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Gonadal function was evaluated in 64 persons homozygous for the HLA-linked hemochromatosis allele. Of 41 men, 10 had reduced libido or impotence and 6 had testicular atrophy. Before treatment, 5 men had below normal testosterone concentrations, 4 of whom also had low gonadotrophin levels. Four hypogonadal men were reevaluated after iron depletion treatment. In 2, 1 with primary and another with secondary hypogonadism, testosterone levels returned to normal after phlebotomy and were accompanied by a return of normal sexual function. None of 23 women with hemochromatosis had loss of libido or had a natural menopause before age 45. Our findings indicate that in some men with hereditary hemochromatosis and hypogonadism of either testicular or central origin, sexual function and sex hormone concentrations can be restored to normal after iron depletion therapy.
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The present trends in the utilization of hormones in the treatment of sterility are reviewed, special reference being made to the utilization of gonadotrophins, hypothalamic hormones and gonadal hormones as well as other substances (clomiphene, epimestrol, cyclophenyl) that are also utilized in this type of treatments.
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The interaction of 14 steroidal and nonsteroidal estrogen agonists and antagonists with the intracellular estrogen receptor system was examined in cell suspensions prepared from the testes of mice that develop malignant Leydig cell tumors after prolonged estrogen administration. The ability of these substances to stimulate DNA synthesis in short-term (3-day) studies and to provoke Leydig cell hyperplasia with prolonged (3-mo) administration was also measured. Our data were consistent with the proposal that, in Leydig cells, the carcinogenic effects of estrogens are mediated through the intracellular receptor complex that results in a localization of hormone bound to chromatin and nuclear matrix. All tested compounds displaced 17 beta-[3H]estradiol from the cytosolic estrogen receptor, but to varying degrees; and there was no discernible relationship between their ability to compete for this receptor and their efficacy in stimulating DNA synthesis. The effect of the test compounds on the levels of estrogen receptor in cytosol and in nuclei was measured by [3H]estradiol exchange. 17 beta-Estradiol, equilin, 17 alpha-ethinylestradiol, diethylstilbestrol, hexestrol, dienestrol, coumestrol, and nafoxidine provoked a complete estrogen receptor response: acutely a decrease in the level of cytosolic estrogen receptor and an increase in the nuclear estrogen receptor. All of these substances acutely stimulated DNA synthesis. Tamoxifen, clomiphene, and nitromifene provoked a decrease in cytosolic receptor but no increase in demonstrable nuclear estrogen receptor. 17 alpha-Estradiol, mestranol, and estriol did not significantly alter the levels of estrogen receptor in cytosol or nuclei. Only those substances that increased measurable nuclear estrogen receptor also acutely stimulated DNA synthesis. Chronic (3-mo) treatment of 2-mo-old male BALB/c mice with diethylstilbestrol, 17 beta-estradiol, ethinylestradiol, and nafoxidine led to Leydig cell hyperplasia. Chronic mestranol treatment also provoked Leydig cell hyperplasia; this is most probably due to induction of liver metabolism of mestranol to ethinylestradiol. Chronic treatment with 17 alpha-estradiol, tamoxifen, and clomiphene failed to produce significant histologic al changes in the testes. Only chronic administration of those substances that exhibited a complete estrogen receptor response and acutely stimulated DNA synthesis produced Leydig cell hyperplasia.
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Meta-analysis of all randomised trials published so far, was performed to compare the effect of additional gonadotropin releasing hormone (GnRH)-agonist treatment to exogenous gonadotropins for ovulation induction in clomiphene-resistant polycystic ovary syndrome (PCOS) patients. Five clinical studies were included, of which only one showed significant differences in pregnancy rate. In addition, pretreatment with GnRH-agonist was once reported to lead more often to cancellation of medication. Combining the results of all five trials, a significant difference in favour of additional GnRH-agonist administration could only be observed for pregnancy rate. No significant differences in ovulation rate could be found. Due to the relative small number of patients in each separate group, no conclusions could be drawn concerning the influence of GnRH-agonist treatment on gonadotropin doses necessary to induce ovulation, and the incidence of multiple pregnancy, abortion and ovarian hyperstimulation.
