Skip to Content

Deferoxamine (Systemic)

Desferrioxamine mesylate {21}

Deferoxamine mesilate {21}

Primary: AD300

Commonly used brand name(s): Desferal.

Another commonly used name is
desferrioxamine .
Note: For a listing of dosage forms and brand names by country availability, see Dosage Forms section(s).


Chelating agent—


Note: Bracketed information in the Indications section refers to uses that are not included in U.S. product labeling.


Toxicity, iron, acute (treatment adjunct)—Deferoxamine facilitates the removal of iron from the body in severe, acute iron poisoning.{55}{58}{67}{68}{69}{70}{71}{72}{73}{74}{75}{76} It is used as an adjunct to, not a substitute for, standard treatment measures, which may include induction of emesis with ipecac syrup; gastric lavage;{43} whole bowel irrigation;{38} suction and maintenance of clear airway; control of shock with intravenous fluids, blood, oxygen, and vasopressors; and correction of acidosis.{24}{43}{44}
—Acute iron poisoning usually follows a biphasic course. During the first phase, vomiting, sometimes bloody and containing partially digested tablets, may occur within the first half hour and recur for up to several hours. However, enteric-coated iron tablets may pass into the small intestine without causing severe gastric symptoms, but may appear on x-ray. Abdominal pain may or may not occur within the first 6 to 12 hours. Tarry stools or bloody diarrhea and lethargy may occur, and in some cases, leukocytosis, hyperglycemia,{42} and fever may be present.{12}{14} A latent period, lasting from a few to 48 hours after ingestion, may occur between the 2 symptomatic phases, during which time the patient may appear to improve clinically. The second phase, not seen in milder cases, is associated with hepatic injury or failure, hypoglycemia, metabolic acidosis, hypotension,{38} shock, seizures, coma, or death.{12}{14} Several weeks to months after the acute episode, late complications of hepatic cirrhosis or duodenal or pyloric stricture may be seen.{14}
—Most iron poisoning cases do not require deferoxamine. However, when deferoxamine is indicated in severe poisoning, the shorter the interval between ingestion of the overdose and administration of deferoxamine, the greater the probability of complete recovery.{05}
—Clinical signs suggesting severe iron poisoning that should be treated with deferoxamine include the following:   • Patient is severely symptomatic.{51}{52} Presence of symptoms warrants treatment with deferoxamine regardless of patient"s serum iron concentrations, unless symptoms are mild (e.g., minor abdominal upset), or they occur after emesis has been induced by ipecac administration.{23}{25}{34}{35}
   • Serum iron concentrations exceeding total iron-binding capacity (TIBC),{43}{48} if obtained within 4 to 6 hours after iron ingestion.{12}{25}
   • Serum iron concentrations > 500 mcg per deciliter (mcg/dL) (90 micromoles per liter [micromoles/L]).{48}{50}{51}{52} Serum iron concentrations above 500 mcg/dL (90 micromoles/L) warrant treatment with deferoxamine even if patient is asymptomatic.{50}{51}{52} Use of deferoxamine in asymptomatic patients with serum iron concentrations of 350 to 500 mcg/dL (63 to 90 micromoles/L) has been recommended by some clinicians.{43}{48}{52}
   • If serum iron concentrations and TIBC are both unavailable, deferoxamine should be used when a combination of the following occur:{38}   —Diarrhea or vomiting occurs spontaneously{23}{43}{45} within 6 hours of ingestion.
   —Leukocyte counts > 15,000 per cubic millimeter (15,000 ×10 9 per liter).{43}{48}
   —Serum glucose > 150 mg per deciliter (8 millimoles per liter).{43}{45}
   —There is a positive deferoxamine provocation test. However, a negative test does not rule out iron toxicity, since false negative tests have been reported with deferoxamine.{20}{39}{45}{48}
   —Abdominal x-ray reveals presence of tablets/capsules.{20}{45}{48}

Toxicity, iron, chronic (treatment)—Deferoxamine is indicated for promotion of iron excretion in patients who have an iron overload secondary to multiple transfusions associated with some chronic anemias, such as thalassemia,{01}{24}{44} and in secondary hemochromatosis.{05}{10} {18} Ascorbic acid may be administered concurrently in small doses to improve the chelating action of deferoxamine and to increase the amount of iron excreted.{05} Since phlebotomy is precluded in patients with transfusional iron overload, chelation with deferoxamine is the only effective therapeutic alternative.{19}

