- Email: [email protected]
Paraoxonase polymorphisms and organophosphates
CORRESPONDENCE
reflect heritability of risk factors of atherosclerotic disease, which is not at all new. In conclusion, increased concentrations of F1+2 and TAT reflect activation of the coagulation system, but there is no evidence that they reflect thrombotic tendency; and concentrations of D-dimer are not specific for thrombotic tendency. We think that Ariëns and colleagues should climb down and merely conclude that activation of the coagulation system has a substantial heritable component. It is still unclear whether this is associated with thrombotic risk. *J G van der Bom, C Kluft *Julius Center for Health Sciences and Primary Care and Van Creveldkliniek, University Medical Hospital Utrecht; and Gaubius Laboratory, TNO-PG, Leiden, Netherlands (e-mail: [email protected]) 1
2
3
4
Ariëns RA, de Lange M, Snieder H, Boothby M, Spector TD, Grant PJ. Activation markers of coagulation and fibrinolysis in twins: heritability of the prethrombotic state. Lancet 2002; 359: 667–71. Van der Bom JG, Bots ML, Haverkate F, et al. Activation products of the haemostatic system in coronary, cerebrovascular and peripheral arterial disease. Thromb Haemost 2001; 85: 234–39. Lowe GD, Rumley A, Sweetnam PM, Yarnell JW, Rumley J. Fibrin D-dimer, markers of coagulation activation and the risk of major ischaemic heart disease in the Caerphilly study. Thromb Haemost 2001; 86: 822–27. Danesh J, Whincup P, Walker M, et al. Fibrin D-dimer and coronary heart disease: prospective study and meta-analysis. Circulation 2001; 103: 2323–27.
Authors’ reply Sir—Although J G van der Bom and C Kluft’s question as to the relation between activation markers and vascular risk is not fully answered by available evidence, we think there is adequate evidence to support our view that markers of activation of the coagulation and fibrinolytic systems are associated with thrombosis. Biochemically, thrombosis is associated with activation of several enzymatic cascades, including the coagulation, fibrinolysis, complement, and kinin systems. The processes preceding thrombosis are complex and may involve longstanding underlying disease such as atherosclerosis of the vessel wall, inflammation, or diabetes. Although pathogenic mechanisms differ between venous or arterial thrombosis, both have in common the formation of a cross-linked fibrin clot that occludes blood vessels. In normal circumstances, low-grade thrombin generation, fibrin deposition, and clot breakdown occur continually.
802
Increased activation of these cascades happens before, during, and after vascular occlusion by a thrombus. Raised concentrations of the fibrin degradation product D-dimer are seen in patients with venous thrombosis, and normal values of this marker are a useful tool with which to exclude deepvein thrombosis.1–3 Other upstream markers of thrombin generation such as F1+2 and TAT are biochemical precursors of D-dimer, and the relation to disease may be less direct. As with most biochemical markers, it is difficult to ascertain whether changes occur before disease symptoms appear and whether they are causative. However, the epidemiological study of atherothrombotic disorders over the past 20 years has thrown up interesting data showing that raised concentrations of coagulation and fibrinolytic zymogens relate to clinical outcome. Indeed, the development of molecular epidemiology in this field was very much predicated on the view that genetic variation might account for this association. In a system that clearly requires activation for thrombin generation and fibrin production to take place, it is difficult to understand how zymogens can be related to thrombosis without their resulting activation markers having a role. Van der Bom and Kluft are correct to point out some of the uncertainties that exist in relation to activation markers and thrombotic risk. For example, markers of activation increase with age, and this in itself does not necessarily show the presence of ongoing thrombosis. However, raised concentrations of F1+2, thrombinantithrombin complexes, and D-dimer have been reported in patients with deep-vein thrombosis and pulmonary embolus4 and an understanding of the mechanisms involved in clot formation, combined with epidemiological studies in this area, suggest that activation of coagulation and fibrinolysis plays a crucial part in thrombotic disorders. *Robert A S Ariëns, Marlies de Lange, Harold Snieder, Tim D Spector, Peter J Grant *Academic Unit of Molecular Vascular Medicine, University of Leeds School of Medicine, G Floor, Martin Wing, L.G.I, Leeds LS1 3EX, UK; and Twin Research and Genetic Epidemiology Unit, St Thomas’ Hospital, London 1
2
3
Kelly J, Hunt BJ. Role of D-dimers in diagnosis of venous thrombosis. Lancet 2002; 359: 456–57. Kraaijenhagen RA, Piovella F, Bernardi E, et al. Simplification of the diagnostic management of suspected deep vein thrombosis. Arch Intern Med 2002; 162: 907–11. Cornuz J, Ghali WA, Hayoz D, Stoianov R,
4
Depairon M, Yersin B. Clinical prediction of deep venous thrombosis using two risk assessment methods in combination with rapid quantitative D-dimer testing. Am J Med 2002; 112: 198–203. Bauer KA. Detection of a prethrombotic state. In: Bloom AL, Forbes CD, Thromas DP, Tuddenham EGD, eds. Haemostasis and thrombosis, 3rd edn. Edinburgh: Churchill Livingstone, 1994: 1189–98.
