Federal Institute for Drugs and Medical Devices, Kurt-Georg-Kiesinger-Allee 3, 53175 Bonn, Germany.
Eur J Med Res. 2010 Nov 4;15 Suppl 2(Suppl 2):164-74. doi: 10.1186/2047-783x-15-s2-164.
Alpha-1-proteinase inhibitor (α1-PI) is the most relevant protease inhibitor in the lung. Patients with hereditary deficiency of α1-PI suffer from an impaired hepatic synthesis of α1-PI in the liver and in consequence an insufficient concentration of the protease inhibitor in the lung followed by development of lung emphysema due to an impaired protease antiprotease balance and a local relative excess of neutrophil elastase (NE). In contrast, patients with cystic fibrosis (CF) are characterised by a normal synthesis of α1-PI and a severe pulmonary inflammation with a strong excess of NE in the lung followed by progressive loss of lung function. In principle, both patient groups may benefit from an augmentation of α1-PI. Intravenous augmentation, which is established in patients with α1-PI deficiency only, is very expensive, subject to controversial discussions and only about 2% of the administered protein reaches lung interstitium. Inhalation of α1-PI may serve as an alternative to administer high α1-PI doses into the lungs of both patient groups to restore the impaired protease antiprotease balance and to diminish the detrimental effects of NE. However, prerequisites of this therapy are the reproducible administration of sufficient doses of active α1-PI into the lung without adverse effects. In our review we describe the results of studies investigating the inhalation of α1-PI in patients with α1-PI deficiency and CF. The data demonstrate the feasibility of α1-PI inhalation for restoration of the impaired protease antiprotease balance, attenuation of the inflammation and neutralisation of the excess activity of NE. Likely, inhalation of α1-PI serves as cheaper and more convenient therapy than intravenous augmentation. However, inhalation will be further optimised by use of novel nebulisers and optimised breathing techniques.
α1-蛋白酶抑制剂(α1-PI)是肺部最重要的蛋白酶抑制剂。遗传性α1-PI 缺乏症患者的肝脏合成α1-PI 受损,因此肺部蛋白酶抑制剂浓度不足,导致蛋白酶-抗蛋白酶平衡受损和中性粒细胞弹性蛋白酶(NE)局部相对过剩,从而发展为肺气肿。相比之下,囊性纤维化(CF)患者的α1-PI 合成正常,但肺部炎症严重,NE 大量过剩,导致肺功能进行性丧失。原则上,这两个患者群体都可能从α1-PI 增强中获益。静脉增强仅在α1-PI 缺乏症患者中建立,非常昂贵,受到争议性讨论的影响,并且只有约 2%的给药蛋白到达肺间质。吸入α1-PI 可以替代静脉给药,将高剂量的α1-PI 递送到两个患者群体的肺部,以恢复受损的蛋白酶-抗蛋白酶平衡,并减少 NE 的有害影响。然而,这种治疗的前提是可重复地将足够剂量的有效α1-PI 递送到肺部而没有不良反应。在我们的综述中,我们描述了研究吸入α1-PI 治疗α1-PI 缺乏症和 CF 患者的结果。这些数据证明了吸入α1-PI 恢复受损的蛋白酶-抗蛋白酶平衡、减轻炎症和中和 NE 活性过剩的可行性。可能,吸入α1-PI 比静脉增强更便宜、更方便。然而,通过使用新型雾化器和优化呼吸技术,吸入将进一步得到优化。