Association of the low 50 g-glucose challenge test in pregnancy and fetal retardation

Citation
Kj. Buhling et al., Association of the low 50 g-glucose challenge test in pregnancy and fetal retardation, Z GEBU NEON, 205(2), 2001, pp. 39-42
Citations number
10
Categorie Soggetti
Reproductive Medicine
Journal title
ZEITSCHRIFT FUR GEBURTSHILFE UND NEONATOLOGIE
ISSN journal
09482393 → ACNP
Volume
205
Issue
2
Year of publication
2001
Pages
39 - 42
Database
ISI
SICI code
0948-2393(200103/04)205:2<39:AOTL5G>2.0.ZU;2-8
Abstract
Background: The connection between elevated blood sugar and macrosomia is s ufficiently well known and studied. The following study, however, examines whether patients with lower blood sugar values - based on the result of the 50 g-glucose screening test - delivered smaller children than patients wit h normal blood sugar based on the current criteria of blood sugar levels. Patients respectively and methods: In this study, all patients were include d who visited our Prenatal Counseling Center between September 21, 1994 and July 31, 1996. Not included were patients with one-hour values greater or equal to 140 mg/dl. For assessing the 50 g-screening tests, percentiles wer e used. Based on the tables of Voigt, children below the 10th percentile we re considered to be growth retarded. The student's t-test and chi-square te st were employed as statistical tests. Results: Of the 1416 participating patients in the study, 868 fulfilled the aforementioned criteria. A significant statistical correlation was shown b etween the development of fetal retardation and nicotine consumption, weigh t gain, and maternal height. It was also shown that patients with a lower ( < 93 mg/dl) 50 g-screening test more often delivered a retarded child than patients with a normal value (23% vs. 12%, p = 0.034). No significant conne ction was found between the screening test groups and the described influen cing factors. The clinical outcome, measured by the Apgar-scores and the tr ansferal rate, was statistically significantly worse with the retarded chil dren. Conclusions: The maternal glucose metabolism influences the fetal growth no t only with respect to macrosomia but also growth retardation. The growth c urves that have been used until now wrongly do not take into consideration the maternal anthropometric data. In light of this, the former ought to be reevaluated. The data of this study emphasize the necessity of need-adapted nutrition. Maybe also pregnant women with a growth retarded child need a d ietary consultation.