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Cyanocobalamin (Vitamin B12) Injection

Cyanocobalamin, also known as vitamin B-12, is found in foods such as fish, shellfish, meats, and dairy products. (Although cyanocobalamin and vitamin B12 are terms used interchangeably, vitamin B12 is also available as hydroxocobalamin, a less commonly prescribed drug product). Cyanocobalamin and hydrocobalamin offer equal biological activity and can be administered nasally, orally, and parenterally. Cyanocobalamin is used to treat pernicious anemia and vitamin B12 deficiency, and is also used to determine vitamin B12 absorption via the Schilling test. B12 Deficiency in healthy individuals is rare; the elderly, those with vegan diets, and patients with malabsorption problems are more likely to become deficient. If vitamin B12 deficiency is not treated, anemia, intestinal problems, and irreversible nerve damage may occur. Oral therapy is not always effective, as some patients lack an endogenous substance produced by the stomach that is necessary for oral B12 absorption. Other patients may not be able to absorb oral vitamin B12 due to compromised intestines in the area where vitamin B12 absorption occurs. Parenteral or nasal therapy may be needed in such cases; however, intranasal therapy should only be applied for maintenance after the condition has been controlled parenterally. Cyanocobalamin was approved by the FDA in 1949.

Mechanism of Action

Vitamin B12, or cyanocolbalamin, is essential for cell reproduction, hematopoiesis, and nucleoprotein and myelin synthesis. Rapidly dividing cells (epithelial cells, bone marrow, myeloid cells) appear to require cyanocobalamin more than others. Vitamin B12 can be converted to coenzyme B12 in tissues; in this form it is essential for the conversion of methylmalonate to succinate and it is also required for the synthesis of methionine from homocysteine. In the absence of B12, tetrahydrofolate cannot regenerate from its inactive storage form, 5-methyl tetrahydrofolate, which results in a folate deficiency. Vitamin B12 also may maintain sulfhydryl (SH) groups in the reduced form required by many SH-activated enzyme systems. Through these reactions, vitamin B12 participates in fat and carbohydrate metabolism and protein synthesis. Vitamin B12 deficiency results in megaloblastic anemia, GI lesions, and neurologic damage. Vitamin B12 requires factor-mediated active transport for absorption; insufficient intrinsic factor results in pernicious anemia.

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