title: Increased mast cell tryptase in sudden infant death - anaphylaxis, hypoxia or artefact?
abstract: BACKGROUND
  Increased concentrations of mast cell tryptase in post mortem blood have frequently been observed in sudden infant deaths but the cause of this has not yet been clarified.
  
  
  OBJECTIVE
  The aim was to evaluate factors (immunological, morphological and anamnestic data) behind the observed increase in mast cell tryptase in sudden infant deaths with elevated tryptase.
  
  
  METHODS
  Mast cell tryptase and total immunoglobulin (Ig) E were measured in post mortem sera from 44 infants younger than 1.5 years. Radioallergosorbent tests were performed for possible allergens (mixture for relevant food allergens, Phadiatop and latex). IgG subclasses, IgM, and complement factors (C3, C4 and factor B) were measured with radial immunodiffusion. Mast cells, labelled with antibodies against mast cell tryptase, were counted in the lungs and heart. The circumstances of death and medical history of the deceased infant and family were obtained through police and hospital records.
  
  
  RESULTS
  In 40% of the SIDS cases tryptase was elevated (>10 microg/L). Total IgE in serum was increased in 33% compared with clinical reference values but showed no association with mast cell tryptase. RAST tests were positive in three cases. In one of these cases both tryptase and total IgE were elevated. The only variable that was associated with high tryptase values was prone position at death (P < or = 0.05 ). Allergy or asthma in the family were alleged in 50% of the cases, but was not associated with elevated tryptase or IgE. Children with elevated total IgE also displayed high concentrations of IgG1 and IgG2. Infants who died in the spring had significantly higher IgE than the others (P < or = 0.05).
  
  
  CONCLUSIONS
  The results do not support the hypothesis that the elevated tryptase concentrations in sudden infant death are caused by allergy. The association between prone position at death and elevated tryptase could hypothetically be explained by mast cell degranulation due to, for example, a hypoxic stimulus in these infants.
authors.affiliation: Department of Forensic Medicine, Linköping, Sweden.
authors.forename: E
authors.initials: E
authors.lastname: Edston
authors.forename: E
authors.initials: E
authors.lastname: Gidlund
authors.forename: M
authors.initials: M
authors.lastname: Wickman
authors.forename: H
authors.initials: H
authors.lastname: Ribbing
authors.forename: M
authors.initials: M
authors.lastname: Van Hage-Hamsten
mesh_terms: D000707:Anaphylaxis / Q000150:complications*; D015550:Cell Degranulation; D053818:Chymases; D003165:Complement System Proteins; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000150:complications*; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D008407:Mast Cells / Q000201:enzymology*; D016684:Prone Position; D011852:Radioallergosorbent Test; D012697:Serine Endopeptidases / Q000097:blood* / Q000276:immunology; D013398:Sudden Infant Death / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D053802:Tryptases
chemical_list: D007074:Immunoglobulin G; D007073:Immunoglobulin E; D003165:Complement System Proteins; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases