emergency contraception: the journey so far

4
CORRESPONDENCE Emergency contraception: the journey so far Sir, In D.N.P. Haggai’s recent review of emergency contraception, 1 the author stated that there was no levonorgestrel-only product licensed in the UK for emergency contraception. In fact, as many readers know, levonorgestrel-only emergency contraception (Levonelle, Schering, UK) has been available for a number of years now, the regime consisting of levonorgestrel 0.75 mg taken 12 hours apart starting within 72 hours of unprotected inter- course. It was granted a license as a ‘prescription-only medicine’ (POM) in November 1999 and was launched in February 2000. In December 2000, it was granted a license as an ‘over-the-counter’ (OTC) medicine, and in January 2001 it was launched 2 despite a move in the House of Lords by Lady Young to ban its sale. In 2002, 523,840 units were sold by pharmacists (35%) compared with 919,541 units prescribed by doctors (65%). OTC requests were made by women with an average age of 24, with 85% over the age of 20 (data from Schering Health Care). We agree with the author that the current rate of unintended pregnancy is too high and that the improved availability of emergency contraception should help to reduce unwanted preg- nancies. However, figures available for the number of abortions undertaken in England during 2000 and 2001 have not shown a decreasing trend, 2 although it may be some time before an effect is seen. References 1. Haggai DNP. Emergency contraception: the journey so far. Br J Obstet Gynaecol 2003;110(4):339 – 345. 2. UK Office of National Statistics. Abortions to Residents (England) 2000 and 2001. Shelley V. Z. Haynes a & Tim J. Dudderidge b a Department of Obstetrics and Gynaecology, Northwick Park Hospital, UK b Royal Free Hospital, London NW3 2QG, UK DOI: 10.1046/j.1471-0528.2003.00020.x Emergency contraception: the journey so far Sir, I wish to correct certain errors and inaccuracies in the review on Emergency Contraception: the Journey so far. 1 The statement that the combined oestrogen – progestogen method is marketed in the UK as PC4 is incorrect as from September 2002, when the manufacturers withdrew PC4 in the UK. The statement that there is no licensed levonorgestrel-only product in the UK is supported by a 4 year old reference. Progestogen-only contraception has been licensed and marketed in the UK as levonelle-2 since February 2000, and a consumer version — levonelle, was licensed in February 2001 for provision by pharmacists to women aged 16 and over. The only form of progestogen-only emergency contraception licensed in the UK consists of two doses of 0.75 mg of levonor- gestrel taken 12 hours apart up to 72 hours of unprotected sexual intercourse 2 and not up to 48 hours! This 48 hour regimen was introduced 10 years ago by Ho and Kwan. 3 It was a pity that the randomised study published in The Lancet in December 2002 was not referenced. This concluded that a single dose of 1.5 mg levonorgestrel was equally effective as a divided dose, 4 and has the advantage of improved compliance. The single-dose levonorgestrel regimen (1.5 mg) has same effect up to 120 hours after unprotected sexual intercourse, and could prevent 82% of expected pregnancies, 4 although women should be aware that usage after 7.2 hours falls outside the current UK license. References 1. Haggai DNP. Emergency contraception: the journey so far. Br J Obstet Gynaecol 2003;110:339 – 345. 2. WHO Task Force on Postovulatory Methods of Fertility Regulation. Randomised trial of the levonorgestrel versus the Yuzpe regimen of combined oral contraceptives for emergency contraception. Lancet 1998;352:428 – 433. 3. Ho PC, Kwan MSW. A prospective randomised comparison of levonorgestrel with the Yuzpe regimen in postcoital contraception. Hum Reprod 1993;8:389 – 392. 4. Vaughan Hertzen H, Piaggio G, Diag J, et al. WHO Research Group on Postovulatory Fertility Regulation. Low dose Mifepristone and two regimens of Levonorgestrel for emergency contraception: a WHO multicentre randomised trial. Lancet 2002;360:1803 – 1810. Sunanda Gupta St Bartholomew and Queen Mary’s School of Medicine and Dentistry, Turner Street, London, UK DOI: 10.1046/j.1471-0528.2003.00021.x Emergency contraception: the journey so far Sir, I read with interest the recent review article on emergency contraception. 1 I was concerned about the statement that an IUD could be inserted between 5 and 7 days postcoitally for contra- ception. It is thought to exert its effect by interfering with fertilisation and possibly implantation and hence both UK and WHO guidelines recommend use up to 120 hours postcoitally. 2,3 Use of an IUD after this time, when implantation may have taken place, is outside its licence for emergency contraception and its use in these circumstances would be as an abortifactent. 3 For anyone requiring evidence-based guidance on emergency contra- ception, I would refer them to the recently published FFPHRC guidelines. 2 References 1. Haggai DNP. Emergency contraception: the journey so far. Br J Obstet Gynaecol 2003;110:339 – 345. D RCOG 2004 BJOG: an International Journal of Obstetrics and Gynaecology www.blackwellpublishing.com/bjog BJOG: an International Journal of Obstetrics and Gynaecology January 2004, Vol. 111, pp. 91–94

