Mast Cell Activation Syndrome: Tools for Diagnosis and Differential Diagnosis

Weiler, Catherine R.

doi:10.1016/j.jaip.2019.08.022

Cited by 27 publications

(38 citation statements)

References 114 publications

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“…This model is consistent with the histopathologic ndings seen at surgery, autopsies, and is supported by clinical pharmacologic ndings suggesting potential bene ts of histamine H2 receptor blockade using famotidine. This model is also supported by the signi cant overlap in the clinical signs and symptoms of the initial phase of COVID-19 disease and those of mast cell activation syndrome (MCAS) [91][92][93][94] as well similarities to Dengue hemorrhagic fever and shock syndrome (including T cell depletion) during the later phase of COVID-19 85,95,96 . The cardiac events, stroke, and related outcomes associated with COVID-19 also appear consistent with the Kounis syndrome [97][98][99] .…”

Section: Famotidine Reaches Functionally Relevant Systemic Concentratmentioning

confidence: 86%

COVID-19: Famotidine, Histamine, Mast Cells, and Mechanisms

Malone

Tisdall²,

Fremont-Smith

et al. 2020

Preprint

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SARS-CoV-2 infection is required for COVID-19, but many signs and symptoms of COVID-19 differ from common acute viral diseases. Currently, there are no pre- or post-exposure prophylactic COVID-19 medical countermeasures. Clinical data suggest that famotidine may mitigate COVID-19 disease, but both mechanism of action and rationale for dose selection remain obscure. We explore several plausible avenues of activity including antiviral and host-mediated actions. We propose that the principal famotidine mechanism of action for COVID-19 involves on-target histamine receptor H2 activity, and that development of clinical COVID-19 involves dysfunctional mast cell activation and histamine release.

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Section: Famotidine Reaches Functionally Relevant Systemic Concentratmentioning

confidence: 86%

COVID-19: Famotidine, Histamine, Mast Cells, and Mechanisms

Malone

Tisdall²,

Fremont-Smith

et al. 2020

Preprint

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“…We identified publications offering new or modified schemes for diagnosing the full range of MCAS (excluding those addressing only subsets, such as monoclonal MCAS). We found nine such publications [7][8][9][19][20][21][22][23][24], reviewed them, and found each to fall into one of two principal schools of thought as defined by their original papers [8,9]. Our analysis proceeded from these groupings, with attempts to assess each "school" for (1) validity of diagnostic criteria, (2) diagnostic accuracy, and (3) practicality.…”

Section: Methodsmentioning

confidence: 99%

“…[31][32][33][34][35]), hinting at commonalities in these diseases' mechanistic roots, and those favoring the consensus-1 criteria have published contrary assertions (e.g. [23,24,36]).…”

Section: Molderings Et Al Proposal For Diagnostic Criteria For Mcasmentioning

confidence: 99%

Diagnosis of mast cell activation syndrome: a global “consensus-2”

Ackerley²,

et al. 2020

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The concept that disease rooted principally in chronic aberrant constitutive and reactive activation of mast cells (MCs), without the gross MC neoplasia in mastocytosis, first emerged in the 1980s, but only in the last decade has recognition of “mast cell activation syndrome” (MCAS) grown significantly. Two principal proposals for diagnostic criteria have emerged. One, originally published in 2012, is labeled by its authors as a “consensus” (re-termed here as “consensus-1”). Another sizable contingent of investigators and practitioners favor a different approach (originally published in 2011, newly termed here as “consensus-2”), resembling “consensus-1” in some respects but differing in others, leading to substantial differences between these proposals in the numbers of patients qualifying for diagnosis (and thus treatment). Overdiagnosis by “consensus-2” criteria has potential to be problematic, but underdiagnosis by “consensus-1” criteria seems the far larger problem given (1) increasing appreciation that MCAS is prevalent (up to 17% of the general population), and (2) most MCAS patients, regardless of illness duration prior to diagnosis, can eventually identify treatment yielding sustained improvement. We analyze these proposals (and others) and suggest that, until careful research provides more definitive answers, diagnosis by either proposal is valid, reasonable, and helpful.

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“…This model is consistent with the histopathologic ndings seen at surgery, autopsies, and is supported by clinical pharmacologic ndings suggesting potential bene ts of histamine H2 receptor blockade using famotidine. This model is also supported by the signi cant overlap in the clinical signs and symptoms of the initial phase of COVID-19 disease and those of mast cell activation syndrome (MCAS)[91][92][93][94] as well similarities to Dengue hemorrhagic fever and shock syndrome (including T cell depletion) during the later phase of COVID-1985,95,96 . The cardiac events, stroke, and related outcomes associated with COVID-19 also appear consistent with the Kounis syndrome97-99 .…”

mentioning

confidence: 87%