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Angiotensinogen gene G-6A polymorphism influences idiopathic pulmonary fibrosis disease progression

¹ Servicio de Neumología, Hospital Clínico, Instituto de Investigaciones Biomédicas Agusti Pi Suñer (IDIBAPS), ⁶ Dept de Patología Experimental, Instituto de Investigaciones Biomédicas de Barcelona, Consejo Superior de Investigaciones Cientificas, ⁹ Servicio de Neumología, Hospital Vall d’Hebron, Barcelona, ⁷ Servicio de Neumología, Hospital La Princesa, Madrid, ⁸ Servicio de Neumología, Hospital Virgen del Rocio, Sevilla, and ² Centro Investigaciones Biomédicas en Red (CIBER) de Enfermedades Respiratorias, Spain, Depts of ³ Physiology, ⁴ Microbiology and Molecular Genetics, and ⁵ Epidemiology, Michigan State University, East Lansing, MI, USA.

CORRESPONDENCE: M. Molina-Molina, Servicio de Neumología, Hospital Clínic, c/Villarroel 170.08036, Barcelona, Spain. Fax: 34 2275455. E-mail: mariamolinamolina{at}hotmail.com

Keywords: Angiotensin system, genetics, interstitial lung disease

Received: February 2, 2008
Accepted May 13, 2008

Angiotensin II is a growth factor that plays a key role in the physiopathology of idiopathic pulmonary fibrosis (IPF). A nucleotide substitution of an adenine instead of a guanine (G-6A) in the proximal promoter region of angiotensinogen (AGT), the precursor of angiotensin II, has been associated with an increased gene transcription rate.

In order to investigate whether the G-6A polymorphism of the AGT gene is associated with IPF development, severity and progression, the present study utilised a case–control study design and genotyped G-6A in 219 patients with IPF and 224 control subjects.

The distribution of G-6A genotypes and alleles did not significantly differ between cases and controls. The G-6A polymorphism of the AGT gene was not associated with disease severity at diagnosis. The presence of the A allele was strongly associated with increased alveolar arterial oxygen tension difference during follow-up, after controlling for the confounding factors. Higher alveolar arterial oxygen tension changes over time were observed in patients with the AA genotype (0.37±0.7 mmHg (0.049±0.093 kPa) per month) compared to GA genotype (0.12±1 mmHg (0.016±0.133 kPa) per month) and GG genotype (0.2±0.6 mmHg (0.027±0.080 kPa) per month).

G-6A polymorphism of the angiotensinogen gene is associated with idiopathic pulmonary fibrosis progression but not with disease predisposition. This polymorphism could have a predictive significance in idiopathic pulmonary fibrosis patients.

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