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CORRESPONDENCE

Emergency contraception: the journey so far

Sir,In D.N.P. Haggai’s recent review of emergency contraception,1

the author stated that there was no levonorgestrel-only productlicensed in the UK for emergency contraception. In fact, as manyreaders know, levonorgestrel-only emergency contraception(Levonelle, Schering, UK) has been available for a number ofyears now, the regime consisting of levonorgestrel 0.75 mg taken12 hours apart starting within 72 hours of unprotected inter-course. It was granted a license as a ‘prescription-only medicine’(POM) in November 1999 and was launched in February 2000.In December 2000, it was granted a license as an ‘over-the-counter’(OTC) medicine, and in January 2001 it was launched2 despite amove in the House of Lords by Lady Young to ban its sale.

In 2002, 523,840 units were sold by pharmacists (35%)compared with 919,541 units prescribed by doctors (65%). OTCrequests were made by women with an average age of 24, with85% over the age of 20 (data from Schering Health Care).

We agree with the author that the current rate of unintendedpregnancy is too high and that the improved availability ofemergency contraception should help to reduce unwanted preg-nancies. However, figures available for the number of abortionsundertaken in England during 2000 and 2001 have not shown adecreasing trend,2 although it may be some time before an effectis seen.

References

1. Haggai DNP. Emergency contraception: the journey so far. Br J Obstet

Gynaecol 2003;110(4):339–345.

2. UK Office of National Statistics. Abortions to Residents (England)

2000 and 2001.

Shelley V. Z. Haynesa & Tim J. DudderidgebaDepartment of Obstetrics and Gynaecology, Northwick ParkHospital, UKbRoyal Free Hospital, London NW3 2QG, UK

DOI: 10.1046/j.1471-0528.2003.00020.x

Emergency contraception: the journey so far

Sir,I wish to correct certain errors and inaccuracies in the review

on Emergency Contraception: the Journey so far.1

The statement that the combined oestrogen–progestogenmethod is marketed in the UK as PC4 is incorrect as fromSeptember 2002, when the manufacturers withdrew PC4 in the UK.

The statement that there is no licensed levonorgestrel-onlyproduct in the UK is supported by a 4 year old reference.Progestogen-only contraception has been licensed and marketedin the UK as levonelle-2 since February 2000, and a consumerversion—levonelle, was licensed in February 2001 for provisionby pharmacists to women aged 16 and over.

The only form of progestogen-only emergency contraceptionlicensed in the UK consists of two doses of 0.75 mg of levonor-

gestrel taken 12 hours apart up to 72 hours of unprotected sexualintercourse2 and not up to 48 hours! This 48 hour regimen wasintroduced 10 years ago by Ho and Kwan.3

It was a pity that the randomised study published in TheLancet in December 2002 was not referenced. This concluded thata single dose of 1.5 mg levonorgestrel was equally effective as adivided dose,4 and has the advantage of improved compliance.

The single-dose levonorgestrel regimen (1.5 mg) has sameeffect up to 120 hours after unprotected sexual intercourse, andcould prevent 82% of expected pregnancies,4 although womenshould be aware that usage after 7.2 hours falls outside the currentUK license.

References

1. Haggai DNP. Emergency contraception: the journey so far. Br J Obstet

Gynaecol 2003;110:339–345.

2. WHO Task Force on Postovulatory Methods of Fertility Regulation.

Randomised trial of the levonorgestrel versus the Yuzpe regimen of

combined oral contraceptives for emergency contraception. Lancet

1998;352:428–433.

3. Ho PC, Kwan MSW. A prospective randomised comparison of

levonorgestrel with the Yuzpe regimen in postcoital contraception.

