Because of the large liver stores (about 5 mg), low turnover rate (0.143%) and small daily requirement (3 micrograms),
vitamin B12 deficiency does not occur under normal circumstances. This is not the case in individuals with chronic inflammatory or trophic changes at
vitamin B12 absorption sites. Without supplementation,
vitamin B12 deficiency can be expected within 5 years of
gastrectomy. Characteristic features of type A
gastritis are hyposecretion and mucosal
atrophy in the fundus and body of the stomach, with absent
intrinsic factor. In the small intestine, active and/or passive absorption is impaired by extensive ileal resection,
exocrine pancreatic insufficiency and chronic inflammatory disorders such as
Crohn's disease. Definitive plasma concentrations cannot be quoted for
vitamin B12 deficiency. Dietary habits, subjective symptoms, hematological laboratory results, function tests and gastrointestinal endoscopic and histological findings must all be taken into account in the diagnosis. Modern diagnostic parameters, such as
methylmalonic acid and
homocysteine serum assays, are useful for achieving early diagnosis and hence optimal treatment. With their assured availability, parenteral
vitamin B12 preparations remain the treatment of choice. Results from
vitamin B12 bioavailability studies in healthy subjects suggest that > 300 micrograms probably suffices as an oral maintenance dose after parenteral loading. Further well-documented cases are needed in order to establish whether these doses are adequate in
malabsorption syndromes and
gastrointestinal diseases. Various case reports indicate the value of prophylactic and therapeutic oral
vitamin B12 administration, especially in disorders of
homocysteine metabolism, a substance postulated as a further important risk factor for
atherosclerosis.