Sudden Infant Death Syndrome Research - SIDS, Causes, Prevention, Statistics

Sudden Infant Death Syndrome Research Today is a free monthly online journal that collates and summarizes the latest research about Sudden Infant Death Syndrome, including details on sids, causes, prevention, statistics.


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Pulmonary neuroendocrine cells and neuroepithelial bodies in sudden infant death syndrome: potential markers of airway chemoreceptor dysfunction.

Cutz E, Perrin DG, Pan J, Haas EA, Krous HF

Pulmonary neuroendocrine cells (PNEC), including neuroepithelial bodies (NEB), are amine- and peptide (for example, bombesin)-producing cells that function as hypoxia/hypercapnia-sensitive chemoreceptors that could be involved in the pathophysiology of sudden infant death syndrome (SIDS). We assessed morphometrically the frequency and size of PNEC/NEB in lungs of infants who died of SIDS (n = 21) and compared them to an equal number PNEC/NEB in lungs of age-matched control infants who died of accidental death or homicide, with all cases obtained from the San Diego SIDS/SUDC Research Project database. As a marker for PNEC/NEB we used an antibody against chromogranin A (CGA), and computer-assisted morphometric analysis was employed to determine the relative frequency of PNEC per airway epithelial area (% immunostained area, %IMS), the size of NEB, the number of nuclei/NEB, and the size of the NEB cells. The lungs of SIDS infants showed significantly greater %IMS of airway epithelium (2.72 +/- 0.28 [standard error of the mean, SEM] versus 1.88 +/- 0.24; P < 0.05) and larger NEB (1557 +/- 153 mum(2) versus 1151 +/- 106 mum(2); P < 0.05) compared to control infants. The size of NEB cells was also significantly increased in SIDS cases compared to the controls (180 +/- 6.39 mum(2) versus 157 +/- 8.0 mum(2); P < 0.05), indicating the presence of hypertrophy in addition to hyperplasia. Our findings support previous studies demonstrating hyperplasia of PNEC/NEB in lungs of infants who died of SIDS. These changes could be secondary to chronic hypoxia and/or could be attributable to maturational delay. Morphometric assessment and/or measurement of the secretory products of these cells (for example, CGA, bombesin) could provide a potential biological marker for SIDS.

Published 23 March 2007 in Pediatr Dev Pathol, 10(2): 106-16.
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Sudden Infant Death Syndrome Research Today Archive:

Volume 1 (2005)
  Issue 1 (September)
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  Issue 3 (November)
  Issue 4 (December)

Volume 2 (2006)
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Volume 3 (2007)
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Volume 4 (2008)
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Sudden Infant Death Syndrome Books

Sudden Infant Death Syndrome: Problems, Progress and Possibilities (Hodder Arnold Publication)

Sudden Infant Death Syndrome: Problems, Progress and Possibilities (Hodder Arnold Publication)