Hum Reprod 1993;8:389–392.

4. Vaughan Hertzen H, Piaggio G, Diag J, et al. WHO Research Group on

Postovulatory Fertility Regulation. Low dose Mifepristone and two

regimens of Levonorgestrel for emergency contraception: a WHO

multicentre randomised trial. Lancet 2002;360:1803–1810.

Sunanda GuptaSt Bartholomew and Queen Mary’s School of Medicine andDentistry, Turner Street, London, UK

DOI: 10.1046/j.1471-0528.2003.00021.x

Emergency contraception: the journey so far

Sir,I read with interest the recent review article on emergency

contraception.1 I was concerned about the statement that an IUDcould be inserted between 5 and 7 days postcoitally for contra-ception. It is thought to exert its effect by interfering withfertilisation and possibly implantation and hence both UK andWHO guidelines recommend use up to 120 hours postcoitally.2,3

Use of an IUD after this time, when implantation may have takenplace, is outside its licence for emergency contraception and itsuse in these circumstances would be as an abortifactent.3 Foranyone requiring evidence-based guidance on emergency contra-ception, I would refer them to the recently published FFPHRCguidelines.2

References

1. Haggai DNP. Emergency contraception: the journey so far. Br J Obstet

Gynaecol 2003;110:339–345.

D RCOG 2004 BJOG: an International Journal of Obstetrics and Gynaecology www.blackwellpublishing.com/bjog

BJOG: an International Journal of Obstetrics and GynaecologyJanuary 2004, Vol. 111, pp. 91–94

2. Faculty of Family Planning and Reproductive Health Care Guidance

Emergency Contraception. UK: RCOG, 2003 (April).

3. Improving access to quality care in family planning: medical eligibility

criteria for contraceptive use. WHO, 2002.

Ruth SwarbrickSpecialist Registrar in Reproductive Health Care, Ella GordonUnit, Portsmouth, UK

DOI: 10.1046/j.1471-0528.2003.00028.x

Serum LH analysis: solutions and problems

Sir,Milsom et al.1 provide a useful reminder of the influence of

biochemical analysis on the diagnosis and interpretation ofresults. The problems in the use of the LH/FSH ratio werereviewed last about 10 years ago.2 –4 The two influences on theratio, the pattern of gonadotrophin isoform secretion by thepituitary and the detection of these isoforms by immunoassaykits differing in their manufacturer’s use of the same Interna-tional Reference Preparation, assay matrix and antibody, cangive different numerical LH (and FSH) results when measure-ment by two different assay kits is made on the same serumsample.

The two problems highlighted1 on the biochemical detectionof PCOS patients and the use of the appropriate reference rangeare still relevant. Recent studies on the diagnosis of PCOS using theLH/FSH ratio have shown favourable diagnostic results,5 – 7 im-plying that LH kits have improved comparability. This may be dueto the use of the Second International Standard 80/552 (not usedin the study1). Some assays may still be using antibodies directedagainst the intact LH molecule.8

Assay-related reference ranges9 can provide an aid to diagnosis,although the criteria used by Milsom et al.1 for patient selectionfor the comparison of LH/FSH ratios does create bias.

References

1. Milsom SR, Sowter MC, Carter MA, Knox BS, Gunn AJ. LH levels in

women with polycystic ovarian syndrome: have modern assays made

them irrelevant. Br J Obstet Gynaecol 2003;110:760–764.

2. Demers LM. Monoclonal antibodies to lutropin: are our immunoassays

too specific? Clin Chem 1991;37:311–312.

3. Jeffcoate SL. Analytical and clinical significance of peptide hormone

heterogeneity with particular reference to growth hormone and lute-

inising hormone in serum. Clin Endocrinol 1993;38:113–121.

4. Taylor AE, Khoury RH, Crowley WF. A comparison of 13 different

immunometric assay kits for gonadotrophins: implications for clinical

investigation. J Clin Endocrinol Metab 1994:79:240–247.

5. Manieri C, Pastorino R, Marolda AR, et al. A new approach in the

evaluation of gonadotrophins for the diagnosis of polycystic ovary

syndrome. Panmin Med 1995;37:115–118.

6. Taylor AE, McCourt B, Martin KA, et al. Determinants of abnormal

gonadotrophin secretion in clinically defined women with polycystic

ovary syndrome. J Clin Endocrinol Metab 1997;82:2248–2256.

