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Query: UMLS:C0003128 (anovulation)
 1,718 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fertility was evaluated in 53 female patients with late-onset adrenal hyperplasia (LAH) due to 21-hydroxylase deficiency. The majority of patients (n = 33) were seen for isolated postpubertal hirsutism, 9 patients consulted for sterility, and 11 for irregular menstrual cycles. At the time of diagnosis, the ages of patients ranged from 15-40 yr (mean +/- SD, 24.6 +/- 5.2). No patient had major signs of virilization. The plasma 17-hydroxyprogesterone level was higher than normal in all patients (26.8 +/- 18.9 nmol/L; range, 3.4-139.4) and dramatically increased to 140.1 +/- 80.6 nmol/L (range, 35.2-324.2) after ACTH treatment. Plasma androgen levels were high (testosterone, 3.25 +/- 2.03 nmol/L; delta 4-androstenedione, 13.65 +/- 5.60 nmol/L). Plasma basal and LHRH-stimulated values were normal for FSH and high for LH. Basal and TRH-stimulated plasma PRL levels were normal. Among these 53 LAH patients, only 20 desired a pregnancy. These had a total of 38 pregnancies. Ten patients became pregnant before the diagnosis of LAH and without any treatment; they had a total of 18 pregnancies, 12 of which were successful. Moreover, 19 normal pregnancies without any spontaneous abortion were carried to term by 14 of 16 hydrocortisone-treated patients. One patient needed the association of one cure of clomiphene citrate. Hypofertility in LAH patients seems, therefore, to be relative. Its mechanism is hormonal, with anovulation or dysovulation, due to the continuous steroid feedback of adrenal origin on the hypothalamo-pituitary axis. Hydrocortisone is the appropriate treatment in most cases, reducing adrenal androgen overproduction and relieving hypothalamic-pituitary gonadotropin function, thereby making possible cyclic ovarian activity and ovulations.
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PMID:Fertility in women with late-onset adrenal hyperplasia due to 21-hydroxylase deficiency. 131 Sep 99

A new case of MURCS association (mullerian duct aplasia, renal aplasia and cervicothoracic somite dysplasia) in an 18 year old patient is reported. In addition to other minor phenotypical features, hypothalamic chronic anovulation was documented. Basal concentrations of PRL, TSH, GH, F and E were within reference values for adult women. Challenges with TRH and ACTH evoked normal responses in terms of TSH and F respectively. Basal levels of LH and FSH and a LHRH stimulation test demonstrated dissociation of both gonadotrophins. Persistent progesterone values within follicular phase levels led us to the diagnosis of hypothalamic chronic anovulation which was confirmed by the induction of ovulation by clomiphene citrate. This finding shows the importance of a detailed endocrinological evaluation in patients with the MURCS association in order to prevent secondary disorders due to endocrinological impairment.
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PMID:MURCS association and hypothalamic anovulation. 152 42

Pregnancy and Cushing's syndrome are seldom found together (40 cases in the literature), since hyperadrenocorticism is often responsible for anovulation by gonadotropin suppression. We report the case of a 25-year old para II woman whose pregnancy was complicated by diabetes and arterial hypertension at 31 weeks and who received the conventional treatments (special diet, insulin therapy, pindolol). Caesarean section, motivated by premature rupture of the membranes, was performed at 37 weeks, delivering a healthy infant. The diagnosis of hypercortisolism with low ACTH level was made post partum. An adrenal tumour (the most frequent cause of Cushing's syndrome occurring during pregnancy) was removed after pre-operative treatment with ketoconazole, and endocrine functions returned to normal.
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PMID:[Adrenal adenoma disclosing after delivery]. 209 25

The relationship between sex hormones and the skin is increasingly considered to be very important. The skin has appropriately been called "A peripheral endocrine gland". In this review some aspects of the cutaneous metabolism of oestrogens, progestogens and particularly androgens are analyzed. Production of skin collagen is markedly enhanced by oestrogens. Progestogens with strong androgenic activity and especially androgens have a powerful stimulating action on all skin elements particularly the epidermis and the dermis the sebaceous glands and the hair. The skin manifestations of hyperandrogenism and disturbances of reproductive functions such as anovulation, oligoamenorrhoea and polycystic ovarian disease are usually the consequences of three main aetiopathogenic factors: the first is an abnormality of GnRH pulsatility related to central nervous system dysfunction and seemingly mediated by an increase in beta Endorphin, possibly related to some extent to changes in body weight and hyperinsulinism. The second aetiopathogenic approach is hyperaestronaemia secondary to obesity. Finally adrenal hyperandrogenism caused by different types of congenital adrenal hyperplasia or by increased sensitivity to ACTH may be implicated in these various clinical manifestations.
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PMID:[Sex hormones and the skin]. 269 19

