NovaFerrum 125 Disease Interactions

There is no excretory mechanism for iron. Iron will correct only hemoglobin abnormalities due to iron deficiency and should not be used to treat conditions such as thalassemia, hemosiderosis, hemochromatosis, normocytic anemia (unless iron deficiency exists), or in patients receiving blood transfusions. Clinical monitoring of erythropoietic function and ferritin levels is recommended.

Vitamin D analogs function to increase serum calcium concentrations and can exacerbate arrhythmias, particularly in patients receiving cardiac glycosides. Therapy with vitamin D analogs should be administered cautiously in patients with or predisposed to cardiac arrhythmias. Clinical monitoring of serum electrolyte concentrations and cardiac function is recommended.

Vitamin D analogs administered in the presence of hyperphosphatemia can result in precipitation of calcium-phosphate deposits within the vascular or renal systems or other soft tissue calcifications. A solubility product (Serum Calcium X Phosphate) should not exceed 70. Serum electrolyte concentrations should be corrected prior to vitamin D analog therapy and monitored during therapy.

Vitamin D analogs such as calciferol and ergocalciferol should not be given to patients with hypercalcemia, malabsorption syndrome, or evidence of vitamin D toxicity.

Ergocalciferol, cholecalciferol, and calcifediol undergo renal biotransformation during metabolic activation. Renal impairment can alter metabolic and therapeutic activity of certain vitamin D analogs. Alternative vitamin D analogs such as dihydrotachysterol (hepatic activation) and calcitriol (active form) may be considered in patients with compromised renal function.

Gastric acidity increases iron bioavailability by maintaining the ingested iron in a reduced form as ferrous ions, which are more readily absorbed than ferric ions. Therefore, when iron therapy is administered orally, higher dosages may be necessary for patients with decreased gastric acid production. Also, a liquid formulation is recommended in these patients because dissolution of the tablet coating depends on normal gastric acidity.

Iron can be irritating and damaging to gastrointestinal mucosa. Iron therapy should be administered cautiously in patients with peptic ulcer disease, enteritis, or ulcerative colitis.

Vitamin D analogs are fat soluble and oral formulations require bile for adequate intestinal absorption. Hepatic and/or biliary dysfunction decrease the absorption of vitamin D analogs. Metabolites of vitamin D analogs are primarily excreted in bile and feces. Ergocalciferol, cholecalciferol, and dihydrotachysterol undergo hepatic hydroxylation during metabolic activation. Hepatic impairment can alter the metabolic and therapeutic activity of certain vitamin D analogs. Alternative vitamin D analogs such as calcifediol (requires renal activation) and calcitriol (active form) may be considered in patients with compromised hepatic function.