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The Dutch Hypothesis* FREE TO VIEW

N. G. M. Orie, MD
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*Dr. Orie is Emeritus Professor of Pulmonary Diseases at the State University of Groningen, Groningen, The Netherlands.

Correspondence to: N. G. M. Orie, MD, Emeritus Professor of Pulmonary Diseases, Kerkstraat 12, 9951AD, Winsum, The Netherlands; e-mail: holloway@inn.nl

Chest. 2000;117(5_suppl_1):299S. doi:10.1378/chest.117.5_suppl_1.299S
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Mr. Chairman, ladies, and gentlemen. First of all, my thanks to Professor Petty and the organizing committee for the kind invitation to participate in the Aspen Conference, and also Tom, for your warm welcome and the support I got in those disturbing days when my wife became ill. I am very glad to be able to give a short survey of the Dutch hypothesis (dubbed by Fletcher); there are too many descriptions that are incomplete and often confusing.

The Dutch Hypothesis

William Wordsworth said, “The child is father of the man,” and this is, in essence, what the Dutch hypothesis is about. The asthmatic child becomes the father of the COPD man.

Childhood respiratory disease occurs in children mainly as a result of pneumonia that has developed as a complication of measles and whooping cough (and perhaps other related infections, such as respiratory syncytial virus). In 1939, it was suggested in the United States1 that bronchitis and bronchiectasis were often found in asthmatic patients. Later observations in Groningen confirmed the existence of bronchial hyperreactivity and reversibility of bronchial obstruction in these patients.

In the Western World, there have been three phases marking the progress of such patients. Before the 1930s, these children often died at an early age. Those affected, in some epidemics, constituted 15% of the childhood population < 3 years old (phase 1). After that, many children survived, but the sequelae of their pneumonia was bronchitis and scattered bronchiectasis (phase 2). This second phase, which is still current in developing countries, occurred in Europe between 1940 and 1970. Children survived as a result of a combined effect of sulfa drugs, vaccinations for whooping cough (1939) and measles (1971), antibiotics, and (probably) corticosteroids. The prevalence of chronic purulent infections dropped. In the third phase, which started in Europe in approximately 1975, the death rate of these (mostly very young) children dropped down to zero. It is probable that no important sequelae were seen any more.

The rate of asthma in children has risen lately, probably as a result of the absence of chronic infections. In older patients, remnants of their childhood illnesses are still seen, although to a decreasing extent. These are the patients who were born in the 1930s, and who fathered the COPD patients we see today.

Watson, SM, Kibler, CS (1939) The role of allergy in bronchiectasis.J Allergy10,364




Watson, SM, Kibler, CS (1939) The role of allergy in bronchiectasis.J Allergy10,364
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