Medicine:Dutch hypothesis
The Dutch hypothesis provides one of several biologically plausible explanations for the pathogenesis of chronic obstructive pulmonary disease (COPD), a progressive disease known to be aetiologically linked to environmental insults such as tobacco smoke.[1] The Dutch hypothesis was originally proposed by Dick Orie and his team in 1961 at the University of Groningen.[2][3] According to Orie, "Bronchitis and Asthma may be found in one patient at the same age but as a rule there is a fluent development from bronchitis in youth to a more asthmatic picture in adults, which in turn develops into bronchitis of elderly patients."[4] This supposition was later named the Dutch hypothesis by a colleague, Professor C. Fletcher.[2] Specifically, clinical characteristics such as allergy and bronchial hyperresponsiveness that are commonly observed in individuals afflicted with asthma were viewed as likely determinants of the life-threatening disease, COPD (in the Netherlands, the term chronic non-specific lung disease was adopted as an umbrella term for asthma and COPD).[citation needed]
More recent molecular biology research suggests that the pathogenesis of asthma and COPD may share overlapping pathways involving innate biological susceptibility, coupled with environmental factors which can trigger the different diseases. Genetic association studies that have uncovered the same polymorphisms in people with asthma and COPD provide support for the notion that the two conditions share some biological characteristics; implicated genes include ADAM33, CCL5 and IL17F.[5]
Although clinically debated,[6][7] the Dutch hypothesis remains one of four main plausible explanations which could help explain the complex pathogenesis of COPD, others being the protease-antiprotease hypothesis (involving alpha 1-antitrypsin overexpression and consequent alpha-1 proteinase deficiency), the British hypothesis (regarding a putative aetiological role of acute bronchial infections), and the autoimmunity hypothesis.[1]
References
- ↑ 1.0 1.1 "Pathobiologic mechanisms of chronic obstructive pulmonary disease". Med. Clin. North Am. 96 (4): 681–98. July 2012. doi:10.1016/j.mcna.2012.04.012. PMID 22793938.
- ↑ 2.0 2.1 "In memoriam Professor Dick Orie". European Respiratory Journal 28 (5): 891–2. 2006. doi:10.1183/09031936.00115706.
- ↑ Kauffmann, Francine; Demenais, Florence (17 October 2002). "Chronic obstructive pulmonory disease - Pathophysiology: biologic basis of genetic susceptibility". in King, Richard A.; Rotter, Jerome I.; Motulsky, Arno G.. The Genetic Basis of Common Diseases. Oxford University Press. pp. 163–171. ISBN 978-0-19-512582-5. https://books.google.com/books?id=xKC4swxJC1UC&pg=PA163. Retrieved 19 November 2012.
- ↑ As quoted in: John A. Goodfellow (31 January 2012). Understanding Medical Research: The Studies That Shaped Medicine. Wiley. p. 13. ISBN 978-1-119-96373-8. https://books.google.com/books?id=tIGPTVuY9jkC&pg=PT133. Retrieved 15 November 2012.
- ↑ Hizawa, N (September 2009). "Genetic backgrounds of asthma and COPD.". Allergology International 58 (3): 315–22. doi:10.2332/allergolint.09-RAI-0105. PMID 19628974.
- ↑ Kraft, M (August 2006). "Asthma and chronic obstructive pulmonary disease exhibit common origins in any country!". American Journal of Respiratory and Critical Care Medicine 174 (3): 238–40; discussion 243–4. doi:10.1164/rccm.2604007. PMID 16864716.
- ↑ Barnes, PJ (August 2006). "Against the Dutch hypothesis: asthma and chronic obstructive pulmonary disease are distinct diseases". American Journal of Respiratory and Critical Care Medicine 174 (3): 240–3; discussion 243–4. doi:10.1164/rccm.2604008. PMID 16864717.
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