Showing posts with label Efficacy. Show all posts
Showing posts with label Efficacy. Show all posts

Saturday, January 22, 2011

Effectiveness of the Different Treatments in Smoking Cessation

Cochrane reviews:

Nicotine Replacement Therapy (NRT): 132 RCTs.

-Overall risk ratio (RR) and 95% confidence interval (CI) of abstinence: 1.58 (1.50 to 1.66); similar for gum, patch, inhaler, and lozenge.

-Adverse events (AEs): local irritation related to product type; no evidence of increased myocardial infarction.

Varenicline: 9 RCTs.

-The RR (95% CI) for cessation at 6 to 12 months over placebo was 2.33 (1.95 to 2.80).

-Varenicline AEs: primarily nausea, insomnia, and abnormal dreams; 10% AE drop-out rate; neuropsychiatric AEs (eg, depression, agitation, suicidal thoughts or behaviour) are infrequent butrequire monitoring.

-Reported benefit of varenicline might be influenced by industry funding and lack of a pragmatic design.

Antidepressants: 49 bupropion and 9 nortriptyline RCTs.

-The RR (95% CI) for cessation over placebo at 6 to 12 months: bupropion 1.69 (1.53 to 1.85); nortriptyline 2.03 (1.48 to 2.78).

-Bupropion AEs: primarily insomnia and dry mouth; 7% to 12% AE drop-out rate; rarely seizure (about 1/1000) and suicidal thoughts or behaviour (association unclear).

-Nortriptyline AEs: primarily dry mouth, drowsiness, light-headedness, and constipation (less at lower doses); 4% to 12% drop-out rate from AEs.

Assuming 10% placebo cessation rates (mean across studies), approximate numbers needed to treat (at 6 to 12 months) are as follows: varenicline 8, nortriptyline 10, bupropion 10, and NRT 16.

Context

Smoking cessation is the most effective preventive manoeuver for high-risk patients: an RCT of aggressive intervention for 209 patients after critical care admission achieved a 2-year quit rate of 39% (9% for placebo) and mortality of 3% (vs 12%); number needed to treat was 11.

Dosing:

-Bupropion: 150 mg is equivalent to 300 mg.

-Varenicline: 0.5 mg twice daily is as effective (or almost as effective),as 1 mg twice daily, but with fewer AEs.

-Nortriptyline: start with 25 mg at bedtime and increase by 25 mg every 3 to 4 days, if the desire to smoke persists, to a maximum of 75 to 100 mg; encourage a quit date 10 days in (or so) and continuefor 10 to 12 weeks.

Bottom line

Nicotine replacement, bupropion, nortriptyline (off label), and varenicline are all effective in smoking cessation; AEs vary (and might relate to quitting smoking), but they are important and require monitoring.


Note

In Malaysia, the recommended (and available) pharmacotherapy for smoking cessation are NRT (gum, lozenges, patch, inhaler) and varenicline.

Nicotine 16hour-patch and varenicline are listed in the Ministry of Health Drug Formulary as A/KK (Category of prescribers: Consultants/ Specialists/Family Physician Specialists).


Reference:

Allan,GM, Ivers N and Els C. Can Fam Physician, 57 (1), January 2011: 47.


Tuesday, January 26, 2010

Comparison of Statin : Chemistry/Functional, Pharmacokinetic, Pharmacodynamic, Cost Effectiveness Differences


As a special offer to whoever viewing this blog, a summary of comparison of statin, from the perspective of chemistry/functional, pharmacokinetics, pharmacodynamic and cost effectivenss, an updated version, is available upon your request to :

1. bpharmer05@gmail.com

OR

2. dmcancw@yahoo.com, direct to me, Mai. I will then send to you after receiving your email.


Wednesday, December 2, 2009

Dutasteride vs Finasteride

My hospital is currently running low for the stock of finasteride, and they changed finasteride 5mg to dutasteride 0.5mg.

Rationale :
1) Preliminary data from a 2-year study comparing dutasteride (0.5-milligram (mg) daily or greater) and finasteride indicated greater decreases in serum dihydrotestosterone with dutasteride after 24 weeks of treatment (at least 95% versus 70%)

Anon: FDC Reports: The Pink Sheet: GSK Dutasteride vs Merck Proscar data for BPH expected by mid-2002. November 26 2001a; 63(48):3

2) Patients with symptomatic BPH who receive dutasteride or finasteride, either as monotherapy or combination therapy with α-blockers, can expect to experience significant prostate gland size reduction, improved symptoms, and reduced risk of progression in terms of long-term adverse outcomes.

Nickel JC. Comparison of Clinical trials with finasteride and dutasteride. Rev Urol 2004; 6: S31-S39.

Sunday, November 22, 2009

Aspirin in Diabetes (in Doubt?)

Extracted from :No benefits of aspirin for primary prevention in diabetics, meta-analysis suggests November 10, 2009 | Shelley Wood (http://www.theheart.org/article/1020401.do)

Another meta-analysis—this one focused on diabetics—is questioning the role of aspirin for the primary prevention of cardiovascular events [1]. Writing in a paper published online November 6, 2009 in BMJ, Dr Giogria De Berardis (Consorzio Mario Negri Sud, Maria Imbaro, Italy) and colleagues conclude that "a clear benefit of aspirin in the primary prevention of major cardiovascular events in people with diabetes remains unproved."

Effect of aspirin compared with placebo or no aspirin on relative risk of clinical events in patients with diabetes

End point
Relative risk
95% CI
p
Major cardiovascular events
0.90
0.81-1.00
0.06
MI
0.86
0.61-1.21
0.37
Stroke
0.83
0.60-1.14
0.25
Cardiovascular death
0.94
0.72-1.23
0.68
All-cause mortality
0.93
0.82-1.05
0.22
Any bleeding
2.50
0.76-8.21
NS

"In the most recent guidelines from the Canadian Diabetes Association, for the first time they fully acknowledged the lack of definite data on the efficacy of aspirin, and they leave to the physician the decision of whether or not to use aspirin based on the characteristics of the individual patients. And the other [guideline groups] are starting to move from certainty to uncertainty as well."

There's strong basic research evidence suggesting that diabetes can represent a particular situation associated with poor response of platelets to aspirin, and there are many reasons for that," Nicolucci noted. "Diabetes is associated with hyperglycemia, hyperinsulinemia, insulin resistance, oxidative stress, and advanced glycation end products, and all these factors can be responsible for activation of platelets [via] different pathways that are not blocked by aspirin."

Related papers:
  1. De Berardis G, Sacco M, Strippoli GFM, et al. Aspirin for primary prevention of cardiovascular events in people with diabetes: Meta-analysis of randomised controlled trials. BMJ 2009; DOI:10.1136/bmj.b4531. Available at: http://www.bmj.com.
  2. Antithrombotic Trialists' (ATT) Collaboration. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials. Lancet 2009; 373:1849-1860.
  3. Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002; 324:71-86.
  4. Haynes R, Bowman L, Armitage J. Aspirin for primary prevention of vascular disease in people with diabetes. BMJ 2009; DOI:10.1136/bmj.b4596. Available at: http://www.bmj.com.
(also in http://gettoknowdrugs.blogspot.com/)