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Safe Drug (safe + drug)
Selected AbstractsEffect of serotonin 1A agonist tandospirone on depression symptoms in senile patients with dementiaHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 4 2002Yutaka Masuda Abstract The treatment of depression in senile patients with dementia is difficult with the drugs used formerly. The effects of a new anxiolytic drug, tandospirone, were investigated on depression symptoms in nine senile patients with dementia using Hamilton Depression Rating Scale (HAM-D) items. Tandospirone improved the symptoms, especially the depressive mood, agitation and anxiety, although a slight gastrointestinal symptom was found in one patient. The findings in the present study may suggest that tandospirone is a useful and comparatively safe drug for depression symptoms in senile patients with dementia. Copyright © 2002 John Wiley & Sons, Ltd. [source] Pretreatment with sufentanil reduces myoclonus after etomidateACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2003L. Hueter Background: Myoclonic movements are a common problem during the induction of general anesthesia with etomidate. We investigated the influence of pretreatment with the opioid sufentanil on the incidence of etomidate-induced myoclonus. Methods: Forty female patients (ASA physical status I,III) were randomly assigned to receive double-blinded either 0.3 µg kg,1 of sufentanil or placebo 150 s before the induction of sleep with 0.3 mg kg,1 of etomidate. The patients were observed for any myoclonic movement. Grade of dizziness, breathing frequency, non-invasive blood pressure and heart rate were measured during the study period. Results: None of the 20 patients receiving sufentanil had myoclonic movements after the administration of etomidate, whereas 16 patients in the placebo group (80%) experienced such movements (P<0.01). No cases of apnoea before induction of sleep were seen in the sufentanil group. Conclusion: Sufentanil 0.3 µg kg,1 is an effective and safe drug to reduce myoclonus after etomidate without causing any harmful side-effect. [source] Atorvastatin in dyslipidaemia of the nephrotic syndromeNEPHROLOGY, Issue 2 2003Pedro VALDIVIELSO SUMMARY: The combined dyslipidaemia that accompanies the nephrotic syndrome increases the cardiovascular risk and appears to worsen long-term renal function. Our aim was to determine the efficacy and safety of 10 mg atorvastatin in the control of dyslipidaemia in these patients. We carried out a prospective, open, 6 month study of 10 patients with primary or secondary nephrotic syndrome (proteinuria >3.5 g/day, hypoalbuminaemia, oedema and hyperlipidaemia). The changes in lipids and plasma lipoproteins were measured, as well as the safety profile (transaminases, creatine phosphokinase, fibrinogen and antithrombin III activity) and parameters of renal function. The addition of 10 mg atorvastatin daily for 6 months resulted in a 41% reduction in low density lipoprotein (LDL) cholesterol and 31% in triglycerides (both P < 0.05), and a 15% increase in high density lipoprotein (HDL) cholesterol (NS). The drug was well tolerated and there was no change in the safety profile or deterioration in renal function. In fact, the levels of proteinuria fell in all but one patient (6.2 ± 2.6 vs 4.8 ± 2.5 g/24 h; P < 0.05). Atorvastatin, at the above dose, and for the time used proved to be a safe drug that effectively reduced dyslipidaemia in patients with nephrotic syndrome. [source] Cocaine-related admissions to an intensive care unit: a five-year study of incidence and outcomesANAESTHESIA, Issue 2 2010S. Galvin Summary Cocaine misuse is increasing and it is evidently considered a relatively safe drug of abuse in Ireland. To address this perception, we reviewed the database of an 18-bed Dublin intensive care unit, covering all admissions from 2003 to 2007. We identified cocaine-related cases, measuring hospital mortality and long-term survival in early 2009. Cocaine-related admissions increased from around one annually in 2003,05 to 10 in 2007. Their median (IQR [range]) age was 25 (21,35 [17,47]) years and 78% were male. The median (IQR [range]) APACHE II score was 16 (11,27 [5,36]) and length of intensive care stay was 5 (3,9 [1,16]) days. Ten patients died during their hospital stay. A further five had died by the time of follow-up, a median of 24 months later. One was untraceable. Cocaine toxicity necessitating intensive care is increasingly common in Dublin. Hospital mortality in this series was 52%. These findings may help to inform public attitudes to cocaine. [source] The clinical use of buprenorphine in opiate addiction: evidence and practiceACTA NEUROPSYCHIATRICA, Issue 5 2004Fergus D. Law Buprenorphine is a partial ,-opioid receptor agonist that is being increasingly used in clinical practice in the treatment of opioid dependence in the UK, USA, and, elsewhere. Its