We found that one-third of the participants who had received a diagnosis of asthma by a physician had no evidence of asthma when their medications were tapered and when they were evaluated with serial assessments of symptoms, lung function and bronchial challenge tests. One obvious interpretation of this observation is that asthma was overdiagnosed in the community. Consequently, overdiagnosis and changes in diagnostic labelling may be contributing to increases in the prevalence of asthma reported in developed countries.
An alternative possibility is that some of the adults in our study may have received an appropriate diagnosis but experienced remission of their asthma since then. Studies involving children have suggested that up to 5% of those aged 7–12 years with asthma may experience persistent remission of their asthma (defined as absence of asthma symptoms without use of asthma medications for more than 1 year).21
However, the situation is different for adults with asthma. A Swedish study involving 300 adults from the community with physiologically confirmed asthma observed an average annual remission rate of less than 1% and an overall remission rate of only 5.8% over 10 years of follow-up.22
A second study in Sweden involving 309 adults with newly diagnosed asthma showed that, after a mean follow-up of 70 months, 95% of the patients still had active asthma (defined as the presence of asthma symptoms or use of asthma medications).23
When the authors included a methacholine challenge test to a maximum dose of 8 mg/mL to rule out asthma, as we did in our study, the rate of spontaneous remission was only 3%. Thus, remission of asthma in adulthood appears to be rare and unlikely accounted for more than a small fraction of the adults in our study whose diagnosis of asthma was excluded.
A study involving Canadians without a previous diagnosis of asthma showed evidence of geographic variability in bronchial hyperresponsiveness.24
Geographic variability could theoretically account for regional differences in the rates of overdiagnosis of asthma. However, we found that study site was not associated with a diagnosis of asthma being confirmed or excluded (p
= 0.22). Similarly, bronchial hyperresponsiveness may vary seasonally; however, we did not find any potential seasonal confounding effects on asthma diagnosis.
Short-and long-term studies have shown that the regular use of inhaled corticosteroids will result in improvements in airway hyperresponsiveness, sometimes with full resolution, and corresponding improvements in clinical status.25
Thus, when trying to exclude a diagnosis of asthma, patients need to be assessed after their anti-inflammatory medicines have been stopped. Previous studies of patients with well-controlled asthma have shown that airway hyperresponsiveness increases significantly within 20 days after discontinuation of inhaled corcitosteroid therapy.26
In our study patients were asked to taper and then stop their asthma medications over 4–6 weeks in order to remove the confounding effects of the medications on the ability to confirm a diagnosis of asthma.
We also assessed the clinical outcomes of patients who were found to have no evidence of asthma. Sixty-six percent of these patients did not need to take any asthma medications and did not seek health care services because of asthma symptoms during the 26-week follow-up period after their asthma medications had been stopped. Only 11 (7.7%) required an unscheduled evaluation by a health care professional because of respiratory symptoms. This observation suggests that our approach to stopping medications in patients in whom asthma was excluded was safe; however, a minority of patients did experience respiratory symptoms that may or may not have been attributable to asthma.
Other studies have suggested an overdiagnosis of asthma in the community. A smaller study involving 90 self-referred individuals with asthma in Canada suggested that 41% did not have asthma when objectively tested.27
Schachter and colleagues studied adults in Australia in a cross-sectional epidemiologic study.28
They found that obesity was a significant risk factor for diagnosis of asthma (OR 2.04), wheezing and use of asthma medications (OR 2.83), but not for airway hyperresponsiveness or airflow obstruction. The authors concluded that, although individuals with severe obesity reported more symptoms consistent with asthma, their lung function tests did not support the suggestion of a higher prevalence of asthma. However, participants in their study did not stop their asthma medications before the lung function testing, which may have confounded the results.
People who are obese are more likely than nonobese people to report dyspnea. In a study involving otherwise healthy younger obese women who did not have asthma, more than 37% reported an elevated intensity of breathlessness during moderate exercise.11
Exertional dyspnea in these individuals was strongly associated with an increased oxygen cost of breathing. This may explain why obese people may report increased breathlessness with exertion, and in turn could explain why asthma is more likely to be diagnosed and treated in obese patients. However, we did not find a significant difference in the rates of overdiagnosis between the obese and nonobese participants in our study. This suggests that the increased prevalence of asthma in association with obesity that has been reported in previous population-based studies is a real phenomenon and not solely due to diagnostic mislabelling.
The recent rise in the prevalence of asthma in developed countries may be a consequence of patients' better education, increased awareness of symptoms and increased readiness to report them to a physician.29
In our study, more than 75% of the participants in whom asthma was eventually excluded reported dyspnea and wheezing in the 12 months before study entry. This increase in reporting of symptoms is probably occurring in concert with physicians' increased willingness to make a diagnosis of asthma in response to respiratory symptoms.
Our study has limitations. First, many potentially eligible individuals did not agree to participate in the study. Volunteer bias could have possibly influenced the study results. Those who agreed to enroll in the study may have doubted their diagnosis of asthma in the first place, either because they had not previously undergone an extensive diagnostic workup, or because their asthma medications were not working to relieve their symptoms. If this were the case, preferential participation by these individuals may have theoretically inflated the overall proportion who were ultimately found to have no asthma.
Second, it was difficult to accurately classify patients with severe restriction due to obesity. Similarly, it was difficult to rule out asthma in participants who may have had fixed airflow obstruction. Three obese participants could not be classified because they had severe restrictive defects and an FEV1 less than 60% of predicted. In addition, 3 of the 150 participants in whom asthma was excluded did have fixed airflow obstruction. These 3 individuals may have been misclassified.
There are obvious consequences associated with a misdiagnosis of asthma, including the lost opportunity to investigate or treat the cause of the patient's respiratory symptoms appropriately, the patient's potential exposure to the adverse effects of asthma medications, the cost of asthma medications, and the social consequences and psychological impact on the patient of being labelled with a chronic respiratory disease. Our study showed that a substantial proportion of people, whether obese or not, may be overdiagnosed with asthma and may be prescribed asthma medications unnecessarily. Physicians should consider objective testing using spirometry and, if necessary, bronchial challenge testing to confirm asthma in patients with respiratory symptoms.
Members of the Steering Committee of the Canadian Respiratory Clinical Research Consortium: Dr. Shawn Aaron, University of Ottawa, Ottawa, Ont.; Dr. Louis-Philippe Boulet, UniversitéLaval, Québec, Que.; Dr. Jean Bourbeau, McGill University, Montréal, Que.; Dr. Penny Brasher, University of British Columbia, Vancouver, BC; Dr. Dina Brooks, University of Toronto, Toronto, Ont.; Dr. Lisa Cicutto, University of Colorado, Denver, USA; Dr. Rajashree Devarakonda, University of British Columbia, Vancouver, BC; Dr. Mark Fitzgerald, University of British Columbia, Vancouver, BC; Dr. John Fleetham, University of British Columbia, Vancouver, BC; Dr. Catherine Lemiere, Université de Montréal, Montréal, Que.; Dr. Brian Rowe, University of Alberta, Edmonton, Alta.; and Ms. Katherine Vandemheen, Ottawa Health Research Institute, Ottawa, Ont.