vitamin-b-12 and Growth-Disorders

Vitamin B12 and folate are key nutrients that help children reach their full potential in growth and development; however, little is known about the status of these vitamins in Brazilian children.. To describe the serum concentrations of vitamin B12 and folate, to investigate the association between high folate concentration (HFC) and vitamin B12 deficiency, and to evaluate the association between vitamin B12 and stunting/underweight in Brazilian children aged 6-59 mo.. Data from 7417 children aged 6-59 mo collected during the Brazilian National Survey on Child Nutrition were used. Serum concentrations of vitamin B12 of <150 pmol/L and folate of <10 nmol/L were classified as deficient, and folate concentrations of >45.3 nmol/L were classified as HFC. Children with length/height-for-age z-score of less than -2 were considered stunted, and those with weight-for-age z-score of less than -2 were underweight. Logistic regression models were performed.. In Brazil, 14.2% (95% CI: 12.2, 16.1) of children aged 6-59 mo had vitamin B12 deficiency, 1.1% (95% CI: 0.5, 1.6) had folate deficiency, and 36.9% (95% CI: 33.4, 40.3) had HFC. Vitamin B12 deficiency was higher in children from the northern region of Brazil (28.5%), between 6 and 24 mo (25.3%), whose mothers had lower formal education (0-7 y; 18.7%). Children with HFC had 62% lower odds (OR: 0.38; 95% CI: 0.27, 0.54) of vitamin B12 deficiency than those with normal/deficient folate. Children with vitamin B12 deficiency and normal/deficient folate had higher odds of stunting (OR: 1.58; 95% CI: 1.02, 2.43) than children without vitamin B12 deficiency and normal/deficient folate.. Vitamin B12 deficiency is a public health problem among Brazilian children aged <2 y with vulnerable socioeconomic status. HFC was inversely associated with vitamin B12 deficiency, and lower odds of stunting were observed in children with HFC and vitamin B12 deficiency than in those with vitamin B12 deficiency and normal/deficient folate.

Topics: Brazil; Child; Female; Folic Acid; Folic Acid Deficiency; Growth Disorders; Humans; Nutritional Status; Thinness; Vitamin B 12; Vitamin B 12 Deficiency

In low-income countries, undernutrition and infections play a major role in childhood anemia. Stunted children may be at particular risk of anemia. In a cross-sectional study nested in a nutrition trial among 12-59-month-old stunted children in eastern Uganda, we measured hemoglobin (Hb) and markers of iron, cobalamin, folate and vitamin A status. We assessed low micronutrient status, socio-demography, stunting severity, inflammation and malaria as correlates of Hb and anemia using linear and logistic regression analyses, respectively. Of 750 stunted children, the mean ± SD age was 32.0 ± 11.7 months and 55% (n = 412) were male. The mean Hb was 104 ± 15 g/L and 65% had anemia, Hb < 110 g/L. In a multivariable model with age, sex and inflammation, the following were associated with lower Hb: serum ferritin < 12 µg/L (-5.6 g/L, 95% CI: -8.6; -2.6), transferrin receptors > 8.3 mg/L (-6.2 g/L, 95% CI: -8.4; -4.0), plasma folate <20 nmol/L (-4.6 g/L, 95% CI: -8.1;-1.1), cobalamin < 222 pmol/L (-3.0 g/L, 95% CI: -5.4; -0.7) and serum retinol-binding protein < 0.7 µmol/L (-2.0 g/L, 95% CI: -4.1; 0.2). In addition, severe stunting, inflammation and malaria were negative correlates. Anemia is common among stunted children in eastern Uganda; micronutrient deficiencies, inflammation and malaria are associated with low Hb.

