Dietary determinants of pregnancy induced hypertension in Isfahan

Pregnancy-induced hypertension [PIH] is a pregnancy-specific condition that occurs after the 20th week of gestation. These physiologic changes can be aggravated by undernutrition. There are some evidence based on the importance of nutrient deficiency in developing this syndrome. Therefore, the aim of present study was to determine the nutritional risk factors for pregnancy induced hypertension in a group of pregnant women in Isfahan. In this case-control study, we recruited 46 Isfahanian pregnant women in two groups [with and without PIH]. They were 19 to 45 year-old and they did not consume any antihypertensive or diuretic medications. Demographic questionnaire and food frequency questionnaire were filled in both groups. There were no significant differences in energy and vitamin E and C intakes between the two groups. Zinc and calcium intakes were lower in women with PIH compared to those without PIH [P = 0.04 and P = 0.007, respectively]. Riboflavin and protein intakes were lower in women with PIH compared to subjects without PIH [P = 0.03 and P = 0.01, respectively]. Lower intake of calcium, zinc, riboflavin and protein should be considered as possible risk factors for PIH. Adequate intake of dairy products which are good sources of mentioned nutrients are recommended to prevent PIH

Antioxidant enzyme levels in the erythrocytes of riboflavin-deficient and Trichinella spiralis-infected rats.

The erythrocyte antioxidant enzyme levels of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) of riboflavin-deficient and Trichinella spiralis-infected rats were investigated. The rats were deprived of riboflavin at the 8th week of the experiment. At that time, the erythrocyte glutathione reductase activity coefficient (EGR AC), as an indicator of riboflavin status, was > or = 1.30 in rats fed a riboflavin-deficient diet and T. spiralis-infected rats fed a riboflavin-deficient diet showed no biochemical sign of riboflavin deficiency. At the 12th week of the experiment, the levels of catalase, SOD and GSH-Px were significantly lower in the riboflavin-deficient, T. spiralis-infected, and combined riboflavin-deficient and T. spiralis-infected, rats, compared to the control group. This may have been due to an increase in free oxygen radicals caused by riboflavin deficiency and parasitic infection.

Glutathione reductase deficiency in Saudi Arabia

Glutathione reductase [GR] is a ubiquitous enzyme required for the conversion of oxidized glutathione [GSSG] to reduced glutathione [GSH] concomitantly oxidizing reduced nicotinamide adenine dinucleotide phosphate [NADPH] in a reaction essential for the stability and integrity of red cells. Mutations in the GR gene and nutritional deficiency of riboflavin, a co-factor required for the normal functioning of GR, can cause GR deficiency. We conducted a study on 1691 Saudi individuals to determine the overall frequency of GR deficiency and to identify whether the deficiency results from genetic or acquired causes or both. The activity of GR was measured in freshly prepared red cell haemolysate in the presence and absence of flavin adenine dinucleotide [FAD] and the activity coefficient [AC] was determined. Samples with low GR activity [> 2.0 IU/g haemoglobin] both in the presence and absence of FAD and an AC between 0.9 and 1.2 were considered GR-deficient. Samples with AC >/= 1.3 were considered riboflavin-deficient. The overall frequency of partial GR deficiency was 24.5% and 20.3% in males and females respectively. In addition, 17.8% of males and 22.4% of females suffered from GR deficiency due to riboflavin deficiency. This could be easily corrected by dietary supplementation with riboflavin. No cases of severe GR deficiency were identified

Revisión bibliográfica actualizada sobre cambios dentofaciales y malformaciones congéticas inducidas por deficiencia aguda de riboflavina / A current review of the literature on dentofacial changes and congenital malformations induced by acute riboflavin deficiency

La riboflavina no es sintetizada por animales superiores en cantidad suficiente como para cubrir las necesidades nutricionales, por lo cual debe ingerirse en los alimentos. La deficiencia aguda de riboflavina en edad embrionaria puede ocasionar malformaciones esqueléticas y alteraciones bucofaciales, siendo el esqueleto membranoso el primero en manifestar los signos de este sindrome. Entre las diferentes anomalías tenemos: braquignacia, fusión de las costillas superiores, ausencia de tibia, atresia del esófago, excenfalia, protrusión de la lengua, incisivos inferiores ausentes, paladar hendido, atrofia de los músculos milhoideo y masetero, sindactilia, abducción de las manos. Se acepta que el agentes causante de estas alteraciones es la hiporriboflavinosis, la cual afecta la multiplicación de células mesenquimatosas durante la vida intrauterina. Si bien estas anomalías no son exclusivas de la deficiencia de riboflavina, se puede afirmar que ciertas deficiencias nutricionales en madres durante el período de gestación pueden causar defectos congénitos en los descendientes.

The relationship between maternal nutritional status and spontaneous abortion.

BACKGROUND: The incidence of pregnancy wastage is high among poor women. Though the aetiology of spontaneous abortion is multifactorial, nutritional deficiency is considered to be an important contributory factor. METHODS: A case-control study was conducted to assess the relationship between maternal vitamin status and spontaneous abortion. RESULTS: The incidence of anaemia (15%), and riboflavin (84%) and folate deficiency (24.5%) were similar among the cases and controls. Vitamin A levels were higher in the study group compared to those in controls. CONCLUSION: The results suggest that various nutrient deficiencies have no correlation with the occurrence of spontaneous abortion. The role of increased vitamin A levels needs to be studied further.

Effect of riboflavin or pyridoxine deficiency on inflammatory response.

Inflammatory response has been assessed in riboflavin or pyridoxine deficient rats. Edema was increased by 54% in pyridoxine deficiency as compared to weight-matched control rats. Food restriction per se reduced the volume of edema by 63%. In pyridoxine deficiency, concentrations of thiobarbituric acid reactive substances (which indicate the extent of lipid peroxidation) increase by 30 and 43% respectively in the edematous tissues of the paw as well as in the wounded skin. Both these parameters were not affected by riboflavin deficiency. Activities of NADPH oxidase and superoxide dismutase in elicited leukocytes from peritoneal cavity were reduced by 54 and 52%, respectively, in riboflavin deficiency but were unaltered in pyridoxine deficiency. Superoxide level and acid phosphatase activity were not influenced by either of the deficiencies, whereas hydrogen peroxide level was increased by 48% in riboflavin deficiency. Food restriction did not affect leukocyte enzymes or the levels of reduced oxygen species. The data suggest that inflammation is enhanced in pyridoxine deficiency but not in riboflavin deficiency.