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Sleeping sickness in Zaire
T H E LANCET
Down’s syndrome screening with nuchal translucency SIR-Hacksaw and colleagues (Dec 21/28, p 1740)’ are concerned that screening for trisomy 21 by a combination of maternal age and fetal nuchal translucency might be introduced into routine practice before they do their own studies to assess this method and compare it with their quadruple test. Wald and colleagues measured inhibin-A in 77 samples (obtained 1973-83) from trisomy 2 1 pregnancies and 385 normal controls at 13-27 weeks of gestation. These samples had been used in previous studies and had undergone several freeze-thaw cycles. Wald and co-workers also measured inhibin in samples from 970 normal pregnancies in white women with known maternal weight, in whom gestation had been dated by ultrasound. On the basis of these data and with various statistical techniques they estimated that screening for trisomy 21 by a combination of maternal serum inhibin-A, a-fetoprotein, unconjugated oestriol, and human chorionic gonadotropin, after adjusting for maternal weight in pregnancies dated by ultrasound, could identify 79% of affected fetuses, for a false positive rate of 5%. They concluded that the fourmarker test is the most effective method of Down’s syndrome screening available for routine use. In a prospective continuing study involving 21 centres in the UIC, 83 327 singleton pregnancies with live fetuses at 10-14 weeks of gestation have been examined so far. The first 61 972 completed pregnancies included 208 with trisomy 21; with a cut-off risk of 1 in 300, estimated from the maternal age and degree of fetal nuchal translucency, the sensitivity for detection of trisomy 21 was 84%. On the basis of the maternal age distribution of our population and the maternal age-related prevalence of trisomy 21 in livebirths, it was estimated that 150 babies with trisomy 21 would have been liveborn but for antenatal screening.’ In reality there were only 26 (13%) live births with trisomy 21 and nine of these were in the screen-positive group (risk more than 1 in 300) but the parents chose not to have prenatal diagnosis or decided to continue with the pregnancy despite the prenatal diagnosis. In addition there were 16 screen-negative pregnancies with trisomy 21 diagnosed antenatally. Even if all these cases had resulted in livebirths had the pregnancies not been terminated, then the live-birth prevalence of trisomy 21 would still have been reduced by at least 78% (1 17 of 150).
438
Screening for chromosomal defects in the first, rather than second trimester, has the advantage of earlier diagnosis and less traumatic termination for couples who choose this option. A potential disadvantage is that earlier screening may preferentially identify those chromosomally abnormal pregnancies that are destined to miscarry. About 40% of affected fetuses die between 12 weeks of gestation and term.’ This issue of intrauterine lethality of chromosomal defects is of course a potential criticism of all methods of antenatal screening, including secondtrimester maternal serum biochemistry; the estimated rate of intrauterine lethality between 16 weeks and term is about 30%.’ *K H Nicolaides, N J Sebire, R J M Snijders Harris Bitthweight Research Centre for Fetal Medicine, Kings College School of Medicine and Denttstiy, London SE5 8RX, UK
Hacksaw AK, Wald NJ, Haddow JE. Down’s syndrome screening with nuchal translucency. Lancet 1996; 348: 1740. George L, Wald NJ, Densem JW, Muttukrishna S, Knight PG. Prenatal screening for Down’s syndrome using inhibin-A as a serum marker. Prenat Diag 1996; 16: 143-53. Snijders RJM, Sebire NJ, Nicolaides I=. Maternal age and gestational age specific risk for chromosomal defects. Fetal Diagn Ther 1995; 10: 356-67.
The rationale for a rapid (3-5 years) and lasting control of T b garnbiense sleeping sickness is a high participation rate, a widespread and judicious application of serological and more refined parasitological techniques, and a closely supervised effective treatment to enhance compliance and to reduce (drug induced) mortality-which is the main reason why the population refrains from participating in the sleeping sickness control surveys. Dirk van Hove Belgian Development Cooperation PO Box 81, Kigali, Rwanda
1 Ekwanzala M, Pepin J, I a o n d e N,
Molisho S , Bruneel H, de Wais P. In the heart of darkness: sleeping sickness in Zaire. Lancet 1996; 348: 1427-30. 2 Epidemiology and control of African trypanosomiasis: report of a WHO expert committee. Geneva: WHO Technical Report Series 1986: 739-67.
