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![]() The case also highlights the need to consider vitamin B12 deficiency in infants with severe anemia even if their hematological parameters do not indicate megaloblastic anemia because the concomitant presence of substantial iron deficiency may modify the characteristics of the anemia.Table 4.1 Effects of various levels of folic acid fortification in bread on. Moreover, the supplementation should be continued during lactation in order to avoid the development of signs of deficiency that may be associated with persistent neurological problems in infants. Dosage Chart.This case underlines the importance of adequately controlling maternal vitamin B12 intake during pregnancy by means of supplementation which, in the case of vegan mothers, should be significantly greater than that usually given. However, most infants with B12 deficiency are born to women with low vitamin B12 levels and have been exclusively breastfed. The most frequent inborn error is cobalamin C disorder, which is caused by a mutation of the MMACHC gene encoding a protein that plays a critical role in the metabolic pathway leading to the formation of succinyl-CoA and methionine. Vitamin B12 deficiency in infancy may be due to an inborn error of absorption and metabolism, or (more frequently) nutritional problems. Vitamin B12 deficiency leads to the accumulation of methylmalonic acid and homocysteine in blood and urine, and the onset of clinical hematological, neurological and psychiatric manifestations. It is required to convert methylmalonyl-CoA to succinyl-CoA (a compound metabolised by the Krebs cycle to produce energy) and to ensure the activity of methionine synthase, an enzyme that catalyses the methylation of homocysteine to form the essential amino acid methionine. Damage undetected.Vitamin B12 plays a major role in human intermediary metabolism. Photoshop for mac number font flat line 3The child was seen by a paediatrician at the age of one month and three months, and physical evaluation resulted normal. The parents reported that some of these signs had been present from the third month of life. The child was exclusively breastfed until the fifth month of life, when he was hospitalised because of poor weight gain, feeding difficulties, severe pallor, muscle hypotonia and somnolence. Unfortunately, this supplementation was stopped after delivery. His mother, who had been vegan for several years, was apparently daily treated with a multivitamin oral preparation with a multivitamin preparation (Multicentrum, Pfizer Consumer Healthcare, Rome, Italy) during the second and third trimester in order to ensure an intake of 2.5 μg of vitamin B12 per day. Consequently, the breast milk of mothers who do not consume such products is frequently poor in vitamin B12, and their newborn infants have low vitamin stores.We describe the case of an exclusively breastfed 5-month-old Italian infant with severe pancytopenia and neurological impairment who was born to a vegan mother who had received B12 supplementation during pregnancy but not during lactation.This five-month-old male Italian infant was born after a normal full-term (41 weeks) pregnancy with a weight of 2,550 g (3rd percentile), length of 48 cm (10 th percentile) and head circumference of 35 cm (25 th percentile). Blood homocysteine was 11 μmol/L (normal value 4–15 μmol/L) and urinary methylmalonic acid 281 mmol/moL creatinine (normal value 29 μg/dL) and serum ferritin of 4 ng/mL (normal value 20–270 ng/mL). His serum vitamin B12 level was 57 pg/mL (normal value 180–500 pg/mL) and serum folate level 12.8 ng/mL (normal value >3 ng/mL). The peripheral blood film showed oval macrocytes, anisopoikilocytosis, hypochromia, anisochromia and hyper-segmented polymorphonuclear leukocytes. His platelet count was 45,000/mm 3. He had a hemoglobin level of 4.7 g/dL with an MCV of 84.2 fL, a white blood cell count of 4,680/mm 3 and neutrophil count of 1,900 mm 3. He was immediately treated with packed red blood cells, intramuscular vitamin B12 injections (at a dose of 1,000 μg/day for two weeks followed by weekly injections at the same dose for six months) and oral iron supplementation (iron sulphate 3 mg/kg/day for 3 months).Table 1 shows the patient’s clinical and laboratory data upon admission and during follow-up. Genetic analyses did not find any MMACHC gene mutations.Magnetic resonance imaging (MRI) of the brain showed mild dilatation of the lateral ventricles with diffuse delayed myelination that was most marked in the brainstem.Maternal investigations showed a hemoglobin level of 9.1 g/dL with an MCV of 96.4 fL, and serum vitamin B12 level of 155 pg/mL (no data on maternal serum vitamin B12 during pregnancy was available).On the basis of these data, the child was diagnosed as having vitamin B12 and iron deficiency due to nutritional inadequacy. A bone marrow examination showed a reduced number of red line cells with some megaloblasts, a small number of dysplastic megakaryocytes, and dysplastic granulopoiesis with asynchronous maturation processes. ![]() ![]()
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