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Clinical Investigations: ASTHMA |

Asthma, Allergy, and Airway Hyperresponsiveness Are Not Linked to the β2-Adrenoceptor Gene*

Charles W. Emala, MD; Christopher K. McQuitty, MD; Scott M. Eleff, MD; Patricia Hopkins-Price, PhD; Carl Lawyer, MD; Josephine Hoh, PhD; Jurg Ott, PhD; Michael A. Levine, MD; Carol A. Hirshman, MD
Author and Funding Information

*From the Departments of Anesthesiology (Drs. McQuitty, Emala, and Eleff), Pediatrics (Dr. Levine), and Environmental Health Sciences (Dr. Hirshman), The Johns Hopkins Medical Institutions, Baltimore, MD; the Department of Internal Medicine (Drs. Hopkins-Price and Lawyer), Division of Pulmonary Medicine, The Southern Illinois University School of Medicine, Springfield, IL; the Division of Biostatistics (Dr. Hoh), The Joseph L. Mailman School of Public Health, Columbia University, New York, NY; and the Laboratory of Statistical Genetics (Dr. Ott), Rockefeller University, New York, NY.

Correspondence to: Charles Emala, MD, Department of Anesthesiology, Columbia University College of Physicians and Surgeons, 630 W. 168th St, PH 525, New York, NY 10032; e-mail: cwe5@columbia.edu



Chest. 2002;121(3):722-731. doi:10.1378/chest.121.3.722
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Study objectives: To exclude genetic linkage between the β2-adrenoceptor gene and asthma, allergy, and methacholine airway hyperresponsiveness.

Design: The current study used six distinct intragene markers within the β2-adrenoceptor gene, and evaluated genetic linkage between the β2-adrenoceptor and asthma, allergy, or methacholine airway hyperresponsiveness in eight multiplex families.

Patients: Forty-nine members of eight multiplex families with a high incidence of asthma.

Interventions: Phenotypes were characterized by history, physical examination, skin testing, pulmonary function tests, and methacholine inhalational challenge. Genetic loci were identified using restriction fragment length polymorphisms, denaturing gradient gel electrophoresis, and restriction enzyme digest of polymerase chain reaction-amplified fragments of the β2-adrenoceptor gene.

Measurements and results: Nonparametric analysis using computer analysis software found no evidence for linkage between these markers within the β2-adrenoceptor gene and asthma. Parametric exclusion analysis using a dominant inheritance model resulted in large negative lod scores (− 6.74, − 19.44, and − 49.9, respectively) for tight linkage between asthma, allergy, or methacholine airway hyperresponsiveness and these polymorphic markers.

Conclusions: These results indicate that asthma, allergy, and methacholine airway hyperresponsiveness are not linked to a dominant β2-adrenoceptor gene with strong effect in these eight families with an inherited pattern of asthma.

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