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Canadian Paediatric Society

Paediatric Allergy Travel Grant

The Paediatric Allergy Travel Grant was created by the Allergy Section. It provides an educational opportunity for young physicians in, or interested in, the field of paediatric allergy, and fosters interest and participation in the section’s activities.  The $750 grant is awarded annually at the section’s business meeting to help offset expenses associated with attending the CPS Annual Conference.

Recipients will write a review of an allergy-related topic that is suitable to publish on the Allergy Section website and/or to submit to a peer-reviewed journal (e.g. Paediatrics & Child Health) (maximum of 500 words). The review is due three months after selection. The grant will be awarded in two installments: $500 upon selection and the remaining $250 upon receipt of the review.

Submission deadline: March 31


To be eligible for this grant, residents/fellows must be members of the CPS Allergy Section and interested in a career in allergy and clinical immunology or be a paediatric allergy fellow.



Applications must be submitted by March 31 to and must include:

  • A letter outlining the applicant’s interest in a career in allergy and clinical immunology. Maximum of 2 pages.
  • A letter of support from an allergy and clinical immunology professional(e.g. division head, department chair, program director). Maximum of 3 pages.

Past recipients

Lucy Li - 2018

“To Prick Or Not To Prick”: Oral Penicillin Challenges without Skin Testing in Diagnosing Penicillin Allergy

by Lucy Li, PY3, University of Toronto, 2018 grant recipient


Beta-lactam antibiotics are one of the most frequently prescribed groups of antibiotics in the paediatric population1-4. Penicillin is also one of the most commonly reported medication allergies with most paediatric patients being diagnosed without further evaluation as being allergic. As a result, paediatric patients may be prescribed alternative antibiotics which often are less effective, more toxic, and more expensive5.

Antibiotic allergies in a sensitized person are mediated by IgE, IgG, or T lymphocytes6. IgE mediated mechanisms are responsible for the immediate reactions that occur within the first hour following drug administration7. Symptoms typically include urticaria, angioedema, rhinitis, bronchospasm, or anaphylaxis7-8. Non-immediate reactions are typically caused by T lymphocyte dependent reactions which occurs at least 1 hour post drug administration. Reactions are typically a macular or papular rash9-11. Serum sickness, Stevens - Johnson syndrome, and toxic epidermal necrolysis are some of the less common, but more severe, non-immediate reactions that can also occur12-13.

Diagnosis of Penicillin Allergy

Currently, diagnosing a penicillin allergy is dependent on both clinical history, skin prick testing, and/or intradermal testing14. This involves the major and minor determinants which are penicillin specific IgE antibodies. As with environmental or food allergy, isolated positive skin test results do not necessarily define clinically significant IgE-mediated penicillin allergy. Furthermore, false-negative as well as false-positive results are possible which can cause significant patient morbidity including adverse reactions to the drug and avoidance of the drug respectively. The current reference standard for documenting acute penicillin tolerance remains an oral challenge, usually with amoxicillin, at a therapeutic dose.

Oral Provocation Challenge

Recent studies have begun to explore the safety of direct oral challenges without preceding skin tests in limited populations with low risk histories of penicillin allergy15-16. In one of the largest paediatric studies, the authors demonstrated that a graded provocation challenge was safe in children with amoxicillin induced rashes with a specificity of 100%, a negative predictive value of 89.1%, and a positive predictive value of 100%.  The study showed that 94% of children tolerated the amoxicillin challenge whereas the remainder developed mild reactions15. A second study showed that a 5 day oral penicillin challenge without antecedent skin testing was safe to exclude clinically significant delayed onset hypersensitivity reactions in patients with previous non-immediate reactions to penicillin16.


