgroup II (n = 7) of idiopathic galactorrhea, and subgroup III (n = 15) induced by drug administration. There were found unexpectedly high frequencies of normoprolactinemic patients (less than 23.7 ng/ml) in 40% of GAS (66.7% in CFS, 40% in ADCS, and 33.3% in DIG). The PRL responsiveness to TRH, evaluated by % delta PRL (peak PRL - basal PRL/basal PRL X 100), tended to be high in ADCS and DIG (group after discontinuation of drugs) compared with those of normal subjects (n = 12) and patients with primary hypothyroidism (n = 21). PRL response was almost normal in CFS or DIG (group during drug administration). Basal level of plasma gonadotropin in GAS was comparable to that of normal subjects. However, responsiveness of gonadotropin to LH-RH in GAS tended to be high compared with that of normal subjects. The patients in group B (subgroup I-III) demonstrated almost parallel responses of PRL and gonadotropin, respectively, to those of corresponded subgroups in group A. From the present results, we concluded that; 1) It seems likely that frequency of normoprolactinemic patients in GAS (Group A) is surprisingly high. 2) A still unclarified mechanism(s) for the occurrence of galactorrhea, not explained solely by plasma radioimmunoassayable PRL level and/or hyperresponsiveness of PRL to stimuli, may operate on a considerably large number of group A patients. 3) Decreased gonadotropin secretion at pituitary level seems not to be a main cause of menstrual abnormality in group A patients. 4) The same mechanism(s) as in group A patients may cause galactorrhea in group B patients.

Adolescent↗
PubMed1992

[A case of type 1 diabetes mellitus with hypothalamic amenorrhea: successful pregnancy following subcutaneous pulsatile administration of LHRH].

A 27-year-old woman with type 1 diabetes mellitus was admitted to the Shimane Medical University Hospital because of secondary amenorrhea. She had been treated with insulin since July, 1986. Fasting plasma glucose and HbA1c levels were controlled within normal limits. However, body weight gradually decreased and amenorrhea started in 1988. Physical examination revealed emaciation with BMI of 17.3. Basal levels of plasma T3, somatomedin C, LH, FSH and estradiol levels were low, whereas HGH levels were slightly elevated. Plasma LH markedly increased in response to LHRH administration. She was diagnosed as having weight loss-related hypothalamic amenorrhea. Induction of ovulation was not obtained with clomiphene citrate. Treatment with subcutaneous pulsatile administration of LHRH (20 micrograms every 120 min) resulted in an increase in plasma levels of LH, FSH and estradiol, which was accompanied by ovulation and corpus luteum formation. Further treatment with pulsatile LHRH administration was followed by conception. Two gestational sacs were detected by ultrasonography. One of them was absorbed at the early stage of pregnancy. She was delivered of one healthy female infant without complications. These findings suggest that it is important not only to control plasma glucose levels but to keep the appropriate weight and support the psychological aspects of the subject in the treatment of diabetes mellitus. Subcutaneous pulsatile LHRH therapy may be effective for the induction of ovulation in clomiphene-resistant hypothalamic amenorrhea; however, it will be necessary to solve the problem of dosage and the interval of LHRH administration in the future.

Adult↗
PubMed1997

Classification of hypothalamic progestin-nonresponsive amenorrhea by secretion pattern of serum LH.

The pathogenesis of hypothalamic progestin-nonresponsive amenorrhea is unclear and this disease often fails to respond to treatment. The pulsatile patterns of diurnal and nocturnal secretion of serum LH as well as serum levels of melatonin were examined to improve the understanding of the pathogenesis and to develop strategies for the management of a severe type of hypothalamic amenorrhea. Four types of LH pulsatile patterns were observed: a) no pulse during the day or night (Group 1); b) more than 1 pulse only at night (Group 2); c) only 1 pulse during the day and more than 2 pulses at night (Group 3); and d) more than 2 pulses during the day and at night (Group 4). Serum estradiol was less than 30 pg/mL, and the serum PRL and PRL response to TRH did not differ among the four groups. The basal level and the pulse amplitude of LH increased successively from Group 1 to Group 4. The serum level of melatonin at night was noticeably increased in Group 1 and correlated negatively with the LH pulse frequency at night. After 6-month hormone replacement therapy with estrogen and progesterone, the rate of improvement in ovarian function were 0%, 33.3%, 57.1% and 67.0% in Groups 1, 2, 3, and 4, respectively. In 5 patients, the LH pulse pattern was re-examined at 6 months, the LH pulsatile pattern was changed from that of Group 1 to that of Group 4, with a decrease in serum concentrations of nocturnal melatonin, indicating improved ovarian function. In conclusion, classification of patients according to the LH secretion pattern is useful in establishing the severity of hypothalamic disturbance in hypothalamic progestin-nonresponsive amenorrhea and in predicting its prognosis; in addition nocturnal melatonin can be used as a marker for severer cases of hypothalamic amenorrhea.

