UMLS:C0016382 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment was interrupted abruptly in 6 hypertensive patients receiving clonidine 0-45-5-4 mg daily. Blood-pressure rose to pretreatment levels within 24-48 h of withdrawal and was accompanied by insomnia, headache, flushing, sweating, and apprehension. These symptoms began 18-20 h after the last dose of clonidine. Plasma-noradrenaline levels and urinary catecholamine excretion increased 24-72 h after withdrawal of clonidine. The subjective symptoms were most prominent in patients on higher doses (greater than 1 mg/day) and in those who had previously been receiving treatment with other antihypertensive drugs. One patient on a very low daily dose (0-15 mg) of clonidine had no symptoms and no significant changes in blood-pressure or catecholamine production after drug withdrawal.
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PMID:Clonidine withdrawal in hypertension. Changes in blood-pressure and plasma and urinary noradrenaline. 6 74

The combination of nifedipine and atenolol must be evaluated in terms of risks and benefits to the hypertensive patient. Disadvantages with single-agent therapy justify trials of combination regimens. beta-Blockers may be unacceptable to some patients because of gastrointestinal upset, musculoskeletal symptoms, tiredness, malaise, insomnia, depression or confusion, sweating, breathlessness or cold extremities. The side effect profile varies from patient to patient and between different beta-blockers. Calcium antagonists also have characteristic side effects, including severe headaches, flushing and oedema, tachycardia and possibly worrying palpitations, and polyuria. Combining a calcium antagonist and a beta-blocker can reduce some side effects; for example, tachycardia is offset by addition of beta-blocker to calcium antagonist therapy, and beta-blocker-induced cold extremities may be reversed with a drug such as nifedipine. Moreover, the antihypertensive efficacy is increased, which is useful in previously resistant patients. However, an excessive fall in blood pressure is a possible adverse effect of the combination. There is also the possibility of precipitating heart failure in patients with cardiomegaly and severely compromised left ventricular function. The combination of nifedipine and atenolol was evaluated in 25 patients in a randomised, crossover trial following a month's treatment with atenolol 50mg twice daily. Patients received either atenolol 50mg twice daily alone, or atenolol 50mg twice daily with sustained release nifedipine 20mg or 40mg twice daily, or placebo twice daily during three 4-week treatment periods. Additional antihypertensive benefit was obtained by addition of the low dose of nifedipine compared with atenolol alone, but no further advantage was obtained with the higher nifedipine dose.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Aims of combination therapy--improved quality of life or better blood pressure control? 337 14

Eleven hypertensive patients in whom clonidine therapy had to be discontinued, were treated prophylactically with labetalol, in order to avoid a possible hypertensive crisis. Most of the known side effects, which are consistent with the withdrawal phenomenon were observed, e.g. tremor, insomnia and apprehension, but headaches and flushing did not occur. Blood pressure levels remained unchanged, despite up to a 20-fold increase in plasma catecholamines. The lack of change in serial measurements of plasma cyclic AMP level appears to indicate that adequate adrenergic blockade was induced by labetalol. Since labetalol is a potent anti-hypertensive drug, and is also effective in avoiding a possible hypertensive crisis due to withdrawal of clonidine, we propose to use it as the drug of choice whenever discontinuation of clonidine therapy is indicated.
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PMID:Use of labetalol in hypertensive patients during discontinuation of clonidine therapy. 627 79

To study the types of patients with climacteric syndrome who respond to conjugated estrogen therapy, we investigated the results of 1- to 2-month therapy in 52 patients by comparing their pre- and post-drug level of blood estradiol (E2), FSH and LH as well as comparing information through a questionnaire on menopausal complaints listed according to Kupperman. Predrug E2 in the patients studied was lower than normal, but the lowering was not significantly specific to any particular climacteric symptom. Blood FSH was higher in the patients complaining of hot flushing, sweating, depression, feeling of something sticking in the throat, and decreased sexual desire, whereas blood LH was higher in the patients with hot flushing and sweating. Changes in various symptom were investigated in relation to hormonal changes found after conjugated estrogen therapy. In the patients whose E2 was increased and FSH and LH were decreased after the therapy, hot flushing, cold sensation, excitability and insomnia were ameliorated at a high rate. Numbness was favorably treated in the patients responding with increased E2, whereas shoulder stiffness, fatigability and headache was reduced in those responding with decreased LH.
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PMID:[Blood levels of estradiol, FSH and LH in women with climacteric syndrome--conjugated estrogen therapy]. 642 67

