Megaloblastic anemia in children from Eastern Odisha, India: A clinical and hematological profile analysis

Background: Anemia can have severe implications on the health of children including motor development, behavioral and cognitive development. Furthermore, morbidity from infectious disease is higher in anemic children. Nutritional anemia is a major concern in rural India. Aim and Objective: We aimed to observe the percentage of megaloblastic anemia among the anemic children and their clinical and hematological parameters. Materials and Methods: After obtaining permission from the Institutional Ethics Committee, this cross-sectional study was conducted from September 2018 to August 2021. The setting was a tertiary care hospital in the eastern part of Odisha, India. Children of 1� years of age presenting with anemia were included in the study. Details clinical examination and blood tests namely mean corpuscular volume, red blood cell count, total leucocyte count, and platelet count were carried out from venous blood. Descriptive statistical analyses were conducted in STATA software version 15.1. Results: Among the total 150 anemic patients, the majority (126 [84%]) were in the 11� years of age group followed by 24 (16%) in 6� years of age (P < 0.0001). Girls were more (94 [62.7%]) than boys (56 [37.3%]), P < 0.0001. Anorexia was the most frequently encountered clinical symptom (99.3%) followed by pallor (94%), weakness (86%), fatigue (62%), and hyperpigmentation (37.4%). According to hemoglobin level, 40% were suffering from severe anemia, 38.7% was having moderate, and 21.3% was having mild anemia. The majority (74%) were having both Vitamin B12 and folic acid deficiency followed by 16.7% Vitamin B12, and 9.3% folic acid deficiency. Conclusion: Girls were presenting with megaloblastic anemia more than boys. Majority of them were suffering from both Vitamin B12 and folic acid deficiency. Children suffering from megaloblastic anemia present with anorexia, pallor, weakness, and fatigue. A proper health promotion program may be designed to aware the parents about the prevention of nutritional anemia.

Mielopatía por causa dual: neurosífilis y deficiencia de ácido fólico: reporte de caso / Dual cause myelopathy: neurosyphilis and folic acid deficiency: case report

RESUMEN La mielitis transversa es una lesión de la médula espinal que causa déficit completo (sensitivo, motor y esfinteriano) desde el nivel en el cual se presenta. Existe una variante denominada longitudinalmente extensa, la cual en la imagen por resonancia magnética (RM) afecta a tres o más cuerpos vertebrales. Se presenta el caso de un paciente con un síndrome medular secundario a neurosífilis y deficiencia de ácido fólico con lesiones medulares extensas.

SUMMARY Transverse myelitis is the spinal cord injury that causes complete deficit (sensory and motor) from the level in which it is present, classically associated with the loss of sphincter control. There is a variant known as longitudinally extensive, which in magnetic resonance imaging (MRI) affects three or more vertebral segments. We present the case of a patient with a medullary syndrome secondary to neurosyphilis with folate deficiency and extensive spinal cord injuries.

Folic acid and birth defects / 国际儿科学杂志

Folic acid deficiency is associated with birth defects such as fetal spina bifida and congenital heart disease.Folic acid supplementation during pregnancy can prevent various birth defects, but excessive folic acid may increase the risk of certain diseases.This article reviews the causes of folate deficiency, single nucleotide polymorphisms of folate metabolism-related enzyme genes, the mechanism of birth defects caused by folic acid deficiency, and the correct supplementation of folic acid to prevent birth defects.

Folic acid and birth defects / 国际儿科学杂志

Folic acid deficiency is associated with birth defects such as fetal spina bifida and congenital heart disease. Folic acid supplementation during pregnancy can prevent various birth defects, but excessive fo-lic acid may increase the risk of certain diseases. This article reviews the causes of folate deficiency, single nu-cleotide polymorphisms of folate metabolism-related enzyme genes, the mechanism of birth defects caused by folic acid deficiency, and the correct supplementation of folic acid to prevent birth defects.

