Calcium/folic acid/ginger/pyridoxine Disease Interactions

Elevated serum concentrations of calcium and phosphate can exceed the solubility level and result in calcium- phosphate precipitates that deposit in vascular and renal systems as well as other soft tissues of the body. Therapy with calcium should be administered with extreme caution in patients with hyperphosphatemia (hypoparathyroidism or severe renal impairment). Administration of oral calcium acetate or calcium carbonate, in addition to providing calcium, complexes phosphates within the GI tract. These complexes are eliminated in the feces. Clinical monitoring of serum calcium and phosphate concentrations is necessary.

Calcium is involved in cardiac muscle contraction and electrical impulse conduction. Therapy with calcium salt formulations (particularly IV) should be administered cautiously to patients with cardiac disease. Patients receiving cardiac glycosides and concomitant IV calcium may experience arrhythmias. Therapy with IV calcium should be administered slowly and at reduced dosages in patients with cardiac disease.

Calcium is absorbed from the intestinal tract by active transport and passive diffusion. Malabsorption syndromes (celiac disease, GI resection), deficiency of vitamin D, parathyroid hormone, or calcitonin, or an alkaline gastric pH (achlorhydria, carbonate or phosphate salts) can decrease the absorption of oral formulations of calcium. Calcium is available in oral and parenteral formulations.

Absorption of oral calcium formulations may be altered and elimination of calcium by the kidney decreased with renal impairment. Hyperphosphatemia occurs during renal failure. Calcium acetate or calcium carbonate, in addition to providing calcium, complexes phosphates within the GI tract. Calcium carbonate can partially correct metabolic acidosis associated with chronic renal failure. Clinical monitoring of renal function and serum calcium and phosphate concentrations is necessary.

Hypercalciuria, with or without hypercalcemia, may occasionally occur in patients with sarcoidosis. Elevated calcium levels may result from increased intestinal absorption of calcium, which is related to the extrarenal production of vitamin D by mononuclear phagocytes present within the sarcoid granuloma. Therapy with calcium salts should be administered cautiously and only if necessary in patients with sarcoidosis.

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.

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.