Several factors have been identified that may increase the risk of cervical neoplasia (Box 43.1). A higher incidence of HPV infection and progression of intraepithelial neo-plasia is seen in immunosuppressed patients, including those infected with HIV as well as those who are organ transplant recipients, who have chronic renal failure or a history of Hodgkin lymphoma, or have undergone immunosuppressive therapy for other reasons. Another factor is cigarette smoking.
More than 1 sexual partner or have a male sexual partner who has had sex with more than 1 person
First intercourse at an early age (younger than 18 years)
Male sexual partner who has had a sexual part-ner with cervical cancer
Human immunodeficiency virus (HIV) infection
Organ (especially kidney) transplant
Diethylstilbestrol (DES) exposure
History of cervical cancer or high-grade squa-mous intraepithelial lesions
Infrequent or absent Pap screening tests
The risk of cervical cancer is 3.5 times greater among smokers than among nonsmok-ers. Carcinogens from cigarette smoke have been found in high concentrations in the cervical mucus of smokers, suggesting a plausible biologic explanation for this asso-ciation. First intercourse at a young age may increase a woman’s risk for cervical neoplasia because of the high rate of metaplasia that occurs in the transformation zone dur-ing adolescence and a higher proportion of new or imma-ture cervical cells in this region.
Persistent HPV infection increases the risk of persistent or progressive cervical dysplasia. HPV 16 infection is more likely to be persistent than infections caused by other oncogenic HPV types. Individuals may possess a genetic suscep-tibility to cervical cancer, but the relative risks are small.