Paraoxonase polymorphisms and organophosphates Sir—In their report on paraoxonase (PON1) polymorphisms, Nicola Cherry and colleagues (March 2, p 763)1 show a genetic variant in people who report ill health after sheep dipping, and that organophosphates contribute to this ill health. Study of sheep dipping has focused attention on mental and physical damage to farm workers who use organophosphates. However, less attention has been given to the effects of organophosphates on children. Babies and young children do not participate in farm work, but at certain times of the year farmhouses may be full of organophosphate vapour drifting in through doors and windows, or being carried in on boots, clothing, and so on. Low-dose exposure has a cumulative effect.2 Developmental disorders in children have been reported among farming families.3 Disorders include: severe learning difficulties, speech impairment, late walking and balance difficulties, poor coordination and absence of tactile movements, lethargy interpreted as laziness, behaviour difficulties such as hyperactivity or aggression, and atypical autism. The Organophosphate Information is collecting Network (OPIN)4 information and has 22 case studies of children affected in this way. In 1998, a group of doctors and members of OPIN met officials of the Health and Safety Executive to discuss the effects of organophosphates on children of farming communities. 3 years later, in April, 2001, the Medical Research Council were asked by the Health and Safety Executive to follow up the cases brought to their attention, and to provide further information, but funding is not yet available. Research is hampered at the outset because the disorder is not recognised. It does not even have a name. Anything without a name is too vague and amorphous for epidemiological study. A name—eg, organophosphate infantile poisoning (OPIP) syndrome—
THE LANCET • Vol 360 • September 7, 2002 • www.thelancet.com
For personal use. Only reproduce with permission from The Lancet Publishing Group.
CORRESPONDENCE
would help to focus attention on the need for research. Jennifer Worth The White House, St John’s Road, Boxmoor, Hertfordshire HP1 1PQ, UK 1
2
3
4
Cherry N, Mackiness M, Durrington P, et al. Paraoxonase (PON1) polymorphisms in farmers attributing ill health to sheep dip. Lancet 2002; 359: 763–64. The Control of Substances Hazardous to Health Regulations 1988. http://www.hmso.gov.uk/si/si1988/Uksi_198 81657_en_1.htm (accessed March 19, 2002). Royal College of Physicians and Royal College of Psychiatrists. Report of a joint working party of the Royal College of Physicians and the Royal College of Psychiatrists. November, 1998. CR67. Organophosphate information network. http://www.op-infonet.org (accessed March 19, 2002).
