Un artículo publicado en la revista New England Journal of Medicine demuestra que los tumores cancerosos de garganta pueden estar provocados por los virus del papiloma humano (VPH), posiblemente contraido con las relaciones sexuales bucogenitales especialmente cuando han existido varias parejas sexuales que han fumado o han bebido alcohol.
Los VPH causan el cáncer de útero y de pene, pero también pueden causar cánceres en la región anal y en la garganta. El contagio se realiza a través de las mucosas a partir de una persona que porta dicho virus. Cuando se han tenido varias parejas sexuales las posibilidades de contagio del virus se incrementan. En el estudio publicado se ha analizado una muestra de 86 varones y 14 mujeres y se calcula que el riesgo de desarrollar cáncer de garganta es 8 veces superior en las personas que han tenido al menos 6 parejas sexuales a lo largo de la vida.
N Engl J Med. 2007;356(19):1944-56.
Case-control study of human papillomavirus and oropharyngeal cancer.
D'Souza G, Kreimer AR, Viscidi R, Pawlita M, Fakhry C, Koch WM, Westra WH, Gillison ML.
Johns Hopkins Bloomberg School of Public Health, Baltimore, USA.
BACKGROUND: Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent. METHODS: We performed a hospital-based, case-control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case-control comparisons. RESULTS: A high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1; 95% confidence interval [CI], 1.5 to 6.5), as was a high lifetime number of oral-sex partners (6 or more) (odds ratio, 3.4; 95% CI, 1.3 to 8.8). The degree of association increased with the number of vaginal-sex and oral-sex partners (P values for trend, 0.002 and 0.009, respectively). Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio, 12.3; 95% CI, 5.4 to 26.4), and seropositivity for the HPV-16 L1 capsid protein (odds ratio, 32.2; 95% CI, 14.6 to 71.3). HPV-16 DNA was detected in 72% (95% CI, 62 to 81) of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio, 19.4; 95% CI, 3.3 to 113.9) and among those without such a history (odds ratio, 33.6; 95% CI, 13.3 to 84.8). The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16. CONCLUSIONS: Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use. Copyright 2007 Massachusetts Medical Society.