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1. |
BevantololA Preliminary Review of its Pharmacodynamic and Pharmacokinetic Properties, and Therapeutic Efficacy in Hypertension and Angina Pectoris |
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Drugs,
Volume 35,
Issue 1,
1988,
Page 1-21
William H. Frishman,
Renée J. Goldberg,
Paul Benfield,
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摘要:
SynopsisBevantolol is a new &bgr;-adrenoceptor antagonist which possesses a relatively high degree of selectivity for &bgr;1-adrenoceptors. It is devoid of intrinsic sympathomimetic activity and possesses only weak local anaesthetic properties. Interestingly, bevantolol has been shown to cause a lowering effect on peripheral vascular resistance. Available clinical data indicate that bevantolol, given once or twice daily, is an effective agent in the management of mild to moderate hypertension and stable angina pectoris. In hypertension bevantolol has been shown to be of comparable therapeutic efficacy to both atenolol and propranolol, while in patients with angina pectoris the drug compared favourably with atenolol. During short and long term administration bevantolol has been well tolerated and few patients have withdrawn from treatment because of adverse effects.However, although the properties of bevantolol may offer theoretical advantages in some patients, only a few comparative studies have been reported, and thus it is presently unclear what advantages bevantolol may offer over existing treatments for hypertension or angina pectoris.Pharmacodynamic PropertiesStudies in animals and man have shown that bevantolol is a relatively selective &bgr;1-adrenoceptor antagonist.In vitroandin vivo, bevantolol inhibited the chronotropic response to isoprenaline (isoproterenol) in various species, and in the anaesthetised dog it also inhibited tachycardia induced by adrenaline (epinephrine), carotid artery occlusion, tyramine and 1,1-dimethyl-4-phenylpiperazinium iodide. Animal studies have shown the &bgr;-adrenoceptor blocking potency of bevantolol to be between 3- and 8-fold less than that of propranolol after intravenous and oral administration. The selectivity of bevantolol for &bgr;1-adrenoceptors was demonstratedin vitroby its significantly greater antagonism of guinea-pig atrialversustracheal response to isoprenaline. In dogs bevantolol produced more selective blockade of the chronotropicversusthe depressor cardiovascular responses to isoprenaline than propranolol. In humans bevantolol 200 mg/day reduced the chronotropic effect of isoprenaline to a similar extent as atenolol 100 mg/day.Bevantolol does not possess intrinsic sympathomimetic activity and it is only a weak local anaesthetic. In receptor binding studies bevantolol displayed weak affinity for &agr;1-adrenoceptors and an antagonist effect has been demonstratedin vitrobut it is not known whether this represents a clinically significant effect.It has been demonstrated in animals and humans that bevantolol, mainly as a result of &bgr;1-adrenoceptor antagonism, exerts a negative chronotropic effect on the heart. In healthy human subjects single oral doses of bevantolol 50 or 100mg reduced tachycardia and elevated blood pressure caused by exercise. In patients with hypertension, administration of bevantolol 200 to 600 mg/day either as single or divided daily doses significantly reduced heart rate over a 24-hour period. In addition, during treatment of patients with angina pectoris heart rate significantly reduced after 2 weeks and this reduction was maintained for up to 12 weeks in treatment with bevantolol 300 mg/day. The results of a study in a small number of healthy subjects and patients with slight to moderate ischaemic heart disease suggest that bevantolol also exerts negative inotropic effects on the myocardium. Administration of bevantolol 200 mg/day orally to healthy subjects for 7 days caused an overall reduction in peripheral vascular resistance. The blood pressure lowering effects of bevantolol have been demonstrated in hypertensive rats, normotensive dogs and in healthy volunteers as well as patients with hypertension. In healthy subjects, administration of bevantolol 200mg daily for 7 days caused a reduction in peripheral resistance.Several studies in animal models of myocardial ischaemia have shown that bevantolol produced increased blood flow and improved contractile function of ischaemic myocardium. It has also been shown that bevantolol decreased the extent of epicardial ST segment shift in dogs and protected the ischaemic myocardium from ventricular fibrillation in