Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0600142 (hot flushes)
 1,242 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen replacement in menopause should be used for specific symptoms such as ovarian failure, hot flushes, vaginal atrophy, atrophy of the vulva, and atrophic urethritis. The dose should be as low as possible to be effective and perscribed for as short as time as possible, since there are possible risks of uterine cancer, breast cancer, increased blood pressure, gallstones, deep vein thrombosis, and thromboembolism. Estrogens should be administered to provide the maximum benefit with the minimum risk involved. Estrogens should not be given to patients with known contraindications such as: suspected breast or uterine cancer; undiagnosed genital bleeding; Dubin-Johnson syndrome; acute hepatic disease; previous or present thromboembolism; or severe thrombophlebitis. Careful evaluation should be made before administering estrogen to women with uterine myomata, hyperlipidemia, hypercholesterolemia, sevare varicose veins, chronic hepatic dysfunction, diabetes mellitus, porphyria, or severe hypertension.
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PMID:Estrogen replacement in the menopause. 39 Apr 56

Oral combined contraceptives did not seem to alter histamine metabolism in females. During treatment with gonadotrophic hormones in four amenorrhoeic patients there was a tendency towards increasing excretion of methylhistamine (MeHi) followed by a sudden decrease corresponding to changes in the urinary estrogen. The excretion of methylimidazoleacetic acid (MeImAA) seemed to parallel that of MeHi. The findings support the hypothesis that an endogenous surge of estrogen may influence histamine turnover in women. Women of post-menopausal age have about the same histamine metabolism as younger menstruating women. Estrogen medication relieved symptoms of hot flushes or sweats but did not seem to affect the histamine turnover.
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PMID:Histamine metabolism and female sex hormones in women. 99 72

Nafarelin, a synthetic agonist of gonadotrophin-releasing hormone (GnRH) [luteinising hormone-releasing hormone (LH-RH); gonadorelin] appears likely to join the other GnRH analogues currently used in a range of conditions reliant on gonadotrophins or sex hormones. With repeated administration, the pituitary becomes desensitised, and gonadotrophin release, and therefore sex hormone synthesis, are inhibited. Nafarelin has proved to be comparable to danazol in the management of women with endometriosis, with fewer potentially harmful adverse effects. Nafarelin has also been used effectively in in vitro fertilisation programmes, and in hirsute women and those with uterine leiomyoma, particularly to induce preoperative fibroid shrinkage. The drug shrinks hypertrophic tissue in men with benign prostatic hyperplasia, although treatment would need to be maintained indefinitely and therefore should probably be reserved for those unsuitable for prostatectomy. Preliminary data suggest that nafarelin is equivalent to diethylstilbestrol (stilboestrol) in terms of disease-free survival in men with prostate cancer. As a reliable method of contraception, nafarelin gives unpredictable results in men and the promising results in women may be offset by hypoestrogenic side effects. Nafarelin may join other GnRH agonists which are now routinely used in the management of children with central or combined precocious puberty. Nafarelin is readily and rapidly absorbed following intranasal delivery, and is protected to some extent from enzymatic degradation. The resultant relatively long elimination half-life allows once- or twice-daily administration. Estrogen depletion accounts for the most common side effects associated with nafarelin, including hot flushes and vaginal dryness, which are mild and tolerable in most patients. Reversible resorption of trabecular bone can occur during nafarelin therapy, perhaps necessitating cyclical treatment to enable bone mass to recover. Nafarelin, therefore, looks likely to find a role in the treatment of women with endometriosis, and results achieved in other conditions dependent on the pituitary-gonadal axis are promising.
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PMID:Nafarelin. A review of its pharmacodynamic and pharmacokinetic properties, and clinical potential in sex hormone-related conditions. 214 Sep 79

