Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002453 (amenorrhea)
 6,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antimitotic chemotherapy and radiation therapy can induce temporary or permanent infertility in men, transitory amenorrhea or premature ovarian failure in women, and genetic mutations responsible of fetal deaths or congenital malformations in the progeny. Alkylating agents and radiotherapy can provoke definitive male infertility and ovarian failure, but individual susceptibility seems quite variable. In man, return of spermatogenesis can still be observed more than 10 years after treatment and pregnancies are obtained with very low sperm counts. In women, the progressive depletion of the follicular pool explains the increasing frequency of ovarian failure, with lower doses of treatment. Antimitotic and immunosuppressive therapy can also induce irreversible lesions in children's gonads.
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PMID:[Fertility after cytostatic treatments]. 826 21

To examine the impact of amenorrhea on bone mineral density in women of reproductive age, we performed a cross sectional study in 190 amenorrheic women, comprising 113 premature ovarian failure, 27 primary hypothalamic amenorrhea, 38 hyperprolactinemia and 12 Sheehan's syndrome. Measurement of bone mineral density was carried out using dual photon absorptiometry at four sites: femur neck, ward's triangle, trochanter and spine (L2-4) and we compared the result with that of 163 normal-cycle control women with age matched. Bone mineral densities was significantly low in patients with primary hypothalamic amenorrhea and premature ovarian failure at all four sites. In those with hyperprolactinemia a decrease in bone mineral density was noted at femur neck and spine while those with Sheehan's syndrome is associated with decreased bone density at femur neck, ward's triangle and trochanter. The degree of bone loss and the affected sites seems differ depending on the type of amenorrhea. In patients with primary hypothalamic amenorrhea, significant bone loss was already noted at all four sites by age 20. The decrement in bone density continued rapidly during the early twenties up to age 25 and then slowed after age 25. In those with premature ovarian failure with secondary amenorrhea there were no decrease in bone mineral density within the first year after onset of amenorrhea, however, in the subsequent 2 years, the reduction in BMD was rapid and thereafter the reduction slowed remarkably. The BMD in this study positively correlated with the body mass index and negatively with the phosphorus intake.
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PMID:Bone mineral density in premenopausal anovulatory women. 859 Nov 16

To examine the impact of amenorrhea on bone mineral density in women of reproductive age, bone mineral density in the lumbar spine (L2-L4) was measured by Dual-energy X-ray absorptiometry in 43 amenorrheal women. There was a significant lower bone mineral density in this test group (0.917 +/- 0.121 g/cm2) than in a normally menstruating control group (1.032 +/- 0.095 g/cm2). In premature ovarian failure, we found lower bone mineral density (0.863 +/- 0.112 g/cm2) than in any other subclass. Seven women with premature ovarian failure received cyclic hormone replacement therapy for 12 months (day 1-28, 0.625 mg conjugated estrogen, and on days 14-28, 5 mg medroxyprogesterone, followed by a seven-day pause). After 12 months, bone mineral density had increased significantly (p < 0.05) compared to the initial bone mineral density. We conclude that amenorrhea is a cause of bone loss in young women and that estrogen therapy is effective in preventing bone loss.
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PMID:[Decreased bone mineral density in premenopausal women with amenorrhea]. 884 Oct 45

