CONFLICTING INDICATORS OF BIOTIN STATUS FROM A CROSS-SECTIONAL STUDY OF NORMAL-PREGNANCY

Citation
Dm. Mock et Dd. Stadler, CONFLICTING INDICATORS OF BIOTIN STATUS FROM A CROSS-SECTIONAL STUDY OF NORMAL-PREGNANCY, Journal of the American College of Nutrition, 16(3), 1997, pp. 252-257
Citations number
31
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
07315724
Volume
16
Issue
3
Year of publication
1997
Pages
252 - 257
Database
ISI
SICI code
0731-5724(1997)16:3<252:CIOBSF>2.0.ZU;2-H
Abstract
Objective: To assess biotin nutritional status during normal human ges tation. Methods: Urine samples were obtained in a cross-sectional desi gn from 16 women in early pregnancy (17 +/- 1 weeks, mean +/- 1 SD) an d from 13 women in late pregnancy (36 +/- 1 weeks). The urinary excret ion of biotin, two metabolites bisnorbiotin (BNB) and biotin sulfoxide (BSO), and the organic acid 3-hydroxyisovaleric acid (3-HIA) were mea sured by HPLC/avidin-binding assay and GC/MS, respectively. Excretion rates were expressed as concentration ratios to urinary creatinine. Re sults: In both early and late pregnancy, 3-HIA excretion was increased compared to controls (p < 0.0001), suggesting decreased activity of a biotin-dependent enzyme caused by tissue biotin depletion. In early p regnancy, urinary excretion of biotin was normal; in late pregnancy, e xcretion was increased (p < 0.0002), suggesting biotin status was not decreased. In late pregnancy, urinary excretion of BNB and BSO were in creased (p < 0.009). Conclusion: The apparent conflict in the indices of biotin status is not explained by this study but could be resolved by two alternate explanations: 1) pregnancy caused an impairment of re nal reclamation of biotin, BNB, and BSO leading to a paradoxical incre ase in biotin excretion. 2) Pregnancy caused metabolic or renal effect s that increased 3-HIA excretion nonspecifically; hence, the increased 3-HIA excretion did not reflect biotin deficiency. We speculate that some of the women studied were marginally biotin deficient and that re nal wasting and accelerated breakdown of biotin contributed to the def iciency.