Volume 89, Issue 3, April (2003), pp. 439-441 © The Author 2003
doi:10.1079/BJN2002828

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Invited commentary

Megaloblastic anaemia in vitamin B₁₂ deficiency

David A. Bender
Department of Biochemistry and Molecular Biology, University College London, Gower Street, London WC1E 6BT, UK

Deficiency of either folic acid or vitamin B₁₂ results in megaloblastic anaemia: the release into the circulation of immature erythrocytes due to a failure of the normal process of erythrocyte maturation in the bone marrow (Wickramasinghe, 1995, 1999). Pernicious anaemia is the megaloblastic anaemia due specifically to vitamin B₁₂ deficiency, in which there is also spinal cord degeneration, leading to peripheral neuropathy. It is a disease of later life; only about 10 % of patients are aged <40 years; by the age of 60 years about 1 % of the population are affected, rising to 2–5 % of people aged >65 years, as a result of atrophic gastritis (commonly due to autoimmune disease) and hence impaired secretion of intrinsic factor, which is required for the absorption of vitamin B₁₂ (Baik & Russell, 1999). Up to one-third of patients develop neurological signs without megaloblastosis, and high intakes of folate may prevent megaloblastosis in vitamin B₁₂ deficiency (Dickinson, 1995; Savage & Lindenbaum, 1995). As discussed later, it has long been believed that only man, and not other animals, develops megaloblastic anaemia as a result of vitamin B₁₂ deficiency, and indeed it is not obvious why vitamin B₁₂ deficiency should affect haematopoiesis.