Friday, February 11, 2011

Workshops on 'Structural Elucidation of Organic Compounds' (1st - 3rd March 2011, IMU Bukit Jalil, Kuala Lumpur)

The main theme of these workshops is how to characterize the organic compounds using NMR and Mass Spectroscopic techniques. The facilitator is Prof. A.I. Gray from University of Strathclyde, UK. He is well known internationally for his expertise in the characterization of organic compounds.

These workshops are unique in the sense that these workshops cover all the basic & advanced techniques in structural elucidation of organic compounds.

These workshops would be very useful to the researchers who are involved in identification of compounds from any source. Also, these workshops would act as a platform to network research collaboration.

The dead line for early bird registration is 15th February 2011.

HURRY!!The number of participants in each workshop is limited to only 25 participants.

Links :
1) MPS :
2) IMU :

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.


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.


-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.


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).


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

Sunday, January 9, 2011

Chapter for Pharmacist-To-be : Pharmaceutical Care Plan for Asthma Patients

Recently, final year pharmacy student or/also known as the pharmacist-to-be, asked me about some questions regarding management of an asthmatic patient.

So to summarise the discussion, When comes to asthmatic patients, there are few things you ned to make it clear before you jump into recommendation:

1) Patient's compliance on inhaler techniques. If non-compliance, there is a bigger issue for u to address before you add in an extra med.

2)How to step up and to step down in asthma management? What parameters you look at ?
If to step up, which agent will you choose ? What monitoring parameters are you interested to look at?
- after corticosteroid, what is next in the list?
- can long acting beta-agonist be given alone?
- what are the up-coming innovation in management of asthma patients, that could improve compliance, improve efficacy and reduce side effect?

3) think about what is the pathophysiology of asthma?
- why we will step up to inhale corticosteroid instead of other agent?

4) How different is the management of asthma vs COPD? why is it so?

5) How the difference of management of acute exacerbation of asthma vs chronic asthma?

6) What is the differences in inhaler corticosteroid and oral corticosteroid?
- why do we have an invention of inhaler?
- When do we oral (systemic) corticosteroid in management of asthma patient?

7) Check the differences in each corticosteroid inhaler (Budesonide, beclomethasone, ciclesonide, fluticasone, betamethasone) By finding the differences, You will then understand why in the market, there is so many different corticosteroid inhalers, and why some inhale corticosteroid were phased out from the market already.

8) can asthma patient be given aspirin?
if can, what would be your concern?
if cant, what would you recommend to your doctor?

If you could find out all the answers, you will have a better understanding of how to manage an asthma patient! But dont forget about his/her other co-morbidity(ies).

Wednesday, January 5, 2011



Stephen R. Hammes
Division of Endocrinology & Metabolism, Department of Medicine, University of Rochester School of Medicine & Dentistry
Laurence L. Brunton
Professor of Pharmacology and Medicine, Department of Pharmacology, University of California San Diego School of Medicine

Related To: Chapter 57. Estrogens and Progestins

View in chapter

The FDA has recently approved ulipristal for post-coital contraception. Ulipristal could be considered “Plan C”, similar in overall effect to the current “Plan B”, mifepristone. Ulipristal can inhibit follicular rupture when administered prior to ovulation (Brache et al, 2010) and is effective post-coitally in preventing pregnancy (Fine et al, 2010; Glasier et al, 2010). The clinical studies with ulipristal have raised some questions about the drug’s equivalence to existing medications (Page and Verhaeghe, 2010) and prompted an interesting discussion of the ethics of including a placebo-control in a study of efficacy of a drug such as this one (Glasier and Gainer, 2010). As may be expected, ulipristal has also provoked an adverse reaction in the United States by opponents of the termination of pregnancy. Ulipristal is included in the recently published 12th edition ofGoodman & Gilman's The Pharmacological Basis of Therapeutics. (Chapter 40, Estrogens and Progestins)

Chemistry. Ulipristal (PubChem CID: 130904) is another derivative of 19-norprogesterone (PubChem CID: 95585) that functions as a selective progesterone receptor modulator (SPRM) with both agonistic and antagonistic effects on the progesterone receptor. Ulipristal has the same dimethyl-aminophenol group at the 11b position as seen in mifepristone (PubChem CID: 55245) with an additional acetoxy group at position 17. Unlike mifepristone, ulipristal appears to be a relatively weak glucocorticoid antagonist.

Pharmacological Actions. Ulipristal is known to have anti-proliferative effects in the uterus at high doses; however, its most relevant actions to date are its ability to inhibit ovulation. While still not clear, ulipristal’s anti-ovulatory actions likely occur due to progesterone regulation at many levels, including inhibition of LH release through the hypothalamus and pituitary, as well as inhibition of LH-induced follicular rupture within the ovary.

Dosing. A 30 mg dose of ulipristral can inhibit ovulation when taken up to five days after intercourse. In fact, ulipristal can block ovarian rupture at or even just after the time of the LH surge, confirming that at least part of its effects are directly in the ovary. Ulipristal may also block endometrial implantation of the fertilized egg, although whether this contributes to its ability to function as an emergency contraceptive (see below) is not clear.

