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E Gidlund

Publications and source records attributed to E Gidlund.

5 recordsLinked to original sources

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

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). CONCLUSION: 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.

Anaphylaxis↗

Enamel incremental lines as recorders for disease in infancy and their relation to the diagnosis of SIDS.

The sudden infant death syndrome (SIDS) is a major diagnosis of post-neonatal mortality in the industrialised countries. The cause of death is, however, still elusive. The development of complementary diagnostic methods widening the possibility to analyse the postmortem findings is therefore important. The aim of this study was to histologically examine the enamel of teeth from children dying suddenly and unexpectedly in order to disclose if the presence of enamel disturbances corresponded to neo- or postnatal disorders. During enamel formation ameloblasts are susceptible to local and systemic disturbances which may be reflected in the fully formed enamel as hypoplasia, hypocalcification or accentuated incremental lines. Nineteen consecutive cases of deaths in infants between 1-19 months of age were investigated at the Department of Forensic Pathology, Stockholm, Sweden. The analyses of anamnestic and postmortem data and the analyses of incremental lines were done independently without knowledge of the conclusion of the other part. The results show a good agreement between enamel changes on one hand and the antemortem history and the autopsy findings on the other. This type of investigation may be a valuable complement to the ordinary postmortem investigations of a child who has suddenly and unexpectedly died.

Autopsy↗

Nicotine and cotinine levels in pericardial fluid in victims of SIDS.

We have analyzed the levels of nicotine and cotinine in pericardial fluid in 24 consecutively autopsied cases of sudden unexpected death in infants aged one to six months. Our aim was to determine to what extent victims of sudden infant death may have been exposed to passive smoking near the time of death. Sixteen of the decreased infants were classified as SIDS at autopsy. Other contributing causes of death, predominantly infections, were found in eight cases. Eight infants (30%) had cotinine levels less than 2 ng, indicating that no significant exposure to nicotine had occurred near the time of death. Of the remaining 70%, five had been moderately exposed, seven markedly exposed and four heavily exposed (cotinine levels 2-10 ng, 10-50 ng and more than 50 ng, respectively). Since only 18% of Swedish women smoke after childbearing we conclude that nicotine exposure in infants who died suddenly was much higher than one would otherwise expect. It is hypothesized that high concentrations of nicotine and nicotine metabolites around the heart may affect cardiac function and thus play a role in the mechanisms causing SIDS or other categories of sudden unexpected death.

Cotinine↗