Maternal and child undernutrition and overweight in low-income and middle-income countries.

Maternal and child malnutrition in low-income and middle-income countries encompasses both undernutrition and a growing problem with overweight and obesity. Low body-mass index, indicative of maternal undernutrition, has declined somewhat in the past two decades but continues to be prevalent in Asia and Africa. Prevalence of maternal overweight has had a steady increase since 1980 and exceeds that of underweight in all regions. Prevalence of stunting of linear growth of children younger than 5 years has decreased during the past two decades, but is higher in south Asia and sub-Saharan Africa than elsewhere and globally affected at least 165 million children in 2011; wasting affected at least 52 million children. Deficiencies of vitamin A and zinc result in deaths; deficiencies of iodine and iron, together with stunting, can contribute to children not reaching their developmental potential. Maternal undernutrition contributes to fetal growth restriction, which increases the risk of neonatal deaths and, for survivors, of stunting by 2 years of age. Suboptimum breastfeeding results in an increased risk for mortality in the first 2 years of life. We estimate that undernutrition in the aggregate--including fetal growth restriction, stunting, wasting, and deficiencies of vitamin A and zinc along with suboptimum breastfeeding--is a cause of 3·1 million child deaths annually or 45% of all child deaths in 2011. Maternal overweight and obesity result in increased maternal morbidity and infant mortality. Childhood overweight is becoming an increasingly important contributor to adult obesity, diabetes, and non-communicable diseases. The high present and future disease burden caused by malnutrition in women of reproductive age, pregnancy, and children in the first 2 years of life should lead to interventions focused on these groups.

La homocisteinemia materna como factor asociado al aborto espontáneo / Maternal homocysteinemia as a factor associated with spontaneous abortion

Introducción. Dentro del concepto de «trombofilia» se agrupan una serie de trastornos hereditarios y/o genéticos del sistema coagulativo capaces de aumentar el riesgo de aborto de repetición. La hiperhomocisteinemia, incluida en este grupo, constituye una de las entidades mejor conocidas. Objetivos. Los objetivos del presente estudio son explorar la asociación de la homocisteinemia materna con el aborto espontáneo (repetido o no), establecer la prevalencia de hiperhomocisteinemia entre las pacientes abortadoras y determinar el efecto que la suplementación preconcepcional y prenatal con folatos y vitamina B12 ejerce sobre la homocisteinemia. Material y métodos. Estudio de casos y controles con apareamiento 1:1 por edad y antecedentes de aborto. Se determinó en todas ellas la homocisteinemia en ayunas, así como aquellas variables que podrían modificarla. Resultados y conclusión. La homocisteinemia es significativamente mayor en abortadoras que en controles, aunque la tasa de pacientes hiperhomocisteinémicas en la serie es muy baja. Los datos sugieren un escaso papel terapéutico para los folatos y la vitamina B12 (AU)

Introduction. The concept of "thrombophilia" encompasses a group of genetic and/or inherited disorders of the coagulative system able to increase the risk of recurrent spontaneous abortion. Hyperhomocysteinemia, an entity included in this group, is one of the best known. Objectives. Our objectives were to explore the association between maternal homocysteinemia and spontaneous (recurrent or isolated) abortion, establish the prevalence of hyperhomocysteinemia among patients with abortion, and determine the effect of preconceptional and prenatal supplementation with folate and vitamin B12 on homocysteinemia. Matherial and methods. We performed a case-control study with 1:1 matching based on maternal age and previous abortions. In all participants, fasting homocysteine levels, as well as the factors that could modify them, were determined. Results and conclusions. Homocysteine concentrations were significantly higher in women with abortion than in controls, although the rate of hyperhomocysteinemia in the series was very low. The data do not suggest an important therapeutic role for folates or vitamin B12 in these patients(AU)

Homocisteína en la clínica humana / Present role of homocysteine in clinical medicine

En las últimas décadas ha existido un especial interés por conocer el significado clínico de los valores elevados de la homocisteína plasmática total (HPT) y, en especial, su posible relación con el riesgo cardiovascular. La determinación de los valores de HPT está claramente indicada cuando existe la sospecha clínica de homocistinuria en adolescentes o adultos (presencia de miopía atípica por su gravedad, rápida evolución o ausencia de fondo de ojo miópico, y/o tromboembolia venosa y/o arteriopatía precoz o atípica) y en el estudio de las deficiencias de vitamina B12 y/o ácido fólico. Por el contrario, dada la evidencia actual, no pueden recomendarse de forma generalizada la determinación de la HPT ni el tratamiento con ácido fólico y/o vitamina B12 en pacientes con enfermedad cardiovascular. Es muy importante recordar que está por demostrar la inocuidad de la administración del ácido fólico durante períodos prolongados y en dosis farmacológicas (AU)