Congenital rubella: down but not out Sir—In a report on congenital rubella, E Sheridan and colleagues (Feb 23, p 674)1 focus on one of about 40 infants reported to the National Congenital Rubella Surveillance Programme (NCRSP) in the UK since 1991. More than 60 terminations for rubella disease or contact in pregnancy were reported in England and Wales in the same period.2 In 1991–96, about 60% of the mothers of infants reported to have congenital rubella had been born abroad. Most had come to the UK as adults, and had not been offered rubella vaccination. 25% of the maternal infections were acquired abroad (imported cases), mostly in Asia, but also one each in the Republic of Ireland, Poland, and Spain.3 No baby born with congenital rubella was reported in 1997 or 1998, one was reported in 1999, and seven more since then. Five of these eight babies were born to women who were infected early in pregnancy in Africa or Asia, before coming to the UK. Another mother acquired her infection in Scotland, although it was epidemiologically linked to an outbreak in Greece in 1999.4 The remaining two maternal infections were acquired in London, one by a UK-born woman, and the other by a Sri Lankan woman who had been in the UK for several years. Almost all infants reported in the past decade had typical rubella defects recognisable at birth or soon after. Congenital rubella is probably underdiagnosed, especially among affected children who have sensorineural hearing loss as the only defect. Before
the start of measles-mumps-rubella (MMR) vaccination, rubella antibodies were useful as a marker for congenital rubella in very young deaf children, since they were unlikely to have acquired natural infection in the first 2–3 years of life. Awareness of congenital rubella is currently low, few younger health professionals will ever have seen a case, and by the time hearing loss has been recognised and investigated, many children already have rubella antibodies from MMR vaccination. As Sheridan and colleagues report, rubella infection in the first 16 weeks of pregnancy can have devastating consequences. The best defence is high uptake of MMR in young children. MMR uptake in the UK has declined notably with substantial variation around the country.5 The current measles outbreaks should serve as a warning that rubella may also be poised to make a comeback. Particular attention should be paid to protecting people who have recently arrived in the UK, and others who are likely to have missed vaccination. Meanwhile, contact with suspected rubella in a susceptible pregnant woman, or rubella-like symptoms in any pregnant woman (irrespective of her recorded rubella status), must be investigated appropriately. If rubella infection is confirmed, women can be advised about the risks, and offered the option of termination of pregnancy if appropriate. Any infant or young child with suspected or confirmed congenital rubella, with or without typical rubella defects, should be reported through the British Paediatric Surveillance Unit’s active reporting scheme for rare disorders of childhood, or direct to the NCRSP. I thank the British Paediatric Surveillance Unit and particularly to paediatricians and all other colleagues who have provided data to the NCRSP. The Public Health Laboratory Service pays for the inclusion of congenital rubella on the BPSU’s orange card.
Pat Tookey National Congenital Rubella Surveillance Programme, Institute of Child Health, London WC1N 1EH, UK (e-mail: [email protected]) 1
2 3
4
5
Sheridan E, Aitken C, Jeffries D, Hird M, Thayalasekaran P. Congenital rubella syndrome: a risk in immigrant populations. Lancet 2002; 359: 674–75. Abortion Statistics 2000: series AB No 27. London: Stationery Office, 2001. Tookey PA, Peckham CS. Surveillance of congenital rubella in Great Britain, 1971–96. BMJ 1999; 318: 769–70. Tookey P, Molyneaux P, Helms P. UK case of congenital rubella can be linked to Greek cases. BMJ 2000; 321: 766–67. PHLS. COVER programme: October to December 2001—vaccination coverage statistics for children up to five years of age
THE LANCET • Vol 360 • September 7, 2002 • www.thelancet.com
in the United Kingdom. http://www.phls.co.uk/publications/CDR %20Weekly/pages/immunisation.html (accessed April 12, 2002).
Sir—We agree with Sheridan and colleagues’ conclusion1 that, despite the success of the UK rubella immunisation programme, congenital rubella syndrome may re-emerge, and that targeted immunisation is required for groups with higher susceptibility rates. They report a rubella susceptibility rate of 6% among Asian women from east London, but our data suggest that the situation in south London may be even worse. After we noticed an unusually high number of rubella-susceptible women from Sri Lanka in 1998, we undertook an audit of rubella susceptibility in pregnant women receiving antenatal care at St George’s Hospital, London, in that year. The overall susceptibility rate was 111 (3%) per 3500, but we noted large variations by country of birth. Of the 142 Sri Lankan women, 23 (16%) of 142 were susceptible compared with 16 (8%) of 195 and 24 (9%) of 276 South Asian and African women, respectively. Only 1% of women born in the UK were susceptible. In a review of the obstetric records for these women, two-thirds from countries without rubella vaccination programmes had already made a total of 85 contacts with obstetric and gynaecology services in the UK before becoming pregnant and testing rubella susceptible in 1998. Moreover, 17% of susceptible Sri Lankan women had previously had terminations done in the UK, yet were not tested for rubella before the procedure. The Sri Lankan women in particular were further disadvantaged by language difficulties, registering with over-worked, singlehanded family physicians more commonly than women of other ethnic origins, and by failures in postpartum immunisation. Despite rubella susceptibility being indicated by laboratory testing, only 85% of women were immunised after birth. The main reason for not being immunised was incorrect recording of rubella status as immune in the notes. With falling rates of MMR uptake in infants and an increase in migration to the UK from resource-poor countries, we are still failing these women in not adhering to the Department of Health’s recommendation that every effort should be made to identify and immunise seronegative women.2 If we are to avoid the re-emergence of congenital rubella syndrome, accurate data on local and national rubella
803
For personal use. Only reproduce with permission from The Lancet Publishing Group.
