IIAIGC Study center, Burlington, Vermont, USA.
Exp Lung Res. 2020 May-Jun;46(5):157-161. doi: 10.1080/01902148.2020.1753266. Epub 2020 Apr 14.
Multiple pharmacological interventions tested over the last decades have failed to reduce ARDS mortality. This short note recounts past data indicating that (i) neutrophils home along an IL-8 gradient, (ii) in ARDS, massive neutrophil accumulation and degranulation in and along bronchoalveolar spaces contributes to damage and hypoxia, (iii) large increases in IL-8 are one of the chemotaxic signals drawing neutrophils to the ARDS lung, and (iv) old data from dermatology and glioblastoma research showed that the old drug against Hansen's disease, dapsone, inhibits neutrophils' chemotaxis to IL-8. Therefore dapsone might lower neutrophils' contributions to ARDS lung pathology. Dapsone can create methemoglobinemia that although rarely problematic it would be particularly undesirable in ARDS. The common antacid drug cimetidine lowers risk of dapsone related methemoglobinemia and should be given concomitantly.
过去几十年的多项药理学干预都未能降低 ARDS 的死亡率。这篇简短的报告回顾了过去的数据,表明:(i) 中性粒细胞沿着 IL-8 浓度梯度归巢;(ii) 在 ARDS 中,大量中性粒细胞在支气管肺泡空间中积聚和脱颗粒,导致损伤和缺氧;(iii) IL-8 的大量增加是吸引中性粒细胞进入 ARDS 肺部的趋化信号之一;(iv) 皮肤科和神经胶质瘤研究的旧数据表明,治疗汉森病的旧药物氨苯砜抑制中性粒细胞对 IL-8 的趋化性。因此,氨苯砜可能降低中性粒细胞对 ARDS 肺部病理的贡献。氨苯砜会引起高铁血红蛋白血症,尽管这种情况很少见,但在 ARDS 中尤其不理想。常用的抗酸药物西咪替丁可降低氨苯砜相关高铁血红蛋白血症的风险,应同时给予。