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factor-I (IGF-I) and fetal growth, consisted with the hypothesis that IGF-I influences maternal constraint upon fetal growth by controlling placental transfer. In sheep, IGF-I infusion to the mother leads to an increase in fetal glucose levels, placental amino acid uptake and pla- cental lactate production which is utilised by the fetus. The results of the paper showed a statistically significant rise in maternal serum IGF-I with advancing gestational age in controls ( r = 0.40; P = O.OOOl), but it did not correlate with the birth weight in that group. This casts doubt about the role of maternal IGF-1 in placental glucose transfer, as mentioned by the authors'.

The IGF-I levels were low in the mothers of growth restricted fetuses (-1.56 SD; P = 0.0001) but not in those with small for gesta- tional age fetuses. The growth restricted fetuses were those small for gestational age fetuses who had an umbilical artery pulsatility index greater than 2SD above the mean. Therefore, the maternal IGF-I lev- els were significantly related to abnormal umbilical artery pulsatility index (placental dysfunction) in growth restricted fetuses. The authors concluded that low maternal IGF-I levels in growth restric- tion may be a cause or consequence of placental dysfunction'. Though the authors did mention that the maternal IGF-I levels increased significantly with advancing gestational age in controls, they did not mention the pattern of changes that occurred to the maternal IGF-I levels in growth restricted fetuses. This may give some clue to answer the question whether low maternal IGF-I level is the cause or consequence of placental dysfunction. If the maternal IGF-I levels decrease with gestational age in growth restricted fetuses (due to placental dysfunction), it may be hypothesised that low IGF-I level in the mother is the consequence of placental dysfunction. On the contrary, if the levels in the mother rise or remain stable with advancing gestational age in growth restricted fetuses, a low level of maternal IGF-I may be a cause of the placental dysfunction which has led to the growth restriction.

Ideally, to show any definite relationship between IGF-I and pla- cental dysfunction (cause or consequence), case-control studies should be done from early pregnancy to determine the absolute levels and the pattern of change in the levels of maternal IGF-I in relation to the onset of placental dysfunction and subsequent growth restriction. In the present paper, maternal IGF-I levels were measured after the onset of growth restriction without any knowledge of the preceding levels, leading to an inconclusive result.

Sudipta Paul Arrowe Park Hospital, Wirral

Reference 1 Holmes RP, Holly JMP, Soothill PW. A prospective study of maternal

serum insulin-like growth factor-I in pregnancies with appropriately grown or growth restricted fetuses. Br J Obstet Gynaecol 1998; 105: 1273-1278.

AUTHORS' REPLY Sir; We thank Dr Paul for the interest in our paper. We agree that whether the low maternal IGF-I levels we reported are the cause or conse- quence of placental dysfunction is a very important question. We also agree that the timing of changes in IGF-I in growth restricted fetuses would give evidence regarding the sequence of events. Indeed, that was an original aim of the study, which is why blood samples were obtained every two weeks after recruitment. However, 21 cases of growth restricted fetuses required delivery within one week, and in the other four cases each had two samples only taken before delivery. In contrast, we were able to collect serial samples from all of the nor- mal small for gestational age cases except for those only identified and recruited at term.

This distinction between the two groups that were characterised according to umbilical artery Doppler measurements has important implications. A small fetus with a normal Doppler measurement invariably indicated that there was no developing placental dysfunc- tion and that these pregnancies could be managed conservatively

until term'. Conversely, in pregnancies with placental dysfunction severe enough to compromise fetal growth, by the time the growth restriction presented the dysfunction was already detectable as an abnormal umbilical artery Doppler. These observations demonstrate the clinical value of umbilical artery Doppler measurements in preg- nancies with small fetuses.

We could not publish the serial data available in pregnancies with growth restricted fetuses because of meagre numbers, but we were intrigued that those four cases were unusual. In three, not only were the maternal IGF-I levels greater than the normal mean for gestation (and this was not so in any other case of growth restriction), but the serial IGF-I SD remained stable (i.e. absolute levels increased consis- tent with control pregnancies) despite all having severely abnormal Dopplers. We hypothesise that a normal or high maternal IGF-I level in a pregnancy with a growth restricted fetus might be protective, allowing these pregnancies to continue long enough for a second blood sample to be collected. Indeed the neonatal outcome of these four cases, as assessed by a neonatologist blinded to the IGF-I results, was excellent. We just feel this speculation cannot be supported by such few data.

We agree that blood samples obtained before the onset of clini- cally apparent growth restriction would be very valuable. This would enable serial samples to be obtained and may clarify the cause or consequence debate. However, since most growth restric- tion occurs in women without specific risk factors in early preg- nancy, large recruitment would be required to achieve adequate numbers. Dr Paul suggests that stable or rising IGF-I levels in FGR would support the hypothesis that low maternal IGF-I is a cause of placental dysfunction. We agree that a causal role is more likely if low IGF-I predates reduced growth than vice versa, but, in our view changes in IGF-I after growth restriction has been established cannot help resolve this issue.

