Vitamin B12 deficiency

Introduction
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By Patrick J Bosque MD

Vitamin B12 deficiency is also known as or subsumes Cobalamin deficiency. -ed.

That B12 deficiency can cause progressive neurologic deficits has been known for many decades, yet 75 years after Minot, Murphy, and Whipple received the Nobel Prize for their pioneering treatment of pernicious anemia, many aspects of B12 deficiency remain poorly understood or in dispute. In this clinical article, Patrick Bosque, Associate Professor of Neurology at Denver Health Medical Center and the University of Colorado, Denver, discusses lesser-known and emerging causes of B12 deficiency, considers a controversial association of B12 deficiency with dementia, and presents recent data demonstrating the lack of efficacy of B12 and other vitamin supplementation in preventing stroke.

Key Points

  • B12 deficiency should be suspected in any patient with otherwise unexplained peripheral neuropathy, myelopathy, optic neuropathy, dementia, ataxia, movement disorder, or psychiatric disturbance.
  • Serum B12 level should be determined in any patient with suspected B12 deficiency; abnormal blood cell indices are neither sensitive nor specific for B12 deficiency.
  • In cases of borderline low B12 levels, finding elevated serum methylmalonic acid and homocysteine levels may confirm a physiological deficiency.
  • Despite suggestive epidemiological data, several clinical trials have now failed to show a therapeutic effect of B12 supplementation in treating dementia associated with low (but not clearly deficient) levels of B12.
  • Similarly, despite an epidemiological link between hyperhomocysteinemia and a risk of ischemic stroke and coronary artery disease, many large, well-designed trials have failed to demonstrate a benefit to B12 and folate supplementation.