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Interventions to Reduce the Impact of Birth Defects Impact of birth defects in developing countries can be reduced through a series of interventions and eventually a comprehensive pro- gram that encompasses prevention, education about reproductive health, diagnosis, treatment, and rehabilitation. Several interventions pre- sented in this chapter involve prevention of common birth defects and have been found to be affordable in even the poorest settings. These high priority interventions can be expanded as other health problems are resolved, as birth defects become a public health priority, and as additional resources become available. The health care provided to children and adults with birth defects should always be equitable with the care provided for other health conditions. In low-resource settings this may be very limited, but as the level of health care improves, the ability to diagnose and treat birth defects can be expanded and the quality of medical support for rehabilita- tion programs can be improved. Once health care has reduced infant mor- tality due to other causes, screening for genetic defects becomes cost-effec- tive and can further reduce the impact of birth defects. Although the number and severity of birth defects pose a challenge to countries with limited health resources, the process of reducing the impact of birth defects can be undertaken in three stages: 1. Introduction of low-cost preventive interventions. 2. Provision of improved treatment for children and adults with birth defects. 3. Introduction of screening to identify genetic birth defects that can be prevented or treated. 68
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INTERVENTIONS TO REDUCE THE IMPACT OF BIRTH DEFECTS 69 Developing countries have a wide range of priorities, capacities, and resources for health care services. Successful implementation of each inter- vention requires that it be matched to the local setting. At each stage of development, health care services also need national leadership and coordi- nation, surveillance to provide a sound evidence base for setting public health priorities, and monitoring of interventions to ensure their clinical- and cost-effectiveness. BASIC REPRODUCTIVE CARE Basic reproductive care, which includes family planning, and precon- ceptional, prenatal, and neonatal care, is the foundation for improving neonatal and infant mortality and reducing birth defects. As infant mortal- ity rates fall, birth rates tend to decline because parents become increasingly confident that the children they conceive will survive childhood. This trend is strongest where family planning is accessible and effective. Family Planning The primary goal of family planning is to provide couples with the knowledge they need to make well-informed decisions concerning whether, when, and under what circumstances to have children. Accomplishing this goal involves education and assistance in preventing unintended pregnan- cies. Planning for a family of the desired size and preventing additional births can substantially reduce the number of children born with birth defects simply by reducing the total number of births. In addition, couples who have an established genetic risk of producing children with birth de- fects can choose whether to have any (or more) children (WorId Health Organization, 19971. Preconceptional Care Maternal education, literacy, and overall socioeconomic status are pow- erful influences on the health of both mother and neonate (Bicego and Boerma, 1993; World Bank, 1993; Rao et al., 1996; van Ginneken et al., 19961. Where both the formal education and the health education of girls are limited, there is an especially acute need for preconceptional health care, which aims to ensure that women and their partners achieve an "op- timal state of physical and emotional health at the onset of pregnancy" (Wallace and Hurwitz, 19981. Preconceptional care identifies risk factors for adverse birth outcomes, including birth defects, and provides the means to minimize those risks.
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70 REDUCING THE IMPACT OF BIRTH DEFECTS Identification of risk factors involves the following assessments (Moos, 19941: · Medical . history to identify preexisting medical conditions, such as 1nsulin-dependent diabetes mellitus, epilepsy, and heart disease, that may pose a threat to the mother and the developing fetus; medications used by the mother; and exposure to rubella and other infectious diseases. · Family history to identify birth defects in close family members. · Reproductive history to identify risk factors that have contributed to previous poor pregnancy outcomes, some of which can be addressed through preconceptional and prenatal care. _ T . · . · 1 /~-1 . 1 . · . 1 · l~utrltlonal profile to Determine the overall nutritional status anu intake of micronutrients, such as iodine and folic acid. · Life-style profile to determine the potential for maternal exposure to infectious agents or recreational drugs such as alcohol. · Maternal occupation should be evaluated for potential teratogenic exposures. Preconceptional care advises on how to prevent certain birth defects that originate during the first weeks of pregnancy often before a mother realizes she is pregnant. At 2 to 8 weeks' gestation, when embryonic cells are dividing rapidly and organ systems and body parts are beginning to differentiate, the embryo is particularly vulnerable to teratogens (Moos, 19941. For example, folic acid supplementation (discussed later in the chap- ter) is only effective in preventing neural tube defects (NTDs) when con- sumed during the periconceptional period. Prenatal Care An early prenatal visit permits the identification and review of risk factors for the pregnancy and prenatal diagnosis if the fetus is at high risk of having a birth defect. As noted above, this is too late for certain preventive measures such as increasing dietary consumption of folic acid to avoid NTDs. Neonatal Care Where possible, neonatal care should include a complete physical ex- amination at birth (or prior to discharge for those born in a clinic or hospital) to diagnose detectable conditions. Early diagnosis followed by timely treatment can minimize some conditions and reduce disability. In- fants with birth defects should receive the best care locally available. This will vary with local resources, the prevalence of specific birth defects, and the cost and effectiveness of potential interventions (Christianson et al.,
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INTERVENTIONS TO REDUCE THE IMPACT OF BIRTH DEFECTS 71 2000; World Health Organization, 1985, l999b; Alwan and Modell, 19971. Low-cost rehabilitation may be less effective than prevention of birth de- fects, but it can reduce dependence and provide a better quality of life for affected individuals and their families. Recommendation 1. Basic reproductive health care services an essen- tial component of primary health care in all countries should be used to reduce the impact of birth defects by providing: · Effective family planning, · Education for couples on avoidable risks for birth defects, · Effective preconceptional and prenatal care and educational cam- paigns to stress the importance of such care, and · Neonatal care that permits the early detection and best care lo- cally available for management of birth defects. LOW-COST PREVENTIVE STRATEGIES These low-cost interventions to prevent birth defects have been found to be affordable in even the poorest settings. They address some important risk factors and involve family planning, public health campaigns, fortification of staple foods, maternal and child health, and infectious disease control. Discouraging Pregnancy in Women Over 35 The simplest means of preventing Down syndrome and other chromo- somal disorders such as trisomies 13 and 18 is to decrease the number of pregnancies among women older than 35 years. This is accomplished by making family planning widely available and providing information about what Down syndrome is and how it is caused (WorId Health Organization, 1997, 2000a). This strategy was shown to be effective in Europe between 1950 and 1975 when family planning programs were expanded and the birth prevalence of Down syndrome decreased from 2.5 to 1.0 per 1,000 live births (Modell and Kuliev, 19901. Recommendation 2. Women should be discouraged from reproducing after age 35 to minimize the risk of chromosomal birth defects such as Down syndrome. Folic Acid Fortification The predominant cause of NTDs is folate deficiency in the early weeks of pregnancy (Oakley, 1993~. Randomized controlled trials in Europe
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72 REDUCING THE IMPACT OF BIRTH DEFECTS showed that folic acid supplementation in early pregnancy reduced NTDs by 70 percent (MRC Vitamin Study Research Group, 1991) and 100 per- cent (Czeize! and Dudas, 19921. A randomized controlled trial from India was halted because of the ethical need to provide folic acid to all partici- pants once its effectiveness had been established. The findings of that study supported the conclusion that folic acid deficiency is the predominant cause of NTDs (Indian Council of Medical Research, 20001. In a large, non- randomized community intervention study in a high-prevalence area (4 to 5 NTDs per 1,000 births) of China, pregnant women received daily supple- ments of 400 micrograms of synthetic folic acid before and during the first 28 days of pregnancy. This prevented 85 percent of NTDs among pregnant women taking folic acid more than 80 percent of the time (Berry et al., 1999) (see Box 3-11. Although folic acid is present in leafy vegetables, legumes, and citrus fruits, it is unlikely that dietary advice alone can adequately increase con-
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INTERVENTIONS TO REDUCE THE IMPACT OF BIRTH DEFECTS 73 gumption of these foods by those at risk. The above studies led the United States to fortify cereal grains with synthetic folic acid to increase consump- tion of the nutrient by an average of 100 micrograms a day (Food and Drug Administration, 19961. Although this amount represents just one-quarter of the daily consumption recommended, it raised blood folate to levels that decreased NTDs by about 20 percent (Green, 2002; Oakley 2002a). The United Kingdom and Chile fortify at about twice the U.S. level. Since Chil- eans consume twice as much wheat as each of the other populations, the average woman in Chile is estimated to receive the recommended level of 400 micrograms of synthetic folic acid daily (Oakley, 2002a). Folic acid fortification is being introduced in several South and Central American countries, many of which already fortify wheat flour with other B vitamins. Folic acid is so inexpensive that the cost of the vitamin premixture hardly changes with its addition. In countries where folic acid fortification is not already under way, its cost is estimated at 0.1 percent of the total cost of flour. Fortification overcomes the logistical problems of supplementation in early pregnancy as well as taking a complete regimen. However, almost universal coverage for women of reproductive age is relatively inexpensive. Fortification is recommended at a level of 240 micrograms per 100 grams of a widely consumed staple food (Oakley, 2002b). Supplementation is useful where fortification is not possible or is below the recommended level (Committee on Medical Aspects of Food and Nutrition Policy, 20001. Recommendation 3. All women of reproductive age should routinely receive 400 micrograms of synthetic folic acid per day for the reduction of neural tube defects. This is best accomplished through fortification of widely consumed staple foods. Where fortification is not feasible or is incomplete, daily supplementation programs should be provided for women before and during pregnancy. Universal Salt Iodization The primary cause of iodine deficiency disorders (IDDs) is insufficient iodine in the diet. The adult requirement for iodine can be met with 100 to 150 micrograms daily, and an additional 50 micrograms daily during preg- nancy (Stanbury, 1998; World Health Organization, 20011. Correction of maternal iodine deficiency before conception is necessary to avoid adverse effects on the fetus. Measurement of urinary iodine is a convenient and reliable method for assessing iodine nutritional status in a community. This method is more accepted and considerably less expensive than the use of
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74 REDUCING THE IMPACT OF BIRTH DEFECTS thyroid-stimulating hormone or other thyroid hormone measurements (Dunn et al., 1994; World Health Organization, 20011. Iodine deficiency may be exacerbated by goitrogens, which interfere with the incorporation of iodine into thyroxine (Geelhoed, 19991. The effects of goitrogens can be mitigated by ensuring a more-than-adequate intake of iodine; avoiding consumption of thiocyanate-containing vegetable products such as cassava; and cooking potentially goitrogenic foods to reduce the goitrogen content (Bourdoux et al., 19821. Soaking foods is also effective in reducing the goitrogen level, but vitamin A and other nutrients are also lost in this process. Vitamin A deficiency can be addressed with dietary supplements (Vanderpas et al., 1993). Iodine, a volatile trace element, is more abundant in the sea than on land. Except in certain geological regions (Li et al., 1989), iodine has been largely depleted from world soils (McClendon, 19391. Plants do not require iodine for healthy growth, and the amount of iodine in plants and animals generally reflects the low levels in soil. Thus to prevent iodine deficiency, most populations need supplementation (Hetze! and Maberly, 19861. The accepted strategy for eliminating iodine deficiency is universal salt iodization (Stanbury, 1998), which is among the most cost-effective health interventions (WorId Bank, 19931. However, since this estimate does not encompass an assessment of the full impact of IDDs, the actual cost is likely to be lower (WorId Health Organization, United Nations Children's Fund, International Council for the Control of Iodine Deficiency Disorders, 19991. The customary level of fortification is 25-50 milligrams of iodine per kilo- gram of salt (WorId Health Organization, 1996b). The fortified salt prod- uct costs only slightly more ($0.02-$0.06 per person annually) than the unfortified product. In populations with endemic cretinism and IDDs, iodized oil has been administered to entire populations as an emergency prophylactic and thera- peutic (Delange, 1996; Geelhoed, 19991. In a Central African population in remote Congo, for example, an intramuscular injection of iodized oil was found to control goiter and cretinism and protect iodine stores for a period of 1 to 5 years, which reduces concerns about compliance (Geelhoed, 19991. Iodization of drinking water and bread has also been shown to provide a safe and cost-effective alternative in some settings (EInager et al., 19971. National leaders at the 1990 World Summit for Children set the goal of virtually eliminating this deficiency by the year 2000. In 1990, less than 20 percent of household salt was iodized, and more than one- third of the worId's population was recognized as having inadequate dietary iodine. By 2002, more than 70 percent of household salt worId- wide was iodized. Annually, this supplementation protects about 85 million infants, but another 35 million infants remain unprotected (Ramalingaswami, 20001. Figure 3-1 shows the percentage of house-
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75 i; :l If . - A ~ —-~t \1. - ~ ~ E ~ ~ ° ~ i o — UD g ~ Ct to to do '>-a .m to to Ct O IL ~ Z O >, Ct U. . o . o 1 U. ~ . 5- Ct O O O ~ as U. ~ O ~ U. U. O - O ~ O O C;, 5- ~ · ~ .= .. V O ~ U)
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76 REDUCING THE IMPACT OF BIRTH DEFECTS holds worldwide that use iodized salt, and efforts are under way to reach those households by 2005. The rapid progress of the last decade has demonstrated the effective- ness of national "ownership" of the challenge (Ramalingaswami, 2000) and close collaboration among public, private, civic, and scientific groups to support the production of good-quality iodized salt, the delivery of only iodized salt, persistent market outreach to all parts of the country, periodic advocacy to sustain political commitment, and continued education to sus- tain public demand. Recommendation 4. A program of universal fortification of salt with 25-50 milligrams of iodine per kilogram of salt used for human and animal consumption should be adopted to prevent iodine deficiency disorders. Immunization Against Rubella Rubella infections are common worldwide and are strongly teratoge- nic. Vaccination programs in several, mostly developed, countries prevent virtually all cases of congenital rubella. Some countries have immunized all young children, some have immunized prepubescent females, and some have used a combined approach with measles-mumps-rubella (MMR) vaccine (Immunization Working Group, 2000; Massad et al., 19951. By 1996, 78 countries worldwide reported national rubella vaccination pro- grams. Included among these were 43 percent of Latin American, 12 per- cent of Eastern Mediterranean, 5 percent of South East Asian, and 11 percent of the Western Pacific populations. Notably absent were African countries (Robertson et al., 19971. The decision to introduce rubella vaccination into a country or region should be based on the susceptibility of women of childbearing age, the burden of disease due to congenital rubella syndrome (CRS), the strength of the measles immunization program, the infrastructure and resources for immunization, the record of injection safety, and other priority uses for limited health resources (WorId Health Organization, 2000b). In countries where more than 80 percent of the population is immunized for other childhood diseases, rubella should be included in the immunization pro- gram. In countries where immunization coverage is lower than 80 percent, overall coverage should be increased before introducing rubella immuniza- tion because vaccination can interrupt natural transmission during child- hood and actually increase the number of women who are not immune (Banatvala, 19981. A vaccination strategy developed and implemented in Brazil was able to eliminate CRS in 2 years (see Box 3-21.
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INTERVENTIONS TO REDUCE THE IMPACT OF BIRTH DEFECTS 77 The most rapid reduction in CRS has been achieved with mass cam- paigns for all women of childbearing age. Checking for rubella antibodies before conception allows those who test negative to be immunized and those who test positive to be reassured. The benefits are considerable, while the main risk is the inappropriate reassurance of women who have false- positive tests (Tookey et al., 19911. All evidence indicates that rubella virus vaccine does not pose a risk to the fetus, so prior screening for pregnancy is unnecessary (Tosefson, 2001; World Health Organization, 2000b). Vacci- nation of women of childbearing age against rubella has been shown to have a benefit-to-cost ratio of 11 to 1 in the United States (Hatziandreu et al., 1994) and a benefit-to-cost ratio of more than 1 in several developing- country studies (Hinman et al., 20021. Eradication of rubella is feasible because it infects only humans and the vaccine is highly immunogenic, highly protective, affordable in all but the poorest countries, and can be administered in conjunction with measles and rubella vaccines and as part of a standard immunization schedule at 9 months of age (Plotkin et al., 19991. Eradicating rubella has not, however, been recognized as a priority in low-income countries (Banatvala, 19981. Combining rubella and measles vaccines can significantly reduce the cost of rubella immunization (Cutts and Vynnycky, 19991. In Latin America and the Caribbean, for example, 20,000 or more infants are born with CRS each year, yet a one-time mass immunization of all females aged 5 to 39 years could control both rubella and CRS (Hinman et al., 19981. Surveillance of rubella and CRS following an eradication campaigns can be a challenge as rubella is often unreported and sometimes asymptom-
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78 REDUCING THE IMPACT OF BIRTH DEFECTS atic. Rubella epidemics are monitored using immunoglobulin M (IgM) test- ing in serum and saliva samples (Perry et al., 19931. Simple hearing tests for infants would improve case ascertainment (Plotkin et al, 1999), while test- ing all infants with microcephaly, developmental delay, hearing loss, mi- crophthalmia, congenital cataracts, and congenital heart disease would cap- ture a more complete estimate of CRS incidence. Recommendation 5. Women should be vaccinated against rubella before they reach reproductive age to prevent congenital rubella syndrome. Preventing Other Congenital Infections Primary prevention of maternal infection with herpes simplex virus and Toxoplasma gondlii is the only way to prevent mother-to-child transmission of these agents. Herpes simplex virus (HSV) Where possible and safe, pregnant women with active genital herpes lesions at the time of delivery should deliver by cesarean section to decrease the risk of neonatal HSV. The risk is decreased to less than 10 percent if performed prior to the rupture of membranes (Nahmias and Schwahn, 19851. Toxoplasmosis Pregnant women can avoid exposure to Toxoplasma gondii by washing their hands after handling raw meat, cooking meat until well done, and avoiding contact with cat feces and soil, insects, or other material contami- nated with cat feces (Essawy et al., 19901. Limiting Alcohol Consumption Alcohol consumption during pregnancy causes fetal alcohol syndrome, which is the most common preventable cause of mental retardation (Vi~joen, 19991. A safe level of maternal alcohol use has not been established. The teratogenic risk of maternal binge drinking during pregnancy is uncertain, but studies suggest that a single heavy binge at a critical period of embry- onic development can damage the fetus (Gladstone et al., 19961. Since the earliest weeks of pregnancy are critical for central nervous system develop- ment, all women should be strongly advised to avoid (Institute of Medicine, 1996) or minimize alcohol consumption before conception as well as dur-
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INTER VENTIONS TO RED UCE THE IMPA CT OF BIR TH DEFE CTS 1 1 1 · Data on causes of death, · Documentation of birth defects using standardized protocols for diagnosis, and · Ongoing monitoring of the common birth defects in a country or region. Many organizations and parts of government can contribute to the strengthening of health care in developing countries. National leadership
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2 REDUCING THE IMPACT OF BIRTH DEFECTS and coordination of these organizations and capabilities can vastly improve the quality and equity of health care, including reproductive health care and care of birth defects. Recommendation 14. Each country should develop a strategy to reduce the impact of birth defects, a framework of activities by which this can be accomplished, and the commitment of health leaders to accomplish these goals. National programs of basic reproductive health should collect and in- terpret surveillance data, set uniform standards for the training and perfor- mance of health care providers, and foster communication among health care providers, researchers, and policy makers. Recommendation 15. Each country should strengthen its public health capacity for recognizing and implementing interventions that have proven effective in reducing the impact of birth defects. This includes monitoring and tuning interventions for clinical- and cost-effectiveness in the local setting. CONCLUSION Despite the existence of low-cost interventions for preventing and treat- ing a number of birth defects, the human, economic, and social burdens associated with these conditions remain high. Obstacles to improving care for birth defects include financial constraints; lack of knowledge on the part of health care workers; poor access to medical facilities; and issues sur- rounding ethnicity, language, religion, and culture. Governments must be educated on the cost-effectiveness of reducing the impact of birth defects through proven methods of prevention and care, which can be adapted to local resources and needs. Providing the best possible care for patients with birth defects begins with the recognition that such care may require signifi- cant financial commitment and that the care that can be provided will vary with the setting(WorI3 Health Organization, 1985, 1997, l999;Carey, 19921. Robust programs of basic reproductive health care and public health campaigns provide a framework for new efforts to reduce the impact of birth defects. Reducing the impact of birth defects in developing countries can be approached through a three-stage process. The first stage of the process involves low-cost interventions to prevent specific birth defects. The second stage addresses improved treatment and rehabilitation for those with birth defects. Although generally more costly than the first stage pre-
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INTER VENTIONS TO RED UCE THE IMPA CT OF BIR TH DEFE CTS 1 1 3 ventive interventions, reducing the disease burden for those with birth de- fects, is key to providing equitable health care as these individuals can suffer from both the burden of disease and an associated burden of lost social and economic opportunity. The third stage is important for countries with comprehensive systems of basic reproductive health care and lower IMRs. The screening and diagnosis of genetic disorders can further reduce infant mortality when they are tailored to national health priorities and address common and severe birth defects that can be accurately detected and effectively prevented or managed. Counseling, with the goal of en- abling individuals to make free and informed health care decisions, is an essential part of screening and diagnostic programs. REFERENCES Adab N. Winterbottom J. Tudur C, Williamson PR. 2001. Common antiepileptic drugs in pregnancy in women with epilepsy. Cochrane Database of Systematic Reviews (2):1-14. Akinyanju OO. 1989. A profile of sickle cell disease in Nigeria. Annals of the New York Academy of Sciences 565:126-136. Alexander M, Ackman JD, Kuo KN. 1999. Congenital idiopathic clubfoot. Orthopaedic Nursing 18(4):47-55; quiz 56-58. Alwan AA, Modell B. 1997. Community control of genetic and congenital disorders. Techni- cal publication series, No 24. Alexandria, Egypt: World Health Organization Regional Office for the Eastern Mediterranean. Angastiniotis M, Kyriakidou S. Hadjiminas M. 1988. The Cyprus Thalassemia Control Pro- gram. Birth Defects Original Article Series 23(5B):417-432. Angastiniotis M, Modell B. Englezos P. Boulyjenkov V. 1995. Prevention and control of haemoglobinopathies. Bulletin of the VDorld Health Organization 73(3):375-386. Baird PA. 1999. Prenatal screening and the reduction of birth defects in populations. Commu- nity Genetics 2(1) :9-17. Balgir RS, Murmu B. Dash BP. 1999. Hereditary hemolytic disorders among the Ashram school children in Mayurbhanj district of Orissa. Journal of the Association of Physi- cians of India 47(10) :987-990. Banatvala JE. 1998. Rubella—could do better. Lancet 351(9106):849-850. Bender PL. 2000. Genetics of cleft lip and palate. Journal of Pediatric Nursing 15(4):242- 249. Berry RJ, Li Z. Erickson JD, Li S. Moore CA, Wang H. Mulinare J. Zhao P. Wong LC, Gindler J. Hong S. Correa A. 1999. Prevention of neural-tube defects with folic acid in China. New England Journal of Medicine 341(20):1485-1490. Beutler E. 1994. Glucose-6-phosphate dehydrogenase deficiency. Blood 84(11):3613-3636. Bicego GT, Boerma JT. 1993. Maternal education and child survival: A comparative study of survey data from 17 countries. Social Science and Medicine 36(9) :1207-1227. Biesecker, BB. 2001. Goals of genetic counseling. Clinical Genetics 60(5):323-330. Bourdoux P. Seghers P. Mafuta M, Vanderpas J. Vanderpas-Rivera M, Delange F. Ermans AM. 1982. Cassava products: HCN content and detoxification processes. In DeLange F. Iteae FB, Ermans EM (eds.). Nutritional Factors Involved in the Goitrogenic Action of Cassava. Ottawa: International Development Research Center. P. 51. Cao A, Rosatelli C, Pirastu M, Galanello, R. 1991. Thalassemias in Sardinia: Molecular pathology, phenology, phenotype-genotoype correlation, and prevention. American Jour- nal of Pediatrica Hematology/Oncology 13(2):179-188.
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114 REDUCING THE IMPACT OF BIRTH DEFECTS Cao A, Rosatelli MC, Galanello R. 1996. Control of beta-thalassaemia by carrier screening, genetic counselling and prenatal diagnosis: The Sardinian experience. Ciba Foundation study group 197:137-151; discussion 151-155. Carey JC. 1992. Health supervision and anticipatory guidance for children with genetic disor- ders (including specific recommendations for trisomy 21, trisomy 18, and neurofibroma- tosis I). Pediatric Clinics in North America 39(1):25-53. Cartmill TB, DuShane JW, McGoon DC, Kirklin JW. 1966. Results of repair of ventricular septal defect. Journal of Thoracic and Cardiovascular Surgery 52(4):486-501. Chapados C. 2000. Experience of teenagers born with cleft lip and/or palate and interven- tions of the health nurse. Issues in Comprehensive Pediatric Nursing 23(1):27-38. Charache S. Terrin ML, Moore RD, Dover GJ, Barton FB, Eckert SV, McMahon RP, Bonds DR. 1995. Effect of hydroxyurea on the frequency of painful crises in sickle cell anemia. Investigators of the Multicenter Study of Hydroxyurea in Sickle Cell Anemia. New England Journal of Medicine 332(20) :1317-1322. Chatterjea JB. 1966. Haemoglobinopathies, glucose-6-phosphate dehydrogenase deficiency and allied problems in the Indian subcontinent. Bulletin of the VDorld Health Organiza- tion 35(6):837-856. Chidyausiku S. Munandi J. Marasha M, Mbazo D, Mhuri F. Oppelstrup H. Nleya C. 1998. Community-based Rehabilitation Programme in Zimbabme. Sida Evaluation 98/15, De- partment for Democracy and Social Development. Stockholm, Sweden: Sida. Christianson AL. 2000. Medical genetics in primary health care. Indian Journal of Pediatrics 67(11):831-835. Christianson AL, Kromberg JR. 1996. Maternal non-recognition of Down syndrome in black South African infants. Clinical Genetics 49(3):141-144. Christianson AL, Mitchell LE. 1996. Familial recurrence-pattern analysis of non-syndromic isolated cleft palate a Danish registry study. American Journal of Medical Genetics 58(1):182-190. Christianson AL, Venter PA, Modiba JH, Nelson MM. 2000. Development of a primary health care clinical genetic service in rural South Africa the Northern Province Experi- ence, 1990-1996. Community Genetics 3(2):77-84. Cockell A, Lees M. 2000. Prenatal diagnosis and management of orofacial clefts. Prenatal Diagnosis 20(2):149-151. Cohen AJ, Tamir A, Houri S. Abegaz B. Gilad E, Omohkidion S. Zabeeda D, Khazin V, Ciubotaru A, Schachner A. 2001. Save a child's heart: We can and we should. The Annals of Thoracic Surgery 71(2):462-468. Committee on Medical Aspects of Food and Nutrition Policy. 2000. Folic acid and the pre- vention of disease. Reports on Health and Social Subjects 50:1-101. Cuckle HS, Wald N. 2000. Principles of screening: Tests using single markers. In Wald N. Leck I (eds.). Antenatal and Neonatal Screening, 2nd edition. New York: Oxford Uni- versity Press. Pp. 274, 473, 510. Cunningham G. 2000. Phenylketonuria and other inherited metabolic defects. In Wald N. Leck I (eds.). Antenatal and Neonatal Screening, 2nd edition. New York: Oxford Uni- versity Press. Pp. 353-369. Cutts FT, Vynnycky E. 1999. Modelling the incidence of congenital rubella syndrome in developing countries. International Journal of Epidemiology 28 (6) :1176-1184. Czeizel AK, Dudas I. 1992. Prevention of the first occurrence of neural-tube defects by periconceptional vitamin supplementation. New England Journal of Medicine 327(26): 1832-1835. Czeizel AK, Hirschberg J. 1997. Orofacial clefts in Hungary. Epidemiological and genetic data, primary prevention. Folia phoniatrica et logopaedica 49(3-4):111-116. Davies S. Oluhohungbe A. 2002. Hydroxyurea for sickle cell disease. Cochrane Database of Systematic Reviews, Issue 4.
