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首页> 外文期刊>COPD: Journal of Chronic Obstructive Pulmonary Disease >Alpha-1 antitrypsin augmentation therapy and biomarkers of elastin degradation
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Alpha-1 antitrypsin augmentation therapy and biomarkers of elastin degradation

机译：Alpha-1抗胰蛋白酶增强疗法和弹性蛋白降解的生物标志物

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Background: Intravenous alpha-1 antitrypsin protein (AAT) augmentation is a prescribed therapy for severe, genetically determined, alpha-1 antitrypsin deficiency (AATD), a genetic basis for pulmonary emphysema. AAT, a predominant systemic inhibitor of neutrophil elastase thus far has not been shown to decrease elastin degradation in a significant number of patients on this therapy. The objective of this study was to compare levels of biomarkers of elastin degradation in plasma, bronchoalveolar lavage (BALF) fluid and urine before and after beginning AAT augmentation therapy in patients with AATD. Methods: Desmosine and isodesmosine (DI), which occur only in elastin, are amino acid cross-links in mature elastin. Levels of DI in body fluids measure degradation of elastin and can be measured more specifically by mass spectrometry. This method was used to measure DI levels in plasma, bronchoalveolar lavage fluid and urine in cohorts of severe AATD patients on augmentation, not on augmentation and before and after the initiation of augmentation therapy. Results: Statistically significant reductions in plasma DI and in BALF DI were demonstrated in AATD patients receiving intravenous (IV) augmentation therapy as compared with those not receiving it. Administration by aerosol also produced statistically significant reductions in levels of DI in BALF. Conclusions: Results indicate that the currently prescribed doses of AAT augmentation inhibit neutrophil elastase adequately to reduce elastin degradation, both systemically and in the lung per se. The currently prescribed doses did not reduce elastin degradation to control levels, which may be possible with higher doses.
机译：背景：静脉注射α-1抗胰蛋白酶（AAT）增强剂是针对严重的，经遗传确定的α-1抗胰蛋白酶缺乏症（AATD）（肺部肺气肿的遗传基础）的处方疗法。迄今为止，尚未显示出AAT是嗜中性粒细胞弹性蛋白酶的主要系统抑制剂，在使用该疗法的大量患者中，AAT并未显示可降低弹性蛋白的降解。本研究的目的是比较AATD患者开始AAT增强治疗前后血浆，支气管肺泡灌洗液（BALF）和尿液中弹性蛋白降解的生物标志物水平。方法：Desmosine和Isodesmosine（DI）仅存在于弹性蛋白中，是成熟弹性蛋白中的氨基酸交联键。体液中DI的含量可测量弹性蛋白的降解，可以通过质谱法进行更具体的测量。该方法用于测量严重AATD患者接受增强治疗时（而非增强治疗时）以及开始增强治疗前后的血浆，支气管肺泡灌洗液和尿液中的DI水平。结果：与未接受静脉内（IV）增强疗法的AATD患者相比，血浆DI和BALF DI的统计学显着降低。通过气雾剂给药还导致BALF中的DI水平在统计学上显着降低。结论：结果表明，目前规定的AAT增强剂量可充分抑制嗜中性白细胞弹性蛋白酶，从而从系统性和在肺部本身减少弹性蛋白的降解。当前规定的剂量并未将弹性蛋白降解降低至对照水平，这可能在较高剂量下可能发生。

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