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)

Hot flushes are frequent among women during natural, surgical, or pharmacological menopause. The available data suggest the involvement of estrogens, progestins, catecholestrogens, catecholamines, dopamine, endorphins, prostaglandins, luteinizing hormone (LH) and luteinizing hormone-releasing hormone (LH-RH) in the pathogenesis of flushes. At present the estrogen withdrawal and pulsatile luteinizing hormone (LH) secretion theories are most commonly accepted for explaining the development of this symptom. The use of LH-RH agonists offers an opportunity to focus on the probable origin and region that regulate the events of this phenomena, since the administration of this drug is associated with hot flushes, in spite of low gonadotropins and normal estrogen levels. Current data may suggest that the origin of this neurovegetative symptom lies in the hypothalamus.
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PMID:Endocrinological basis of hot flushes. 266 75

The aim of this study was to investigate circadian and ultradian variations in menopausal hot flash. The number of hot flashes per 2-hr period was collected from 25 diurnally-active, perimenopausal women for 1 week in January or February of each year for 3 consecutive years. Fourteen women were experiencing natural menopause (NM) (mean age 51.9 years) and 11 were experiencing surgically-induced menopause (SIM) (mean age 52.0 years). The difference in the number of hot flashes between the two types of menopause at each clock time was not statistically significant; neither was the mean number of hot flashes per 24 hr different between the two groups (Student's t-test). Data when normalized for each woman and placed end-to-end revealed by cosinor analysis circadian rhythmicity in the SIM group (P = 0.02) but not in the NM group. A 12-hr periodicity was detected in both groups (P less than 0.001 for both). An 8-hr rhythm was detected only for the NM group (P = 0.04). Both groups combined exhibited statistically significant rhythmicities with periods of 24 hr (P = 0.003), 12 hr (P less than 0.001) and 8 hr (P = 0.005). Regardless of the type of menopause, the women could be separated into two groups based on the temporal pattern of hot flashes during the day. One group was defined by the occurrence of peak frequency of flashes during the morning (0400-0959), while the second group was defined by the occurrence of the peak in the evening (1600-2159).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circadian rhythms in hot flashes in natural and surgically-induced menopause. 280 56

Hot flushes are not caused by hypergonadotrophinaemia. This is apparent because peaks of gonadotrophin in the serum do not coincide with cutaneously measured hot flushes while such flushes still occur in hypophysectomized women. Gonadotrophin-releasing hormone and other neurotransmitters (possibly beta-endorphin) affect thermoregulation. The following hypothesis is advanced. During the climacteric period neurotransmitter changes, a decrease in catechol oestrogens, a decrease in alpha-2-adrenoceptor activity and cessation of ovarian steroid production may lead to alterations in endogenous opiate activity and thus to disturbances of thermoregulation, resulting in the occurrence of hot flushes. Low beta-endorphin levels in the peripheral plasma, which rise again following oestrogen treatment, are observed during the climacteric. On the other hand, women with severe hot flushes caused by a stress event show enormously increased beta-endorphin values, which are normalized by hormone substitution therapy acting via still unknown neuroendocrinological feedback mechanisms.
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PMID:Beta-endorphin levels during the climacteric period. 284 May 57

Eight menstrually cycling women with proven endometriosis were treated with a delayed-release preparation of the superactive agonist D-Trp-6-LH-RH in biodegradable microcapsules, administered intramuscularly at intervals of 16 to 36 days for a period of 3 to 5 months. After the first injection which caused a transient stimulatory response, a sustained hypogonadal state, characterized by an estradiol (E2) level less than 50 pg/mL, was induced in all patients by day +14.7 (range 7.19). Subsequent injections caused no more stimulation, but a continuous decrease in E2 levels was observed. In all patients, E2 levels fell to zero after the second or third injection. Gonadotropins remained in the normal range throughout the course of treatment. Hot flashes and severe dyspareunia (related to vaginal dryness) were the main side effects. Resumption of normal pituitary-ovarian activity was documented in all patients after the last injection; the end of the hypogonadal state, ovulation and menses, occurred on days 41 (range 32-59), 58 (range 51-64) and 70 (range 65-76), respectively. All patients showed a clinical improvement. Our results demonstrate that a long-lasting, reversible hypogonadism can be induced in cyclic women by intramuscular injections of D-Trp-6-LH-RH microcapsules at monthly intervals. This simple and convenient treatment should be useful in treating endometriosis and other conditions.
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PMID:Therapeutic hypogonadism induced by a delayed-release preparation of microcapsules of D-Trp-6-luteinizing hormone-releasing hormone: a preliminary study in eight women with endometriosis. 290 72

