2001, Number 5
<< Back Next >>
Cir Cir 2001; 69 (5)
Upper and Lower Neural Tube Defect at Birth in the Hospital Civil “Juan I. Menchaca”
Pérez-Molina NJ, Meza-López C, Pando-Moreno M, Valadéz-Figueroa I, Ruiz-Gómez A
Language: Spanish
References: 26
Page: 232-235
PDF size: 36.09 Kb.
ABSTRACT
Goals: This study was undertaken to determine the prevalence of upper and lower neural tube defects (NTD) at birth and frequency of exposure to flu, and use of contraceptives and analgesics during the first trimester of pregnancy.
Introduction: Neural tube defects are associated to genetics and environment risk factors. Although some have been identified, there is a hypothesis that upper neural tube defects have a different etiology from lower neural tube defects.
Material and method: A descriptive cross-sectional study was carried out. All live births and stillbirths between January 1989 and March 1997 weighing >500 g and >20 weeks of gestational age were included. The study was undertaken at the Dr. Juan I. Menchaca, Civil Hospital. Demographic variables, flu, and use of contraceptives and analgesics, as well as newborn characteristics, were included.
Results: Of 56,926 newborns, 166 had NTD with a general prevalence of 25 x 10,000 newborns; upper NTD showed a prevalence of 18.8 x 10,000, while lower NTD showed a prevalence of 10.4 x 10,000. Anencephaly was the most frequent upper NTD with a prevalence of 14 x 10,000, while myelomeningocele was the most frequent lower NTD with a rate of 6.5 x 10,000. Acetaminophen intake was three times greater among cases of upper NTD. Flu presence and use of contraceptives showed no differences between the two groups. Weight, height, and newborn gestational age were lower in the group with upper NTD. In this group, births were predominately accomplished by vaginal delivery, while in the group with lower NTD Cesarean section was more predominant.
Discussion: We found differences between upper and lower NTD, mainly demonstrated by frequency of myelocele and myelomeningocele and use of acetaminophen, as well as type of delivery.
REFERENCES
Godfrey P, Oakley JR. Frequency of human congenital malformation. Clin Perinatol 1986; 13(3): 545-54.
Mutchinick O, Orozco E, Lisker R, Babinsky V, Nuñez C. Factores de riesgo asociados a los defectos de cierre de tubo neural: exposición durante el primer trimestre de la gestación. Gac Med Mex 1990; 126: 227-33.
Moore K. Embriología clínica. 3rd. ed. México: Interamericana; 1987. p. 400-439.
Kulkarni M, Mathew M, Reddy V. The range of neural tube defects in Southern India. Arch Dis Child 1989; 64: 201-4.
Yen IH, Khoury MJ, Erickson JD, James LM, Waters GD, Berry RJ. The changing epidemiology of neural tube defects. Am J Dis Child 1992; 146: 857-61.
Pérez MJ, Alfaro AN. Defectos del cierre del tubo neural: prevalencia y búsqueda de asociación con algunos factores de riesgo durante el primer trimestre del embarazo. Bol Med Hosp Infant Mex 1988; 5: 435-42.
Keneth FS. Pediatric neurology, principles and practice. St. Louis, MO, USA: Mosby Company; 1989. 317-28.
Wilkins H. Neurosurgery: congenital structural defects. Philadelphia PA, USA: McGraw-Hill Co.; 1985. p. 17-41.
Frecker MF, Fraser FC, Heneghan WD. Are “upper” and “lower” neural tube defects aetiologically different? J Med Genet 1988; 25: 503-4.
Seller MJ. Neural tube defects: are neurulation and canalization forms causally distinct? Am J Med Genet 1990; 35: 394-6.
Garabedian BH, Fraser FC. Upper and lower neural tube defects: an alternate hypothesis. J Med Genet 1993; 30: 849-51.
Park CH, Stewart W, Khoury MJ, Mulinare J. Is there etiologic heterogeneity between upper and lower neural tube defects? Am J Epidemiol 1992; 136: 1493-1501.
Insel PA. Analgésicos antipiréticos y antiinflamatorios y fármacos antigotosos. In: Hardman JG, Limbird LF, Molinoff PB, Rudson RA, Goodman AG, editors. Goodman y Gilman. Las bases farmacológicas de la terapéutica. 9a Ed. México: McGraw-Hill Interamericana; 1996. p. 661-705.
Collins E. Salicylates and acetaminophen in the pregnancy. Obstet Gynecol 1981; 58: 575-625.
Kotwani A, Mehta VL, Lyengar B. Mechanism of aspirin induced neural tube defects in chick embryo. Indian J Med Res 1994; 99: 289-94.
Shepard TH. Catalog of teratogenic agents. 7th. ed. Baltimore, MD, USA: The Johns Hopkins University Press; 1992: 15.
Aselton PA, Jick H, Milunsky A, Hunter JR, Stergachis A. First trimester drug use and congenital disorders. Obstet Gynecol 1985; 65: 451-5.
Kramer MS. Clinical epidemiology and bioestatistics. New York: Springer-Verlag; 1988. p. 113-6.
Alfaro AN, Prado AC, López ZC et al. Malformaciones congénitas en 75,788 nacimientos consecutivos en cuatro hospitales de Guadalajara, México. Perinatol Reprod Hum 1994; 8: 91-100.
Slattery ML, Janerich DT. The epidemiology of neural tube defects: a review of dietary intake and related factors as etiologic agents. Am J Epidemiol 1991; 133: 526-40.
Walls R, Garnica A, Acosta A, Remusat J. Epidemiología de los defectos congénitos de DTN en la ciudad de Torreón, Coahuila. Rev Med IMSS (Mex) 1990; 28: 265-68.
Zhang J, Cai W. Association of the common cold in the first trimester of pregnancy with birth defects. Pediatrics 1993; 92: 559-63.
Lynberg M, Khoury M, Lu X, Cocian T. Maternal flu, fever, and the risk of neural tube defects: a population-based case control study. Am J Epidemiol 1994; 140: 244-55.
Pérez Molina JJ. La exposición a analgésicos no narcóticos durante el primer trimestre de embarazo, como factor de riesgo para el desarrollo de defectos de cierre del tubo neural (Tesis doctoral). Jalisco, México: Universidad de Guadalajara; 2001.
Seller MJ. Sex, neural tube defects, and multisite closure of human neural tube. Am J Med Genet 1995; 58: 332-6.
Martínez F. Sex ratios in neural tube defects. Lancet 1986; 6: 871-2.