非原发性α1抗胰蛋白酶（α1-AT）缺乏且慢性肝病已代偿患者的血清α1抗胰蛋白酶水平低与气流阻塞风险
Low serum levels of alpha1 anti-trypsin (α1-AT) and risk of airflow obstruction in non-primary α1-AT-deficient patients with compensated chronic liver disease.
作者信息
Rodríguez-Romero Elizabeth, Suárez-Cuenca Juan Antonio, Elizalde-Barrera César Iván, Mondragón-Terán Paul, Martínez-Hernández José Enrique, Gómez-Cortés Eduardo, Pérez-Cabeza de Vaca Rebeca, Hernández-Muñoz Rolando E, Melchor-López Alberto, Jiménez-Saab Nayeli Gabriela
机构信息
Department of Internal Medicine, Xoco General Hospital, and Ticomán General Hospital, Mexico City, Mexico.
Biomedical Research Division, "20 de Noviembre" National Medical Centre, ISSSTE and Mexican Group for Basic and Clinical Research in Internal Medicine, Mexico City, Mexico.
出版信息
Med Sci Monit. 2015 Apr 27;21:1194-9. doi: 10.12659/MSM.893350.
BACKGROUND
Alpha1 anti-trypsin (α1-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 α1-AT as a biomarker of airflow performance in chronic liver disease (CLD).
MATERIAL/METHODS: Serum α1-AT levels and lung function (spirometry) were evaluated in non-primary α1-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 α1-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 α1-AT increased the risk of airflow obstruction in CLD patients without primary α1-AT deficiency.
背景
α1抗胰蛋白酶（α1-AT）是一种在肝脏中合成的丝氨酸蛋白酶抑制剂，是主要的循环抗蛋白酶，可保护多个组织免受蛋白水解损伤。其缺乏与气流阻塞有关。本研究旨在探讨α1-AT作为慢性肝病（CLD）气流表现生物标志物的作用。
材料/方法：对无明显呼吸受限的非原发性α1-AT缺乏的酒精性CLD患者进行血清α1-AT水平和肺功能（肺活量测定）评估。
结果
34例气流阻塞患者（n = 11）、气流受限患者（n = 12）和气流正常患者（n = 11，年龄匹配的对照组）符合条件。气流阻塞组中α1-AT降低。ROC曲线下α1-AT = 24 mg/dL可有效区分气流阻塞（AUC = 0.687），且与风险高10倍相关（p = 0.0007）。
结论
在无原发性α1-AT缺乏的CLD患者中，较低的α1-AT增加了气流阻塞的风险。
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