Interactions between Dimercaprol and Iron sucrose

Dimercaprol has a moderate potential interaction with Allergies.

Dimercaprol ampules are formulated with peanut oil. Peanut oil may cause allergic reactions in some individuals. Physicians should use caution in prescribing dimercaprol ampules for peanut-sensitive patients. Medication and equipment necessary to treat allergic reactions should be available if the product is administered to peanut-allergic patients.

Dimercaprol has a moderate potential interaction with G-6-PD Deficiency.

Dimercaprol-associated hemolysis has been reported in patients with glucose-6-phosphate dehydrogenase deficiency. Therapy with dimercaprol should be administered with caution in patients with G6PD deficiency. Clinical monitoring of erythropoietic function including hemolysis is recommended.

Iron sucrose has a major potential interaction with Hemoglobinopathy.

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.

Dimercaprol has a moderate potential interaction with High Blood Pressure.

Dose-related increase in systolic and diastolic blood pressure, with or without accompanying tachycardia, is the most frequently reported adverse effect of dimercaprol therapy. Blood pressure may rise 15 to 30 minutes following injection and usually returns to normal within 2 hours. Therapy with dimercaprol should be administered cautiously in patients with hypertension. Clinical monitoring of blood pressure is recommended.

Dimercaprol has a major potential interaction with Liver Disease.

The use of dimercaprol is contraindicated in patients with impaired hepatic function, except for arsenic- associated jaundice. Dimercaprol, not complexed to heavy metals, is metabolized by the liver to inactive forms in patients with normal hepatic function. Hepatic impairment decreases the metabolism of dimercaprol and can result in elimination of potentially nephrotoxic dimercaprol as well as increased CNS toxicity and hypertension.

Dimercaprol has a major potential interaction with Renal Dysfunction.

Dimercaprol is primarily eliminated by the kidney complexed with a heavy metal (lead, arsenic, mercury, gold). Dimercaprol and heavy metals are nephrotoxic and dissociate at an acid pH. Urinary alkalinization during dimercaprol therapy is necessary. The serum concentration of dimercaprol is elevated in patients with oliguria and CNS toxicity and hypertension are possible. Dimercaprol should be discontinued or used only with extreme caution if acute renal insufficiency develops during therapy. Therapy with dimercaprol should be administered very cautiously and dosages reduced in patients with oliguria. Close clinical monitoring of urine pH and renal function is necessary.