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The Cochrane Database of Systematic... Mar 2014Smokers have a substantially increased risk of postoperative complications. Preoperative smoking intervention may be effective in decreasing this incidence, and surgery... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Smokers have a substantially increased risk of postoperative complications. Preoperative smoking intervention may be effective in decreasing this incidence, and surgery may constitute a unique opportunity for smoking cessation interventions.
OBJECTIVES
The objectives of this review are to assess the effect of preoperative smoking intervention on smoking cessation at the time of surgery and 12 months postoperatively, and on the incidence of postoperative complications.
SEARCH METHODS
We searched the Cochrane Tobacco Addiction Group Specialized Register in January 2014.
SELECTION CRITERIA
Randomized controlled trials that recruited people who smoked prior to surgery, offered a smoking cessation intervention, and measured preoperative and long-term abstinence from smoking or the incidence of postoperative complications or both outcomes.
DATA COLLECTION AND ANALYSIS
The review authors independently assessed studies to determine eligibility, and discussed the results between them.
MAIN RESULTS
Thirteen trials enrolling 2010 participants met the inclusion criteria. One trial did not report cessation as an outcome. Seven reported some measure of postoperative morbidity. Most studies were judged to be at low risk of bias but the overall quality of evidence was moderate due to the small number of studies contributing to each comparison.Ten trials evaluated the effect of behavioural support on cessation at the time of surgery; nicotine replacement therapy (NRT) was offered or recommended to some or all participants in eight of these. Two trials initiated multisession face-to-face counselling at least four weeks before surgery and were classified as intensive interventions, whilst seven used a brief intervention. One further study provided an intensive intervention to both groups, with the intervention group additionally receiving a computer-based scheduled reduced smoking intervention. One placebo-controlled trial examined the effect of varenicline administered one week preoperatively followed by 11 weeks postoperative treatment, and one placebo-controlled trial examined the effect of nicotine lozenges from the night before surgery as an adjunct to brief counselling at the preoperative evaluation. There was evidence of heterogeneity between the effects of trials using intensive and brief interventions, so we pooled these separately. An effect on cessation at the time of surgery was apparent in both subgroups, but the effect was larger for intensive intervention (pooled risk ratio (RR) 10.76; 95% confidence interval (CI) 4.55 to 25.46, two trials, 210 participants) than for brief interventions (RR 1.30; 95% CI 1.16 to 1.46, 7 trials, 1141 participants). A single trial did not show evidence of benefit of a scheduled reduced smoking intervention. Neither nicotine lozenges nor varenicline were shown to increase cessation at the time of surgery but both had wide confidence intervals (RR 1.34; 95% CI 0.86 to 2.10 (1 trial, 46 participants) and RR 1.49; 95% CI 0.98 to 2.26 (1 trial, 286 participants) respectively). Four of these trials evaluated long-term smoking cessation and only the intensive intervention retained a significant effect (RR 2.96; 95% CI 1.57 to 5.55, 2 trials, 209 participants), whilst there was no evidence of a long-term effect following a brief intervention (RR 1.09; 95% CI 0.68 to 1.75, 2 trials, 341 participants). The trial of varenicline did show a significant effect on long-term smoking cessation (RR 1.45; 95% CI 1.01 to 2.07, 1 trial, 286 participants).Seven trials examined the effect of smoking intervention on postoperative complications. As with smoking outcomes, there was evidence of heterogeneity between intensive and brief behavioural interventions. In subgroup analyses there was a significant effect of intensive intervention on any complications (RR 0.42; 95% CI 0.27 to 0.65, 2 trials, 210 participants) and on wound complications (RR 0.31; 95% CI 0.16 to 0.62, 2 trials, 210 participants). For brief interventions, where the impact on smoking had been smaller, there was no evidence of a reduction in complications (RR 0.92; 95% CI 0.72 to 1.19, 4 trials, 493 participants) for any complication (RR 0.99; 95% CI 0.70 to 1.40, 3 trials, 325 participants) for wound complications. The trial of varenicline did not detect an effect on postoperative complications (RR 0.94; 95% CI 0.52 to 1.72, 1 trial, 286 participants).
AUTHORS' CONCLUSIONS
There is evidence that preoperative smoking interventions providing behavioural support and offering NRT increase short-term smoking cessation and may reduce postoperative morbidity. One trial of varenicline begun shortly before surgery has shown a benefit on long-term cessation but did not detect an effect on early abstinence or on postoperative complications. The optimal preoperative intervention intensity remains unknown. Based on indirect comparisons and evidence from two small trials, interventions that begin four to eight weeks before surgery, include weekly counselling and use NRT are more likely to have an impact on complications and on long-term smoking cessation.