Experimental research of mechanism of hearing impairment cause by lack of folic acid in mouse / 中国耳鼻咽喉头颈外科

OBJECTIVE To clarify the influence factors of hearing impairment in mice caused by lack of folic acid and the mechanism.METHODS Mice were randomly divided into 2 groups,fed with no folic acid diet and normal diet for 10 weeks.Hearing was tested by ABR.Serum homocysteine,folic acid were detected.Immune imprint method was used to analyze the expression of related protein.Cochlear tissue was tested by histological method to observe morphological changes.At the same time using the TUNEL method was used to analyse the cochlear tissue cell apoptosis.RESULTS Analysis showed that serum folate levels in mice fed without folic acid diet dropped than that of the normal group,while homocysteine levels elevated.Through the brain stem auditory records and cochlear cell apoptosis of mice severe hearing loss was found in folate deficiency group.Western blot detection showed enzyme catalysis homocysteine products increased by 50％ in folate deficiency group than that of the normal diet group.CONCLUSION The high homocysteine levels,and folate deficiency can cause hearing loss in mice and are related with the inner ear homocysteine metabolic disorders.

Serum homocysteine levels of retinal vein occlusion patients with different ages and types / 中华眼底病杂志

Objective To observe serum homocysteine (Hcy) levels in retinal vein occlusion (RVO) patients with different ages and types.Methods A total of 79 patients (79 eyes) diagnosed with RVO were enrolled.There were 33 females and 46 males,the mean age was (57.00± 9.29) years.Eighty-two age-and sex-matched patients (82 eyes) without retinal vascular disease were included as controls.There were 32 females and 50 males,the mean age was (60.00± 10.15) years.Among RVO patients,there were 24 patients younger than 50 years old (young patients) and 55 patients older than 50 years old (elderly patients);35 patients with central RVO (CRVO) and 44 patients with branch RVO (BRVO).Fasting plasma Hcy,serum vitamin (Vit) B6,B12 and folate levels were measured in all patients.The relationship of high Hcy,low VitB6,low folate and RVO with different age were analyzed.Results Hcy level was significantly higher in RVO patients than control subjects (t =2.946,P ＜ 0.01).Blood concentration of folate and VitB6 were significantly lower in RVO patients than control subjects (t=2.641,2.889;P＜0.01).Blood level of VitB12 was significantly different in RVO patients from control subjects (t =1.665,P＞0.05).Concentrations of Hcy,folate,VitB12 and VitB6 were not different between patients with CRVO and BRVO (t =0.756,1.306,0.682,1.306;P＞ 0.05).Hcy level was significantly higher in the young RVO patients than in the elderly RVO patients (t=2.394,P＜0.05).Blood concentration of folate and VitB6 were lower in the young RVO patients than in the elderly RVO patients,but the difference were not significant(t=1.318,1.694;P＞0.05).The number of patients with high Hcy [x2=13.67,odds ratio (OR) =3.327,95％ confidence interval (CI) =1.742-6.354],low VitB6 (x2 =5.28,OR =2.068,95％CI=1.103-3.878) and low folate status (x2 =8.642,OR=2.546,95％CI=1.349-4.806) in RVO patients were more than control subjects (P=0.0001,0.023,0.004).Conclusions High Hcy,low folate and low VitB6 were risk factors for the onset of RVO.Hcy may play more important role in young patients with RVO.Hcy,folate and VitB6 levels were similar in CRVO and BRVO patients.