Twenty-seven patients with metastatic adenocarcinoma of the prostate were treated with the new luteinizing hormone-releasing hormone analog, Zoladex (ICI 118,630) for up to ninety-eight weeks. Initially, treatment was randomized between Zoladex 250 micrograms and 500 micrograms self-injected subcutaneously every day for a minimum period of twelve weeks following which a sustained-release, once-monthly depot formulation of Zoladex 3.6 mg s.c. was used. Acute rises in serum gonadotropins and testosterone during the first two days were followed by declines in hormone levels over the following three weeks. Median time to castration with 500 micrograms/day was twenty-two days compared with forty-three days with 250 micrograms/day (p = 0.06). No significant endocrinologic changes occurred during the transfer to the depot, and serum testosterone remained 95 per cent suppressed throughout the duration of the study. After three months the median daily serum Zoladex concentrations ranged between 0.47 and 0.53 ng/ml and were not significantly different among the three dosage forms. No specific correlation among serum Zoladex concentrations, endocrinologic parameters, and tumor response rates were found. Hot flashes initially, and decreased libido were the only common complaints. Zoladex was well tolerated, and no side effects required dose-modification or removal from the study. Tumor response rates up to one year appeared to be comparable to the conventional endocrine therapies. This analog in monthly depot formulation is recommended for further clinical evaluation.
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PMID:Zoladex (ICI 118,630): clinical trial of new luteinizing hormone-releasing hormone analog in metastatic prostatic carcinoma. 294 17

A total of 113 women who presented with climacteric symptoms participated in the study. They were randomly allocated to seven groups of 10-27 subjects, who received for 6 mth the following therapies, respectively: conjugated oestrogens (CE) 0.625 mg/day for 21 days + norethisterone (NET) 5 mg/day from day 12 to day 21; CE + cyproterone acetate (CPA) 12.5 mg/day from day 1 to day 10; oestradiol valerate (EV) 2 mg/day for 21 days + NET; EV + CPA; oestriol (E3) 2-4 mg/day; tibolone (ORG OD14) 2.5 mg/day; and placebo, one tablet/day. Hot flushes decreased significantly over the treatment period in all seven groups. However, E3 was less effective at the dose used than CE, EV or ORG OD 14. At the end of the 6 month treatment period histological examination revealed no changes in endometrial morphology in any of the patients treated. Indeed, the addition of a progestogen even induced regression of endometrial hyperplasia in 8 cases. No significant variation in the plasma levels of triglycerides, total cholesterol, high-density lipoprotein (HDL) or low-density lipoprotein (LDL) was observed after the second and sixth months of treatment with E3 or ORG OD 14. After 6 months, treatment with CE/EV + CPA produced a significant increase in HDL, while treatment with CE/EV + NET brought about a reduction in total cholesterol and HDL and an increase in LDL.
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PMID:Benefits and risks of different hormonal replacement therapies in post-menopausal women. 303 44

In a randomized, prospective trial, 199 previously untreated patients with Stage D2 prostatic cancer were treated with 3 mg/day diethylstilbestrol (DES) or 1 mg/day leuprolide acetate, a luteinizing hormone releasing hormone analog. Both DES and leuprolide suppressed testosterone to the desired castrate levels. Objective measures of disease, such as acid phosphatase levels, and subjective measures, such as bone pain, performance status, and mobility, showed similar decreases in both groups. No progression of disease was seen in 86 per cent of the leuprolide-treated group, compared with 85 per cent of the DES-treated group. The time to disease progression, development of adverse reaction requiring discontinuation of treatment, or death was identical for the two groups. Hot flashes were more common with leuprolide than with DES. Gynecomastia and breast tenderness, nausea and vomiting, and peripheral edema occurred more often in the DES group. Of those taking DES, 13 per cent discontinued treatment because of side effects, compared with 3 per cent of those taking leuprolide.
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PMID:Leuprolide versus diethylstilbestrol for previously untreated stage D2 prostate cancer. Results of a prospectively randomized trial. 307 35

A comparative study was done in 59 recently diagnosed Stage D2 prostatic cancer patients treated with either long-term GnRH-A (Buserelin) (N = 42) or with orchiectomy (N = 17) and followed up for three years. The suppressed limits of plasma testosterone and estradiol levels after eight-week follow-up as well as the objective clinical response and disease outcome were found to be similar with either treatment. Hot flushes and loss of libido were noticed in both groups throughout the follow-up period; however, there were no other side effects. Analysis of Stage D2 patients based on their time of death enables us to identify nonhormonal variables which, in the form of an aggressiveness score, correlated well with both clinical response and disease outcome. These data confirm that (1) Buserelin is an effective and safe alternative to orchiectomy in advanced prostatic cancer, and (2) in clinical studies a multifactor aggressiveness score is useful for analyzing clinical efficacy data. Prospective application of that score may enable predictability of patient response and influence patient management.
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PMID:Objective response and disease outcome in 59 patients with stage D2 prostatic cancer treated with either Buserelin or orchiectomy. Disease aggressivity and its association with response and outcome. 308 58