A limitation of clonidine therapy is the syndrome of rebound hypertension and sympathetic overactivity after withdrawal. Ten patients, four male, six female, aged 28--64 years, with essential hypertension, were treated for one year with an imidazoline derivative, tiamenidine. Blood pressure fell from an average of 178/108 mm Hg pretreatment to 152/86 mm Hg after 1 year. Tiamenidine was then withdrawn in hospital, replaced by identical placebo under single blind conditions and observations made over 96 h. The study was interrupted in five patients (4 patients within 36 h) because blood pressure rose to greater than 30 mm Hg (systolic) or greater than 20 mm Hg (diastolic) above pretreatment values. For the group, blood pressure was maximal at 194/112 mm Hg, 18 h post withdrawal, significantly higher than pretreatment (p less than 0.005). Headache, tremor, flushing and insomnia were noted. Saliva production rose 100% at 24 h. Plasma noradrenaline rose within 24 h with an accompanying rise in urinary metanephrine and catecholamine excretion. Tiamenidine appears to share with other imidazolines rebound cardiovascular and autonomic effects following abrupt withdrawal.
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PMID:Changes in blood pressure, heart rate, and sympathetic activity on abrupt withdrawal of tiamenidine (HOE 440) in essential hypertension. 746 Oct 12

Yohimbine was used in four men and four women ranging in age from 21 to 64 years with nocturnal polysomnography and multiple sleep latency test-verified narcolepsy. All achieved a stimulant response in doses ranging from 2.7 to 16.2 mg/day. The effective dose was defined as the amount of medication required to maintain subjective wakefulness for 8 consecutive working hours. The average effective dose was approximately 8 mg/day. While one subject became immediately tolerant, others maintained a response for several weeks. The first subject continued to have good control of sleepiness for 17 months. Mild and transient side effects were insomnia, diarrhea, dyspepsia, flushing, and tremor. Alpha-2 adrenergic receptor abnormalities are suspected in narcolepsy, which could explain the improvement in sleepiness for these patients.
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PMID:Effectiveness of yohimbine in treating narcolepsy. 797 85

Gonadotropin-releasing hormone (GnRH) agonists are widely administered to treat endometriosis, but generally are not prescribed for more than 6 months since they are associated with vasomotor symptoms and bone loss. A GnRH agonist and steroid add-back therapy can be given for longer times without flare-up or significant hypoestrogenic symptoms. We examined the efficacy and safety of a weak estrogenic steroid, OD14, with prolonged goserelin treatment in seven regularly menstruating women (age 26-33 yrs) with laparoscopically diagnosed, symptomatic endometriosis. The women received goserelin 3.65 mg subcutaneously/month and 2.5 mg OD14 2.5 mg/day beginning in the fourth cycle for 18 to 20 months. The frequency and severity of hot flushes, sweating, irritability, loss of libido, nervousness, and sleeplessness were scored by the women on a scale of 0 to 6 and compared. Samples of blood and urine were obtained to measure serum estradiol (E2) levels, lipids, and urinary calcium:creatinine (Ca:Cr) ratios at the start of treatment and monthly thereafter. The vasomotor scores, serum E2 levels, and urine Ca:Cr ratios were consistent with the hypoestrogenism induced by goserelin (24.2 ± 3.1, 18.5 ± 7.2 pg/ml, and 0.063 ± 0.008, respectively). The decreases in vasomotor scoring with regard to hot flushing, sweating, and urinary Ca:Cr ratios were significant after adding OD14 (14.8 ± 2.2, 0.031 ± 0.005, p <0.05), whereas E2 levels remained below 40 pg/ml (23.1 ± 8.2 pg/ml, p >0.05) throughout therapy. The increased low-density:high-density lipoprotein ratio with goserelin improved with OD14, remaining at the lower limit of normal. Thus, OD14 add-back to GnRH agonist therapy enabled us to extend medical therapy of endometriosis longer than 6 months, preventing hypoestrogenic side effects, and with adequate suppression endometriosis symptoms.
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PMID:Effectiveness and Long-Term Safety of Prolonged Gosereline and Tibolone in Women with Endometriosis 907 53

