Heritability of Respiratory Infection with Pseudomonas aeruginosa in Cystic Fibrosis - 24/07/12
Reprint requests: Garry R. Cutting, MD, The Johns Hopkins Medical Institutions, 733 North Broadway, BRB 559, Baltimore, MD 21205.Abstract |
Objective |
To quantify the relative contribution of factors other than cystic fibrosis transmembrane conductance regulator genotype and environment on the acquisition of Pseudomonas aeruginosa (Pa) by patients with cystic fibrosis.
Study design |
Lung infection with Pa and mucoid Pa was assessed using a co-twin study design of 44 monozygous (MZ) and 17 dizygous (DZ) twin pairs. Two definitions were used to establish infection: first positive culture and persistent positive culture. Genetic contribution to infection (ie, heritability) was estimated based on concordance analysis, logistic regression, and age at onset of infection through comparison of intraclass correlation coefficients.
Results |
Concordance for persistent Pa infection was higher in MZ (0.83; 25 of 30 pairs) than DZ twins (0.45; 5 of 11 pairs), generating a heritability of 0.76. Logistic regression adjusted for age corroborated genetic control of persistent Pa infection. The correlation for age at persistent Pa infection was higher in MZ twins (0.589; 95% CI, 0.222-0.704) than in DZ twins (0.162; 95% CI, −0.352 to 0.607), generating a heritability of 0.85.
Conclusion |
Genetic modifiers play a significant role in the establishment and timing of persistent Pa infection in individuals with cystic fibrosis.
Le texte complet de cet article est disponible en PDF.Mots-clés : CF, CFTR, DZ, FEV1, MBL2, MPa, MZ, Pa
Plan
| Supported by National Institutes of Health Grants NHLBI T32 HL072748 (to D.G.), NHLBI HL068927 (to G.C.), and NIDDK DK076446 (to S.B). The National Institutes of Health had no role in the study design; collection, analysis, and interpretation of data; writing of the manuscript; or the decision to submit the manuscript for publication. The authors declare no conflicts of interest. |
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| This work was published in part in abstract form in Pediatric Pulmonology 2008, Supplement 31 (abstract 232) and Pediatric Pulmonology 2009, Supplement 32 (abstract 170). |
Vol 161 - N° 2
P. 290 - août 2012 Retour au numéro
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