Abstract □ 68

Approximately half of all SIDS victims have had slight infections prior to death. There is a co-incidence between pertussis - and other epidemics and increased SIDS rates. The risk to die from SIDS is significantly increased when prone sleeping position is combined with slight infection and overwrapping. Furthermore, the reduction in SIDS occurrence after 1990 is most pronounced in the group of small infants with signs of slight infections prior to death.

Immunohistochemical studies in SIDS victims have shown signs of immune stimulation in the airways and the intestinal tract: salivary glands IgA, IgM, IgG, CD45, T-cell, HLA-DR; tonsills: IgG, IgM; tracheal wall: IgM; duodenal mucosa: IgA, and by ELISA IL-6 is found in the CSF. IL-6 induces fever.

Furthermore, immunohistochemical studies in stillborn fetuses, full term infants and infants who died during the first 6 months after birth have revealed that humoral immunity and epithelial expression of secretory component and HLA-DR in the respiratory- and the intestinal tract show a very rapid increase in the first months after birth. This rapid development may make some infants vulnerable to an "overreaction" of the mucosal immune system. In favour of a link between SIDS and infectious deaths is also the similar distribution of vitreous humour hypoxanthine levels and CSF-IL-6 levels. Both groups have significantly higher levels than sudden violent deaths.

Factors that may explain why some infants "overreact" immunologically to slight infections are as follows:

1) SIDS takes place during a period of rapid development of both the CNS and the immune system. Developmental delay of the CNS may cause disturbance in temperature regulation and the rapid development of mucosal immunity may make the infants vulnerable to simple infections - both factors leading to hyperthermia and death.

2) A genetic predisposition may make infants react inadequately to infections; SIDS-victims with slight upper airway infections prior to death more often have deletions of either the complement factor C4A- or C4B-gene than both SIDS-victims without such infections and normal controls. This may be of significance since the complement system is important for defence against micro-organisms. Recently, it has been focused on a genetically determined deficient energy production. This view fit well with the observation that infants who later succumb to SIDS tend to be more sleepy and less reactive than age matched controls, and it may be explained by reduced ATP production. ATP deficiency could also explain why slight infections may be disastrous in situations of increased stress. Muscular weakness may make the infant placed prone with the face down unable to turn the head to the side, or impair breathing when the diaphragmatic muscle is affected. In fact, SIDS victims show more substitutions in the hypervariable D-loop of mitochondrial DNA than controls and further studies in mt-DNA are underway.

3) A simple infection may trigger the death mechanism; epidemiological data support this hypothesis.

Supported by the Norwegian SIDS Society