Cases reported "Amenorrhea"

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1/7. Premature ovarian failure in the early age 20s: 3 case reports.

    Premature ovarian failure in the early age 20s is a very rare phenomenon. In a woman presenting with amenorrhea and symptoms of hypoestrogenism, the confirmatory diagnosis of premature ovarian failure relies upon the finding of postmenopausal level of the follicle-stimulating hormone (FSH > 40 mIU/ml). Three women at the age of 25, 30 and 32 years presented with 5, 6 and 10 years secondary amenorrhea, respectively. They used to have regular menses, and two of them gave birth to a healthy baby(ies). Although the etiology remains enigmatic, their gonadotropin and estradiol serum values were found to be in the postmenopausal range. serum FSH values in the three cases were 135.4, 41.9 and 86.5 mlU/ml. Both combined oral contraceptive pills and progesterone challenge test were administered but couldn't bring about recommencement of menstrual flow. These three women who were diagnosed as a case of premature ovarian failure, evidenced by long standing secondary amenorrhea, secondary infertility, signs and symptoms of postmenopause and biochemical evidences of hypergonadotropic hypoestrogenism, were put on continuous combined oral contraceptive pills and felt better. literature on the potential serious complications of premature menopause and treatment options in low setting areas is revised.
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2/7. Secondary amenorrhoea due to autoimmune ovarian failure.

    A case of spontaneous premature menopause due to autoimmune ovarian failure is described. This report emphasises that this uncommon condition is important to diagnose because of its association with other autoimmune endocrine disorders including Addison's disease. In addition, in the present case, the marked increase in luteinizing hormone with relatively normal follicle stimulating hormone raises the possibility of a non-steroidal inhibitory feedback of follicle stimulating hormone.
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3/7. The phenotypic effects of small, distal Xq deletions.

    The effects of small, distal Xq deletions (Xq26   qter) have been reviewed in light of three cases of our own and five from the literature. The symptoms caused by such deletions range from apparently none through irregular menstruation to secondary amenorrhea (or premature menopause) to primary amenorrhea. That the abnormal chromosome has any effects when it is inactivated may best be explained by one or by a combination of the following hypotheses. (1) the Xq-chromosome might exert an effect during development when cells in which it is active compete with cells in which it is inactivated, assuming that the inactivation of the two X chromosomes is originally random. (2) a more probable hypothesis is that there is a position effect when a break has occurred in the critical region Xq13   q27 which apparently must be intact in both X chromosomes to allow normal development of the ovaries. (3) this position effect might, in turn, affect the oocytes (and thus the ovary) after the inactive x chromosome is reactivated before meiosis or the deletion as such might have a direct effect on the ovaries.
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4/7. The role of follicle-stimulating hormone in the depletion of follicular reserve: menopause in a woman with hypogonadotropic hypoestrogenic amenorrhea: a case report.

    OBJECTIVE: To investigate the role of FSH in the depletion of follicular reserve in a human being. DESIGN: Prospective evaluation of a very rare case. SETTING: Academic research environment. PATIENT: A 43-year-old woman with primary hypogonadotropic hypoestrogenic amenorrhea, with very low levels of plasma FSH throughout her life. INTERVENTIONS: Pulsatile GnRH was administered IV at the dose of 4 micrograms every 90 minutes for 20 days. blood samples were collected every 3 to 4 days. MAIN OUTCOME MEASURES: plasma levels of E2, FSH, and LH. RESULTS: During the 20 days of treatment there was no increase in E2 plasma levels. On the contrary, FSH and LH levels began to rise after 3 days and reached postmenopausal levels within 20 days. CONCLUSIONS: Depletion of follicular reserve may occur also when the levels of FSH are very low throughout a woman's life. Thus FSH seems only able to rescue follicles from atresia without interfering with the onset of menopause.
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5/7. Reversal of amenorrhoea after Mectizan treatment.

    Plausible reversal of secondary amenorrhoea in three women infected with onchocerciasis after Mectizan treatment in Imo State, nigeria, is presented. The women aged 30, 28, and 32 years with drastic reduction in mean microfilaria scores had reversed amenorrhoea 8, 13 and 10 days post Mectizan treatment, respectively. They had typical manifestation of onchocerciasis including nodules, pruritic rash, body itching and musculo-skeletal pains. The manifestations eased off 4 days post treatment. The plausible link between loss of fertility due to premature menopause in women and onchocerciasis is discussed.
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6/7. Spontaneous pregnancy after 13 years of amenorrhea in a patient with a voluminous ovarian dysgerminoma and submitted to left adnexectomy and radiotherapy.

    The authors illustrate the case of a 17-year-old patient who was submitted to left adnexectomy in view of an ovarian dysgerminoma 24 cm in diameter and weighing 2,800 g. She was subsequently submitted to two cycles of radiotherapy. Following a period of amenorrhea lasting 13 years and characterized by high serum levels of gonadotropins, the patient had a spontaneous pregnancy and at 33 weeks of gestation delivered a live and vital fetus. Therefore the occurrence of post-radiotherapy amenorrhea, characterized by high serum gonadotropin levels, should not always be considered pathognomonic of precocious menopause. The possibility that radiotherapy causes only a temporary alteration in ovarian activity should also be taken into consideration.
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7/7. A familial case of X chromosome deletion ascertained by cytogenetic screening of women with premature ovarian failure.

    The association between x chromosome deletions and premature ovarian failure is well established. Previous anecdotal reports however, have not documented the prevalence of X deletions in women with premature ovarian failure. We therefore performed cytogenetic analyses on 79 women with primary or secondary amenorrhoea to assess the utility of screening for a genetic marker for familial premature ovarian failure. A normal karyotype was found in 77 women. One woman with primary amenorrhoea had an XY karyotype and a woman with secondary amenorrhoea had a deletion at Xq 26.1. This second case had a family history of premature ovarian failure, and her mother who underwent premature ovarian failure at 28 years shared this deletion. The early diagnosis of familial X deletions causing premature ovarian failure allowed for the prediction of impending menopause and the implementation of manoeuvres to advance conception. Although cytogenetic aberrations are rare in secondary amenorrhoea, the ability to predict premature ovarian failure can be vital.
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