Riboflavin deficiency and preeclampsia

被引:23
作者
Wacker, J
Frühauf, J
Schulz, M
Chiwora, FM
Volz, J
Becker, K
机构
[1] Univ Mannheim, Womens Hosp, D-68135 Mannheim, Germany
[2] Ctr Biochem, Heidelberg, Germany
[3] Mpilo Hosp, Dept Obstet & Gynecol, Bulawayo, Zimbabwe
[4] Univ Heidelberg, Womens Hosp, Heidelberg, Germany
关键词
D O I
10.1016/S0029-7844(00)00847-4
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective: To examine in a prospective study riboflavin deficiency as a predisposing factor for preeclampsia in a high-risk collective of pregnant women in Zimbabwe. Methods: At an antenatal clinic in Bulawayo, Zimbabwe, 154 women at increased risk for preeclampsia were observed prospectively until delivery. Riboflavin status was determined using the erythrocyte glutathione reductase activation coefficient test on the day of antenatal booking. Riboflavin deficiency was expressed by erythrocyte glutathione reductase activation coefficient of 1.4 or greater. Results: Riboflavin deficiency was frequently found among the study population (33.8%). Incidence rose toward the end of pregnancy (27.3% at 29-36 weeks' gestation compared with 53.3% at over 36 weeks). In the riboflavin-deficient group, mothers were more likely to develop preeclampsia (28.8%) than in the riboflavin-adequate group (7.8%; P <.001, odds ratio [OR] 4.7, 95% confidence interval [CI] 1.8-12.2). The calculated concentrations of intracellular free flavin adenine dinucleotide were significantly lower in patients who developed preeclampsia than in normal pregnancies (P <.05). Conclusion: Riboflavin deficiency should be considered a possible risk factor for preeclampsia. Insufficient concentrations of the riboflavin-derived cofactors flavin adenine dinucleotide and flavin adenine mononucleotide could contribute to the established pathophysiologic changes including mitochondrial dysfunction, enhanced oxidative stress, and disturbances in nitric oxide release. (Obstet Gynecol 2000; 96:38-44. (C) 2000 by The American College of Obstetricians and Gynecologists.).
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页码:38 / 44
页数:7
相关论文
共 41 条
[1]  
ADIGA PR, 1997, HUM REPROD UPDAE, V3, P299
[2]  
AGGETT N, 1989, S AFR MED J, V76, P342
[3]   The mechanism of thioredoxin reductase from human placenta is similar to the mechanisms of lipoamide dehydrogenase and glutathione reductase and is distinct from the mechanism of thioredoxin reductase from Escherichia coli [J].
Arscott, LD ;
Gromer, S ;
Schirmer, RH ;
Becker, K ;
Williams, CH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (08) :3621-3626
[4]  
Bates C J, 1987, World Rev Nutr Diet, V50, P215
[5]  
BATES CJ, 1994, EUR J CLIN NUTR, V48, P660
[6]   RIBOFLAVIN STATUS IN GAMBIAN PREGNANT AND LACTATING WOMEN AND ITS IMPLICATIONS FOR RECOMMENDED DIETARY-ALLOWANCES [J].
BATES, CJ ;
PRENTICE, AM ;
PAUL, AA ;
SUTCLIFFE, BA ;
WATKINSON, M ;
WHITEHEAD, RG .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1981, 34 (05) :928-935
[7]   GLUTATHIONE AND ASSOCIATED ANTIOXIDANT SYSTEMS IN PROTEIN-ENERGY MALNUTRITION - RESULTS OF A STUDY IN NIGERIA [J].
BECKER, K ;
LEICHSENRING, M ;
GANA, L ;
BREMER, HJ ;
SCHIRMER, RH .
FREE RADICAL BIOLOGY AND MEDICINE, 1995, 18 (02) :257-263
[8]   Enzyme inactivation through sulfhydryl oxidation by physiologic NO-carriers [J].
Becker, K ;
Savvides, SN ;
Keese, M ;
Schirmer, RH ;
Karplus, PA .
NATURE STRUCTURAL BIOLOGY, 1998, 5 (04) :267-271
[9]  
BECKER K, 1991, INT J VITAM NUTR RES, V61, P180
[10]   Reduction of placental nitric oxide synthase activity in pre-eclampsia [J].
Brennecke, SP ;
Gude, NM ;
DiIulio, JL ;
King, RG .
CLINICAL SCIENCE, 1997, 93 (01) :51-55