![]() ![]() Such measures remove the need for long-term administration of cyanocobalamin.ġ2 in excess of normal (due to pregnancy, thyrotoxicosis, hemolytic anemia, hemorrhage, malignancy, hepatic and renal disease) can usually be met with oral supplementation.Ĭyanocobalamin Injection, USP is also suitable for the vitamin B It may be possible to treat the underlying disease by surgical correction of anatomic lesions leading to small bowel bacterial overgrowth, expulsion of fish tapeworm, discontinuation of drugs leading to vitamin malabsorption (seeĭrug Interactions), use of a gluten-free diet in nontropical sprue, or administration of antibiotics in tropical sprue. Gastrointestinal pathology, dysfunction, or surgery, including gluten enteropathy or sprue, small bowel bacteria overgrowth, total or partial gastrectomy.Hydroxycobalamin is equally as effective as cyanocobalamin, and they share the cobalamin molecular structure.Ĭyanocobalamin is indicated for vitamin Bġ2 deficiencies due to malabsorption which may be associated with the following conditions: Oral absorption is considered too undependable to rely on in patients with pernicious anemia or other conditions resulting in malabsorption of vitamin BĬyanocobalamin is the most widely used form of vitamin Bġ2, and has hematopoietic activity apparently identical to that of the antianemia factor in purified liver extract. A small amount (approximately 1% of the total amount ingested) is absorbed by simple diffusion, but this mechanism is adequate only with very large doses. It is then transported by the transcobalamin binding proteins. In people with normal absorption, deficiencies have been reported only in strict vegetarians who consume no products of animal origin (including no milk products or eggs).ġ2 is bound to intrinsic factor during transit through the stomach separation occurs in the terminal ileum in the presence of calcium, and vitamin Bġ2 enters the mucosal cell for absorption. Vitamin Bġ2 is not present in foods of plant origin, but is abundant in foods of animal origin. The average diet supplies about 5 to 15 mcg/day of vitamin Bġ2 in a protein-bound form that is available for absorption after normal digestion. Prompt parenteral administration of vitamin Bġ2 prevents progression of neurologic damage. Intrinsic factor deficiency causes pernicious anemia, which may be associated with subacute combined degeneration of the spinal cord. Intravenous administration results in even more rapid excretion with little opportunity for liver storage.ġ2 depends on the presence of sufficient intrinsic factor and calcium ions. ![]() The major portion is excreted within the first eight hours. Within 48 hours after injection of 100 or 1000 mcg of vitamin Bġ2, 50 to 98% of the injected dose may appear in the urine. The liver is the main organ for vitamin B ![]() Absorbed vitamin Bġ2 binding proteins, transcobalamin I and II to the various tissues. ![]() 12 is essential to growth, cell reproduction, hematopoiesis, and nucleoprotein and myelin synthesis.Ĭyanocobalamin is quantitatively and rapidly absorbed from intramuscular and subcutaneous sites of injection the plasma level of the compound reaches its peak within 1 hour after intramuscular injection. ![]()
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