Topics: Benzazepines; Humans; Nicotine; Nicotinic Agonists; Postoperative Complications; Preoperative Care; Quinoxalines; Randomized Controlled Trials as Topic; Smoking; Smoking Cessation; Tobacco Use Cessation Devices; Varenicline
PubMed: 24671929
DOI: 10.1002/14651858.CD002294.pub4 -
The Cochrane Database of Systematic... Jan 2014There are at least three reasons to believe antidepressants might help in smoking cessation. Firstly, nicotine withdrawal may produce depressive symptoms or precipitate... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
There are at least three reasons to believe antidepressants might help in smoking cessation. Firstly, nicotine withdrawal may produce depressive symptoms or precipitate a major depressive episode and antidepressants may relieve these. Secondly, nicotine may have antidepressant effects that maintain smoking, and antidepressants may substitute for this effect. Finally, some antidepressants may have a specific effect on neural pathways (e.g. inhibiting monoamine oxidase) or receptors (e.g. blockade of nicotinic-cholinergic receptors) underlying nicotine addiction.
OBJECTIVES
The aim of this review is to assess the effect and safety of antidepressant medications to aid long-term smoking cessation. The medications include bupropion; doxepin; fluoxetine; imipramine; lazabemide; moclobemide; nortriptyline; paroxetine; S-Adenosyl-L-Methionine (SAMe); selegiline; sertraline; St. John's wort; tryptophan; venlafaxine; and zimeledine.
SEARCH METHODS
We searched the Cochrane Tobacco Addiction Group Specialised Register which includes reports of trials indexed in the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, and PsycINFO, and other reviews and meeting abstracts, in July 2013.
SELECTION CRITERIA
We considered randomized trials comparing antidepressant medications to placebo or an alternative pharmacotherapy for smoking cessation. We also included trials comparing different doses, using pharmacotherapy to prevent relapse or re-initiate smoking cessation or to help smokers reduce cigarette consumption. We excluded trials with less than six months follow-up.
DATA COLLECTION AND ANALYSIS
We extracted data and assessed risk of bias using standard methodological procedures expected by the Cochrane Collaboration.The main outcome measure was abstinence from smoking after at least six months follow-up in patients smoking at baseline, expressed as a risk ratio (RR). We used the most rigorous definition of abstinence available in each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed-effect model.
MAIN RESULTS
Twenty-four new trials were identified since the 2009 update, bringing the total number of included trials to 90. There were 65 trials of bupropion and ten trials of nortriptyline, with the majority at low or unclear risk of bias. There was high quality evidence that, when used as the sole pharmacotherapy, bupropion significantly increased long-term cessation (44 trials, N = 13,728, risk ratio [RR] 1.62, 95% confidence interval [CI] 1.49 to 1.76). There was moderate quality evidence, limited by a relatively small number of trials and participants, that nortriptyline also significantly increased long-term cessation when used as the sole pharmacotherapy (six trials, N = 975, RR 2.03, 95% CI 1.48 to 2.78). There is insufficient evidence that adding bupropion (12 trials, N = 3487, RR 1.9, 95% CI 0.94 to 1.51) or nortriptyline (4 trials, N = 1644, RR 1.21, 95% CI 0.94 to 1.55) to nicotine replacement therapy (NRT) provides an additional long-term benefit. Based on a limited amount of data from direct comparisons, bupropion and nortriptyline appear to be equally effective and of similar efficacy to NRT (bupropion versus nortriptyline 3 trials, N = 417, RR 1.30, 95% CI 0.93 to 1.82; bupropion versus NRT 8 trials, N = 4096, RR 0.96, 95% CI 0.85 to 1.09; no direct comparisons between nortriptyline and NRT). Pooled results from four trials comparing bupropion to varenicline showed significantly lower quitting with bupropion than with varenicline (N = 1810, RR 0.68, 95% CI 0.56 to 0.83). Meta-analyses did not detect a significant increase in the rate of serious adverse events amongst participants taking bupropion, though the confidence interval only narrowly missed statistical significance (33 trials, N = 9631, RR 1.30, 95% CI 1.00 to 1.69). There is a risk of about 1 in 1000 of seizures associated with bupropion use. Bupropion has been associated with suicide risk, but whether this is causal is unclear. Nortriptyline has the potential for serious side-effects, but none have been seen in the few small trials for smoking cessation.There was no evidence of a significant effect for selective serotonin reuptake inhibitors on their own (RR 0.93, 95% CI 0.71 to 1.22, N = 1594; 2 trials fluoxetine, 1 paroxetine, 1 sertraline) or as an adjunct to NRT (3 trials of fluoxetine, N = 466, RR 0.70, 95% CI 0.64 to 1.82). Significant effects were also not detected for monoamine oxidase inhibitors (RR 1.29, 95% CI 0.93 to 1.79, N = 827; 1 trial moclobemide, 5 selegiline), the atypical antidepressant venlafaxine (1 trial, N = 147, RR 1.22, 95% CI 0.64 to 2.32), the herbal therapy St John's wort (hypericum) (2 trials, N = 261, RR 0.81, 95% CI 0.26 to 2.53), or the dietary supplement SAMe (1 trial, N = 120, RR 0.70, 95% CI 0.24 to 2.07).