unique pharmacological properties mean it is a relatively safe drug, it can be given by alternate day dispensing, and it is associated with relatively mild symptoms on withdrawal. The interpretation of the research literature on buprenorphine is however, complex, and often appears to be in conflict with how buprenorphine is used in clinical practice. This article describes these apparent contradictions, their likely explanations, and how these may further inform our clinical practice. The article also describes the clinically relevant pharmacological properties of buprenorphine, compares it to methadone, relates the evidence to clinical experience, and provides practical advice on how to manage the most common clinical techniques. The best quality evidence suggests that very rapid buprenorphine induction is not associated with a higher drop-out rate than methadone, that buprenorphine is probably as good as methadone for maintenance treatment, and is superior to methadone and ,-2 adrenergic agonists for detoxification. However, buprenorphine cannot yet be considered the ,gold standard' treatment for opiate dependence because of the higher drop-out rates that may occur on induction using current techniques, its high-cost relative to methadone, and because the place of buprenorphine in treatment is still continuing to evolve. [source] Therapeutics for alcoholism: what's the future?DRUG AND ALCOHOL REVIEW, Issue 1 2007ANDREW J. LAWRENCE Abstract As with other addictions, human alcoholism is characterised as a chronically relapsing condition. Consequently, the therapeutic goal is the development of clinically effective, safe drugs that promote high adherence rates and prevent relapse. These products can then be used in conjunction with psychosocial approaches. In this review, preclinical studies are highlighted that indicate the mechanism of action of currently used anti-craving medications or demonstrate the potential of novel pharmacological agents for the treatment of alcohol use disorders. While current pharmacological strategies are far from ideal, there are a number of candidate molecules that may ultimately be developed into therapeutic agents. In addition, prescribing clinicians should also consider strategies such as combinations of various drugs to aid in the regulation of aberrant alcohol consumption. [source] Guide to drug porphyrogenicity prediction and drug prescription in the acute porphyriasBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 5 2007Stig Thunell What is already known about this subject ,,Many drug safety lists for acute porphyrias, largely based on anecdotal evidence, are put forward, but no methods or rationale for the risk estimates are given. ,,Many unexplained discrepancies between the lists exist. What this study adds ,,A standardized method for assessment of the risk that a certain drug may activate these diseases has been developed. ,,It also allows risk assessments for drugs lacking porphyria related clinical experience. ,,About one thousand therapeutic drugs have been classified with regard to porphyrogenicity by the proposed method, which is most valuable for the care of porphyria patients. Aims This paper addresses two common problems in the care of carriers of acute porphyria: the choice of safe drugs for pharmacotherapy and the strategy to apply when potentially unsafe drugs cannot be avoided. Methods and results A technique is presented for prediction of risk that a certain drug may activate the disease in a gene carrier for acute porphyria. It is based on a model explaining the clinical manifestations as a result of the acute overloading of a deficient enzyme within the hepatic heme biosynthetic chain. The capacity of the drug for induction of the rate-limiting enzyme in heme biosynthesis, e.g. housekeeping 5-aminolevulinate synthase (ALAS1), is assessed by critical appraisal of reports of the outcomes of clinical use of the drug, and by theoretical criteria. The assessment occurs within the frame of a flow-scheme employing variables of increasing specificity, i.e. endocrine properties of the drug, structure and metabolism pointing to affinity to cytochrome P450, hepatic load in therapeutic use, recognized affinity to major CYP species, capacity for CYP-induction or irreversible inhibition, and capacity to activate or modulate the transduction mechanisms of nuclear receptors affecting ALAS1-gene transcription. It is proposed that in the absence of a safer alternative, an urgently needed drug not should be withheld on the grounds of potential porphyrogenicity. After risk-benefit analysis it should be prescribed, but individualized preventive measures adapted to patient vulnerability may be needed. Conclusions About 1000 therapeutic drugs categorized with regard to porphyrogenicity by the technique proposed are presented on the internet (http://www.drugs-porphyria.org). [source] | |||||||||||||||||||