Document Type
Article
Publication Date
2020
Publication Title
Journal of Thoracic Disease
Volume
12
Issue
Supplement 1
Pages
S54-S65
DOI
10.21037/jtd.2019.12.85
Abstract
Sepsis affects 30 million people worldwide, leading to 6 million deaths every year (WHO), and despite decades of research, novel initiatives are drastically needed. According to the current literature, oxidative imbalance and mitochondrial dysfunction are common features of septic patients that can cause multiorgan failure and death. Melatonin, alongside its traditionally accepted role as the master hormonal regulator of the circadian rhythm, is a promising adjunctive drug for sepsis through its anti-inflammatory, antiapoptotic and powerful antioxidant properties. Several animal models of sepsis have demonstrated that melatonin can prevent multiorgan dysfunction and improve survival through restoring mitochondrial electron transport chain (ETC) function, inhibiting nitric oxide synthesis and reducing cytokine production. The purpose of this article is to review the current evidence for the role of melatonin in sepsis, review its pharmacokinetic profile and virtual absence of side effects. While clinical data is limited, we propose the adjunctive use of melatonin is patients with severe sepsis and septic shock.
Original Publication Citation
Colunga Biancatelli, R. M. L., Berrill, M., Mohammed, Y. H., & Marik, P. E. (2020). Melatonin for the treatment of sepsis: the scientific rationale. Journal of Thoracic Disease, 12 (1 Suppl.), S54-S65. https://doi.org/10.21037/jtd.2019.12.85
Repository Citation
Colunga Biancatelli, Ruben Manuel Luciano; Berrill, Max; Mohammed, Yassen H.; and Marik, Paul E., "Melatonin for the Treatment of Sepsis: The Scientific Rationale" (2020). Bioelectrics Publications. 334.
https://digitalcommons.odu.edu/bioelectrics_pubs/334
ORCID
0000-0002-1174-3876 (Colunga Biancatelli)
Included in
Amino Acids, Peptides, and Proteins Commons, Endocrine System Commons, Hormones, Hormone Substitutes, and Hormone Antagonists Commons
Comments
Published under an Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license.