OCR for page 115
INTER VENTI ONS TO RED UCE THE IMPA CT OF BIR TH DEFE CTS 1 1 5 De Azevedo Neto RS, Silveira AS, Nokes DJ, Yang HM, Passos SD, Cardoso MR, Massad E. 1994. Rubella seroepidemiology in a non-immunized population in Sao Paulo, Brazil. E pidemiology and Infection 113 (1): 161-173. Delange F. 1996. Administration of iodized oil during pregnancy: A summary of the pub- lished evidence. Bulletin of tI7e World HealtI7 Organization 74(1):101-108. Dunn JT. 1994. Societal implications of iodine deficiency and the value of its prevention. In Stanbury JB (ed.). TI7e Damaged Brain of Iodine Deficiency. New York: Cognizant Communications. Pp. 309-314. Durkin MS, Khan NZ, Davidson LL, Huq S. Munir S. Rasul I, Zaman SS. 2000. Prenatal and postnatal risk factors for mental retardation among children in Bangladesh. American Journal of Epidemiology 152(11):1024-1033. Elnager B. Eltom M, Karlsson FA, Bourdoux PP, Gebre-Mehdin M. 1997. Control of iodine deficiency using iodination of water in a goiter endemic area. International Journal of Food Sciences and Nutrition 48(2):119-127. Essawy M, Khashaba A, Magda A, el-Kholy M, Elmeya S. Samy G. 1990. Study of congenital toxoplasmosis in Egyptian newborns. Journal of tI7e Egyptian Public HealtI7 Association 65(5-6):669. Eyre-Brook AL. 1986. An appropriate approach to orthopaedics in developing countries. International OrtI7opedics 10(1):5-10. Frossard PM, Lestringant G. Girodon E, Goossens M, Dawson KP. 1999. Determination of the prevalence of cystic fibrosis in the United Arab Emirates by genetic carrier screening. Clinical Genetics 55(6):496. Geelhoed GW. 1999. Metabolic maladaptation: Individual and social consequences of medi- cal intervention in correcting endemic hypothyroidism. Nutrition 14(11-12):908-932. Gladstone J. Nulman I, Koren G. 1996. Reproductive risks of binge drinking during preg- nancy. Reproductive Toxicology 10(1):3-13. Gosden C, Tabor A, Leck I, Grant A, Alfirevic Z. Wald N. 2000. Amniocentesis and chori- onic villus sampling. In Wald N. Leck I (eds.). Antenatal and Neonatal Screening, 2nd edition. New York: Oxford University Press. Pp. 470-516. Granda H. Gispert S. Dorticos A, Martin M, Cuadras Y. Calvo M, Martinez G. Zayas MA, Oliva JA, Heredero L. 1991. Cuban programme for prevention of sickle cell disease. Lancet 337(8734):152-153. Green NS. 2002. Folic acid supplementation and prevention of birth defects. Journal of Nutrition 132(8 suppl):2356S-2360S. Groce NE. 1999. Disability in cross-cultural perspective: Rethinking disability. Lancet 354(9180):756-757. Grody WW, Cutting GR, Klinger KW, Richards CS, Watson MS, Desnick RJ. 2001. Labora- tory standards and guidelines for population-based cystic fibrosis carrier screening. Ge- netics in Medicine 3(2):149-154. Haddad E. 1990. VDorld Declaration Education for All. Paris: United Nations Educational, Scientific and Cultural Organization. Haddow JE, Bradley LA, Palomaki GE, Doherty RA, Berhardt BA, Brock DJ, Cheuvront B. Cunningham GC, Donnenfeld AK, Erickson JL, Erlich HA, Ferrie RM, FitzSimmons SC, Greene MF, Grody WW, Haddow PK, Harris H. Holmes LB, Howell, RR, Katz M, Klinger KW, Kloza EM, LeFevre ML, Little S. Loeben G. McGovern M, Pyeritz RE, Rowley PT, Saiki RK, Short MP, Tabone J. Wald NJ, Wilker NL, Witt DR. 1999. Issues in implementing prenatal screening for cystic fibrosis: Results of a working conference. Genetics in Medicine 1 (4): 129-135. Hadidi H. 1974. Management of congenital talipes equinovarus. OrtI7opedic Clinics of NortI7 America 5(1):53-58.
OCR for page 116
116 REDUCING THE IMPACT OF BIRTH DEFECTS Handin RI. 1998. Disorders of coagulation and thrombosis. In Fauci AS, Eugene B. Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser SL, Longo DL (eds.). Harrison's Prin- ciples of Internal Medicine, 14th edition. Vol. 1. New York: McGraw-Hill. Pp. 737- 738. Hardman J. Goodman A, Gilman L, Limbird L. 1996. Goodman and Gilman's: The Pharma- cological Basis of Therapeutics, 9th edition. New York: McGraw-Hill Professional. Hatziandreu EJ, Brown RE, Halpern MT. 1994. A Cost Benefit Analysis of the Measles- Mumps-Rubella (MMR) Vaccine: Final Report. Arlington, VA: Battelle. Helander E, Mendis P. Nelson G. 1989. Training Disabled People in the Community. Geneva: World Health Organization. Heredero L. 1992. Comprehensive national genetic program in a developing country Cuba. Birth Defects Original Article Series 28 (3) :52-57. Hetzel BS, Maberly GF. 1986. Iodine. In Mertz (ed.). Trace Elements in Human and Animal Nutrition 2:139-208. Hill K. 1999. Levels and trends in perinatal and neonatal mortality in developing countries. In Reducing Perinatal and Neonatal Mortality: Report of a Meeting. Baltimore, Maryland. May 10-12, 1999. Hinman AR, Hersh BS, de Quadros CA. 1998. Rational use of rubella vaccine for prevention of congenital rubella syndrome in the Americas. Pan American Journal of Public Health 4(3):156-160. Hinman AR, Irons B. Lewis M, Kandola K. 2002. Economic analyses of rubella and rubella vaccines: A global review. Bulletin of the VDorld Health Organization 80(4):264-270. Hitzeroth HW, Niehaus CE, Brill DC. 1995. Phenylketonuria in South Africa. A report on the status quo. South African MedicalJournal 85(1):33-36. Hogge JS, Hogge WA. 1996. Preconception genetic counseling. Clinical Obstetrics and Gyne- cology 39(4):751-762. House H. McAlister M, Naidoo C. 1990. Zimbabme Steps Akead. Nottingham, UK: Catholic Institute for International Relations. immunization Working Group of the Mexico-United States Binational Commission. 2000. Measles, rubella, and congenital rubella syndrome United States and Mexico, 1997- 1999. Morbidity and Mortality VDeekly Report 49(46):1048-1050, 1059. International Labor Organization, United Nations Educational, Scientific and Cultural Orga- nization, World Health Organization (ILO, UNESCO, WHO). 1994. Community Based Rehabilitation for and with People with Disabilities. Joint Position Paper. Geneva: World Health Organization. Institute of Medicine (IOM). 1996. Fetal Alcobol Syndrome: Diagnosis, Epidemiology, Pre- vention, and Treatment. Washington, DC: National Academy Press. Jaovisidha A, Ajjimarkorn S. Panburana P. Somboonsub O. Berabutya Y. Rungsiprakarn R. 2000. Prevention and control of thalassemia in Ramathibodi Hospital, Thailand. South- east Asian Journal of Tropical Medicine and Public Health 31(3):561-565. Jellis J. 1988. Taking orthopaedics to the people. Baillie're's Clinical and Tropical Medicine Community Discussion 3:257-263. Jenkins T. 1990. Medical genetics in South Africa. Journal of Medical Genetics 27(12):760- 779. J lonsson T. 1994. OMAR in rehabilitation: A Guide on Operations Monitoring and Results. UNDP Interregional Programme for Disabled People. Geneva: United Nations Develop- ment Program. Josefson D. 2001. Rubella vaccine may be safe in early pregnancy. British Medical Journal 322(7288):695. Kale JS. 1999. Haemophilia: Scope for rehabilitation in India. Journal of Postgraduate Medi- cine 45(4):127.
OCR for page 117
INTERVENTIONS TO REDUCE THE IMPACT OF BIRTH DEFECTS 117 Kaneko S. Battino D, Andermann E, Wada K, Kan R. Takeda A, Nakane Y. Ogawa Y. Avanzini G. Fumarola C, Granata T. Molteni F. Pardi G. Minotti L, Canger R. Dansky L, Oguni M, Lopes-Cendas I, Sherwin A, Andermann F. Seni MH, Okada M, Teranishi T. 1999. Congenital malformations due to antiepileptic drugs. Epilepsy Research 33(2- 3):145-158. Kate SL. 2001. Health problems of tribal population groups from the state of Maharashtra. Indian Journal of Medical Sciences 55(2):99-108. Kavakli K, Nisli G. Aydinok Y. Oztop S. Cetingul N. Aydogdu S. Yalman O. 1997. Prophy- lactic therapy for hemophilia in a developing country, Turkey. Pediatric Hematology and Oncology 14(2):151-152, 158. Keskin A, Turk T. Polat A, Koyuncu H. Saracoglu B. 2000. Premarital screening of beta- thalassemia trait in the province of Denizli, Turkey. Acta Haematology 104(1):31-33. Kim NH, Park BM, Lee HM. 1990. Congenital dislocation of the hip a long-term follow-up in Korea. Yonsei Medical Journal 3 1 (2 ): 1 34-1 43. King RA, Hearing VJ, Creel DJ, Oetting WS. 1996. Abnormalities of pigmentation. In Emery AEH, Rimoin DL (eds.). Emery and Rimoin's Principles and Practice of Medical Genet- ics. New York: Churchill Livingstone. Pp. 1193-1194. Kirklin JW, Barrat-Boyes BG (eds.). 1993. Coarctation of the Aorta, and Interrupted Aortic Arch. Cardiac Surgery, 2nd edition. Vol. 2. New York: Churchill Livingstone. P. 1274. Koren A, Segal-Kupershmit D, Zalman L, Levin C, Abu Hana M, Palmor H. Luder A, Attias D. 1999. Effect of hydroxyurea in sickle cell anemia and sickle cell beta-thalassemia. Pediatric Hematology and Oncology 16(3):221-232. Kromberg J. 1992. Albinism in the South African negro: IV. Attitudes and the death myth. Birth Defects Original Article Series 28 (1) :159-166. Kyzer S. 1991. Congenital idiopathic clubfoot. Orthopaedic Nursing 10(4):11-18. Leck I. 2000. Congenital dislocation of the hip. In Wald N. Leck I (eds.). 2000. Antenatal and Neonatal Screening, 2nd edition. New York: Oxford University Press. Pp. 398-424. Lees CM, Davies S. Dezateux C. 2000. Neonatal screening for sickle cell disease. Cochrane Database System Review (2):CD0001913. Li M, Qian QD, Qu CY, Liu DR, Zhang CD, Jia QZ, Wang HX, Zhang PY, Eastman CJ, Boyages SC, Maberly GF. 1989. A Survey of inland iodine excess goiter in Taiyuan suburbs and its immunological changes. Journal of Chinese Endocrinology and Metabo- lism 5:75-76. Loukopoulos D. 1996. Current status of thalassemia and the sickle cell syndromes in Greece. Seminars in Hematology 33(1):76-86. Lugovska R. Vevere P. Andrusaite R. Kornejeva A. 1999. Newborn screening for PKU and congenital hypothyroidism in Latvia. Southeast Asian Journal of Tropical Medicine and Public Health 30(suppl 2):52-53. Lund PM. 1998. Living with albinism: A study of affected adults in Zimbabwe. Journal of Social Biology and Human Affairs 63:3-10. Lund PM. 2001. Health and education of children with albinism in Zimbabwe. Health Edu- cation and Research 1 6( 1 ): 1-7. Macri CN, de Gentile AS, Manterola A, Tomezzoli S. Reis FC, Garcia IL, Fernandez JLL. 1991. Epidemiology of cystic fibrosis in Latin America: Preliminary communication. Pediatric Pulmonology 10(4):250. Mahashur AA. 1993. Cystic fibrosis. Journal of Association of Physicians of India 41(2):71- 72. Mariga L, Phachaka L. 1993. Integrating Children with Special Education Needs into Regu- lar Schools in Lesotho. Report of a Feasibility Study. Lesotho: United Nations Children's Fund.
