cyanocobalamin (generic name)
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Interactions with Drugs
Excessive alcohol intake lasting longer than two weeks can decrease vitamin B12 absorption from the gastrointestinal tract.
Aminosalicylic acid can reduce oral vitamin B12 absorption, possibly by as much as 55%, as part of a general malabsorption syndrome. Megaloblastic changes, and occasional cases of symptomatic anemia, have occurred. Vitamin B12 levels should be monitored in people taking aminosalicylic acid for more than one month.
An increased bacterial load can bind significant amounts of vitamin B12 in the gut, preventing its absorption. In people with bacterial overgrowth of the small bowel, antibiotics such as metronidazole (Flagyl®) can actually improve vitamin B12 status. The effects of most antibiotics on gastrointestinal bacteria are unlikely to have clinically significant effects on vitamin B12 levels.
The data regarding the effects of oral contraceptives on vitamin B12 serum levels are conflicting. Some studies have found reduced serum levels in birth control pill users, but others have found no effect despite the use of birth control pills for up to six months. When birth control pill use is stopped, normalization of vitamin B12 levels usually occurs. Lower vitamin B12 serum levels seen with birth control pills probably are not clinically significant.
Limited case reports suggest that chloramphenicol can delay or interrupt the reticulocyte response to supplemental vitamin B12 in some patients. Blood counts should be monitored closely if this combination cannot be avoided.
Cobalt irradiation of the small bowel can decrease gastrointestinal (GI) absorption of vitamin B12.
Colchicine can disrupt normal intestinal mucosal function, leading to malabsorption of several nutrients, including vitamin B12. Lower doses do not seem to have a significant effect on vitamin B12 absorption after three years of colchicine therapy. The significance of this interaction is unclear. Vitamin B12 levels should be monitored in people taking large doses of colchicine for prolonged periods.
Colestipol (Colestid®) and Cholestyramine (Questran®) resins can decrease gastrointestinal (GI) absorption of vitamin B12. It is unlikely that this interaction will deplete body stores of vitamin B12 unless there are other factors contributing to deficiency. In a group of children treated with cholestyramine for up to 2.5 years, there was not any change in serum vitamin B12 levels. Routine supplements are not necessary.
H2-blockers include cimetidine (Tagamet®), famotidine (Pepcid®), nizatidine (Axid®), and ranitidine (Zantac®). Reduced secretion of gastric acid and pepsin produced by H2-blockers can reduce absorption of protein-bound (dietary) vitamin B12, but not of supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Clinically significant vitamin B12 deficiency and megaloblastic anemia are unlikely, unless H2-blocker therapy is prolonged (two years or more) or the person's diet is poor. It is also more likely if the person is rendered achlorhydric (lacking hydrochloric stomach acid), which occurs more frequently with proton pump inhibitors than H2-blockers. Vitamin B12 levels should be monitored in people taking high doses of H2 blockers for prolonged periods.
Metformin may reduce serum folic acid and vitamin B12 levels. These changes can lead to hyperhomocysteinemia (abnormally large levels of homocysteine in the blood), adding to the risk of cardiovascular disease in people with diabetes. There are also rare reports of megaloblastic anemia in people who have taken metformin for five years or more. Reduced serum levels of vitamin B12 occur in up to 30% of people taking metformin chronically. However, clinically significant deficiency is not likely to develop if dietary intake of vitamin B12 is adequate. Deficiency can be corrected with vitamin B12 supplements even if metformin is continued. The metformin-induced malabsorption of vitamin B12 is reversible by oral calcium supplementation. A multivitamin preparation may also be valuable for some patients. Patients should be monitored for signs and symptoms of vitamin B12 and folic acid deficiency. People taking metformin chronically should be advised to include adequate amounts of vitamin B12 in their diet, and have their serum vitamin B12 and homocysteine levels checked annually.
Nicotine can reduce serum vitamin B12 levels. The need for vitamin B12 supplementation has not been adequately studied.
Nitrous oxide inactivates the cobalamin form of vitamin B12 by oxidation. Symptoms of vitamin B12 deficiency, including sensory neuropathy, myelopathy, and encephalopathy can occur within days or weeks of exposure to nitrous oxide anesthesia in people with subclinical vitamin B12 deficiency. Symptoms are treated with high doses of vitamin B12, but recovery can be slow and incomplete. People with normal vitamin B12 levels have sufficient vitamin B12 stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (nitrous oxide abuse). Vitamin B12 levels should be checked in people with risk factors for vitamin B12 deficiency prior to using nitrous oxide anesthesia.
Phenytoin (Dilantin®), phenobarbital, and primidone (Mysoline®) anticonvulsants have been associated with reduced vitamin B12 absorption and reduced serum and cerebrospinal fluid levels in some patients. This may contribute to the megaloblastic anemia, primarily caused by folate deficiency, associated with these drugs. It has also been suggested that reduced vitamin B12 levels may contribute to the neuropsychiatric side effects of these drugs. Patients should be encouraged to maintain adequate dietary vitamin B12 intake. Folate and vitamin B12 status should be checked if symptoms of anemia develop.
Proton pump inhibitors (PPIs) include omeprazole (Prilosec®, Losec®), lansoprazole (Prevacid®), rabeprazole (Aciphex®), pantoprazole (Protonix®, Pantoloc®), and esomeprazole (Nexium®). The reduced secretion of gastric acid and pepsin produced by PPIs can reduce absorption of protein-bound (dietary) vitamin B12, but not supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Reduced vitamin B12 levels may be more common with PPIs than with H2-blockers, because they are more likely to produce achlorhydria (complete absence of gastric acid secretion). However, clinically significant vitamin B12 deficiency is unlikely, unless PPI therapy is prolonged (two years or more) or dietary vitamin intake is low. Vitamin B12 levels should be monitored in people taking high doses of PPIs for prolonged periods.
Reduced serum vitamin B12 levels may occur when zidovudine (AZT, Combivir®, Retrovir®) therapy is started. This adds to other factors that cause low vitamin B12 levels in people with HIV and might contribute to the hematological toxicity associated with zidovudine. However, data suggests vitamin B12 supplements are not helpful for people taking zidovudine.
Interactions with Herbs and Dietary Supplements
Folic acid, particularly in large doses, can mask vitamin B12 deficiency. In vitamin B12 deficiency, folic acid can produce hematologic improvement in megaloblastic anemia, while allowing potentially irreversible neurological damage to progress. Vitamin B12 status should be determined before folic acid is given as a monotherapy.
Potassium supplements can reduce absorption of vitamin B12 in some people. This effect has been reported with potassium chloride and, to a lesser extent, with potassium citrate. Potassium might contribute to vitamin B12 deficiency in some people with other risk factors, but routine supplements are not necessary.
Preliminary evidence suggests that vitamin C supplements can destroy dietary vitamin B12. However, other components of food, such as iron and nitrates, might counteract this effect. Clinical significance is unknown, and it can likely be avoided if vitamin C supplements are taken at least two hours after meals.