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α-1抗胰蛋白酶缺乏症:一种再度出现的成人肝脏疾病。

Alpha-1 antitrypsin deficiency: A re-surfacing adult liver disorder.

作者信息

Fromme Malin, Schneider Carolin V, Trautwein Christian, Brunetti-Pierri Nicola, Strnad Pavel

机构信息

Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Health Care Provider of the European Reference Network on Rare Liver Disorders (ERN RARE LIVER), Aachen, Germany.

Telethon Institute of Genetics and Medicine, Pozzuoli, 80078 Naples, Italy; Department of Translational Medicine, Federico II University of Naples, Naples, Italy.

出版信息

J Hepatol. 2022 Apr;76(4):946-958. doi: 10.1016/j.jhep.2021.11.022. Epub 2021 Nov 27.

Abstract

Alpha-1 antitrypsin deficiency (AATD) arises from mutations in the SERPINA1 gene encoding alpha-1 antitrypsin (AAT) that lead to AAT retention in the endoplasmic reticulum of hepatocytes, causing proteotoxic liver injury and loss-of-function lung disease. The homozygous Pi∗Z mutation (Pi∗ZZ genotype) is responsible for the majority of severe AATD cases and can precipitate both paediatric and adult liver diseases, while the heterozygous Pi∗Z mutation (Pi∗MZ genotype) is an established genetic modifier of liver disease. We review genotype-related hepatic phenotypes/disease predispositions. We also describe the mechanisms and factors promoting the development of liver disease, as well as approaches to evaluate the extent of liver fibrosis. Finally, we discuss emerging diagnostic and therapeutic approaches for the clinical management of this often neglected disorder.

摘要

α-1抗胰蛋白酶缺乏症(AATD)源于编码α-1抗胰蛋白酶(AAT)的SERPINA1基因突变,这些突变导致AAT在肝细胞内质网中滞留,引起蛋白毒性肝损伤和功能丧失性肺病。纯合子Pi∗Z突变(Pi∗ZZ基因型)是大多数严重AATD病例的病因,可引发儿童和成人肝病,而杂合子Pi∗Z突变(Pi∗MZ基因型)是已确定的肝病遗传修饰因子。我们综述了与基因型相关的肝脏表型/疾病易感性。我们还描述了促进肝病发展的机制和因素,以及评估肝纤维化程度的方法。最后,我们讨论了针对这种常被忽视的疾病的临床管理的新兴诊断和治疗方法。

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