Clitidine

Background: Clonidine was originally used to lower blood pressure. It acts on the central nervous system and may reduce withdrawal symptoms in various addictive behaviours, including tobacco use. Objectives: The aim of this review is to determine clonidine's effectiveness in helping smokers to quit. Search strategy: We searched the Cochrane Tobacco Addiction Group trials register for trials of clonidine. Date of the most recent search: May 2004. Selection criteria: We considered randomized trials of clonidine versus placebo with a smoking cessation endpoint assessed at least 12 weeks following the end of treatment. Data collection and analysis: We extracted data in duplicate on the type of subjects, the dose and duration of clonidine therapy, the outcome measures, method of randomization, and completeness of follow up. The main outcome measure was abstinence from smoking after at least 12 weeks follow up in patients smoking at baseline. We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed effect model. Main results: Six trials met the inclusion criteria. There were three trials of oral, and three of transdermal clonidine. Some form of behavioural counselling was offered to all participants in five of the six trials. There was a statistically significant effect of clonidine in one of these trials. The pooled odds ratio for success with clonidine versus placebo was 1.89 (95% confidence interval 1.30 to 2.74). There was a high incidence of dose-dependent side-effects, particularly dry mouth and sedation. Reviewers' conclusions: Based on a small number of trials, in which there are potential sources of bias, clonidine is effective in promoting smoking cessation. Prominent side-effects limit the usefulness of clonidine for smoking cessation.

Clonidine, an α(2)-adrenergic agonist, is approved in the US as an extended-release (XR) tablet for the treatment of attention-deficit hyperactivity disorder (ADHD) in children and adolescents (aged 6-17 years). In two, randomized, double-blind, multicenter, phase III trials of 8 weeks' duration, clonidine XR improved the symptoms of ADHD in children and adolescents. Significantly greater reductions from baseline in ADHD rating scale IV (ADHD-RS-IV) total scores at week 5 (primary endpoint) were achieved by recipients of clonidine XR 0.2 and 0.4 mg/day monotherapy than by recipients of placebo. When added to patients' normal stimulant regimen, significantly greater reductions from baseline in ADHD-RS-IV total scores at week 5 (primary endpoint) were achieved with a flexible dose of clonidine XR 0.1-0.4 mg/day than with placebo. Symptomatic improvement of ADHD was achieved following 2 weeks' treatment with clonidine XR. In both trials, significantly greater reductions from baseline in ADHD-RS-IV total scores were apparent at week 2 onwards for recipients of clonidine XR than for recipients of placebo. Clonidine XR was generally well tolerated as monotherapy and as adjunctive therapy with stimulant regimens in clinical trials in children and adolescents.

Background: Clonidine was originally used to lower blood pressure. It acts on the central nervous system and may reduce withdrawal symptoms in various addictive behaviours, including tobacco use. Objectives: The aim of this review is to determine clonidine's effectiveness in helping smokers to quit. Search strategy: We searched the Cochrane Tobacco Addiction Group trials register. Date of the most recent search: October 1998. Selection criteria: We considered randomised trials of clonidine versus placebo with a smoking cessation endpoint assessed at least 12 weeks following the end of treatment. Data collection and analysis: We extracted data in duplicate on the type of subjects, the dose and duration of clonidine therapy, the outcome measures, method of randomisation, and completeness of follow-up. The main outcome measure was abstinence from smoking after at least twelve weeks follow-up in patients smoking at baseline. We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed effects model. Main results: Six trials met the inclusion criteria. There were three trials of oral, and three of transdermal clonidine. Some form of behavioural counselling was offered to all participants in five of the six trials. There was a statistically significant effect of clonidine in one of these trials. The pooled odds ratio for success with clonidine vs placebo was 1.89 (95% confidence interval 1.30 to 2.74). There was a high incidence of dose-dependent side-effects, particularly dry mouth and sedation. Reviewer's conclusions: Based on a small number of trials, in which there are potential sources of bias, clonidine is effective in promoting smoking cessation. Prominent side-effects limit the usefulness of clonidine for smoking cessation.