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)

Twenty-six women, most of them with advanced endometriosis (Stage III according to Acosta), were treated for six months with the LH-RH agonist Buserelin. After initially increased liberation both of the gonadotropins as well as of the sexual steroids there was consecutive inhibition of gonadal function, especially after inhibition of FSH secretion. Within two to four weeks estradiol production was completely and lastingly suppressed in 21 of the 26 women. In three women it lasted for three months and in two women estradiol again rose up to three times during the period of observation. Correspondingly, 22 of the women suffered from hot flushes as early as within the first two months. Twenty of the 26 women became completely free of symptoms within four to six weeks, and a clear regression of the pain was recorded in another four. In two women the complaints persisted without change. Withdrawal bleeding of short duration occurred simultaneously with the intermittent increases in estradiol levels; however, this bleeding usually caused little or no pain. Eleven of the 19 endometrium biopsies performed during therapy revealed a dormant endometrium, and only in one case was proliferated endomedium found, in the third month of treatment, in a stage of transition to hyperplasia. The remaining seven biopsies were insufficient for assessment. In seven women with advanced endometriosis, laparotomies were performed after drug treatment. Histologic study of the endometriosis tissue thus obtained revealed, except in the two nonresponders, cicatrized tissue with atrophic glands and severely reduced stroma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Initial results in the treatment of endometriosis with the LH-RH analog buserelin]. 309 11

Buserelin [D-Ser(TBU)6-des Gly NH2(10) LHRH ethylamide], an LHRH agonist, was administered intranasally at two dose levels, 200 micrograms t.d.s or 300 micrograms t.d.s., to 20 women with proven endometriosis, many with recurrent disease. Both dose schedules achieved significant suppression of circulating 17 beta-oestradiol levels often to within the postmenopausal range, the larger dose inducing significantly greater suppression (P less than 0.05). Serum FSH values were suppressed below baseline but serum LH remained at pretreatment levels or above, whilst on treatment. Complete resolution of endometriotic deposits was achieved in 68% of cases following 6 months treatment with dramatic and long-standing relief of symptoms with no apparent dose difference. In all other subjects there was significant reduction in the extent of endometriotic deposits and improvement in American Fertility Society classification of disease stage. The most commonly occurring side effect was hot flushes; their intensity and frequency related to the degree of suppression of serum oestradiol and the dose of Buserelin administered.
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PMID:Reversible pituitary ovarian suppression induced by an LHRH agonist in the treatment of endometriosis--comparison of two dose regimens. 310 12

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

This study was designed to evaluate the long-term effect (6 months) of the luteinizing hormone-releasing hormone (LH-RH) agonist buserelin on pituitary and ovarian function in a group of 14 patients presenting with the polycystic ovarian (PCO) syndrome. Buserelin was given subcutaneously 200 micrograms three times daily for the first 7 days followed by 500 micrograms once daily. Blood samples were taken weekly for the first month and then every month for radioimmunoassay of LH, FSH and sex steroids. While LH levels were stimulated during the first 2 weeks and then declined towards baseline, serum FSH levels were reduced after only 1 week (P less than 0.05). Serum oestradiol levels were maximally suppressed to the menopausal range after 1 month and testosterone levels were also significantly inhibited (P less than 0.05) after 2 weeks of therapy. Dehydroepiandrosterone (DHEA) sulphate did not show any significant change while 17-hydroxyprogesterone was suppressed after the first month of buserelin administration (P less than 0.01). The apparent divergent response of the gonadotrophins and the reduction of ovarian steroids in spite of lack of suppression of LH levels can be explained by the marked inhibition of the bioactivity of LH assessed by dispersed mouse Leydig cells assay. The clinical evaluation of hirsutism did not detect any change during the 6 month period. No patient had any menstrual bleeding or spotting after the sixth week of buserelin. The monthly incidence of hot flushes varied between 50 to 66%. This study shows that LH-RH agonist administration can selectively inhibit ovarian function and could be an interesting approach to evaluate the respective contribution of the ovary and adrenal on the pathophysiology of the polycystic ovarian disease. Polycystic ovarian (PCO) syndrome is characterized by tonic and exaggerated secretion of LH leading to an excessive stimulation of the ovarian stroma and an increased production of androgens (Yen et al., 1970; DeVane et al., 1975; Rebar et al., 1976). The androgen precursor delta 4 androstenedione is transformed in peripheral tissues into oestrone (Siiteri & MacDonald, 1973), thus maintaining the state of pituitary hypersensitivity and creating a positive feedback (Yen et al., 1976). The starting point of this vicious circle is still controversial; some argue for a hypothalamic abnormality (Vaitukaitis, 1983) while others support the peripheral origin of the hypersecretion of steroids (Reyniak, 1983). The importance of the adrenal contribution in this syndrome is still unclear.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Ovarian suppression in polycystic ovarian disease during 6 month administration of a luteinizing hormone-releasing hormone (LH-RH) agonist. 313 52

