- Email: [email protected]
Poverty and HIV in sub-Saharan Africa
CORRESPONDENCE
number of elective caesarean sections might be partly contributing to the rise, since the rate of 20·3% is among the highest in more-developed countries. The findings of two Australian studies have strengthened the evidence pointing to women requesting caesarean section. More than 20% of women who had had caesarean sections in a large south Australian hospital said that they had insisted on or were keen to have this procedure.2 In Western Australia, in 633 women 27% of caesarean sections were done solely because of maternal request, even when vaginal birth was judged safe.3 We believe, however, that the issue of lowering rates might be more complicated than implied by Wagner. We did a study in a tertiary-referral hospital in South Australia. In a crosssectional survey of 15 staff specialists and medical specialists (response rate 75%), only 40% agreed that the optimum rate of caesarean section should be 15–20%. A third of these specialists did not know what the rate should be, a third stated that the current rate in Australia (20·3%) should be the optimum rate, and 13% said that the rate should be 20–30%. The lowering of caesarean-section rates needs more than reversing the marginalisation of midwives in maternity care, as Wagner argues. We have critically reviewed more than 25 studies done in many countries in the past decade, including randomised controlled trials, systematic reviews, and quasiexperimental studies. The lowering of caesarean-section rates proved difficult in all studies, but midwife-managed models of care, compared with standard care, did not reduce rates. One-to-one care from a support person during labour can, however, affect the rate of caesarean section.
Sir—We have some Greek data that support the views expressed by Marsden Wagner.1 We did two national perinatal surveys in 1983 and 1998, with 11 059 and 14 549 consecutive birth cohorts, respectively. The total caesarean section rate rose from 13% to 31% between surveys. Elective caesarean sections more than doubled (7% vs 15·5%), and the birthweight distribution curve shifted significantly to the left, with a loss of 100 g mean birthweight. Since the intrauterine weight gain by gestational week did not differ significantly between the two studies, we compared gestational age and birthweight for newborn babies delivered vaginally or by elective caesarean section. A third of those delivered by elective caesarean in 1998 were born at less than 38 weeks’ gestational age compared with 18% born after spontaneous delivery. In addition, 12% of neonates delivered by elective caesarean section had low birthweight (less than 2500 g) compared with 6% of those delivered spontaneously, whereas in 1983, the respective proportions were equal. Thus iatrogenic prematurity was fully confirmed in our data sets. The incidence of caesarean sections varied greatly between women of Greek origin and refugees (33% vs 24·5%), between private hospitals and public hospitals (39 vs 28%), and between urban centres and the suburbs (36 vs 26%). As Wagner points out, the better-off women receive less-safe care. *C Bakoula, N Matsaniotis First Department of Paediatrics, Hospital for Sick Children “Aghia Sophia”, Athens 115-27, Greece 1
*Ruth Walker, Eleni Golois, Deborah Turnbull, Chris Wilkinson
1 2
3
Wagner M. Choosing caesarean section. Lancet 2000; 356: 1677–80. Turnbull DA, Wilkinson C, Yaser A, Carty V, Svigos JM, Robinson JS. Women’s role and satisfaction in the decision to have a caesarean section. Med J Aust 1999; 170: 580–83. Quinlivan JA, Petersen RW, Nichols CN. Patient preference the leading indication for elective caesarean section in public patients: results of a 2-year prospective audit in a teaching hospital. Aust NZ J Obstet Gynaecol 1999; 174: 199–205.
