4CPS-238 Role of HLA-DQA1*05 in the persistence of adalimumab in the management of inflammatory bowel disease

<h3>Background and Importance</h3> Anti-tumour necrosis factor (anti-TNF) drugs are the most used biological therapies for treating Inflammatory Bowel Disease (IBD). However, their efficacy is significantly reduced due to the formation of anti-drug antibodies which can lead to treatment failure. HLA-DQA1*05 haplotype has been linked as a possible biomarker of immunogenicity and loss of response to anti-TNF treatment. <h3>Aim and Objectives</h3> To analyse persistence after 48 weeks of treatment with adalimumab (ADA) in biologic-naive patients with IBD starting ADA in 2022 who had HLA-DQA1*05 determined. <h3>Material and Methods</h3> Descriptive retrospective and single-centre study including biologic-naive patients diagnosed with IBD who started ADA in 2022. Sex, age, type of IBD (Crohn’s disease (CD) or ulcerative colitis (UC)), smoking status and previous immunosuppressant (IS) treatment were collected from the electronic medical records. It was also documented (according to the presence or absence of HLA-DQA1*05 haplotype): persistence after 48 weeks of treatment, time (days) to failure, reason for withdrawal, immunogenicity, dose or interval intensification and pre- and post-intensification ADA levels. The target therapeutic interval of ADA was established between 5 and 12 mcg/mL during maintenance. <h3>Results</h3> 39 patients were included, female (56%), median age (IQR) 51 (39–60), CD (74%), UC (26%), smokers (26%), ex-smokers (31%), previous IS treatment (30%). These variables did not influence persistence at 48 weeks in the study population. HLA-DQA1*05 haplotype was present in 43% of the patients in the study. Results are shown in table 1. <h3>Conclusion and Relevance</h3> The persistence at 48 weeks was 69.2% in the total study population after ADA initiation, being 1.8 times lower in patients with HLA-DQA1*05. These data are consistent with those published in the literature. Further studies are needed to analyse the impact of HLA-DQA1*05 in the loss of response to ADA in order to support the determination of HLA-DQA1*05 prior to initiation of therapy. <h3>References and/or Acknowledgements</h3> <h3>Conflict of Interest</h3> No conflict of interest