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(Chest. 2005;127:1537-1543.)
© 2005 American College of Chest Physicians

Glutathione S-Transferase P1 and Lung Function in Patients With {alpha}1-Antitrypsin Deficiency and COPD*

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

* 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{at}clinic.ub.es

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 {alpha}1-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.

Key Words: {alpha}1-antitrypsin deficiency • COPD • genetics • glutathione S-transferase • smoking




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 Eur Respir JHome page
O. Senn, E. W. Russi, M. Imboden, and N. M. Probst-Hensch
{alpha}1-Antitrypsin deficiency and lung disease: risk modification by occupational and environmental inhalants
Eur. Respir. J., November 1, 2005; 26(5): 909 - 917.
[Abstract] [Full Text] [PDF]


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