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Precancerous changes in the cervix and risk of subsequent preterm birth

Sir, We applaud the attempts of Bruinsma et al.1 to address the relationship between precancerous cervical change, its treatment and preterm birth (PTB). Nevertheless, we have concerns that their guarded conclusions may result in some women declining potentially life-saving treatments or demanding unnecessary or unproven screening tests (fetal fibronectin or transvaginal ultrasound of cervical length) and potentially damaging intervention such as cervical cerclage in subsequent pregnancies. The span of such a retrospective study which started some 25 years ago fails to address advances in definition and calculation (using fetal sonographic biometry) of PTB rates2 and fails to take into account changes in our knowledge of the aetiology, prediction, prevention, diagnosis and management of spontaneous preterm labour which leads to PTB. While they correct for some confounding variables associated with PTB, they did not correct for race or bacterial vaginosis both of which are independent risk factors for PTB and also associated with cervical intraepithelial neoplasia (CIN). There were 92 multiple pregnancies excluded from the analysis which constitutes an excess of some 33% over expected which suggests a contribution ofmedically assisted conception, which, even correcting for fetal number, is associated with an increased risk of PTB. By their own admission, less than 10% recorded their smoking status, and smoking doubles the risk of PTB. Treatment increased the risk of PTB by 23%; yet, the neonatal mortality and morbidity at this gestational age (>32 weeks) is low. Overall, the perinatal mortality rate in the treatment group (14/1000) was less than that in the untreated nonpregnant group (16/1000). With respect to the amount of cervical tissue excised, the authors used unhelpful terms such as ‘excessive’ or ‘substantive’ without definition; yet, they do not record the number of women who had repeated excision which is likely to be approximately 5%, which is a more objective measure. Following local ablative therapy, cervical damage may cause cervical weakness in the second trimester or cervical dystocia in labour. Cervical dystocia did not appear to be significant because there was no difference in the rate of emergency caesarean section. With respect to cervical weakness, two to three times as many women in the treatment group had cervical sutures inserted; yet, there is no mention of whether they received antibiotic cover which is known to reduce the incidence of PTB in at-risk women by some 60%.3 There is no mention of late miscarriage as an outcome, and the incidence of preterm prelabour rupture of the membranes which is associated with cervical weakness was no different between the treated and untreated groups. The authors claim to be ‘lumpers’ rather than ‘splitters’ with respect to the aetiology of PTB; yet, one of the co-authors (J.L.) has most eloquently demonstrated that PTB is a heterogeneous condition with different aetiologies and hence different management modalities and different risks of recurrence.4 Finally, the authors claim that ‘treatment offers a small additional risk’. What we really need to know is how this is likely to affect the perinatal mortality rate. Bearing in mind that 50% (1125/1951) of treated women and 15% (569/3597) of untreated women had high grades of CIN, how many cases of PTB occurred for each case of cervical cancer prevented? The true message of this study is ‘around Melbourne in the 1980s, using suboptimal retrospective data, Australian women