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dc.contributor.advisorReel, Sally J.en_US
dc.contributor.authorSteffen, Priscilla
dc.creatorSteffen, Priscillaen_US
dc.date.accessioned2011-12-06T13:27:32Z
dc.date.available2011-12-06T13:27:32Z
dc.date.issued2010en_US
dc.identifier.urihttp://hdl.handle.net/10150/194842
dc.description.abstractPurpose/Aims: The American Thoracic Society (ATS) published recommendations for alpha-1 antitrypsin deficiency (AATD) testing in 2003. This descriptive project evaluates the outcomes of ATS AATD guideline use in the setting of the pulmonary function testing (PFT) lab.The specific aims met by this descriptive project describe the prevalence of AATD cases and carriers in the sample, examine to what degree the established clinical guideline promoted accurate patient selection for the alpha-1 test in the sample, and aimed to determine whether alpha-1 antitrypsin blood levels are reduced in current smokers compared to former or never smokers.Background: Alpha-1 antitrypsin prevents lung tissue breakdown by attenuating excess elastase released from neutrophils during the inflammatory response. Smoking impairs alpha-1 antitrypsin protection at the site of lung inflammation promoting emphysema development. In the case of genetic mutation, protective alpha-1 antitrypsin levels are reduced, causing emphysema even in non-smokers. Significantly reduced protective levels of alpha-1 antitrypsin increase the odds for morbidity and early mortality from emphysema. The literature provides support for targeted testing in the population most affected.Sample/Methods: The sample population included adults 21 through 79 years completing pulmonary function testing over 18 months in a metropolitan pulmonary medicine practice and was retrospectively reviewed.Of the 521 in the sample, 190 were tested for AATD, and 24 were found to carry an abnormal genotype. However, using Table 11 from the ATS CPG failed to provide structured, consistent guidance in selecting patients for AATD testing. Still, the prevalence of the abnormal genotypes MS, MZ, SZ, and ZZ was increased in this pulmonary population compared to the published estimated prevalence for the general population.A structured decision-tree, developed from the original guideline for diagnostic testing, may provide superior guidance for AATD test patient selection in this setting. Increased case finding by targeted testing of patients in the setting of the pulmonary function lab can serve to integrate this clinical practice guideline in a consistent streamlined fashion.In this sample, no difference between AAT blood levels among ever, never, and current tobacco smokers was detected. A more powerful sample is needed.
dc.language.isoENen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.subjectalpha-1 antitrypsinen_US
dc.subjectalpha-1 antitrypsin deficiencyen_US
dc.subjectclinical practice guidelineen_US
dc.subjectemphysemaen_US
dc.subjectpulmonary function laben_US
dc.titleClinical Practice Guideline Implementation for Alpha-1 Antitrypsin Deficiency Testing: Evaluation of an Innovative Methoden_US
dc.typetexten_US
dc.typeElectronic Dissertationen_US
dc.contributor.chairReel, Sally J.en_US
dc.identifier.oclc659754810en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.leveldoctoralen_US
dc.contributor.committeememberRitter, Leslieen_US
dc.contributor.committeememberRigney, Teden_US
dc.identifier.proquest10914en_US
thesis.degree.disciplineNursingen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.nameD.N.P.en_US
refterms.dateFOA2018-06-24T11:30:44Z
html.description.abstractPurpose/Aims: The American Thoracic Society (ATS) published recommendations for alpha-1 antitrypsin deficiency (AATD) testing in 2003. This descriptive project evaluates the outcomes of ATS AATD guideline use in the setting of the pulmonary function testing (PFT) lab.The specific aims met by this descriptive project describe the prevalence of AATD cases and carriers in the sample, examine to what degree the established clinical guideline promoted accurate patient selection for the alpha-1 test in the sample, and aimed to determine whether alpha-1 antitrypsin blood levels are reduced in current smokers compared to former or never smokers.Background: Alpha-1 antitrypsin prevents lung tissue breakdown by attenuating excess elastase released from neutrophils during the inflammatory response. Smoking impairs alpha-1 antitrypsin protection at the site of lung inflammation promoting emphysema development. In the case of genetic mutation, protective alpha-1 antitrypsin levels are reduced, causing emphysema even in non-smokers. Significantly reduced protective levels of alpha-1 antitrypsin increase the odds for morbidity and early mortality from emphysema. The literature provides support for targeted testing in the population most affected.Sample/Methods: The sample population included adults 21 through 79 years completing pulmonary function testing over 18 months in a metropolitan pulmonary medicine practice and was retrospectively reviewed.Of the 521 in the sample, 190 were tested for AATD, and 24 were found to carry an abnormal genotype. However, using Table 11 from the ATS CPG failed to provide structured, consistent guidance in selecting patients for AATD testing. Still, the prevalence of the abnormal genotypes MS, MZ, SZ, and ZZ was increased in this pulmonary population compared to the published estimated prevalence for the general population.A structured decision-tree, developed from the original guideline for diagnostic testing, may provide superior guidance for AATD test patient selection in this setting. Increased case finding by targeted testing of patients in the setting of the pulmonary function lab can serve to integrate this clinical practice guideline in a consistent streamlined fashion.In this sample, no difference between AAT blood levels among ever, never, and current tobacco smokers was detected. A more powerful sample is needed.


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