636
Sir—International Development agencies and donors are increasingly adopting aid programmes directed towards poverty alleviation in subSaharan Africa. One of the goals of this policy is to reduce the prevalence of HIV. Colin Butler (Oct 21, p 1445)1 concludes that povety is a major underlying causal factor for the scale of the African AIDS epidemic, but the relation between HIV and poverty is complex and there is little evidence that poverty-reduction policies are likely to succeed. HIV prevalence and gross national product (GNP) vary substantially between countries throughout subSaharan Africa. To investigate the relation between HIV and GNP in the region, we gathered data for HIV antenatal prevalences in the capital or major city, obtained by accessing the US Bureau of the census website (www.census.gov/ipc/www/hiv1.html, accessed on 15 Jan, 2001). For GNP, data were obtained from the World Bank website org (www.worldbank. org/data/countrydata/adi/adi1-1.pdf, accessed on 15 Jan, 2001), which reports the GNP for 1998. Data for HIV prevalencies (range 0–43%) and GNP (range US$140–3600) were available from these sources for 40 countries. The years in which HIV prevalence studies were done were 1998–99 (21), 1996–97 (16), and 1993–94 (3). Data for both variables were not available for Cape Verde, Djibouli, Liberia, Niger, Sao Tome, Seychelles, Sierra Leone, and Somalia. A scatter plot of HIV prevalence in antinatal-clinic attenders and GNP is shown in the figure. There is a weak positive correlation between HIV prevalence and GNP (Pearson correlation coefficient 0·29, p=0·07).
4500 4000 GNP per caput 1998 (US$)
Departments of Public Health and General Practice, Psychology, and *General Practice and Psychology, Adelaide University, Adelaide, South Australia 5005, Australia; and Department of Obstetrics and Gynaecology, Women’s and Children’s Hospital, Adelaide (e-mail: [email protected])
Wagner M. Choosing caesarean section. Lancet 2000; 356: 1677–80.
Poverty and HIV in sub-Saharan Africa
3500 3000 2500 2000 1500 1000 500 0 0
10
20 30 HIV prevalence in ANC attenders (%)
40
50
Relation between GNP and HIV prevalence in antenatal-clinic (ANC) attenders in sub-Saharan Africa
THE LANCET • Vol 357 • February 24, 2001
For personal use only. Reproduce with permission from The Lancet Publishing Group.
CORRESPONDENCE
This correlation is due to a few countries with high HIV prevalence and high GNP. The correlation disappears when the analysis is restricted to countries with GNPs lower than $1000 (n=32, Pearson correlation coefficient 0·04, p=0·82). These results show that there is no correlation between a low GNP and a high HIV antenatal HIV prevalence. In two of the countries with the largest GNP—Botswana and South Africa—two of the highest HIV prevalences, 43%, and 32·5% respectively, are reported. Although there may be reasons at the individual level that predispose the poor to HIV, interventions to raise GNP at the macro level might not reduce new HIV transmissions. Clearly, we must continue to seek to implement HIV prevention interventions that target people at highest risk of HIV as early as possible in the epidemic. Alleviation of poverty alone, however politically acceptable and justifiable, will divert attention away from biological risk factors such as male circumcision status and poor genital hygiene in core groups that may be the determining influences that drive high-prevalence HIV epidemics.2 Nigel O’Farrell Pasteur Suite, Infection and Immunity Unit, Genitourinary Medicine, Ealing Hospital, Southall, Middlesex UB1 3HW, UK 1 2
Butler C, HIV and AIDS, poverty, and causation. Lancet 2000; 356: 1445–46. O’Farrell N. Enhanced efficiency of female to male HIV transmission in core groups in developing countries: the need to target men. Sex Transm Dis 2001; 28: 84–91.
Vitamin K in anticoagulation therapy Sir—M Crowther and colleagues (Nov 4, p 1551)1 recommend routine use of low dose oral vitamin K to rapidly lower international normalised ratios (INR) of 4·5–10·0. Difficulties with warfarin coagulopathy are frequently encountered in patients treated with oral anticoagulation. For those with an INR above 10, there is agreement on vitamin K use because of the high risk of bleeding,2 but for the management of those receiving warfarin with INR value of 4·5–10·0 there are no recognised standards. Crowther and colleagues state that a symptomless moderate increase of INR is frequently associated with serious bleeding, and that low dose oral vitamin K does not raise the risk of thrombosis and is more effective than placebo for rapid lowering of raised INR values, as shown by their results.