In 103 sexually mature women with disturbance of ovulation, a possible relationship between Kupperman menopausal complaints and endocrinological status was investigated to find the cause of climacteric syndrome. The Kupperman index was increased as the disturbance of ovulation was advanced from the stage of anovulatory cycle to amenorrhea I and further to amenorrhea II. In parallel with the advance in disturbance of ovulation, serum FSH and LH levels rose significantly, and serum estrone (E1) and estradiol (E2) levels dropped. Prolactin (PRL) showed a tendency to decrease. There were some hormonal patterns characteristic of individual complaints; hot flush was associated with increased FSH and LH, and decreased E1 and E2; difficulty in falling asleep, excitability, and fatigability, with increased FSH and LH, and decreased E2; nervousness, with increased LH and decreased E2; headache, with increased LH and PRL, and decreased E2; feeling of cold, with decreased E2 and PRL; and numbness and shoulder stiffness, with decreased E2. In sexually mature women, the complaints associated with abnormal levels of two or more kinds of hormones seemed to be most specifically related with decreased E2, followed by increased LH. Fatigability and headache developed specifically in the ovulatory phase of women with normal menstrual cycles (105 subjects), suggesting that these two complaints are closely related to increased LH. These results indicate that the majority of Kupperman menopausal complaints have their individually specific endocrinological cause, and that they may develop even in sexually mature women if those specific conditions exist. In climacteric syndrome in a narrow sense (i.e., dysautonomic type), each complaint may also have its specific endocrinological cause.
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PMID:[Serum hormone level and Kupperman menopausal complaints in sexually mature women with disturbance of ovulation]. 391 22

21 women with menopausal disorders were given veralipride, which is a benzamide derivative having a central anti-dopaminergic action. The LH, FSH and PRL plasma levels were controlled before and after treatment. Treatment, using veralipride at a daily dose of 100 mg for 20 days, improved the climacteric syndrome, and, in particular, the sudden hot flushes. The FSH plasma levels remained unchanged, the LH levels were reduced, although they remained high, and the PRL levels increased during the course of the treatment.
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PMID:[Effect of veralipride on LH, FSH, and PRL levels and on the climacteric syndrome]. 392 34

A 25-year-old woman developed hot flushes due to the artificial menopause induced by cytotoxic chemotherapy (MOPP) during five years for Hodgkin's disease. Plasma FSH levels were found to be greatly elevated while those af 17 beta-oestradiol were markedly diminished. Veralipride was prescribed as one tablet (100 mg) daily for 20 days. Hot flushes disappeared completely, and no recurrence was observed during the 4-month follow-up period after discontinuation of treatment. Tolerance was excellent. This result is in agreement with those of studies reported in the published literature, relating to the treatment of hot flushes and psychofunctional disorders associated with both the natural and artificial menopause.
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PMID:[Iatrogenic menopause: a case report (author's transl)]. 626 10

Twenty post-menopausal women (10 natural and 10 surgical menopauses) with climateric manifestations consisting mainly in hot flushes were given veralipride. Overall satisfactory results obtained in two-thirds of cases evidence the value of tis non-hormonal therapy, especially in cases of natural menopause which responded consistently. Clinical tolerance of veralipride proved satisfactory. Biological investigations (total and differential blood cell counts, glucid and lipid metabolism, BUN, transaminases) before and after three twenty-day courses of veralipride showed no modifications. Hormonal assays done in four patients showed no action of veralipride on FSH and LH.
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PMID:[Veralipride and menopause]. 631 85

To examine the relationship between the occurrence of menopausal hot flashes and the pulsatile release of LH, we have investigated the serum hormone levels and the occurrence of hot flashes by objective recordings in five women with endometriosis given daily injections of a long-acting GnRH agonist (GnRH-a) for 28 days. Results were compared to the findings made in 25 young women 6-8 weeks after bilateral oophorectomy. Serum levels of estrone and estradiol were similar in the subjects given GnRH-a and the women who underwent a surgical castration. In comparison with values before GnRH-a administration, the mean FSH level was lower whereas the mean LH concentration was significantly higher (P less than 0.01) on the last day of therapy. The coefficients of variations of both gonadotropins measured during 4-h sampling periods at 20-min intervals before and at the end of GnRH-a administration were significantly reduced (P less than 0.01) with therapy. During the total of 20 h of frequent sampling in the 5 subjects, 15 pulses (20% rise from nadir) of LH and 12 pulses of FSH were detected before GnRH-a, whereas only 2 and 8 pulses, respectively, were observed on day 28 of treatment. Hot flashes were observed in both groups of patients. The proportion of women experiencing hot flashes, the rate of occurrence/h and the characteristics of the physiological changes were similar in the 2 groups of women. These data indicate that hot flashes can occur in the absence of prominent LH pulses, suggesting the pulsatile release of this hormone is merely associated with the hot flash rather than being etiological.
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PMID:Induction of hot flashes in premenopausal women treated with a long-acting GnRH agonist. 640 56

Hot flashes have a close temporal relationship with the initiation of LH pulses, suggesting that factors stimulating gonadotropin release are involved in the mechanism of this disturbance. It has been reported that the opiate antagonist naloxone acutely blocked subjective hot flashes, a seemingly paradoxical effect, since the use of this agent in premenopausal women increases the magnitude and frequency of LH pulses. We, therefore, studied the effects of naloxone in 16 postmenopausal women with frequent hot flashes using continuous recordings of finger temperature and skin resistance as objective indices of flushing and perspiration, respectively. After baseline recordings, the subjects were randomized into equal groups, and the recordings were repeated during 8-h infusion of either saline or naloxone (22 micrograms/min). Serum gonadotropin levels were measured at 15-min intervals before and during the last 4 h of the infusion. Naloxone did not change the rate of objectively measured hot flashes, mean serum LH or FSH levels, or the frequencies or amplitudes of gonadotropin pulses. These data suggest that there is a very low input of endogenous opiates on gonadotropin secretion in postmenopausal women and that opioid peptides do not play a role in the initiation of the postmenopausal hot flash.
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PMID:The effects of naloxone on hot flashes and gonadotropin secretion in postmenopausal women. 642 Apr 45


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