Topics: Child, Preschool; Cross-Sectional Studies; Female; Folic Acid; Growth Disorders; Hemoglobins; Humans; Infant; Inflammation; Male; Malnutrition; Micronutrients; Trace Elements; Uganda; Vitamin B 12

To evaluate the prevalence of vitamin B12 deficiency and factors associated with vitamin B12 status in Amazonian children.. Genetic risk score (GRS), socio-economic and nutritional status, and morbidity data were the independent variables used in multiple linear regression models to evaluate factors associated with vitamin B12 status in a population-based cross-sectional study. GRS was created by summing a number of known risk alleles for low serum vitamin B12.. Acrelândia, western Brazilian Amazon.. Children (n 988) aged <10 years.. Overall prevalence of vitamin B12 deficiency (<150 pmol/l) was 4·2 (95 % CI 3·0, 5·6) % and was highest in children aged <24 months: 13·6 (95 % CI % 8·8, 19·7) %. For children <24 months, wealth index (β=0·017, P=0·030) and animal protein intake (β=0·219, P=0·003) were positively associated with vitamin B12 status. GRS (β=-0·114, P<0·001) and serum homocysteine (β=-0·049, P<0·001) were negatively associated. Among children aged ≥24 months, vitamin B12 status was positively associated with wealth index (β=0·012, P<0·001), height-for-age Z-score (β=0·024, P=0·033) and serum vitamin A (β=0·089, P<0·001). Age≥60 months (β=-0·118, P<0·001), GRS (β=-0·048, P<0·001), maternal schooling <5 years (β=-0·083, P<0·001), low intake of animal-derived foods (β=-0·050, P=0·030), serum homocysteine (β=-0·053, P<0·001), serum folate ≥23·6 nmol/l (β=-0·055, P=0·012) and geohelminth infection (β=-0·141, P=0·017) were negatively associated with vitamin B12 status.. GRS, poverty, low intake of animal-derived foods, geohelminth infection, vitamin A and folate status were important factors associated with vitamin B12 status of children in our study.

Topics: Alleles; Body Mass Index; Body Weight; Brazil; Child; Child, Preschool; Cross-Sectional Studies; Folic Acid; Gene-Environment Interaction; Genotyping Techniques; Growth Disorders; Homocysteine; Humans; Infant; Linear Models; Nutrition Assessment; Nutritional Status; Overweight; Polymorphism, Single Nucleotide; Prevalence; Risk Factors; Socioeconomic Factors; Vitamin A; Vitamin B 12; Vitamin B 12 Deficiency

Vitamin B12 (cobalamin, Cbl) deficiency can cause metabolic, hematological, and neurological abnormalities. Adequate levels of succinyl-coenzyme A (CoA) cannot be synthesized from methylmalonyl-CoA because of the decreased activity of the methylmalonyl-CoA mutase enzyme that uses Cbl as the cofactor. Succinyl-CoA synthesis deficiency leads to decreased heme synthesis and gluconeogenesis. The reason of growth retardation can be gluconeogenesis deficiency together with heme synthesis deficiency whereas the reason of the neurological abnormalities can be glycine increase in the tissue due to decreased heme synthesis. We present 7 infants diagnosed with severe nutritional Cbl deficiency and discuss the role of succinyl-CoA and glycine in the possible pathogenesis in this article. Patients brought to our clinic with a complaint of growth retardation and diagnosed with nutritional Cbl deficiency were included in the study. There were 5 females and 2 males. The mean age was 11 ± 2.30 (range 6-13) months. All patients had general muscular hypotonia and 4 had growth retardation. Neuromotor growth retardation was found in 4 of the children who had previously shown normal neuromotor development for age. The mean Cbl level was 83.8 ± 27.6 (45.6-114) pg/mL. The mean Cbl level of the mothers was 155 ± 56.6 (88-258) pg/mL. Six of the patients had anemia and 1 had thrombocytopenia. Mean corpuscular volume value was 91.5 ± 12.2 fL. Following treatment, the muscle tonus of the patients improved, the anemia and growth retardation decreased, and the lost neuromotor abilities were recovered. Severe nutritional Cbl deficiency is an important nutritional disease where complications can be prevented with early treatment. When evaluating the pathogenesis, it should be noted that nutritional Cbl deficiency is a succinyl-CoA synthesis deficiency.

