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A Practical Risk Measure for Identification of Adults With Oncogenic Oral Human Papillomavirus: Potential Use in Primary Care.
Family Medicine 2020 January
BACKGROUND AND OBJECTIVES: Oral human papillomavirus (HPV) infection is the main cause of oropharyngeal cancer. However, there is no assessment tool for early detection and prevention of oropharyngeal cancer in practice. The purpose of the study was to develop and validate a risk assessment tool to predict the presence of HPV associated with oropharyngeal cancer.
METHODS: Using data from the National Health and Nutrition Examination Survey 2011-2014, 6,978 US adults aged 18 to 59 years who were tested for oral HPV infection were included for this study. We carried out an analysis to test and validate risk predictive models for oral HPV infection. Presence of one of the 20 HPV subtypes associated with oropharyngeal cancer was used for the outcome.
RESULTS: Of 6,978 participants aged 18-59, 303 (4.3%; 6.6 million) were found to have oncogenic HPV subtypes. Our final model included sex, income-to-poverty ratio, current smoking, and the lifetime number of oral sex partners. The discriminatory power of the oral HPV risk score to predict the presence of oncogenic HPV was good (C-statistic=0.73). The risk score performed comparably in the validation population (C-statistic=0.72). The comparison between observed and estimated proportions of population with oncogenic oral HPV demonstrated excellent calibration.
CONCLUSIONS: We developed and validated the oral HPV risk score that predicts the risk of oral HPV requiring only self-reported data and no laboratory testing. The Oral HPV risk score has the potential to provide clinicians with a no-cost, easy way to screen for patients at greater risk for oncogenic HPV infection.
METHODS: Using data from the National Health and Nutrition Examination Survey 2011-2014, 6,978 US adults aged 18 to 59 years who were tested for oral HPV infection were included for this study. We carried out an analysis to test and validate risk predictive models for oral HPV infection. Presence of one of the 20 HPV subtypes associated with oropharyngeal cancer was used for the outcome.
RESULTS: Of 6,978 participants aged 18-59, 303 (4.3%; 6.6 million) were found to have oncogenic HPV subtypes. Our final model included sex, income-to-poverty ratio, current smoking, and the lifetime number of oral sex partners. The discriminatory power of the oral HPV risk score to predict the presence of oncogenic HPV was good (C-statistic=0.73). The risk score performed comparably in the validation population (C-statistic=0.72). The comparison between observed and estimated proportions of population with oncogenic oral HPV demonstrated excellent calibration.
CONCLUSIONS: We developed and validated the oral HPV risk score that predicts the risk of oral HPV requiring only self-reported data and no laboratory testing. The Oral HPV risk score has the potential to provide clinicians with a no-cost, easy way to screen for patients at greater risk for oncogenic HPV infection.
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