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Low Serum Levels of Alpha(1) Anti-trypsin (α(1)-AT) and Risk of Airflow Obstruction in Non-Primary α(1)-AT-Deficient Patients with Compensated Chronic Liver Disease

BACKGROUND: Alpha(1) anti-trypsin (α(1)-AT), a serine protease inhibitor synthesized in the liver, is a major circulating antiprotease that provides defense against proteolytic damage in several tissues. Its deficiency is associated with airflow obstruction. The present study aimed to explore the ro...

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Detalles Bibliográficos
Autores principales: Rodríguez-Romero, Elizabeth, Suárez-Cuenca, Juan Antonio, Elizalde-Barrera, César Iván, Mondragón-Terán, Paul, Martínez-Hernández, José Enrique, Gómez-Cortés, Eduardo, de Vaca, Rebeca Pérez-Cabeza, Hernández-Muñoz, Rolando E., Melchor-López, Alberto, Jiménez-Saab, Nayeli Gabriela
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424928/
https://www.ncbi.nlm.nih.gov/pubmed/25913248
http://dx.doi.org/10.12659/MSM.893350
Descripción
Sumario:BACKGROUND: Alpha(1) anti-trypsin (α(1)-AT), a serine protease inhibitor synthesized in the liver, is a major circulating antiprotease that provides defense against proteolytic damage in several tissues. Its deficiency is associated with airflow obstruction. The present study aimed to explore the role of α(1)-AT as a biomarker of airflow performance in chronic liver disease (CLD). MATERIAL/METHODS: Serum α(1)-AT levels and lung function (spirometry) were evaluated in non-primary α(1)-AT-deficient, alcoholic CLD patients without evident respiratory limitations. RESULTS: Thirty-four patients with airflow obstruction (n=11), airflow restriction (n=12), and normal airflow (n=11, age-matched controls) were eligible. α1-AT was decreased in the airflow obstruction group. ROC-cutoff α(1)-AT=24 mg/dL effectively discriminated airflow obstruction (AUC=0.687) and was associated with a 10-fold higher risk (p=0.0007). CONCLUSIONS: Lower α(1)-AT increased the risk of airflow obstruction in CLD patients without primary α(1)-AT deficiency.