7. Turhan NO, Toppare MF, Seckin NC, Dilmen G. The predictive power

of endocrine tests for the diagnosis of polycystic ovaries in women with

oligoamenorrhea. Gynecol Obstet Invest 1999;48:183–186.

8. Petterson K, Ding Y-Q, Huhtaniemi I. Monoclonal antibody-based

discrepancies between two-site immunometric tests for lutropin. Clin

Chem 1991;37:1745–1748.

9. Andrew CE, Hanning I, McBain AM, Moody D, Price A. A model for a

muticentre approach to the derivation of reference intervals for thyroid

hormones and testosterone for laboratories using identical analysers.

Clin Chem Lab Med 2000;38:1013–1019.

A. M. FieldingDepartment of Chemical Pathology, Swansea NHS Trust,Morriston Hospital, Swansea SA6 6NL, UK

DOI: 10.1046/j.1471-0528.2003.00022.x

Cerebral palsy and clinical negligence litigation: acohort study

Sir,Greenwood et al.1 applied parts of the template from the

1999 cerebral palsy consensus statement,2 which helps definewhether an acute hypoxic event around birth was sufficientto cause cerebral palsy. As members of that task force thereis much in their discussion with which we agree. However,in assessing the prevalence of the available evidence in their1984–1993 cohort, they have applied the template in a mannerthat was not quite intended. Of the eight recommended crite-ria in the template, the first three ‘essential’ criteria helpedto prove the existence of a severe hypoxia (metabolic acidosis)at birth rather than acute hypoxia. If hypoxia at birth waslikely, the next five criteria, when present or mostly absent asa group, helped differentiate whether the hypoxia was acute orchronic.

The consensus statement acknowledged that some evidencemight often be missing and that in assessing the remainingevidence it could not be claimed that the missing criteria wouldor would not have been met. The more evidence that was missingthe more the diagnosis was in doubt. Missing peripartum gases isnot a failure of the criteria but the failure to have measured cordor early neonatal gases around or after a delivery with perinatalrisk factors. Prospective documentation of all eight criteria in highrisk cases will improve obstetric audits. The template was alsopublished to define strong research criteria that are necessary tovalidate that sequelae, such as specific brain imaging patterns inlater life, actually correlate with acute hypoxic events at birth andare not confused with chronic hypoxic and non-hypoxic condi-tions, which often manifest themselves for the first time arounddelivery.

Those considering offering expert medico-legal opinion in thiscomplicated area, where the antenatal origins of much of theneuropathology of cerebral palsy are beginning to be understood,should read the latest Neonatal Encephalopathy and CerebralPalsy Task Force report, published this year by the AmericanCollege of Obstetricians and Gynecologists. It largely endorsesthe 1999 report and its template, but has updated and modified it.When properly applied, the template helps exclude non-hypoxicand chronic hypoxic causes of cerebral palsy and encouragesmore thorough examination of possible antenatal causes that maynot be suspected until labour or birth. Until better tests are avail-able, it provides more objective criteria than ‘expert’ opinionthat sometimes mistakenly assumes that the non-specific signs ofmeconium staining, non-reassuring cardiotocograms, low Apgarscores and neonatal encephalopathy mean that there must havebeen an intrapartum hypoxic event that should have been pre-vented. As pointed out by Greenwood et al. and the consensusstatement, there is often little proof that cerebral palsy caused byan acute intrapartum event necessarily is preventable and criti-cism of details of labour management may not link cause andeffect.

D RCOG 2004 Br J Obstet Gynaecol 111, pp. 91–94

CORRESPONDENCE92

References

1. Greenwood C, Newman S, Impey L, Johnson A. Cerebral palsy and

clinical negligence litigation: a cohort study. Br J Obstet Gynaecol

2003;110:6–11.

2. MacLennan AH for the International Cerebral Palsy Task Force. A

template for defining a casual relation between acute intrapartum events

and cerebral palsy: international consensus statement. BMJ 1999;319:

1054–1059.

3. Task force of the American College of Obstetricians and Gynecologists

and the American Academy of Pediatrics. Neonatal Encephalopathy and

Cerebral Palsy. Defining the Pathogenesis and Pathophysiology. The

American College of Obstetricians and Gynecologists, Washington, DC,

2003.

