Deficiency of vitamin B12 can result in both anemia and neurological changes. The anemia is characterized by large red blood cells and some immature red blood cells. Neurologically, patients may experience signs and symptoms compatible with Alzheimer's type dementia.
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The neurologic changes may well precede any evidence of anemia. There are also many other medical conditions that will mimic B12 deficiency.
B12 deficiency affects up to 25% of the general population age 65 and older. By a simple blood test these patients may be identified as having low / borderline B12 levels. The reasons patients may become low in B12 is generally secondary to decreased oral intake, or decreased absorption from the intestinal tract. The only dietary sources of vitamin B12 are meat, eggs, and dairy (animal) products.
Many different types of gastric disease can result in B12 deficiency. These include autoimmune processes and pernicious anemia, as well as infection with Helicobacter pylori. Successful treatment of Helicobacter infection will result in resolution of the B12 deficiency.
Other factors contributing to poor B12 absorption include intestinal bacterial overgrowth, secondary to antibotic treatment, medications (antiacids, H2 receptor agonists, and proton pump inhibitors), chronic alcholism, gastric surgery, pancreatic problems, and Sjogren's syndrome. Deficiency of folic acid may also be associated risk factors.
Fortunately, once B12 deficiency is identified, treatment is quite simple and straightforward. B12 deficiency is usually fully reversible if treated without undue delay. Treatment consists of injections of B12 and repeat blood test confirming normal B-12 blood levels. Alternately, using high-doses of B12 orally will produce similar results. This requires a conscientious and complaint patient.
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