Rationale for the Dutch hypothesis. Allergy and airway hyperresponsiveness as genetic factors and their interaction with environment in the development of asthma and COPD.
The Dutch hypothesis, formulated in the 1960s, holds that the various forms of airway obstruction are different expressions of a single disease entity. It suggests that genetic factors (eg, airway hyperresponsiveness [AHR] and atopy), endogenous factors (eg, sex and age), and exogenous factors (eg, allergens, infections, and smoking) all play a role in the pathogenesis of chronic nonspecific lung disease. This review finds evidence that AHR and smoking are common risk factors for asthma and COPD. To prove the Dutch hypothesis definitively, however, genetic studies, preferably longitudinal, must be performed. Such studies must include subjects who have airway obstruction that does not necessarily meet the current strict definitions of asthma or COPD (ie, the extremes of these conditions) that are used in clinical studies.
Department of Pulmonology, University Hospital, University of Groningen, Postbus 30001, Hanseplein 1, 9700 RB Groningen, the Netherlands.
Dirkje S
DS
Postma
H Marike
HM
Boezen
D000393:Air Pollutants / Q000009:adverse effects*; D001249:Asthma / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000503:physiopathology; D004781:Environmental Exposure / Q000009:adverse effects*; D005541:Forced Expiratory Volume / Q000502:physiology; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D012130:Respiratory Hypersensitivity / Q000209:etiology* / Q000235:genetics* / Q000503:physiopathology; D012907:Smoking / Q000009:adverse effects / Q000235:genetics / Q000503:physiopathology
D000393:Air Pollutants