Colchicine, Aspirin, and Montelukast - A Case of Successful Combined Pharmacotherapy for Adult Multisystem Inflammatory Syndrome in COVID-19.
Colchicine, Aspirin, and Montelukast - A Case of Successful Combined Pharmacotherapy for Adult Multisystem Inflammatory Syndrome in COVID-19.
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DOI：
10.4103/jgid.jgid_296_20
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发表时间：
2020-10
影响因子：
1.6
通讯作者：
Stawicki SP
中科院分区：
文献类型：
--
作者：
Downing S;Chauhan V;Chaudry IH;Galwankar S;Sharma P;Stawicki SP
自COVID-19大流行开始以来，已尝试了许多治疗策略，以预防和治疗COVID-19中的成人多系统炎症综合征（Vdd-COVID-19），结果喜忧参半。这背后的原因可能是SARS-CoV-2感染和相应的人体全身反应中涉及的高度交织的病理生理机制的复杂网络，导致终末器官损伤，残疾和死亡。目前正在研究秋水仙碱、高剂量阿司匹林和孟鲁司特作为Vdd-COVID-19的潜在调节剂，用于传统治疗方法未能改善的患者。在这里，我们提出了一个病人谁提出了高热，极度疲劳和呼吸困难，并持续恶化。作为我们临床方法的一部分，我们使用了上述三种药物的同时组合，利用它们各自不同的抗Vdd-COVID-19作用机制。开始治疗后，患者在24小时内表现出症状改善，在持续三联治疗72小时后能够恢复日常活动。基于这一经验，我们回顾了该方案的免疫调节基础，包括它可以预防细胞因子释放综合征（CRS）及其临床表现--COVID-19发展的潜在途径。通过阻断炎症反应的早期阶段，通过不同的机制途径，所讨论的方案可能被证明有效地阻止CRS和Vdd-COVID-19在急性症状，无改善的COVID-19患者中的升级。
Since the beginning of the COVID-19 pandemic, many therapeutic strategies have been tried, with mixed results, to prevent and treat adult multisystem inflammatory syndrome in COVID-19 (AMIS-COVID-19). The reason behind this may the complex web of highly intertwined pathophysiologic mechanisms involved in the SARS-CoV-2 infection and the corresponding human systemic response, leading to end-organ damage, disability, and death. Colchicine, high-dose aspirin, and montelukast are being investigated currently as potential modulators of AMIS-COVID-19 in patients who fail to improve with traditional therapeutic approaches. Here, we present a patient who presented with high fevers, extreme fatigue and dyspnea, and ongoing deterioration. As part of our clinical approach, we used the simultaneous combination of the three agents listed above, capitalizing on their different respective mechanisms of action against AMIS-COVID-19. Following the initiation of therapy, the patient showed symptomatic improvement within 24 h, with the ability to return to daily activities after 72 h of continued triple-agent approach. Based on this experience, we have reviewed the immunomodulatory basis of this regimen, including potential avenues in which it may prevent the development of cytokine release syndrome (CRS) and its clinical manifestation, AMIS-COVID-19. By blocking the early stages of an inflammatory response, via diverse mechanistic pathways, the regimen in question may prove effective in halting the escalation of CRS and AMIS-COVID-19 in acutely symptomatic, nonimproving COVID-19 patients.