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)

10 examine the relationship between obesity and chronic anovulation, we compared basal serum LH, FSH, and PRL levels, determined at 20-min intervals, and basal C21 [progesterone, 17- hydroxyprogesterone , pregnenolone, 17-hydroxypregnenolone ( 17Pe ), and cortisol], C19 [testosterone (T), delta 4-androstenedione (A), and dehydroepiandrosterone] and C18 (estrone and estradiol) steroid hormone concentrations measured at 1- to 2-h intervals for a 24-h period in five normal weight cycling women (NC) and in two groups of weight-matched obese women. Five of the obese women were regularly cycling (OC), and six were amenorrheic (OA). Sex hormone-binding globulin (SHBG) and non-SHBG-bound T and estradiol concentrations were also measured in each woman. Compared to NC women, OC women had normal basal protein and steroid hormone concentrations, except for reduced 17Pe levels (P less than 0.05). Mean SHBG concentrations were reduced by approximately 30%, and non-SHBG-bound T was increased by 70%, although the differences were not significant. In addition, when six precursors of testosterone (pregnenolone, 17Pe , dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, and A) were considered together as a group and the data analyzed by the kappa 2 test, a reduction in basal levels of these precursors was found in OC women relative to those in NC women (P less than 0.005). In OA women, mean concentrations of SHBG were markedly reduced and those of total T, A, estrone, and non-SHBG-bound T were significantly increased compared to those in both NC and OC women. Mean 24-h concentrations of LH tended to be greatest and FSH lowest in this group, but were not significantly different from those in the other groups. The mean LH pulse frequency was significantly greater in OA than in OC women (P less than 0.05). Mean 24-h PRL and cortisol levels were also reduced in OA women relative to those in NC women. These data suggest the possibility of a compensatory decline in total T production in OC women in an attempt to maintain normal hormonal homeostasis; as a consequence, ovulation continues in a cyclic fashion. In OA women, such compensatory mechanisms are no longer operative. Instead, a central and/or peripheral defect, resulting in overproduction of androgen, may also exist and lead to anovulation in OA women. In conclusion, our data imply that obesity is not a primary factor causing chronic anovulation. However, obesity may aggravate an already existing subtle defect in some women and result in amenorrhea.
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PMID:Endocrine comparison of obese menstruating and amenorrheic women. 642 58

An alteration of the hypothalamic dopaminergic regulation of LH secretion has been implicated in the abnormal LH secretion of polycystic ovarian syndrome (PCOS). To investigate this, the acute effect of dopamine (DA) receptor blockade on LH, FSH, PRL and TSH secretion was determined. No effect was observed on either LH or FSH secretion in the PCOS patients or in normal women and LH pulsatility appeared to be maintained. When the PCOS patients were divided into those who ovulated in the preceding cycle and those who were anovulatory, it was observed that the ovulatory patients had a normal PRL and TSH response; whereas in the anovulatory patients, the PRL rise was blunted and the TSH response was absent. We conclude that this study gives no evidence to support the hypothesis of altered hypothalamic DA regulation of LH secretion in PCOS. The lack of LH response to DA blockade suggests that a physiological role of DA in the control of LH secretion seems unlikely as determined under these experimental conditions. The differences in PRL and TRH response may reflect anovulation rather than a fundamental abnormality in PCOS.
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PMID:The acute effects of a dopamine antagonist (domperidone) on luteinising hormone, follicule stimulating hormone, prolactin and thyrotrophin secretion in polycystic ovarian syndrome: differential effect of ovulation. 643 39

