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• W2036133704 abstract "Sir, We read with interest the paper by Sigurdsson and colleagues recently published in AOGS (1). They cleverly integrated different data to answer some of the most urgent questions about screening in the vaccine era and about efficacy of the vaccine in sexually active women. Most of their deductive conclusions are sound. However, in our opinion two points need deeper insight: (1) the lower age limit for screening in vaccinated cohorts, and (2) the effect of the length of follow-up on the estimates of vaccine efficacy in a young sexually active population of unknown HPV infection status. On point (1), the authors state that the reduction of CIN2+ in younger women is similar to (and not greater than) that in older women. Therefore, they suggest not raising the lower age limit for screening. Actually, screening programs are there for the interest in preventing invasive cancers, rather than CIN2 or CIN3, particularly in younger women whose probability of regression is very high. In public health, in fact, we are more interested in absolute risk than relative measures: even if the relative proportion of 16/18 HPV vs. non-16/18 cancer is the same in younger and older women, the absolute risk of non-16/18 in the former is extremely low. Consequently, in a vaccinated population, the lower age limit for screening should not be modified if the predicted number of cases not prevented through vaccination in 22–29–year-old women justifies a mass screening in that age group. On point (2) we ask: Is it safe to quantify the impact of a vaccine on a sexually active population using the results of a trial with a short follow-up? It is well established that the median time from infection to CIN3 is quite long (2, 3). If we look at the intention-to-treat efficacy results in the FUTURE-II study, we note that most lesions in the placebo group were due to infections already present at enrollment (4). Since the vaccine has no therapeutic effect (5), the baseline prevalence of infection and of disease in the vaccination group is similar. The final effect dilutes the vaccine's efficacy. As time passes, the proportion of lesions due to newly acquired infections increases, accentuating the differences between placebo and vaccination groups, which maintains the vaccine's efficacy. To quantify this effect we have to rely on some parameters of the natural progression of the disease, namely the length of the latency period from infection to disease and the age-specific transition probabilities, i.e. the probability of infection, of progression from infection to high-grade lesions, and then to cancer. Figure 1 shows that shorter latency times and lower variances mean greater vaccine efficacy in sexually active women at longer follow-up, and vice versa. The graph A shows the proportion of prevented cases and estimates of efficacy at two different follow-up times under a given latency time; graph B and C, respectively, show the effects of a reduction in latency time and an increase in latency variance." @default.
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• W2036133704 date "2010-06-01" @default.
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• W2036133704 title "Efficacy of HPV 16/18 vaccines on sexually active young women and the impact on organized cervical cancer screening" @default.
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• W2036133704 doi "https://doi.org/10.3109/00016340903134221" @default.
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