pigs.Bevantolol, administered as single or cumulative doses, has been shown to reduce the FEV1in small numbers of patients with asthma but the risk of bronchospasm occurring in such patients during treatment for hypertension is not known.During 12 weeks' administration to patients with angina pectoris bevantolol 300 mg/day reduced the serum low density lipoprotein concentration and increased the high density lipoprotein/low density lipoprotein ratio. However, bevantolol affected neither fasting plasma insulin concentrations in these patients nor fasting blood glucose concentrations in patients with both hypertension and mild diabetes. These apparently beneficial effects of bevantolol on the blood lipid profile were not confirmed in patients with hypertension treated for 6 months.Pharmacokinetic PropertiesAfter single doses of bevantolol 100 to 400mg in fasted healthy subjects, peak plasma concentrations occur between 1 and 2 hours. While absorption of bevantolol is nearly complete, it undergoes presystemic metabolism - about 60% of an orally administered dose reaches the systemic circulation in unchanged form. Although food may slow the rate of absorption of bevantolol, the total amount of drug absorbed is not significantly affected. Distribution is rapid and extensive. In man, the apparent volume of distribution is 1.5 L/kg. Over 95% of plasma bevantolol is bound to glycoproteins.Less than 10% of an oral dose of bevantolol appears unchanged in the urine. Several metabolites have been identified, although none are considered to be of clinical importance. Most (72%) of a radioactive dose of bevantolol is renally excreted over 5 days. In healthy subjects the mean elimination half-life of bevantolol was about 1.5 hours and there were no recorded changes in pharmacokinetic variables after 7 daily doses of 100 or 200mg.Current evidence suggests that the pharmacokinetic properties of bevantolol do not change to a clinically significant extent in the elderly or patients with renal impairment.Therapeutic TrialsIn patients with mild to moderate hypertension single or divided daily doses of bevantolol 200, 300 or 400mg reduced diastolic blood pressure to a significantly greater extent than placebo. After up to 11 weeks' treatment with bevantolol 100 to 400 mg/day between 66 and 79% of patients had attained a clinical response compared with 23 to 33% of patients administered placebo. Daily doses of bevantolol 200, 300 and 400mg appear to be therapeutically equivalent in patients with mild to moderate hypertension. Using 24-hour blood pressure recordings, it was shown that the antihypertensive effects of once or twice daily administration are similar. In addition, bevantolol blunted the early morning increase in blood pressure. Administration of twice daily doses of bevantolol 100 to 300mg or propranolol 80 to 240mg for 6 months produced equivalent antihypertensive effects. In addition, bevantolol 400 mg/day appears to be similar in antihypertensive efficacy to atenolol 100 mg/day, when both are administered as once daily regimens.In patients with stable angina pectoris bevantolol 75 or 150mg twice daily significantly reduced both the myocardial oxygen demand during maximum workload and the proportion of patients who stopped exercising because of angina pain or ST segment depression. In addition, the frequency of angina attacks was reduced and the patients' ‘quality of life’ improved after bevantolol. Another study showed that indices of antianginal efficacy were similarly improved after bevantolol 200 mg/day was administered as a once or twice daily dosage regimen.Bevantolol 150mg twice daily and atenolol 100mg once daily displayed similar antianginal effects when administered over 12 weeks, with the exception that both resting and exercise heart rate were reduced to a greater extent after atenolol. Another study showed that once daily administration of bevantolol 400mg or atenolol 100mg for 4 weeks caused significant antianginal effects with no between-treatment differences.Side EffectsBevantolol has been well tolerated during short and long term studies in hypertension and angina pectoris. The most frequently reported side effects were fatigue, headache, dizziness, oedema and gastrointestinal upsets. These have generally been mild, causing only few patients to withdraw from treatment.Dosage and AdministrationMost patients with mild to moderate hypertension or angina pectoris should respond to doses of bevantolol within the ranges of 200 to 400 mg/day or 150 to 300 mg/day, respectively. A once or twice daily dosage regimen, individually titrated for optimum efficacy, may be used.