The last few years have seen the isolation, characterization and synthesis of two new hypothalamic peptides, the growth-hormone releasing factor (GRF) and the corticotrophin-releasing factor (CRF). GRF selectively stimulates pituitary growth hormone. It is interesting to note that GRF was isolated from two pancreatic tumors which were responsible for an acromegalic condition in the two patients. Hypothalamic GRF (1-44) has been found to be identical to this pancreatic GRF. CRF was isolated first from ovine hypothalamus and later characterized in several species and in the human. CRF specifically stimulates the secretion of ACTH and of beta-endorphins, and other fragments of the common precursor named pro-opiomelanocortin. Chemical synthesis of analogues of hypothalamic peptides, and in particular of GnRH (gonadotrophin-releasing hormone), has made available new molecules which form agonists as well as antagonists. After a short period of gonadotrophin stimulation GnRH agonists induce desensitization of the pituitary and a decrease in secretion of the gonadotrophins and the sex steroids by the gonads. Their usefulness is presently being tested in several conditions such as prostate cancer, endometriosis, breast cancer and idiopathic precocious puberty, and as a contraceptive method. On the other hand, pulsatile administration of GnRH restores deficient reproductive functions in certain conditions such as anovulation or azoospermia.
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PMID:[Hypothalamic factors: current findings]. 300 38

Depressive illness has been associated with reversible abnormalities in the pituitary response of growth hormone, prolactin, and ACTH-cortisol. We saw similar neuroendocrine abnormalities in a patient with pseudocyesis. Normalization of the hormonal responses occurred with resolution of the pseudocyesis. Ovarian responsiveness to HCG suggests pseudocyesis to be of central hypothalamic-pituitary origin similar to polycystic ovarian disease, with neuroendocrine data consistent with reversible depression. In patients with affective illness, ovulatory disturbances may be the presenting symptom. Thorough psychosocial evaluation may be an important tool in the diagnosis of and therapy for anovulation.
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PMID:Neuroendocrine indices of depression in pseudocyesis. A case report. 670 24

Secondary PCOS may occur in association with disorders characterized by adrenal androgen excess, e.g. congenital adrenal hyperplasia. Primary PCOS is associated frequently with more subtle abnormalities in adrenal androgen status. However, it has not been established that the mild adrenal androgen occurring in PCOS is causally involved in the development of PCOS, although adrenal hyperresponsiveness to stimulation appears to be characteristic of PCOS. It remains to be clarified whether this is due to excess stimulation of the adrenal by the putative CASH, which with ACTH probably coordinates adrenal androgen steroidogenesis, or whether adrenal hyperresponsiveness occurs as a consequence of increased cortisol clearance with compensatory hypersecretion of ACTH, which is associated with excessive adrenal androgen production. The possibility also exists that the enzyme system responsible for 17-hydroxyprogesterone production and its conversion to androgens is excessively active and may occur as a common defect in the adrenal and ovaries as a consequence of a congenital disorder. For at least some patients, treatment with a nocturnal low-dose glucocorticoid is an effective form of treatment. Indeed, this is the only hormonal form of treatment for hirsutism that also facilitates fertility and pregnancy. It is possible that PCOS may occur as a consequence of any disorder in which anovulation is associated with normal or elevated oestrogen levels. For some patients with PCOS, mild adrenal androgen excess is probably primary to development of the disorder. Thus, a trial of treatment with low-dose glucocorticoid at night appears to be a reasonable option in susceptible patients who can probably be recognized by demonstration of an excessive androgen response to ACTH or metyrapone.
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PMID:Adrenal androgen production in polycystic ovary syndrome. 758 58