THE LANCET • Vol 357 • February 24, 2001
For patients on warfarin with a symptomless increase in the INR to between 4·5 and 10, the difficulty is to rapidly lower the INR and keep it in the therapeutic range. We were concerned with the significantly higher number of patients in the vitamin K group who had INR values lower than 1·5. Crowther and colleagues do not discuss this point. During the 5 days after treatment was given, 13 of 141 patientdays in the placebo group and 24 of 121 in the vitamin K group were at this infra-therapeutic level. The investigators are reassuring about the absence of risks of thromboembolic events attributable to rapid lowering of the INR after vitamin K treatment. However, their study, which included a small number of patients (44 in the placebo group, 45 in the vitamin K group), was probably not powerful enough to detect an increase in the risk of thrombosis in patients whose INR fell to lower than 1·5. Moreover, they state that other studies that have shown that low dose vitamin K was safe were non-randomised, small, or did not use a clinically applicable protocol.3–5 Medical decisions should be individually based. The benefit of preventing serious bleeding has to be balanced with the individual’s risk of thrombosis induced by the excessive correction of the INR by low-dose oral vitamin K. For example, in a patient with distal vein thrombosis whose INR value is 9, the risk of serious bleeding justifies the use of oral low-dose vitamin K and outweighs the risk of thrombosis. In a patient with a mechanical heart valve whose INR is 5, however, thrombosis could lead to devastating disease and might not be outweighed by the risk of serious bleeding. These issues must be addressed before recommending low-dose oral vitamin K for any patients with a symptomless increase in the INR to between 4·5 and 10. Otherwise, clinicians may (correctly) continue not to reverse with vitamin K any moderate symptomless increase of the INR in all patients. *Thomas Hanslik, Cecile Viboud, Marie L Chadenat, Vincent Jubault, Jacques Prinseau *Service de Médecine Interne, CHU Ambroise Paré, Université Paris 5, Boulogne Billancourt, France; and Institut National de la Santé et de la Recherche Médicale, Unit 444, Université Paris. (e-mail: [email protected]) 1
2
Crowther MA, Julian J, McCarty D, et al. Treatment of warfarin-associated coagulopathy with oral vitamin K: a randomised controlled trial. Lancet 2000; 356: 1551–53. Hirsch J, Dalen JE. Anderson DR, et al. Oral anticoagulants; mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 1998; 114: 445S–69S.
3
4
5
Crowther MA, Donovan D, Harrison L, McGinnis J, Ginsberg J. Low-dose oral vitamin K reliably reverses overanticoagulation due to warfarin. Thromb Haemost 1998; 79: 1116–18. Pengo V, Banzato A, Garelli E, Zasso A, Biasiolo A. Reversal of excessive effects of regular anticoagulation: low dose of phytonadione (vitamin K) compared with warfarin discontinuation. Blood Coagul Fibrinolysis 1993; 4: 739–41. Weibert RT, Le DT, Kayser SR, Rapaport SI. Correction of excessive anticoagulation with low-dose oral vitamin K1. Ann Intern Med 1997; 126: 959–62.
Sir—We are concerned that M Crowther and colleagues1 should state so positively that their findings “. . . provide a strong case for the routine use of low-dose oral vitamin K in patients on warfarin with a symptomless increase in INR”. They do, of course, refer to a study by Hylek and colleagues2 to support their argument, but their own report contains several questionable features that cast serious doubt on the firmness of this conclusion. First, the defined primary endpoint was “a comparison of the proportion of patients in the two treatment groups with INR values of 1·8–3·2 on the day after receiving the study drug. What is the clinical relevance of this outcome? Why is it so important, especially since Crowther and colleagues report (table 2) that mean INR values of the two groups did not differ significantly by day 3? Second, any occurrence of the most relevant clinical endpoint—namely a new bleeding episode, was determined by follow-up by telephone or clinic visits. The researchers do not state what proportion of these episodes were ascertained by telephone and what steps they took to validate the patients’ reports of episodes of bleeding that were obtained in this way. In the intention-to-treat analysis the odds ratio for bleeding seems impressive at 0·187 in favour of vitamin K, but the CI are wide and the p value is only barely significant. The only major bleeding episode occurred in a patient who had been given vitamin K and whose INR, at the time of the haemorrhage, was 2·0. All other bleeding episodes were described as minor and occurred between 6 days and 3 months after administration of the study drug. Given that the INR values for the two groups became similar a mere 3 days after the giving of the study drug, these findings are confusing, as is the rather mysterious statement about the two thrombotic episodes noted. It seems to us that Crowther and colleagues’ confident statement is not justified by the evidence presented, and we would suggest that most physicians will wish to see further studies reported
637
For personal use only. Reproduce with permission from The Lancet Publishing Group.
