PULMONARY IMMUNOPATHOLOGY OF SUDDEN-INFANT-DEATH-SYNDROME

Citation
Wj. Howat et al., PULMONARY IMMUNOPATHOLOGY OF SUDDEN-INFANT-DEATH-SYNDROME, Lancet, 343(8910), 1994, pp. 1390-1392
Citations number
31
Categorie Soggetti
Medicine, General & Internal
Journal title
LancetACNP
ISSN journal
01406736
Volume
343
Issue
8910
Year of publication
1994
Pages
1390 - 1392
Database
ISI
SICI code
0140-6736(1994)343:8910<1390:PIOS>2.0.ZU;2-K
Abstract
Sudden infant death syndrome (SIDS) is the most common cause of postne onatal mortality in the UK. Pathological investigations have shown evi dence suggestive of respiratory obstruction with subsequent hypoxia le ading to death. We examined 48 infants who died of SIDS and 30 who die d of other, non-pulmonary, causes and identified pulmonary eosinophil and neutrophil leucocytes, mast cells, and T and B lymphocytes by immu nocytochemistry. Positively stained cells were counted in the parenchy ma and around the bronchi without knowledge of the tissue source. The results showed three times more eosinophils in the lungs of infants wh o died of SIDS (27.61 vs 7.91 [99% CI 1.76-5.87] cells/mm(2) for paren chyma) accompanied by increased T lymphocytes and B lymphocytes. There were more peribronchial mast cells in the SIDS group (22.1 vs 14.7 [1 .03-2.10] cells/mm(2)) and insignificant differences in neutrophils an d parenchymal mast cells. There were significant associations between eosinophil, B lymphocyte, and T lymphocyte numbers. These findings pro vide evidence for an abnormal T lymphocyte-mediated pulmonary inflamma tory response In SIDS. Products of eosinophil degranulation can cause epithelial damage and pulmonary oedema, which could cause the respirat ory obstruction and hypoxia associated with SIDS.