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.

BACKGROUND: Brutons tyrosine kinase (BTK) is important in B-cell signalling. Efficacy has been reported for BTK inhibitors (BTKi) in human autoimmune diseases. Canine pemphigus foliaceus (cPF) is one of the most common canine autoimmune skin diseases. OBJECTIVES: To determine the safety and efficacy of the BTKi PRN1008 in the treatment of cPF. ANIMALS: Four privately owned dogs. METHODS AND MATERIALS: Four dogs diagnosed with PF were administered BTKi PRN1008. Initial dosages approximated to 15 mg/kg once daily, increased to twice daily if inadequate response was seen. Treatment continued for 20 weeks, attempting to decrease to every other day. Dogs were monitored with complete blood counts, serum biochemistry panels and urinalyses, and evaluated with a modified version of a validated human Pemphigus Disease Activity Index (cPDAI). Serum anti-desmocollin-1 (DSC-1) and desmoglein-1 (DSG-1) immunoglobulin (Ig)G titres were performed before and after the treatment period. Drug bound to target was measured in peripheral blood mononuclear cells (PBMC). RESULTS: All four dogs showed reduction in lesions and cPDAI score during the first two weeks of treatment. Three dogs continued to improve and sustained near complete remission by 20 weeks, at which point three responses were considered good and one fair. Final daily dosages were in the range 17-33 mg/kg. Anti-DSC-1 IgG titre decreased dramatically in one dog, was undetectable in two and was uninterpretable in one dog. No dogs had detectable IgG to DSG1. A possible adverse event occurred in one dog. CONCLUSIONS AND CLINICAL IMPORTANCE: BTKi PRN1008 monotherapy may have some beneficial effects in some cases of cPF.