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Riboflavin Deficiency and Preeclampsia

From the University Women’s Hospital and the Center of Biochemistry, Heidelberg; the University Women’s Hospital, Mannheim, Germany; and the Department of Obstetrics and Gynecology, Mpilo Hospital, Bulawayo, Zimbabwe.

Address reprint requests to: Johannes Frühauf, MD, University Women’s Hospital, Theodor Kutzer Ufer 10, Mannheim D-68135, Germany, E-mail: johannes.fruehauf{at}gyn.ma.uni-heidelberg.de

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.