number of elective caesarean sections might be partly contributing to the rise, since the rate of 20·3% is among the highest in more-developed countries. The findings of two Australian studies have strengthened the evidence pointing to women requesting caesarean section. More than 20% of women who had had caesarean sections in a large south Australian hospital said that they had insisted on or were keen to have this procedure.2 In Western Australia, in 633 women 27% of caesarean sections were done solely because of maternal request, even when vaginal birth was judged safe.3 We believe, however, that the issue of lowering rates might be more complicated than implied by Wagner. We did a study in a tertiary-referral hospital in South Australia. In a crosssectional survey of 15 staff specialists and medical specialists (response rate 75%), only 40% agreed that the optimum rate of caesarean section should be 15–20%. A third of these specialists did not know what the rate should be, a third stated that the current rate in Australia (20·3%) should be the optimum rate, and 13% said that the rate should be 20–30%. The lowering of caesarean-section rates needs more than reversing the marginalisation of midwives in maternity care, as Wagner argues. We have critically reviewed more than 25 studies done in many countries in the past decade, including randomised controlled trials, systematic reviews, and quasiexperimental studies. The lowering of caesarean-section rates proved difficult in all studies, but midwife-managed models of care, compared with standard care, did not reduce rates. One-to-one care from a support person during labour can, however, affect the rate of caesarean section.
Sir—We have some Greek data that support the views expressed by Marsden Wagner.1 We did two national perinatal surveys in 1983 and 1998, with 11 059 and 14 549 consecutive birth cohorts, respectively. The total caesarean section rate rose from 13% to 31% between surveys. Elective caesarean sections more than doubled (7% vs 15·5%), and the birthweight distribution curve shifted significantly to the left, with a loss of 100 g mean birthweight. Since the intrauterine weight gain by gestational week did not differ significantly between the two studies, we compared gestational age and birthweight for newborn babies delivered vaginally or by elective caesarean section. A third of those delivered by elective caesarean in 1998 were born at less than 38 weeks’ gestational age compared with 18% born after spontaneous delivery. In addition, 12% of neonates delivered by elective caesarean section had low birthweight (less than 2500 g) compared with 6% of those delivered spontaneously, whereas in 1983, the respective proportions were equal. Thus iatrogenic prematurity was fully confirmed in our data sets. The incidence of caesarean sections varied greatly between women of Greek origin and refugees (33% vs 24·5%), between private hospitals and public hospitals (39 vs 28%), and between urban centres and the suburbs (36 vs 26%). As Wagner points out, the better-off women receive less-safe care. *C Bakoula, N Matsaniotis First Department of Paediatrics, Hospital for Sick Children “Aghia Sophia”, Athens 115-27, Greece 1
*Ruth Walker, Eleni Golois, Deborah Turnbull, Chris Wilkinson
1 2
3
Wagner M. Choosing caesarean section. Lancet 2000; 356: 1677–80. Turnbull DA, Wilkinson C, Yaser A, Carty V, Svigos JM, Robinson JS. Women’s role and satisfaction in the decision to have a caesarean section. Med J Aust 1999; 170: 580–83. Quinlivan JA, Petersen RW, Nichols CN. Patient preference the leading indication for elective caesarean section in public patients: results of a 2-year prospective audit in a teaching hospital. Aust NZ J Obstet Gynaecol 1999; 174: 199–205.
636
Sir—International Development agencies and donors are increasingly adopting aid programmes directed towards poverty alleviation in subSaharan Africa. One of the goals of this policy is to reduce the prevalence of HIV. Colin Butler (Oct 21, p 1445)1 concludes that povety is a major underlying causal factor for the scale of the African AIDS epidemic, but the relation between HIV and poverty is complex and there is little evidence that poverty-reduction policies are likely to succeed. HIV prevalence and gross national product (GNP) vary substantially between countries throughout subSaharan Africa. To investigate the relation between HIV and GNP in the region, we gathered data for HIV antenatal prevalences in the capital or major city, obtained by accessing the US Bureau of the census website (www.census.gov/ipc/www/hiv1.html, accessed on 15 Jan, 2001). For GNP, data were obtained from the World Bank website org (www.worldbank. org/data/countrydata/adi/adi1-1.pdf, accessed on 15 Jan, 2001), which reports the GNP for 1998. Data for HIV prevalencies (range 0–43%) and GNP (range US$140–3600) were available from these sources for 40 countries. The years in which HIV prevalence studies were done were 1998–99 (21), 1996–97 (16), and 1993–94 (3). Data for both variables were not available for Cape Verde, Djibouli, Liberia, Niger, Sao Tome, Seychelles, Sierra Leone, and Somalia. A scatter plot of HIV prevalence in antinatal-clinic attenders and GNP is shown in the figure. There is a weak positive correlation between HIV prevalence and GNP (Pearson correlation coefficient 0·29, p=0·07).
