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216 Risk of ovarian cancer in women with pelvic inflammatory disease under 55: a prospective study in UK biobank database
  1. Chenzhao Feng,
  2. Wanwan Luo,
  3. Gang Chen and
  4. Chaoyang Sun
  1. Tongji Hospital, Wuhan, China


Introduction/Background Ovarian cancer is a heterogeneous disease with perplexing pathogenesis mechanism and prevention strategies are limited. Pelvic inflammatory disease (PID) has been suggested to increase the risk of developing ovarian cancer (OC), but existing literature have been inconclusive and large prospective cohort studies are inadequate.

Methodology We conducted a prospective cohort study of 261624 women participants in the UK Biobank. During a median of 12.8 years of follow-up, we included 901 incident OC cases. Germline homologous recombination (gHR) mutations carriers were determined using paired whole-exome-sequencing data. We used Cox’s regression models to assess the hazard ratios (HRs) of risk of developing OC under PID, with adjustment for confunding factors. We also conducted subgroup analysis by tumor histology subtyping and age. The interactive effect of gHR and PID history was determined using cox regressions.

Results We identified 4054 women with PID and 257570 controls in this large prospective cohort study. Among participants 901 had developed ovarian cancer during a median of 12.8 years follow-up period. The adjusted hazard ratio for ovarian cancer in patients with PID was 1.45 (95% CI 0.90–2.32) compared with controls. However, in the age subgroup analysis, we found a positive relation between history of PID and risk of OC in aged younger than 55 years (1.92, 95% CI 1.02–3.63). Furthermore, participants who had a PID history and gHR mutations have the highest risk of developing OC (7.40, 95% CI 1.03–53.10).

Conclusion In our study, we found that PID is a potential precursor for ovarian cancer, especially in participants aged younger than 55 years with gHR mutation, as participants who had a PID history and HRD mutations have the highest risk of developing OC. The mechanism between genetic susceptibility, PID and OC remains still obscure and needs to be further investigated.

Disclosures The authors declare no competing interests.

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