Prevalence of iron, folate, and vitamin B12 deficiencies in 20 to 49 years old women: Ensanut 2012 / Prevalencia de deficiencias de hierro, folato y vitamina B12 en mujeres de 20 a 49 años: Ensanut 2012

Objective. To describe the prevalence of iron, folate, and B12 deficiencies in Mexican women of reproductive age from the National Health and Nutrition Survey (Ensanut) 2012. Materials and methods. Data came from a national probabilistic survey, representative from rural and urban areas, and different age groups. Blood samples were obtained from 4 263, 20 to 49 years old women for serum ferritin, vitamin B12 and serum folate concentrations. The prevalence of deficiencies, was assessed using adjusted logistic regression models. Results. The deficiency of folate was 1.9% (95%CI 1.3-2.8), B12 deficiency was 8.5% (95%CI 6.7-10.1) and iron deficiency was 29.4% (95%CI 26.5-32.2). No differences were found when compared with 2006, 24.8% (95%CI 22.3-27.2). Conclusions. The vitamin B12 deficiency is still a problem for women of reproductive age and their offspring in Mexico, while folate deficiency disappeared as a problem. Iron deficiency needs prevention and fortification strategies.

Objetivo. Describir las prevalencias de deficiencias de hierro, folato y B12 en mujeres mexicanas en edad reproductiva de la Encuesta Nacional de Salud y Nutrición (Ensanut) 2012. Material y métodos. Datos derivados de una encuesta probabilística nacional, representativa del área rural y urbana por grupos de edad. Se obtuvo una submuestra de sangre en 4 263 mujeres de 20 a 49 años de edad para medir las concentraciones séricas de ferritina, vitamina B12 y folato. Las deficiencias fueron evaluadas mediante regresiones logísticas múltiples ajustadas. Resultados. La prevalencia de deficiencias de folatos fue de 1.9% (IC95% 1.3-2.8) y vitamina B12 de 8.5% (IC95% 6.7-10.1). La deficiencia de hierro no fue diferente a la de 2006: 29.4% (IC95% 26.5-32.2) vs 24.8% (IC95% 22.3-27.2). Conclusiones. La prevalencia de deficiencias de hierro y vitamina B12 todavía representan un problema en mujeres mexicanas (20-49), mientras que la deficiencia de folato ha dejado de ser un problema de salud pública. Aún se requieren estrategias de prevención en México.

Effect of folate deficiency on experimental colitis in mice induced by dextran sodium sulfate / 中华消化杂志

Objective To investigate whether folate deficiency cause high expression level of interferon gamma (IFN-γ) resulted from IFN-γ gene ( IFNG) hypomethylation and then promote the pathogenesis and development of ulcerative colitis (UC ) in a dextran sulfate sodium (DSS )-induced experimental colitis model in mice .Methods A total of 24 female BALB/c mice were divided into four groups ,six mice in each group , including folate deficient/DSS+ group , standard diet/DSS+ group , standard diet/DSS - group and folate deficient/DSS- group .At the beginning of the sixth week since fed , the mice of model groups were treated with 5% DSS to establish experimental colitis .By the end of the sixth week ,disease activity index (DAI) of colitis and histological changes were evaluated .The folate level of peripheral blood serum of mice were detected by enzyme-linked immunosorbent assay (ELISA ) . The expression of IFN-γ in colonic mucosa of mice was examined by immunohistochemistry . The methylation level of CpG island in the promoter region of IFNG was determined by methylation specific polymerase chain reaction (MSP) .The t test was used for measurement data .Chi square test was performed for comparison between groups of count data . Spearman correlation analysis was used for correlation analysis .Results The folate levels of peripheral blood serum of folate deficiency/DSS+ group and folate deficiency/DSS- group ((2 .70 ± 0 .19) and (2 .80 ± 0 .25)μg/L) were significantly lower than those of standard diet/DSS+ group and standard diet/DSS- group ((13 .62 ± 0 .38 ) and (13 .52 ± 0 .77)μg/L ,t= -63 .33、32 .27 ,both P< 0 .05) ,resepectively .The expression of IFN-γ in colonic mucosa of folate deficiency/DSS+ group and standard diet/DSS+ group were significantly higher than those of folate deficiency/DSS- group and standard diet/DSS- group (χ2 = 22 .18 ,P< 0 .05 ) . And the expression of IFN-γ in colonic mucosa of folate deficiency/DSS+ group was also higher than that of standard diet/DSS+ group (χ2 = 12 .00 ,P< 0 .05) .The expression level of IFN-γ of folate deficiency/DSS+ group and standard diet/DSS+ group was positively correlated with (r=0 .998、0 .953 ,both P<0 .01) .The folate levels of peripheral blood serum of folate deficiency/DSS+ group was negatively correlated with IFN-γexpression level and DAI (r= -0 .880 and -0 .926 ,both P<0 .05) .No abnormal methylation was detected in IFNG promoter CpG island in colonic mucosa tissues of mice of each group . Conclusion In the mice model of DSS induced acute experimental colitis ,folate deficiency may increace the expression of inflammatory factor IFN-γand enhance the inflammation activity of colonic mucosa .

