Vitamin B12, or cobalamin, is derived from foods of animal origin ^[5,6]. The main sources of vitamin B12 and B6 in the student s diet were chicken white meat (51.8-53.7 %), beef (45-63 %), cream (62.2 -72.1 %), sardines in oil (47.9-52.2 %), tuna (55.2 -60.4 %), cheese edamer (80.1%) and cheese feta (67.4%-73%) 5. In the United States, the estimated average daily intake of vitamin B12 is about 5 µg/d for men and 3.5 µg/d for women. The recommended intake for vitamin B12 is 2.4 µg/d 7. Its deficiency is one of the most common vitamin deficiencies. Deficits can occur at any age 18. The mean age of the patients was 8±4.8 months 9. In our two patients, the signs of deficiency were found after infant age. Indeed, during the first 1,000 days, the vitamin B12 needs of both children are covered by breast milk and dietary intake by diversification 10. Ablactation could be the cause of this deficiency in the context of an overall intake deficit in our 2 patients. The tendency towards late revelation in these two cases should prompt prevention of micronutrient deficiencies in children after weaning.

Vitamin B12 is a cofactor such as pyridoxine (vitamin B6) and folic acid (vitamin B9) in the conversion of homocysteine to methionine. It plays several other roles including structural and functional integrity of myelin, hematopoiesis and DNA and RNA synthesis 67. Its deficiency is mainly revealed by haematological and neurological signs 1112. Epilepsy is a rare condition in children and adults with VB12 deficiency 9. However, other organs may be affected 1314. In our two patients, the disease was manifested by hematological and cutaneous signs. Anemia was more profound when associated with martial deficiency in case 2 requiring transfusion. The disappearance of melanoderma that led to the diagnosis in our two patients was correlated with the biological cure of the disease.

Several etiologies of vitamin B12 deficits are founded in children. These are mainly lack of intake, malabsorption, lack of intracellular use, and metabolic disorders 15161718.

Malabsorption is the most common cause of cobalamin deficiency. Diseases Leading to Insufficient Cobalamin Absorption are Imerslund-Grasbeck syndrome, atrophic gastritis or partial gastrectomy, inadequate functional gastric mucosa, atrophy of the gastric parietal cells, Lacking or inhibition of pancreatic proteases, competition in the intestines with vitamin B12 by parasites or Small Intestinal bacterial overgrowth (SIBO), transcobalamin II deficiency. Also long-term anti-acid therapy, insufficient pepsin or gastric secretion and inadequate proteolytic digestion, are others causes of cobalamin deficiency due to malabsorption 161718.

Biermer s disease is a relatively common autoimmune gastritis affecting mostly women. All age groups can be affected and it is often associated with other autoimmune diseases including type 1 diabetes, thyroiditis or vitiligo. It is characterized with fundic atrophy by involvement of parietal cells leading to achlorhydia and reactive hypergastrinemia. Antibodies are directed against gastric parietal cells (sensitivity 90%, specificity 50%) and against intrinsic factor (sensitivity 50%, specificity 90%). Iron deficiency is frequently associated due to achlorhydria 8910. In our two patients, gastric biopsy and anti-parietal cell antibodies assay were not indicated in this context of undernutrition. Indeed, in view of the clinical signs, the results of the medullogram and the dietary investigation, undernutrition was the most probable hypothesis.

Imerslund-Grasbeck disease is a congenital and elective malabsorption of cobalamins, with autosomal recessive transmission, by mutation of 2 different genes (cubulin and amnionless) coding for 2 subunits of the physiological receptor of the intrinsic factor-vitamin B12 complex in the ileal mucosa. These 2 proteins are also present in the renal proximal tubule, which explains the presence of non-selective proteinuria in the majority of cases 1920. During this disease, the intrinsic factor activity increased 21. We also ruled out this disease in our two patients because of the favorable clinical response to replacement therapy.

Defects in intracellular utilization due to congenital transcobalamin II deficiency are also a cause of vitamin B12 deficiency in children 2223. Intrinsic factor activity assay and genetic study were not performed in view of the favorable clinical response after therapeutic testing.

Intake deficiency was the cause of vitamin B12 deficiency in our two patients. The clinical signs, which are most often, are at the origin of the diagnosis as in our 2 cases (failure to thrive, melanoderma and anemia) 13. In contrast to adults, this deficiency in children has rapid and sometimes irreversible repercussions, particularly on the neurological system 10. In our two reported cases, we did not found neurological signs. Psychomotor development was normal in our patients. However, neurological damage is more severe in infants with a predominant cerebral atrophy, while in our two patients it is mainly bone marrow and skin damage.

Intake deficiency is generally reported in children breastfed by strictly vegetarian mothers or mothers with undiagnosed or untreated Biermer's disease . Anemia appears very early and the diagnosis is carried out with dietary investigation and maternal exploration (NFS, vitamin B12 assay, intrinsic anti-factor antibody assay). Health screening is therefore essential to specify the maternal diet, family and personal history in order to identify dysimmune condition 10. A case of Biermer s disease in a woman explaining vitamin B12 deficiency in exclusively breastfed children was reported by Cariou et al 19. The deficiency occured after a few months of exclusive breastfeeding. A study of 40 exclusively breastfed children with vitamin B12 deficiency showed an average age at diagnosis at 4.4 2.5 months 1924. In our two reported cases, vitamin B12 deficiency was related to lack of intake after weaning, hence the interest of primary prevention in our often unfavourable socio-economic context.