Covid-19 hyperinflammation, post-Covid illness may start in mast cell activation syndrome

 

Lawrence B.Afrina, Leonard B.WeinstockbGerhard J.Molderingsc 

DOI: https://doi.org/10.1016/j.ijid.2020.09.016

PDF: https://www.sciencedirect.com/science/article/pii/S1201971220307323/pdfft?md5=7af57d7248552203969bd62f626d851c&pid=1-s2.0-S1201971220307323-main.pdf

Highlights

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Much of Covid-19 hyperinflammation is consistent with mast-cell-driven inflammation.

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Prevalence of severe Covid-19 is similar to that of mast cell activation syndrome (MCAS).

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Drugs inhibiting mast cells (MCs) and their mediators show promise in Covid-19.

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None of the authors currently treated MCAS patients with Covid-19 had severe forms or mortality.

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The dysfunctional MCs of MCAS may underlie severe acute and chronic Covid-19 illness.

Abstract

Objectives

One-fifth of Covid-19 patients suffer a severe course of Covid-19 infection; however, the specific causes remain unclear. Mast cells (MCs) are activated by SARS-CoV-2. Although only recently recognized, MC activation syndrome (MCAS), usually due to acquired MC clonality, is a chronic multisystem disorder with inflammatory and allergic themes, and an estimated prevalence of 17%. This paper describes a novel conjecture explaining how MCAS might cause a propensity for severe acute Covid-19 infection and chronic post-Covid-19 illnesses.

Methods

Observations of Covid-19 illness in patients with/without MCAS were compared with extensive clinical experience with MCAS.

Results

The prevalence of MCAS is similar to that of severe cases within the Covid-19-infected population. Much of Covid-19’s hyperinflammation is concordant with manners of inflammation which MC activation can drive. Drugs with activity against MCs or their mediators have preliminarily been observed to be helpful in Covid-19 patients. None of the authors’ treated MCAS patients with Covid-19 suffered severe infection, let alone mortality.

Conclusions

Hyperinflammatory cytokine storms in many severely symptomatic Covid-19 patients may be rooted in an atypical response to SARS-CoV-2 by the dysfunctional MCs of MCAS rather than a normal response by normal MCs. If proven, this theory has significant therapeutic and prognostic implications.

https://www.sciencedirect.com/science/article/pii/S1201971220307323