The rate of positive penicillin skin testing in patients with a history of penicillin allergy has declined over the years from >10% to ~5%17. The incidence of anaphylactic reactions after penicillin administration is very low – only 1 in 225 00018. The studies above demonstrate that for a certain population of patients who have low risk histories of penicillin allergy, direct oral challenges with penicillin may be safe without preceding skin testing. In the paediatric population, this can overcome the difficulty associated with administering skin prick testing/intradermal testing to patients who are often needle phobic and uncooperative. It also avoids the pain associated with testing. Nonetheless, more research is required to help establish guidelines and protocols for the safety of administering a direct drug challenge without antecedent skin testing for patients presenting with a query penicillin allergy. Defining exactly what constitutes a clinically significant challenge reaction is also important and further work is needed to standardize reporting of challenge reactions. Should centres choose to proceed to a direct drug challenge, such challenges should be performed in settings where personnel and resources are available to manage anaphylaxis should it occur.


  1. Pichichero ME. Otitis media. Pediatr Clin North Am 2013; 60:391-407.
  2. Brook I. Acute sinusitis in children. Pediatr Clin North Am 2013; 60: 409-24.
  3. Caubet JC, Kaiser L, Lemaitre B, Fellay B, Gervaix A, Eigenmann PA. The role of penicillin in benign skin rashes in childhood: a prospective study based on drug rechallenge. J Allergy Clin Immunol 2011; 127: 218-22.
  4. Ponvert C, Perrin Y, Bados-Albiero A, Le Bourgeois M, Karila C, Delacourt C, Scheinmann P, De Blic J. Allergy to beta-lactam antibiotics in children: results of a 20 year study based on clinical history, skin and challenge tests. Pediatr Allergy Immunol 2011; 22:411-8.
  5. Seitz CS, Brocker EB, Trautmann A. Diagnosis of drug hypersensitivity in children and adolescents: Discrepancy between physician-based assessment and results of testing. Pediatr Allergy Immunol. 2011; 22(4): 405-410.
  6. Gueant JL, Gueant-Rodriguez RM, Gastin IA, Cornejo-Garcia JA, Viola M, Barbaud A, Mertes PM, Blanca M, Romano A. Pharmacogenetic determinants of immediate and delayed reactions of drug hypersensitivity. Curr Pharm Des.2008; 14(27): 2770-2777.
  7. Bousquet PJ, Kvedariene V, Co-Minh HB, Martins P, Rongier M, Arnoux B, Demoly P. Clinical presentation and time course in hypersensitivity reactions to beta-lactams. Allergy. 2007;62(8):872-876.
  8. Saxon A, Beall GN, Rohr AS, Adelman DC. Immediate hypersensitivity reactions to beta-lactam antibiotics. Ann Intern Med. 1987; 107 (2): 204-215.
  9. Pichler WJ. Delayed drug hypersensitivity reactions. Ann Intern Med. 2003; 139(8):683-693.
  10. Pavlos R, Mallal S, Ostrov D, Buus S, Metushi I, Peters B, Phillips E. T cell-mediated hypersensitivity reactions to drugs. Ann Rev Med. 2015; 66:439-454.
  11. Hari Y, Frutig-Schnyder K, Hurni M, Yawalkar N, Zanni MP, Schnyder B, Kappeler A, von Greyerz S, Braathen LR, Pichler WJ. T cell involvement in cutaneous drug eruptions. Clin Exp Allergy. 2001; 31(9): 1398-1408.
  12. Caubet JC, Eigenmann P. Managing possible antibiotic allergy in children. Curr Opin Infect Dis. 2012; 25(3): 279-285
  13. Atanaskovic-Markovic  M, Velickovic TC, Gavrovic-Jankulovic M, Vuckovic O, Nestorovic B. Immediate Allergic Reactions to Cephalosporins and Penicillins and Their Cross-Reactivity in Children. Pediatr Allergy Immunol. 2005; 16(4):341-347.
  14. Torres MJ, Romano A, Celik G, Demoly P, Khan DA, Macy E, Park M, Blumenthal K, Aberer W, Castells M, Barbaud A, Mayorga C, Bonadonna P. Approach to the diagnosis of drug hypersensitivity reactions: similarities and differences between Europe and North America. Clin Transl Allergy. 2017; 7(7): 1-13
  15. Mill C, Primeau MN, Medoff E, Lejtenyi C, et al. Assessing the Diagnostic Properties of a Graded Oral Provocation Challenge for the Diagnosis of Immediate and Nonimmediate Reactions to Amoxicillin in Children. JAMA Pediatr. 2016; 170(6):1-8.
  16. Confino-Cohen R, Rosman Y, Meir-Shafrir K, Stauber T, Lachover-Roth I, Hershko A, Goldberg A. Oral Challenge without Skin Testing Safely Excludes Clinically Significant Delayed-Onset Penicillin Hypersensitivity.
  17. Macy E, Schatz M, Lin CK, Poon KY. The Falling Rate of Positive Penicillin Skin Tests from 1995 to 2007. Perm J 2009; 13:12-8.
  18. Macy E, Chen LH. The incidence of anaphylaxis associated with oral and parenteral penicillin-class antibiotic exposures. J Allergy Clin Immunol. 2017; 139(2): 1

