Effects of Tocilizumab on Inflammation and Iron Metabolism in Critically Ill Patients with COVID-19

Author:

Szabo Robert123ORCID,Petrișor Cristina23,Bodolea Constantin24,Dobre Vlad2,Tranca Sebastian23ORCID,Clichici Simona1ORCID,Szabo Iulia5ORCID,Melinte Razvan Marian67ORCID,Mocan Teodora18

Affiliation:

1. Physiology Department, “Iuliu Hatieganu” University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania

2. 2nd Anesthesia Department, “Iuliu Hatieganu” University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania

3. Department of Anesthesia and Intensive Care, Clinical County Emergency Hospital, 400000 Cluj-Napoca, Romania

4. Municipal Clinical Hospital, 400139 Cluj-Napoca, Romania

5. Department of Rheumatology, “Iuliu Hațieganu” University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania

6. Department of Orthopedics, Regina Maria Health Network, 540098 Targu Mures, Romania

7. Department of Orthopedics, Humanitas Medlife Hospital, 400664 Cluj-Napoca, Romania

8. Nanomedicine Department, Regional Institute of Gastroenterology and Hepatology, 400000 Cluj-Napoca, Romania

Abstract

COVID-19 produces cytokine-mediated persistent inflammation and is associated with elevated iron stores and low circulating iron. It is believed that central to the pathophysiological mechanism is interleukin 6 and hepcidin. A state of iron overload, termed hyperferritinemia, and inflammatory anemia take place. Both conditions are linked to a worse result in critically ill patients. Blocking the interleukin 6—hepcidin pathway with Tocilizumab could present favorable outcomes. The aim of this study was to evaluate if Tocilizumab influences survival, the occurrence of sepsis, anemia and transfusions in critically ill patients suffering from COVID-19. This prospective observational study focused on levels of interleukin 6, hepcidin and blood iron parameters in patients treated with Tocilizumab. Data were compared before and after therapy as well as between treated and control groups. Results indicate that there is no difference in terms of survival nor in the rate of anemia or sepsis occurrence. Hepcidin was elevated and anemia ensued after treatment, which could indicate alternative pathways. In conclusion, when the classic interleukin 6—hepcidin pathway is blocked, inflammation seems to use alternative routes. Further understanding of these pathways is required and new pharmacological therapies need to be developed to treat persistent inflammation.

Funder

“Iuliu Hatieganu” University of Medicine and Pharmacy Cluj-Napoca

National Authority for Scientific Research and Innovation Romania

Publisher

MDPI AG

Subject

Pharmaceutical Science

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