Introduction

Our aim is to establish the feasibility and response rate of a population-based screening programme for Vietnamese women aged over 50. Almost all cervical cancers in post-menopausal women are caused by HPV infection acquired before age 50 and about 80% of cervical cancer deaths occur after age 50. A single HPV test after menopause with treatment of HPV positive women either immediately or after retesting a year later to exclude transient infections is therefore a practicable means of achieving a large reduction in lifetime cancer risk.

Methods

Women aged 50-64 resident in 10 small districts in Ho Chi Minh City will be invited. Recruitment will continue until 300 have been screened. A sample of 100 current or former female sex workers will also be invited. Younger women are at substantial risk of acquiring a new HPV infection, so a single test cannot confer high lifelong protection, and radical cervical treatment can predispose to subsequent premature delivery.

Participants will attend a district health centre to complete a questionnaire and provide a self-administered vaginal swab followed by a nurse-taken LBC sample. Cytology will be done only on HPV+ samples.

HPV+ women with abnormal cytology will be referred for colposcopy and management according to hospital guidelines. Other HPV+ women will retested after a year. Those still HPV+ (with or without cervical abnormality) will be offered colposcopy and LEEP if deemed feasible.

Results

Preliminary results will be presented on recruitment, HPV prevalence, and attitudes and knowledge on HPV and screening. The main outcomes at follow-up will be the proportion of HPV+ women who attend for retesting, the HPV clearance rate within a year and the proportion of those still HPV positive in whom LEEP can be performed.

Conclusions

We hope to demonstrate that national HPV screening of older women is feasible and affordable

Introduction

HPV testing protocols should be based on the simplest plausible model of cervical carcinogenesis.

Methods

Model assumptions

1. Each new HPV infection has a fixed probability (averaged over HPV types) of progressing to precancer before it disappears or becomes latent.

2. Precancer persists, conferring a constant lifelong cancer rate.

3. Genetics and neoplasm characteristics determine a woman’s probability and rate.

4. From HPV infection to precancer plus from malignancy to cancer diagnosis averages 7.5 years, and is rarely less than 5 years.

The age-distribution of HPV acquisition at entry to the ARTISTIC trial was assumed. The reduction in precancer prevalence, and hence cancer incidence, per screening round was modelled in English birth cohorts.

Results

English cervical cancer incidence rates, including the unexpected large increase at age 25-29 since the screening age was raised from 20 to 25, were predicted with remarkable accuracy assuming 40% precancer elimination per test since organised cytology began. The model also explains the dependence on age and age at first intercourse of cancer incidence in unscreened women.

Conclusions

The simplest model that accounts for the evidence defines the best scientific theory. Our age-independent model of the relationship between HPV infection rates and cancer incidence rates contradicts several current assumptions. The 5-year delay between screening at age 20 and detectable cancer prevention reflects the diagnostic lag, not some peculiar natural history of HPV infection in young women. Precancer is often latent after the initiating HPV infection has cleared or become latent, undetectable by cytology and sometimes shedding HPV below the cut-off of standard HPV tests. Cancer incidence is therefore the only useful measure of precancer prevalence.

5-yearly HPV screening from age 20 instead of 25 would reduce cervical cancer risk below age 30 in unvaccinated English women from ~0.1% to 0.02% or less, and would reduce their lifelong risk from ~0.2% to ~0.1% compared to 3.3% without screening.