Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003128 (anovulation)
 1,718 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Competitive swimmers were followed over a 2-year period when they trained at different levels of exercise which coincided with distinct changes in their menstrual history. Oligomenorrhea was identified in 5 of 13 of these athletes when they swam approximately 100,000 yards per week. Weight and percentage of body fat were not significantly different between the period of oligomenorrhea and regular menstrual function (P = 0.24). Mean and median levels of luteinizing hormone, follicle-stimulating hormone, prolactin, and 17beta-estradiol were decreased and catechol estrogens and beta-endorphins were increased in serum during the strenuous, when compared with the moderate, training period. The serum levels of the steroid and protein hormones were similar to those of normal cycling, nonexercising control subjects during moderate exercise (60,000 yards per week). The significant differences between beta-endorphins and catechol estrogens during periods of strenuous exercise suggest an explanation for oligomenorrhea in female athletes. These hormonal changes result in hypothalamic anovulation, which appears to be reversible, because the hormone levels and menstrual cycles return to normal when the exercise is reduced.
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PMID:The role of beta-endorphins and catechol estrogens on the hypothalamic-pituitary axis in female athletes. 609 53

We hypothesize that the Stein-Leventhal syndrome (type 1 polycystic ovarian disease: SLS-PCOD-I) results from an aberrant puberty. Abnormal neural development in the brain decreases the hypophyseal set-point for negative and positive ovarian hormone feedback. This generates a condition whereby hypophyseal luteinizing hormone (LH) secretion is inappropriately elevated compared to hypophyseal follicle-stimulating hormone (FSH) secretion and is thus termed inappropriate gonadotropin secretion (IGS). The events which create an initial state of IGS are referred to as the "generator" stage. IGS is maintained by ovarian-derived hyperandrogenemia and increased peripheral aromatization of androgens yielding elevated free serum estrone (E1) and unbound estradiol (E2) levels. E1 suppresses release of hypophyseal FSH while E2 exerts positive feedback on LH pulsatile release by increasing pituitary sensitivity to gonadotropin-releasing hormone (GnRH). Diminished circulating FSH levels decrease granulosa cell aromatase activity sufficiently to cause suboptimal ovarian conversion of LH-induced thecal androgens into estrogens. Consequently, chronic local ovarian hyperandrogenemia with associated arrested follicle maturation results in chronic anovulation. Furthermore, an elevated circulating LH/FSH ratio stimulates early development and proliferation of immature follicles causing the appearance of polyfollicular ovaries. In this effector stage of PCOD-I, a vicious cycle is fashioned wherein IGS causes polyfollicular ovaries and increased ovarian androgen production which, in turn, promotes IGS. We suggest that the etiology of this disease involves an aberrant puberty that establishes a persistent faulty hypothalamic-hypophyseal-ovarian axis.
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PMID:Hypothesis: aberrant puberty and the Stein-Leventhal syndrome. 614 82

Serum measurements of bioactive (bio) luteinizing hormone (LH), immunoreactive (i) LH, iLH/follicle-stimulating hormone (FSH) ratios, serum androgens and estradiol (E2) were determined in 20 women with the clinical diagnosis of the polycystic ovary syndrome (PCO), and compared with the levels of 10 women with chronic anovulation (CA) and 10 control subjects in the early follicular phase. Women with CA and control subjects had similar levels of E2, androgens, bioLH, iLH, and iLH/FSH ratios. Fourteen of 20 women with PCO had levels of iLH exceeding 3 standard deviations (SD) of the levels of control women (21 mIU/ml), and 13 of 20 had iLH/FSH ratios above 3.2 (3 SD of control levels). Nineteen of 20 women, however, had bioLH levels above 70 mIU/ml (3 SD of control levels). Mean levels for bioLH were 131 +/- 18 in PCO, 39 +/- 3 in control subjects, and 40 +/- 3 in women with CA. The ratio of bioLH/iLH was 3.5 +/- 0.4 in control subjects and 3.2 +/- 0.3 in women with CA but significantly elevated in PCO (4.6 +/- 0.4, P less than 0.05). There was, however, a significant positive correlation between bioLH and iLH values in PCO (r = 0.64, P less than 0.01). A significant correlation was found between bioLH and serum testosterone as well as between bioLH and serum dehydroepiandrosterone sulfate (DHEA-S) (P less than 0.05), although no correlation was found between iLH and serum DHEA-S. Weight and obesity also did not correlate with either iLH or bioLH in women with PCO and CA. These data suggest that bioLH may be an important hormonal marker in the clinical diagnosis of PCO.
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PMID:Elevated bioactive luteinizing hormone in women with the polycystic ovary syndrome. 622 Sep 24

