Vitamin B12 (B12), a member of the corrin family, is a cofactor for the conversion of methylmalonyl Coenzyme-A (CoA) to succinoyl CoA. In addition, B12 is a cofactor in the synthesis of methionine from
homocysteine, is implicated in the formation of myelin, and, along with folate, is required for DNA synthesis.
B12 is absorbed from food after binding to a protein called intrinsic factor which is produced by the stomach. Causes of vitamin B12 deficiency can be divided into three classes: nutritional deficiency, malabsorption
syndromes, and other gastrointestinal causes. B12 deficiency can cause megaloblastic anemia (MA), nerve damage and degeneration of the spinal cord. Lack of B12, even mild deficiencies, damages the myelin sheath that surrounds and protects nerves, which may lead to peripheral neuropathy.
The nerve damage caused by a lack of B12 may become permanently debilitating, if the underlying condition is not treated. People with intrinsic factor defects who do not get treatment eventually develop a MA called pernicious anemia (PA). The relationship between B12 levels and MA is not always clear in that some
patients with MA will have normal B12 levels; conversely, many individuals with B12 deficiency are not afflicted with MA. Despite these complications, however, in the presence of MA (e.g., elevated mean corpuscular volume (MCV)) there is usually serum B12 or folate deficiency.
There are a number of conditions that are associated with low serum B12 levels, including iron deficiency, normal near-term pregnancy, vegetarianism, partial gastrectomy/ileal damage, celiac disease, use of oral contraception, parasitic competition, pancreatic deficiency, treated epilepsy, and advancing age. Disorders associated with elevated serum B12 levels include renal failure, liver disease, and myeloproliferative diseases.
Manufacturer’s Reagent package insert Architect Vitamin B12, November 2015, Abbott Ireland,
Diagnostics Division Lisnamuck Longford Co., Ireland.