Shama Sud - 2017

Probiotics and the Prevention of Allergic Disease


The prevalence of allergic disease such as atopic dermatitis, asthma and allergic rhinitis continues to rise around the globe, particularly in developed countries1.  Studies suggest 1 in 5 people worldwide suffer from an allergic disorder2. Identifying methods of reducing the incidence of allergic diseases is of paramount importance.  It has been estimated that 1.4 billion Canadian dollars are spent annually on the management of atopic dermatitis alone3. Uncontrolled allergic disease has also been shown to have a negative impact on quality of life4.

The microbial flora in the intestine plays a pivotal role in mucosal immunity and may be important in the pathogenesis of allergic disease.  Normal microbial flora favours a Th1 cell response to allergens while abnormal gut flora favours the allergic pathway of a Th2 response with increased production of IgE and Th2 cytokines5.   Probiotics have the potential to favour the production of Th1 cytokines and reduce the Th2 response by regulating the immune system6.   

Probiotics and Atopic Disease

Multiple studies have been done looking at the administration of probiotics from the antenatal to the postnatal period as a method of preventing atopic disease.  Most have not found any benefits in terms of preventing asthma or atopic sensitization7, 8.  The most promising data appears to be in the area of atopic dermatitis with several papers showing a significantly lower prevalence with the use of probiotics9, 10, 11. This is not true for all studies, however.  Differences in the strain of probiotic administered, vehicle, dose, duration of treatment, inclusion criteria and length of follow-up may explain some of the variability in findings.

The strain Lactobacillius rhamnosus has been identified in the literature as having a protective effect.  Multiple studies have shown a significantly reduced prevalence of atopic dermatitis in children treated with probiotics containing this strain as compared with those given placebo7, 9, 12, 13. The benefit of early administration appears to be persistent with some studies still showing a significantly reduced prevalence of atopic dermatitis at 4-6 years of age14, 15.  Treatment of the mother prior to delivery and the baby following birth appears to be important and consistent amongst all trials with positive findings.  Three studies using Lactobacillus rhamnosus have had negative results.  Two of these studies were done looking at administration of probiotics solely in the prenatal or postnatal period16, 17.  A third study with negative results did administer probiotics in both the pre and postnatal period but found no significant difference in the prevalence of atopic dermatitis18.  Additional trials are needed to clarify optimal administration standards and populations most likely to benefit from their use. 


Probiotics have a relatively safe side effect profile and are easy to administer19. Given the growing body of evidence to suggest that certain strains may be protective against the development of atopic dermatitis, the incorporation of their use into prenatal care for children at high risk is an area that may warrant further exploration.    


1. Asher MI, Montefort S, Bjorksten B, Lai CK, Strachan DP, Welland SK et al. Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and eczema in childhood: ISAAC Phases One and Three repeat multicountry cross-sectional surveys. Lancet. 2006;368(9537):733-43.

2. Warner JO, Kaliner MA, Crisci CD, Del Giacco S, Frew AJ, Liu GH et al. Allergy practice worldwide: a report by the World Allergy Organization Specialty and Training Council. Int Arch Allergy Immunol. 2006;139(2):166-74.