4500 4000 GNP per caput 1998 (US$)
Departments of Public Health and General Practice, Psychology, and *General Practice and Psychology, Adelaide University, Adelaide, South Australia 5005, Australia; and Department of Obstetrics and Gynaecology, Women’s and Children’s Hospital, Adelaide (e-mail: [email protected])
Wagner M. Choosing caesarean section. Lancet 2000; 356: 1677–80.
Poverty and HIV in sub-Saharan Africa
3500 3000 2500 2000 1500 1000 500 0 0
10
20 30 HIV prevalence in ANC attenders (%)
40
50
Relation between GNP and HIV prevalence in antenatal-clinic (ANC) attenders in sub-Saharan Africa
THE LANCET • Vol 357 • February 24, 2001
For personal use only. Reproduce with permission from The Lancet Publishing Group.
CORRESPONDENCE
This correlation is due to a few countries with high HIV prevalence and high GNP. The correlation disappears when the analysis is restricted to countries with GNPs lower than $1000 (n=32, Pearson correlation coefficient 0·04, p=0·82). These results show that there is no correlation between a low GNP and a high HIV antenatal HIV prevalence. In two of the countries with the largest GNP—Botswana and South Africa—two of the highest HIV prevalences, 43%, and 32·5% respectively, are reported. Although there may be reasons at the individual level that predispose the poor to HIV, interventions to raise GNP at the macro level might not reduce new HIV transmissions. Clearly, we must continue to seek to implement HIV prevention interventions that target people at highest risk of HIV as early as possible in the epidemic. Alleviation of poverty alone, however politically acceptable and justifiable, will divert attention away from biological risk factors such as male circumcision status and poor genital hygiene in core groups that may be the determining influences that drive high-prevalence HIV epidemics.2 Nigel O’Farrell Pasteur Suite, Infection and Immunity Unit, Genitourinary Medicine, Ealing Hospital, Southall, Middlesex UB1 3HW, UK 1 2
Butler C, HIV and AIDS, poverty, and causation. Lancet 2000; 356: 1445–46. O’Farrell N. Enhanced efficiency of female to male HIV transmission in core groups in developing countries: the need to target men. Sex Transm Dis 2001; 28: 84–91.
Vitamin K in anticoagulation therapy Sir—M Crowther and colleagues (Nov 4, p 1551)1 recommend routine use of low dose oral vitamin K to rapidly lower international normalised ratios (INR) of 4·5–10·0. Difficulties with warfarin coagulopathy are frequently encountered in patients treated with oral anticoagulation. For those with an INR above 10, there is agreement on vitamin K use because of the high risk of bleeding,2 but for the management of those receiving warfarin with INR value of 4·5–10·0 there are no recognised standards. Crowther and colleagues state that a symptomless moderate increase of INR is frequently associated with serious bleeding, and that low dose oral vitamin K does not raise the risk of thrombosis and is more effective than placebo for rapid lowering of raised INR values, as shown by their results.
