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Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour

Research paper by H. Storm, T. O. Rognum, O. D. Saugstad, K. L. Reichelt

Indexed on: 01 Nov '93Published on: 01 Nov '93Published in: European Journal of Pediatrics



Abstract

Beta-endorphin (BEND) may induce respiratory depression. Elevated levels of beta-endorphin immunoreactivity (BENDI) in the CSF are found in children with apnoea and in about 50% of sudden infant death (SID) victims. Premortal hypoxia in SID victims has been indicated by elevated hypoxanthine (HX) levels in the vitreous humour (VH). In this study we correlated BENDI in CSF with HX in VH in SID victims (n=19) and controls (n=18). BEND in CSF was measured by RIA, and HPLC was used for identification of BENDI. HX in VH was measured by HPLC. All the SID victims had elevated levels of HX in VH. The BENDI in CSF divided the SID victims into two subpopulations (P<0.01); one with undetectable levels (<4.3 fmol/ml) (n=10) and one with high levels (160–400 fmol/ml) (n=9).In the SID subpopulation with high levels of BENDI in CSF,we found a correlation between BENDI in CSF and HX in VH (r=0.92). Control infants who died a stressful death, such as during heart operations (n=2), had high levels of BENDI in CSF and low levels of HX in VH. Controls who died of infections (n=11) had low levels of BENDI in CSF and elevated levels of HX in VH. Because hypoxia in itself does not increase BENDI in CSF, increased BENDI in CSF is probably not secondary to hypoxia but may be of aetiological significance. We therefore suggest that SID victims with high levels of BENDI in CSF, which correlate with the elevated levels of HX in VH, may die from premortal hypoxia possibly induced by BEND.