Cyanocobalamin/folic acid/pyridoxine/strontium gluconate Disease Interactions

Hypokalemia (resulting in death) has occurred during vitamin B12 therapy as a result of increased red blood cell requirements during hematopoiesis. Clinical monitoring and correction of potassium levels prior to and during vitamin B12 therapy is necessary.

The use of cyanocobalamin is contraindicated in patients with Leber's disease (hereditary optic nerve atrophy). Cyanocobalamin has induced severe and rapid optic nerve atrophy in patient's with early Leber's disease.

The use of folic acid is contraindicated in patients with undiagnosed anemia. Folic acid in dosages above 1 mg/day can obscure the diagnosis of pernicious anemia by alleviating the hematologic abnormalities while allowing the progression of neurologic complications. In addition, folic acid alone is improper therapy in the treatment of pernicious anemia and other megaloblastic anemias where vitamin B12 is deficient.

Absorption of vitamin B12 is decreased in malabsorption syndromes and in pernicious anemia without coadministration of intrinsic factor (IF). Cyanocobalamin is rapidly absorbed following IM or subcutaneous injections. Hydroxocobalamin (cyanocobalamin analog) functions the same a cyanocobalamin, but has induced antibody formation to the hydroxocobalamin-transcobalamin II complex. The use of cyanocobalamin may be preferred in patients with these conditions.

Cyanocobalamin products contain aluminum that may be toxic and may reach toxic levels with prolonged parenteral administration if kidney function is impaired. Premature neonates are particularly at risk because their kidneys are immature, and they require large amounts of calcium and other solutions which also contain aluminum. Research indicates that patients with impaired kidney function, including premature neonates, who receive parenteral levels of aluminum greater than 4-5 mcg/kg/day accumulate aluminum at levels associated with central nervous system and bone toxicity. Caution and monitoring are recommended.

The B vitamins are readily absorbed in the GI tract following oral administration. However, GI absorption may be decreased in patients with malabsorption syndromes and other conditions. For example, the absorption of thiamine and pyridoxine may commonly be decreased in alcoholics and in patients with cirrhosis. Likewise, riboflavin absorption may be impaired in patients with hepatitis, cirrhosis, or biliary obstruction. When malabsorption of these vitamins is suspected, parenteral administration may be appropriate.