Estrogen therapy is extremely effective in relieving menopausal symptoms such as hot flushes, night sweats, urogenital atrophy and certain psychological symptoms. The short term side effects from this therapy are usually mild and self-limiting. They are more common in women who commence hormone replacement therapy some years after the menopause than in those who start treatment at about the time of the ovarian failure. Pre-existing gynaecological conditions such as fibroids and endometriosis can be worsened by estrogen therapy. The majority of published studies suggest a beneficial effect of postmenopausal estrogen therapy on cardiovascular and cerebrovascular disease. These effects may be mediated by favourable changes in lipids, but other mechanisms may also be involved. It is uncertain whether the adverse changes in lipids caused by progestogen therapy will reduce any of the benefits of estrogen therapy on the cardiovascular system. Osteoporosis is the major bone disease of the Western world; long term estrogen therapy will prevent its development in most postmenopausal women. The risk of endometrial carcinoma is increased with unopposed estrogen therapy; this increased risk appears to be abolished if a progestogen is added at an adequate dose and duration for each cycle. The risk of ovarian or cervical cancer is not increased with estrogen therapy. There may be an increased risk of breast carcinoma with long term postmenopausal estrogen use, but the studies show inconsistent results.
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PMID:A risk-benefit assessment of estrogen therapy in postmenopausal women. 222 68

Premenopausal breast cancer patients frequently develop amenorrhea during adjuvant chemotherapy. Despite psychic distress and severe weight loss are possible causes for secondary amenorrhea in cancer patients, it is in this case due to the gonadotoxicity of the cytostatic drugs. Alkylating agents, such as cyclophosphamide, damage ovaries directly, resulting in ovarian fibrosis, atretic follicles and decline in estrogen production. Elevated plasma levels of LH and FSH show adequate reaction of the hypothalamohypophyseal unit. There is no change in the androgen production of stromal cells as well as in the plasma levels of prolactin and adrenal androgen precursors. Ovarian damage goes along with hot flushes, loss of libido and dyspareunia. The onset of amenorrhea is age- and dose-related. Commonly the changes are irreversible. Estrogen replacement therapy promptly removes menopausal symptoms but is contra-indicated regarding the possible hormone-dependence of the tumor. In this case low dose medroxy-progesterone acetate is indicated.
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PMID:[Effects of adjuvant chemotherapy of breast cancer on gonadal function]. 223 81

The average life span of women living in the United States is approximately 80 years of age, with one-third of those years spent after menopause. Of the approximately 35-40 million postmenopausal American women, only 10% are currently using estrogen replacement therapy. Atrophy of the genitourinary system may be prevented or reversed with estrogen therapy. In addition, 75% of all postmenopausal women have vasomotor symptoms severe enough to lead them to seek medical consultation. For 65%, these symptoms persist for at least 1 year, and for 20%, the hot flushes are present for more than 5 years. Estrogen replacement therapy is the treatment of choice for the management of vasomotor symptoms, with or without additional behavior symptoms, and should be considered safe for most postmenopausal women. It protects the bones and, most important, the cardiovascular system.
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PMID:The menopausal syndrome. 305 Jun 57

Buserelin (B) is a synthetic nonapeptide analogue of native LHRH. Upon continued administration it reliably lowers the serum testosterone level to less than 100 ng/dl. It has been used in a clinical trial for the treatment of patients with stage C, D1, and D2 prostate cancer. Analysis of efficacy of testosterone suppression and toxicity included all 207 buserelin-treated patients. A comparison with historical controls from two National Prostate Cancer Project (NPCP) studies considered only the 147 evaluable patients with distant metastases (stage D2). All patients received buserelin, 500 micrograms q 8 hours subcutaneously (s.c.) for the first 7 days and then elected to take 200 micrograms s.c. daily or 400 micrograms q 8 hours by the intranasal (i.n.) route. Seventy-three percent elected s.c. administration. Only 2% changed the route of administration. The serum testosterone (T) level increased during week 1 in both the s.c. (426 ng/dl) and the i.n. (521 ng/dl) group but reached castrate (less than 100 mg/dl) levels by 4 weeks in 90% of patients. Subsequently, the likelihood of having a T level greater than 100 was higher for those treated by the i.n. than the s.c. route. The mean T level 4 and 12 months after therapy for the s.c. treated patients was 29 and 28. These values were 61 and 53 for those taking i.n. buserelin. This difference may in part be due to poor compliance. Toxicity was minor. Twelve percent of 151 s.c. treated patients had at least one episode of reaction at the injection site. None required discontinuation of the agent. Seventy-two percent experienced hot flushes; this was the same for both the s.c. and i.n. groups. Only 2 of 207 patients had a severe exacerbation of symptoms (spinal cord compression) during the first week of therapy. The criteria for response to therapy were those of the NPCP. There was no significant difference in the percentage of patients achieving a response when comparing the B-treated D2 patients to the NPCP D2 patients treated with DES, 3 mg daily, or orchiectomy. More of the B-treated patients entered with pain, a poor performance status, and weight loss than the DES/orchiectomy group. Nonetheless, the progression-free survival did not differ among the treatments. In summary, buserelin reliably lowers the serum T level by week 4 in 95% of men. Treatment efficacy is equivalent to a historical group treated with either DES or orchiectomy.
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PMID:Efficacy of buserelin in advanced prostate cancer and comparison with historical controls. 313 44

