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The best asthma care is not good enough if the patient is nonadherent. Applied "humanomics" as an approach to chronic care was discussed this week at CHEST 2015.
A panel presentation on evolution in asthma care at the ACCP 2015 meeting (CHEST 2015) in Montreal began with an overview by Professor Mark FitzGerald, MD, the Head of Respiratory Medicine at University of British Columbia, of results from “Preventable Burden of Productivity Loss Due to Suboptimal Asthma Control Study.” The study’s bottom line revealed substantial gains in productivity obtained by achieving tight and consistent asthma control.1 Dr Fitzgerald then cited a nationwide study on medication adherence in chronic disease2 that found between 2002 and 2007 there was a 300% increase in the use of combination therapy for asthma. That is the good news. Unfortunately, that improvement in prescribed therapy was associated with only a 44% reduction in hospitalizations from poorly controlled asthma.2 This discrepancy was largely explained by data showing poor patient adherence to medications. There also were data suggesting poor adherence by physicians to guidelines.2
Professor FitzGerald concluded that one of the many challenges to effective asthma care is poor health literacy which impacts patient adherence. What is needed? The creation of customized, patient-friendly treatments that anticipate and accommodate individual patient behaviors and medication beliefs will help. It’s a tall order, but asthma care that targets patient-specific needs in multiple domains is more likely to achieve the desired goal of disease control.3
The full title of this session, “Evolutions in Adult and Pediatric Asthma Care: From Guidelines to Humanomics” is meant to remind that even with the explosion of medical technology that allows therapeutic interventions never dreamed of, we must fully acknowledge the cultural and behavioral aspects of providing care-the “humanomics” of medicine-because we deal with individual humans, each with a unique blend of characteristics that together can thwart the best evidence-based treatments we have.
At the same session, Professor Stephen Lazarus, MD from the Department of Medicine (Pulmonary and Critical Care), at UCSF, talked about the development of better biomarkers for diagnosis of asthma as well as monitoring disease control. Early in the 21st century, severe asthma was divided pathologically into two inflammatory subtypes (eosinophil positive and eosinophil negative), each having distinct physiologic and clinical characteristics.4 The distinction is critical since corticosteroids are considered useful in treatment of chronic asthma provided the sputum contains large number of eosinophils. In the absence of eosinophils, a response to steroids is less likely-and, thus, effective symptom control elusive.
Earlier in the session, data were presented that suggest better biomarkers indeed are coming (eg, fractional exhaled nitric oxide, blood total eosinophil count, sputum eosinophilic cationic protein, and serum IgE).5
In a randomized controlled trial, Jayaram et al, demonstrated that patients whose treatment was managed by sputum cell counts have reductions in the number of eosinophilic exacerbations and reductions in the severity of both eosinophilic and noneosinophilic exacerbations of asthma without an increase in total corticosteroid dose.6 Wagener et al proposed monitoring blood eosinophils as a surrogate for sputum eosinophils.7
Professor Lazarus concluded that alongside the rapid development of several biologic agents for the treatment of asthma, parallel progress is being made with additional biomarkers in the pipeline for monitoring disease severity, patient responses to therapy, and predicting future exacerbations.8
What does all of this mean to primary care? First, since not all patients with asthma are the same, we can anticipate future treatments that are tailored to an individual patient’s “type” of asthma. Those with eosinophils will receive therapy different from those individuals without eosinophils. Also, there will be better ways to determine if a patient is responding to therapy (biomarkers). Right now, one treatment approach (Ã-agonist inhalers, corticosteroid inhalers, and oral or parenteral steroids) is the backbone for all therapy. In the future, that approach will be expanded and focused more on individual patient characteristics. In the meanwhile, follow treatment guidelines and for patients who are not adherent, apply some humanomics to the problem by considering everything you know about each one-and exploring where the communication is weak.
1. Sadatsafavi M, Rousseau R, Chen W, Zhang W, Lynd L, FitzGerald JM; Economic Burden of Asthma Study Team. The preventable burden of productivity loss due to suboptimal asthma control: a population-based study. Chest. 2014;145:787-793. doi:10.1378/chest.13-1619. http://www.ncbi.nlm.nih.gov/pubmed/?term=10.1378%2Fchest.13-1619
2. Thier SL1, Yu-Isenberg KS, Leas BF, et al. In chronic disease, nationwide data show poor adherence by patients to medication and by physicians to guidelines. Manage Care. 2008;17:48-52, 55-7. PMID: 18361259 http://www.managedcaremag.com/linkout/2008/2/48
3. Bateman ED. Treatment adherence in asthmatic patients: the last frontier? J Allergy Clin Immunol. 2014 Dec;134(6):1269-70. doi: 10.1016/j.jaci.2014.08.004. PMID: 25258141 http://www.ncbi.nlm.nih.gov/pubmed/?term=10.1016%2Fj.jaci.2014.08.004.
4. Wenzel SE1, Schwartz LB, Langmack EL Evidence that severe asthma can be divided pathologically into two inflammatory subtypes with distinct physiologic and clinical characteristics. Am J Respir Crit Care Med. 1999;160:1001-8. http://www.ncbi.nlm.nih.gov/pubmed/?term=Am+J+Respir+Crit+Care+Med.+1999+Sep%3B160%283%29%3A1001-8.
5. Martin RJ1, Szefler SJ, King TS. The Predicting Response to Inhaled Corticosteroid Efficacy (PRICE) trial. J Allergy Clin Immunol. 2007 Jan;119(1):73-80. http://www.ncbi.nlm.nih.gov/pubmed/?term=J+Allergy+Clin+Immunol.+2007+Jan%3B119%281%29%3A73-80.
6. L. Jayaram, M. M. Pizzichini, R. J. Cook, et al. Determining asthma treatment by monitoring sputum cell counts: effect on exacerbations. Eur Respir J. 2006;27:483-94. http://erj.ersjournals.com/content/27/3/483.long
7. Wagener AH, de Nijs SB, Lutter R, et al. External validation of blood eosinophils, FE(NO) and serum periostin as surrogates for sputum eosinophils in asthma. Thorax. 2015;70:115-20. doi: 10.1136/thoraxjnl-2014-205634. http://www.ncbi.nlm.nih.gov/pubmed/?term=10.1136%2Fthoraxjnl-2014-205634.
8. Gauthier M, Ray A, Wenzel SE. Evolving concepts of asthma. Am J Respir Crit Care Med. 2015; 192:660-8. doi: 10.1164/rccm.201504-0763PP. http://www.ncbi.nlm.nih.gov/pubmed/?term=10.1164%2Frccm.201504-0763PP.