Previously, we reported that short term administration of a highly potent GnRH agonist (GnRHa) for 1 month to patients with polycystic ovarian disease (PCO) resulted in complete suppression of ovarian steroidogenesis without measurable effects on adrenal steroid production. This new study was designed to evaluate the effects of long term GnRHa administration in PCO patients with respect to their hormone secretion patterns and clinical responses. Eight PCO patients and 10 ovulatory women with endometriosis were treated daily with sc injections of [D-His6-(imBzl]),Pro9-NEt]GnRH (GnRHa; 100 micrograms) for 6 months. Their results were compared to hormone values in 8 women who had undergone bilateral oophorectomies. In response to GnRHa, PCO and ovulatory women had rises of serum LH at 1 month, after which it gradually declined to baseline. In both groups FSH secretion was suppressed throughout treatment. Serum estradiol, estrone, progesterone, 17-hydroxyprogesterone, androstenedione, and testosterone levels markedly decreased to values found in oophorectomized women by 1 month and remained low thereafter. In contrast, serum pregnenolone and 17-hydroxypregnenolone were partially suppressed, and dehydroepiandrosterone, dehydroepiandrosterone sulfate, and cortisol levels did not change. Clinically, hyperplastic endometrial histology in three PCO patients reverted to an inactive pattern, and proliferative endometrium in two other PCO patients became inactive in one and did not change in the other. Regression of proliferative endometrial histology occurred in all ovulatory women. Vaginal bleeding occurred in all women studied during the first month of GnRHa administration, after which all but one PCO patient became amenorrheic. Hot flashes were noted by all ovulatory women and by four of eight PCO patients. All PCO patients noted subjective reduction of skin oiliness, and five had decreased hair growth. We conclude that in premenopausal women: 1) chronic GnRHa administration results in apparently complete persistent suppression of ovarian steroid secretion; 2) adrenal steroid secretion is not influenced directly or indirectly; and 3) its use may be helpful in the treatment of endometrial hyperplasia and ovarian androgen excess in women with PCO.
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PMID:Clinical and hormonal effects of chronic gonadotropin-releasing hormone agonist treatment in polycystic ovarian disease. 311 31

We compared the transdermal and subdermal routes of estrogen administration with respect to the constancy of estrogen delivery and metabolic effects. Twenty postmenopausal women were randomized to receive either two 25 mg estradiol pellets subdermally (n = 10) or a 0.1 mg estradiol transdermal patch twice weekly (n = 10). Blood was sampled at 0, 2, 4, 6, 8, 12, 24, and 72 hours and 1, 2, 4, 8, 12, 16, 20, and 24 weeks (fasting samples at 0, 12, and 24 weeks), and a fasting urine was obtained after diuresis at 0, 12, and 24 weeks. In a 72-hour profile, serum estradiol levels (mean +/- SE) were highest at 24 hours (179 +/- 20 pg/ml) and fell to 139 +/- 16 pg/ml at 72 hours in the pellet group. In the patch group, estradiol levels rose rapidly to 152 +/- 33 pg/ml at 4 hours, remained relatively constant over 8 hours, and fell to 46 +/- 10 pg/ml at 72 hours. At 1 week, estradiol levels in the pellet group were 113 +/- 12 pg/ml and remained relatively constant for 24 weeks. In contrast, estradiol levels in the patch group were 52 +/- 11 pg/ml at 1 week and then varied widely until 24 weeks, when the levels were 89 +/- 26 pg/ml. The mean estradiol/estrone ratio ranged between 1 and 2.5 in both groups but fluctuated widely in the patch group. Follicle-stimulating hormone was suppressed in both groups; however, the decrement in the pellet group was greater (p less than 0.002). There was a significant increase in high-density lipoprotein cholesterol and a decrease in total cholesterol/high-density lipoprotein cholesterol at 12 weeks with the pellet but only at 24 weeks with the patch. The urinary calcium/creatinine ratio was reduced more consistently with the pellet than with the patch. Hot flushes were eliminated in all subjects.
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PMID:A randomized comparison of nonoral estradiol delivery in postmenopausal women. 314 19


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