Deferoxamine Mesylate (deferoxamine mesylate)

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Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

Iron Chelators/Exagamglogene Autotemcel

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: Treatment with exagamglogene autotemcel requires hematopoietic stem cell (HSC) mobilization which can suppress the immune system.

CLINICAL EFFECTS: Iron chelators should be held prior to and after infusion with exagamglogene autotemcel.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Iron chelators should be discontinued 7 days prior to initiation of mobilization or conditioning. Avoid myelosuppressive iron chelators for six months after exagamglogene autotemcel infusion. Avoid non-myelosuppressive iron chelators for three months after exagamglogene autotemcel infusion. If iron chelation is needed, consider phlebotomy in lieu of iron chelation when appropriate.(1)

DISCUSSION: In preparation for infusion of exagamglogene autotemcel, iron chelation should be discontinued 7 days prior to initiation of mobilization or conditioning.(1)

Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

Myelosuppressives; Immunomodulators/Sodium Iodide I 131

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Sodium iodide I 131 can cause depression of the hematopoetic system. Myelosuppressives and immunomodulators also suppress the immune system.(1)

CLINICAL EFFECTS: Concurrent use of sodium iodide I 131 with agents that cause bone marrow depression, including myelosuppressives or immunomodulators, may result in an enhanced risk of hematologic disorders, including anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia. Bone marrow depression may increase the risk of serious infections and bleeding.(1)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The US manufacturer of sodium iodide I 131 states that concurrent use with bone marrow depressants may enhance the depression of the hematopoetic system caused by large doses of sodium iodide I 131.(1) Sodium iodide I 131 causes a dose-dependent bone marrow suppression, including neutropenia or thrombocytopenia, in the 3 to 5 weeks following administration. Patients may be at increased risk of infections or bleeding during this time. Monitor complete blood counts within one month of therapy. If results indicate leukopenia or thrombocytopenia, dosimetry should be used to determine a safe sodium iodide I 131 activity.(1)

DISCUSSION: Hematologic disorders including death have been reported with sodium iodide I 131. The most common hematologic disorders reported include anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia.(1)

Moderate Interaction: Assess the risk to the patient and take action as needed.

Deferoxamine/Ascorbic Acid (VITAMIN C)

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: It is believed that ascorbic acid increases the iron available for chelation from an labile intracellular iron pool. Ascorbic acid may then facilitate iron-induced oxidative tissue damage.(1)

CLINICAL EFFECTS: Dietary ascorbic acid may increase the absorption of dietary iron. Supplemental ascorbic acid therapy given during chelation therapy may improve iron output;(1-9) however, excessive dosages may result in cardiac toxicity from iron-induced oxidative tissue damage.(1,2,11-13)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Ascorbic acid intake is often restricted in patients with iron overload; however, it has been used in conjunction with deferoxamine to increase iron excretion.(2) Supplemental ascorbic acid therapy should only be initiated after one month of deferoxamine therapy. Ascorbic acid therapy should only be given in patients receiving deferoxamine regularly and the dose should be given after the infusion has started. The dosage of ascorbic acid should be limited to 50 mg daily in children under 10 years of age; 100 mg daily in older children; and 200 mg daily, in divided doses, in adults.(2) Cardiac function should be monitored in patients receiving concurrent therapy. Discontinue ascorbic acid therapy in patients who develop cardiac dysfunction.(2)

DISCUSSION: Supplemental ascorbic acid therapy given during chelation therapy has been shown to improve iron output,(1-9) possibly by increasing iron available for chelation from an labile intracellular iron pool.(1) However, dosages in excess of 500 mg daily have been associated with cardiac dysfunction.(1,2,11-13)

Deferoxamine/Prochlorperazine

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Although the exact mechanism is unclear, the combination of deferoxamine and prochlorperazine appears to have additive or synergistic pharmacodynamic effects on central nervous system(CNS) dopamine activity.(1) Iron is required for normal dopamine cycling in central nervous system (CNS) neurons; iron deficiency has been associated with dopamine-mediated neuropsychiatric disease.(2-5) Deferoxamine chelation of iron in dopamine neurons may lead to diminished neural activity(1) while prochlorperazine may further decrease dopamine activity via blockade of dopamine binding sites.(6)

CLINICAL EFFECTS: Concurrent treatment with therapeutic doses of deferoxamine and prochlorperazine has resulted in loss of consciousness.(7,8)

PREDISPOSING FACTORS: Patients with normal or low iron stores may have an increased risk for toxicity.(7) The elderly are more susceptible to adverse effects from prochlorperazine.(6)

PATIENT MANAGEMENT: Although the incidence of this interaction is unknown, given the potential severity of the interaction it would be prudent, particularly in patients with normal or low iron stores, to use alternative antiemetics (e.g. ondansetron or other 5-HT3 receptor antagonists) in patients receiving deferoxamine. The Australian manufacturer of prochlorperazine states that simultaneous administration of deferoxamine and prochlorperazine is contraindicated.(9)

