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DOI 10.1111/j.1365-3016.1989.tb00510.x

Медицинская библиотека · Paediatric and perinatal epidemiology · 1989

Assessment of in utero hypoxia and risk of sudden infant death syndrome.

Buck G M, Cookfair D L, Michalek A M, Nasca P C, Standfast S J, Sever L E

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

Few data are available on the role of hypoxia in sudden infant death syndrome (SIDS). The purpose of this study was to assess whether 10 antenatal factors consistent with in utero hypoxia were associated with an increased risk of SIDS. Cases and two sets of controls were chosen from the Upstate New York Live Birth Cohort for 1974 (n = 132,948). One hundred and forty-eight SIDS cases were identified, along with 114 dead controls made up of all other sudden deaths. Randomly selected live controls were frequency-matched to cases on mother's age, race, residence, parity, and infant's birthdate (n = 355). Data were collected from vital certificates (97% response), hospital delivery records (89%), and autopsy reports (100%). Odds ratios and 95% confidence intervals were calculated using Mantel-Haenszel techniques and logistic regression. Abnormal uterine bleeding was the only statistically significant (P less than 0.05) risk factor observed when dead controls were used (OR = 5.4). When live controls were used, statistically significant increases in risk were found for: placenta praevia (OR = 21.8), abruptio placentae (OR = 3.7), multiple birth (OR = 29.6), pregnancy interval less than or equal to 12 months (OR = 3.8), sexually transmitted disease (OR = 6.4), and eclampsia (OR = 17.7). These results lend support to a possible hypoxic aetiology of SIDS; however, differences by control group suggest that some factors are not specific to SIDS alone but may be risk factors for infant mortality in general.

Для цитирования: Buck G M, Cookfair D L, Michalek A M, Nasca P C, Standfast S J, Sever L E. Assessment of in utero hypoxia and risk of sudden infant death syndrome.. Paediatric and perinatal epidemiology. 1989. DOI: 10.1111/j.1365-3016.1989.tb00510.x.

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