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)

Premature ovarian failure is defined as amenorrhea with hypo-oestrogenism and elevated gonadotrophins occurring before the age of 40 years. In theory, ovarian failure may occur because of a decreased pool of primordial follicles, because ovarian apoptosis is increased or accelerated or because the follicle maturation is interrupted before the preovulatory stage. The mechanisms inducing premature ovarian failure have been described in a few number of cases. Atm or c-kit gene mutations induce a very low pool of primordial follicles. In chromosome X abnormalities, chemotherapy, galactosemia and blepharophimosis syndrome apoptosis is increased. Follicle maturation is interrupted in FSH and LH receptor mutations or in autoimmunity. However, in most cases, the etiology remains idiopathic. A better knowledge in genes involved in ovarian apoptosis should enhance our understanding of premature ovarian failure. Meanwhile, the best treatment is to give hormonal replacement therapy and send the patient to oocyte donation program when they desire to be pregnant.
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PMID:[Premature ovarian insufficiency]. 1048 61

The effect of hormone replacement therapy on the bone mineral content of hypoestrogenic subjects depends on the pathogenesis of the disease as well as on the dosage and route of administration. This is particularly true in hypoestrogenism related to eating disorders. We present a longitudinal study of 26 young women with diet-induced amenorrhea compared with a group of subjects with POF. The study protocol included the quantification of weight loss, the endocrine profile (follicle-stimulating hormone, luteinizing hormone, prolactin, E2, FT3, FT4, thyroid-stimulating hormone, and cortisol), the evaluation of markers of bone turnover (GLA, OSTK-PR, ALP, OHP, and DPYR), and spinal bone density by DEXA at observation and after weight recovery. No hormone replacement therapy was administered. Mean BMD and Z scores before and after recovery do not differ significantly; OHP and DPYR appear significantly higher during basal evaluation, whereas GLA and ALP do not. Data on the impact of oral contraceptive use on bone mineral density are controversial. We particularly discuss the question of long-term treatment with 20 micrograms ethinyl estradiol pills on peak bone mass acquisition during adolescence.
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PMID:Estrogen replacement therapy in the management of osteopenia related to eating disorders. 1081 31

Premature ovarian failure is characterized by secondary oligomenorrhoea or amenorrhoea and serum follicle stimulating hormone (FSH) levels above 40 IU/l before or at the age of 40. The incidence is 1:1000 below age 30 and 1:100 below age 40. In the majority of cases a cause can not be identified. The chance to conceive spontaneously after premature ovarian failure is estimated at 5-10%. There is no treatment available to restore ovarian function and increase the pregnancy rate. In vitro fertilisation using oocyte donation is the only successful fertility treatment option. Climacteric symptoms can be treated with hormone replacement therapy. In the absence of symptoms and when bone mineral density is normal there is no need for hormone replacement therapy. In the near future cryopreservation of ovarian tissue will offer some hope to women at risk to develop premature ovarian failure, e.g. women from families with familial premature ovarian failure and women scheduled to undergo chemotherapy or radiotherapy at a young age.
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PMID:[Premature ovarian failure]. 1108 87

Issues of long-term toxicity from treatment for breast cancer, including the induction of premature ovarian failure, appear to be of increasing importance for breast cancer survivors. The incidence of treatment-related amenorrhea is related to patient age and to the treatment regimen. Whereas the induction of ovarian failure may be advantageous with respect to breast cancer outcome, it is not clear that there is any advantage to permanent menopause over reversible hormonal manipulations. In addition, menopause may be associated with a variety of adverse health effects. Although nonhormonal therapies are available to manage many of the consequences of menopause, avoidance of chemotherapy-related ovarian toxicity may provide the best prospects for fertility after treatment. Pregnancy after breast cancer is a realistic consideration for some breast cancer survivors and is not clearly detrimental to either the mother or her offspring.
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PMID:Fertility and the impact of systemic therapy on hormonal status following treatment for breast cancer. 1112 97

Objective of this case-control study was to investigate the potential risk factors for premature ovarian failure (POF). Seventy-three patients with secondary hypergonadotropic amenorrhea and, as control group, 144 women with acute, non-gynecological, non-neoplastic, non-hormone-related diseases were included in the study. Information was obtained on sociodemographic characteristics, gynecological and obstetric data, general lifestile habits, smoking habits and history of selected gynecological and other clinical conditions. A statistically significant association between high education level and POF was found (p = 0.03). Parity was related to a reduced risk of POF and this reduction increased with the number of live births (p = 0.02). No association emerged between POF risk and age at menarche, cycle length and oral contraceptive use. Women with POF could not be distinguished from control women by behavioral and reproductive history, except for lower fertility. The minor influence that reproductive and lifestyle factors have on the occurrence of POF suggests that genetic inheritance plays a more important role.
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PMID:Case-control study on risk factors for premature ovarian failure. 1115 Aug 74

The objective of this study was to evaluate the psychological side effects of a transvaginal natural progesterone gel in hormone replacement therapy (HRT). This 3-month preliminary study was part of a multicenter study previously performed in our center. We enrolled 49 women (ages 18-45 years) with hypothalamic amenorrhea (HA) (n = 40) and premature ovarian failure (POF) (n = 9). Estrogenized patients applied vaginal progesterone gel (4% or 8%) every other day for six doses per month. The Hopkins Symptom Checklist (HSCL), a psychometric profile test, was administered at baseline, day 13 of cycle 2, day 24 of cycle 2, and day 24 of cycle 3. Application of the progesterone gel caused no significant change in HSCL total scores or individual symptom scores for somatization, obsession-compulsion, interpersonal sensitivity, depression, and anxiety. Natural vaginal progesterone gel can be an effective alternative to oral progesterone for women on HRT.
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PMID:Natural vaginal progesterone is associated with minimal psychological side effects: a preliminary study. 1178 9