Secondary side-effects often occur in women undergoing hormonal stimulation treatment with clomiphene citrate. In general 10.4% of women experience hot flushing, 5.5% have complaints caused by enlargement of the ovaries and 3.5% experience central nervous symptoms (nervousness, sleeplessness, headaches, visual disturbances, vertigo). During ovarian stimulation with clomiphene citrate for in-vitro fertilization, a 32 year old patient developed psychotic symptoms, commencing 3 days after initiation of treatment. Hospitalization in the psychiatric ward became necessary when severe formal and rational thought disturbances arose together with perceptory and sensory delusions. Under neuroleptic treatment the symptoms improved. Nevertheless, follow-up psychiatric care on an outpatient basis was deemed necessary. The infertility treatment was continued with human menopausal gonadotrophin stimulation. Psychiatric instability occurred neither at this point nor during the 2 year follow-up observation period. Both an exogenous psychosis (ICD F23.9) as well as the exacerbation of an endogenous psychosis (ICD F29) may be considered for the differential diagnosis. The stimulation with clomiphene citrate in connection with the physical and psychic stress of the infertility therapy can be regarded as the trigger factor. For patients with evidence of psychiatric illness in their case history, ovulation-inducing substances such as clomiphene citrate should be implemented with particular care.
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PMID:Clomiphene citrate as a possible cause of a psychotic reaction during infertility treatment. 915 29