3. Barbeau M, Lalonde H. Burden of Atopic dermatitis in Canada. International Journal of Dermatology. 2006;46:31-36.

4. Lewis-Jones S. Quality of life and childhood atopic dermatitis: the misery of living with childhood eczema.  Int J Clin Pract. 2006;60(8):984-992.

5. Kirjavainen PV, Arvola T, Salminen SJ, Isolauri E. Aberrant composition of gut microbiota of allergic infants: a target of bifidobacterial therapy at weaning? Gut. 2002;51(1):51–55.

6. Winkler P, Ghadimi D, Schrezenmeir J, Kraehenbuhl JP. Molecular and cellular basis of microflora-host interactions. J Nutr. 2007;137(3 suppl 2):756S–72S.

7. Dotterud CK, Storrø O, Johnsen R, Oien T. Probiotics in pregnant women to prevent allergic disease: a randomized, double-blind trial. Br J Dermatol. 2010 Sep;163(3):616-23.

8. Simpson MR, Dotterud CK, Storro O, Johnsen R, Oien T. Perinatal probiotic supplementation in the prevention of allergy related disease: 6 year follow up of a randomised controlled trial. BMC Dermatology. 2015;15:13.

9. Kalliomäki M, Salminen S, Arvilommi H, Kero P, Koskinen P, Isolauri E. Probiotics in primary prevention of atopic disease: a randomised placebo-controlled trial. Lancet. 2001;357(9262):1076-9.

10.  Kim JY, Kwon JH, Ahn SH, Lee SI, Han YS, Choi YO, et al. Effect of probiotic mix (Bifidobacterium bifidum, Bifidobacterium lactis, Lactobacillus acidophilus) in the primary prevention of eczema: a double-blind, randomized, placebo-controlled trial.  Pediatric Allergy & Immunology. 2010;21(2 Pt 2):e386-93.

11. Niers L, Martin R, Rijkers G, Sengers F, Timmerman H, van Uden N, et al. The effects of selected probiotic strains on the development of eczema (the PandA study). Allergy. 2009;64(9):1349-58.

12. Wickens K, Black PN, Stanley TV, Mitchell E, Fitzharris P, Tannock GW, et al. A differential effect of 2 probiotics in the prevention of eczema and atopy: a double-blind, randomized, placebo-controlled trial. Journal of Allergy & Clinical Immunology. 2008;122(4):788-94.

13. Rautava S, Kainonen E, Salminen S, Isolauri E. Maternal probiotic supplementation during pregnancy and breast-feeding reduces the risk of eczema in the infant. J Allergy Clin Immunol. 2012;130(6):1355-60.

14. Wickens K, Black P, Stanley TV, Mitchell E, Barthow C, Fitzharris P, et al. A protective effect of Lactobacillus rhamnosus HN001 against eczema in the first 2 years of life persists to age 4 years. Clinical & Experimental Allergy. 2012; 42(7):1071-9.

15. Wickens K, Stanley TV, Mitchell EA, Barthow C, Fitzharris P, Purdie G, et al. Early supplementation with Lactobacillus rhamnosus HN001 reduces eczema prevalence to 6 years: does it also reduce atopic sensitization?.  Clin Exp Allergy. 2013;43(9):1048-57.

16. Boyle RJ, Ismail IH, Kivivuori S, Licciardi PV, Robins-Browne RM, Mah LJ, et al. Lactobacillus GG treatment during pregnancy for the prevention of eczema: a randomized controlled trial. Allergy. 2011;66(4):509-16.

17. Soh SE, Aw M, Gerez I, Chong YS, Rauff M, Ng YP, et al. Probiotic supplementation in the first 6 months of life in at risk Asian infants—effects on eczema and atopic sensitization at the age of 1 year. Clin Exp Allergy. 2009;39(4):571-8.

18. Ou CY, Kuo HC, Wang L, Hsu TY, Chuang H, Liu CA, et al. Prenatal and postnatal probiotics reduces maternal but not childhood allergic diseases: a randomized, double-blind, placebo-controlled trial.  Clinical & Experimental Allergy. 2012;42(9):1386-96.