To examine the mechanism by which obesity influences ovulation, 55 patients with oligo- or anovulation were studied. Parameters measured in serum were sex steroid-binding globulin (SSBG), testosterone (T), PRL, LH, FSH, and estradiol (E2). The women were divided into 2 groups: an obese group (group 1), greater than 145% of ideal body weight, and a normal weight group, less than 120% ideal body weight. SSBG was measured by saturation analysis T, LH, FSH, PRL, and E2 were measured by RIA. SSBG group 1 levels were 7.14 ng dihydrotestosterone bound/ml compared to 14.7 ng dihydrotestosterone bound/ml in group 2 (P less than 0.05). There were no significant differences in FSH, T, or E2. The correlation of body weight vs. SSBG in all patients was r = -0.62. In these 2 groups, the SSBG was significantly lower in the obese patients compared to that in the normal weight patients, independent of T or E2 levels. SSBG correlated negatively with body weight, suggesting that obesity has an influence on SSBG levels independent of hormonal status. When SSBG is lowered, there may be an increase in free T which, by inhibiting follicular maturation, may begin the sequence of events seen in polycystic ovary syndrome.
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PMID:Obesity and its role in polycystic ovary syndrome. 678 98

Several investigators have reported that CB-154 induces ovulation in patients with normoprolactinemic anovulation as well as those with hyperprolactinemic amenorrhea. In the present research, the ovulation-inducing effects of CB-154 were studied in normoprolactinemic subjects with special reference to the feedback effect of estradiol on LH release. Thirty female subjects aged 20 approximately 32 years with ovulatory disturbances were studied. Basal serum PRL, LH and FSH were determined by radioimmunoassay, and both hyperprolactinemic and hypergonadotropic anovulatory patients were excluded. A 2mg dose of estradiol benzoate was administered intramuscularly to each subject and 8ml samples of venous blood were taken at 0, 6, 24, 30, 48, 54, 72, 78 hr. The subjects under study were divided into two groups, A and B, according to the effect the estradiol benzoate had an LH release. Group A subjects (nine in all) failed to show any positive feedback release of LH in response to the estradiol benzoate. Group B subjects (twenty-one in all) showed a more than twofold increase in circulating LH as compared with the initial serum LH value, and this was taken as an indication of positive feedback release. All the subjects in group B were given clomiphene (50 approximately 100mg daily for five days). The clomiphene therapy was effective in eleven subjects, and four became pregnant (three in the first or second cycle of treatment and one in the third). The therapy was ineffective in the remaining six subjects, four of whom were diagnosed as suffering from polycystic ovary syndrome. Clomiphene was judged to be effective when the subjects undergoing therapy with this drug ovulated during three successive treatment cycles, and ineffective when the subjects did not fulfill this criterion (criterion for effectiveness of clomiphene). With the exception of four cases of polycystic ovary syndrome and three pregnancies which occurred in the first or second cycle, the rate of effectiveness of clomiphene in group B was 12 out of 14. It was concluded from these results that clomiphene was effective in group B subjects except in cases of polycystic ovary syndrome. Treatment with clomiphene alone was effective in none of the seven subjects in group A. However, administration of CB-154 for several weeks prior to and during the clomiphene treatment cycle (combined therapy of CB-154 and clomiphene) led to remarkably improved ovulation rates in five subjects in group A. Four patients in group A were selected, and given estradiol benzoate prior to (control) and during (study) CB-154 administration. In each case administration of CB-154 elicited marked positive feedback release of LH as compared with the control period, that is to say, CB-154 transformed group A patients into group B patients. This effect of CB-154 may explain why therapy combining CB-154 and clomiphene improved ovulation rates in group A...
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PMID:[The ovulation-inducing effect of CB-154 on normoprolactinemic anovulatory subjects (author's transl)]. 680 83

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).
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PMID:Metergoline in the management of hyperprolactinemic amenorrhea and anovulation. 703 5

