Wiklund L, George M, Nord C E, Ronquist G, Saldeen T
Uppsala University, Uppsala, Sweden.
Eur J Clin Invest. 1998 Nov;28(11):958-68. doi: 10.1046/j.1365-2362.1998.00385.x.
A hypothesis suggesting an inducible inability of the enteric bacteria to metabolize urea in infants, resulting in metabolic alkalosis and subsequent respiratory insufficiency, has been proposed as the cause of sudden infant death syndrome (SIDS).
Microbiological cultivation and determination of faecal urease activity and faecal urea content were carried out in 30 cases of unexpected infant 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.
The SIDS subjects differed significantly from the control cases in two respects: they had low or no sigmoid faecal urease activity and an unmetabolized sigmoid faecal urea content, whereas the control subjects had normal faecal urease activity and none, or very little, remaining faecal urea. The NO concentration in faeces was correlated with the faecal content of urea in the SIDS cases.
The present findings lend support to the hypothesis of an insufficient metabolism of enteric urea in infants with SIDS.
一种假说认为，婴儿肠道细菌代谢尿素的能力存在诱导性缺陷，导致代谢性碱中毒及随后的呼吸功能不全，这被认为是婴儿猝死综合征（SIDS）的病因。
对30例婴儿意外死亡病例进行微生物培养，并测定粪便脲酶活性和粪便尿素含量，其中22例被认为死于SIDS，8例死于其他原因。将粪便在生理盐水中孵育后，测定密封试管中一氧化氮（NO）的浓度。
SIDS组与对照组在两个方面存在显著差异：SIDS组乙状结肠粪便脲酶活性低或无，乙状结肠粪便尿素未代谢，而对照组粪便脲酶活性正常，粪便尿素残留无或极少。SIDS组粪便中NO浓度与粪便尿素含量相关。
目前的研究结果支持SIDS婴儿肠道尿素代谢不足的假说。