19. Smilowitz JT, Moya J, Breck MA, Cook C, Fineberg A, Angkustsiri K, et al.  Safety and tolerability of Bifidobacterium longum subspecies infantis EVC001 supplementation in healthy term breastfed infants: a phase I clinical trial.  BMC Pediatr. 2017;17(1):133.

Herman Tam - 2015

Updates on early peanut introduction and prevention of peanut allergy


Peanut allergy is estimated to affect 1-3% of the population1 and its prevalence has substantially increased in the past 10-15 years2. It is the leading cause of anaphylaxis and death related to food allergy3. Recent studies have explored the relationship between dietary introduction and prevention of peanut allergy.

In 2008, the American Academy of Pediatrics retracted previous recommendations, and concluded that there was no convincing evidence for early food avoidance to prevent development of allergy4. In 2011, the Canadian Paediatric Society issued a joint position statement with the Canadian Society of Allergy and Clinical Immunology5 with a recommendation to not delay introduction of solid food beyond six months while active introduction at four to six months of age is ‘still under investigation’.

Results from LEAP study

A landmark United Kingdom study, Learning Early About Peanut Allergy (LEAP)6, investigated whether early introduction of peanut-based products prevented allergy in high-risk infants. 640 infants (4-11months) with severe eczema and/or egg allergy were stratified to cohorts based on preexisting sensitization assessed using skin prick test (SPT): 542 non-sensitized (0mm wheal) and 98 sensitized (1-4mm wheal). 76 infants with SPT wheal greater than 4mm were excluded due to high-risk of severe reactions. The two groups were randomized to regularly consume or completely avoid peanut products until 60 months of age, when peanut allergy was determined using an oral challenge with peanut protein.

The prevalence of peanut allergy showed a striking difference of 17% in the avoidance group compared to 3% in the consumption group, with a corresponding number needed to treat of 7.1. This effect was demonstrated in both the non-sensitized group (primary prevention) as well as the sensitized group (secondary prevention).


Current Recommendations and Implications

The LEAP study is the first prospective, randomized trial that clearly demonstrates early introduction reduces the risk of peanut allergy. An interim guidance from international allergy collaborations was issued to highlight the potential benefits7. It supports dietary introduction of peanut products in high-risk infants between 4 and 11 months of age (Level 1 evidence). It also recommends healthcare providers to consider evaluation by allergists (including SPT and food challenge) in infants with early-onset allergic diseases before initiating peanut introduction, similar to the screening procedures in the LEAP study.


Current Canadian guidelines are being revised to reflect new evidence and raise awareness. Changing the culture from ‘not delay’ to ‘active introduction’ for primary prevention is vital in the setting of increasing peanut allergy. However, healthcare resources must be ready to accommodate these applications, especially the increasing need for evaluation by an allergist in the large number of high-risk infants at an early age. Further research is required to address the optimum dose to prevent allergy, the prevalence of allergy after cessation of regular consumption, and applications to other allergenic foods.


For high-risk infants, early feeding at 4-6 months can be an effective intervention in primary prevention of peanut allergy. For non high-risk infants, delayed introduction beyond 6 months is not recommended routinely.


1. Ben-Shoshan M, Harrington DW, Soller L, Fragapane J, Joseph L, St Pierre Y, Godefroy SB, Elliott SJ, Clarke AE. A population-based study on peanut, tree nut, fish, shellfish, and sesame allergy prevalence in Canada. J Allergy Clin Immunol 2010;125(6):1327-35.

2. Sicherer SH, Muñoz-Furlong A, Godbold JH, Sampson HA. US prevalence of self-reported peanut, tree nut, and sesame allergy: 11-year follow-up. J Allergy Clin Immunol 2010;125:1322-6.

3. Bock SA, Muñoz-Furlong A, Sampson HA. Further fatalities caused by anaphylactic reactions to food, 2001-2006. J Allergy Clin Immunol. 2007;119(4):1016-8.