[Toxicity, aluminum (treatment)]—Deferoxamine, administered intravenously or intraperitoneally, is used to treat aluminum-induced encephalopathy, osteomalacia,{03} and aluminum overload in children and adults with chronic renal failure, but only those{52}{53} who are maintained with hemodialysis or continuous ambulatory peritoneal dialysis (CAPD).{02}{04}{15}{16}{17}{23}{43}

[Toxicity, aluminum (diagnosis)]—Deferoxamine is used to diagnose aluminum toxicity in patients with end-stage renal disease.{43}

Deferoxamine is not indicated for the treatment of primary hemochromatosis, since phlebotomy is more effective and is the treatment of choice for this indication.{24}{44}

Deferoxamine is not used to remove iron deposits from the cornea and subconjunctiva in the treatment of ocular siderosis, nor to remove rust stains after penetration of the eye by a foreign body.{23}


Physicochemical characteristics:
Molecular weight—
    656.79 {21} {44}

Mechanism of action/Effect:

Iron toxicity—Deferoxamine has a strong affinity for trivalent (ferric) iron, binding with it to form ferrioxamine, a stable, water-soluble complex, which is eliminated via the kidneys. {39} {43} Theoretically, 100 mg of deferoxamine is capable of binding approximately 8.5 mg of ferric iron. {05} {43} {44} Deferoxamine can remove iron from ferritin and hemosiderin in vitro and to a lesser extent from transferrin; {06} {24} {44} however, the iron in hemoglobin, myoglobin, {05} {24} or cytochromes is not removed by deferoxamine. {06} {44}

Aluminum toxicity—Deferoxamine combines with tissue-bound aluminum to form aluminoxamine, a stable, water-soluble complex. {43} The formation of aluminoxamine causes blood concentrations of aluminum to rise, resulting in an increased concentration gradient between the blood and dialysate, with the net effect of an increased removal of aluminum during dialysis. {15} Theoretically, 100 mg of deferoxamine is capable of binding approximately 4.1 mg of aluminum. {43}

Other actions/effects:

Deferoxamine has a low affinity for ferrous iron {05} and a very low affinity for calcium. {06} Studies in man and animals have shown no increase in the excretion of electrolytes or trace metals. {24} {44}


Poorly absorbed from gastrointestinal tract after oral administration; therefore, parenteral administration is required. {06}


Rapidly metabolized by tissues {05} and by plasma enzymes, but exact mechanism is not known. {06} {24} {44}


Distribution—About 1 hour. {05} {61}

Elimination—About 6 hours. {61}

    Renal—Deferoxamine is rapidly excreted by the kidneys after intramuscular injection, often without binding any iron. {13} The water-soluble complexes, ferrioxamine and aluminoxamine, pass easily through the kidneys, with ferrioxamine possibly imparting a characteristic orange-rose (vin rosé) color to the urine. {24} {43} {44}
    Fecal—About one-third the total quantity of iron excreted in response to deferoxamine therapy is excreted through the bile into the feces. {05}
    In dialysis—Dialysis is of no value in removing serum iron alone but may be used to increase excretion of ferrioxamine, the deferoxamine-iron complex. Deferoxamine is readily dialyzable. {23} {24} {43} {44}

Precautions to Consider


Problems in humans have not been documented; however, deferoxamine is not recommended for women of child-bearing potential or for use during early pregnancy.{24}{43} However, in cases of moderate to severe, acute iron intoxication, deferoxamine should be used, since iron is also toxic to the fetus.

Skeletal abnormalities were observed in the fetuses of 2 animal species when deferoxamine was administered in doses 4.5 times the maximum daily{23}{44} human dose.{24}{44}

FDA Pregnancy Category C.{44}


It is not known whether deferoxamine is distributed into breast milk.{43}{44} However, problems in humans have not been documented.{23}{24}


Deferoxamine is used after acute overdose,{55} but is not usually used as chronic therapy in children up to 3 years of age. Younger patients are more likely to experience auditory and ocular toxicity with long-term, high-dose therapy.{07}{08}{09}


In patients with iron overload, when ascorbic acid is administered concurrently with deferoxamine to improve chelation and increase ferrioxamine excretion, older patients may be more prone to cardiac decompensation due to increased tissue iron toxicity; therefore, this regimen should be used with caution in older patients.{05}{13}

Drug interactions and/or related problems
The following drug interactions and/or related problems have been selected on the basis of their potential clinical significance (possible mechanism in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

Note: Combinations containing any of the following medications, depending on the amount present, may also interact with this medication.