There has been a great interest in the last decades about the clinical significance of elevated total plasma homocysteine (tHcy), and especially its possible association with an increased cardiovascular risk. Measurement of tHcy is clearly indicated when homocystinuria is suspected in young or adult patients (in the presence of a severe, atypical or progressive miopia with ectopia lentis and/or venous thromboembolism and/or severe, premature or atypical atherosclerotic vascular disease) and in the evaluation of vitamin B12 and/or folic acid deficiencies. The current evidence does not support either the screening measurement of tHcy or the treatment with vitamin B12 and/or folic acid supplementation in patients with cardiovascular disease. It is important to remember that it remains to be proved whether the long-term administration of folic acid at pharmacological doses is safe (AU)

Prevalencia de la mutación C677T del gen de la metilentetrahidrofolato reductasa en pacientes con patología isquémica cerebrovascular aguda en la Comunidad Autónoma Aragonesa / Prevalence of methylenetetrahydrofolate reductase C677T mutation among patients with acute ischemic cerebrovascular disease in Aragon

Fundamentos: La mutación C677T de la metilentetrahidrofolato reductasa (MTHFR) es la principal causa de hiperhomocisteinemia moderada en nuestro medio. La hiperhomocisteinemia es un factor reconocido de riesgo para aterotrombosis. Los pacientes con la mutación MTHFR C677T padecen hiperhomocisteinemia moderada en situaciones de carencia de folatos. Métodos: Se revisaron retrospectivamente resultados de los estudios de la mutación C677T MTHFR en pacientes con accidentes cerebrovasculares isquémicos agudos (ACVA) menores de 50 años y mayores de 50 años sin factores clásicos de riesgo vascular o historia familiar o personal sugerente de trombofilia, en un periodo de 3 años. Se realizaron estudios de la misma mutación en 90 donantes de sangre voluntarios sanos, como grupo control. Se realizó estadística descriptiva en base de datos informatizada. Resultados: Se recogieron muestras de 99 pacientes y de 90 controles. Edad media: 44,3 con desviación estándar de 13,9 años en pacientes y 39,1 con DS de 8,3 años en controles. Encontramos 19 (19,19%) homocigosis MTHFR C677T en el grupo de pacientes y 14 (15,55%) en el grupo de controles . Conclusiones: La homocigosis MTHFR C667T es más frecuente en el grupo de pacientes con ACVA que en los controles, si bien no encontramos diferencias significativas. Sin embargo, sugerimos que, dada la alta prevalencia poblacional encontrada en nuestro medio para la mutación MTHFR C677T, su estudio debe realizarse dentro de los estudios de trombofilia, pues es capaz de identificar pacientes con un factor de riesgo reversible mediante la administración de folatos

Background: Mutation C677T of the methylenetetrahydrofolate reductase (MTHFR) is the main cause of mild hyperhomocysteinemia. Hyperhomocysteinemia is a recognized risk factor for aterothrombosis. MTHFR C677T patients have higher levels of homocysteine in absence of dietary folates. Methods: Retrospective study over data from patients studied for MTHFR C677T diagnosed of ischemic stroke (IS) younger 50 or older 50 without classic vascular risk factors or with familiar or personal history suggesting thrombophilia in a period of 3 years. MTHFR C677T was screened in 90 healthy blood donors as a control group. Computer database was used for descriptive statistics. Results: Blood simples from 99 patients and from 90 donors (control). Mean age: 44.3 with Standard desviation (SD) 13.9 years in IS group and 39.1 with SD 8.3 years in control group. We found 19 (19.19%) homozygotes for MTHFR C677T in IS group and 14 (15.55%) in control group. Conclusions: Homozygosis for MTHFR C667T is more frequent in the IS group than in the control one, although there is no significant differences. Anyway, we suggest that, because of the high prevalence of the mutation MTHFR C677T found, screening should be made in the thombophilia studies, so that we could find patients with a risk factor that could be lowered by folates in the diet