Introduction and Objectives: Raloxifene, a novel selective estrogen receptor modulator (SERM), is under investigation for the prevention of osteoporosis in postmenopausal women. Like traditional estrogen replacement therapy, raloxifene has beneficial effects on bone and on serum lipids whereas, in contrast to estrogen's adverse effects in the breast and uterus, raloxifene is an estrogen antagonist in the breast and is nonstimulatory in the uterus. This study examines the effects of raloxifene 60 mg/day compared with placebo on: 1) the incidence of vasomotor symptoms: hot flashes (flushing) and sweating (including night sweats), 2) the severity and time course of hot flashes, and 3) the relation of hot flashes to baseline subject characteristics and study discontinuations. Additionally, the study explores the effects of raloxifene 60 mg/day compared with placebo on other climacteric symptoms that affect the quality of life of postmenopausal women, such as depression, insomnia, mood lability and genitourinary complaints.Methods: Integrated data from five randomized, placebo-controlled studies involving 1,165 healthy, postmenopausal women, with up to 30 months of study drug exposure, were analyzed. The incidence and severity of hot flashes and other climacteric symptoms were compared in patients treated with placebo or raloxifene (60 mg/day) via open-ended, non-directed subject self-assessment questionnaires. Data were analyzed for subgroup-by-therapy interactions using many baseline subject characteristics such as age, body mass index, smoking, alcohol, and years post-menopause, as well as preexisting conditions such as hot flashes, sweating, insomnia, depression, and history of hysterectomy. The overall incidence of other climacteric symptoms were reported as adverse events.Results: The increase in overall incidence of hot flashes in raloxifene-treated (24.6%) and placebo-treated (18.3%) subjects was modest, but statistically significant. However, this difference was significant only during the first 6 months of therapy, raloxifene (20.1%) compared with placebo (14.4%). After 6 months of treatment, there was no statistically significant difference in the incidence of hot flashes between the two treatment groups. The majority of hot flashes in raloxifene-treated subjects were subject-assessed as "mild-to-moderate" in severity (89%). The incidence of hot flashes reported as "severe" did not differ significantly in raloxifene- or placebo-treated subjects. Subgroup analyses revealed the overall incidence of hot flashes to be highest for both raloxifene and placebo-treated subjects, in younger (age < 55 years) women (P =.004), in women who had previously experienced hot flashes (P =.031), and in women having had hysterectomies (P <.001). Within each of these subgroups, there was no statistical difference in the incidence of hot flashes between the raloxifene and placebo groups. Between the two treatment groups, there was no difference in the overall incidence of subject discontinuations from study due to hot flashes. The occurrence of the other common vasomotor symptom, sweating (which includes night sweats), was not statistically different for the raloxifene- or placebo-treated subjects.Genitourinary complaints are often symptoms related to vaginal dryness, such as dyspareunia and decreased libido, as well as other symptoms of vaginitis and leukorrhea. No statistically significant differences occurred for raloxifene- or placebo-treated subjects in reports of these genitourinary symptoms. Similarly, for the other common climacteric symptoms; depression, insomnia, and mood lability, no significant differences in incidence between the raloxifene and placebo treatment groups were observed.Conclusions: Raloxifene (60 mg/day) treatment modestly increased the incidence of hot flashes compared with placebo, however, this difference was only statistically significant during the first 6 months of treatment. There were no differences in the severity of hot flashes between treatment groups, and this symptom did not adversely affect subjects' study participation. In both the raloxifene and placebo treatment groups, young postmenopausal women (age < 55), those with baseline hot flashes, and those with histories of hysterectomy were most likely to experience hot flashes. Raloxifene therapy did not affect the occurrence of other climacteric symptoms commonly affecting the quality of life of women after menopause.
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PMID:Raloxifene effects on vasomotor and other climacteric symptoms in postmenopausal women. 1083 11

Safety and tolerability of sildenafil citrate was assessed in a population subset of 60 Singaporean men with erectile dysfunction taken from the Asian Sildenafil Efficacy and Safety Study (ASSESS-I), a double-blind, placebo-controlled, flexible-dose study. The men, from two centres, with > or = 6 months' history of erectile dysfunction, were randomized to two treatment arms for 12 weeks. One group (30 patients) received sildenafil (initial dose 50 mg taken 1 h before sexual activity for the first 2 weeks, increased to 100 mg or decreased to 25 mg, according to efficacy and/or tolerability). The remaining 30 patients received a matching placebo. Incidence and type of adverse effects were evaluated at 2, 4, 8 and 12 weeks. Nine patients (30.0%) on sildenafil (33.1% in the full ASSESS-I study) and one patient (3.3%) on placebo (22.8% in the full ASSESS-I study) experienced treatment-related adverse events, the most frequent being headache in the sildenafil group (reported by five patients [16.7%]; 11.0% in the full ASSESS-I study). Flushing, visual disturbance, dizziness, insomnia, myalgia and back pain each occurred in one patient in the sildenafil group (3.3%); in the placebo group, one patient (3.3%) had headache. Importantly, the incidence of cardiovascular and respiratory system adverse events were relatively less than in the full ASSESS-I population (cardiovascular 3.3% in the present study versus 10.2% in the full ASSESS-I population; respiratory 3.3% versus 5.5%). All adverse events were transient and mild, and did not lead to treatment withdrawal. There was no effect on sitting blood pressure, heart rate or standard laboratory parameters; more importantly, there was no incidence of myocardial infarction, stroke or priapism. These results should reassure Singaporean patients and their physicians of the safety of sildenafil for erectile dysfunction.
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PMID:Clinical safety profile of sildenafil in Singaporean men with erectile dysfunction: pre-marketing experience (ASSESS-I evaluation). 1202 21

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