Overview
Clinical Frame
A B12 result is evidence, not the diagnosis. The clinical question has two parts: is cobalamin function impaired, and what caused that impairment?
CNPLE
CNPLE
A B12 result is evidence, not the diagnosis. The clinical question has two parts: is cobalamin function impaired, and what caused that impairment? Total serum B12 is useful but imperfect; laboratory cut-offs vary, Canadian results are usually reported in pmol/L, and the concentration correlates poorly with the severity of neurological injury. Testing should be targeted rather than used as routine screening. Look for a compatible symptom, examination finding, or blood abnormality together with a risk factor such as restrictive intake, gastrointestinal surgery or disease, metformin, acid suppression, or nitrous oxide exposure. A normal haemoglobin or MCV does not make neurological B12 deficiency safe to dismiss. Conversely, an isolated low result without clinical context should prompt confirmation and assessment of cause rather than automatic injection therapy. The most useful interpretation combines the history, neurological examination, CBC, total B12, and—when the result is indeterminate—methylmalonic acid (MMA) and/or homocysteine. MMA is generally the more specific functional marker, but reduced kidney function can elevate both metabolites and weaken their diagnostic value.
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