Increased mast cell tryptase in sudden infant death - anaphylaxis, hypoxiaor artefact?

Background Increased concentrations of mast cell tryptase in post mortem bl ood 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 sud den 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. Radioallergosorbe nt tests were performed for possible allergens (mixture for relevant food a llergens, Phadiatop and latex). IgG subclasses, IgM, and complement factors (C3, C4 and factor B) were measured with radial immunodiffusion. Mast cell s, labelled with antibodies against mast cell tryptase, were counted in the lungs and heart. The circumstances of death and medical history of the dec eased infant and family were obtained through police and hospital records. Results In 40% of the SIDS cases tryptase was elevated (> 10 mu g/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 ele vated. The only variable that was associated with high tryptase values was prone position at death (P less than or equal to 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 si gnificantly higher IgE than the others (P less than or equal to 0.05). Conclusion The results do not support the hypothesis that the elevated tryp tase concentrations in sudden infant death are caused by allergy. The assoc iation between prone position at death and elevated tryptase could hypothet ically be explained by mast cell degranulation due to, for example, a hypox ic stimulus in these infants.