Alastair MacLennan & Jeffrey RobinsonDepartment of Obstetrics and Gynaecology, University ofAdelaide, Australia

DOI: 10.1046/j.1471-0528.2003.00023.x

Factor V Leiden in pregnancies complicated byplacental abruption

Sir,Prochazka et al. [Prochazka M, Happach C, Marsal K, Dahlback

B, Lindqvist PG. Factor V Leiden in pregnancies complicatedby placental abruption. Br J Obstet Gynaecol 2003;110(May):462–466] found a carrier rate for factor V Leiden of 16% inwomen with placental abruption, which did not differ significantlyfrom the control population (11%), perhaps because this rate incontrols is very high.

A 4.4% rate value is expected in Europeans.1 In our recentstudy on Italian Caucasian women, 102 controls showed a prev-alence of 3% compared with 22% among 51 cases of placentalabruption.2 This rate in cases is similar to two other studies, 30%3

and 25%.4

In a case–control study, controls should be well defined, in afixed ratio with cases and matched for the main confoundingvariables. In our series, as well as in those of Wiener-Megnagiet al.3 andKupferminc et al.,4 controls were womenwith previouslyuncomplicated pregnancies, matched for age, parity and ethnicity.In the article of Prochazka et al., none of the above features wasrespected. Indeed, their control group included patients with pre-eclampsia and IUGR, both conditions associated with a higher riskof thrombophilia. Moreover, the geographical origin of the subjectswas not mentioned and no matching for age and parity was done.

The role played by thrombophilia in obstetric disorders remainscontroversial. However, among the various disorders of pre-eclampsia, IUGR, unexplained fetal loss and placental abruption,controlled studies suggest that factor V Leiden is most prevalent inthe latter condition. In other words, a personal history of placentalabruption is the sole obstetric condition warranting thrombophiliascreening.

References

1. Rees CD, Cox M, Clegg JB. World distribution of factor V Leiden.

Lancet 1995;346:1133–1134.

2. Facchinetti F, Marozio L, Grandone E, Pizzi C, Volpe A, Benedetto C.

Thrombophilic mutations are a main risk factor for placental abruption.

Haematologica 2003;88(7):785–788.

3. Wiener-Megnagi Z, Ben-Shlomo I, Goldberg Y, Shalev E. Resistance to

activated protein C and the Leiden mutation: high prevalence in patients

with abruptio placentae. Am J Obstet Gynecol 1998;179:1565–1567.

4. Kupferminc MJ, Eldor A, Steinman N, et al. Increased frequency of

genetic thrombophilia in women with complications of pregnancy.

N Engl J Med 1999;340:9–13.

Fabio FacchinettiMother–Infant Department, University of Modena and ReggioEmilia, Via del Pozzo 71, 41100 Modena, Italy

DOI:10.1016/j.1471-0528.2003.00003.x

AUTHOR’S REPLY

Sir,Professor Facchinetti suggests that our lack of significance

might be due to an unexpectedly high prevalence of factor VLeiden in the control group and that the control group might notbe properly drawn. He states that we have not matched forconfounding variables such as age, parity, ethnicity and pregnancycomplications like pre-eclampsia, IUGR and fetal loss. He claimsthat other controlled studies have found factor V Leiden related topregnancy complications such as pre-eclampsia, IUGR, fetal lossand placental abruption in a homogenous manner.

First, we believe that the prevalence of our control group is whatwe expected. From larger population-based series, the prevalenceof factor V Leiden shows a north to south ratio with a carrier rate ofaround 3% in Italy, 9% in Germany and between 10% and 15% inSweden.1–4 The reason we have a lower prevalence of factor VLeiden in Malmo as compared with the Kristianstads study (15%)is that we have a 31% non-Scandinavian population, which haveclearly been declared in the detailed description of our controlgroup.4

