Preamble

PREAMBLE PREAMBLE

Preamble HPV Guidelines Committee Chairs: Deborah M. Money, MD, FRCSC, Vancouver BC Michel Roy, MD, FRCSC, Quebec City QC he development of new HPV vaccines has re-energized the evaluation of HPV-related disease and greatly increased the need to clearly understand the biologic features of HPV and related disease so as to inform decision-making on the role of HPV vaccination. These guidelines are designed to summarize the key aspects of HPV infection and allow the clinician to be well informed in managing HPV-related disease in the new era of vaccine availability.

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Abbreviations Used in This Guideline ACIS

adeno-carcinoma in situ

AGC

atypical glandular cells

AGCUS atypical glandular cells of undetermined significance ASC-H

atypical squamous cells—cannot exclude high-grade squamous intraepithelial lesion

ASC-US atypical squamous cells of undetermined significance CI

confidence interval

CIN

ervical intraepithelial neoplasia

EGWs

external genital warts

HIV

human immunodeficiency virus

HPV

human papillomavirus

HSIL

high-grade squamous intraepithelial lesion

HSV

herpes simplex virus

LBC

liquid-based cytology

LSIL

low-grade squamous intraepithelial lesion

Pap

Papanicolaou

PCR

polymerase chain reaction

RRP

recurrent respiratory papillomatosis

SCC

squamous cell carcinoma

STI

sexually transmitted infection

VIN

vulvar intraepithelial neoplasia

HPV infection is the most common STI, affecting approximately 550 000 Canadians annually. The virus is spread by skin-to-skin contact. HPV infection is so common that most women are likely to be in contact with one or more of the subtypes of this virus at some time in their lives. Herpes simplex and bacterial vaginosis may facilitate cutaneous and mucosal entry of the virus. The prevalence of HPV infection rises rapidly after the onset of sexual activity and then declines with age. Most infections are unnoticed and resolve spontaneously within 24 months. Classic genital HPV lesions include benign genital warts and cervical, vaginal, anal, and vulvar cancers. Concurrent oral, hand, and genital HPV infection is frequent. Drugs (steroids), diseases (such as diabetes, renal failure, and HIV infection), and cigarette smoking compromise the immune system and may potentiate the problem. Persistent infection with HPV 16 or 18, although infrequent, may lead to cervical dysplasia and cancer. Almost all cervical and vaginal cancers and a large proportion of vulvar, anal, and oral cancers are associated with high-risk, oncogenic strains of HPV. Low-risk HPV types cause genital warts, RRP, and oral or conjunctival papillomas. HPV infection is difficult to prevent in sexually active adults, and preventing transmission is much more difficult to achieve with HPV infection than with other STIs. Vaccination may represent the best primary prevention method, as condoms have limited efficacy without consistent use, and abstinence is unacceptable to many. Pap testing may represent the best secondary prevention method. New paradigms for prevention and diagnosis will evolve as scientists, regulatory agencies, and private-sector companies share agendas. Since Canada provides universal health care to its population, it is our responsibility to seek sound information and promote constructive strategies. Canadian researchers have a strong international presence in the fight against HPV. Integration of HPV vaccination and screening registries would contribute to the study of HPV infection and profoundly affect the history of cervical cancer. AUGUST JOGC AOÛT 2007 l

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