Considerations on the food fortification policy in Brazil

Government health authorities approved, in December 2002, the ANVISA (National Sanitary Vigilance Agency) resolution number 344, making the addition of iron and folic acid to all wheat and maize flours industrialized in Brazil obligatory. After a brief review of iron deficiency, iron overload and folic acid deficiency several questions and remarks need to be made about this universal food fortification program. Iron salts and folic acid are drugs widely used in medicine and they may present undesirable side effects. There are potential risks with offering iron to the normal population for a long period of time and to patients with iron overload. Other important remarks are: there is no medical follow up of this treatment in the Brazilian population; patients can decide the quantity of foods (and of these nutrients) that they want to ingest; fortified foods may correct iron deficiency anemia but not necessarily the causes, which include gastrointestinal neoplasms; and folic acid in the diet may interfere with several treatment protocols that use folic acid antagonists, such as methotrexate. Finally, with the exception of some social programs, the costs of treatment using fortified foods are passed on to the population. Considering that Brazil has 330,000 active medical doctors it is suggested that our Health Ministry should invite them to take care of these important medical conditions.

Megaloblastic anemia: Back in focus.

Megaloblastic anemia (MA), in most instances in developing countries, results from deficiency of vitamin B12 or folic acid. Over the last two to three decades, incidence of MA seems to be increasing. Of the two micronutrients, folic acid deficiency contributed to MA in a large majority of cases. Now deficiency of B12 is far more common. In addition to anemia, occurrence of neutropenia and/or thrombocytopenia is increasingly being reported. Among cases presenting with pancytopenia, MA stands out as an important (commonest cause in some series) cause. This article focuses on these and certain other aspects of MA. Possible causes of increasing incidence of MA are discussed. Observations on other clinical features like neurocognitive dysfunction, associated hyperhomocysteinemeia and occurrence of tremors and thrombocytosis during treatment are highlighted.

Effects of folic acid deficiency on plasma homocysteine level and arterial lesions in rats / 中华老年医学杂志

Objective To observe effects of the folic acid deficient diet on plasma homocysteine(Hcy) level and lesions of aorta in rats. Methods Twenty male Wistar rats were divided into two groups, folic acid deficent group (FD) and control group (Ctl).The rats were fed with folic acid deficient diet and normal diet for 3 months,respectively. The levels of serum folic acid and plasma Hcy as well as the activities of superoxide dismutase(SOD) and glutathione peroxidase (GPX) in erythrocytes were measured.The histological changes of aorta were also examined by light microscope. Results After 3 months treated with folic acid deficient diet, serum folic acid level 〔(6 08?1 84)?g/L〕 decreased significantly in rats of FD group compared either with pre experimental level 〔(13 32?2 02)?g/L〕 or with control one 〔(12 17?1 67)?g/L〕. Meanwhile, plasma homocycteine level increased significantly in rats of FD group 〔(28 66?6 07)?mol/L〕 compared either with pre experimental level 〔(9 75?1 86)?mol/L〕 or with control one 〔(9 49?1 77)?mol/L〕. The activity of erythrocytic SOD increased but GPX decreased obviously. The morphology lesions were also observed in aortic tissue. Conclusions Folic acid deficient diet induced hyperhomocysteinemia and arterial lesions.The high oxidant stress induced by hyper homocysteinemia may be one of mechanisms of arterial lesion.