AUTHORS' CONCLUSIONS
The antidepressants bupropion and nortriptyline aid long-term smoking cessation. Adverse events with either medication appear to rarely be serious or lead to stopping medication. Evidence suggests that the mode of action of bupropion and nortriptyline is independent of their antidepressant effect and that they are of similar efficacy to nicotine replacement. Evidence also suggests that bupropion is less effective than varenicline, but further research is needed to confirm this finding. Evidence suggests that neither selective serotonin reuptake inhibitors (e.g. fluoxetine) nor monoamine oxidase inhibitors aid cessation.
Topics: Anti-Anxiety Agents; Antidepressive Agents; Bupropion; Humans; Nortriptyline; Randomized Controlled Trials as Topic; Selective Serotonin Reuptake Inhibitors; Smoking; Smoking Cessation; Tobacco Use Cessation Devices
PubMed: 24402784
DOI: 10.1002/14651858.CD000031.pub4 -
The Cochrane Database of Systematic... May 2013Smoking is the leading preventable cause of illness and premature death worldwide. Some medications have been proven to help people to quit, with three licensed for this... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Smoking is the leading preventable cause of illness and premature death worldwide. Some medications have been proven to help people to quit, with three licensed for this purpose in Europe and the USA: nicotine replacement therapy (NRT), bupropion, and varenicline. Cytisine (a treatment pharmacologically similar to varenicline) is also licensed for use in Russia and some of the former socialist economy countries. Other therapies, including nortriptyline, have also been tested for effectiveness.
OBJECTIVES
How do NRT, bupropion and varenicline compare with placebo and with each other in achieving long-term abstinence (six months or longer)? How do the remaining treatments compare with placebo in achieving long-term abstinence? How do the risks of adverse and serious adverse events (SAEs) compare between the treatments, and are there instances where the harms may outweigh the benefits?
METHODS
The overview is restricted to Cochrane reviews, all of which include randomised trials. Participants are usually adult smokers, but we exclude reviews of smoking cessation for pregnant women and in particular disease groups or specific settings. We cover nicotine replacement therapy (NRT), antidepressants (bupropion and nortriptyline), nicotine receptor partial agonists (varenicline and cytisine), anxiolytics, selective type 1 cannabinoid receptor antagonists (rimonabant), clonidine, lobeline, dianicline, mecamylamine, Nicobrevin, opioid antagonists, nicotine vaccines, and silver acetate. Our outcome for benefit is continuous or prolonged abstinence at least six months from the start of treatment. Our outcome for harms is the incidence of serious adverse events associated with each of the treatments. We searched the Cochrane Database of Systematic Reviews (CDSR) in The Cochrane Library, for any reviews with 'smoking' in the title, abstract or keyword fields. The last search was conducted in November 2012. We assessed methodological quality using a revised version of the AMSTAR scale. For NRT, bupropion and varenicline we conducted network meta-analyses, comparing each with the others and with placebo for benefit, and varenicline and bupropion for risks of serious adverse events.
MAIN RESULTS
We identified 12 treatment-specific reviews. The analyses covered 267 studies, involving 101,804 participants. Both NRT and bupropion were superior to placebo (odds ratios (OR) 1.84; 95% credible interval (CredI) 1.71 to 1.99, and 1.82; 95% CredI 1.60 to 2.06 respectively). Varenicline increased the odds of quitting compared with placebo (OR 2.88; 95% CredI 2.40 to 3.47). Head-to-head comparisons between bupropion and NRT showed equal efficacy (OR 0.99; 95% CredI 0.86 to 1.13). Varenicline was superior to single forms of NRT (OR 1.57; 95% CredI 1.29 to 1.91), and to bupropion (OR 1.59; 95% CredI 1.29 to 1.96). Varenicline was more effective than nicotine patch (OR 1.51; 95% CredI 1.22 to 1.87), than nicotine gum (OR 1.72; 95% CredI 1.38 to 2.13), and than 'other' NRT (inhaler, spray, tablets, lozenges; OR 1.42; 95% CredI 1.12 to 1.79), but was not more effective than combination NRT (OR 1.06; 95% CredI 0.75 to 1.48). Combination NRT also outperformed single formulations. The four categories of NRT performed similarly against each other, apart from 'other' NRT, which was marginally more effective than NRT gum (OR 1.21; 95% CredI 1.01 to 1.46). Cytisine (a nicotine receptor partial agonist) returned positive findings (risk ratio (RR) 3.98; 95% CI 2.01 to 7.87), without significant adverse events or SAEs. Across the 82 included and excluded bupropion trials, our estimate of six seizures in the bupropion arms versus none in the placebo arms was lower than the expected rate (1:1000), at about 1:1500. SAE meta-analysis of the bupropion studies demonstrated no excess of neuropsychiatric (RR 0.88; 95% CI 0.31 to 2.50) or cardiovascular events (RR 0.77; 95% CI 0.37 to 1.59). SAE meta-analysis of 14 varenicline trials found no difference between the varenicline and placebo arms (RR 1.06; 95% CI 0.72 to 1.55), and subgroup analyses detected no significant excess of neuropsychiatric events (RR 0.53; 95% CI 0.17 to 1.67), or of cardiac events (RR 1.26; 95% CI 0.62 to 2.56). Nortriptyline increased the chances of quitting (RR 2.03; 95% CI 1.48 to 2.78). Neither nortriptyline nor bupropion were shown to enhance the effect of NRT compared with NRT alone. Clonidine increased the chances of quitting (RR 1.63; 95% CI 1.22 to 2.18), but this was offset by a dose-dependent rise in adverse events. Mecamylamine in combination with NRT may increase the chances of quitting, but the current evidence is inconclusive. Other treatments failed to demonstrate a benefit compared with placebo. Nicotine vaccines are not yet licensed for use as an aid to smoking cessation or relapse prevention. Nicobrevin's UK license is now revoked, and the manufacturers of rimonabant, taranabant and dianicline are no longer supporting the development or testing of these treatments.
