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Diseases represent extremes of continuously distributed characteristics, and defining exactly where and why in that distribution normality ends and disease begins may be difficult. The use of objective markers can be helpful, but these often force us to change our concept of a disease to accommodate the new information they provide—such as the identification of subclinical disease or adverse prognostic factors in otherwise healthy people. These conceptual changes are part of the natural evolution of disease definition and are justified if, in the long run, patients benefit. Asthma has always been a clinical diagnosis, recognised on the basis of a characteristic history of variable wheezing, cough, and breathlessness and supported by objective, though non-standardised, evidence of variations in airflow. Many attempts have been made to define this diagnosis. Since 19581 all have highlighted the fundamental abnormality of variable airflow obstruction, and some have also invoked concepts such as airway hyperresponsiveness2 or airway pathology.3 None has yet provided objective criteria for the component parts of this process, and there remains no standardised definition of the …
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Britton et al. (1998) studied this question.
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