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Race affects timely access to infertility care, diagnosis, and treatment cycle characteristics but not outcomes. Considering the nation's growing multiracial population, understanding the effect of race on fertility care becomes increasingly important.
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To evaluate the pregnancy rate (PR) of unstimulated intrauterine insemination (IUI).
Retrospective cohort study.
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In total, 30 non-obese PCOS women with clomiphene citrate (CC) resistance from the Medical College's Reproductive Health Center were enrolled and randomly assigned to be treated with placebo (Group 1) or metformin (850 mg) (Group 2) twice daily for 3 months as the pre-treatment. Then, metformin alone was administered with CC, human menopausal gonadotropin (HMG) and human chorionic gonadotropin (HCG) to induce ovulation for 3 months in Group 1. In Group 2, CC/HMG/HCG was used to induce ovulation for 3 months without metformin. Follicle-stimulating hormone, luteinizing hormone, estradiol and TT levels before and after ovulation in pregnant cycles and non-pregnant cycles were evaluated over the course of treatment.
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In ovariectomized rats, treatment with CC is seen as effective as estrogen treatment in preventing osteoporosis, without causing uterin hyperstimulation. Nevertheless, further investigations on more rats are needed to assess whether it is an alternative treatment method to estrogen.
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The results are presented of clomiphene treatment of 22 patients with functional lactorrhea-amenorrhea. Lower therapeutic effect of this drug in comparison with that of parlodel was demonstrated in hyperprolactinemia. Combined clomiphene-parlodel treatment of lactorrhea-amenorrhea was studied in 12 patients, including 4 subjects with hypophyseal adenomas. It was shown that the combined use of these drugs enhances therapeutic activity without potentiating side effects.
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Polyspermy is a potential complication of attempts at in vitro fertilization. Nine polyspermic oocytes were identified among 169 oocytes obtained from 67 cycles stimulated by human menopausal gonadotropin. Cleavage to the 2-, 3-, and 4-cell stage was observed. Four polyspermic oocytes were identified among 85 oocytes obtained from 47 cycles stimulated by clomiphene citrate. Cleavage was not observed. Careful dispersion of cumulus cells at 15 to 18 hours and examination of the oocytes for polyspermy is essential, because the condition may not be apparent at 40 hours from insemination, when normal-appearing cleavage stages may be observed.
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Male fertility clinic.
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The effects of clomiphene on the pituitary response to LRF in eugonadal men were studied to investigate the role of estradiol in the feedback modulation of gonadotropin secretion in men. 150 mcg LRF was given to 6 healthy men (20-28 years) and luteinizing hormone (LH) and follicle stimulating hormone (FSH) evaluated. A 5-day course of clomiphene (100 mg daily) was then given and the LRF test repeated. Serum FSH, LH, estradiol, and testosterone (T) were determined. Clomiphene caused a significant elevation in the basal levels of LH, FSH, Estradiol, and T. Pituitary release of LH and FSH in response to LRF was markedly reduced by clomiphene treatment indicating that estradiol provides feedback regulation of gonadotropin output by the pituitary.
Women were randomized to receive either 1 mg anastrozole or 100 mg clomiphene citrate for 5 days (cycle days 3-7) followed by FSH injections (days 7-11) for ovulation induction. A subset participated in a crossover arm of the study.
After randomization, six women conceived before starting treatment and another patient postponed treatment. The remaining 65 women received the treatment (33 underwent LOD and 32 received CC). After the primary treatment, more pregnancies (44%) occurred in women receiving CC than in those undergoing LOD (27%), although the difference did not reach statistical significance [P = 0.13, OR 2.1 (0.7 - 5.8)]. After adding the second treatment, the pregnancy rate was still higher, but to a less extent, in the CC group [63% versus 52%, P = 0.2, OR 1.6 (0.6 - 4.2)].