AUTHORS' CONCLUSIONS
NRT, bupropion, varenicline and cytisine have been shown to improve the chances of quitting. Combination NRT and varenicline are equally effective as quitting aids. Nortriptyline also improves the chances of quitting. On current evidence, none of the treatments appear to have an incidence of adverse events that would mitigate their use. Further research is warranted into the safety of varenicline and into cytisine's potential as an effective and affordable treatment, but not into the efficacy and safety of NRT.
Topics: Adult; Alkaloids; Antidepressive Agents, Second-Generation; Azocines; Benzazepines; Bupropion; Humans; Nicotinic Agonists; Nortriptyline; Quinolizines; Quinoxalines; Randomized Controlled Trials as Topic; Review Literature as Topic; Smoking; Smoking Cessation; Tobacco Use Cessation Devices; Varenicline
PubMed: 23728690
DOI: 10.1002/14651858.CD009329.pub2 -
The Cochrane Database of Systematic... Feb 2013Individuals with schizophrenia smoke more heavily than the general population and this contributes to their higher morbidity and mortality from smoking-related... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Individuals with schizophrenia smoke more heavily than the general population and this contributes to their higher morbidity and mortality from smoking-related illnesses. It remains unclear what interventions can help them to quit or to reduce smoking.
OBJECTIVES
To evaluate the benefits and harms of different treatments for nicotine dependence in schizophrenia.
SEARCH METHODS
We searched electronic databases including MEDLINE, EMBASE and PsycINFO from inception to October 2012, and the Cochrane Tobacco Addiction Group Specialized Register in November 2012.
SELECTION CRITERIA
We included randomised trials for smoking cessation or reduction, comparing any pharmacological or non-pharmacological intervention with placebo or with another therapeutic control in adult smokers with schizophrenia or schizoaffective disorder.
DATA COLLECTION AND ANALYSIS
Two reviewers independently assessed the eligibility and quality of trials, as well as extracted data. Outcome measures included smoking abstinence, reduction in the amount smoked and any change in mental state. We extracted abstinence and reduction data at the end of treatment and at least six months after the intervention. We used the most rigorous definition of abstinence or reduction and biochemically validated data where available. We noted any reported adverse events. Where appropriate, we pooled data using a random-effects model.
MAIN RESULTS
We included 34 trials (16 trials of cessation; nine trials of reduction; one trial of relapse prevention; eight trials that reported smoking outcomes for interventions aimed at other purposes). Seven trials compared bupropion with placebo; meta-analysis showed that cessation rates after bupropion were significantly higher than placebo at the end of treatment (seven trials, N = 340; risk ratio [RR] 3.03; 95% confidence interval [CI] 1.69 to 5.42) and after six months (five trials, N = 214, RR 2.78; 95% CI 1.02 to 7.58). There were no significant differences in positive, negative and depressive symptoms between bupropion and placebo groups. There were no reports of major adverse events such as seizures with bupropion.Smoking cessation rates after varenicline were significantly higher than placebo, at the end of treatment (2 trials, N = 137; RR 4.74, 95% CI 1.34 to 16.71). Only one trial reported follow-up at six months and the CIs were too wide to provide evidence of a sustained effect (one trial, N = 128, RR 5.06, 95% CI 0.67 to 38.24). There were no significant differences in psychiatric symptoms between the varenicline and placebo groups. Nevertheless, there were reports of suicidal ideation and behaviours from two people on varenicline.Two studies reported that contingent reinforcement (CR) with money may increase smoking abstinence rates and reduce the level of smoking in patients with schizophrenia. However, it is uncertain whether these benefits can be maintained in the longer term. There was no evidence of benefit for the few trials of other pharmacological therapies (including nicotine replacement therapy (NRT)) and psychosocial interventions in helping smokers with schizophrenia to quit or reduce smoking.
AUTHORS' CONCLUSIONS
Bupropion increases smoking abstinence rates in smokers with schizophrenia, without jeopardizing their mental state. Varenicline may also improve smoking cessation rates in schizophrenia, but its possible psychiatric adverse effects cannot be ruled out. CR may help this group of patients to quit and reduce smoking in the short term. We failed to find convincing evidence that other interventions have a beneficial effect on smoking in schizophrenia.