Topics: 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Acyl Coenzyme A; Amino Acid Metabolism, Inborn Errors; Anemia; Female; Gluconeogenesis; Glycine; Growth Disorders; Hematopoiesis; Humans; Infant; Male; Mothers; Motor Skills; Muscle Hypotonia; Nervous System Diseases; Pregnancy; Pregnancy Complications; Vitamin B 12; Vitamin B 12 Deficiency

Both maternal and offspring-derived factors contribute to lifelong growth and bone mass accrual, although the specific role of maternal deficiencies in the growth and bone mass of offspring is poorly understood. In the present study, we have shown that vitamin B12 (B12) deficiency in a murine genetic model results in severe postweaning growth retardation and osteoporosis, and the severity and time of onset of this phenotype in the offspring depends on the maternal genotype. Using integrated physiological and metabolomic analysis, we determined that B12 deficiency in the offspring decreases liver taurine production and associates with abrogation of a growth hormone/insulin-like growth factor 1 (GH/IGF1) axis. Taurine increased GH-dependent IGF1 synthesis in the liver, which subsequently enhanced osteoblast function, and in B12-deficient offspring, oral administration of taurine rescued their growth retardation and osteoporosis phenotypes. These results identify B12 as an essential vitamin that positively regulates postweaning growth and bone formation through taurine synthesis and suggests potential therapies to increase bone mass.

Topics: Animals; Bone Density; Bone Development; Female; Growth; Growth Disorders; Growth Hormone; Insulin-Like Growth Factor I; Intrinsic Factor; Liver; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Osteoporosis; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; STAT5 Transcription Factor; Taurine; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Animals; Bone Density; Female; Fetal Development; Growth Disorders; Humans; Insulin-Like Growth Factor I; Mice; Pregnancy; Taurine; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Adult; Anus, Imperforate; Ectodermal Dysplasia; Growth Disorders; Hearing Loss, Sensorineural; Humans; Hypothyroidism; Intellectual Disability; Male; Nose; Pancreatic Diseases; Pancytopenia; Vitamin B 12; Vitamin B 12 Deficiency; Young Adult

Seizures and epilepsy are a common problem in childhood. Nonepileptic paroxysmal events are conditions that can mimic seizure and frequent in early childhood. Nonepileptic paroxysmal events can be due to physiological or exaggerated physiological responses, parasomnias, movement disorders, behavioral or psychiatric disturbances, or to hemodynamic, respiratory, or gastrointestinal dysfunction. Vitamin B12 deficiency is a treatable cause of failure to thrive and developmental regression, involuntary movements, and anemia. Involuntary movements rarely may appear a few days after the initiation of vitamin B12 treatments and might be misdiagnosed as seizure. Here, we report 2 patients who presented with involuntary movements with his video image.

Topics: Atrophy; Brain; Breast Feeding; Clonazepam; Diagnostic Errors; Dyskinesia, Drug-Induced; Electroencephalography; Emergencies; Epilepsies, Partial; Female; Growth Disorders; Humans; Infant; Injections, Intramuscular; Magnetic Resonance Imaging; Male; Milk, Human; Psychomotor Agitation; Status Epilepticus; Vitamin B 12; Vitamin B 12 Deficiency

The Imersland-Gräsbeck Syndrome (IGS) is a rare inherited disorder characterized by megaloblastic anemia due to a selective Vitamin B₁₂ malabsorption in association with mild proteinuria. This syndrome can be diagnosed and treated easily. Herein, we describe an infant with IGS as a rare etiology of growth retardation with diarrhea, vomiting and therapy-resistant proteinuria.

Topics: Anemia, Megaloblastic; Diarrhea, Infantile; Growth Disorders; Humans; Infant; Malabsorption Syndromes; Male; Proteinuria; Recurrence; Respiratory Tract Infections; Treatment Outcome; Vitamin B 12; Vitamin B 12 Deficiency; Vitamin B Complex; Vomiting

In 2004, Bogotá's Secretary of Education (SED) initiated a snack program in public primary schools. A midmorning food ration was provided free of charge to children to supplement 30 and 50% of their daily requirements of energy and iron, respectively. The purpose of this study, an observational investigation of 3202 children ages 5-12 y, was to examine whether the snack program improved children's nutritional and health status. We measured micronutrient levels (plasma ferritin and vitamin B-12, and erythrocyte folate), anthropometry, and reported morbidity during the first semester of the 2006 school year. After adjusting for socioeconomic status and other school interventions, children at schools receiving the snack (n = 1803) had greater increases in plasma vitamin B-12 (42 pmol/L; P < 0.0001) from baseline to 3 mo of follow-up than children at schools not receiving the snack (n = 1399). They also experienced a smaller decrease in height-for-age Z-scores than children who did not receive the snack (P = 0.001). Provision of the SED snack was associated with significantly fewer reported days with morbidity symptoms (e.g. cough with fever, diarrhea with vomiting), 44% fewer doctor visits (P = 0.02), and 23% fewer days of school absenteeism (P = 0.03). The snack was not related to ferritin or folate levels. In conclusion, provision of a school-administered snack was related to improved vitamin B-12 status and linear growth and decreased reported morbidity. Although provision of the snack was not related to BMI changes over a 4-mo period, snack components such as candy and sugar-sweetened beverages should be replaced with healthier options, as the rates of child overweight in Colombia are not negligible.

