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- Sara Mastaglio, Annalisa Ruggeri, Antonio M Risitano, Piera Angelillo, Despina Yancopoulou, Dimitrios C Mastellos, Markus Huber-Lang, Simona Piemontese, Andrea Assanelli, Cecilia Garlanda, John D Lambris, and Fabio Ciceri.
- Hematology and Bone Marrow Transplantation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
- Clin. Immunol. 2020 Jun 1; 215: 108450.
AbstractAcute respiratory distress syndrome (ARDS) is a devastating clinical manifestation of COVID-19 pneumonia and is mainly based on an immune-driven pathology. Mounting evidence suggests that COVID-19 is fueled by a maladaptive host inflammatory response that involves excessive activation of innate immune pathways. While a "cytokine storm" involving IL-6 and other cytokines has been documented, complement C3 activation has been implicated as an initial effector mechanism that exacerbates lung injury in preclinical models of SARS-CoV infection. C3-targeted intervention may provide broader therapeutic control of complement-mediated inflammatory damage in COVID-19 patients. Herein, we report the clinical course of a patient with severe ARDS due to COVID-19 pneumonia who was safely and successfully treated with the compstatin-based complement C3 inhibitor AMY-101.Copyright © 2020 Elsevier Inc. All rights reserved.
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