4. Greer FR, Sicherer SH, Burks AW, American Academy of Pediatrics Committee on Nutrition; American Academy of Pediatrics Section on Gastroenterology, Hepatology, and Nutrition: Effects of early nutritional interventions on the development of atopic disease in infants and children: The role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics 2008;121(1):183191.

5. Chan ES, Cummings C. Canadian Paediatric Society, Community Paediatrics Committee and Allergy Section. Dietary exposures and allergy prevention in high-risk infants: a joint statement with the Canadian Society of Allergy and Clinical Immunology. Paediatr Child Health 2013;18:545-54.

6. Du Toit G, Roberts G, Sayre PH, Bahnson HT, Radulovic S, Santos AF, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med 2015;372:803-13.

7. Fleischer DM, et al. Consensus communication on early peanut introduction and the prevention of peanut allergy in high-risk infants. J Allergy Clin Immunol. 2015 Aug;136(2):258-61.

Andrea Fong - 2011

Review Article: Long-acting ß2-adrenergic Agonists

ß2-adrenergic agonists have been the mainstay treatment for relief of acute asthma exacerbations since its introduction in the 1960’s. The introduction of long-acting ß2-adrenergic agonists (LABAs) in the 1990’s subsequently provided clinicians with another ‘tool’ in the management of uncontrolled asthma. LABAs have not been without its fair share of controversy however. This article aims to review the controversy surrounding LABAs as well as their physiology and current recommended use in the pediatric population.


The ß2-receptor is a G-protein coupled receptor widely distributed throughout the body. It is most densely located in airway smooth muscle1. The bronchodilating effect occurs when the ß2-agonists bind to and stabilize the ß2-receptor in its activated form. The ß2-receptor is in the activated form when it is associated with the α-subunit of the G-protein, together with guanosine triphosphate (GTP). This leads to an increase in cyclic adenosinemonophosphate (cAMP). Although the mechanism by which an increase in cAMP leads to bronchodilation is not fully understood, it is thought that it catalyzes the activation of protein kinase A (PKA), which in turn phosphorylates key regulatory proteins involved in the control of muscle tone1.


Formoterol fumarate is moderately lipophilic and is taken up into the cell membrane. It acts like a “depot” and progressively releases into the aqueous environment to interact with the ß2-receptor. Its onset is 2-3 minutes. This is due to some of the drug remaining in the aqueous phase outside of the cell allowing it to interact immediately with the ß2-receptors1. Its duration is approximately 12 hours.

Salmeterol xinafoate is even more lipophilic and as such has a longer time of onset (30 minutes) as compared to fomoterol. It diffuses laterally in the cell membrane to approach the activity site of the ß2-receptor1. Its duration is also approximately 12 hours.


The US Food and Drug Administration (FDA) black box warning on LABAs was issued in 2006 following several studies which showed an increase in serious adverse events (SAEs) with the use of LABAs2. The mechanism by which LABAs could potentially cause harm were postulated to be due to its cardiac side effects, desensitization of the ß2-receptors, delay in seeking help due to the masking of the severity of the exacerbation and/or reduction in the use of inhaled corticosteroids (ICS)3. The controversy at the time was due to the fact that the black box warning was issued for both monotherapy and combination ICS/LABA use. Although the evidence was quite clear that there was a significant increase in SAEs with LABA monotherapy, the evidence against combination ICS/LABA use was not as clear. Criticisms for the studies used leading to the FDA warning include undertreatment with ICS and differential dosing of ICS in many of the trials4. As an example, in the SMART study which was the largest study conducted at the request of the FDA to examine LABA safety, less than 50% of their study population were on an ICS at baseline5. Since then, various meta-analyses have struggled to clearly identify a significant increase in SAEs with the use of combination ICS/LABA therapy, as the majority of the study populations were either not on ICS at baseline or were not assigned to consistent ICS plus LABA use6. Subsequently, the FDA re-issued an updated warning in 2010 stating that LABAs should always be used with an ICS in the treatment of asthma2. Furthermore, in the pediatric and adolescent population, the medication should be delivered in a fixed-dose combination product to ensure that LABA monotherapy does not occur2. The latest Cochrane Review examining the safety of LABAs in children estimates that there are probably an additional three children per 1000 over three months who suffer a non-fatal SAE on combination therapy in comparison to ICS use alone3. The authors emphasized that this estimated risk needs to be balanced against the symptomatic benefit obtained by each child. They also stated that there was insufficient information to make any conclusion in relation to the risks of mortality in children on regular LABA therapy.

