Vitamin B12 deficiency in school‑aged children is a common but underdiagnosed condition. Depending on the region and dietary habits, the prevalence of subclinical deficiency in at‑risk groups reaches 20-40%, which globally corresponds to tens of millions of children. The main causes of deficiency are nutritional factors (insufficient intake of animal products), malabsorption due to gastrointestinal diseases (coeliac disease, Crohn's disease, autoimmune gastritis), competitive consumption (small intestinal bacterial overgrowth, parasitic infestations), drug‑induced causes (proton pump inhibitors, metformin), as well as rare hereditary disorders of cobalamin transport and metabolism. The key clinical feature of B12 deficiency in schoolchildren is its ability to present as isolated cognitive impairment (reduced attention, working memory, and information processing speed) in the absence of anaemia and with normal total serum B12 levels. The most sensitive diagnostic method is the measurement of active B12 (holotranscobalamin) in combination with homocysteine. Treatment includes parenteral (500-1000 µg of cyanocobalamin or methylcobalamin) or oral (500-1000 µg/day) administration of the vitamin depending on the severity of deficiency and the presence of malabsorption. Neurological manifestations are reversible with timely therapy. The main barriers to timely diagnosis are low awareness among physicians and the general public regarding the cognitive manifestations of B12 deficiency, the absence of screening protocols for at‑risk groups, and insufficient laboratory provision. Vitamin B12 is one of those micronutrients whose deficiency can be completely corrected by affordable means; timely detection and adequate therapy can restore cognitive function and prevent long‑term consequences for academic performance and psychoemotional development in children.