ISSN:0012-6667
出版商:ADIS
年代:1988
数据来源: ADIS
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2. |
BitolterolA Preliminary Review of its Pharmacological Properties and Therapeutic Efficacy in Reversible Obstructive Airways Disease |
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Drugs,
Volume 35,
Issue 1,
1988,
Page 22-41
Heather A. Friedel,
Rex N. Brogden,
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摘要:
SynopsisBitolterol is a &bgr;-adrenoceptor agonist which is hydrolysed to colterol by tissue esterases present at high concentrations in the lung. Animal studies indicate that bitolterol has significant &bgr;2-selectivity. In initial clinical trials transient cardiovascular effects have occurred in about 5% of patients. The spectrum of other adverse reactions with bitolterol is similar to that found with other &bgr;-adrenoceptor agonists.Preliminary therapeutic trials of bitolterol administered by aerosol or nebuliser in adult patients with asthma have shown variable but significant improvements in forced expiratory volume in 1 second (FEV1) and a duration of action of up to 8 hours in some patients. Bitolterol has been shown to provide similar maximum increases in FEV1to isoprenaline (isoproterenol) and to be significantly longer acting in long term comparative trials. Either alone or in combination with oral theophylline, bitolterol aerosol produces greater and more prolonged bronchodilation than oral theophylline alone but more consistently in non-steroid-dependent patients. Duration of bronchodilation with bitolterol in patients receiving steroids is less than in those who are not steroid dependent, perhaps due to more severe disease in the former group. More long term trials in larger groups of patients are clearly needed to assess the efficacy and safety of bitolterol in comparison with other long acting &bgr;-adrenoceptor agents, and to define the role of bitolterol in the combination regimens of antiasthmatic agents which are becoming increasingly popular. Nevertheless, bitolterol appears to be a well tolerated and relatively long acting alternative to other &bgr;-adrenoceptor agonists in the treatment of reversible obstructive airways disease.Pharmacodynamic StudiesBitolterol is a relatively selective &bgr;2-adrenoceptor agonist. Animal studies have shown a greater separation of bronchodilator and cardiovascular activities in comparison with salbutamol (albuterol) and terbutaline. In animals, bronchodilator response to bitolterol after histamine or carbachol challenge or injection of immune complexes is considerable, with effects lasting 4 to 5 hours. Cardiovascular response, on the other hand, is less than that seen with the other drugs studied and returns to baseline values while bronchodilation continues. In animals the separation of bronchodilator and cardiovascular effects has been explained by greater concentration of bitolterol and of esterase (to form the active metabolite colterol) in lung as opposed to heart tissue.In adult asthmatic patients the onset of bronchodilator activity occurs within 3 to 5 minutes of bitolterol inhalation and a peak effect is attained at 30 to 90 minutes. Mean peak improvement in forced expiratory volume in 1 second (FEV1) following administration of 700 to 1100&mgr;g by aerosol and higher doses by nebuliser ranges from 20 to 56% and may be greater in non-steroid-dependent than in steroid-dependent patients. However, doses above 1000&mgr;g administered by closed nebuliser do not generally provide further improvement in FEV1. Duration of activity is also variable, ranging from 4 to 8 hours after a single inhaled dose, and is longer with higher doses and in patients not on steroids. Preliminary studies in small groups of paediatric patients suggest similar results. Preliminary results suggest that bitolterol is effective in preventing exercise-induced asthma but optimum dose and timing in relation to exercise, and duration of protective effect, have not been determined.Cardiovascular effects of inhaled bitolterol during treatment of adult asthma patients for periods of up to 3 months have been generally mild and transient in nature. These have included small increases in heart rate (usually less than 10 beats/min), minor blood pressure changes, palpitations and chest discomfort. No cardiotoxicity, based on 24-hour electrocardiogram readings using Holter monitors, has been demonstrated during combined use with theophylline. However, only small numbers of fairly young, reasonably well controlled asthmatics have been studied. More work is needed to assess risks of toxicity in older patients and/or those with severe asthma or other intercurrent illness.PharmacokineticsAfter oral dosing with bitolterol, both in animals and in human volunteers, partial hydrolysis to active colterol occurs in the gastrointestinal tract and liver during the absorption process. After 1 hour peak plasma colterol levels are reached and inactive metabolites are also present. In the rat the greatest tissue uptake is in the liver with little difference in uptake by blood, heart or lung tissue.Upon intravenous dosing, on the other hand, bitolterol is preferentially distributed to lung tissue in both rat and dog. That, plus