Estrogen replacement therapy is effective for the prevention and treatment of postmenopausal osteoporosis and should be offered to all women at high risk for osteoporosis. Such therapy is particularly beneficial for prevention of spinal compression fractures; in addition, it alleviates menopausal symptoms (hot flushes, genitourinary symptoms, and changes in mood). In each patient, these benefits must be weighted against the potential risks of endometrial hyperplasia and carcinoma, breast tenderness, hypertension, vascular headaches, and the inconvenience of menstrual bleeding if the uterus is intact. The risk of endometrial cancer associated with estrogen replacement therapy can be considerably reduced by the addition of a progestin, and other side effects can be diminished or eliminated by use of the new transdermal estrogen preparations. Thus, estrogen replacement therapy should be considered in all women who have experienced natural or surgically induced menopause, and it is advisable in women who have osteoporosis or an increased risk for this disorder and no contra-indications to its use. Estrogen replacement therapy should be instituted as soon after menopause as possible and seems to be well tolerated until at least 75 years of age.
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PMID:Estrogen replacement therapy: current recommendations. 328 71

Symptoms due to estrogen deficiency begin in the perimenopausal years and progress as serum levels of this hormone decrease Vasomotor instability, manifested by hot flushes or night sweats, may persist for several months to a few years. Psychologic symptoms include anxiety, tension, depression, insomnia, palpitations, and headaches. Atrophy of the genital epithelium may result in senile vaginitis with symptoms of irritation, burning, pruritus, dyspareunia, and even vaginal bleeding. Even the lower urinary tract mucosa is dependent upon estrogen. Postmenopausal osteoporosis affects 25 to 50% of older women and increases the risk for vertebral, hip, and other fractures. Estrogen therapy for menopausal complaints has received adverse publicity because several reports have indicated that unopposed estrogens increase the risk of endometrial cancer. Added progestogen not only negates this risk but reduces the incidence of endometrial adenocarcinoma in estrogen-progestogen users to less than that observed in untreated women. Estrogen replacement therapy does not increase the risk of breast cancer; the incidence of this malignancy, however, was also less in the estrogen-progestogen users when compared with either the untreated women or from that expected from the national cancer surveys. In evaluating postmenopausal women for hormone replacement, the benefits of estrogen-progestogen therapy must be weighed against possible risks.
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PMID:The menopause. 351 23

Hot flushes occur in the vast majority of women at menopause or after bilateral oophorectomy. Yet only in the last decade have the physiologic changes associated with hot flushes been identified. It is now clear that hot flushes occur together with pulsatile release of luteinizing hormone. Available data implicate the anterior hypothalamus in the pathogenesis of the hot flush and suggest involvement of catecholamines and endogenous opiates. Estrogen withdrawal appears to be the stimulus to the development of hot flushes in susceptible women, and likewise estrogen is the most effective agent in reducing the frequency and intensity of the hot flush.
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PMID:The physiology and measurement of hot flushes. 357 49


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