Topics: Adult; Antidepressive Agents, Second-Generation; Benzazepines; Bupropion; Humans; Nicotine; Nicotinic Agonists; Quinoxalines; Randomized Controlled Trials as Topic; Reinforcement, Psychology; Schizophrenia; Schizophrenic Psychology; Smoking Cessation; Smoking Prevention; Tobacco Use Cessation Devices; Varenicline
PubMed: 23450574
DOI: 10.1002/14651858.CD007253.pub3 -
Addiction (Abingdon, England) Feb 2013To update our prior meta-analysis that showed past major depression (MD+) to be unrelated to smoking cessation outcome. (Meta-Analysis)
Meta-Analysis Review
AIMS
To update our prior meta-analysis that showed past major depression (MD+) to be unrelated to smoking cessation outcome.
METHODS
Eligible trials included 14 from our original review and 28 identified through an updated systematic review (2000-2009). We coded for assessment of past MD, exclusion for recent MD episode (MDE; ≤6 months versus no exclusion), duration/modality of cognitive behavioral treatment (CBT; face-to-face versus self-help) and other factors. To minimize influence of experimental treatments that may selectively benefit MD+ smokers we analyzed placebo/lowest intensity control arms only. Study-specific ORs for the effect of past MD on short-term (≤3 months) and long-term (≥6 months) abstinence were estimated and combined using random effects. Two-way interaction models of past MD with study methodology and treatment factors were used to evaluate hypothesized moderators of the past MD-abstinence association.
RESULTS
MD+ smokers had 17% lower odds of short-term abstinence (n = 35, OR = 0.83, 95% CI = 0.72-0.95, P = 0.009) and 19% lower odds of long-term abstinence (n = 38, OR = 0.81, 95% CI = 0.67-0.97, P = 0.023) than MD- smokers after excluding the sole study of varenicline because of its antidepressant properties. The association between past MD and abstinence was affected by methodological (recent MDE exclusion, type of MD assessment) and treatment (CBT modality) factors.
CONCLUSIONS
Past major depression has a modest adverse effect on abstinence during and after smoking cessation treatment. An increased focus on the identification of effective treatments or treatment adaptations that eliminate this disparity in smoking cessation for MD+ smokers is needed.
Topics: Cognitive Behavioral Therapy; Depressive Disorder, Major; Humans; Smoking; Smoking Cessation; Smoking Prevention; Time Factors; Treatment Outcome
PubMed: 23072580
DOI: 10.1111/add.12009 -
Annals of Medicine Sep 2012This review compared the effect of high-dose nicotine replacement therapy (NRT) and combinations of NRT for increasing smoking abstinence rates compared to standard-dose... (Comparative Study)
Comparative Study Meta-Analysis Review
Comparisons of high-dose and combination nicotine replacement therapy, varenicline, and bupropion for smoking cessation: a systematic review and multiple treatment meta-analysis.
AIM
This review compared the effect of high-dose nicotine replacement therapy (NRT) and combinations of NRT for increasing smoking abstinence rates compared to standard-dose NRT patch, varenicline, and bupropion on smoking abstinence.
METHODS
Ten electronic databases were searched (up to January 2012) for randomized controlled trials (RCT) of standard-dose (≤ 22 mg) or high-dose nicotine patch therapy (> 22 mg), combination NRT (e.g. nicotine patch + nicotine inhaler), bupropion, and varenicline. Analysis consisted of random-effects pairwise meta-analysis and a Bayesian multiple treatment comparison (MTC).
RESULTS
We identified 146 RCTs (65 standard-doses of the nicotine patch (≤ 22 mg); 6 high-dose NRT patch (> 22 mg); 5 high versus standard-dose NRT patch; 5 combination NRT versus inert controls; 6 combination versus single NRT patch; 48 bupropion; and 11 varenicline). The MTC found that all therapies offered treatment benefits at most time points over controls. Combination NRT and higher-dose NRT did not demonstrate consistent effects over other interventions. With the exception of varenicline, the benefits of treatments over standard-dose NRT were not retained in the long term.
CONCLUSIONS
All pharmacologic treatments were significantly more effective than inert controls. Varenicline was the only treatment demonstrating effects over other options. These results should be considered in the development of clinical practice guidelines.
Topics: Benzazepines; Bupropion; Databases, Bibliographic; Dose-Response Relationship, Drug; Drug Therapy, Combination; Humans; Nicotinic Antagonists; Quinoxalines; Smoking Cessation; Tobacco Use Cessation Devices; Varenicline
PubMed: 22860882
DOI: 10.3109/07853890.2012.705016 -
The Cochrane Database of Systematic... May 2012Smoking contributes to reasons for hospitalisation, and the period of hospitalisation may be a good time to provide help with quitting. (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Smoking contributes to reasons for hospitalisation, and the period of hospitalisation may be a good time to provide help with quitting.
OBJECTIVES
To determine the effectiveness of interventions for smoking cessation that are initiated for hospitalised patients.