Topics: Body Height; Child; Child, Preschool; Colombia; Dietary Services; Female; Growth; Growth Disorders; Health Status; Humans; Longitudinal Studies; Male; Nutritional Status; Observation; School Health Services; Socioeconomic Factors; Vitamin B 12

Seven cases of total colonic aganglionosis were reviewed with a follow-up period of 10 to 26 years, focusing on the relationship between the length of aganglionic ileum and postoperative metabolic disorders. Pulled-through ileum ranged from 0 to 65 cm from the ileocecal valve, and suprapelvic side-to-side anastomosis was performed between the pulled-through ileum and 17 to 40 cm of aganglionic colon (left side and transverse colon, four; right side colon, one; no colonic patch, two). Hemoglobin level in three out of four patients with ileal involvement of more than 25 cm was below 11 g/dL (10.9, 7.7, 6.6 g/dL, respectively). Serum iron level was less than 30 micrograms/dL (27, 21, 20, 18 micrograms/dL, respectively) in four out of five patients with ileal involvement of more than 10 cm. Serum vitamin B12 level was below 100 (100, 46 pg/dL, respectively) in two patients whose pulled-through ileum was 45 cm and 65 cm, respectively from the ileocecal valve. One patient needs periodical parenteral iron therapy and one was treated as megaloblastic anemia. In the patients with ileal involvement of more than 25 cm, both weight and height for age are very low at less than the fifth percentile, except for one patient whose side patch was at the right colon. One patient still needs parenteral nutritional support. Severe iron deficiency anemia, low level of B12, and growth retardation are apparent in the patients with total colonic aganglionosis with ileal involvement. Colonic side-to-side anastomosis does not substitute for the loss of terminal ileum.

Topics: Anastomosis, Surgical; Anemia, Iron-Deficiency; Anemia, Megaloblastic; Body Height; Body Weight; Colon; Follow-Up Studies; Growth Disorders; Hemoglobins; Hirschsprung Disease; Humans; Ileal Diseases; Infant; Iron; Male; Parenteral Nutrition; Postoperative Complications; Vitamin B 12; Vitamin B 12 Deficiency

Based on localization studies of the GH receptor/binding protein (BP) in the gastrointestinal tract, we have recently demonstrated growth hormone regulation of gastric intrinsic factor. In order to define the role of GH in the submandibular gland (SMG) we have investigated the effect of GH on SMG structure and function with particular reference to haptocorrin. Bovine GH (65 micrograms/100 g body weight) was administered twice daily to adult male dwarf rats for 6 days (DW+) while control animals received vehicle (DW-). Administration of GH produced a significant increase in body weight (P < 0.001) and allometric increase in SMG weight (P = 0). There was no change in RNA or protein content per g SMG and GH administration produced a small decrease in DNA content normalized to SMG weight. Morphometric analysis of the SMG revealed a significant increase in the percentage area of the gland occupied by tubular (GH receptor/BP expressing) structures and a significant increase in the diameter of both the intralobular striated and granular convoluted tubules. The effect of GH on cellular proliferation in the ductular and acinar components was determined by the immunohistochemical detection of nuclear 5'-bromo-2'-deoxyuridine (BrdU) incorporated during a 2-h pulse of BrdU. GH treatment induced a 5.5-fold increase in the labelling index of tubular cells whereas the acinar cell labelling index increased only 3.3-fold. Soluble extracts of SMG were prepared for estimation of 57Co-cyanocobalamin (vitamin B12) binding. GH administration resulted in an increase in total 57Co-cyanocobalamin (CBL) binding per mg SMG protein. To determine the contribution of haptocorrin (R-protein) the amount of cobinamide dicyanide (CD) displaceable binding was calculated. GH administration produced a 70% increase in CD displaceable CBL binding per mg SMG indicating GH regulation of haptocorrin. A comparison of total SMG CBL binding and CD displaceable CBL binding between male and female rats detected no sex difference. Therefore sex-specific GH secretory profiles are unlikely to be of importance in the regulation of haptocorrin. In conclusion we have demonstrated that GH stimulates hypertrophy and hyperplasia of components of the SMG in the dwarf rat. The observed upregulation of haptocorrin may synergize with the GH-stimulated increase in intrinsic factor to facilitate absorption of CBL during the anabolic state.