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Laboratory research setting.
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Metformin is not always beneficial when given to clomiphene resistant infertile women with PCOS in clinical practice.
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Six trials met the inclusion criteria. There were three trials of oral, and three of transdermal clonidine. Some form of behavioural counselling was offered to all participants in five of the six trials. There was a statistically significant effect of clonidine in one of these trials. The pooled odds ratio for success with clonidine vs placebo was 1.89 (95% confidence interval 1.30 to 2.74). There was a high incidence of dose-dependent side-effects, particularly dry mouth and sedation.
Tertiary fertility and IVF center.
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The search strategy to identify RCTs consisted of (1) the Group's Specialised Register of Controlled Trials using the search strategy developed for the Menstrual Disorders and Subfertility Group as a whole (see the Review Group details for more information), (2) additional specific electronic Medline searches and (3) bibliographies of identified studies and narrative reviews.
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Endometrial morphology and ultrastructure are studied in 17 spontaneous, 23 stimulated, and 18 artificial cycles in cases of primary ovarian failure. Normal light-microscopic aspect was found, but impaired development of nucleolar channel system and stronger intercellular junction have been observed by electron-microscopic studies in stimulated cycles with relative excess of luteal estrogen. Normal glandular maturation can be obtained in patients with premature menopause, given adequate steroid replacement, but an abnormally dense fibrocytic aspect of the stroma is characteristic of the first treatment cycles.
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(1) P:E2 ratios at the time of implantation were similar after CC with or without hCG and hMG and hCG treatment; (2) high luteal P:E2 ratio was associated with ongoing pregnancies; and (3) lower P:E2 ratio was seen in cycles leading to spontaneous abortion.
All patients received oral CC. In 362 of the cycles, a single dose of gonadotropin was administered on cycle day 9 (MinStim). A transvaginal ultrasound was performed on cycle day 10, 11, or 12.
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The mechanism of hypogonadism was studied in a 63-year-old man with idiopathic hemochromatosis. Basal levels of thyroid, prolactin, cortisol, and growth hormones were normal and responded normally to appropriate provocative stimuli. Basal testosterone and gonadotropin levels were low. There was inadequate gonadotropin response to luteinizing hormone-releasing hormone and clomiphene citrate stimulation. Testosterone response to human chorionic gonadotropin was normal. Hypothalamic-pituitary dysfunction resulting in impaired gonadotropin secretion appears to be the cause of hypogonadism in hemochromatosis.
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University research laboratory.
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Clomiphene at concentrations between 10 and 75 microM increased [Ca2+]i in a concentration-dependent manner and the signal saturated at 50 microM. The [Ca2+]i signal was biphasic with an initial rise and a slow decay. Ca2+ removal inhibited the Ca2+ signal by about 40-50% in maximum [Ca2+]i. Adding 3 mM Ca2+ increased [Ca2+]i in cells pretreated with 50 microM clomiphene in Ca2+-free medium, suggesting that clomiphene induced capacitative Ca2+ entry. In Ca2+-free medium, pretreatment with 50 microM brefeldin A (to disrupt the Golgi complex Ca2+ store), 1 microM thapsigargin (to inhibit the endoplasmic reticulum Ca2+ pump), and CCCP (to uncouple mitochondria) inhibited 85% of clomiphene-induced intracellular Ca2+ release. Conversely, pretreatment with 50 microM clomiphene in Ca2+-free medium abolished the [Ca2+]i increase induced by brefeldin, thapsigargin or CCCP. The intracellular Ca2+ release was unaltered by inhibiting formation of inositol-1,4,5-trisphosphate (IP3) with 2 mM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122; a phospholipase C inhibitor).
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Netherlands Trial register NTR1449.
To determine the accuracy of diagnosing polycystic ovarian syndrome (PCOS) predominantly on clinical features and the response to metformin therapy.