<HashMap><database>biostudies-literature</database><scores/><additional><submitter>EPIFEVER-2 investigators</submitter><funding>National Institute for Health Research (NIHR)</funding><pagination>134-140</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12226748</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>135(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Genetically predicted higher levels of the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL1-Ra) might reduce the risk of developing epidural-related maternal fever, a phenomenon that occurs exclusively in women having epidural analgesia in labour. We hypothesised that in women having epidural analgesia, the absence of specific alleles that lower circulating levels of IL1-Ra would be associated with the development of epidural-related maternal fever, administration of intrapartum antibiotics, or both.&lt;h4>Methods&lt;/h4>We prospectively enrolled women ≥18 yr of age receiving epidural analgesia during labour, excluding those with pre-existing fever, antibiotic therapy, or immunodeficiency. Allele scores were constructed from genotyping the C-allele frequency a</pubmed_abstract><journal>British journal of anaesthesia</journal><pubmed_title>Interleukin-1 receptor antagonist polymorphisms in women receiving epidural analgesia who develop maternal intrapartum fever: a prospective, multicentre Mendelian randomised study.</pubmed_title><pmcid>PMC12226748</pmcid><funding_grant_id>NIHR300097</funding_grant_id><pubmed_authors>Thompson C</pubmed_authors><pubmed_authors>Patel A</pubmed_authors><pubmed_authors>Rodriguez Sierra EP</pubmed_authors><pubmed_authors>Brunnen D</pubmed_authors><pubmed_authors>Patrick A</pubmed_authors><pubmed_authors>Raja J</pubmed_authors><pubmed_authors>Wilson V</pubmed_authors><pubmed_authors>Phull M</pubmed_authors><pubmed_authors>Stephenson L</pubmed_authors><pubmed_authors>Arumugaum A</pubmed_authors><pubmed_authors>Razzaque M</pubmed_authors><pubmed_authors>Wilson M</pubmed_authors><pubmed_authors>Wray S</pubmed_authors><pubmed_authors>Tanqueray T</pubmed_authors><pubmed_authors>Frowd R</pubmed_authors><pubmed_authors>Tripurneni V</pubmed_authors><pubmed_authors>Blake H</pubmed_authors><pubmed_authors>Weist S</pubmed_authors><pubmed_authors>Martin T</pubmed_authors><pubmed_authors>Leary R</pubmed_authors><pubmed_authors>Canclini L</pubmed_authors><pubmed_authors>Wikner M</pubmed_authors><pubmed_authors>Kwok S</pubmed_authors><pubmed_authors>Kennedy N</pubmed_authors><pubmed_authors>Noakes I</pubmed_authors><pubmed_authors>De Freixo L</pubmed_authors><pubmed_authors>David AL</pubmed_authors><pubmed_authors>Achempong Y</pubmed_authors><pubmed_authors>Pinder A</pubmed_authors><pubmed_authors>Sarmiento L</pubmed_authors><pubmed_authors>Borg LX</pubmed_authors><pubmed_authors>Berger P</pubmed_authors><pubmed_authors>Noblett J</pubmed_authors><pubmed_authors>Longbottom R</pubmed_authors><pubmed_authors>Carey A</pubmed_authors><pubmed_authors>Nicklin A</pubmed_authors><pubmed_authors>Begum S</pubmed_authors><pubmed_authors>Al-Maiyah F</pubmed_authors><pubmed_authors>Hoodless S</pubmed_authors><pubmed_authors>Tsun J</pubmed_authors><pubmed_authors>Sousi E</pubmed_authors><pubmed_authors>Bruce-Hickman K</pubmed_authors><pubmed_authors>Mak K</pubmed_authors><pubmed_authors>George D</pubmed_authors><pubmed_authors>Kim J</pubmed_authors><pubmed_authors>Barrett A</pubmed_authors><pubmed_authors>Odor P</pubmed_authors><pubmed_authors>Costa AV</pubmed_authors><pubmed_authors>Valori L</pubmed_authors><pubmed_authors>Bourke M</pubmed_authors><pubmed_authors>Usman N</pubmed_authors><pubmed_authors>Sharp T</pubmed_authors><pubmed_authors>Ali A</pubmed_authors><pubmed_authors>Abbott TEF</pubmed_authors><pubmed_authors>Hoe M</pubmed_authors><pubmed_authors>Newth O</pubmed_authors><pubmed_authors>Coulter C</pubmed_authors><pubmed_authors>Gutierrez Del Arroyo A</pubmed_authors><pubmed_authors>Smith C</pubmed_authors><pubmed_authors>Waspe J</pubmed_authors><pubmed_authors>Wong R</pubmed_authors><pubmed_authors>Khan A</pubmed_authors><pubmed_authors>Singh A</pubmed_authors><pubmed_authors>Ciechanowicz S</pubmed_authors><pubmed_authors>Warrington A</pubmed_authors><pubmed_authors>Chapman A</pubmed_authors><pubmed_authors>Meroz MR</pubmed_authors><pubmed_authors>Verma P</pubmed_authors><pubmed_authors>Stretch B</pubmed_authors><pubmed_authors>Ali J</pubmed_authors><pubmed_authors>Quereshi N</pubmed_authors><pubmed_authors>Collins E</pubmed_authors><pubmed_authors>Folorunsho M</pubmed_authors><pubmed_authors>Eiben P</pubmed_authors><pubmed_authors>Dias P</pubmed_authors><pubmed_authors>Papoutsos C</pubmed_authors><pubmed_authors>Vishwanathan A</pubmed_authors><pubmed_authors>Sritharan P</pubmed_authors><pubmed_authors>Weber V</pubmed_authors><pubmed_authors>Das A</pubmed_authors><pubmed_authors>Palfreeman C</pubmed_authors><pubmed_authors>Mazzoli I</pubmed_authors><pubmed_authors>Bramley P</pubmed_authors><pubmed_authors>Black R</pubmed_authors><pubmed_authors>EPIFEVER-2 investigators</pubmed_authors><pubmed_authors>Ackland G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Interleukin-1 receptor antagonist polymorphisms in women receiving epidural analgesia who develop maternal intrapartum fever: a prospective, multicentre Mendelian randomised study.</name><description>&lt;h4>Background&lt;/h4>Genetically predicted higher levels of the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL1-Ra) might reduce the risk of developing epidural-related maternal fever, a phenomenon that occurs exclusively in women having epidural analgesia in labour. We hypothesised that in women having epidural analgesia, the absence of specific alleles that lower circulating levels of IL1-Ra would be associated with the development of epidural-related maternal fever, administration of intrapartum antibiotics, or both.&lt;h4>Methods&lt;/h4>We prospectively enrolled women ≥18 yr of age receiving epidural analgesia during labour, excluding those with pre-existing fever, antibiotic therapy, or immunodeficiency. Allele scores were constructed from genotyping the C-allele frequency a</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jul</publication><modification>2026-05-26T20:09:33.601Z</modification><creation>2026-05-26T03:06:33.109Z</creation></dates><accession>S-EPMC12226748</accession><cross_references><pubmed>40368685</pubmed><doi>10.1016/j.bja.2025.03.037</doi></cross_references></HashMap>