Poster Presentations: Wednesday, October 26, 2011 |

Alpha-1-Antitrypsin (AAT) Deficiency Prevalence Is Greater Than Expected but Does Not Impact on Spirometry FREE TO VIEW

Ronald Dandurand, MD; Jean Bourbeau, MD; David Eidelman, MD
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Montreal Chest Institute and Royal Victoria Hospital, McGill University, Montreal, QC, Canada

Chest. 2011;140(4_MeetingAbstracts):566A. doi:10.1378/chest.1112394
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PURPOSE: COPD causes non-fully reversible airways obstruction, respiratory and systemic symptoms, progressive disability, and is the fourth leading cause of death worldwide. An interaction of environment, largely through tobacco smoke exposure, and genetic host factors is felt to cause disease in affected individuals. Currently, the only well defined genetic abnormality is AAT deficiency which is said to be present in 0.5-2.5% of COPD patients and is actively sought in those with early onset disease beginning in the fourth or fifth decade. We wished to determine the prevalence of AAT deficiency within a community based respirology practice.

METHODS: All new and returning patients with symptoms compatible with the diagnosis of COPD, >10 pack-year smoking history and a post bronchodilator FEV1/FVC < 0.70 seen over a 4 month period were evaluated. Patients resided in the West-Island suburbs of Montreal, Quebec, population 349,849 or Cornwall, Ontario, population 45,965. All subjects underwent spirometry respecting ATS criteria, met the ATS/ERS definition/criteria for COPD, were treated according to Canadian Thoracic Society guidelines and had serum samples assayed in the community laboratories. Local normal range values were used to separate non-AAT deficient (non-AATD) patients from AAT deficient (AATD) patients.

RESULTS: 20 out of 162 patients had low serum AAT levels (AATD mean 0.76±0.04SE g/L vs. non-AATD 1.53±0.03) for a prevalence of 12%. AATD patients when compared with non-AATD patients, showed no differences in age (74 years±2 vs. 72±1), smoking history (43 pack-years±3 vs. 49±2), FEV1 (60% of predicted±4 vs. 61±2) or FEV1/FVC (54%±3 vs. 54±1).

CONCLUSIONS: In this small population, AAT deficiency prevalence was almost 5 times greater than expected, yet no acceleration of FEV1 decline was detected in those with AAT deficiency. Genotype distribution and the prevalence of hepatic disease in these ATTD patients, and the false positive rate of our serum AAT assays remain to be determined.

CLINICAL IMPLICATIONS: Whether the benign course of AAT deficiency without replacement therapy in these patients was due to strict smoking cessation and/or medication compliance is unclear.

DISCLOSURE: The following authors have nothing to disclose: Ronald Dandurand, Jean Bourbeau, David Eidelman

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