Abstract
Skeletal muscle channelopathy: a new risk for sudden infant death syndrome
Highlights
Sudden infant death syndrome (SIDS) remains a leading cause of infant mortality, despite a steadily decreasing incidence since the 1990s.1 The reasons for this decline are debated, but it could be due to methodological reasons or a reduction of risks, such as an increase in supine sleeping position for infants, as advocated by the Back to Sleep campaign.[2]
About 10% of infants who die of SIDS have ion channel-related arrhythmias, half of which are caused by mutations in the cardiac sodium channel gene (SCN5A) or one of its subunits (SCN1B–4B).[5]
The authors postulated that SCN4A variants capable of disrupting muscle excitability might be over-represented in SIDS
Summary
Sudden infant death syndrome (SIDS) remains a leading cause of infant mortality, despite a steadily decreasing incidence since the 1990s.1 The reasons for this decline are debated, but it could be due to methodological reasons (eg, changes in reporting or advances in diagnosis of specific diseases) or a reduction of risks, such as an increase in supine sleeping position for infants, as advocated by the Back to Sleep campaign.[2]. In The Lancet, Roope Männikkö and colleagues[3] identify a new risk factor for SIDS: a skeletal muscle genetic channelopathy that could compromise respiratory and laryngeal function.
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