title: Hypothesis: new concepts concerning the pathophysiology of the sudden infant death syndrome due to magnesium deficiency shock.
abstract: There appear to be many contributing factors to sudden infant death syndrome (SIDS). One final common pathway that may explain some cases of SIDS is presented as a hypothesis: SIDS occurs as a shock-like event in a stressed infant with congenital or acquired magnesium deficiency with respect to calcium, or with genetically determined high magnesium requirements. Increased calcium and stress-related catecholamines favour platelet aggregation and release of mediators, chief of which appears to be thromboxane A2 (TXA2). TXA2, a major vasoconstrictor, bronchoconstrictor, and platelet aggregator is relatively unopposed during shock by prostacyclin, a vasodilator, bronchodilator, and platelet disaggregator which normally counterbalances its effects. The shock episode is self-limited. Infants who recover have suffered an apparent life threatening event (ALTE); those who die have insufficient pathology to explain the cause of death; the diagnosis is SIDS.
authors: Department of Pediatrics, Jefferson Medical College, Thomas Jefferson University, Philadelphia.
authors: J L
authors: JL
authors: Caddell
mesh_terms: D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008275:Magnesium Deficiency / Q000150:complications* / Q000473:pathology; D013398:Sudden Infant Death / Q000209:etiology*