DISCUSSION: In a pilot study,(7) deferoxamine was prescribed for patients with progressive rheumatologic disease based upon proposed antiinflammatory effects. Deferoxamine was administered subcutaneously over 8-12 hours, 5 days per week, for a maximum of 3 weeks. Two patients who experienced nausea received prochlorperazine resulting in a loss of consciousness. Case details: - A 75 year old woman with symmetrical synovitis had pretreatment tests which included C-reactive protein (CRP) 155 mg/L, ferritin 88 mcg/L, hemoglobin (Hb) 9.2 g/dL. She received 42 grams of deferoxamine over three weeks. During the last day of treatment she complained of nausea and took 5 doses of 5 mg oral prochlorperazine over 29 hours. Twelve hours after the last dose she became drowsy, progressing to a significant impairment of consciousness; at times she was only partially responsive to painful stimuli. Electrolyte, liver function, blood glucose tests and CT of the brain were normal during this time. The patient recovered after 3 days without apparent long term sequelae. - A 58 year old, 67kg man with severe peripheral polyarthritis had pretreatment tests which included CRP 10 mg/L, ferritin 78 mcg/L and Hb 15 g/dL. He received twelve 3 gram deferoxamine infusions during the study period. On the last day of treatment he complained of nausea during the infusion and received 2 doses of prochlorperazine 12.5mg IM in a 13 hour period. The deferoxamine was stopped early due to mental status changes. He gradually lost consciousness over a 6 hour period and was only minimally responsive to painful stimuli for 2 days. During this time brisk reflexes, spontaneous limb movement and clonus were observed. Electrolyte, liver function and blood glucose tests, lumbar puncture, and CT of the brain were normal during this time. Subsequently he gradually returned to normal over a 4 day period. These cases of unexpected toxicity prompted an interaction study with iron-deficient and iron-replete rats who were given intraperitoneal deferoxamine and prochlorperazine. Given individually, neither drug impaired consciousness, but the combination led to either movement only in response to stimuli, or total loss of consciousness. Consciousness was regained by 36 hours in the iron-deficient group and 12 hours in the iron-replete group.(7)

Iron Chelators/Lovotibeglogene Autotemcel

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Treatment with lovotibeglogene autotemcel requires hematopoietic stem cell (HSC) mobilization which can suppress the immune system.

CLINICAL EFFECTS: Iron chelators should be held prior to and after infusion with lovotibeglogene autotemcel.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Iron chelators should be discontinued 7 days prior to initiation of mobilization or conditioning. Avoid myelosuppressive iron chelators for six months after lovotibeglogene autotemcel infusion. Avoid non-myelosuppressive iron chelators for three months after lovotibeglogene autotemcel infusion. If iron chelation is needed, consider phlebotomy in lieu of iron chelation when appropriate.(1)

DISCUSSION: In preparation for infusion of lovotibeglogene autotemcel, iron chelation should be discontinued 7 days prior to initiation of mobilization or conditioning.(1)

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• Lactation

• Anuria
• Chronic kidney disease stage 4 (severe) GFR 15-29 ml/min
• Chronic kidney disease stage 5 (failure) GFr<15 ml/min
• Mucormycosis
• Optic neuritis
• Pyelonephritis

• Aluminum toxicity
• Cataracts
• Hearing loss
• Seizure disorder
• Tinnitus

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More Frequent

• Auditory neurotoxicity
• Hypotension
• Mucormycosis
• Shock
• Tachycardia
• Yersinia pseudotuberculosis infection

Less Frequent

• Hypocalcemia
• Thrombocytopenic disorder

Rare or Very Rare

• Abnormal hepatic function tests
• Acute respiratory distress syndrome
• Angioedema
• Cataracts
• Leukopenia
• Night blindness
• Optic neuritis
• Seizure disorder
• Urticaria

More Frequent

• Blurred vision
• Injection site sequelae
• Pruritus of skin
• Skin rash

Less Frequent

• Acute abdominal pain
• Diarrhea
• Dysuria
• Fever
• Flushing
• Urine discoloration

Rare or Very Rare

• Acute renal failure
• Corneal opacity
• Dizziness
• Injection site inflammation
• Muscle spasm
• Nausea
• Paresthesia
• Peripheral motor neuropathy
• Peripheral sensory neuropathy
• Visual field defect

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In teratogenicity studies, deferoxamine mesylate appeared to cause delayed ossification and skeletal anomalies in 2 animal species at dosages up to 4.5 times the maximum dosage recommended for humans. For this reason, the drug should not be administered to pregnant women (especially during early pregnancy) or women who may become pregnant unless the potential benefits outweigh the possible risks to the fetus.

It is not known whether deferoxamine is distributed into milk. Because many drugs are distributed into milk, caution should be exercised when deferoxamine is used in nursing women.

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