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Prenatal exposure to H 2 blockers and to proton pump inhibitors and asthma development in offspring
Author(s) -
YitshakSade Maayan,
Gorodischer Rafael,
Aviram Micha,
Novack Lena
Publication year - 2016
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1002/jcph.574
Subject(s) - asthma , medicine , offspring , etiology , pregnancy , pediatrics , confounding , lansoprazole , relative risk , risk factor , asthma exacerbations , obstetrics , confidence interval , genetics , biology , helicobacter pylori
Fetal exposure to H 2 blockers (H 2 Bs) or proton pump inhibitors (PPIs) has been reported to be associated with asthma in children. We evaluated the risk of asthma in offspring following prenatal H 2 Bs. We enrolled 91 428 children and their mothers who resided in southern Israel during 1998–2011. The computerized medications database was linked with records from the district hospital. Of the eligible children, 11 227 developed asthma, and overall 5.5% had been exposed to H 2 Bs or PPIs prenatally. The risk of developing asthma was slightly higher in the group exposed to H 2 Bs or PPIs (RR, 1.09; P = .023). At greater risk were children whose mothers purchased these medications more than 3 times (RR, 1.22; P = .038) or exposed to >20 defined daily doses or prenatally exposed to lansoprazole. The statistical association was significant and depended on magnitude of exposure and specific medication, but the absolute risk was low. The association between maternal consumption of H 2 Bs or PPIs and asthma and childhood remained statistically significant 2 years after delivery, raising the possibility of confounding by the indication phenomenon. In view of the findings, a causal relationship could not be ascertained, and an unidentified etiological factor could be operative.