Medication Summary
Vitamin B12 is available for therapeutic use parenterally as either cyanocobalamin or hydroxocobalamin. [26] Both are equally useful in the treatment of vitamin B12 deficiency, and they are nontoxic (except for rare allergic reactions). Theoretical advantages exist to using hydroxocobalamin because it is retained better in the body and is more available to cells; both chemical forms of cobalamin provide prompt correction.
Vitamins
Class Summary
Cobalamin is an essential vitamin. The inability to absorb adequate quantities of the vitamin from the diet leads to hematologic and neurologic complications.
Cyanocobalamin (CaloMist, Ener-G, Nascobal)
Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitamin B12 in humans. Microbes, but not humans or plants, synthesize vitamin B12. Vitamin B12 deficiency may result from intrinsic factor (IF) deficiency (pernicious anemia), partial or total gastrectomy, or diseases of the distal ileum.
Cyanocobalamin may be administered either intramuscularly (IM) or subcutaneously (SC). At the initiation of therapy, large daily doses are administered in order to replenish body stores with cobalamin.
With certain hereditary defects of cobalamin, metabolism doses of cobalamin (eg, 1000 µg SC every week) may be required to obtain a response.
Hydroxocobalamin
Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitamin B12 in humans. Vitamin B12 synthesized by microbes but not humans or plants. Vitamin B12 deficiency may result from intrinsic factor deficiency (pernicious anemia), partial or total gastrectomy, or diseases of the distal ileum. This agent is used to treat conditions caused by altered cobalamin metabolism that may cause secondary carnitine deficiency (ie, cobalamin C deficiency).
Multivitamins (MVI-12, Cernevit-12)
Multivitamins are used as dietary supplements.
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Pernicious anemia. The structure of cyanocobalamin is depicted. The cyanide (Cn) is in green. Other forms of cobalamin (Cbl) include hydroxocobalamin (OHCbl), methylcobalamin (MeCbl), and deoxyadenosylcobalamin (AdoCbl). In these forms, the beta-group is substituted for Cn. The corrin ring with a central cobalt atom is shown in red and the benzimidazole unit in blue. The corrin ring has 4 pyrroles, which bind to the cobalt atom. The fifth substituent is a derivative of dimethylbenzimidazole. The sixth substituent can be Cn, CC3, hydroxycorticosteroid (OH), or deoxyadenosyl. The cobalt atom can be in a +1, +2, or +3 oxidation state. In hydroxocobalamin, it is in the +3 state. The cobalt atom is reduced in a nicotinamide adenine dinucleotide (NADH)–dependent reaction to yield the active coenzyme. It catalyzes 2 types of reactions, which involve either rearrangements (conversion of l methylmalonyl coenzyme A [CoA] to succinyl CoA) or methylation (synthesis of methionine).
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Pernicious anemia. Inherited disorders of cobalamin (Cbl) metabolism are depicted. The numbers and letters correspond to the sites at which abnormalities have been identified, as follows: (1) absence of intrinsic factor (IF); (2) abnormal Cbl intestinal adsorption; and (3) abnormal transcobalamin II (TC II), (a) mitochondrial Cbl reduction (Cbl A), (b) cobalamin adenosyl transferase (Cbl B), (c and d) cytosolic Cbl metabolism (Cbl C and D), (e and g) methyl transferase Cbl utilization (Cbl E and G), and (f) lysosomal Cbl efflux (Cbl F).
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Pernicious anemia. Cobalamin (Cbl) is freed from meat in the acidic milieu of the stomach where it binds R factors in competition with intrinsic factor (IF). Cbl is freed from R factors in the duodenum by proteolytic digestion of the R factors by pancreatic enzymes. The IF-Cbl complex transits to the ileum where it is bound to ileal receptors. The IF-Cbl enters the ileal absorptive cell, and the Cbl is released and enters the plasma. In the plasma, the Cbl is bound to transcobalamin II (TC II), which delivers the complex to nonintestinal cells. In these cells, Cbl is freed from the transport protein.
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Peripheral smear of blood from a patient with pernicious anemia. Macrocytes are observed, and some of the red blood cells show ovalocytosis. A 6-lobed polymorphonuclear leucocyte is present.
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Bone marrow aspirate from a patient with untreated pernicious anemia. Megaloblastic maturation of erythroid precursors is shown. Two megaloblasts occupy the center of the slide with a megaloblastic normoblast above.
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Response to therapy with cobalamin (Cbl) in a previously untreated patient with pernicious anemia. A reticulocytosis occurs within 5 days after an injection of 1000 mcg of Cbl and lasts for about 2 weeks. The hemoglobin (Hgb) concentration increases at a slower rate because many of the reticulocytes are abnormal and do not survive as mature erythrocytes. After 1 or 2 weeks, the Hgb concentration increases about 1 g/dL per week.
Tables
Patient Condition |
Methylmalonic Acid |
Homocysteine |
Healthy |
Normal |
Normal |
Vitamin B12 deficiency |
Elevated |
Elevated |
Folate deficiency |
Normal |
Elevated |
Patient Condition |
Stage I No Intrinsic Factor |
Stage II Intrinsic Factor |
Stage III Antibiotic |
Stage IV Pancreatic Extract |
Healthy |
Normal |
… |
… |
… |
Pernicious anemia |
Low |
Normal |
… |
… |
Bacterial overgrowth |
Low |
Low |
Normal |
… |
Pancreatic insufficiency |
Low |
Low |
Low |
Normal |
Defect in ileum |
Low |
Low |
Low |
Low |
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- Overview
- Presentation
- DDx
- Workup
- Approach Considerations
- CBC and Peripheral Blood Smear
- Indirect Bilirubin and Serum Lactate Dehydrogenase
- Evaluation of Gastric Secretions
- Serum Cobalamin
- Serum Folic Acid, Methylmalonic Acid, and Homocysteine
- Intrinsic Factor Antibodies
- Schilling Test
- Clinical Trial of Vitamin B12
- Bone Marrow Aspiration and Biopsy
- Other Tests
- Show All
- Treatment
- Medication
- Questions & Answers
- Media Gallery
- Tables
- References
