The pathogenesis of sudden infant death syndrome (SIDS) is elusive and
probably multifactorial. The occurrence of mast cell activation in SI
DS was assessed in this study by measuring concentrations of tryptase,
a neutral protease produced mainly by mast cells, in postmortem sera
from term infants with SIDS and from age-matched control infants who d
ied unexpectedly at home from a known-cause. Tryptase levels were sign
ificantly higher in the 50 infants with SIDS than in the 15 control in
fants (p = 0.0004). Forty percent of the infants with SIDS and none of
the control infants had a tryptase level greater than 10 ng/ml, the t
hreshold chosen to indicate premortem mast cell activation. An infant
with SIDS had a 20-fold higher chance of having an elevated tryptase l
evel compared with a control infant. The postmortem interval did not i
nfluence these results. Thus mast cell-mediated anaphylaxis is likely
to be the pathogenetic mechanism involved in some but not all SIDS cas
es. Recognition of this pathway as operative in SIDS should facilitate
a more precise identification of the allergens involved, the processe
s leading to mast cell activation, and procedures to identify those in
fants at risk for anaphylaxis, and should, in time, lead to better the
rapeutic interventions aimed at preventing this specific cause of SIDS
.