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Megaloblastic anaemia and miscellaneous deficiency anaemias 

Megaloblastic anaemia and miscellaneous deficiency anaemias
Chapter:
Megaloblastic anaemia and miscellaneous deficiency anaemias
Author(s):

A.V. Hoffbrand

DOI:
10.1093/med/9780198746690.003.0536
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date: 28 February 2021

Megaloblastic anaemias are characterized by red blood cell macrocytosis. They arise because of inhibition of DNA synthesis in the bone marrow, usually due to deficiency of one or other of vitamin B12 (cobalamin) or folate, but sometimes as a consequence of a drug or a congenital or acquired biochemical defect that disturbs vitamin B12 or folate metabolism, or affects DNA synthesis independent of vitamin B12 or folate. Acquired pernicious anaemia—antibodies in serum and gastric juice directed against parietal cells (85–90% of cases) and intrinsic factor (50%), and raised serum gastrin are associated with autoimmune gastritis and failure of absorption of vitamin B12. Treatment and prevention of megaloblastic anaemia—vitamin B12 deficiency—may be treated with intramuscular hydroxocobalamin (1-mg doses, six given in the first 2–3 weeks, then every 3 months). Oral therapy is practised by a minority and is unlikely to be useful in pernicious anaemia. Neurological complications are irreversible unless treated early. Folate deficiency—high-dose oral folic acid (5 mg daily) overcomes folate malabsorption, but this should not be given alone where vitamin B12 deficiency coexists because neurological disease may be precipitated or exacerbated (although the haematological abnormalities improve). Where folate metabolism is disturbed by methotrexate, oral or parenteral folinic acid is given to restore DNA synthesis. Prevention—dietary folate fortification is an accepted and highly effective public health measure in many countries (none in Europe) for reducing the incidence of neural tube birth defects.

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