{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T12:28:21Z","timestamp":1790166501296,"version":"4.1.0"},"reference-count":44,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2012,3,22]],"date-time":"2012-03-22T00:00:00Z","timestamp":1332374400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Aliment Pharmacol Ther"],"published-print":{"date-parts":[[2012,5]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Proton pump inhibitors (<jats:styled-content style=\"fixed-case\">PPIs<\/jats:styled-content>) may activate the immune system and cause asthma.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aim<\/jats:title><jats:p>To investigate the association of prenatal exposure to <jats:styled-content style=\"fixed-case\">PPIs<\/jats:styled-content> and histamine 2\u2010receptor antagonists (<jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">RAs<\/jats:styled-content>) with risk of asthma.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>In this cohort study, 197\u00a0060 singletons born between 1996 and 2008 in northern <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>enmark were followed until the end of 2009. Data were obtained through <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>anish medical registries. Asthma in offspring was defined as at least two prescriptions of both a \u03b2\u2010agonist and an inhaled glucocorticoid and\/or a hospital diagnosis of asthma during the follow\u2010up. Cox proportional\u2010hazard regression was used to compute incidence rate ratios, adjusting for covariates.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A total of 2238 (1.1%) children were prenatally exposed to <jats:styled-content style=\"fixed-case\">PPIs<\/jats:styled-content> and 24\u00a0506 (12.4%) children developed asthma during follow\u2010up (median follow\u2010up\u00a0=\u00a06.8\u00a0years). The adjusted <jats:styled-content style=\"fixed-case\">IRR<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">aIRR<\/jats:styled-content>) of asthma associated with prenatal exposure to <jats:styled-content style=\"fixed-case\">PPIs<\/jats:styled-content> was 1.41 (95% confidence interval (<jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>): 1.27\u20131.56), compared with those unexposed. The association did not vary by trimester of exposure, and prenatal exposure to <jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>s was associated with similar increase in risk. The <jats:styled-content style=\"fixed-case\">aIRR<\/jats:styled-content> for maternal <jats:styled-content style=\"fixed-case\">PPI<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content> use in the year after, but not during pregnancy was 1.32 (95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 1.20\u20131.46) and 1.13 (0.93\u20131.36), respectively, compared with non\u2010use during and in the year after pregnancy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Prenatal exposure to both <jats:styled-content style=\"fixed-case\">PPIs<\/jats:styled-content> and H2<jats:styled-content style=\"fixed-case\">RAs<\/jats:styled-content> was associated with an increased risk of asthma in our study. Because the observed association is not drug specific and also observed for maternal postnatal use it may be explained by a \u2018class effect\u2019 or maternal underlying condition.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1365-2036.2012.05073.x","type":"journal-article","created":{"date-parts":[[2012,3,23]],"date-time":"2012-03-23T10:58:08Z","timestamp":1332500288000},"page":"1190-1198","source":"Crossref","is-referenced-by-count":39,"title":["Prenatal exposure to acid\u2010suppressive drugs and the risk of childhood asthma: a population\u2010based <scp>D<\/scp>anish cohort study"],"prefix":"10.1111","volume":"35","author":[{"given":"A. B. 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