SEARCH METHODS
We searched the Cochrane Tobacco Addiction Group register which includes papers identified from CENTRAL, MEDLINE, EMBASE and PsycINFO in December 2011 for studies of interventions for smoking cessation in hospitalised patients, using terms including (hospital and patient*) or hospitali* or inpatient* or admission* or admitted.
SELECTION CRITERIA
Randomized and quasi-randomized trials of behavioural, pharmacological or multicomponent interventions to help patients stop smoking, conducted with hospitalised patients who were current smokers or recent quitters (defined as having quit more than one month before hospital admission). The intervention had to start in the hospital but could continue after hospital discharge. We excluded studies of patients admitted to facilities that primarily treat psychiatric disorders or substance abuse, studies that did not report abstinence rates and studies with follow-up of less than six months. Both acute care hospitals and rehabilitation hospitals were included in this update, with separate analyses done for each type of hospital.
DATA COLLECTION AND ANALYSIS
Two authors extracted data independently for each paper, with disagreements resolved by consensus.
MAIN RESULTS
Fifty trials met the inclusion criteria. Intensive counselling interventions that began during the hospital stay and continued with supportive contacts for at least one month after discharge increased smoking cessation rates after discharge (risk ratio (RR) 1.37, 95% confidence interval (CI) 1.27 to 1.48; 25 trials). A specific benefit for post-discharge contact compared with usual care was found in a subset of trials in which all participants received a counselling intervention in the hospital and were randomly assigned to post-discharge contact or usual care. No statistically significant benefit was found for less intensive counselling interventions. Adding nicotine replacement therapy (NRT) to an intensive counselling intervention increased smoking cessation rates compared with intensive counselling alone (RR 1.54, 95% CI 1.34 to 1.79, six trials). Adding varenicline to intensive counselling had a non-significant effect in two trials (RR 1.28, 95% CI 0.95 to 1.74). Adding bupropion did not produce a statistically significant increase in cessation over intensive counselling alone (RR 1.04, 95% CI 0.75 to 1.45, three trials). A similar pattern of results was observed in a subgroup of smokers admitted to hospital because of cardiovascular disease (CVD). In this subgroup, intensive intervention with follow-up support increased the rate of smoking cessation (RR 1.42, 95% CI 1.29 to 1.56), but less intensive interventions did not. One trial of intensive intervention including counselling and pharmacotherapy for smokers admitted with CVD assessed clinical and health care utilization endpoints, and found significant reductions in all-cause mortality and hospital readmission rates over a two-year follow-up period. These trials were all conducted in acute care hospitals. A comparable increase in smoking cessation rates was observed in a separate pooled analysis of intensive counselling interventions in rehabilitation hospitals (RR 1.71, 95% CI 1.37 to 2.14, three trials).
AUTHORS' CONCLUSIONS
High intensity behavioural interventions that begin during a hospital stay and include at least one month of supportive contact after discharge promote smoking cessation among hospitalised patients. The effect of these interventions was independent of the patient's admitting diagnosis and was found in rehabilitation settings as well as acute care hospitals. There was no evidence of effect for interventions of lower intensity or shorter duration. This update found that adding NRT to intensive counselling significantly increases cessation rates over counselling alone. There is insufficient direct evidence to conclude that adding bupropion or varenicline to intensive counselling increases cessation rates over what is achieved by counselling alone.
Topics: Counseling; Hospitalization; Humans; Inpatients; Patient Education as Topic; Randomized Controlled Trials as Topic; Sensitivity and Specificity; Smoking Cessation; Smoking Prevention
PubMed: 22592676
DOI: 10.1002/14651858.CD001837.pub3 -
BMJ (Clinical Research Ed.) May 2012To examine the risk of treatment emergent, cardiovascular serious adverse events associated with varenicline use for tobacco cessation. (Meta-Analysis)
Meta-Analysis Review
OBJECTIVE
To examine the risk of treatment emergent, cardiovascular serious adverse events associated with varenicline use for tobacco cessation.
DESIGN
Meta-analysis comparing study effects using four summary estimates.
DATA SOURCES
Medline, Cochrane Library, online clinical trials registries, and reference lists of identified articles.
REVIEW METHODS
We included randomised controlled trials of current tobacco users of adult age comparing use of varenicline with an inactive control and reporting adverse events. We defined treatment emergent, cardiovascular serious adverse events as occurring during drug treatment or within 30 days of discontinuation, and included any ischaemic or arrhythmic adverse cardiovascular event (myocardial infarction, unstable angina, coronary revascularisation, coronary artery disease, arrhythmias, transient ischaemic attacks, stroke, sudden death or cardiovascular related death, or congestive heart failure).
