Publication Date:
2020
abstract:
Acute 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.
Iris type:
1.1 Articolo in rivista
Keywords:
Aged; Antiviral Agents; Atrial Fibrillation; Betacoronavirus; Complement Activation; Complement C3; Complement Inactivating Agents; Coronavirus Infections; Humans; Hypercholesterolemia; Hypertension; Lung; Male; Pandemics; Peptides, Cyclic; Pneumonia, Viral; Treatment Outcome
List of contributors:
Mastaglio, S.; Ruggeri, A.; Risitano, A. M.; Angelillo, P.; Yancopoulou, D.; Mastellos, D. C.; Huber-Lang, M.; Piemontese, S.; Assanelli, A.; Garlanda, C.; Lambris, J. D.; Ciceri, F.
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