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Clinical Asthma Syndromes and Important Asthma Mimics

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Clinical Asthma Syndromes and Important Asthma Mimics Clinical Asthma Syndromes and Important Asthma Mimics Christopher S King MD and Lisa K Moores MD Introduction Clinical Phenotypes Severity-Defined Exacerbation-Prone Asthma With Chronic Airflow Obstruction Treatment-Resistant Asthma Asthma Defined by Age at Onset Trigger-Related Phenotypes Inflammatory Phenotypes Why Do Phenotypes Matter? Asthma Mimics Chronic Obstructive Pulmonary Disease Vocal Cord Dysfunction Summary Asthma is a heterogeneous disorder with multiple clinical phenotypes. Phenotypes can be grouped into clinical or physiological, trigger-defined, and inflammatory phenotypes. Treatment based on inflammatory phenotyping improves clinical measures of asthma morbidity. Further study of in- dividual asthma phenotypes will improve understanding of their immunologic and pathologic char- acteristics and improve diagnosis and therapy. Because asthma is a common disorder with non- specific presenting features, other disorders are often misdiagnosed as asthma. A high index of suspicion for alternative diagnoses must be maintained when evaluating a patient who presents with clinical features suggestive of asthma, particularly if the patient presents with atypical symptoms or fails to respond to therapy. Key words: asthma; phenotypes; asthma, etiology; asthma, genetics; asthma, mimics; vocal cord dysfunction. [Respir Care 2008;53(5):568–580] Introduction are poorly characterized, with little known about the un- derlying pathophysiology. The recent development of tar- Asthma is probably not a single disease, but rather a complex of multiple, separate syndromes that overlap. Sev- eral classification schemes have been proposed, but many The opinions and assertions in this report are the private views of the authors and are not to be construed as official or as the views of the Department of the Army or the Department of Defense. Christopher S King MD is affiliated with the Pulmonary, Critical Care, and Sleep Medicine Service, Department of Medicine, Walter Reed Army Dr Moores presented a version of this paper at the 41st RESPIRATORY Medical Center, Washington DC. Lisa K Moores MD is affiliated with CARE Journal Conference, “Meeting the Challenges of Asthma,” held the Department of Medicine, Uniformed Services University of the Health September 28–30, 2007, in Scottsdale, Arizona. Sciences, Bethesda, Maryland. Correspondence: Lisa K Moores MD, Office for Student Affairs, Uni- The authors report no conflicts of interest related to the content of this formed Services University of the Health Sciences, 4310 Jones Bridge paper. Road, Bethesda MD 20814. E-mail: [email protected]. 568 RESPIRATORY CARE • MAY 2008 VOL 53 NO 5 CLINICAL ASTHMA SYNDROMES AND IMPORTANT ASTHMA MIMICS geted asthma therapies has raised renewed interest in asthma Table 1. Potential Asthma Phenotypes phenotypes. However, there is no standardized method or agreed-upon classification system to define asthma phe- Clinical or Physiological Phenotypes Severity-defined notypes. Focus has recently shifted to classification of Exacerbation-prone asthma based on immunopathology, specifically the cel- Defined by chronic airflow obstruction lular makeup of the inflammatory response. Studies have Treatment-resistant shown clinical improvement with management strategies Defined by age at onset that target inflammation rather than symptoms and peak Trigger-Related Phenotypes flow.1,2 Better defining asthma phenotypes may improve Aspirin or nonsteroidal anti-inflammatory drug understanding of the underlying pathobiology of the phe- Environmental allergens notypes and lead to targeted therapies for individual phe- Occupational allergens notypes. In this article we will explore the characteristics Menses of 3 categories of asthma phenotypes: clinical phenotypes, Exercise trigger-defined phenotypes, and inflammatory phenotypes. Inflammatory Phenotypes We will then discuss conditions that commonly mimic Eosinophilic asthma, with particular attention to chronic obstructive Neutrophilic pulmonary disease (COPD) and vocal cord dysfunction. Paucigranulocytic The 2007 National Asthma Education and Prevention (Adapted from Reference 4.) Program’s Expert Panel Report 3, Guidelines for the Di- agnosis and Management of Asthma, defines asthma as “a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, Clinical Phenotypes airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation.”3 This purposefully broad defi- The clinically or physiologically defined phenotypes pro- nition encompasses the many phenotypes of asthma, but posed by Wenzel include: severity-defined asthma, exac- poorly accentuates important differences. The current strat- erbation-prone