Abstract
Introduction Elevated concentration of proinflammatory cytokines followed by hyperinflammation is one of the hallmarks of severe and critical COVID-19. In the short term, this may result in ARDS and lung injury; subsequently, this may cause pulmonary fibrosis—a disease with poor prognosis—in the long run. Among the cytokines, interleukin-1β (IL-1β) is one of the most overexpressed in COVID-19. We speculate that administration of intravenous activated autologous platelet-rich plasma (aaPRP), which contains interleukin-1 receptor antagonist (IL-1RA), would lower IL-1β levels and benefit the severe and critical COVID-19 patients. Methods After acquiring ethical clearance, we recruited 12 adult COVID-19 patients of both sexes from the Koja Regional Hospital (Jakarta, Indonesia) ICU. After selection, seven patients were included and divided into two groups, severe and critical. In addition to three doses of aaPRP, both groups received the same treatment of antiviral, steroid, and antibiotics. Quantification of plasma IL-1β levels was performed by beads multiplex assay a day before the first aaPRP administration and a day after the second and third aaPRP administration. PaO2/FiO2 ratio and lung injury scores were evaluated a day before and a day after each aaPRP administration. Results Severe and critical patients' initial plasma IL-1β concentration was 4.71 pg/mL and 3.095 pg/mL, respectively. After 2 treatments with aaPRP, severe patients' plasma IL-1β concentration decreased 12.48 pg/mL, while critical patients' plasma IL-1β concentration increased to 18.77 pg/mL. Furthermore, after 3 aaPRP treatments, significant amelioration of patients' PaO2/FiO2 ratio from 71.33 mmHg at baseline to 144.97 mmHg was observed (p < 0.05). However, no significant improvement in lung injury score was observed in severe and critical groups. All severe patients and one critical patient recovered. Conclusion The use of aaPRP may prevent pulmonary fibrosis in severe COVID-19 patients through the reduction of patients' plasma IL-1β concentration and the amelioration of PaO2/FiO2 ratio.
Highlights
Elevated concentration of proinflammatory cytokines followed by hyperinflammation is one of the hallmarks of severe and critical COVID-19
COVID-19 causes mortality through the process of cytokine storm, which is hyperinflammation and multiorgan damage triggered by uncontrolled release of cytokines. [1] e elevated concentration of proinflammatory cytokines is associated with severe COVID-19 and may result in complications such as acute respiratory distress (ARDS), sepsis, and respiratory failure [1,2,3]
Oxygen therapy and antibiotics were given . e patients received intravenous (IV) activated autologous platelet-rich plasma (aaPRP) on day 1, 3, and 5, while quantification of plasma IL-1β levels was conducted by the FMUI Integrated Laboratory on day 0, 4, and 6 with PaO2/ FiO2 ratio and lung injury scores recorded with the same intervals. e quantification method was MILLIPLEX®
Summary
Elevated concentration of proinflammatory cytokines followed by hyperinflammation is one of the hallmarks of severe and critical COVID-19. E use of aaPRP may prevent pulmonary fibrosis in severe COVID-19 patients through the reduction of patients’ plasma IL-1β concentration and the amelioration of PaO2/FiO2 ratio. [1] e elevated concentration of proinflammatory cytokines is associated with severe COVID-19 and may result in complications such as acute respiratory distress (ARDS), sepsis, and respiratory failure [1,2,3]. Such cytokine storms can cause acute lung injury, which, in turn, may induce pulmonary fibrosis [4, 5]. No definitive cure exists for the condition except for lung transplantation. [9]
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