RESULTS
We identified 22 trials; all were double blinded and placebo controlled; two included participants with active cardiovascular disease and 11 enrolled participants with a history of cardiovascular disease. Rates of treatment emergent, cardiovascular serious adverse events were 0.63% (34/5431) in the varenicline groups and 0.47% (18/3801) in the placebo groups. The summary estimate for the risk difference, 0.27% (95% confidence interval -0.10 to 0.63; P = 0.15), based on all 22 trials, was neither clinically nor statistically significant. For comparison, the relative risk (1.40, 0.82 to 2.39; P = 0.22), Mantel-Haenszel odds ratio (1.41, 0.82 to 2.42; P = 0.22), and Peto odds ratio (1.58, 0.90 to 2.76; P = 0.11), all based on 14 trials with at least one event, also indicated a non-significant difference between varenicline and placebo groups.
CONCLUSIONS
This meta--analysis--which included all trials published to date, focused on events occurring during drug exposure, and analysed findings using four summary estimates-found no significant increase in cardiovascular serious adverse events associated with varenicline use. For rare outcomes, summary estimates based on absolute effects are recommended and estimates based on the Peto odds ratio should be avoided.
Topics: Adult; Benzazepines; Cardiovascular Diseases; Female; Humans; Male; Nicotinic Agonists; Quinoxalines; Randomized Controlled Trials as Topic; Risk Factors; Tobacco Use Cessation; Tobacco Use Disorder; Treatment Outcome; Varenicline
PubMed: 22563098
DOI: 10.1136/bmj.e2856 -
The Cochrane Database of Systematic... Jan 2012Most people who stop smoking gain weight. There are some interventions that have been designed to reduce weight gain when stopping smoking. Some smoking cessation... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Most people who stop smoking gain weight. There are some interventions that have been designed to reduce weight gain when stopping smoking. Some smoking cessation interventions may also limit weight gain although their effect on weight has not been reviewed.
OBJECTIVES
To systematically review the effect of: (1) Interventions targeting post-cessation weight gain on weight change and smoking cessation.(2) Interventions designed to aid smoking cessation that may also plausibly affect weight on post-cessation weight change.
SEARCH METHODS
Part 1 - We searched the Cochrane Tobacco Addiction Group's Specialized Register and CENTRAL in September 2011.Part 2 - In addition we searched the included studies in the following "parent" Cochrane reviews: nicotine replacement therapy (NRT), antidepressants, nicotine receptor partial agonists, cannabinoid type 1 receptor antagonists and exercise interventions for smoking cessation published in Issue 9, 2011 of the Cochrane Library.
SELECTION CRITERIA
Part 1 - We included trials of interventions that were targeted at post-cessation weight gain and had measured weight at any follow up point and/or smoking cessation six or more months after quit day.Part 2 - We included trials that had been included in the selected parent Cochrane reviews if they had reported weight gain at any time point.
DATA COLLECTION AND ANALYSIS
We extracted data on baseline characteristics of the study population, intervention, outcome and study quality. Change in weight was expressed as difference in weight change from baseline to follow up between trial arms and was reported in abstinent smokers only. Abstinence from smoking was expressed as a risk ratio (RR). We used the most rigorous definition of abstinence available in each trial. Where appropriate, we performed meta-analysis using the inverse variance method for weight and Mantel-Haenszel method for smoking using a fixed-effect model.
MAIN RESULTS
Part 1: Some pharmacological interventions tested for limiting post cessation weight gain (PCWG) resulted in a significant reduction in WG at the end of treatment (dexfenfluramine (Mean difference (MD) -2.50 kg, 95% confidence interval (CI) -2.98 to -2.02, 1 study), phenylpropanolamine (MD -0.50 kg, 95% CI -0.80 to -0.20, N=3), naltrexone (MD -0.78 kg, 95% CI -1.52 to -0.05, N=2). There was no evidence that treatment reduced weight at 6 or 12 months (m). No pharmacological intervention significantly affected smoking cessation rates.Weight management education only was associated with no reduction in PCWG at end of treatment (6 or 12m). However these interventions significantly reduced abstinence at 12m (Risk ratio (RR) 0.66, 95% CI 0.48 to 0.90, N=2). Personalised weight management support reduced PCWG at 12m (MD -2.58 kg, 95% CI -5.11 to -0.05, N=2) and was not associated with a significant reduction of abstinence at 12m (RR 0.74, 95% CI 0.39 to 1.43, N=2). A very low calorie diet (VLCD) significantly reduced PCWG at end of treatment (MD -3.70 kg, 95% CI -4.82 to -2.58, N=1), but not significantly so at 12m (MD -1.30 kg, 95% CI -3.49 to 0.89, N=1). The VLCD increased chances of abstinence at 12m (RR 1.73, 95% CI 1.10 to 2.73, N=1). There was no evidence that cognitive behavioural therapy to allay concern about weight gain (CBT) reduced PCWG, but there was some evidence of increased PCWG at 6m (MD 0.74, 95% CI 0.24 to 1.24). It was associated with improved abstinence at 6m (RR 1.83, 95% CI 1.07 to 3.13, N=2) but not at 12m (RR 1.25, 95% CI 0.83 to 1.86, N=2). However, there was