THE LANCET • Vol 357 • February 24, 2001
For patients on warfarin with a symptomless increase in the INR to between 4·5 and 10, the difficulty is to rapidly lower the INR and keep it in the therapeutic range. We were concerned with the significantly higher number of patients in the vitamin K group who had INR values lower than 1·5. Crowther and colleagues do not discuss this point. During the 5 days after treatment was given, 13 of 141 patientdays in the placebo group and 24 of 121 in the vitamin K group were at this infra-therapeutic level. The investigators are reassuring about the absence of risks of thromboembolic events attributable to rapid lowering of the INR after vitamin K treatment. However, their study, which included a small number of patients (44 in the placebo group, 45 in the vitamin K group), was probably not powerful enough to detect an increase in the risk of thrombosis in patients whose INR fell to lower than 1·5. Moreover, they state that other studies that have shown that low dose vitamin K was safe were non-randomised, small, or did not use a clinically applicable protocol.3–5 Medical decisions should be individually based. The benefit of preventing serious bleeding has to be balanced with the individual’s risk of thrombosis induced by the excessive correction of the INR by low-dose oral vitamin K. For example, in a patient with distal vein thrombosis whose INR value is 9, the risk of serious bleeding justifies the use of oral low-dose vitamin K and outweighs the risk of thrombosis. In a patient with a mechanical heart valve whose INR is 5, however, thrombosis could lead to devastating disease and might not be outweighed by the risk of serious bleeding. These issues must be addressed before recommending low-dose oral vitamin K for any patients with a symptomless increase in the INR to between 4·5 and 10. Otherwise, clinicians may (correctly) continue not to reverse with vitamin K any moderate symptomless increase of the INR in all patients. *Thomas Hanslik, Cecile Viboud, Marie L Chadenat, Vincent Jubault, Jacques Prinseau *Service de Médecine Interne, CHU Ambroise Paré, Université Paris 5, Boulogne Billancourt, France; and Institut National de la Santé et de la Recherche Médicale, Unit 444, Université Paris. (e-mail: [email protected]) 1
2
Crowther MA, Julian J, McCarty D, et al. Treatment of warfarin-associated coagulopathy with oral vitamin K: a randomised controlled trial. Lancet 2000; 356: 1551–53. Hirsch J, Dalen JE. Anderson DR, et al. Oral anticoagulants; mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 1998; 114: 445S–69S.
3
4
5
Crowther MA, Donovan D, Harrison L, McGinnis J, Ginsberg J. Low-dose oral vitamin K reliably reverses overanticoagulation due to warfarin. Thromb Haemost 1998; 79: 1116–18. Pengo V, Banzato A, Garelli E, Zasso A, Biasiolo A. Reversal of excessive effects of regular anticoagulation: low dose of phytonadione (vitamin K) compared with warfarin discontinuation. Blood Coagul Fibrinolysis 1993; 4: 739–41. Weibert RT, Le DT, Kayser SR, Rapaport SI. Correction of excessive anticoagulation with low-dose oral vitamin K1. Ann Intern Med 1997; 126: 959–62.
Sir—We are concerned that M Crowther and colleagues1 should state so positively that their findings “. . . provide a strong case for the routine use of low-dose oral vitamin K in patients on warfarin with a symptomless increase in INR”. They do, of course, refer to a study by Hylek and colleagues2 to support their argument, but their own report contains several questionable features that cast serious doubt on the firmness of this conclusion. First, the defined primary endpoint was “a comparison of the proportion of patients in the two treatment groups with INR values of 1·8–3·2 on the day after receiving the study drug. What is the clinical relevance of this outcome? Why is it so important, especially since Crowther and colleagues report (table 2) that mean INR values of the two groups did not differ significantly by day 3? Second, any occurrence of the most relevant clinical endpoint—namely a new bleeding episode, was determined by follow-up by telephone or clinic visits. The researchers do not state what proportion of these episodes were ascertained by telephone and what steps they took to validate the patients’ reports of episodes of bleeding that were obtained in this way. In the intention-to-treat analysis the odds ratio for bleeding seems impressive at 0·187 in favour of vitamin K, but the CI are wide and the p value is only barely significant. The only major bleeding episode occurred in a patient who had been given vitamin K and whose INR, at the time of the haemorrhage, was 2·0. All other bleeding episodes were described as minor and occurred between 6 days and 3 months after administration of the study drug. Given that the INR values for the two groups became similar a mere 3 days after the giving of the study drug, these findings are confusing, as is the rather mysterious statement about the two thrombotic episodes noted. It seems to us that Crowther and colleagues’ confident statement is not justified by the evidence presented, and we would suggest that most physicians will wish to see further studies reported
637
For personal use only. Reproduce with permission from The Lancet Publishing Group.