Fe-Tinic 150 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.

Acute hemolysis following administration of high doses of ascorbic acid in patients with glucose-6-phosphate deficiency (G6PD) has been reported. Ascorbic acid should be administered cautiously and dosages modified in patients with G6PD.

Large doses of ascorbic acid have lead to hyperoxaluria in 5% of patients. Ascorbic acid can acidify urine resulting in precipitation of urate, cystine, or oxalate stones. Ascorbic acid should be administered cautiously and dosages modified in patients predisposed to renal stones. Clinical monitoring of urinalysis for pH and crystal formation is recommended.

Ascorbic acid preparations contain sodium. The sodium content should be considered when used in patients with sodium restricted diets and conditions require sodium restriction, such as congestive heart failure, hypertension, and fluid retention.

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.

Ascorbic acid is removed by dialysis.