Emarceepy disease &-The evocative ballad by Marshall (Dec 21/28 p 1718)‘ prompts an educational comment on verse four: Besides inducing abject terror An MCQ can imprint error Mair Thornas 2 1 Park Avenue, Golders Green, London N W l l 7SL. UK
Sleeping sickness in Zaire SIR-Ekwanzala and colleagues (November 23, p 1427)’ point out that the only way to break the epidemiological chain of Tgpansoma bmcei gambiense transmission and to reduce the human reservoir is to identify patients through mass screening, and to treat symptom-free individuals-an approach that gave excellent results in Zaire during the first half of the century. Before field-adapted serological tests became available in 1976, mass screening was done by cervical gland palpation followed by classic parasitological techniques having somewhat low sensitivity.’ In my experience in southern Sudan (Lirangu, 1990) this method did not diagnose-and consequently left untreated-numerous symptom-free individuals; this may explain why it took three decades to break the chain of transmission and to reduce the total number of new cases in Zaire from 33 562 in 1930 to about 1000 in 1959. Although serodiagnostic field tests and treatment of symptom-free individuals, are useful, these strategies are unlikely to compensate for a very low (50%) participation rate of exposed populations in case-finding surveys.
1 Marshall S. Emarceepy disease. Lancet 1996; 348: 1718.
SIR-The poem “Emarceepy disease”’ and the accompanying cartoon about t$ paper on venous thrombosis in iambic pentameter are reminders of that other older disease that results from the frustration of physicians’ literary ambitions by the dry prose adopted for most scientific writing. This disease breaks out in more sporadic form. It was believed by all my student class, at the University of the Witwatersrand Medical School, that our professor of psychiatry had during his anatomy examinations composed and submitted all his essay answers in iambic pentameter, and that he had taken the prize in anatomy for his efforts. The anatomical poems were never produced in evidence and I am afraid it is too late now for him to enjoy this poem and cartoon, and to tell us finally whether his reasoning was indeed rhymed. Alan Wilkinson 200 UCLA Medical Plaza, Box 951693. Los Angeles, CA 90095, USA
1 Marshall S. Emarceepy disease. Lancet 1996; 348: 1718.
Vo1349 * February 8, 1997
Down’s syndrome screening with nuchal translucency SIR-Hacksaw and colleagues (Dec 21/28, p 1740)’ are concerned that screening for trisomy 21 by a combination of maternal age and fetal nuchal translucency might be introduced into routine practice before they do their own studies to assess this method and compare it with their quadruple test. Wald and colleagues measured inhibin-A in 77 samples (obtained 1973-83) from trisomy 2 1 pregnancies and 385 normal controls at 13-27 weeks of gestation. These samples had been used in previous studies and had undergone several freeze-thaw cycles. Wald and co-workers also measured inhibin in samples from 970 normal pregnancies in white women with known maternal weight, in whom gestation had been dated by ultrasound. On the basis of these data and with various statistical techniques they estimated that screening for trisomy 21 by a combination of maternal serum inhibin-A, a-fetoprotein, unconjugated oestriol, and human chorionic gonadotropin, after adjusting for maternal weight in pregnancies dated by ultrasound, could identify 79% of affected fetuses, for a false positive rate of 5%. They concluded that the fourmarker test is the most effective method of Down’s syndrome screening available for routine use. In a prospective continuing study involving 21 centres in the UIC, 83 327 singleton pregnancies with live fetuses at 10-14 weeks of gestation have been examined so far. The first 61 972 completed pregnancies included 208 with trisomy 21; with a cut-off risk of 1 in 300, estimated from the maternal age and degree of fetal nuchal translucency, the sensitivity for detection of trisomy 21 was 84%. On the basis of the maternal age distribution of our population and the maternal age-related prevalence of trisomy 21 in livebirths, it was estimated that 150 babies with trisomy 21 would have been liveborn but for antenatal screening.’ In reality there were only 26 (13%) live births with trisomy 21 and nine of these were in the screen-positive group (risk more than 1 in 300) but the parents chose not to have prenatal diagnosis or decided to continue with the pregnancy despite the prenatal diagnosis. In addition there were 16 screen-negative pregnancies with trisomy 21 diagnosed antenatally. Even if all these cases had resulted in livebirths had the pregnancies not been terminated, then the live-birth prevalence of trisomy 21 would still have been reduced by at least 78% (1 17 of 150).
