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Vitamin B12, also known as cobalamin, is a water-soluble vitamin which is found mostly in animal foods in fortified cereals. It cannot be synthesized in the human body.
Dietary cobalamin is liberated from ingested animal protein by gastric hydrochloric acid. The free vitamin is then complexed with intrinsic factor, released from gastric parietal cells, and the complex is absorbed in the terminal ileum.
Cobalamin has several functions in the human body, including neurologic development, red blood cell production, and DNA synthesis.
There are three important reactions which require this vitamin as a cofactor:
Clinical features of vitamin B12 deficiency are subtle at first. Plasma levels sink slowly because of the large reserve in the liver. More sensitive and early markers of deficiency include a rise in the levels of homocysteine and of methylmalonic acid.
These include hematologic, neurologic, and psychiatric features.
Vitamin B12 deficiency is classically associated with megaloblastic macro-ovalocytic anemia. The hemoglobin concentration is elevated, rather than reduced in most patients, while total hemoglobin levels fall. However, almost a third of patients show a normal hemoglobin level.
Pancytopenia develops at a later stage. Folate deficiency is also known to cause megaloblastic anemia, and this should be checked for. Patients with anemia have pallor, tachycardia, weakness, and easy fatigability, and may complain of palpitations.
Vitamin B12 deficiency can cause paresthesia, peripheral neuropathy, and a serious irreversible deficiency disease known as subacute combined degeneration of the spinal cord, with demyelination damage to both the corticospinal and dorsal columns of the spinal tract. Weakness and gait impairment may result.
It is important in cases of suspected folate deficiency to first rule out vitamin B12 deficiency. This is because folate supplementation produces a correction in the hematologic indices which may mask the deficit in vitamin B12, while acutely worsening neurologic symptoms, or precipitating subacute degeneration.
Vitamin B12 deficiency can cause poor memory, cognitive loss, irritability and personality changes, depression, and dementia. Psychosis is rare but has been known to occur.
Vitamin B12 deficiency can cause hyperpigmentation or vitiligo.
Vitamin B12 deficiency manifests in the digestive tract as inflammation of the tongue, or glossitis, with or without jaundice.
Neural tube defects are more common in children born to women with low vitamin B12 levels. Infants who are exclusively breastfed by women with vitamin B12 deficiency have a higher risk of failure to thrive, and show slow development, anemia, weakness, and hypotonia or ataxia.
Vitamin B12 deficiency causes an early and sustained rise in serum homocysteine levels – this is a known risk factor for atherosclerotic disease.