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Clinical Investigations: COPD |

Glutathione S-Transferase P1 and Lung Function in Patients With α1-Antitrypsin Deficiency and COPD*

Francisco Rodriguez, MD; Cristian de la Roza, MD; Rosendo Jardi, MD; Melanie Schaper, RN; Rafael Vidal, MD; Marc Miravitlles, MD
Author and Funding Information

*From the Departments of Biochemistry (Drs. Rodriguez and Jardi, and Ms. Schaper) and Pneumology (Dr. Vidal), Hospital Vall d’Hebron; and Department of Pneumology (Drs. de la Roza and Miravitlles), Clinical Institute of Pneumology and Thoracic Surgery, Hospital Clínic (IDIBAPS). Barcelona, Spain.

Correspondence to: Marc Miravitlles, MD, Department of Pneumology, Clinical Institute of Pneumology and Thoracic Surgery, Hospital Clínic, C/ Villarroel 170 (UVIR, esc 2, planta 3), Barcelona 08036, Spain; e-mail: marcm@clinic.ub.es



Chest. 2005;127(5):1537-1543. doi:10.1378/chest.127.5.1537
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Background: The glutathione S-transferase P1 (GSTP1) gene is involved in detoxification of electrophilic substances of tobacco smoke. A polymorphism at nucleotide 315 of this gene alters its enzymatic activity.

Objective: We analyzed the association between the variability in the GSTP1 gene and impairment in lung function in smokers with and without α1-antitrypsin (AAT) deficiency and COPD.

Population and method: The study population consisted of 99 patients with smoking-related COPD and 69 patients with AAT deficiency; 198 healthy volunteers provided the frequency of the different polymorphisms in the general population. GSTP1 genotyping was performed by a real-time polymerase chain reaction amplification assay.

Results: The frequency (0.28) of the 105Val polymorphism was identical in COPD patients and the general population. However, the frequency was significantly increased (0.44) in patients with AAT deficiency (odds ratio [OR], 2.09; 95% confidence interval [CI], 1.17 to 3.72 compared to control subjects; and OR, 2.41; 95% CI, 1.27 to 4.59 compared to COPD). FEV1 percentage of predicted was significantly impaired in AAT-deficient carriers of 105Val. This effect was not observed in COPD patients.

Conclusions: These findings suggest that the frequency of the GSTP1 105Val polymorphism is increased in patients with AAT deficiency. Globally, GSTP1 genotypes, age, and tobacco smoking explained 41% of total FEV1 percentage of predicted variability in patients with AAT deficiency. The modulatory role of GSTP1 in lung disease has only been observed in smokers lacking AAT.


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