OCR for page 118
118 REDUCING THE IMPACT OF BIRTH DEFECTS Massad E, Burattini MN, de Azevedo Neto RS, Yang HM, Coutinho FAB, Zanetta DMT. 1994. A model-based design of a vaccination strategy against rubella in a non-immu- nized community of Sao Paulo State, Brazil. Epidemiology and Infection 112:579-594. Mass ad E, Azevedo-Neto RS , Burattini MN, Zanetta DM, Coutinho FA, Yang HM, Moraes JC, Pannuti CS, Souza VA, Silveira AS, Struchiner CJ, Oselka GW, Camargo MC, Omoto TM, Passos SD. 1995. Assessing the efficacy of a mixed vaccination strategy against rubella in Sao Paulo, Brazil. International Journal of Epidemiology 24(4):842- 850. McClendon JF. 1939. Iodine and the incidence of goiter. Minneapolis: University of Minne- sota Press. Pp. 3-57. McConachie H. Huq S. Munir S. Ferdous S. Zaman SS, Khan NZ. 2000. A randomized controlled trial of alternative modes of service provision for children with cerebral palsy in Bangladesh. Journal of Pediatrics 137(6):769-776. McConkey R. O'Toole B. 1999. Towards the new millennium. In O'Toole B. McConkey R. (eds.). Developing Countries for People with Disabilities. Chorley, Lancashire, UK: Lisieux Hall Publications. P. 8. McIntosh GC, Olshan AF, Baird PA. 1995. Paternal age and the risk of birth defects in offspring. Epidemiology 6(3) :282-288. McKay DW. 1982. New concept approach to clubfoot treatment. Section I. Principles and morbid anatomy. Journal of Pediatric Orthopaedics, 2, 347-356. Medb0 IU. 1961. Early diagnosis and treatment of the hip joint dysplasia. Acta Orthopaedica Scandinavica 31:282-315. MEDLINEplus Medical Encyclopedia. 2001a. Cystic Fibrosis. Available online at www. nlm.nih.gov/medlineplus/ency/article/000107.htm. MEDLINEplus Medical Encyclopedia. 2001b. Toxoplasmosis. Available online at www. nlm.nih.gov/medlineplus/ency/article/000637.htm. Meloni T. Forteleoni G. Meloni GF. 1992. Marked decline of favism after neonatal glucose-6- phosphate dehydrogenase screening and health education: The northern Sardinian expe- rience. Acta Haematologica 87(1-2):29-31. Mendes DG, Roffman M. 1980. Early detection and treatment of congenital dislocation of the hip in the newborn. Israel Journal of Medical Sciences 16(4):247-249. Modell B. Kuliev A. 1990. Changing paternal age distribution and the human mutation rate in Europe. Human Genetics 86(2):198-202. Moos MK. 1994. Preconceptional Health Promotion: March of Dimes Nursing Modules. New York: March of Dimes Birth Defects Foundation. MRC (Medical Research Council) Vitamin Study Research Group. 1991. Prevention of neural tube defects: Results of the Medical Research Council Vitamin Study. Lancet 338(8760):135. Munir KM, Beardslee WR. 1999. Developmental psychiatry: Is there any other kind? Harvard Review of Psychiatry 6(5):250-262. Nahmias AJ, Schwahn MG. 1985. Neonatal herpes simplex: A worldwide disease which is potentially preventable and treatable. Progress in Clinical and Biological Research 163B:355-362. Oakley GP. 1993. Folic acid-preventable spine bifida and anencephaly (editorial). Journal of the American Medical Association 269(10):1292-1293. Oakley GP Jr. 2002a. Inertia on folic acid fortification: Public health malpractice. Teratology 66(1):44-54. Oakley GP Jr. 2002b. Delaying folic acid fortification of flour. British Medical Journal 324(7350):1348-1349. Operation Smile. 2001. Available online at http://www.operationsmile.org.
OCR for page 119
INTERVENTIONS TO REDUCE THE IMPACT OF BIRTH DEFECTS 119 Ounap K, Lillevali H. Metspalu A, Lipping-Sitska M. 1998. Development of the phe- nylketonuria screening programme in Estonia. Journal of Medical Screening 5(1):22- 23. Parekh PK. 1985. Prevalence and management of congenital club-feet (talipes equinobarus) in Zambia. East African MedicalJournal 62(1):38-47. Perry KR, Brown DW, Parry JV, Panday S. Pipkin C, Richards A. 1993. The detection of measles, mumps, and rubella antibodies in saliva using antibody capture radioimmu- noassays. Journal of Medical Virology 40(3 ) :235-240. Pilu G. Reece E, Romero R. Bovicelli L, Hobbins J. 1986. Prenatal diagnosis of craniofacial malformations with ultrasonography. American Journal of Obstetrics and Gynecology 155(1):45-50. Plotkin SA, Katz M, Cordero JF. 1999. The eradication of rubella. Journal of the American Medical Association 281(6):561-562. Porter RW. 1987. Congenital talipes equinovarus: II. A staged method of surgical manage- ment. Journal of Bone and Joins Surgery 69(5):826-831. Poustie VJ, Rutherford P. 2001. Dietary interventions for phenylketonuria. Cochrane Data- base of Systematic Reviews, Issue 2. Powell G. 2000. Report on Childhood Disability in Sub-Sabaran Africa. Harare: Department of Pediatrics and Child Health, University of Zimbabwe Medical School. Rabbi-Bortolini E, Bernardino AL, Lopes AL, Ferri AS, Passos-Bueno MR, Zatz M. 1998. Sweat electrolyte and cystic fibrosis mutation analysis allows early diagnosis in Brazilian children with clinical signs compatible with cystic fibrosis. American Journal of Medical Genetics 76(4):288-290. Ramalingaswami V. 2000. The public health imperative of permanent elimination of iodine deficiency. In Geertman RM (ed.). Eighth VDorld Salt Symposium. Vol. 1. Amsterdam: Elsevier. Pp. 3-11. Ramsey PL, Lasser S. MacEwen GD. 1976. Congenital dislocation of the hip. Use of the Pavlik harness in the child during the first six months of life. Journal of Bone and Joint Surgery 58(7):1000. Rao RS, Chakladar BK, Nair NS, Kutty PR, Acharya D, Bhat V, Chandrasekhar S. Rodrigues VC, Kumar P. Nagaraj K, Prasad KN, Krishnan L. 1996. Influence of parental literacy and socio-economic status on infant mortality. Indian Journal of Pediatrics 63(6):795- 800. Robertson SE, Cutts FT, Samuel R. Diaz-Ortega JL. 1997. Control of rubella and congenital rubella syndrome (CRS) in developing countries, Part 2: Vaccination against rubella. Bulletin of the VDorld Health Organization 75(1):69-80. Rodriguez L, Sanchez R. Hernandez J. Carrillo L, Oliva J. Heredero L. 1997. Results of 12 years' combined maternal serum alpha-fetoprotein screening and ultrasound fetal moni- toring for prenatal detection of fetal malformations in Havana City, Cuba. Prenatal Diagnosis 17(4):301-304. Ross HL, Elias S. 1997. Maternal serum screening for fetal genetic disorders. Obstetrics and Gynecology Clinics in North America 24(1):33-47. Rygg IH, Olesen K, Boesen I. 1971. The life history of teratology of Fallot. Danish Medical Bulletin 18(suppl 2):25-30. Saborio M. 1992. Experience in providing genetic services in Costa Rica. Birth Defects Origi- nal Article Series 28(3):96-102. Scott R. Evans S. 1997. Non-specialist management of tropical talipes. Tropical Doctor 27(1):22-25. Sengupta A. 1987. The management of congenital talipes equinovarus in developing coun- tries. International Orthopaedics 11(3):183-187.