asthma, asthma defined by chronic airflow egy of “lumping” asthma phenotypes together, with treat- obstruction, treatment-resistant asthma, and asthma defined ment based solely on asthma severity, hinders efforts to- by age at onset.4 ward therapy specifically targeted at the underlying etiology. Despite the call for a new taxonomy of asthma, Severity-Defined there is no current consensus regarding categorization of asthma by phenotype. We believe that the categorization The severity-defined phenotype is advocated by the ma- proposed in a recent review by Wenzel, the preeminent jor national and international guidelines and therefore is expert on asthma phenotyping, is the most comprehensive among the most commonly used clinically.3,6 The Global 4 and descriptive. Wenzel describes 3 potential phenotypic Initiative for Asthma guidelines6 recommend classifying categories: clinical or physiological, trigger-related, and asthma as intermittent, mild persistent, moderate persis- inflammatory (Table 1). tent, or severe persistent when making initial assessment Phenotype is defined as “the observable characteristics, and treatment decisions. Though severity-defined assess- at the physical, morphologic, or biochemical level, of an ment may help develop an initial treatment strategy, it individual, as determined by the genotype and the envi- does not adequately predict the clinical course and re- ronment.”5 This definition yields 2 key points: (1) pheno- sponse to therapy. Bateman and colleagues assessed the typic characteristics of asthmatic patients are only those efficacy of escalating doses of either salmeterol/flutica- that are observable, and (2) asthma phenotypes are deter- sone or fluticasone in achieving symptom control, as de- mined by the complex interaction between environmental fined by the Global Initiative for Asthma 2002 guidelines.7 and genetic factors. Note that there is substantial overlap Despite escalating doses of inhaled corticosteroids and rig- between phenotypic categories. An example of this is mod- orous follow-up, only 71% of patients were well-controlled erately persistent allergen-induced asthma in a child. One and a mere 31% achieved total control in the salmeterol/ could phenotype based on severity, age of onset, type of fluticasone arm. An even lower success rate was achieved trigger, or the underlying inflammatory phenotype. All of in the fluticasone arm. Though those authors concluded these approaches are valid, but the optimal approach would that the goal of guideline-derived asthma control was consider all of these phenotypes in an effort to get at the achieved in a majority of patients, a substantial minority underlying pathobiologic mechanisms of asthma in this did not achieve control, despite appropriate medication particular patient. and follow-up. RESPIRATORY CARE • MAY 2008 VOL 53 NO 5 569 CLINICAL ASTHMA SYNDROMES AND IMPORTANT ASTHMA MIMICS Another disadvantage of severity phenotyping is dispar- steroid-dependent patients with severe asthma. They found ity in the assessment of severity. Miller et al8 compared 2 distinct inflammatory milieus: 14 patients had nearly physician assessment of asthma severity to those estab- absent eosinophils; the remainder were considered eosino- lished by the National Asthma Education and Prevention phil-positive. Both groups had similar baseline FEV1 and Program and the Global Initiative for Asthma groups in bronchodilator response, but the eosinophil-positive group 2,927 patients enrolled in the Epidemiology and Natural had more intubations than the eosinophil-negative group History of Asthma: Outcomes and Treatment Regimens (12/20 vs 1/14, p Ͻ 0.001).14 Another recent study, by Qiu cohort. They found a clear lack of agreement among asthma et al, assessed endobronchial biopsy specimens from pa- severity assessment modalities, though patients considered tients with severe asthma exacerbations. They found both to have severe asthma by all 3 assessments had greater bronchial neutrophilia and eosinophilia.15 Given the above health-care and medication usage. In conclusion, severity- studies, it seems that the baseline level of eosinophilic defined phenotypes are widely used and have some utility inflammation plays a key role in exacerbation-prone in predicting health-care utilization and medication usage; asthma. Further studies are needed to clarify this issue. however, they cannot adequately predict clinical course or response to therapy. Asthma With Chronic Airflow Obstruction Exacerbation-Prone Asthma has classically been thought of as a disorder A subgroup of asthmatics predisposed to frequent and characterized by reversible airflow obstruction; however, sometimes severe exacerbations despite adequate treatment irreversible obstruction develops in a portion of both adult has been recognized
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