Adolescent↗
PubMed2000

Hypothalamic amenorrhea with normal body weight: ACTH, allopregnanolone and cortisol responses to corticotropin-releasing hormone test.

OBJECTIVE: Hypothalamic amenorrhea (HA) is a functional disorder caused by disturbances in gonadotropin-releasing hormone (GnRH) pulsatility. The mechanism by which stress alters GnRH release is not well known. Recently, the role of corticotropin-releasing hormone (CRH) and neurosteroids in the pathophysiology of HA has been considered. The aim of the present study was to explore further the role of the hypothalamic-pituitary-adrenal axis in HA. DESIGN: We included 8 patients (aged 23.16+/-1.72 years) suffering from hypothalamic stress-related amenorrhea with normal body weight and 8 age-matched healthy controls in the follicular phase of the menstrual cycle. METHODS: We measured basal serum levels of FSH, LH, and estradiol and evaluated ACTH, allopregnanolone and cortisol responses to CRH test in both HA patients and healthy women. RESULTS: Serum basal levels of FSH, LH, and estradiol as well as basal levels of allopregnanolone were significantly lower in HA patients than in controls (P<0.001) while basal ACTH and cortisol levels were significantly higher in amenorrheic patients with respect to controls (P<0.001). The response (area under the curve) of ACTH, allopregnanolone and cortisol to CRH was significantly lower in amenorrheic women compared with controls (P<0.001, P<0.05, P<0.05 respectively). CONCLUSIONS: In conclusion, women with HA, despite the high ACTH and cortisol levels and, therefore, hypothalamus-pituitary-adrenal axis hyperactivity, are characterized by low allopregnanolone basal levels, deriving from an impairment of both adrenal and ovarian synthesis. The blunted ACTH, allopregnanolone and cortisol responses to CRH indicate that, in hypothalamic amenorrhea, there is a reduced sensitivity and expression of CRH receptor. These results open new perspectives on the role of neurosteroids in the pathogenesis of hypothalamic amenorrhea.

Adrenocorticotropic Hormone↗
PubMed1977

Effect of exogenous estrogens on LH and FSH secretion in women with hypothalamic amenorrhea.

The effect of estradiol on FSH and LH secretion in 5 women with hypothalamic amenorrhea are presented. The functional capacity of the pituitary to secrete FSH and LH had been proved by testing with synthetic luteinizing hormone-releasing hormone (LH-RH) 100 mug i.m. The thyroid and adrenal functions were normal. In 3 patients estrogens were low-normal and in the other 2 extreme hypoestrogenism was found. Twelve days after the appearance of withdrawal bleeding each patient was given 10 mg estradiol benzoat (EB) i.m. In 3 patients a significant increase in the LH and a slightly smaller increase in the FSH concentration were noted, with an LH peak 60 to 84 hours after injection of EB. The first of these 3 patients became pregnant, in the second the biphasic BBT curve, urine pregnanediol excretion above 2.5 mg/24 hr and the histological finding of secretory endometrium indicated that ovulation had been successfully induced, while in the third patient, despite a satisfactory increase in the LH and FSH concentration, ovulation could not be induced. In the remaining 2 patients no increase in the LH and FSH concentrations was noted even as late as 96 hours after the injection of EB. In these women bleeding began on the 18th and 22nd day of the cycle, respectively, when histological examination revealed proliferative endometrium. The first 3 cases are classified as hypothalamic amenorrhea with dysfunction of the cyclic centre and the other 2 as hypothalamic amenorrhea with dysnfunction of the tonic centre. The effect of exogenous estrogens in patients with hypothalamic amenorrhea depends both on the functional capacity of the hypophysis and the capacity and condition of the tonic and cyclic centres in the hypothalamus.

Adult↗