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In refugee populations the most common cause is low intake - typically a diet low in animal products, due to chronic food insecurity in the country of origin.
B12 deficiency can cause life threatening disease due to megaloblastic anaemia with cytopaenias or neurological abnormalities (regression/seizures). Findings in children include delay or regression of developmental milestones, feeding difficulties, hypotonia, lethargy or hyperirritability, microcephaly and coma. Other patients may be asymptomatic or diagnosed incidentally. There are associations with decreased cognitive function, mental health and long-term cardiovascular outcomes.
If B12 deficiency is confirmed:
Seek specialist advice for patients with symptomatic B12 deficiency. At RCH management is usually in consultation with the Haematology and/or the Metabolic units.
For infants and those with neurological involvement, standard replacement is intramuscular B12 (cyanocobalamin). Although oral doses are poorly absorbed (0.5-4% absorbed), high doses can be effective for lower-risk cases - i.e. older children/adults without evidence of tissue deficiency (i.e. no clinical features and normal homocysteine/MMA).
Rapid clinical improvement is usually seen with replacement, but neurological impairment may persist if there has been prolonged deficiency. Long term developmental follow-up may be required if presentation included neurological features (seizures and neurocognitive deficits are common).
Immigrant health resources Author: Daniel Engelman. Initial - November 2013, reviewed and updated Sophie Oldfield, April 2020. Contact: email@example.com