Cytokine storm
Cytokine storm | |
---|---|
Other names | hypercytokinemia |
Specialty | Immunology |
A cytokine storm, also called hypercytokinemia, is a pathological reaction in humans and other animals in which the innate immune system causes an uncontrolled and excessive release of pro-inflammatory signaling molecules called cytokines. Cytokines are a normal part of the body's immune response to infection, but their sudden release in large quantities may cause multisystem organ failure and death.[1]
Cytokine storms may be caused by infectious or non-infectious
Cytokine storm syndrome is a diverse set of conditions that can result in a cytokine storm. Cytokine storm syndromes include familial
Cytokine storms versus cytokine release syndrome
The term "cytokine storm" is often loosely used interchangeably with cytokine release syndrome (CRS) but is more precisely a differentiable syndrome that may represent a severe episode of cytokine release syndrome or a component of another disease entity, such as macrophage activation syndrome. When occurring as a result of a therapy, CRS symptoms may be delayed until days or weeks after treatment. Immediate-onset (fulminant) CRS appears to be a cytokine storm.[7]
Research
Nicotinamide (a form of vitamin B3) is a potent inhibitor of proinflammatory cytokines.[8][9] Low blood plasma levels of trigonelline (one of the metabolites of vitamin B3) have been suggested for the prognosis of SARS-CoV-2 death (which is thought to be due to the inflammatory phase and cytokine storm).[10][11]
Magnesium decreases inflammatory cytokine production by modulation of the immune system.[12][13]
History
The first reference to the term cytokine storm in the published
It is believed that cytokine storms were responsible for the disproportionate number of healthy young adult deaths during the
In 2006, a study at
Relationship to COVID-19
During the
ARDS was shown to be the cause of mortality in 70% of COVID-19 deaths.
Early recognition of a cytokine storm in COVID-19 patients is crucial to ensure the best outcome for recovery, allowing treatment with a variety of biological agents that target the cytokines to reduce their levels. Meta-analysis suggests clear patterns distinguishing patients with or without severe disease. Possible predictors of severe and fatal cases may include "
Due to the increased levels of cytokines and interferons in patients with severe COVID-19, both have been investigated as potential targets for SARS-CoV-2 therapy. An
Short-term use of dexamethasone, a synthetic corticosteroid, has been demonstrated to reduce the severity of inflammation and lung damage induced by a cytokine storm by inhibiting the severe cytokine storm or the hyperinflammatory phase in patients with COVID-19.[34]
Clinical trials continue to identify causes of cytokine storms in COVID-19 cases.[35][36] One such cause is the delayed Type I interferon response that leads to accumulation of pathogenic monocytes. High viremia is also associated with exacerbated Type I interferons response and worse prognosis.[37] Diabetes, hypertension, and cardiovascular disease are all risk factors of cytokine storms in COVID-19 patients.[38]
References
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