Topics: Animals; Body Weight; DNA; Growth Disorders; Growth Hormone; Male; Nuclear Proteins; Organ Size; Protein Binding; Proteins; Rats; Rats, Inbred Lew; RNA; Submandibular Gland; Vitamin B 12

A 33-month-old boy with an inborn error of vitamin B12 metabolism characterized by methylmalonic aciduria, homocystinuria, cystathioninuria , and hypomethioninemia had poor vision and a progressive retinal pigmentary degeneration. The child had early growth retardation with microcephaly, developmental delay, and a megaloblastic anemia. The retinal lesions were first noted when he was 1 year of age and, by ophthalmoscopy and by electroretinographic testing, have progressed. Treatment with hydroxocobalamin and L-methionine improved the anemia and the biochemical abnormalities but apparently did not halt the retinal degeneration. We believe the retinopathy is a feature of this disease, particularly in patients with infantile involvement. The retinal lesion may be caused by an unidentified abnormality of sulfur amino acid metabolism.

Topics: Amino Acid Metabolism, Inborn Errors; Amino Acids, Sulfur; Child, Preschool; Cystathionine; Growth Disorders; Homocystinuria; Humans; Hydroxocobalamin; Male; Malonates; Methionine; Methylmalonic Acid; Retinal Degeneration; Vitamin B 12

Topics: Anemia; Animals; Female; Gastrectomy; Growth Disorders; Iron; Stomach; Swine; Vitamin B 12

Topics: Anemia, Pernicious; Developmental Disabilities; Growth Disorders; Humans; Infant; Male; Neurologic Manifestations; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Achlorhydria; Anemia, Pernicious; Celiac Disease; Child; Eye Manifestations; Gastric Mucosa; Glossitis; Growth Disorders; Humans; Injections, Intramuscular; Intestinal Mucosa; Intrinsic Factor; Male; Neurologic Manifestations; Paresthesia; Skin Diseases; Skin Manifestations; Vitamin B 12; Vitiligo

Topics: Anemia, Macrocytic; Anemia, Sickle Cell; Child; FIGLU Test; Folic Acid; Folic Acid Deficiency; Growth Disorders; Hemoglobinometry; Histidine; Humans; Intestinal Absorption; Male; Recurrence; Vitamin B 12

Topics: Acidosis; Agranulocytosis; Blood Glucose; Cephalometry; Child Development; Diet Therapy; Electroencephalography; Female; Growth Disorders; Humans; Infant; Intelligence; Isoleucine; Lymphocytosis; Malonates; Metabolism, Inborn Errors; Methionine; Otitis Media; Threonine; Valine; Vitamin B 12

Topics: Animals; Chickens; Diet; Female; Folic Acid; Glutamates; Growth Disorders; Male; Poultry Diseases; Pyridoxine; Serine; Vitamin B 12

Topics: Anemia, Macrocytic; Anemia, Pernicious; Child, Preschool; Female; Growth Disorders; Humans; Intrinsic Factor; Vitamin B 12

Topics: Female; Growth; Growth Disorders; Humans; Infant Nutrition Disorders; Infant, Newborn; Infant, Premature, Diseases; Male; Vitamin B 12

Topics: Adolescent; Adrenocorticotropic Hormone; Child; Developmental Disabilities; Gonadotropins; Growth; Growth Disorders; Humans; Hypopituitarism; Ileum; Jejunum; Male; Postoperative Complications; Vitamin A; Vitamin B 12