Therapeutic Uses. Ulipristal acetate, which is sold as ella and ellaOne, has recently been licensed in Europe and the United States as an emergency contraceptive. Studies comparing ulipristal to levonorgestrel (progesterone-only emergency contraception, or POEC) have found that ulipristal is at least as effective when taken up to 72 hours after unprotected sexual intercourse. Most importantly, while levonorgestrel does not work well beyond 72 hours after unprotected intercourse, ulipristal remains effective up to 120 hours (5 days) after intercourse, making ulipristal a more versatile emergency contraceptive. The most severe side effect in clinical trials using ulipristal has been a self-limited headache and some abdominal pain. The drug should not be taken by women who are breastfeeding or who are pregnant and wish to remain so.


Brache V, Cochon L, Jesam C, et al. Immediate pre-ovulatory administration of 30 mg ulipristal acetate significantly delays follicular rupture. Hum Reprod 2010;25:2256-63. [PMID: 20634186]

Fine P, Mathé H, Ginde S, et al. Ulipristal acetate taken 48-120 hours after intercourse for emergency contraception. Obstet Gynecol 2010;115:257-63. [PMID: 20093897]

Glasier A, Gainer E. Correspondence: Ulipristal acetate for emergency contraception? Authors’ reply. Lancet 2010;375:1608. [PMID: 20452518]

Glasier AF, Cameron ST, Fine PM, et al. Ulipristal acetate versus levonorgestrel for emergency contraception: a randomised non-inferiority trial and meta-analysis. Lancet 2010;375: 555-562. [PMID: 20116841]

Page GH, Verhaeghe V. Correspondence: Ulipristal acetate for emergency contraception? Lancet 2010;375:1608. [PMID: 20452519]

Hammes Stephen R, Brunton Laurence L, "ella: a Newly-Approved Selective Progesterone Receptor Modulator" (Update). Laurence L. Brunton, John S. Lazo, Keith L. Parker: Goodman & Gilman's The Pharmacological Basis of Therapeutics, 11e:

Thursday, December 23, 2010

FAPA 2010: Community Pharmacy Visit

Find out more about the community pharmacy in Taiwan HERE!

Thursday, December 2, 2010

Some Facts about Eye Drops

On 28th November 2010, I attended the CPD Pharmacists' Workshop on Ophthalmology at the Saujana Hotel with several friends. This workshop is a breath of fresh air indeed-while the lunch is sponsored by Allergan, the workshop is not heavily laden with product talks; not only that, the invited speakers comprise consultant ophthalmologist and experienced pharmacists, sharing practical points on various topics:red eyes, dry eye, glaucoma and nutritional supplments for age-related macular disease.

Some learning points from the workshop that I would like to share with you all:
When instilling eye drops, 1 drop is sufficient as the ideal volume of a drop that the eye can hold, especially the conjunctiva cul de sac is 10-15uL and the typical volume of an eye drop is 40uL.

Sequence of instillation (if more than one type of topical drugs are to be used):
1) solution 2) suspension 3) Suspension/Gel

For contact lens wearer, instill the eye drop first, then wait for 15 minutes before putting on the contact lens.

Tear film is a barrier to effective drug delivery. Tear film penetration can be increased by manually blocking the nasolacrimal duct and tilting the head backwards. Occlusion of the nasolacrimal ducta after instillation of eye drop, minimises systemic absorption.Examples of systemic side effects: Gutt chloramphenicol may cause aplastic anaemia, Gutt timolol may cause acute exacerbation of bronchial asthma.

Once an eye drop passes the tear film, it penetrates the cornea which is the major site of absorption for topical drugs.

1 drop of eye drop: only 50% reach the site of action.

The iris acts as a reservoir for drugs instilled into the eye. Prostaglandin analogues used for glaucoma may change colour of iris as they stay in the iris.

Hydrophilic drugs do not enter the retina easily. They are prevented by tight junctions complexes at the retinal pigment epithelium, hence retinal toxicity is seen in certain drugs. E.g. Gutt. chloramphenicol may cause optic nerve toxicity.

Caution must be taken when recommending/prescribing steroid eye drops as they have contraindications and adverse effects. Adverse effects include: elevation of intraocular presure and possibly glaucoma with nerve damage, cataract formation, delayed wound healing, worsening corneal ulcers especially if bacterial or fungal.

One of the points to consider when recommending eye drop to patient-the types of preservatives used.

Wednesday, December 1, 2010

Mechanism-Based Therapies for Heart Failure and Cardiac Arrhythmias

Mechanism-Based Therapies for Heart Failure and Cardiac Arrhythmias


Introduction to excitation-contraction coupling - History of the field of EC coupling - Introduction to the ryanodine receptor/calcium release channel (RyR2) - Mechanisms that regulate the RyR2 channel during stress - Defective regulation of RyR2 in heart failure - Evidence that diastolic sarcoplasmic reticulum (SR) calcium leak causes heart failure and arrhythmias in vivo - Novel therapeutic approaches to treating heart failure and preventing sudden cardiac death by fixing the leak in RyR2 channels

How to cite this talk:
Marks, A. (2007), "Mechanism-Based Therapies for Heart Failure and Cardiac Arrhythmias", in Simpson, A. (ed.),Calcium Signaling: Regulation, Mechanisms, Effectors, Role in Disease and Recent Advances, The Biomedical & Life Sciences Collection, Henry Stewart Talks Ltd, London (online at