reflect heritability of risk factors of atherosclerotic disease, which is not at all new. In conclusion, increased concentrations of F1+2 and TAT reflect activation of the coagulation system, but there is no evidence that they reflect thrombotic tendency; and concentrations of D-dimer are not specific for thrombotic tendency. We think that Ariëns and colleagues should climb down and merely conclude that activation of the coagulation system has a substantial heritable component. It is still unclear whether this is associated with thrombotic risk. *J G van der Bom, C Kluft *Julius Center for Health Sciences and Primary Care and Van Creveldkliniek, University Medical Hospital Utrecht; and Gaubius Laboratory, TNO-PG, Leiden, Netherlands (e-mail: [email protected]) 1
2
3
4
Ariëns RA, de Lange M, Snieder H, Boothby M, Spector TD, Grant PJ. Activation markers of coagulation and fibrinolysis in twins: heritability of the prethrombotic state. Lancet 2002; 359: 667–71. Van der Bom JG, Bots ML, Haverkate F, et al. Activation products of the haemostatic system in coronary, cerebrovascular and peripheral arterial disease. Thromb Haemost 2001; 85: 234–39. Lowe GD, Rumley A, Sweetnam PM, Yarnell JW, Rumley J. Fibrin D-dimer, markers of coagulation activation and the risk of major ischaemic heart disease in the Caerphilly study. Thromb Haemost 2001; 86: 822–27. Danesh J, Whincup P, Walker M, et al. Fibrin D-dimer and coronary heart disease: prospective study and meta-analysis. Circulation 2001; 103: 2323–27.
Authors’ reply Sir—Although J G van der Bom and C Kluft’s question as to the relation between activation markers and vascular risk is not fully answered by available evidence, we think there is adequate evidence to support our view that markers of activation of the coagulation and fibrinolytic systems are associated with thrombosis. Biochemically, thrombosis is associated with activation of several enzymatic cascades, including the coagulation, fibrinolysis, complement, and kinin systems. The processes preceding thrombosis are complex and may involve longstanding underlying disease such as atherosclerosis of the vessel wall, inflammation, or diabetes. Although pathogenic mechanisms differ between venous or arterial thrombosis, both have in common the formation of a cross-linked fibrin clot that occludes blood vessels. In normal circumstances, low-grade thrombin generation, fibrin deposition, and clot breakdown occur continually.
802
Increased activation of these cascades happens before, during, and after vascular occlusion by a thrombus. Raised concentrations of the fibrin degradation product D-dimer are seen in patients with venous thrombosis, and normal values of this marker are a useful tool with which to exclude deepvein thrombosis.1–3 Other upstream markers of thrombin generation such as F1+2 and TAT are biochemical precursors of D-dimer, and the relation to disease may be less direct. As with most biochemical markers, it is difficult to ascertain whether changes occur before disease symptoms appear and whether they are causative. However, the epidemiological study of atherothrombotic disorders over the past 20 years has thrown up interesting data showing that raised concentrations of coagulation and fibrinolytic zymogens relate to clinical outcome. Indeed, the development of molecular epidemiology in this field was very much predicated on the view that genetic variation might account for this association. In a system that clearly requires activation for thrombin generation and fibrin production to take place, it is difficult to understand how zymogens can be related to thrombosis without their resulting activation markers having a role. Van der Bom and Kluft are correct to point out some of the uncertainties that exist in relation to activation markers and thrombotic risk. For example, markers of activation increase with age, and this in itself does not necessarily show the presence of ongoing thrombosis. However, raised concentrations of F1+2, thrombinantithrombin complexes, and D-dimer have been reported in patients with deep-vein thrombosis and pulmonary embolus4 and an understanding of the mechanisms involved in clot formation, combined with epidemiological studies in this area, suggest that activation of coagulation and fibrinolysis plays a crucial part in thrombotic disorders. *Robert A S Ariëns, Marlies de Lange, Harold Snieder, Tim D Spector, Peter J Grant *Academic Unit of Molecular Vascular Medicine, University of Leeds School of Medicine, G Floor, Martin Wing, L.G.I, Leeds LS1 3EX, UK; and Twin Research and Genetic Epidemiology Unit, St Thomas’ Hospital, London 1
2
3
Kelly J, Hunt BJ. Role of D-dimers in diagnosis of venous thrombosis. Lancet 2002; 359: 456–57. Kraaijenhagen RA, Piovella F, Bernardi E, et al. Simplification of the diagnostic management of suspected deep vein thrombosis. Arch Intern Med 2002; 162: 907–11. Cornuz J, Ghali WA, Hayoz D, Stoianov R,
4
Depairon M, Yersin B. Clinical prediction of deep venous thrombosis using two risk assessment methods in combination with rapid quantitative D-dimer testing. Am J Med 2002; 112: 198–203. Bauer KA. Detection of a prethrombotic state. In: Bloom AL, Forbes CD, Thromas DP, Tuddenham EGD, eds. Haemostasis and thrombosis, 3rd edn. Edinburgh: Churchill Livingstone, 1994: 1189–98.
