PMID- 38541678
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240330
IS  - 2075-1729 (Print)
IS  - 2075-1729 (Electronic)
IS  - 2075-1729 (Linking)
VI  - 14
IP  - 3
DP  - 2024 Mar 7
TI  - VAERS Vasculitis Adverse Events Retrospective Study: Etiology Model of Immune 
      Complexes Activating Fc Receptors in Kawasaki Disease and Multisystem 
      Inflammatory Syndromes.
LID - 10.3390/life14030353 [doi]
LID - 353
AB  - BACKGROUND: Vasculitis diseases include Kawasaki disease (KD), Kawasaki disease 
      shock syndrome (KDSS), Multisystem Inflammatory Syndrome (MIS), Henoch-Schonlein 
      purpura (HS), or IgA vasculitis, and additional vasculitis diseases. These 
      diseases are often preceded by infections or immunizations. Disease incidence 
      rates are higher in children than in adults. These diseases have been extensively 
      studied, but understanding of the disease etiology remains to be established. 
      OBJECTIVE: Many studies have failed to demonstrate an association between 
      vasculitis diseases and vaccination; this study examines possible associations. 
      METHODS: Herein, the Vaccine Adverse Event Reporting System (VAERS) database is 
      retrospectively examined for associations between vasculitis diseases and 
      immunizations. RESULTS: For some vaccines, the number of rare cases of KD, MIS, 
      and HS are higher than the background rates. These rare cases are predicted to 
      occur in individuals with (1) genetic risk factors with (2) antibody titer levels 
      above the primary immune response level. Herein, the model of humoral immune 
      response antibodies bound to antigens (pathogen or vaccine) creating immune 
      complexes is proposed. These immune complexes are proposed to bind Fc receptors 
      on immune cells and platelets, resulting in cell activation and the release of 
      inflammatory molecules including histamine and serotonin. Immune complexes and 
      inflammatory molecules including serotonin and histamine likely trigger 
      vasculitis. Elevated serotonin and possibly histamine drive initial 
      vasoconstrictions, disrupting blood flow. Increased blood flow pressure from 
      cardiac capillary vasoconstrictions is predicted to trigger coronary artery 
      aneurysms (CAA) or lesions (CAL) in some patients. For KDSS and MIS patients, 
      these cardiac capillary vasoconstrictions are predicted to result in ischemia 
      followed by ventricular dysfunction. Ongoing ischemia can result in long-term 
      cardiac damage. Cases associated with pathogens are likely to have persistent 
      infections triggering disease onset. CONCLUSION: The proposed model of immune 
      complexes driving disease initial disease etiology by Fc receptor activation of 
      immune cells and platelets, resulting in elevated histamine and serotonin levels, 
      is testable and is consistent with disease symptoms and current treatments.
FAU - Ricke, Darrell O
AU  - Ricke DO
AUID- ORCID: 0000-0002-2842-2809
AD  - Lincoln Laboratory, Massachusetts Institute of Technology, Lexington, MA 02421, 
      USA.
FAU - Smith, Nora
AU  - Smith N
AD  - Lincoln Laboratory, Massachusetts Institute of Technology, Lexington, MA 02421, 
      USA.
LA  - eng
GR  - FA8702-15-D-0001/United States Air Force/
PT  - Journal Article
DEP - 20240307
PL  - Switzerland
TA  - Life (Basel)
JT  - Life (Basel, Switzerland)
JID - 101580444
PMC - PMC10971466
OTO - NOTNLM
OT  - Henoch-Schonlein purpura
OT  - Kawasaki disease
OT  - Kawasaki disease shock syndrome
OT  - MIS-A
OT  - MIS-C
OT  - MIS-N
OT  - MIS-V
OT  - Multisystem Inflammatory Syndrome
OT  - vaccines
COIS- The authors declare no conflicts of interest. The funders had no role in the 
      design of the study; in the collection, analyses, or interpretation of data; in 
      the writing of the manuscript; or in the decision to publish the results.
EDAT- 2024/03/28 06:46
MHDA- 2024/03/28 06:47
PMCR- 2024/03/07
CRDT- 2024/03/28 01:14
PHST- 2024/01/10 00:00 [received]
PHST- 2024/02/22 00:00 [revised]
PHST- 2024/03/05 00:00 [accepted]
PHST- 2024/03/28 06:47 [medline]
PHST- 2024/03/28 06:46 [pubmed]
PHST- 2024/03/28 01:14 [entrez]
PHST- 2024/03/07 00:00 [pmc-release]
AID - life14030353 [pii]
AID - life-14-00353 [pii]
AID - 10.3390/life14030353 [doi]
PST - epublish
SO  - Life (Basel). 2024 Mar 7;14(3):353. doi: 10.3390/life14030353.