greater lung tissue esterase activity, is probably responsible for the good bronchodilator: cardiovascular separation ratio found in animals. It is not known whether these factors are present in humans. Nevertheless, upon aerosol administration in humans it is known that bitolterol is only slowly hydrolysed to colterol with serum concentrations of the latter too low to be measured by available methods.By all routes of administration the pharmacological activity of bitolterol is terminated by further metabolism of colterol through methylation and subsequent conjugation. In healthy subjects over 85% of a dose of bitolterol is eliminated in the urine and 8% in the faeces over a period of 72 hours. No parent compound is recovered. Plasma elimination half-life is 3 hours.Therapeutic TrialsIn single-dose studies in adult patients with asthma, inhaled bitolterol has produced similar degrees of improvement in various parameters of respiratory function to that produced by salbutamol, orciprenaline (metaproterenol) and isoprenaline. Bitolterol aerosol 1050 and 1100&mgr;g was significantly longer acting than isoprenaline 250&mgr;g, and longer acting than salbutamol 180&mgr;g by the same route in some initial studies. The duration of action of a lower dose of bitolterol (700&mgr;g) was equal to that of orciprenaline in a single study.In long term studies (1 to 3 months) comparing bitolterol administered by aerosol or nebuliser with isoprenaline given by the same route, in parallel groups of adult asthmatics, bitolterol was at least as effective as isoprenaline in improving FEV1response and was significantly longer acting. Adverse effects were minor and not different between the 2 drugs. No data are available comparing bitolterol with other &bgr;-adrenoceptor agonists.In 1 small study bitolterol aerosol, either alone or in combination with oral theophylline, produced a greater and more prolonged improvement in FEV1than did oral theophylline alone in parallel groups of patients over a 6-week period. However, results were consistent only in patients not receiving inhaled corticosteroids concomitantly. In steroid-dependent patients, likely to have more severe disease, there was a smaller degree of bronchodilation and a shorter duration of effect, and one regimen was not clearly superior over another. There was no difference in the number of asthma attacks among all groups of patients studied. Acute bronchodilator studies may not adequately reflect the efficacy of slow release oral theophylline. Further work in much larger groups of patients is needed to adequately assess the long term efficacy of bitolterol relative to that of other &bgr;2-adrenoceptor agonists.In one multicentre study in adult patients with chronic obstructive pulmonary disease, bitolterol aerosol 740&mgr;g produced a greater and more prolonged improvement in respiratory parameters than isoprenaline 170&mgr;g 3 times daily, which was maintained for the 3-month study period. Further studies are needed to determine the efficacy of bitolterol relative to that of established therapy in this type of patient.Side EffectsThe side effects most commonly associated with bitolterol therapy are tremor (14%), nervousness (5%), throat irritation (5%), headache (4%), cough (4%), dizziness (3%), lightheadedness (3%), nausea (3%) and palpitations (3%). Cardiovascular effects (including palpitations) occur in about 5% of patients. Effects are usually mild and transient but are occasionally moderate to severe. However, few patients have required withdrawal from treatment.Dosage and AdministrationThe usual aerosol dose for relief of bronchospasm is 2 inhalations (370 &mgr;g/actuation) given at an interval of 1 to 3 minutes and followed by a third inhalation if needed. For prevention of bronchospasm the usual dose is 2 inhalations every 8 hours but not exceeding 3 inhalations every 6 hours or 2 inhalations every 4 hours. By nebuliser the dose needed to produce maximum bronchodilation is 1.0 to 1.5mg using a closed intermittent flow system with an actuator valve and 2.5mg using an open continuous-flow system.
ISSN:0012-6667
出版商:ADIS
年代:1988
数据来源: ADIS
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3. |
QuazepamA Preliminary Review of its Pharmacodynamic and Pharmacokinetic Properties, and Therapeutic Efficacy in Insomnia |
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Drugs,
Volume 35,
Issue 1,
1988,
Page 42-62
Stephen I. Ankier,
Karen L. Goa,
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摘要:
SynopsisQuazepam is a trifluoroethyl benzodiazepine hypnotic with a half-life of 27 to 41 hours, which has been shown to induce and maintain sleep in the short to long term (up to 4 weeks) treatment of patients with chronic or transient insomnia.Although its hypnotic efficacy has been well characterised against placebo, there are few clinical studies in comparison with established hypnotics, particularly over long term administration. However, preliminary evidence suggests that quazepam 15 to 30mg is as effective as flurazepam and triazolam in usual therapeutic doses, and causes minimal rebound insomnia following its withdrawal, unlike rapidly eliminated benzodiazepines such as triazolam. The lack of rebound phenomena is likely to be attributable to the ‘carryover’ effects occurring after discontinuation of quazepam, which has pharmacologically active metabolites with half-lives of elimination similar to or longer than that of the parent drug. Probably because of the long half-lives of quazepam's metabolites, daytime sedation, fatigue and lethargy are the most frequently reported side effects. These side effects are most intense with the 30mg dose and least with the 7.5mg dose, which has not been studied extensively.Hence, quazepam is an effective hypnotic which may be particularly suitable for short or medium term use in patients in whom withdrawal effects or rebound insomnia may be espectally bothersome. Further definition of certain characteristics of its profile - such as its long term use and potential for development of tolerance or dependence, effects on psychomotor skills, efficacy of the 7.5mg dose, and suitability in elderly patients and patients with chronic organic diseases - will assist in more clearly defining its ultimate place in therapy.Pharmacodynamic StudiesIn comparison with baseline established by the administration of placebo, quazepam in doses of 7.5 to 45mg decreases sleep latency and percentage of stage 1 sleep, and facilitates sleep maintenance as measured by reductions in number of awakenings, wake time after sleep onset and total wake time, and prolonged total sleep time. These effects are usually apparent following a single dose. The percentage of sleep spent in stage 2 increases, whereas that of rapid eye movement (REM) sleep and slow wave sleep (stages 3 and 4) is shortened.Comparative parallel group sleep laboratory studies reveal that the profile of sleep induction and maintenance with quazepam 15 and 30mg is similar to that of flurazepam. Unlike the more rapidly eliminated benzodiazepines triazolam and temazepam, the hypnotic effects of quazepam persist throughout the first night or more of drug withdrawal. Thus, rebound insomnia has not been shown to occur with quazepam, in contrast to the effects of the short acting benzodiazepines. To what extent, if any, that tolerance or dependence may occur with quazepam has not yet been established with certainty.A few studies in small numbers of volunteers in which the effects of single doses of quazepam on psychomotor performance have been investigated, suggest that the 15mg dose produces impairment to a similar extent as placebo and nitrazepam 5mg, but causes less deterioration than triazolam 0.25 to 1mg, nitrazepam 10mg and flunitrazepam 1mg. However, the effects of quazepam 30mg on psychomotor function appear to be equivalent to those of triazolam 0.5mg and nitrazepam 10mg.Animal studies demonstrate that quazepam possesses anxiolytic, anticonvulsant and muscle relaxant activity typical of the benzodiazepine profile, with low toxicity. In antagonising foot-shock aggression and pentylenetetrazol seizures in mice, quazepam was equipotent to flurazepam, but was more potent for inhibition of isoniazid-induced seizures.Selective binding by quazepam to the benzodiazepine receptor type I (BZ1) is characteristic of benzodiazepines with a trifluoroethyl moiety in position 1, and it has been postulated that the lack of ataxia seen with quazepam in animal studies may result from this property. While the biochemical events responsible for hypnotic activity are uncertain, evidence obtained in cats suggests that quazepam may act through facilitation of mechanisms in the lower brain which contribute to physiological EEG synchronisation and sleep induction.Pharmacokinetic PropertiesFollowing oral administration, peak plasma quazepam concentrations of about 30 &mgr;g/L are attained within 2.5 hours, and may be subject to diurnal variation. The drug is distributed to most body tissues including the placenta, and is excreted in breast milk. The apparent volume of distribution of the central compartment is 5.0 L/kg after a night-time dose; this is a reflection of the high lipophilicity of the drug. Quazepam is reported to be greater than 95% bound to plasma proteins.Extensive metabolism of quazepam by substitution of the sulphur group with oxygen yields 2-oxoquazepam (OQ), a pharmacologically active metabolite. OQ is further biotransformed by hydroxylation, or byN-dealkylation toN-desalkyl-2-oxoquazepam (DOQ), which is identical toN-desalkylflurazepam and is also pharmacologically active. The appearance of OQ in plasma is rapid and parallels the absorption of the parent drug. Although the concentration of DOQ is higher in brain than those of quazepam and OQ, in mice hypnotic activity is better correlated with the concentrations of the latter 2 compounds.Quazepam is excreted slowly in the urine and the faeces as metabolites; only trace amounts of the parent drug are recoverable unchanged. The half-lives of elimination of quazepam and OQ in young and elderly subjects are similar (about 27 to 40 hours). However, the half-life of DOQ (about 70 hours) is twice as long in the elderly.Therapeutic TrialsSeveral placebo-controlled studies involving mainly young or elderly outpatients taking single or repeated night-time doses of quazepam 15 or 30mg have clearly demonstrated its hypnotic efficacy, with some residual