Premature ovarian failure is classically defined as menopause occurring before age 40 and is associated with elevated serum FSH levels. If elevated FSH levels indicate lack of ovarian feedback and depletion of primordial follicles, women with prematurely elevated FSH levels should have infertility. However, there are many reports of pregnancies in affected women occurring during estrogen therapy leading to the hypothesis that estrogen may have a salutary effect on folliculogenesis and conception. This randomized, controlled trial was designed to investigate whether estrogen replacement therapy offered a significant therapeutic benefit in hypergonadotropic amenorrhea and to evaluate the potential pathophysiologic mechanisms that would explain the reported pregnancies. Thirty seven women, aged 16 to 40, with menstrual dysfunction and documented FSH levels elevated above the 95% confidence limits of the mid-cycle gonadotropin peak of the normal menstrual cycle (> 40 IU/L 2nd IRP hMG in our RIA) on at least two occasions, entered the study. The average duration of their amenorrhea was 15.9 months (range 2-96 months). Subjects were randomized to begin estradiol replacement (micronized estradiol [Estrace TM], 2 mg orally each day) or no therapy for 6 weeks in a 12-week, cross-over design with weekly monitoring by both pelvic ultrasonography and serum hormone levels. Thirty-one women completed the entire randomized study. As expected, estradiol therapy increased mean serum estradiol levels by 98 pg/mL and was associated with a significant decrease in mean LH and FSH levels (LH: 45.4 IU/L 2nd IRP hMG vs. 37.1 IU/L, FSH: 63.4 IU/L vs. 40.6 IU/L, geometric means). However, there was no effect of estradiol replacement on mean ovarian volume, the number or size of new follicles, or the ovulation rate in all subjects or in the subset with no identified cause for their hypergonadotropic hypogonadism (n = 20). Two pregnancies occurred during the randomized trial, one on and one off estradiol. In both arms of the study, the majority of subjects developed cystic ovarian structures by ultrasound that were temporally associated with increasing serum estradiol levels, indicating functional ovarian follicles. Seventy-eight percent of all subjects grew at least one new follicle over 10 mm in diameter and 46% ovulated at least once, as determined by a serum progesterone level more than 4 ng/mL. Although ovulations were significantly more common in the 10 women subjects who had less than 3 months of amenorrhea (all of whom ovulated) than in the 27 with greater than 3 months of amenorrhea (only 7 of whom ovulated (26%), P < 0.001), there was no significant difference in eventual pregnancies (2 of the 10 women with less than 3 months of amenorrhea vs. 3 of the 27 with greater than 3 months of amenorrhea, P = 0.47). We conclude that in hypergonadotropic women with amenorrhea: 1) folliculogenesis occurs often but is less frequently followed by ovulation and rarely by pregnancy, suggesting that elevated FSH is a marker of oocyte dysfunction occurring distinct from and earlier than granulosa cell or follicular dysfunction; and 2) estrogen therapy does not improve the rate of folliculogenesis or ovulation.
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PMID:A randomized, controlled trial of estradiol replacement therapy in women with hypergonadotropic amenorrhea. 885 11

Spinal bone density of 41 girls with diet-induced amenorrhea (DA) was compared with that of the density of 22 subjects with premature ovarian failure (POF) of comparable age. The Z score values, as well as the estradiol levels, were not significantly different in the two groups. The duration of amenorrhea was significantly correlated to bone mass density in the DA population, especially when considering subjects with amenorrhea that had lasted longer than 20 months. A similar correlation between weight loss and BMD was evident. Although estradiol concentrations did not seem to be correlated to the Z score, FT3 and cortisol values exhibited, respectively, a negative and a positive correlation with spinal density. Cortisol seemed to act precociously, whereas FT3 acted later than cortisol.
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PMID:Bone mineral metabolism in diet-induced amenorrhea. 923 75

Autoimmunity may be involved in idiopathic premature ovarian failure (POF). However, the frequency, physiopathology and potential reversibility of autoimmune oophoritis needs clarification. Using an ELISA against whole tissue homogenate as antigen, from human ovaries at different ages, positive circulating ovarian antibodies (AOA) were found in 59% of patients with primitive idiopathic POF (27/46); 20/27 were positive for IgG isotype, 9/27 for IgM and 8/27 for IgA. Specificity of AOA was examined (i) by comparison to different control groups; mean values of the three subclasses of immunoglobins were significantly higher in POF women than in normally cycling fertile young women (n = 23) and fertile young men (n = 17), in untreated Grave's disease (n = 35) or in women with positive antinuclear factor (n = 25); and (ii) by assessing possible cross-reaction; only six out of the 27 positive sera reacted with other tissues (thyroid, pancreas, adrenal), including four clinical polyendocrinopathies. Significance of AOA was explored (i) by comparison with postmenopausal women (n = 40) and older women (n = 15), who did not have enhanced ratios of AOA, thereby excluding a potential role of high FSH values; (ii) by analysing the factors time and surgery; no relation could be found either with the duration of amenorrhoea (6 months to 21 years) or with the history of an ovarian biopsy (12/47) in the absence of any associated pelvic surgery; and (iii) by screening for other immunological factors; familial or personal autoimmune disease (8/46), HLA DR3 (10/42), HLA DR4 (11/42), associated autoantibodies (thyroperoxidase, adrenal, beta islets, parathyroid, DNA, smooth muscles) (12/42). If one positive AOA isotype was present, a second immunological factor was found in 45% of cases. Spontaneous pregnancies during oestrogen therapy occurred in four cases, including three women with positive AOA. Circulating AOA detected by an ELISA may represent a practical and suitable marker for diagnosis of POF. Its use for prognosis and rational treatment needs further evaluation.
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PMID:Prevalence, specificity and significance of ovarian antibodies during spontaneous premature ovarian failure. 945 25