438
Screening for chromosomal defects in the first, rather than second trimester, has the advantage of earlier diagnosis and less traumatic termination for couples who choose this option. A potential disadvantage is that earlier screening may preferentially identify those chromosomally abnormal pregnancies that are destined to miscarry. About 40% of affected fetuses die between 12 weeks of gestation and term.’ This issue of intrauterine lethality of chromosomal defects is of course a potential criticism of all methods of antenatal screening, including secondtrimester maternal serum biochemistry; the estimated rate of intrauterine lethality between 16 weeks and term is about 30%.’ *K H Nicolaides, N J Sebire, R J M Snijders Harris Bitthweight Research Centre for Fetal Medicine, Kings College School of Medicine and Denttstiy, London SE5 8RX, UK
Hacksaw AK, Wald NJ, Haddow JE. Down’s syndrome screening with nuchal translucency. Lancet 1996; 348: 1740. George L, Wald NJ, Densem JW, Muttukrishna S, Knight PG. Prenatal screening for Down’s syndrome using inhibin-A as a serum marker. Prenat Diag 1996; 16: 143-53. Snijders RJM, Sebire NJ, Nicolaides I=. Maternal age and gestational age specific risk for chromosomal defects. Fetal Diagn Ther 1995; 10: 356-67.
The rationale for a rapid (3-5 years) and lasting control of T b garnbiense sleeping sickness is a high participation rate, a widespread and judicious application of serological and more refined parasitological techniques, and a closely supervised effective treatment to enhance compliance and to reduce (drug induced) mortality-which is the main reason why the population refrains from participating in the sleeping sickness control surveys. Dirk van Hove Belgian Development Cooperation PO Box 81, Kigali, Rwanda
1 Ekwanzala M, Pepin J, I a o n d e N,
Molisho S , Bruneel H, de Wais P. In the heart of darkness: sleeping sickness in Zaire. Lancet 1996; 348: 1427-30. 2 Epidemiology and control of African trypanosomiasis: report of a WHO expert committee. Geneva: WHO Technical Report Series 1986: 739-67.
Emarceepy disease &-The evocative ballad by Marshall (Dec 21/28 p 1718)‘ prompts an educational comment on verse four: Besides inducing abject terror An MCQ can imprint error Mair Thornas 2 1 Park Avenue, Golders Green, London N W l l 7SL. UK
Sleeping sickness in Zaire SIR-Ekwanzala and colleagues (November 23, p 1427)’ point out that the only way to break the epidemiological chain of Tgpansoma bmcei gambiense transmission and to reduce the human reservoir is to identify patients through mass screening, and to treat symptom-free individuals-an approach that gave excellent results in Zaire during the first half of the century. Before field-adapted serological tests became available in 1976, mass screening was done by cervical gland palpation followed by classic parasitological techniques having somewhat low sensitivity.’ In my experience in southern Sudan (Lirangu, 1990) this method did not diagnose-and consequently left untreated-numerous symptom-free individuals; this may explain why it took three decades to break the chain of transmission and to reduce the total number of new cases in Zaire from 33 562 in 1930 to about 1000 in 1959. Although serodiagnostic field tests and treatment of symptom-free individuals, are useful, these strategies are unlikely to compensate for a very low (50%) participation rate of exposed populations in case-finding surveys.
1 Marshall S. Emarceepy disease. Lancet 1996; 348: 1718.
SIR-The poem “Emarceepy disease”’ and the accompanying cartoon about t$ paper on venous thrombosis in iambic pentameter are reminders of that other older disease that results from the frustration of physicians’ literary ambitions by the dry prose adopted for most scientific writing. This disease breaks out in more sporadic form. It was believed by all my student class, at the University of the Witwatersrand Medical School, that our professor of psychiatry had during his anatomy examinations composed and submitted all his essay answers in iambic pentameter, and that he had taken the prize in anatomy for his efforts. The anatomical poems were never produced in evidence and I am afraid it is too late now for him to enjoy this poem and cartoon, and to tell us finally whether his reasoning was indeed rhymed. Alan Wilkinson 200 UCLA Medical Plaza, Box 951693. Los Angeles, CA 90095, USA
1 Marshall S. Emarceepy disease. Lancet 1996; 348: 1718.
Vo1349 * February 8, 1997