significant statistical heterogeneity.Part 2: We found no evidence that exercise interventions significantly reduced PCWG at end of treatment (MD -0.25 kg, 95% CI -0.78 to 0.29, N=4) however a significant reduction was found at 12m (MD -2.07 kg, 95% CI -3.78 to -0.36, N=3).Both bupropion and fluoxetine limited PCWG at the end of treatment (bupropion MD -1.12 kg, 95% CI -1.47 to -0.77, N=7) (fluoxetine MD -0.99 kg, 95% CI -1.36 to -0.61, N=2). There was no evidence that the effect persisted at 6m (bupropion MD -0.58 kg, 95% CI -2.16 to 1.00, N=4), (fluoxetine MD -0.01 kg, 95% CI -1.11 to 1.10, N=2) or 12m (bupropion MD -0.38 kg, 95% CI -2.00 to 1.24, N=4). There were no data on WG at 12m for fluoxetine.Overall, treatment with NRT attenuated PCWG at the end of treatment (MD -0.69 kg, 95% CI -0.88 to -0.51, N=19), with no strong evidence that the effect differed for the different forms of NRT. There was evidence of significant statistical heterogeneity caused by one study which reported a 4.3 kg reduction in PCWG due to NRT. With this study removed, the difference in weight change at end of treatment was -0.45 kg (95% CI -0.66 to -0.27, N=18). There was no evidence of an effect on PCWG at 12m (MD -0.42 kg, 95% CI -0.92 to 0.08, N=15).We found evidence that varenicline significantly reduced PCWG at end of treatment (MD -0.41 kg, 95% CI -0.63 to -0.19, N=11), but this effect was not maintained at 6 or 12m. Three studies compared the effect of bupropion to varenicline. Participants taking bupropion gained significantly less weight at the end of treatment (-0.51 kg (95% CI -0.93 to -0.09 kg), N=3). Direct comparison showed no significant difference in PCWG between varenicline and NRT.
AUTHORS' CONCLUSIONS
Although some pharmacotherapies tested to limit PCWG show evidence of short-term success, other problems with them and the lack of data on long-term efficacy limits their use. Weight management education only, is not effective and may reduce abstinence. Personalised weight management support may be effective and not reduce abstinence, but there are too few data to be sure. One study showed a VLCD increased abstinence but did not prevent WG in the longer term. CBT to accept WG did not limit PCWG and may not promote abstinence in the long term. Exercise interventions significantly reduced weight in the long term, but not the short term. More studies are needed to clarify whether this is an effect of treatment or a chance finding. Bupropion, fluoxetine, NRT and varenicline reduce PCWG while using the medication. Although this effect was not maintained one year after stopping smoking, the evidence is insufficient to exclude a modest long-term effect. The data are not sufficient to make strong clinical recommendations for effective programmes to prevent weight gain after cessation.
Topics: Antidepressive Agents; Benzazepines; Exercise; Female; Humans; Male; Nicotine; Nicotinic Agonists; Piperidines; Pyrazoles; Quinoxalines; Randomized Controlled Trials as Topic; Smoking Cessation; Weight Gain
PubMed: 22258966
DOI: 10.1002/14651858.CD006219.pub3 -
CMAJ : Canadian Medical Association... Sep 2011There have been postmarketing reports of adverse cardiovascular events associated with the use of varenicline, a widely used smoking cessation drug. We conducted a... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
There have been postmarketing reports of adverse cardiovascular events associated with the use of varenicline, a widely used smoking cessation drug. We conducted a systematic review and meta-analysis of randomized controlled trials to ascertain the serious adverse cardiovascular effects of varenicline compared with placebo among tobacco users.
METHODS
We searched MEDLINE, EMBASE, the Cochrane Database of Systematic Reviews, websites of regulatory authorities and registries of clinical trials, with no date or language restrictions, through September 2010 (updated March 2011) for published and unpublished studies. We selected double-blind randomized controlled trials of at least one week's duration involving smokers or people who used smokeless tobacco that reported on cardiovascular events (ischemia, arrhythmia, congestive heart failure, sudden death or cardiovascular-related death) as serious adverse events asociated with the use of varenicline.
RESULTS
We analyzed data from 14 double-blind randomized controlled trials involving 8216 participants. The trials ranged in duration from 7 to 52 weeks. Varenicline was associated with a significantly increased risk of serious adverse cardiovascular events compared with placebo (1.06% [52/4908] in varenicline group v. 0.82% [27/3308] in placebo group; Peto odds ratio [OR] 1.72, 95% confidence interval [CI] 1.09-2.71; I(2) = 0%). The results of various sensitivity analyses were consistent with those of the main analysis, and a funnel plot showed no publication bias. There were too few deaths to allow meaningful comparisons of mortality.
INTERPRETATION
Our meta-analysis raises safety concerns about the potential for an increased risk of serious adverse cardiovascular events associated with the use of varenicline among tobacco users.
Topics: Benzazepines; Cardiovascular Diseases; Humans; Nicotinic Agonists; Product Surveillance, Postmarketing; Quinoxalines; Randomized Controlled Trials as Topic; Risk; Varenicline
PubMed: 21727225
DOI: 10.1503/cmaj.110218