Paraoxonase polymorphisms and organophosphates Sir—In their report on paraoxonase (PON1) polymorphisms, Nicola Cherry and colleagues (March 2, p 763)1 show a genetic variant in people who report ill health after sheep dipping, and that organophosphates contribute to this ill health. Study of sheep dipping has focused attention on mental and physical damage to farm workers who use organophosphates. However, less attention has been given to the effects of organophosphates on children. Babies and young children do not participate in farm work, but at certain times of the year farmhouses may be full of organophosphate vapour drifting in through doors and windows, or being carried in on boots, clothing, and so on. Low-dose exposure has a cumulative effect.2 Developmental disorders in children have been reported among farming families.3 Disorders include: severe learning difficulties, speech impairment, late walking and balance difficulties, poor coordination and absence of tactile movements, lethargy interpreted as laziness, behaviour difficulties such as hyperactivity or aggression, and atypical autism. The Organophosphate Information is collecting Network (OPIN)4 information and has 22 case studies of children affected in this way. In 1998, a group of doctors and members of OPIN met officials of the Health and Safety Executive to discuss the effects of organophosphates on children of farming communities. 3 years later, in April, 2001, the Medical Research Council were asked by the Health and Safety Executive to follow up the cases brought to their attention, and to provide further information, but funding is not yet available. Research is hampered at the outset because the disorder is not recognised. It does not even have a name. Anything without a name is too vague and amorphous for epidemiological study. A name—eg, organophosphate infantile poisoning (OPIP) syndrome—
THE LANCET • Vol 360 • September 7, 2002 • www.thelancet.com
For personal use. Only reproduce with permission from The Lancet Publishing Group.
CORRESPONDENCE
would help to focus attention on the need for research. Jennifer Worth The White House, St John’s Road, Boxmoor, Hertfordshire HP1 1PQ, UK 1
2
3
4
Cherry N, Mackiness M, Durrington P, et al. Paraoxonase (PON1) polymorphisms in farmers attributing ill health to sheep dip. Lancet 2002; 359: 763–64. The Control of Substances Hazardous to Health Regulations 1988. http://www.hmso.gov.uk/si/si1988/Uksi_198 81657_en_1.htm (accessed March 19, 2002). Royal College of Physicians and Royal College of Psychiatrists. Report of a joint working party of the Royal College of Physicians and the Royal College of Psychiatrists. November, 1998. CR67. Organophosphate information network. http://www.op-infonet.org (accessed March 19, 2002).
