Rapid review explores the relationship between inflammation and infection risk in SIDS, indicating potential vulnerabilities in infants.
Within sudden infant death syndrome (SIDS) reside several primary phenomena. These include a state of immune immaturity, susceptibility to infection, and an inflammatory state. Most SIDS risk factors increase the risk of infection (prematurity, lack of breastfeeding, low or absent transplacental antibody, ethnicity, genetics, specific gene polymorphisms associated with susceptibility to infection, poverty, etc.). Most SIDS cases display evidence of an inflammatory state (raised inflammatory markers and inflammatory cytokines). The pattern of inflammation is very similar to that observed following vaccination. The complex relationship between reactogenicity and immunogenicity is examined. Under certain circumstances, reactogenicity can cause immune paralysis and may leave a vulnerable infant open to infection and systemic inflammatory response syndrome, leading to shock. This mechanism is explored in this rapid review in the context of the aetiopathogenesis of SIDS.
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Paul N. Goldwater (2026) studied this question.
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