Both hyper- and hypothyroidism may result in menstrual disturbances. In hyperthyroidism, amenorrhea was described as early as 1840 by von Basedow. The most common manifestation is simple oligomenorrhea (decreased menstrual flow). Anovulatory cycles are very common. Increased bleeding may occur, but is rare in hyperthyroidism. Nowadays hyperthyroidism is diagnosed earlier than it once was, and so the clinical picture is generally milder. So, menstrual disorders are less common than in previous series. In a recent paper, 21.5% of 214 patients had disturbances in their cycle, compared to 50% in some older series. In hypothyroidism, on the contrary, polymenorrhea (increased menstrual bleeding) is more common. Defects in hemostasis may contribute to this. Anovulation may be represent. Fertility is reduced in both hyper- and hypothyroidism, and the outcome of pregnancy is more often abnormal than in euthyroid women. It is of interest that in juvenile hypothyroidism precocious puberty has been described. This is probably due to a "spillover" effect of the glucoprotein hormones: TSH, which is markedly increased in hypothyroidism, has a small FSH- and LH-like effect. Galactorrhea may also be present in hypothyroidism, possibly because TSH, the hypophyseal TSH-releasing hormone, increases the secretion of both TSH and PRL.
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PMID:Disturbances of menstruation in thyroid disease. 923 78

Mice carrying a null mutation of the progesterone receptor gene exhibit several reproductive abnormalities, including anovulation, attenuated lordotic behavior, uterine hyperplasia, and lack of mammary gland development. The hormonal correlates of these abnormalities are unknown, however, and were the focus of these studies. Serum samples from female wild-type (WT) and progesterone receptor knockout (PRKO) mice were obtained and analyzed by RIA for LH, FSH, PRL, estrogen (E2), and progesterone. Hypothalamic tissues were also processed for measurement of LHRH by RIA. Serum LH levels in PRKO mice were found to be elevated by approximately 2-fold over basal (metestrus) values in WT mice. By contrast, basal FSH levels were not different in PRKO and WT mice. Basal levels of E2 and progesterone in serum were likewise similar in the two groups, as were hypothalamic LHRH concentrations. Basal PRL levels were slightly higher in PRKO vs. WT mice. Ovariectomy of both groups of mice was accompanied by significant increases in both LH and FSH. At 5 days following ovariectomy, LH levels were elevated in both groups by 2-fold over PRKO basal and 4-fold over WT basal levels; however, by 10 days postovariectomy LH levels had continued to rise to a greater extent in PRKO mice than in WT animals. The FSH response to ovariectomy was greater for the PRKO mice at 5 days, but was no different from WT at 10 days. Of seven PRKO mice that were exposed to male odor, none exhibited preovulatory surges 3 days later, on the day of presumptive proestrus; this was in marked contrast with WT females, in which 100% exhibited robust LH surges. These results confirm the essential role of progesterone receptors in the regulation of hypothalamic and/or pituitary processes that govern gonadotropin secretion. The finding that basal LH levels are elevated in PRKO mice confirms that circulating progesterone normally conveys a significant portion of the total ovarian negative feedback control of the gonadotropin. That gonadotropin responses to ovariectomy are slightly enhanced in PRKO mice suggests that adrenal progesterone may contribute to the imposition of negative feedback control. The apparent inability of PRKO mice to respond to male odor suggests that anovulation in these mice may not be solely due to reproductive abnormalities within the ovary itself; rather, PRKO mice additionally harbor neuroendocrine defects that render them incapable of mounting normal preovulatory gonadotropin surges. It remains to be determined how the absence of PR in brain and pituitary of PRKO mice may produce this hormonal acyclicity and, conversely, how the presence of PR in brain and pituitary of WT mice may be obligatory in the generation of gonadotropin surges.
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PMID:Endocrine defects in mice carrying a null mutation for the progesterone receptor gene. 932 23