drowsiness (particularly with the higher dose) the following day, as assessed by the indices of Hypnotic Activity and Sleep Quality, and ‘Freedom from Hangover’. In most trials, quazepam 15mg given for 5 days provided satisfactory sleep in patients with transient or chronic insomnia. However a single 30mg dose was more effective than placebo in presurgical patients on the night prior to surgery. Furthermore, global evaluations by both patients and physicians favoured quazepam over placebo, indicating subjective as well as objective improvement in sleep.Although some comparisons have been made with triazolam, temazepam and flurazepam under sleep laboratory conditions (see Pharmacodynamic Studies), there are few repeat dose and long term studies comparing quazepam with established benzodiazepines in an adequate number of insomniac patients within the clinical setting.Following a single night's administration, quazepam 30mg but not 15mg appeared to be as effective as flunitrazepam 1 and 2mg in evoking sleep in presurgical patients in a single study. In another trial, quazepam 30mg was rated as ‘satisfactory’ treatment by a similar proportion of patients with chronic insomnia as those who were given flurazepam 30mg (70%vs75%, respectively), for a mean duration of 9.5 weeks. Finally, quazepam 15mg was equally efficacious as triazolam 0.5mg in improving sleep induction and maintenance compared with placebo.Side EffectsQuazepam at doses of 15mg is generally well tolerated although a 30mg dose is associated with an increase in side effects, particularly daytime somnolence. Side effects such as drowsiness, fatigue, and daytime somnolence are predictable from its pharmacological profile. The incidence of these effects with quazepam (usually 15mg) is similar to that with placebo (about 25 to 50% of patients), while their intensity is more severe than occurs with temazepam, and comparable to that seen with flurazepam.Quazepam 30mg administration has very rarely been shown to be associated with any of the unexpected side effects - such as hyperexcitability, confusion or amnesia - which have been reported to occur with benzodiazepines of the triazolo group such as triazolam and alprazolam. Moreover, these effects have not occurred with quazepam 15mg. Further, quazepam withdrawal has not been shown to result in rebound insomnia which may occur following the withdrawal of rapidly eliminated benzodiazepine hypnotics. Following repeat dose administration these effects may become attenuated. Ataxia has been reported infrequently with quazepam.Dosage and AdministrationQuazepam 15mg given orally prior to retiring to bed provides satisfactory hypnotic effects in patients with chronic or transient insomnia. In elderly patients it is possible that 7.5mg may be a more appropriate dose, but this has yet to be determined.Since the effects of quazepam on psychomotor skills and cognitive performance have not been adequately characterised, it seems prudent to caution patients against performing such skills while receiving quazepam therapy. Patients should also avoid concomitant use of alcohol with quazepam, as is generally recommended with all hypnotic agents.
ISSN:0012-6667
出版商:ADIS
年代:1988
数据来源: ADIS
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4. |
GnRH Agonists and AntagonistsCurrent Clinical Status |
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Drugs,
Volume 35,
Issue 1,
1988,
Page 63-82
Marco Filicori,
Carlo Flamigni,
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摘要:
Gonadotrophin-releasing hormone (GnRH) analogues offer a novel approach for the non-steroidal manipulation of the reproductive endocrine axis. GnRH agonists are now effectively employed in the management of precocious puberty, prostate and breast cancer, endometriosis, uterine leiomyoma, polycystic ovarian disease, and various other disorders. Unfortunately, contraceptive applications of GnRH agonists have been disappointing. The availability of slow release depot formulations of GnRH agonists, and the development of GnRH antagonists may further optimise and extend the clinical application of these compounds.
ISSN:0012-6667
出版商:ADIS
年代:1988
数据来源: ADIS
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5. |
Alopecia and HirsutiesCurrent Concepts in Pathogenesis and Management |
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Drugs,
Volume 35,
Issue 1,
1988,
Page 83-91
Julian H. Barth,
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摘要:
Hirsuties and androgenic alopecia are the patterns of hair growth in women which develop in a similar manner to that normally seen in men. This process is mediated by androgens. It may be due to increased hormone production or increased target organ sensitivity.The majority of patients with hirsuties may be adequately managed with a careful explanation of their condition and advice about depilatory techniques. Some will benefit from a course of systemic antiandrogen therapy, but hair growth will resume on cessation of therapy.There have been few objective studies to evaluate the benefits of antiandrogen therapy in female baldness and none with minoxidil.
ISSN:0012-6667
出版商:ADIS
年代:1988
数据来源: ADIS
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