We agree with Professor Facchinetti that the selection ofcontrols is of vital importance for the validity of the results.Since we know that carriers of factor V Leiden confer anevolutionary advantage, we spent a considerable amount of timedeciding how to draw a representative control group. We foundtwo ways that would not introduce bias. One was the method ofZoller et al.3 using a population register to draw unselectedcontrols. The other was to prospectively draw all womenattending the maternal health clinic, which is the method thatwe used. It includes unselected pregnant women, which webelieve is a representative sample of our population. In mostother ways, there is a risk of introducing bias. For example, ifthe control group is drawn from women at the postpartum ward,a too low prevalence would be found.4 We believe our materialis very well defined.4 In the case of an heritable condition likecarriership of factor V Leiden, there are no indications of orreason for age or parity to be confounding variables. In addition,in our large unselected control group, there were no differencesin the proportion of factor V Leiden carriers in the subgroups ofpre-eclampsia, IUGR or fetal loss. Therefore, we used the entirecontrol group in analysis.4 Regarding ethnicity, women of Scan-dinavian origin probably have a higher prevalence compared withnon-Scandinavians. However, our ethics committee does notpermit sampling data on ethnicity without special permission.We have clearly declared in the article that this is a drawbackof our study. Furthermore, not mentioned by Dr Facchinetti, thereis a need for adjusting for other thrombophilias. However, we didnot have the women’s permission to do so. In a case–controlstudy like ours, there is no need for fixed ratio between cases andcontrols.

D RCOG 2004 Br J Obstet Gynaecol 111, pp. 91–94

CORRESPONDENCE 93

Finally, we disagree with Professor Facchinetti’s contentionthat carriership of factor V Leiden is more common in pregnancieswith pre-eclampsia, IUGR, fetal loss and placental abruption forthese reasons.

The results of most studies are heterogenic, larger studies showless relation than small studies and most studies are too small toassess the question. The studies quoted by Professor Facchinettimight have been designed for other reasons, but our ethicalcommittee would not permit a study designed to assess a rela-tionship between factor V Leiden and placental abruption withoutsufficient size to detect a reasonable outcome. For example, thepower to detect a doubled prevalence among carriers as comparedwith non-carriers are as follows: Weiner-Megnagi et al. 8%,Kupferminc et al. 18%, Aliferevic et al. 14%, Facchinetti et al.15%, and our 73%.3–9

We conclude that our results regarding factor V Leiden andplacental abruption are valid and our finding of an odds ratio of1.5 (0.9–2.6) is within the 95% confidence limits of all four otherstudies on the subject.

References

1. Rodeghiero F, Tosetto A. Activated protein C resistance and factor V

Leiden mutation are independent risk factors for venous thromboem-

bolism. Ann Intern Med 1999;130(8):643–650.

2. Ehrcnforth S, Klinke S, von Depka Prondzinski M, Kreuz W, Ganser A,

Scharrer I. Activated protein C resistance and venous thrombophilia:

molecular genetic prevalence study in the German population. Dtsch

Med Wochenschr 1999;124(25–26):783–787.

3. Zoller B, Norlund L, Leksell H, et al. High prevalence of the FVR506Q

mutation causing APC resistance in a region of southern Sweden with a

high incidence of venous thrombosis. Thromb Res 1996;83(6):475–477.

4. Lindqvist PG, Svensson PJ, Marsal K, Grennert L, Lutherkort M,

Dahlback B. Activated protein C resistance (FV:Q506) and pregnancy.

Thromb Haemost 1999;81:532–537.

5. Wiener-Megnagi Z, Ben Shlomo I, Goldberg Y, Shalev E. Resistance to

activated protein C and the Leiden mutation: high prevalence in pa-

tients with abruptio placentae. Am J Obstet Gynecol 1998;179(6 Pt 1):

1565–1567.

6. Kupferminc MJ, Eldor A, Steinman N, et al. Increased frequency of

genetic thrombophilia in women with complications of pregnancy.

N Engl J Med 1999;340(1):9–13.

7. Alfirevic Z, Mousa HA, Martlew V, Briscoe L, Perez-Casal M, Toh

CH. Postnatal screening for thrombophilia in women with severe

pregnancy complications. Obstet Gynecol 2001;97(5 Pt 1):753–759.

8. Facchinetti F, Marozio L, Grandone E, Pizzi C, Volpe A, Benedetto C.

Thrombophilic mutations are a main risk factor for placental abruption.

Haematologica 2003;88(7):785–788.

9. Prochazka M, Happach C, Marsal K, Dahlback B, Lindqvist PG. Factor

V Leiden in pregnancies complicated by placental abruption. Br J

Obstet Gynaecol 2003;110(5):462–466.

Pelle LindqvistOn the behalf of all authors

DOI:10.1016/j.1471-0528.2003.00003.x

D RCOG 2004 Br J Obstet Gynaecol 111, pp. 91–94

CORRESPONDENCE94