Human Papillomavirus and Risk of Colorectal Cancer: An Analysis of Nationwide Claims Data

Background and Objectives: Although human papillomavirus (HPV) is a major etiology of cervical and anogenital cancers, whether it is associated with colorectal carcinogenesis is yet undetermined. Materials and Methods: The longitudinal association of HPV infection with colorectal cancer (CRC) was ev...

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Published inMedicina (Kaunas, Lithuania) Vol. 58; no. 10; p. 1461
Main Authors Hsu, Chih-Hsiung, Lin, Yu-Jyun, Chen, Yong-Chen, Liu, I-Lan, You, San-Lin, Hu, Je-Ming, Lin, Tzu-Chiao, Chang, Pi-Kai, Chen, Chao-Yang, Chou, Yu-Ching, Sun, Chien-An
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 01.10.2022
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Summary:Background and Objectives: Although human papillomavirus (HPV) is a major etiology of cervical and anogenital cancers, whether it is associated with colorectal carcinogenesis is yet undetermined. Materials and Methods: The longitudinal association of HPV infection with colorectal cancer (CRC) was evaluated using 2000–2013 data from a nationwide Taiwanese claims database. In this retrospective cohort study, 358 patients with primary HPV diagnoses (HPV-infected cohort) and 1432 patients without such a diagnosis (HPV-uninfected cohort) were recruited between 2000 and 2006. Both cohorts were followed up to identify CRC incidences from 2006 to 2013. Hazard ratios (HRs) and their 95% confidence intervals (CIs) derived from Cox proportional hazards models were used to estimate the association between HPV and CRC risk. Results: The HPV-infected cohort had a significantly higher cumulative incidence of CRC than the HPV-uninfected cohort. The presence of HPV was associated with an increased risk of CRC (adjusted HR, 1.63; 95% CI, 1.02–3.62). Furthermore, the significant HPV–CRC risk association was evident in both sexes. Conclusions: This population-based cohort study reveals longitudinal evidence that HPV is associated with an increased risk of CRC. Further studies are required to verify the role of HPV in colorectal carcinogenesis.
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ISSN:1648-9144
1010-660X
1648-9144
DOI:10.3390/medicina58101461