We have evaluated daily blood levels of gonadal steroids and trophic hormones in the cycles of four ovulatory and six anovulatory patients with a luteinizing hormone (LH) surge. The cycles of anovulatory nonhirsute patients were characterized by a premature and blunted LH surge and by low levels of follicle-stimulating hormone (FSH) throughout the study period in the face of normal tonic and peak levels of estrone and estradiol (E2). These observations, together with decreased levels of prolactin, suggest a hypothalamic pituitary abnormality as the cause of anovulation in these patients. The cycles of anovulatory hirsute patients were marked by a decrease in E2 production and a blunted and delayed E2 peak. Androgen levels were elevated throughout the cycle and may have a direct inhibitory effect on ovarian folliculogenesis. The LH/FSH ratio in the follicular phase was high in both groups of anovulatory patients when compared with ovulatory controls; however, the shifts in gonadotropin levels producing the increase in this ratio were different for these two groups.
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PMID:Daily blood hormone levels related to the luteinizing hormone surge in anovulatory cycles. 640 Dec 51

The 24-hour mean plasma concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured during the follicular phase of the menstrual cycle in 15 healthy, regularly cycling obese women (59-218% above desirable weight) and 9 healthy, regularly cycling nonobese women (14% below to 14% above desirable weight). The obese women showed slightly but not significantly higher FSH values (12.5 vs. 9.6 mIU/ml), definitely and significantly lower LH values (11 vs. 17 mIU/ml; p less than 0.005) and markedly and very significantly higher FSH/LH ratios (1.2 vs. 0.62; p less than 0.0005). These abnormalities may represent a human counterpart of the slow-GnRH-pulsing model of primates: monkeys in which the GnRH secretory centers have been ablated and that receive GnRH infusions at subnormal pulsing rates show slightly elevated FSH levels, markedly decreased LH levels, greatly elevated FSH/LH ratios and anovulation.
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PMID:Subnormal 24-hour mean plasma LH concentration and elevated plasma FSH/LH ratio in obese premenopausal women. A possible human counterpart of the slow-GnRH-pulsing model in primates. 642 May 58

This study was designed to characterize pituitary function in premenopausal women during hypothyroid and euthyroid periods. Six subjects with basal thyroid-stimulating hormone (TSH) levels above 10 microU/ml were studied. Estradiol (E2), prolactin (PRL), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) levels were measured by radioimmunoassay at 30, 15, and 0 minutes before infusion. Pituitary function was evaluated by rapid infusion of 10 micrograms of luteinizing hormone-releasing hormone (LHRH) every 2 hours for a total of 6 hours. Samples were then obtained for FSH and LH every 30 minutes for the duration of the 6-hour study. A significant elevation in basal gonadotropins was observed during the hypothyroid period regardless of basal E2 levels in all 6 subjects (P < .01). Basal PRL levels were not significahtly different during the 2 periods (P > .05). In all 6 patients pituitary sensitivity and reserve correlated significantly with basal E2 levels (P < .05), but were not altered by the hypothyroid condition. It is concluded that pituitary responsiveness to LHRH is not altered in hypothyroid women, but that chronic elevation of basal gonadotropins may in part explain the anovulation that so often accompanies this disorder.
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PMID:Pituitary response to LHRH in hypothyroid women. 677 59

Parturition in the sow is followed by a period of anovulation which is prolonged by lactation. Follicular development and luteinizing hormone (LH) secretion are depressed during the last month of pregnancy. After parturition, LH secretion increases but is again inhibited by the establishment of lactation. Lactating sows are submitted to stimuli originating from the young, whose intensity culminates 3-14 d post-partum (pp), and to high nutrient requirements for milk production. The inhibitory effects of sucklings are imposed during the first 3 d pp and seem to be mediated by the action of opioids at the hypothalamic level. The nutritional deficit constitutes an additional inhibitory factor. As lactation continues, LH secretion progressively increases. A further rise in LH occurs at weaning. Variations in follicle-stimulating hormone (FSH) profiles are less marked. The divergence observed between LH and FSH might be explained by different mechanisms of control; FSH secretion depends mainly on ovarian inhibition whereas LH secretion depends mainly on factors related to lactation. Folliculogenesis progressively resumes during lactation and follicles acquire the ability to respond to the weaning-associated stimuli and begin preovulatory growth. Hormones modified by lactation, such as prolactin, insulin, growth hormone and insulin-like growth factor I, may influence folliculogenesis directly at the ovarian level or via modifications of gonadotrophin secretions. In conclusion, the inhibition of the hypothalamo-pituitary-ovarian axis during lactation is mainly due to suckling-induced neuroendocrine reflexes. We hypothesize that the nutritional deficit becomes relatively more important during the third and fourth weeks pp.
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PMID:Endocrine bases of lactational anoestrus in the sow. 754 31

