Enzymic evaluation of thiamin, riboflavin and pyridoxine status of parturient mothers and their newborn infants in a Mediterranean area of Spain.
OBJECTIVE
To determine the biochemical status of thiamin, riboflavin and pyridoxine in parturient mothers and their newborn infants in a Mediterranean region.


METHODS
Transveral study.


METHODS
St Joan University Hospital and Faculty of Medicine & Health Sciences, Universitat Rovira i Virgili, Reus, Spain.


METHODS
131 healthy parturient mothers, with normal pregnancies and deliveries in St Joan University Hospital, and their newborn infants.


METHODS
Erythrocyte haemolysates were prepared from maternal blood at delivery and infants' umbilical cord blood and used to measure micronutrient status using the transketolase, glutathione reductase and aspartate aminotransferase coenzyme stimulation tests.


RESULTS
Maternal and infant coenzyme activities were significantly correlated, but infant coenzyme status was better than maternal, with significantly higher basal and stimulated activity (P < 0.001) and significantly lower activation coefficients (P < 0.001). Inadequate thiamin, riboflavin or pyridoxine status occured in 38.2 62.6% (50-82) of the mothers and 3.1-37.4% (4 49) of the infants; 85.2% (46/54), 12.9% (4/31) and 24.1% (12/54) of infants born to mothers with biochemical deficiency of either thiamin, riboflavin or pyridoxine, respectively also had inadequate status. Maternal deficiencies in more than one vitamin further increased the risk of infant thiamin and pyridoxine deficiency. Maternal and infant riboflavin status were significantly correlated with fetal development (e.g. length at birth, P < 0.001). The incidence of thiamin deficiency in paturient mothers in Spain was the highest out of a 12-country comparison.


CONCLUSIONS
Inadequate status for each vitamin was evident in mothers and infants. Maternal status of each individual vitamin, but especially riboflavin, was affected by maternal status of the other vitamins. Infant thiamin status was the most adversely affected by maternal deficiencies in more than one vitamin. Infant riboflavin status, however, was apparently protected from adverse maternal status.
Sánchez
D J
DJ
Department de Ciècies Mèdiques Bàsiques, Facultat de Medicina i Ciencies de la Salut, Universitat Rovira i Virgili, Reus, Spain.
Murphy
M M
MM
Bosch-Sabater
J
J
Fernández-Ballart
J
J
D000293:Adolescent; D000328:Adult; D001219:Aspartate Aminotransferases / Q000097:blood; D005260:Female; D005312:Fetal Blood / Q000201:enzymology; D005182:Flavin-Adenine Dinucleotide / Q000737:chemistry; D005980:Glutathione Reductase / Q000097:blood; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007227:Infant Nutritional Physiological Phenomena; D007231:Infant, Newborn / Q000097:blood / Q000502:physiology*; D008297:Male; D009752:Nutritional Status; D049590:Postpartum Period / Q000097:blood / Q000502:physiology*; D011247:Pregnancy; D011732:Pyridoxal Phosphate / Q000737:chemistry; D011736:Pyridoxine / Q000097:blood*; D012256:Riboflavin / Q000097:blood*; D013030:Spain; D018709:Statistics, Nonparametric; D013831:Thiamine / Q000097:blood*; D013835:Thiamine Pyrophosphate / Q000737:chemistry; D014174:Transketolase / Q000097:blood
D001219:Aspartate Aminotransferases; D005182:Flavin-Adenine Dinucleotide; D005980:Glutathione Reductase; D006442:Glycated Hemoglobin; D011732:Pyridoxal Phosphate; D011736:Pyridoxine; D012256:Riboflavin; D013831:Thiamine; D013835:Thiamine Pyrophosphate; D014174:Transketolase