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AnnuAl Congress of MAlAysiAysi An ThorAC iC soCieTy anniversary MALAYSIAN THORACIC SOCIETY Advancing Thoracic Medicine in Malaysia for 25 years aCknowledgeMents The Organising Committee of the MTS Annual Congress 2011 expresses its deep appreciation to the following for their support and contributions: PLAtinuM PArtners GlaxoSmithKline Pharmaceutical Sdn Bhd Merck Sharp & Dohme Novartis Corporation (M) Sdn Bhd goLD PArtners AstraZeneca Sdn Bhd Roche (Malaysia) Sdn Bhd siLver PArtner Bayer Healthcare other PArtners Acucare System (M) Sdn Bhd Boehringer Ingelheim (Malaysia) Sdn Bhd Daya Cergas (M) Sdn Bhd Delta Medisains (M) Sdn Bhd Easmed Sdn Bhd Edaran Bio-Medik Sdn Bhd Eli Lilly (M) Sdn Bhd Endodynamics (M) Sdn Bhd First Pharmaceuticals Sdn Bhd Goodlabs Medical (M) Sdn Bhd Healol Pharmaceuticals Sdn Bhd Insan Bakti Sdn Bhd Janssen-Cilag Novartis Corporation (M) Sdn Bhd Nycomed Malaysia Sdn Bhd Pahang Pharmacy Sdn Bhd Pfizer (Malaysia) Sdn Bhd Rigel Pharma Sdn Bhd Screen Diagnostics Somnotec (M) Sdn Bhd SymbioMed Sdn Bhd Unipress Distributor Sdn Bhd 15
Annual Congress of Malaysian Thoracic Society Plenary Lecture 1 CURRENT UNDERSTANDING OF ASTHMA PHENOTYPES Philip Thompson Australia Asthma is a common condition worldwide. Allergic asthma and other allergic diseases are increasing in the Western World for reasons that are not entirely clear. Definitions of asthma are not robust and this remains a challenge. The prevailing paradigm has been that asthma is one disease entity but has often subdivided into atopic and non atopic. Symptomatic improvement is provided by Beta 2 adrenergic receptor antagonists, while inhaled corticosteroids are assumed to be the mainstay of preventing asthma. Severe asthma affects at least 10% of the asthma population but accounts for up to 60% of asthma care health costs. Clinical trials in which inhaled corticosteroids are used frequently show 30% or more get worse while on inhaled steroid. Patient’s symptom complex can vary from one patient to another and drug responsiveness also varies. Many patients have both atopic and non atopic triggers. Large scale attempts to find genes relevant to asthma have on the whole been disappointing. Despite protracted stability patients can deteriorate quickly with infection. As such it is more likely that there are multiple forms of asthma, with differing mechanisms and that they can coexist in the one patient. Phenotypic descriptions are only as good as the variables chosen and then how they are applied. Cluster analysis is potentially useful but the same caveats apply. The variables that can be applied to derive phenotypic descriptions may include the following variables: epidemiology data, triggers, clinical features, physiology, induced sputum/exhaled mediators, genetic criteria and treatment responsiveness. Some suggested phenotypes include: allergic; aspirin/NSAID; alcohol; food additives; cold air/exercise/acute stress; reflux; small airways asthma; fixed airway obstruction; inhaled chemicals; post viral syndromes; sputum producing, hyper-eosinophilic; steroid resistant; and obesity syndromes. It is likely that interaction occurs between these phenotypes. It is likely that as one phenotype improves a beneficial bystander effect will occur for other phenotypes. Secondary disease states such as ABPA and Churg Strauss serve only to complicate matters for physicians. Ultimately it is only by linking mechanistic pathways to phenotypic descriptions that we will develop appropriate treatment strategies for the difficult asthma patient. 16
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