The goal of the study was to compare cardiovascular heart disease risk factors in women with polycystic ovary syndrome (PCOS) and matched control subjects. Women with PCOS have risk factors, including anovulation, hyperandrogenism, and insulin resistance, that suggest a male coronary heart disease risk-factor profile. A total of 206 women with PCOS were recruited by using records from a large reproductive endocrinology practice. A clinical diagnosis of PCOS was made if there was a history of chronic anovulation in association with either clinical evidence of androgen excess (hirsutism) or if total testosterone level was > 2 nm/L or the luteinizing hormone/follicle-stimulating hormone ratio was greater than 2. The overall response rate for cases was 76%. A control population was obtained by using a combination of area voters' registration tapes and directories of households. A control subject was matched to each case subject by age +/- 5 years, race, and neighborhood. The response rate for recruitment of the first or second eligible control subject was 83.6%. The average age at initial interview was 35.9 +/- 7.4 years for case and 37.2 +/- 7.8 years for control subjects. Women with PCOS had significantly increased cardiovascular disease risk factors compared with control women. These included increases in body mass index, insulin, and triglyceride levels (P < .001), decreased total HDL and HDL2 levels (P < .01), and increased total cholesterol and fasting LDL levels, waist/hip ratio, and systolic blood pressure (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary heart disease risk factors in women with polycystic ovary syndrome. 760 Jan 12

A total of 82 normogonadotrophic clomiphene-resistant anovulatory patients were treated with exogenous gonadotrophins according to a step-down dose regimen during 234 cycles. In 43 (18%) cycles co-treatment with gonadotrophin-releasing hormone analogues was applied. The initial dose was between 1.5 and 2.5 ampoules (75 IU follicle-stimulating hormone each) per day (dependent on body weight), and decreasing steps of 0.5 ampoules/day were based on sonographic findings. The overall ovulation rate was 91% (213 cycles). The median treatment period was 11 days and a total of 14 ampoules of gonadotrophin were needed. In 131 (62%) of the ovulatory cycles not more than one, and in 208 (98%) cycles not more than two, follicles > or = 16 mm were present on the day human chorionic gonadotrophin was given. A total of 37 pregnancies occurred of which two were twins and one was a triplet (multiple pregnancy rate 8%). The pregnancy rate per cycle was 17% and the cumulative pregnancy rate after 7 months was 47%. The abortion rate was 19%. There were four (1.7%) cases of mild ovarian hyperstimulation, of which none became pregnant. In conclusion, this study shows that the applied step-down regimen for gonadotrophin induction of ovulation can be a safe and effective treatment alternative for patients with clomiphene-resistant anovulation. The duration of ovarian stimulation and the amount of exogenous gonadotrophin required is limited. Pregnancy rates are comparable with those reported for step-up regimens, and a low incidence of complications (i.e. multiple gestation and ovarian hyperstimulation) was noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gonadotrophin induction of ovulation using a step-down dose regimen: single-centre clinical experience in 82 patients. 765 39

From a longitudinal prospective study, 160 women with spontaneous menopause and without steroid medication were followed during the transition from pre- to postmenopause. After 12 years 152 women were still participating in the study. Blood samples were drawn every 6 months until 1 year after the menopause and every 12 months thereafter. Measurements of bone mineral density (BMD) on the forearm were performed every second year. All women routinely completed a questionnaire concerning symptoms frequently attributed to the climacteric period. All data were grouped around the onset of the menopause, thereby allowing longitudinal evaluation of the changes in the variables from the premenopausal to the postmenopausal period. The beginning of the perimenopausal period was characterized by transitory elevations of follicle-stimulating hormone (FSH). A significant increase in serum levels of gonadotropins was observed for both FSH and luteinizing hormone (LH) from about 5 years before the menopause. Within the 6 month period around the menopause there was a further increase which culminated within the first postmenopausal year for LH and 2-3 years postmenopause for FSH. Thereafter, a continuous decrease in LH occurred over the following 8 years. With respect to FSH, there was a slight decline starting about 4 years postmenopause. During the premenopausal period an increasing frequency of inadequate luteal function or anovulation occurred and, in the postmenopausal years, the serum levels of progesterone (P) were invariably low. Gradually, the ratio between estrone (E1) and 17-beta-estradiol (E2) increased, reflecting the declining follicular steroidogenesis. A marked decrease in estrogen levels occurred during the 6 month period around the menopause, most pronounced in E2. During the next 3 years, the levels of E2 and E1 showed an essentially parallel, moderate decline. Around the menopause, serum levels of testosterone (T), delta 4-androstenedione (A) and sex hormone-binding globulin (SHBG) showed small but significant decreases. From about 3 years postmenopause, the levels were relatively constant over the following 5 years. A decrease in BMD was observed in the postmenopause, and from about 3 years postmenopause, estradiol correlated positively with BMD. Before, as well as after the menopause, body mass index (BMI) showed an inverse correlation with SHBG. Postmenopausal androstenedione correlated positively with E1, E2 and T. BMI correlated positively with E1 and E2. The concentrations of the free fraction of E2 and T are dependent on the levels of SHBG, which in turn has a negative correlation with BMI. The impact of this will influence the severity of symptoms, the degree of bone loss and the need for supplementary therapy.
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PMID:A longitudinal study of the perimenopausal transition: altered profiles of steroid and pituitary hormones, SHBG and bone mineral density. 1943 80


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