Congenital rubella: down but not out Sir—In a report on congenital rubella, E Sheridan and colleagues (Feb 23, p 674)1 focus on one of about 40 infants reported to the National Congenital Rubella Surveillance Programme (NCRSP) in the UK since 1991. More than 60 terminations for rubella disease or contact in pregnancy were reported in England and Wales in the same period.2 In 1991–96, about 60% of the mothers of infants reported to have congenital rubella had been born abroad. Most had come to the UK as adults, and had not been offered rubella vaccination. 25% of the maternal infections were acquired abroad (imported cases), mostly in Asia, but also one each in the Republic of Ireland, Poland, and Spain.3 No baby born with congenital rubella was reported in 1997 or 1998, one was reported in 1999, and seven more since then. Five of these eight babies were born to women who were infected early in pregnancy in Africa or Asia, before coming to the UK. Another mother acquired her infection in Scotland, although it was epidemiologically linked to an outbreak in Greece in 1999.4 The remaining two maternal infections were acquired in London, one by a UK-born woman, and the other by a Sri Lankan woman who had been in the UK for several years. Almost all infants reported in the past decade had typical rubella defects recognisable at birth or soon after. Congenital rubella is probably underdiagnosed, especially among affected children who have sensorineural hearing loss as the only defect. Before
the start of measles-mumps-rubella (MMR) vaccination, rubella antibodies were useful as a marker for congenital rubella in very young deaf children, since they were unlikely to have acquired natural infection in the first 2–3 years of life. Awareness of congenital rubella is currently low, few younger health professionals will ever have seen a case, and by the time hearing loss has been recognised and investigated, many children already have rubella antibodies from MMR vaccination. As Sheridan and colleagues report, rubella infection in the first 16 weeks of pregnancy can have devastating consequences. The best defence is high uptake of MMR in young children. MMR uptake in the UK has declined notably with substantial variation around the country.5 The current measles outbreaks should serve as a warning that rubella may also be poised to make a comeback. Particular attention should be paid to protecting people who have recently arrived in the UK, and others who are likely to have missed vaccination. Meanwhile, contact with suspected rubella in a susceptible pregnant woman, or rubella-like symptoms in any pregnant woman (irrespective of her recorded rubella status), must be investigated appropriately. If rubella infection is confirmed, women can be advised about the risks, and offered the option of termination of pregnancy if appropriate. Any infant or young child with suspected or confirmed congenital rubella, with or without typical rubella defects, should be reported through the British Paediatric Surveillance Unit’s active reporting scheme for rare disorders of childhood, or direct to the NCRSP. I thank the British Paediatric Surveillance Unit and particularly to paediatricians and all other colleagues who have provided data to the NCRSP. The Public Health Laboratory Service pays for the inclusion of congenital rubella on the BPSU’s orange card.
Pat Tookey National Congenital Rubella Surveillance Programme, Institute of Child Health, London WC1N 1EH, UK (e-mail: [email protected]) 1
2 3
4
5
Sheridan E, Aitken C, Jeffries D, Hird M, Thayalasekaran P. Congenital rubella syndrome: a risk in immigrant populations. Lancet 2002; 359: 674–75. Abortion Statistics 2000: series AB No 27. London: Stationery Office, 2001. Tookey PA, Peckham CS. Surveillance of congenital rubella in Great Britain, 1971–96. BMJ 1999; 318: 769–70. Tookey P, Molyneaux P, Helms P. UK case of congenital rubella can be linked to Greek cases. BMJ 2000; 321: 766–67. PHLS. COVER programme: October to December 2001—vaccination coverage statistics for children up to five years of age
THE LANCET • Vol 360 • September 7, 2002 • www.thelancet.com
in the United Kingdom. http://www.phls.co.uk/publications/CDR %20Weekly/pages/immunisation.html (accessed April 12, 2002).
Sir—We agree with Sheridan and colleagues’ conclusion1 that, despite the success of the UK rubella immunisation programme, congenital rubella syndrome may re-emerge, and that targeted immunisation is required for groups with higher susceptibility rates. They report a rubella susceptibility rate of 6% among Asian women from east London, but our data suggest that the situation in south London may be even worse. After we noticed an unusually high number of rubella-susceptible women from Sri Lanka in 1998, we undertook an audit of rubella susceptibility in pregnant women receiving antenatal care at St George’s Hospital, London, in that year. The overall susceptibility rate was 111 (3%) per 3500, but we noted large variations by country of birth. Of the 142 Sri Lankan women, 23 (16%) of 142 were susceptible compared with 16 (8%) of 195 and 24 (9%) of 276 South Asian and African women, respectively. Only 1% of women born in the UK were susceptible. In a review of the obstetric records for these women, two-thirds from countries without rubella vaccination programmes had already made a total of 85 contacts with obstetric and gynaecology services in the UK before becoming pregnant and testing rubella susceptible in 1998. Moreover, 17% of susceptible Sri Lankan women had previously had terminations done in the UK, yet were not tested for rubella before the procedure. The Sri Lankan women in particular were further disadvantaged by language difficulties, registering with over-worked, singlehanded family physicians more commonly than women of other ethnic origins, and by failures in postpartum immunisation. Despite rubella susceptibility being indicated by laboratory testing, only 85% of women were immunised after birth. The main reason for not being immunised was incorrect recording of rubella status as immune in the notes. With falling rates of MMR uptake in infants and an increase in migration to the UK from resource-poor countries, we are still failing these women in not adhering to the Department of Health’s recommendation that every effort should be made to identify and immunise seronegative women.2 If we are to avoid the re-emergence of congenital rubella syndrome, accurate data on local and national rubella
803
For personal use. Only reproduce with permission from The Lancet Publishing Group.