{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T17:10:26Z","timestamp":1788887426001,"version":"build-2803163510"},"reference-count":33,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"133","license":[{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    Gestational diabetes mellitus (GDM) may exacerbate hyperbilirubinemia-induced auditory neurotoxicity via oxidative stress, whereas genetic susceptibility (e.g., GJB2 variants) heightens cochlear vulnerability. However, the tripartite interplay among maternal metabolic dysregulation, neonatal hyperbilirubinemia and genetic predisposition remains poorly characterized.\n                    <jats:bold>Objective:<\/jats:bold>\n                    This study aimed to investigate the synergistic interaction between GDM and neonatal hyperbilirubinemia in auditory dysfunction, focusing on the modifying role of deafness-associated genetic variants (GJB2, SLC26A4, and mtDNA).\n                    <jats:bold>Methods:<\/jats:bold>\n                    In this prospective cohort study (our hospital, 2023\u20132025), 350 neonates were classified by an exposure-based 2\u2009\u00d7\u20092 factorial design into four groups: GDM-exposed hyperbilirubinemia (\n                    <jats:italic toggle=\"yes\">n<\/jats:italic>\n                    \u2009=\u200998), non-GDM hyperbilirubinemia (\n                    <jats:italic toggle=\"yes\">n<\/jats:italic>\n                    \u2009=\u2009185), GDM-only (\n                    <jats:italic toggle=\"yes\">n<\/jats:italic>\n                    \u2009=\u200942) and healthy controls (\n                    <jats:italic toggle=\"yes\">n<\/jats:italic>\n                    \u2009=\u200925). Genetic screening was performed via Sanger sequencing. Serial audiological assessments (automated auditory brainstem response) and brainstem auditory evoked potential [BAEP]) and biochemical monitoring (bilirubin-to-albumin [B\/A]), malondialdehyde [MDA] and superoxide dismutase) were conducted at birth, 72\u2009h, 1 month, and 3 months. Cox proportional hazards models, multivariable logistic regression and bootstrapped causal mediation analysis were used to evaluate risk factors and oxidative stress-mediated pathways.\n                    <jats:bold>Results:<\/jats:bold>\n                    GDM-exposed hyperbilirubinemia neonates exhibited a 2.3-fold higher incidence of severe hearing loss compared with those with hyperbilirubinemia alone (34.7% vs. 15.1%,\n                    <jats:italic toggle=\"yes\">P<\/jats:italic>\n                    &lt; 0.001). GJB2 variant carriers showed significantly greater BAEP threshold elevation (\u0394\u2009=\u20099.2\u2009\u00b1\u20093.1\u2009dB vs. 3.1\u2009\u00b1\u20091.8\u2009dB,\n                    <jats:italic toggle=\"yes\">P<\/jats:italic>\n                    \u2009=\u20090.002) than their counterparts. The B\/A ratio was a GDM-dependent prognostic marker, with B\/A &gt; 5.5 predicting hearing loss only in the GDM subgroup (odds ratio\u2009=\u20094.17, 95% confidence interval [CI]: 2.33\u20137.45). MDA accounted for 38% of the total effect of GDM\u2013hyperbilirubinemia on auditory impairment (indirect effect\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    \u2009=\u20090.28, 95% CI: 0.19\u20130.39).\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    GDM significantly modifies hyperbilirubinemia-induced auditory toxicity through oxidative stress and genetic interaction, particularly in GJB2 carriers. Integrated screening of maternal glycemic status, neonatal bilirubin dynamics, and deafness-associated genes is warranted.\n                  <\/jats:p>","DOI":"10.4103\/nah.nah_83_26","type":"journal-article","created":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T10:03:36Z","timestamp":1788343416000},"page":"885-894","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Maternal Gestational Diabetes Mellitus as an Independent Risk Factor for Hearing Impairment in Hyperbilirubinemia Newborns: A Prospective Birth Cohort With Genetic Profiling"],"prefix":"10.4103","volume":"28","author":[{"given":"LiQin","family":"Ruan","sequence":"first","affiliation":[{"name":"Department of Obstetrics, Yuhuan People\u2019s Hospital, Yuhuan Branch, The First Affiliated Hospital of Wenzhou Medical University, Yuhuan 317600, Zhejiang, 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