Inactivating mutations of the FSH receptor (FSHR) are known to cause ovarian failure with amenorrhea and infertility in women. The first mutation identified in the FSHR gene was a missense mutation (566C-->T, predicting Ala189Val transition) found in several Finnish patients with primary amenorrhea due to ovarian failure. Only five additional, partially or totally inactivating, mutations of the FSHR have been reported. Here, we report a novel FSHR mutation, 1255G-->A, in a Finnish female with primary amenorrhea. The patient was a compound heterozygote for two mutations in the FSHR gene: 566C-->T, the Finnish founder mutation, and 1255G-->A, a previously unidentified mutation. The new mutation is located in exon 10 in the second transmembrane stretch of the FSHR, and it predicts an Ala419Thr change in the protein structure. In functional testing, the mutation was shown to have minimal effect on ligand binding capacity and affinity, but it almost totally abolished the cAMP second messenger response. Neither of the two FSHR mutations (566C-->T or1255G-->A) was identified in 40 other Finnish patients with premature ovarian failure. Based on this and previous studies, FSHR mutations remain a rare cause of ovarian failure.
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PMID:A Novel mutation in the FSH receptor inhibiting signal transduction and causing primary ovarian failure. 1188 79

Premature ovarian failure is defined by the association of amenorrhea, elevated levels of serum gonadotropins and hypoestrogenism occuring before the age of forty. In a growing number of these cases, genetic disorders have been shown to be involved. Cytogenetic abnormalities predominantly concern the X chromosome, including Turner syndrome, but also rearrangements such as deletions and X-autosome translocations. Molecular investigation of these abnormalities has led to the identification of a number of candidate genes most of them still having unknown functions. Testing for premutation of the FMR1 gene, whose full mutation determines the fragile X syndrome, is particularly worthwhile in these patients because of its high frequency, not only among the patients with ovarian failure but also in the general population. Other, much less frequent mutations have been located for example in the gonadotropin and gonadotropin receptor genes and their study contributes to the understanding of ovarian physiology. Here we review most of the etiologies which have to be taken in account in the genetic screening of premature ovarian failure patients.
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PMID:[The genetic basis of premature ovarian failure]. 1205 37

Of 410 cases of spontaneous or induced abortion in the first or second trimester that were followed up, 95 were infertile. 18 of these had amenorrhea and 12 had oligomenorrhea. Amenorrhea and oligorrhea were more prevalent among the women who were over 31. Amenorrhea, oligomenorrhea, and infertility were more frequent after spontaneous than after induced abortion. Asymptomatic tubal block resulting from reflux of blood from the uterus into the fallopian tube after spontaneous abortion could have been responsible in a number of other cases. Definite causal link with abortion could not be established in any of the other cases of infertility without amenorrhea or oligorrhea. Amenorrhea following abortion was most often due to an endocrinal or mechanical defect (often uterine synechiae). Partial pituitary necrosis, premature ovarian failure, and endometrial tuberculosis were other postabortal causes of amenorrhea and oligomenorrhea.
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PMID:Infertility and amenorrhoea following abortions. 1225 18

Persistent amenorrhea, an uncommon sequela of oral contraceptive (OC) use, would not be a major problem except for the fact that an estimated 50 million women worldwide use OCs. Following OC use, women often experience some delay in resuming normal menses, but according to most studies, fewer than 1% fail to begin menstruating regularly within 6 months. In about 1/2 of this small percentage of women, failure to resume normal menses within 6 months is caused by an identifiable underlying disorder. The remaining 1/2 are considered to have "postpill amenorrhea," the result of a disruption of the normal hypothalamic-pituitary-ovarian feeding mechanism, which may be reversible with appropriate treatment. In evaluating patients with postpill amenorrhea, it is important to rule out premature ovarian failure, polycystic ovary syndrome, weight loss, and hyperprolactinemia before arriving at a diagnosis of idiopathic postpill amenorrhea. Prior to 6 months, detailed laboratory evaluation is not indicated, but after 6 months of amenorrhea, the history and physical status should again be carefully evaluated. Any history of weight change, galactorrhea, hirsutism, headaches, or "hot flashes" should be noted. On examination, evidence of hirsutism, virilization, expressible galactorrhea, or ovarian enlargement should be sought. The presence of any of these findings warrants laboratory testing. Pregnancy should always be excluded before further testing. If the patient shows no clinical evidence of premature ovarian failure, polycystic ovaries, anorexia nervosa, or hyperprolactinemia, or if laboratory evaluation fails to confirm clinical suspicions, it is appropriate to wait another 6 months before further evaluation. These disorders may be differentiated from idiopathic postpill amenorrhea by measuring serum levels of gonadotropins, estradiol, testosterone, and prolactin and by sella polytomography. It is important to define whether the treatment objective is resumption of a normal menstrual pattern or restoration of fertility, or both, for therapy will differ depending upon the objective. Ovulation can be induced with clomiphene or bromocriptine in 50-75% of women. Rarely, human menopausal gonadotropin and human chorionic gonadotropin may be needed. If fertility is not an issue, cyclic estrogen and progesterone may be useful to maintain adequate estrogen effects but will obviously continue to suppress the hypothalamic-pituitary-ovarian axis.
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PMID:Management of post-pill amenorrhea. 1227 95


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