Mast cell activation may explain many cases of chemical intolerance View Full Text


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Article Info

DATE

2021-11-17

AUTHORS

Claudia S. Miller, Raymond F. Palmer, Tania T. Dempsey, Nicholas A. Ashford, Lawrence B. Afrin

ABSTRACT

BackgroundThis paper explores the relationship between chemical intolerance (CI) and mast cell activation syndrome (MCAS). Worldwide observations provide evidence for a two-stage disease process called toxicant-induced loss of tolerance (TILT) as a mechanism for CI. TILT is initiated by a major exposure event or a series of lower-level exposures. Subsequently, affected individuals report that common chemical inhalants, foods, and drugs (i.e., various xenobiotics) trigger multi-system symptoms.PurposeTo determine whether MCAS provides a plausible biological mechanism for CI/TILT.MethodsUsing the validated Quick Environmental Exposure and Sensitivity Inventory (QEESI), we compared patients diagnosed with MCAS (n = 147) to individuals who reported chemical intolerances (CI/TILT) following various exposures (n = 345) and to healthy controls (n = 76). Using ANOVA, we compared QEESI scores across groups. Clinical scores for the MCAS patient group were used to predict CI status using logistic regression.ResultsMore than half (59%) of the MCAS group met criteria for CI. A logistic regression model illustrates that as the likelihood of patients having MCAS increased, their likelihood of having CI/TILT similarly increased, to a near-perfect correspondence at the high ends of the QEESI and clinical MCAS scores. Symptom and intolerance patterns were nearly identical for the CI and MCAS groups.DiscussionWe present data suggesting that xenobiotic activation of mast cells may underlie CI/TILT. The strikingly similar symptom and intolerance patterns for MCAS and TILT suggest that xenobiotics disrupt mast cells, leading to either or both of these challenging conditions. Faced with patients suffering from complex illness affecting multiple organ systems and fluctuating inflammatory, allergic, and dystrophic symptoms, clinicians can now ask themselves two questions: (1) Could MCAS be at the root of these problems? (2) Could environmental exposures be driving MC activation and mediator release? Increasing our understanding of the connection between TILT and MCs has the potential to expose a new link between environmental exposures and illness, offering new opportunities for improving individual and public health.ConclusionThe close correspondence between QEESI scores and symptom patterns for MCAS and TILT patients supports xenobiotic-driven mast cell activation and mediator release (i.e., MCAS) as a plausible unifying biological mechanism for CI/TILT, with profound implications for medicine, public health, and regulatory toxicology. More... »

PAGES

129

References to SciGraph publications

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  • 2018-04-17. Mast Cell Interactions and Crosstalk in Regulating Allergic Inflammation in CURRENT ALLERGY AND ASTHMA REPORTS
  • 2011-03-22. Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options in JOURNAL OF HEMATOLOGY & ONCOLOGY
  • 2016-04-30. Pharmacological treatment options for mast cell activation disease in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
  • 2009-07-15. Evaluation of subjective symptoms of Japanese patients with multiple chemical sensitivity using QEESI© in ENVIRONMENTAL HEALTH AND PREVENTIVE MEDICINE
  • 2010-09-14. Comparative analysis of mutation of tyrosine kinase kit in mast cells from patients with systemic mast cell activation syndrome and healthy subjects in IMMUNOGENETICS
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    http://scigraph.springernature.com/pub.10.1186/s12302-021-00570-3

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    45 affected individuals
    46 biological mechanisms
    47 cases
    48 cell activation
    49 cells
    50 challenging conditions
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    71 food
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    74 health
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    81 intolerance
    82 likelihood
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    84 link
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    87 loss
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    89 low-level exposure
    90 mast cell activation
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    92 mast cells
    93 mechanism
    94 mediator release
    95 medicine
    96 model
    97 multi-system symptoms
    98 multiple organ systems
    99 new links
    100 new opportunities
    101 observations
    102 opportunities
    103 organ systems
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    105 patient group
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    109 plausible biological mechanisms
    110 potential
    111 present data
    112 problem
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    114 profound implications
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