Anemias megaloblásticas / Megaloblastic anemias

Las anemias megaloblásticas son producidas por una alteración en la síntesis del DNA con una síntesis normal de ARN. Se origina por un déficit de vitamina b12 ó de folatos. Las alteraciones afectan no solamente a la médula ósea sino también a las células epiteliales, sobre toda las del tracto digestivo. Se acompañan de alteraciones neurológicas específicas. El déficit se corrige mediante la corrección de la dieta (AU)

Megaloblastic anemias are produced by an alteration in the synthesis of DNA with a normal synthesis of RNA. It arises due to a vitamin B12 of folate deficit. The alterations not only affect the bone marrow but also the epithelial cells, above all those of the digestive tract. They are accompanied by specific neurologic alterations. The deficit is corrected by correcting the diet (AU)

Optimization of daily folate, vitamin B12 and vitamin B6 supplements in paediatric patients with sickle cell disease

We determined optimal folate, vitamin B12 and vitamin B6 dosages in 21 sickle cell disease (SCD) patients (11 HbSS, 10 HbSC; mean 7 years, range 7-16), using plasma homocysteine (Hcy) as functional marker. They received daily 400 g (0-3 weeks), 700 g (3-6) and 1000 g (6-70) folate; 1 (0-21), 3 (21-45 and 5 RDA (45-70) vitamin B12; and 1 RDA vitamin B6 (0-70). Blood was taken at baseline (P0) and after 3 (PI), 6 (P2), 9 (P3), 21 (P4), 33 (P5), 45 (P6), 57 (P7) and 70 (P8) weeks for measurement of erythrocyte (RBC), serum folate, plasma vitamin B12, whole blood vitamin B6 and plasma Hcy. Vitamin B6 increased from P0 to P1 and P1 to P2; vitamin B12 from P4 to P8; serum folate from P0 to P1 and P1 to P2; RBC folate from P0 to P1, P1 to P2 and P2 to P3. Hcy decreased from P1 to P2 and P4 to P6. Most pronounced Hcy decreases occurred from P0 to P1 (43 percent of patients), P1 to P2 (14 percent) and P4 to P5 (24 percent). Haematological indices did not change. Patients with HbSS had higher RBC folate at P1, P2 and P8. The entire group exhibited inverse relations between RBC folate and haemoglobin on P1, P2, P3, P6, P7 and P8. We conclude that RBC folate is less valuable for folate status assessment in SCD patients. The optimal daily supplement is 700 g folate (3.5-7 RDA vitamin B12 (4.2-6.0 g) and 1 RDA vitamin B6 (1.4-2.0 mg). This combination causes Hcy levels that do not decrease further upon higher dosages and may reduce by simple and relatively inexpensive means their inherently high risk of endothelial damage.(Au)

Evidence for pteridine regulation of lead-mediated inhibition of uroporphyrinogen and heme formation in rat bone marrow.

Uroporphyrin I (URO I) accumulation has been reported in the bone marrow of rats exposed to lead, suggesting a sensitivity of uroporphyrinogen III cosynthase (COSYN) to this heavy metal. Furthermore, it has been reported that a polyglutamated folate derivative may serve as a coenzyme for the catalytic action of hepatic uroporphyrinogen III cosynthase. These findings raised the question of whether depletion of polyglutamated folate could enhance the susceptibility of bone marrow COSYN to lead and potentially interfere with the formation of heme. Nitrous oxide, an anesthetic agent capable of causing bone marrow tetrahydrofolate deficiency, depressed total bone marrow polyglutamated folate content by 42% with significant reductions in all three chain lengths (5-7) identified in the bone marrow during an exposure period of 7 days at 4 hr/day. Lead acetate (15 mg/kg) administered by ip injection at Days 0 and 2 during a 7-day exposure to nitrous oxide resulted in an 84% increase of bone marrow URO I content, which was markedly higher than the increases of 22 and 38% seen with sole administration of lead or nitrous oxide, respectively. The combination of agents also produced a 48% rise in COPRO I, a 39 and 43% decrease in COPRO III and protoporphyrin, respectively, and a 42% decline in the activity of microsomal 7-ethoxycoumarin O-deethylase, which is hemoprotein, cytochrome P-450 mediated. Heme oxygenase activity was not altered by nitrous oxide, lead, or their combination. These results suggest that bone marrow folate deficiency may render COSYN more sensitive to lead as characterized by increased uroporphyrin I and coproporphyrin I isomer content, decreased coproporphyrin III and protoporphyrin content, and depressed microsomal hemoprotein, cytochrome P-450-mediated drug-metabolizing capability.