In 1% of women, premature ovarian failure develops by 40 years of age, a condition causing amenorrhea, infertility, sex steroid deficiency, and elevated gonadotropins. Early loss of ovarian function has significant psychosocial sequelae and major health implications. These young women have a nearly two-fold age-specific increase in mortality rate. Among women with spontaneous premature ovarian failure who have a normal karyotype, half have ovarian follicles remaining in the ovary that function intermittently. Indeed, pregnancies have occurred after the diagnosis of premature ovarian failure. Thus, premature ovarian failure should not be considered as a premature menopause. Young women with this disorder have a 5% to 10% chance for spontaneous pregnancy. Attempts at ovulation induction using various regimens fail to induce ovulation rates greater than those seen in untreated patients; however, oocyte donation for women desiring fertility is an option. Young women with premature ovarian failure need a thorough assessment, sex steroid replacement, and long-term surveillance to monitor therapy. Estrogen-progestin replacement therapy should be instituted as soon as the diagnosis is made. Androgen replacement should also be considered for women with low libido, persistent fatigue, and poor well-being despite taking adequate estrogen replacement. Women with premature ovarian failure should be followed up for the presence of associated autoimmune endocrine disorders such as hypothyroidism, adrenal insufficiency, and diabetes mellitus.
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PMID:Premature ovarian failure. 992 18

A cDNA was cloned from human testis cDNA library by the use of rat FSH receptor cDNA as a probe. Transformation of 293 cells with the cloned cDNA led to expression of specific human FSH binding sites with high affinity (Kd: 1.5 x 10(-9) M), ligand dose-dependent production of cAMP and promotion of phosphatidyl inositol turnover, indicating that the cloned cDNA must encode a human FSH receptor. Northern blot analysis using human ovarian tissues revealed a high expression of mRNA at the stage of early follicular phase, but not luteal phase. Cross-linking of ligand with the expressed human FSH receptor showed that the molecular mass of the receptor should be 76 kDa, consistent with the estimated size of deduced amino acid sequence from the cloned cDNA. A polymorphism was found at 680th amino acid Ser or Asn, in the C-terminal region of the receptor although the influence of this difference upon the receptor function was not determined obviously in this study yet. The incidence of the polymorphism in the C-terminal region was not significantly correlated to the reproductive failures in 70 female cases of endometriosis, hyperprolactinemia, amenorrhea, PCOD or POF. However, elucidation of the structure and function in human FSH receptor using the cDNA will be applicable to diagnosis of some clinical cases associated with abnormal FSH receptor gene in the future.
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PMID:[cDNA cloning of human testicular follicle-stimulating hormone receptor and analysis of its in vitro function]. 1003 19

We examined the prevalence of anti-nuclear antibodies (ANA) in 32 consecutive patients with premature ovarian failure with and without chromosomal abnormalities. Blood samples were taken for karyotype determination as well as detection of autoantibodies, X-terminal microdeletions and spontaneous follicular growth. The correlation between ANA positivity and the age at onset of amenorrhoea, as well as the presence of karyotype abnormalities, X-terminal microdeletions and follicular growth was determined. Ten of the 24 patients with normal karyotype and none of the 8 patients with karyotype abnormalities were ANA positive. ANA were found more frequently in patients with premature ovarian failure with normal karyotypes than in control amenorrhoeic patients (42 versus 6, P < 0.01). ANA were found in 77% (10/13) of premature ovarian failure patients with normal karyotypes who developed amenorrhoea at or under the age of 30 years, but not in the patients who developed amenorrhoea later in life. Follicular growth was evident in 50% (5/10) of karyotypically normal patients with ANA, 71% (10/14) of karyotypically normal patients without ANA and 38% (3/8) of patients with karyotype abnormalities. X-terminal microdeletions were not found in any of the patients studied. These results suggest that patients with premature ovarian failure and ANA are an aetiologically and clinically distinct group.
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PMID:Anti-nuclear antibodies in patients with premature ovarian failure. 1037 97

Pregnancy in patients with hypergonadotropic amenorrhea, although previously reported, remains quite rare. Women may conceive spontaneously or following different regimens of ovulation induction, thus indicating that ovarian failure is not always permanent. The case of an 18-year-old woman with premature ovarian failure, who conceived during hormone-replacement therapy, is reported. During hormone-replacement therapy, elevated gonadotropin levels returned to the physiologically normal range. It is suggested that this restored the receptors to luteinizing hormone and to follicle-stimulating hormone, which might have been downregulated. This hypothesis is supported by previous results from clinical trials and experimental work on a rat model.
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PMID:Unexpected pregnancy during hormone-replacement therapy in a woman with elevated follicle-stimulating hormone levels and amenorrhea. 1039 52


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