» Ascorbic acid    (vitamin C given orally in doses of 150 to 250 mg per day may improve the chelating action {05} {43} of deferoxamine and increase the amount of iron excreted; however, concurrent use may cause exacerbation of tissue iron toxicity, {43} especially in the heart, causing cardiac decompensation; therefore, this regimen should be used with caution in older patients and patients with cardiac problems; {13} the need for ascorbic acid supplementation should be completely documented by measurements of iron excretion before and after supplements, and the oral dose of ascorbic acid should be given an hour or two after the deferoxamine infusion has been initiated when adequate concentrations of deferoxamine have been achieved {22})

Epoetin{43}    (aluminum toxicity may reduce erythropoiesis; therefore, dialysis patients with aluminum toxicity may require an adjustment in epoetin dosage)

Laboratory value alterations
The following have been selected on the basis of their potential clinical significance (possible effect in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

With diagnostic test results
Colorimetric iron assay    (deferoxamine may interfere with test, resulting in falsely low concentrations of serum iron {11})

» Total iron-binding capacity (TIBC)    (deferoxamine may cause a falsely high TIBC {45} {47} {48})

Medical considerations/Contraindications
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)— not necessarily inclusive (» = major clinical significance).

Risk-benefit should be considered when the following medical problems exist
» Anuria or oliguria or{24}{44}
» Renal disease, severe{24}{43}{44}    (decreases the excretion of deferoxamine and its chelates; dialysis may be used to increase excretion of the iron-deferoxamine and aluminum-deferoxamine complexes {05} {43})

Sensitivity to deferoxamine{43}

Patient monitoring
The following may be especially important in patient monitoring (other tests may be warranted in some patients, depending on condition; » = major clinical significance):

» Ferritin concentrations, serum{43}{64} or
» Iron concentrations, serum    (recommended periodically to adjust dose of deferoxamine in relation to iron burden; {08} in acute toxicity, blood samples should be obtained within 4 hours after iron ingestion, and repeated, because iron undergoes rapid redistribution into tissues; {05} serum drawn early [within 2 hours after ingestion] may have artificially high concentrations of iron; but achievement of peak serum concentrations is delayed if the iron was in extended-release form, if the patient had a significant amount of food in his/her stomach, and if the dose of iron was large; serum iron concentrations obtained beyond 6 hours after ingestion may not be elevated, even in the presence of severe poisoning; {14} in chronic iron overload, chelation treatment should be continued until the serum iron concentration is < 100 mcg per deciliter [18 micromoles per liter]; {20} it may be important to monitor serum ferritin concentrations in patients with chronic iron overload {64})

Iron excretion, urinary, 24-hr{08}{43}{46}    (recommended periodically for dosage adjustment and to determine duration of therapy {05})

Total iron-binding capacity (TIBC){25}{43}    (may be useful if evaluated prior to administration of deferoxamine; {46} {54} following deferoxamine therapy, TIBC should not be relied upon as an indicator of acute iron overdose {45} {48} {54} because it cannot provide information on the saturation of iron-binding proteins, {48} and it may be falsely elevated {45} {47} {48})

In chronic iron overload only
» Audiovisual examinations    (complete eye examinations, {40} including visual-evoked potentials, and audiologic testing recommended every 3 months, since patients on chronic subcutaneous therapy may be asymptomatic with the loss identified only by careful auditory testing or ophthalmologic examination; slit-lamp eye examinations recommended periodically to detect cataracts in patients treated for chronic iron overload; deficits are usually reversible upon immediate dosage reduction or discontinuation of deferoxamine therapy {07} {08} {24} {43} {44})

In aluminum toxicity only
Aluminum concentrations, serum{43}    (recommended before and after administration of deferoxamine; a rise in serum aluminum concentration of > 150 mcg per L, measured 18 to 48 hours after the baseline measurement, is diagnostic of aluminum toxicity {66})

Side/Adverse Effects

Note: Iron overload increases susceptibility of patients to Yersinia enterocolitica this susceptibility may be enhanced by deferoxamine therapy.{24} {26}{27}{28}{29}{36}{43}{44} Mucormycosis has also been reported in patients receiving deferoxamine while undergoing hemodialysis.{24}{30}{31}{32} {33}{36}{43}{44}{56}

The following side/adverse effects have been selected on the basis of their potential clinical significance (possible signs and symptoms in parentheses where appropriate)—not necessarily inclusive:

Those indicating need for medical attention
More frequent
Allergic reaction (hives; itching; skin rash; wheezing){24}{43}{44}
auditory neurotoxicity (hearing problems){43}{44}— especially in younger patients
convulsions {20}{43}{55}
fast heartbeat {20}{24}{43}{44}
flushing {20}{44}{55}
hives, itching, or skin rash {24}{43}{44}{55}
low blood pressure or shock {24}{43}{44}{55}
ocular toxicity (blurred vision ; decreased acuity; impaired peripheral, color, and night vision; retinal pigmental abnormalities ){24}{43}{44}—more frequent in younger patients
pain or swelling at site of injection {24}{43}
respiratory distress syndrome (cyanosis; difficult or fast breathing){55}{69}—with excessively high intravenous doses for more than 1 day {43}

Note: Auditory neurotoxicity may occur in patients on chronic, high-dose therapy. Onset may be acute and may accompany ocular problems. High-frequency hearing loss may occur in some patients after the serum ferritin returns to normal.{07}{08} Usually, but not always,{38} reversible upon reduction of dose.
Allergic reaction, convulsions, fast heartbeat, flushing, or low blood pressure or shock may be due to too-rapid a rate of intravenous injection in acute iron intoxication;{44}{55} skin problems may also occur in patients on chronic therapy as an allergic-type reaction.
Ocular toxicity may occur in patients with low ferritin levels who are on chronic, high-dose therapy. {44} Onset may be acute within 4 to 17 days of initiation of therapy{09} and may accompany hearing loss. Usually reversible upon reduction of dose or discontinuation of deferoxamine.{44} Cataracts have been observed on rare occasions in patients on long-term therapy.{08}{09}

Less frequent
—with chronic therapy     
Abdominal or stomach discomfort {24}{43}{44}
diarrhea {24}{43}{44}
difficult urination {24}{43}{44}
fever {24}{44}
hypocalcemia (abdominal and muscle cramps)—only when used for aluminum toxicity{61}{62}{63}
leg cramps {24}{43}{44}
thrombocytopenia (unusual bleeding or bruising){25}{43}

Those not indicating need for medical attention
Urine color change to orange-rose or “vin rosé” color {24}{44}

Patient Consultation
As an aid to patient consultation, refer toAdvice for the Patient, Deferoxamine (Systemic).

In providing consultation, consider emphasizing the following selected information (» = major clinical significance):

Before receiving this medication
»   Conditions affecting use, especially:
Sensitivity to deferoxamine

Pregnancy—Not recommended for use by women of child-bearing potential or during early pregnancy, unless iron poisoning becomes life-threatening

Use in children—Used after acute overdose, but not usually used as chronic therapy in children up to 3 years of age; also, younger patients on chronic, high-dose therapy are more likely to develop hearing and ocular toxicity

Use in the elderly—Caution when ascorbic acid used concurrently with deferoxamine; older patients more prone to cardiac decompensation with this regimen
Other medications, especially ascorbic acid
Other medical problems, especially renal disease

Proper use of this medication
» Importance of clear understanding and careful following of physician"s directions when using medication at home

» Proper dosing

» Proper storage

Precautions while using this medication
» Regular visits to physician to check progress of therapy and to prevent adverse effects

» Checking with doctor as soon as possible if any hearing or vision problems are noticed

Not taking vitamin C unless ordered by physician

Side/adverse effects
Signs of potential side effects, especially allergic reaction; hearing impairment; convulsions; fast heartbeat; flushing; hives, itching, or skin rash; low blood pressure or shock; vision impairment; pain or swelling at site of injection; respiratory distress syndrome; abdominal or stomach discomfort; diarrhea; difficult urination; fever; hypocalcemia; leg cramps; or thrombocytopenia

Urine color may change to orange-rose.