Robert Holmes, Jeffery Holly & Peter Soothill Fetal Medicine Research Unit, University of Bristol, St Michael's Hospital

Reference 1 Bobrow CS, Holmes R, Soothill PW. Small for gestational age is not a

diagnosis. Ultrasound Obsret Gynecol1999. In press.

Prevalence of faecal incontinence among women with urinary incontinence (Received 25 January 1999)

Sic We read with interest the paper by Khullar et al. (Vol 105, Novem- ber 1998)' which showed a strong relationship between urinary incontinence and faecal incontinence. However, given that they are postulating an alternative mechanism to link faecal incontinence with detrusor instability, we were disappointed that they did not report the incidence of incontinence of flatus in the sample popula- tion, especially since there was a question referring to it in the ques- tionnaire used in the study. Weakness of the internal sphincter may result in incontinence of the flatus without faecal incontinence. MacArthur et aL2 reported that had incontinence of flatus been included in their study then the prevalence of faecal symptoms would have been much higher. A weak voluntary sphincter may result in faecal urgency but not incontinence in many not willing to put their continence to the test. Therefore a question on urgency would have been an interesting addition to the questionnaire used in the study.

We were pleased that Khullar et al. highlighted the importance of self completed questionnaires: the incidence of faecal incontinence was 15.3% on direct questioning compared with 26% on completion of the questionnaire. Faecal incontinence is a deeply embarrassing problem, consequently few patients seek help. For these reasons we are developing a condition-specific quality of life questionnaire for

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faecal incontinence in women, along similar lines to that of Kelleher eta/.’.

G. Bugg & G. Hosker St Mary’s Hospital, Whirworth Park, Manchester E. Kiff Wythenshawe Hospital, Wythenshawe, Manchester

References 1 Khullar V, Damiano R, Toozs-Hobson P, Cardozo L. Prevalence of

faecal incontinence among women with urinary incontinence. Br J Obstet Gynaecol1998; 105: 1211-1213.

2 MacArthur et al. Faecal incontinence after childbirth. Br J Obstet Gynaecol 1997; 104: 4650.

3 Kelleher Cl. A new questionnaire to assess the quality of life or urinary incontinent women. Br J Obstet Gynaecol 1997; 104: 1374-1379.

Maternal intensive care and near-miss mortality in obstetrics (Received 7 April 1999)

Sir; In their interesting paper, Baskett and Sternadel (Vol 105, September 1998)’ have proposed to define maternal near-miss cases as those women requiring critical care or transfer to an intensive care unit. We are very happy that that definition has retained their attention because three years ago, we used the same to estimate the frequency of severe morbidity, its causes and risk factors’. In our study we included all pregnant women and women in the puerperium who had been treated in an intensive care unit from three different regions in France. Like Baskett and Sternadel we classified our cases according to the pri- mary indication for maternal transfer to the intensive care unit. Despite the difference in the collection of data and methods, the fre- quency of causes is close to those published by Baskett and Sternadel: hypertension 29.7% (Baskett and Sternadel 25.4%); haemorrhage

22.6% (2143%); embolism 7.6% (7.3%); respiratory diseases 6.0% (5.4%); and cardiac diseases 3.4% (3.6%).

We would like to emphasise three points. Firstly, the definition of near-miss cases by transfer to an intensive care unit may depend on the health care organisation and may therefore not comparable between countries or regions with different levels of care or styles of clinical practice. Secondly, all near-miss cases do not result in an admission to an intensive care unit; for example, a severe haemor- rhage can threaten the life of a patient and be cared without transfer to an intensive care unit. In order to compare the frequency and poten- tial mortality of sever obstetric complications in several countries, the European Concerted Action selected three conditions using standard- ised criteria: haemorrhage; pre-eclampsia; and sepsis3. The analysis is continuing and results have not yet been published. Thirdly, we dis- agree with the authors when they assume “that the conditions requu- ing intensive care tend to mirror the causes of maternal deaths” because maternal momlity varies greatly between these conditions, as we found in our survey’. In consequence, with the aim of evaluat- ing the quality of obstetric care, we proposed to retain the potential maternal mortality calculated by condition or disease as an important indicator.

Marie-HClkne Bouvier-CoUe Unite de Recherches Epidemiologiques sur la Sante des Femmes et des Enfants, INSEM, Paris, France

References 1 Baskett TF, Sternadel J. Maternal intensive care and near-miss mortal-

ity in obstetrics. Br J Obstet Gynaecol1998; 105: 981-984. 2 Bouvier-Colle MH, Vamoux N, Salanave B, Ancel PY, Brdart G and

the Maternal Morbidity Group. Case control study of risk factors for obstetric patients’ admission to intensive care. Eur J Obstet Gynecol Rep Biol1997; 7 4 173-77.

3 Alexander S, Bouvier-Colle MH, Salanave B and the MOMS-B team. The European survey MOMS B: a regional study of prevalence of three severe maternal morbid conditions: methodological problems and adopted solutions [abstract]. Confrbs conjoint ADELF-IEA, Bor- deaux Sept 1998? Rev Epidemiol Santipublique 1998; 46: S104.

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