OUGH, WHEEZING (AND
other respiratory noises),and dyspnea are common respiratory symptomsthat potentially have an extensive differential diagnosis.
Because asthma is an exceedingly common disorder,such symptoms are often a result of this recurring andchronic respiratory disorder. Although there is demon-strable underdiagnosis of asthma,
the purpose of thisreview is to increase awareness of common and uncom-mon entities that have resulted in inappropriate diag-noses of asthma.
Asthma is a disease that is characterized by hyperrespon-siveness of the airways to various stimuli, which resultsin airway obstruction that is reversible either spontane-ously or as a result of treatment. The airway obstructionis from variable components of bronchial smooth musclespasm and inﬂammation that result in edema of therespiratory mucosa and mucous secretions. Althoughthe diagnosis of asthma is frequently readily apparent,we have encountered several clinical entities that have been misdiagnosed as asthma and consequently treatedinappropriately. In this review we describe these clinicalentities, identify how their clinical presentation is con-fused with asthma, and indicate the diagnostic methodsfor identifying these pseudo-asthma syndromes.
Asthma is diagnosed clinically and is suspected whenthere is cough, wheezing, or dyspnea. However, thesame symptoms may be results of other causes. Al-though for some patients the presenting clinical picturecan readily identify the problem as being somethingother than asthma, there can also be legitimate diagnos-tic uncertainty with others. The distinguishing charac-teristic of asthma is the response to bronchodilator orcorticosteroids when the patient is symptomatic. Forpatients who are old enough to perform a pulmonary-function test, substantial improvement of airway ob-struction from an aerosol bronchodilator or a shortcourse of reasonably high-dose systemic corticosteroid, 2mg/kg twice daily to a maximum of 40 mg twice daily(reduced to once daily in the morning if insomnia orirritability becomes problematic), supports diagnosis ofasthma. Failure to observe substantial improvementwithin 5 to 7 days with complete relief of symptoms andsubstantial improvement in lung function after a maxi-mum of 10 days argues against asthma as the etiology,assuming, of course, that the patient has taken the med-ication.
Asthma is the most common cause of chronic or recur-rent inﬂammatory airway disease and a major cause ofcough. Although there are causes of cough that areunlikely to be confused with asthma, there are severalthat characteristically are confused with asthma and re-sult in overdiagnosis of asthma with consequent inap-propriate treatment.
Pertussis, known in the past as the100-day cough, causes a prolonged period of cough, andwe have seen several cases in which the primary carephysician prescribed antiasthmatic medication becausepertussis was not adequately considered. Characteristi-cally spasmodic and associated with posttussive gaggingor emesis, the classical clinical symptoms are often notpresent in an immunized population.
However, thediagnosis is important to prevent spread to contacts, andpertussis should be suspected for any cough that persistsfor
2 weeks in those with no previous history ofasthma or other causes of chronic cough. Diagnosis ismade most readily by polymerase chain reaction from aproperly collected nasal swab to detect pertussis antigen.
Cystic ﬁbrosis is the second most common chronic in-ﬂammatory airway disease, at least among the whitepopulation. It occurs in
1 in 2500 live births in popu-lations of northern European descent with variablelesser incidence in other ethnic groups and races. Al-though the mechanisms of airway inﬂammation are dif-ferent in these 2 diseases, both cause airway obstruction,cough, wheezing, and dyspnea. The classical clinical pre-sentation of malabsorption is not always present, andthe severity and progression of the airway disease ishighly variable. There is a variability in the extent towhich the
1500 mutations of the cystic ﬁbrosis trans-membrane regulator gene alters the chloride channeland results in clinical manifestations.
Consequently,some people do not present with respiratory symptomsuntil adolescence or even adulthood.
Some degree of bronchodilator response may even be present, althoughthe physiology of the airway responsiveness differs fromthat in asthma.
Also, asthma can coexist with cysticﬁbrosis.Cystic ﬁbrosis should be suspected when symptomsand signs of airway inﬂammatory disease persist despitea short course of high-dose systemic corticosteroid. Thediagnosis of cystic ﬁbrosis is made most reliably by per-forming a sweat chloride measurement using the classi-cal quantitative pilocarpine iontophoresis method. Mostof the various screening methods that assess by theconductivity of sweat are unreliable, because they canhave both false-positive and false-negative results.
Forthe test to be valid, duplicate collections of at least 75 mgare required for the ﬁlter-paper discs or gauze pads, andduplicate 15-
L samples are sufﬁcient with the Macro-duct collection coil (Wescor, Logan, UT).
Measurementof 60 mEq/L chloride with substantial agreement in bothsamples is generally diagnostic of cystic ﬁbrosis. Sweatchloride concentrations of
40 mEq/L are generally re-assuring that cystic ﬁbrosis is not the cause of the pa-tient’s airway inﬂammatory disease. Levels of 40 to 60