Abstract

Cervical screening within organised screening programmes has dramatically reduced the incidence and mortality from cervical cancer. In England, screening used to start from the age of 20 years but, for the last decade, screening has begun at 25 years of age. The other home countries within the UK have some autonomy on the delivery of NHS screening programmes and as a result there are often differences in practice with other countries adopting a more conservative approach; Northern Ireland introduced this change in 2011, Wales in late 2013 and in Scotland it is envisaged that this will be achieved by 2015. The initial change to the age at which screening starts in England was not readily accepted by many health professionals and many suggested that this change would put young women's lives at risk. However, the evidence base from the NHS screening programmes suggests that cervical cancer is very rare in women under the age of 25 years and, with the majority of these cancers being quick to develop, screening is unlikely to benefit younger women. Furthermore, it is now apparent that infection with high-risk human papillomavirus (HPV) is often transitory—particularly in young women—and as a consequence many early epithelial neoplastic changes are also transitory. Only women with persistent oncogenic HPV infection and disease are likely to benefit from screening (i.e. women aged over 25 years), particularly as treatment might be associated with adverse outcomes. Currently, there is little opposition to screening only women aged 25 years or more in the UK. In this month's BJOG, further evidence from the Canadian screening programme supporting the delayed onset of screening is debated by Professor Dickinson and colleagues on page 255. A proposed change to the starting age of screening to reflect current UK practice (and many other European countries) is not being warmly received by many Canadian health professionals. In a mini-commentary, Professor Massad also illustrates that there is a wide variation in practice in the USA and guidelines are often not adhered to. Hopefully, the commentaries will give our international readers an insight into why there might be variations in practice in the western world. Although there is always scope for improving the evidence base for guidelines, the implementation of such recommendations is often evolutionary as illustrated by the UK experience. There is a growing body of evidence suggesting that a history of pelvic inflammatory disease (PID) may predispose to pelvic malignancy. Reactive free radicals produced by inflammation can cause damage to DNA, pro-inflammatory molecules can promote neoplastic transformation by paracrine modulation, and chronically activated innate immune cells suppress adaptive immune responses. Ovarian cancer has been directly associated with asbestos and talc exposure, and also by epidemiological studies comparing cohorts of women with a history of PID and controls. In an epidemiological study Hsu and Lin in Taiwan demonstrate a potential association between PID and colorectal carcinoma on page 337. These are interesting findings and, if proven by larger studies, are further evidence for the importance of primary prevention of PID (Figure 1). Finally, Jayaprakasan et al., based in the UK, have investigated the effect of ethnicity on live birth rates after in vitro fertilisation (IVF) or intracytoplasmic sperm injection (ICSI) treatment in a retrospective single institution study (page 300). Live birth rates following IVF/ICSI treatment were significantly lower in the ethnic minority group compared with white European women, which suggests that ethnicity is a major determinant of live birth following IVF treatment (Figure 2). Ideally, ethnic-minority-specific evidence should be available when counselling couples on fertility outcomes.

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