OCR for page 120
120 REDUCING THE IMPACT OF BIRTH DEFECTS Simpson JL, Golbus MS. 1992. Spectrum of autosomal chromosome abnormalities. In Genet- ics in Obstetrics and Gynecology, 2nd edition. Philadelphia: W.B. Saunders Co. Pp. 53- 59, 61-78, 207. Sinha SN. 1987. A simple guide to management of club foot. Papua New Guinea Medical Journal 30(2):165-168. Smith HW, Keen M, Edwards E. 1991. Cleft lip and palate surgery in La Ceiba, Honduras. Archives of Otolaryugology- Head and Neck Surgery 117(12):1356-1359. Stanbury JB. 1998. Prevention of iodine deficiency. In Howson CP, Kennedy ET, Horowitz A. (eds.). Prevention of Micronutrient Deficiencies: Tools for Policymakers and Public HealtI7 Workers. Washington, DC: National Academy Press. Pp. 177-179. Steensma DP, Hoyer JD, Fairbanks VF. 2001. Hereditary red blood cell disorders in Middle Eastern patients. Mayo Clinic Proceedings 76(3):285-293. Stolk EA, Post HA, Rutten FF, Molenaar JC, Busschbach JJ. 2000. Cost-effectiveness of neonatal surgery: A review. Journal of Pediatric Surgery 35(4):588-592. Thorburn MJ. 1993. Recent developments in low-cost screening and assessment of childhood disabilities in Jamaica. Part I: Screening. VDest Indian Medical Journal 42(1):10-20. Thorburn MJ. 2000. Training of CBR personnel: Current issues and future trends. Asia Pacific Disability Rel7abilitation Journal 11:12-17. Thorburn M, Desai P. Paul TJ, Malcolm L, Durkin M, Davidson L. 1992. Identification of childhood disability in Jamaica: The ten question screen. International Journal of Rel7a- bilitation ResearcI7 15(2):115-127. Thorburn MJ, Paul TJ, Malcolm LM. 1993. Recent developments in low-cost screening and assessment of childhood disabilities in Jamaica. Part 2: Assessment. VDest Indian Medical Journal 42(2):46-52. Tookey PA, Jones G. Miller BH, Peckham CS. 1991. Rubella vaccination in pregnancy. Communicable Disease Report (London:Review) 1(8):R86-R88. Turco VT. 1974. Discussion. OrtI7opedic Clinics of NortI7 America 5(1):58. United Nations Educational, Scientific and Cultural Organization (UNESCO) and the Minis- try of Education and Science, Spain. 1994. TI7e Salamanca Statement. TI7e Final Report of tI7e VDorld Conference on Special Needs Education, Access and Quality. Paris. United Nations Children's Fund (UNICEF). 2000a. Ending Iodine Deficiency Forever: A Goal VDitI7in Our Grasp. New York: United Nations Children's Fund and the World Health Organization. United Nations Children's Fund (UNICEF). 2000b. TI7e State of tI7e VDorld's CI7ildren 2001. New York: United Nations Children's Fund. U.S. Food and Drug Administration. 1996. Food standards: Amendment of standards of identity for enriched grain products to require addition of folic acid. Federal Register 61(44):8781-8807. Vanderpas JB, Contempre B. Duale NL, Deckx H. Bebe N. Longombe AO, Thilly CH, Diplock AT, Dumont JE. 1993. Selenium deficiency mitigates hypothyroxinemia in iodine-defi- cient subjects. American Journal of Clinical Nutrition 57(2 suppl):271S-275S. van Ginneken JK, Lob-Levyt J. Gove S. 1996. Potential interventions for preventing pneumo- nia among young children in developing countries: Promoting maternal education. Tropi- cal Medicine and International HealtI7 1(3):283-294. Verjee ZH. 1993. Glucose 6-phosphate dehydrogenase deficiency in Africa review. East African Medical Journal 70(4 suppl):40, 42-43. Vichinsky EP, Styles LA, Colangelo LH, Wright EC, Castro O. Nickerson B. 1997. Coopera- tive Study of Sickle Cell Disease. Acute chest syndrome in sickle cell disease: Clinical presentation and course. Blood 89(5):1787-1792. Viljoen D.1999. Fetal alcohol syndrome. SoutI7 African Medical Journal 89(9):958-960.
OCR for page 121
INTERVENTIONS TO REDUCE THE IMPACT OF BIRTH DEFECTS 121 Wald NJ, Hackshaw AK. 2000. Advances in antenatal screening for Down syndrome. Best Practice and Research in Clinical Obstetrics and Gynecology 14(4):543-551, 563-580. Wald N. Leck I, Gray JAM. 2000. Ethics of antenatal and neonatal screening. In Wald N. Leck I (eds.). Antenatal and Neonatal Screening, 2nd edition. New York: Oxford Uni- versity Press. Pp. 543-555. Wald NJ, Huttly WJ, Hackshaw AK. 2003. Antenatal screening for Down's syndrome with the quadruple test. Lancet 361(9360):835-838. Wallace M, Hurwitz B. 1998. Preconception care: Who needs it, who wants it, and how should it be provided? British Journal of General Practice 48:963-966. Weatherall D, Letsky EA. 2000. Genetic haematological disorders. In Wald N. Leck I (eds.). Antenatal and neonatal screening, 2nd edition. New York: Oxford University Press. Pp. 260-261. Werner D. 1987. Disabled Village Children. Palo Alto, CA: Hesperian Foundation. World Bank. 1993. World Development Report 1993: Investing in HealtI7. New York: World Bank. World Health Organization (WHO). 1980. International Classification of Impairments, Dis- abilities and Handicaps. Geneva: WHO. World Health Organization (WHO). 1985. Community Approaches to tI7e Control of He- reditary Diseases. Geneva: WHO. World Health Organization (WHO). 1993. Promoting tI7e Development of Young Children witI7 Cerebral Palsy: A Guide for Mid-Level Rehabilitation Workers. Geneva: WHO. World Health Organization (WHO). 1996a. Control of Hereditary Diseases: Report of a WHO Scientific Working Group. WHO Technical Report Series. Geneva: WHO. World Health Organization (WHO). 1996b. Recommended Iodine Levels in Salt and Guide- lines for Monitoring their Adequacy and Effectiveness. Geneva: WHO/UNICEF/ICCIDD. World Health Organization (WHO). 1997. Human genetics. Proposed International Guide- lines on Ethical Issues in Medical Genetics and Genetic Services. Available online at http://www.who.int/ncd/hgn/hgnethic.htm. World Health Organization (WHO). 1999. Human Genetics: Services for tI7e Prevention and Management of Genetic Disorders and BirtI7 Defects in Developing Countries: Report of a Joint VDHO/VDOAPBD Meeting. Geneva: WHO. World Health Organization (WHO). 2000a. Primary HealtI7 Care Approaches for tI7e Pre- vention and Control of Congenital Genetic Disorders: Report of a WHO Meeting. World Health Organization (WHO). 2000b. Preventing congenital rubella syndrome. Weekly Epidemiology Record 75(36):290-295. World Health Organization (WHO). 2001. Assessment of Iodine Deficiency Disorders and Monitoring Their Elimination. A Guide for Program Managers, 2nd edition. Geneva: WHO. Pp. 1-122. World Health Organization, United Nations Children's Fund, International Council for the Control of Iodine Deficiency Disorders (WHO, UNICEF, ICCIDD). 1999. Progress to- wards elimination of iodine deficiency disorders. Geneva: WHO (unpublished docu- ment) WHO/NHD/99.4. Yang YH, Ju KS, Kim SB, Cho YH, Lee JH, Lee SH, Choi OH, Chun JH, Kim JI, Kim HJ, Sohn YS. 1999. The Korean Collaborative Study on 11,000 prenatal genetic amniocen- tesis. Yonsei Medical Journal 40(5):460-466. Zaman SS, Khan NZ, Islam S (eds.). 1996. From Awareness to Action: Ensuring HealtI7, Education and RigI7ts of Disabled. Dhaka: Bangladesh Protibondhi Foundation. Zar HJ, Bateman E, Ramsay M. 1998. New advances in cystic fibrosis implications for developing countries. SoutI7 A frican Medical Journal 88 (8) :968. Zimbabwe Ministry of Education, Sports and Culture. 1998. School Psychological Services and Special Needs Education. Annual Report.
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