ADAM33 gene polymorphisms in chronic obstructive pulmonary disease
<p>Abstract</p> <p>Study objective</p> <p>The pathogenesis of chronic obstructive pulmonary disease (COPD) is characterized by an interaction of environmental influences, particularly cigarette smoking, and genetic determinants. Given the global increase in COPD, resear...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2009-12-01
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| Series: | European Journal of Medical Research |
| Subjects: | |
| Online Access: | http://www.eurjmedres.com/content/14/S4/182 |
| _version_ | 1811284158993924096 |
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| author | Pabst S Touron C Pizarro Gillissen A Lennarz M Tuleta I Nickenig G Skowasch D Grohé C |
| author_facet | Pabst S Touron C Pizarro Gillissen A Lennarz M Tuleta I Nickenig G Skowasch D Grohé C |
| author_sort | Pabst S |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Study objective</p> <p>The pathogenesis of chronic obstructive pulmonary disease (COPD) is characterized by an interaction of environmental influences, particularly cigarette smoking, and genetic determinants. Given the global increase in COPD, research on the genomic variants that affect susceptibility to this complex disorder is reviving. In the present study, we investigated whether single nucleotide polymorphisms in 'a disinter-grin and metalloprotease' 33 (ADAM33) are associated with the development and course of COPD.</p> <p>Patients and design</p> <p>We genotyped 150 German COPD patients and 152 healthy controls for the presence of the F+1 and S_2 SNPs in ADAM 33 that lead to the base pair exchange G to A and C to G, respectively. To assess whether these genetic variants are influential in the course of COPD, we subdivided the cohort into two subgroups comprising 60 patients with a stable and 90 patients with an unstable course of disease.</p> <p>Results</p> <p>In ADAM33, the frequency of the F+1 A allele was 35.0% among stable and 43.9% among unstable COPD subjects, which was not significantly different from the 35.5% found in the controls (P = 0.92 and P = 0.07, respectively). The frequency of the S_2 mutant allele in subjects with a stable COPD was 23.3% (P = 0.32), in subjects with an unstable course 30.6% (P = 0.47).</p> <p>Conclusion</p> <p>The study shows that there is no significant difference in the distribution of the tested SNPs between subjects with and without COPD. Furthermore, these polymorphisms appear to have no consequences for the stability of the disease course.</p> |
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| format | Article |
| id | doaj.art-1c3319fb49774cb5bddff0992e153fdd |
| institution | Directory Open Access Journal |
| issn | 2047-783X |
| language | English |
| last_indexed | 2024-04-13T02:24:31Z |
| publishDate | 2009-12-01 |
| publisher | BMC |
| record_format | Article |
| series | European Journal of Medical Research |
| spelling | doaj.art-1c3319fb49774cb5bddff0992e153fdd2022-12-22T03:06:49ZengBMCEuropean Journal of Medical Research2047-783X2009-12-0114Suppl 418218610.1186/2047-783X-14-S4-182ADAM33 gene polymorphisms in chronic obstructive pulmonary diseasePabst STouron C PizarroGillissen ALennarz MTuleta INickenig GSkowasch DGrohé C<p>Abstract</p> <p>Study objective</p> <p>The pathogenesis of chronic obstructive pulmonary disease (COPD) is characterized by an interaction of environmental influences, particularly cigarette smoking, and genetic determinants. Given the global increase in COPD, research on the genomic variants that affect susceptibility to this complex disorder is reviving. In the present study, we investigated whether single nucleotide polymorphisms in 'a disinter-grin and metalloprotease' 33 (ADAM33) are associated with the development and course of COPD.</p> <p>Patients and design</p> <p>We genotyped 150 German COPD patients and 152 healthy controls for the presence of the F+1 and S_2 SNPs in ADAM 33 that lead to the base pair exchange G to A and C to G, respectively. To assess whether these genetic variants are influential in the course of COPD, we subdivided the cohort into two subgroups comprising 60 patients with a stable and 90 patients with an unstable course of disease.</p> <p>Results</p> <p>In ADAM33, the frequency of the F+1 A allele was 35.0% among stable and 43.9% among unstable COPD subjects, which was not significantly different from the 35.5% found in the controls (P = 0.92 and P = 0.07, respectively). The frequency of the S_2 mutant allele in subjects with a stable COPD was 23.3% (P = 0.32), in subjects with an unstable course 30.6% (P = 0.47).</p> <p>Conclusion</p> <p>The study shows that there is no significant difference in the distribution of the tested SNPs between subjects with and without COPD. Furthermore, these polymorphisms appear to have no consequences for the stability of the disease course.</p>http://www.eurjmedres.com/content/14/S4/182COPDADAM33genetics |
| spellingShingle | Pabst S Touron C Pizarro Gillissen A Lennarz M Tuleta I Nickenig G Skowasch D Grohé C ADAM33 gene polymorphisms in chronic obstructive pulmonary disease European Journal of Medical Research COPD ADAM33 genetics |
| title | ADAM33 gene polymorphisms in chronic obstructive pulmonary disease |
| title_full | ADAM33 gene polymorphisms in chronic obstructive pulmonary disease |
| title_fullStr | ADAM33 gene polymorphisms in chronic obstructive pulmonary disease |
| title_full_unstemmed | ADAM33 gene polymorphisms in chronic obstructive pulmonary disease |
| title_short | ADAM33 gene polymorphisms in chronic obstructive pulmonary disease |
| title_sort | adam33 gene polymorphisms in chronic obstructive pulmonary disease |
| topic | COPD ADAM33 genetics |
| url | http://www.eurjmedres.com/content/14/S4/182 |
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