|
|
| A B C D E F G H I J K L M N O P Q R S T U V W X Y Z # |
Vitamin B12
Test CodeVTB12
Alias/See Also
VB12, cobalamin
Preferred Specimen
1.0 mL plasma (0.5 mL minimum)
Instructions
Protect samples from light.
Transport Container
PST (light green top). Red top and SST also acceptable
Specimen Stability
Room temperature: 24 hours, Refrigerated: 48 hours, Frozen: 7 days
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
Hemolyzed specimens are unacceptable.
Report Available
24 hours
Reference Range
193 - 986 pg/mL
Clinical Significance
Vitamin B12, or cobalamin, is found in a variety of foods such as fish, shellfish, meats and dairy products. Intrinsic factor (IF), transcobalamin II (TCII) and haptocorrin (HC) are binding proteins necessary for the assimilation, transport and delivery of B12 to the blood and body tissues. Vitamin B12 is primarily stored in the liver and released on demand. The body uses B12 very efficiently, reabsorbing B12 from the small intestine and returning it to the liver so little is excreted and nutritional deficiency is extremely rare. Vitamin B12 is necessary for DNA synthesis, normal red blood cell maturation and myelin sheath formation and maintenance. It is a coenzyme in the conversion of methylmalonic acid to succinic acid and in the synthesis of methionine.
Vitamin B12 deficiency is one of the causes of megaloblastic anemia, a disease in which red blood cells are larger than normal and the ratio of nucleus size to cell cytoplasm is increased. Since folic acid deficiency can also cause megaloblastic anemia, measurement of serum B12 levels is an important part of the differential diagnosis. Vitamin B12 deficiency also causes macrocytic anemias which are characterized by abnormal red blood cell maturation and early release from the bone marrow. Pernicious anemia is a macrocytic anemia. In this disease, an absence of IF prevents normal absorption of B12. In both megaloblastic anemia caused by B12 deficiency and pernicious anemia, treatment with B12 is the therapeutic course.
Vitamin B12 deficiency can also lead to abnormal neurologic and psychiatric symptoms such as ataxia, muscle weakness, dementia, psychosis and mood disturbances. Many patients show neurological changes without developing macrocytic anemia. Populations at risk for B12 deficiency include strict vegetarians, the elderly and populations with increased B12 requirements associated with pregnancy, thyrotoxicosis, hemolytic anemia, hemorrhage, malignancy and liver or kidney disease. Early diagnosis of B12 deficiency is crucial because of the latent nature of this disorder and the risk of irreversible neurological damage. Recent studies suggest that in addition to serum B12 levels, folic acid, methylmalonic acid and homocysteine should be measured to improve the specificity of the diagnosis. Elevated B12 levels are seen in hematological disorders (chronic myelogenous leukemia, promyelocytic leukemia, polycythemia vera) and in liver disorders (acute hepatitis, cirrhosis, hepatocellular carcinoma).
Vitamin B12 deficiency is one of the causes of megaloblastic anemia, a disease in which red blood cells are larger than normal and the ratio of nucleus size to cell cytoplasm is increased. Since folic acid deficiency can also cause megaloblastic anemia, measurement of serum B12 levels is an important part of the differential diagnosis. Vitamin B12 deficiency also causes macrocytic anemias which are characterized by abnormal red blood cell maturation and early release from the bone marrow. Pernicious anemia is a macrocytic anemia. In this disease, an absence of IF prevents normal absorption of B12. In both megaloblastic anemia caused by B12 deficiency and pernicious anemia, treatment with B12 is the therapeutic course.
Vitamin B12 deficiency can also lead to abnormal neurologic and psychiatric symptoms such as ataxia, muscle weakness, dementia, psychosis and mood disturbances. Many patients show neurological changes without developing macrocytic anemia. Populations at risk for B12 deficiency include strict vegetarians, the elderly and populations with increased B12 requirements associated with pregnancy, thyrotoxicosis, hemolytic anemia, hemorrhage, malignancy and liver or kidney disease. Early diagnosis of B12 deficiency is crucial because of the latent nature of this disorder and the risk of irreversible neurological damage. Recent studies suggest that in addition to serum B12 levels, folic acid, methylmalonic acid and homocysteine should be measured to improve the specificity of the diagnosis. Elevated B12 levels are seen in hematological disorders (chronic myelogenous leukemia, promyelocytic leukemia, polycythemia vera) and in liver disorders (acute hepatitis, cirrhosis, hepatocellular carcinoma).