Current Recommendations:

Currently, the Canadian Thoracic Society (CTS) 2012 Asthma guideline update recommends the use of combination ICS/LABA use in those >/= 12 years whose asthma is not controlled on low-dose ICS and upon review of adherence, technique and avoidance of triggers7. ICS/LABA use is recommended in children 6-11 years whose asthma is uncontrolled on moderate-dose ICS and upon review of adherence, technique and avoidance of triggers7. Although salmeterol is approved for patients as young as four, use of a combination ICS/LABA in the preschool group should probably be reserved for those whose asthma is uncontrolled despite the use of moderate to high-dose ICS and leukotriene receptor antagonist and in consultation with a specialist8. The CTS has also commented that the FDA statement to “Stop [the] use of the LABA, if possible, once asthma control is achieved and maintain the use of an asthma-controller medication, such as an inhaled corticosteroid,” is not evidence-based and that withdrawing the LABA may result in loss of symptom control4,9.

Future directions:

Ultra-long ß2-adrenergic agonists (uLABAs) such as indacaterol have now entered the market in Canada as of 2012 although it is not indicated for asthma. The duration of uLABAs are approximately 24 hours and would only require once daily dosing which may help improve adherence to the medication. Since LABA monotherapy is contraindicated in asthma, perhaps it will not be too long before a combination ICS/uLABA product may be seen in the future for the treatment of asthma.


It is clear that LABA monotherapy should not be used in any age group for the treatment of asthma. There is a role however for LABAs as add-on therapy in asthma, in combination with ICS as recommended in the CTS guidelines7. As clinicians, we must continue to weigh the benefits with the risks of using any therapy. Until there is stronger evidence to suggest the contrary, for some patients the risks of uncontrolled asthma outweigh the potential risk of using ICS/LABA therapy.


1. Johnson M, Molecular mechanisms of beta2-adrenergic receptor function, response, and regulation, J Allergy Clin Immunol. 2006 Jan; 117(1):18-24

2. Chowdhury B et al, The FDA and safe use of long-acting beta-agonists in the treatment of asthma N Engl J Med 2010; 362:1169-1171

3. Cates CJ et al, Safety of regular formoterol or salmeterol in children with asthma: an overview of Cochrane reviews, Cochrane Database Syst Rev. 2012 Oct 17;10:CD010005

4. Sears M, Safe use of long-acting β-agonists: what have we learnt?, Expert Opin Drug Saf. 2011 Sep;10(5):767-78.

5. Nelson H et al, The Salmeterol Multicenter Asthma Research Trial: A Comparison of Usual Pharmacotherapy for Asthma or Usual Pharmacotherapy Plus Salmeterol, CHEST, January 2006, Vol 129, No. 1

6. McMahon A et al, Age and Risks of FDA-Approved Long-Acting β2-Adrenergic Receptor Agonists, Pediatrics Vol. 128 No. 5 November 1, 2011

7. Lougheed M et al, Canadian Thoracic Society 2012 guideline update: Diagnosis and management of asthma in preschoolers, children and adults, Can Respir J Vol 19 No 2 March/April 2012

8. Kovesi T et al, Achieving Control of Asthma in Preschoolers, CMAJ March 9, 2010 vol. 182 no. 4

9. Lougheed MD et al, Canadian Thoracic Society Asthma Committee commentary on long-acting beta-2 agonist use for asthma in Canada. Canadian Respiratory Journal 2010;17(2):57–58.

Last updated: Aug 10 2018