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Is excess male infant mortality from sudden infant death syndrome and other respiratory diseases X‐linked?
Author(s) -
Mage David T,
Donner E Maria
Publication year - 2014
Publication title -
acta paediatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/apa.12482
Subject(s) - medicine , sudden infant death syndrome , infant mortality , pediatrics , excess mortality , cause of death , respiratory system , disease , mortality rate , population , environmental health
Abstract Aim Male excess infant mortality is well known but unexplained. In 2004, we reported sudden infant death syndrome ( SIDS ) and other infant respiratory deaths showed a ~50% male excess in the United States between 1979 and 2002. This study analyses expanded US data from 1968 to 2010 to see whether infant respiratory deaths still show similar ~50% male excess and may be X‐linked. Methods The analysis compared infant mortality data from the US Centers for Disease Control and Prevention, 1968–2010, with 11 World Health Organization International Classification of Diseases ( ICD ) rubric groups for respiratory deaths by accidents, congenital anomalies, respiratory diseases and causes unknown. Results The 11 ICD groupings presented male excesses of ~50% and combining the 453 953 US cases produced a male fraction of 0.6034, a 52.1% male excess. A further 72 380 non‐ US respiratory cases showed a similar 0.6055 male fraction, a 53.5% male excess. Conclusion The constant ~50% male excess for quite different causes of respiratory death suggests they all have a common terminal event and that is acute anoxic encephalopathy. We hypothesise that this constant male excess phenomenon must be caused by a single X‐linked gene, with a recessive condition, leading to a predisposition to succumb to acute anoxic encephalopathy.