To characterize the episodic fluctuations of serum LH, FSH and PRL in women with normally cycling, secondary amenorrhea and polycystic ovary syndrome (PCOS), four groups of women were studied: group I (N = 8) consisted of normal women in the follicular phase of the cycle; group II (N = 10) of women with secondary amenorrhea and positive progesterone withdrawal bleeding; group III (N = 8) of women with secondary amenorrhea and negative progesterone withdrawal bleeding; group IV (N = 9), women with polycystic ovary syndrome (PCOS). Blood samples were obtained at 15 minute intervals for 4 hours during one admission day. Ovarian steroids were measured to evaluate the baseline endocrine environment in each group. Distinct pulsatile fluctuations of serum LH, FSH and PRL were observed in all subjects. These pulses showed a high degree of coincidence in LH with FSH and LH with PRL in each group. However, the mean (+/- SD) frequencies of LH in group III and group IV were significantly lower (P < 0.01) and higher (P < 0.01) than in group I, respectively. The mean frequencies of FSH in groups III and IV were lower (P < 0.05), as compared with those of group I. The mean amplitude of LH in group IV was significantly higher (P < 0.001) than in group I. These results suggest that loss of the regulatory pulsatility of gonadotropin releases may be a contributory cause to anovulation and secondary amenorrhea. The concomitant pulsatile releases of gonadotropin and PRL are essential to reproductive function and their regulatory controls in the follicular phase may be mediated through a common neuroendocrine mechanism in normal and hypogonadal women.
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PMID:Characterization of pulsatile secretion of gonadotropin and prolactin in women with normal menstrual cycle, secondary amenorrhea and polycystic ovary syndrome (PCOS). 954 61

To evaluate the level of hormones before and after female renal transplantation, we measured pituitary gonadal hormones, estrovite, progestin, and prolactin in 25 renal transplant recipients (RTR) and 25 cases of chronic renal failure (CRF) using engyme immunoassay (EIA). The results indicated that serum RRL, FSH and LH level were reduced in RTR females compared with CRF, whereas E2 and P were normal. Serum PRL levels were elevated in CRF females whereas P levels were significantly lower compared with those of other groups. After clomiphene stimulation test, the plasma levels of LH FSH and E2 elevated, suggesting hypothalamic anovulation. Following successful renal transplantation, uremic hypothalamic disfunction was ameliorated and normal menstrual cycle, fertility was restored. During dialysis, treatment was given using suit therapy rather than trigger the ovulatory. Renal transplantation is the best treatment.
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PMID:[Fertility and related hormones before and after female successful renal transplantation]. 1067 50

Hypertrichosis, characterized by increased hair growth located in non-androgen-dependent areas, does not justify the monitoring of hormone levels, conversely to hirsutism, with increased hair growth in androgen-dependent areas of the female genitals. Adult hypertrichosis is iatrogenic (minoxidil, ciclosporine, diazoxide or glucocorticosteroids), of metabolic origin (porphyria), nutritional (anorexia) or paraneoplastic (hypertrichosis lanuoginosa). Metabolic or general assessment can help clinical diagnosis. In non-iatrogenic hirsutism the following must be eliminated: 1) a virilizing tumor (ovarian, adrenal) when confronted with rapid progression or recent hirsutism, plasma testosterone (T)>1.5ng/ml and/or (adrenal tumor) DHEA-sulfate (DHEAS)>700 microgram/dl and associated with hypertension; 2) when confronted with characteristic signs of hirsutism, Cushing's syndrome (post-dexamethasone cortisol), hyperprolactinemia (pooled PRL), or acromegalia (IGF1). Measurement of 17-OH-progesterone at 8 am on the 4th day of the cycle detects the late manifestation homozygous forms of a 21-hydroxylase (21OHD) block. The more frequent forms are: 1) ovarian polymicrocystic or hirsutism-anovulation syndromes without other causes (LH/FSH, T, hyperinsulinemia, sonography); 2) functional adrenal hyperandrogenia (increased DHEAS without organic cause); 3) idiopathic hirsutism. Treatment can be local (discoloration, depilation, diathermo-coagulation, laser). Treatment of hirsutism of organic origin is etiologic. The inhibitory effects of glucocorticosteroids are mediated by 21OHD. The most effective treatments are anti-androgenic: cyproterone acetate, progesterone-like and anti-gonadotropic (contraceptive) agents; and the only product in France officially indicated in hirsutism , spironolactone (anti-mineralocorticosteroid); and flutamide, pure anti-androgen (probably hepatoxic). Finasteride (type II 5 alpha-reductase inhibitor) appears less effective. Estrogen-progestagen-like agents can be associated with anti-androgens. We should also mention the GnRH-agonists, and finally, dietetics and metformine (in cases of insulin-resistance).
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PMID:[Hirsutism and hypertrichosis in adults: investigations and treatment]. 1222 63


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