Baranovski Boris M, Schuster Ronen, Nisim Omer, Brami Ido, Lior Yotam, Lewis Eli C
Department of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Chronic Obstr Pulm Dis. 2018 Sep 19;5(4):267-276. doi: 10.15326/jcopdf.5.4.2017.0161.
Alpha-1 antitrypsin deficiency (AATD) is a genetic disorder which most commonly manifests as pulmonary emphysema. Accordingly, alpha-1 antitrypsin (AAT) augmentation therapy aims to reduce the progression of emphysema, as achieved by life-long weekly slow-drip infusions of plasma-derived affinity-purified human AAT. However, not all AATD patients will receive this therapy, due to either lack of medical coverage or low patient compliance. To circumvent these limitations, attempts are being made to develop lung-directed therapies, including inhaled AAT and locally-delivered AAT gene therapy. Lung transplantation is also an ultimate therapy option. Although less common, AATD patients also present with disease manifestations that extend beyond the lung, including vasculitis, diabetes and panniculitis, and appear to experience longer and more frequent hospitalization times and more frequent pneumonia bouts. In the past decade, new mechanism-based clinical indications for AAT therapy have surfaced, depicting a safe, anti-inflammatory, immunomodulatory and tissue-protective agent. Introduced to non-AATD individuals, AAT appears to provide relief from steroid-refractory graft-versus-host disease, from bacterial infections in cystic fibrosis and from autoimmune diabetes; preclinical studies show benefit also in multiple sclerosis, ulcerative colitis, rheumatoid arthritis, acute myocardial infarction and stroke, as well as ischemia-reperfusion injury and aberrant wound healing processes. While the current augmentation therapy is targeted towards treatment of emphysema, it is suggested that AATD patients may benefit from AAT augmentation therapy geared towards extrapulmonary pathologies as well. Thus, development of mechanism-based, context-specific AAT augmentation therapy protocols is encouraged. In the current review, we will discuss extrapulmonary manifestations of AATD and the potential of AAT augmentation therapy for these conditions.
α-1抗胰蛋白酶缺乏症(AATD)是一种遗传性疾病,最常见的表现为肺气肿。因此,α-1抗胰蛋白酶(AAT)增强疗法旨在减缓肺气肿的进展,这是通过每周一次、持续终身的缓慢静脉滴注血浆来源的亲和纯化人AAT来实现的。然而,并非所有AATD患者都能接受这种治疗,原因要么是缺乏医保覆盖,要么是患者依从性低。为了克服这些限制,人们正在尝试开发针对肺部的治疗方法,包括吸入AAT和局部递送AAT基因疗法。肺移植也是一种终极治疗选择。虽然不太常见,但AATD患者还会出现肺部以外的疾病表现,包括血管炎、糖尿病和脂膜炎,而且似乎住院时间更长、更频繁,肺炎发作也更频繁。在过去十年中,基于新机制的AAT治疗临床适应症已经出现,表明它是一种安全的抗炎、免疫调节和组织保护剂。在非AATD个体中,AAT似乎能缓解类固醇难治性移植物抗宿主病、囊性纤维化中的细菌感染以及自身免疫性糖尿病;临床前研究表明,它对多发性硬化症、溃疡性结肠炎、类风湿性关节炎、急性心肌梗死和中风以及缺血再灌注损伤和异常伤口愈合过程也有好处。虽然目前的增强疗法针对的是肺气肿的治疗,但有人认为AATD患者可能也会从针对肺外病变的AAT增强疗法中受益。因此,鼓励制定基于机制、针对具体情况的AAT增强治疗方案。在本综述中,我们将讨论AATD的肺外表现以及AAT增强疗法对这些病症的治疗潜力。