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12 May 2009

B12 deficiency: A look beyond pernicious anemia

If an image of an elderly patient with pernicious anemia is the first thing that comes to mind when you think of B12 deficiency, take note: That image could obfuscate a more common case of B12 deficiency—one caused by food-B12 malabsorption.

Food-B12 malabsorption, characterized by the inability to release B12 from food or its binding proteins, is actually the leading cause of B12 malabsorption, especially in elderly patients.1-4 And unlike pernicious anemia, it’s more likely to be associated with mild, preclinical B12 deficiency.1,5

Spotting this form of B12 deficiency requires that you focus on its nuances, such as its link to Helicobacter pylori infection and long-term antacid and biguanide use. It also requires that you consider not only a patient’s serum B12 levels, but his homocysteine and methylmalonic acid levels, since they are considered more sensitive indicators of cobalamin deficiency.6 Keying in on these indicators early will ensure prompt treatment, which typically includes intramuscular injections of the vitamin, but which could revolve around a more convenient option: oral B12.

A common problem that comes in many shades
B12 deficiency is common in elderly patients7 and its incidence increases with age.7,8 The Framingham study revealed a prevalence of 12% among elderly people living in the community.8 Other studies focusing on those who are in institutions or who are sick and malnourished, have suggested a higher prevalence of 30% to 40%.3,9

The clinical manifestations of B12 deficiency are highly polymorphic and of varying severity ranging from milder conditions such as the common sensory neuropathy and isolated anomalies of macrocytosis and hypersegmentation of neutrophils, to severe disorders, including combined sclerosis of the spinal cord, hemolytic anemia and even pancytopenia (TABLE 1).1,5,6,10-13

B12 deficiency is often unrecognized or not investigated because the clinical manifestations can be very subtle. In fact, one of its manifestations—mild memory loss—can mimic the early stages of dementia.14

Further muddying the waters is the fact that B12 deficiency appears to be more common among patients who have a variety of chronic neurologic conditions such as stroke, Parkinson’s disease, dementia, Alzheimer’s disease, and depression—although it is unclear if these are causal relationships.1,15 In our own studies in which we administered B12 to patients with dementia, we did not observe any improvement.2,5 Other studies have had similar results.16,17

B12 deficiency is typically defined in terms of the serum concentration of B12, as well as the concentration of homocysteine and methyl malonic acid—2 components of the cobalamin metabolic pathway. A deficiency exists if the patient’s blood work reveals the following:2,18

Serum B12 levels <150 pmol/L and either total serum homocysteine levels >13 μmol/L or methylmalonic acid levels >0.4 μmol/L (in the absence of renal failure and folate and vitamin B6 deficiencies).

Low serum holotranscobalamin levels <35 pmol/L.

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