Sudden infant death syndrome and nitrogen metabolism: further development of a hypothesis

Citation
L. Wiklund et al., Sudden infant death syndrome and nitrogen metabolism: further development of a hypothesis, EUR J CL IN, 28(11), 1998, pp. 958-965
Citations number
31
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
ISSN journal
00142972 → ACNP
Volume
28
Issue
11
Year of publication
1998
Pages
958 - 965
Database
ISI
SICI code
0014-2972(199811)28:11<958:SIDSAN>2.0.ZU;2-F
Abstract
Background A hypothesis suggesting an inducible inability of the enteric ba cteria to metabolize urea in infants, resulting in metabolic alkalosis and subsequent respiratory insufficiency, has been proposed as the cause of sud den infant death syndrome (SIDS). Methods Microbiological cultivation and determination of faecal urease acti vity and faecal urea content were carried out in 30 cases of unexpected inf ant deaths out of which 22 were considered to be due to SIDS and eight from other causes. The concentration of nitric oxide (NO) in sealed test tubes was determined after incubation of faeces in normal saline. Results The SIDS subjects differed significantly from the control cases in two respects: they had low or no sigmoid faecal urease activity and an unme tabolized sigmoid faecal urea content, whereas the control subjects had nor mal faecal urease activity and none, or Very little, remaining faecal urea. The NO concentration in faeces was correlated with the faecal content of u rea in the SIDS cases. Conclusion The present findings lend support to the hypothesis of an insuff icient metabolism of enteric urea in infants with SIDS.