Abstract
Vitamin B12 deficiency causes a wide range of hematological, gastrointestinal, psychiatric and neurological disorders. Hematological presentation of cobalamin deficiency ranges from the incidental increase of mean corpuscular volume and neutrophil hypersegmentation to symptoms due to severe anemia, such as angor, dyspnea on exertion, fatigue or symptoms related to congestive heart failure, such as ankle edema, orthopnea and nocturia. Neuropsychiatric symptoms may precede hematologic signs and are represented by myelopathy, neuropathy, dementia and, less often, optic nerve atrophy. The spinal cord manifestation, subacute combined degeneration (SCD), is characterized by symmetric dysesthesia, disturbance of position sense and spastic paraparesis or tetraparesis. The most consistent MRI finding is a symmetrical abnormally increased T2 signal intensity confined to posterior or posterior and lateral columns in the cervical and thoracic spinal cord. Isolated peripheral neuropathy is less frequent, but likely overlooked. Vitamin B12 deficiency has been correlated negatively with cognitive functioning in healthy elderly subjects. Symptoms include slow mentation, memory impairment, attention deficits and dementia. Optic neuropathy occurs occasionally in adult patient. It is characterized by symmetric, painless and progressive visual loss. Parenteral replacement therapy should be started soon after the vitamin deficiency has been established.
Highlights
Vitamin B12 or cobalamin is produced by bacteria in the large bowel of humans and by external bacteria and fungi
Several conditions can falsely elevate or decrease serum cobalamin concentrations, but a normal methylmalonic acid (MMA) and homocysteinemia concentration suggest the absence of vitamin B12 deficiency [18]
Megaloblastic anemia is a common early symptom leading to the diagnosis, neurological symptoms may occur in the absence of hematological abnormalities
Summary
Vitamin B12 or cobalamin (formerly known as cyanocobalamin, because of an artifactual cyano group added to the cobalamin molecule during the original extraction procedure from the liver) is produced by bacteria in the large bowel of humans and by external bacteria and fungi. Cobalamin from the former source is not absorbed, and humans need to introduce it solely from the diet [1]. An average non-vegetarian diet in western countries contains 5 to 8 μg of cobalamin per day. Since the total-body cobalamin content is two to 5 mg in adults, a complete discontinuation in the absorption will take 3–5 years to deplete cobalamin stores
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