To determine how continued presence of a calf affected duration of postpartum anovulation, 23 udder-intact cows and their calves were assigned to three treatments on d 4 to 9 postpartum (experimental d 0). The treatments were 1) calf present with unlimited contact with its dam (n = 8), 2) calf restricted to noninguinal contact with its dam (n = 8), and 3) calf weaned from its dam (n = 7). Calves in the calf-present and calf-restricted treatments were weaned after 5 wk. Based on daily measurements of blood progesterone, days to first ovulation after onset of treatments were 35.4 +/- 2.2, 22.5 +/- 2.2, and 14.3 +/- 2.2 for the calf-present, calf-restricted, and calf-weaned treatments, respectively; each one differed (P < .01) from the others. Mean concentrations of LH were greater (P < .05) in the calf-restricted treatment and tended (P = .13) to be greater in the calf-weaned treatment than in the calf-present treatment on d 7 after the onset of treatments. On d 7 and 21, calves in the calf-present and calf-restricted (calves could not suckle) treatments were returned to their dams after overnight separation. Blood samples were collected to assess changes in cortisol, ACTH, prolactin, and oxytocin. No treatment effects were detected on d 7, but on d 21, the calf-present and calf-restricted cows had a greater (P < .05) increase in cortisol after calf return than the calf-weaned cows (calves were not returned), whereas prolactin was increased (P < .05) after calf return in the calf-present cows only. We conclude that calf presence is associated with an increase in cortisol and calf presence without suckling is one factor that delays the onset of first postpartum ovulation in beef cows.
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PMID:Restricting calf presence without suckling compared with weaning prolongs postpartum anovulation in beef cattle. 877

We report a case of a 34-year-old woman affected with ovarian arrhenoblastoma characterized by very high testosterone (T) levels (34.0-60.0 ng/ml; n.v.0.2-0.9) and suppressed gonadotropin levels. The physical examination revealed: severe hirsutism, acne, amenorrhea and other virilization signs. Basal hormonal evaluation also showed a markedly elevated 17-hydroxyprogesterone (17-OHP) and a mild delta 4 Androstenedione (A) and dehydroepiandrosterone sulfate (DHEAs) increase. ACTH test induced only slight changes in androgen secretion. By contrast, dexamethasone test greatly decreased A and DHEAs whereas T levels were only partially suppressed. Moreover, hCG test was clearly stimulatory for T and A. Suppressed gonadotropin levels did not respond to LHRH stimulation. The removal of the neoplasia was followed by normalization of T levels and increase of serum gonadotropins with subsequent restoration of a normal responsiveness to LHRH and resumption of an ovulatory menstrual cycle. This observation suggests that the high T levels played a primary role in the pathogenesis of the gonadotropin suppression and anovulation. Recovery of acne was complete whereas hirsutism score was reduced but still elevated after one year. This may be due to postoperative A and DHEAs levels slightly above the normal range, indicating the presence of adrenal hyperandrogenism.
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PMID:Clinical features and hormonal characteristics in a case of ovarian arrhenoblastoma. 888 44

The etiology of hyperandrogenic chronic anovulation is heterogeneous and relatively unknown in the majority of cases. Affected individuals in this latter segment are considered to have polycystic ovary syndrome (PCOS) of which 50 to 60% exhibit androgen excess of adrenal origin. An understanding of normal adrenal function provides insight into the factors that contribute to adrenal androgen excess in PCOS. Since pituitary ACTH secretion promotes developmental growth and overall steroidogenic efficiency within the adrenal cortex, it is probable that these actions of ACTH along with the adrenal's unique centripetal circulation play a major role in the induction of adrenarche. This latter phenomenon is characterized by alterations in adrenocortical morphology and steroidogenic enzyme activities culminating in increases in adrenal androgens to normal circulating adult levels. Thus, it is not surprising that adrenal dynamic testing has revealed increased 17,20 lyase activity or adrenal androgen hyper-responsiveness to ACTH as the two abnormalities leading to adrenal androgen excess in PCOS. Whereas 17,20 lyase hyperactivity diagnosed by defined criteria in response to pharmacological ACTH may be an intrinsic genetic defect, increases in 17,20 lyase activity and adrenal androgen hyper-responsiveness to ACTH in response to physiological ACTH may be promoted by the functional elevation of estrogen of ovarian origin in PCOS. The latest in vitro data suggest the estrogen may elicit its effect on the adrenal cortex through a receptor mediated mechanism. Therefore, the currently available data indicate that adrenal androgen excess in PCOS is also heterogeneous in etiology.
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PMID:Adrenal involvement in polycystic ovary syndrome. 916 58


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