General Dosing Information

For acute iron intoxication
Slow intravenous infusion should be used for patients in a state of cardiovascular collapse. {20} {44} The rate of infusion should not exceed 15 mg per kg of body weight (mg/kg) per hour. {24} {43} {44} If it is difficult to establish an intravenous line, then the medication may be administered intramuscularly. {51} {57}

Although severe symptoms of iron toxicity do not usually occur when iron measures between 300 and 500 mcg per deciliter (54 and 90 micromoles per liter), a trial dose of deferoxamine may be administered intramuscularly (40 mg/kg) or by intravenous infusion (0.5 to 1 gram) over 4 hours, between 2 to 4 hours {12} after ingestion of iron and after the gastrointestinal tract has been cleaned out. The patient should be observed for ferrioxamine in the urine (orange-rose color change of urine) {12} until the results of serum iron and total iron binding capacity (TIBC) determinations are available, since the color change usually denotes a significant ingestion of iron. {14} If the serum iron and TIBC results are not available, monitoring of urine color change should continue. {23} If the color does not appear by 2 hours after the injection and the patient is asymptomatic, usually no further dose is needed. However, in some cases, the urine color may never change, even in the presence of severe, acute iron poisoning. {05} {11} {12} {45}

Dialysis is of no value in removing serum iron but may be useful in removing the iron-deferoxamine complex in patients who develop renal failure during treatment. {11} {43}

After treatment for acute iron intoxication, some physicians recommend that all treated patients be observed for a minimum of 24 hours after they become asymptomatic {18} and that they be seen again in 2 weeks. This is to check for gastrointestinal symptoms and for iron deficiency caused by blood loss and/or excessive therapy. {12} Delayed effects may include shock (24 to 48 hours) and gastrointestinal obstruction (weeks to months). Residual damage may be ruled out with liver and upper gastrointestinal studies. {18}

For chronic iron overload
The route of administration, either intramuscular or subcutaneous, must be individualized for each patient.

Because of the short serum half-life of deferoxamine, most of the drug may be rapidly excreted after a single intramuscular injection without binding any iron. However, continuous subcutaneous infusion may be almost as effective in mobilizing iron as continuous intravenous infusion. {19} Therefore, a small mechanical infusion pump may be used to administer deferoxamine into the subcutaneous tissue of the abdomen. Deferoxamine is then infused very slowly over 8 to 16 hours on an outpatient basis. {13} The duration of subcutaneous infusion with a portable mini-infusion pump must be individualized, depending on the rate of the patient's iron excretion. This regimen may remove 2 to 3 times more iron than a single daily intramuscular injection. {13}

Patients who do not tolerate deferoxamine therapy because of cutaneous pain and swelling or hives may receive the medication via an infusion pump in an indwelling central venous line at an adult dose of 2 to 4 grams (40 to 80 mg/kg of body weight) administered over 12 to 16 hours. {65}

If a net negative iron balance in response to deferoxamine can be achieved, long-term therapy should be considered in patients with transfusional iron overload.

If blood is transfused during deferoxamine therapy, it must not be mixed in the same container with deferoxamine. {24} {44}

Parenteral Dosage Forms

Note: Bracketed uses in the Dosage Forms section refer to categories of use and/or indications that are not included in U.S. product labeling.


Usual adult and adolescent dose
Iron toxicity, acute
Intramuscular, initially, 90 mg per kg of body weight, followed by 45 mg per kg of body weight, up to a maximum of 1 gram per dose, every four to twelve hours; not to exceed 6 grams per day.{43}{50}{59}

Intravenous, 15 mg per kg of body weight per hour, up to a total of 90 mg per kg of body weight every eight hours; not to exceed 6 grams per day.{50}{59}

Note: The intravenous infusion rate should not exceed 15 mg per kg of body weight per hour.{24}{43}{44}

Iron toxicity, chronic
Intramuscular, 500 mg to 1 gram a day.{24}{43}{44}

Intravenous, in addition to intramuscular administration, 2 grams infused at a rate not to exceed 15 mg per kg of body weight per hour. This is administered at the same time each unit of blood is transfused, but through a separate line.{24}{44}

Subcutaneous, 1 to 2 grams (20 to 40 mg per kg of body weight) a day administered over a period of eight to twenty-four hours by means of a portable, continuous mini-infusion pump.{23}{24}{43}{44}

[Aluminum toxicity]
Dosage must be individualized;{37}{43} theoretically, 100 mg of deferoxamine can bind 4.1 mg of aluminum.{37}{43}

Note: In hemodialysis or hemofiltration patients with moderate aluminum toxicity, and no concomitant iron toxicity, 1 gram of deferoxamine once a week has been given by slow intravenous infusion during the last two hours of every third dialysis session. {43}
In peritoneal dialysis patients, 1 to 1.5 grams of deferoxamine have been given in the dialysis fluid once or twice a week, by slow intravenous infusion, or by the intramuscular or subcutaneous route.{37}{43}

[Aluminum toxicity, diagnosis of]
Intravenous, 1 gram infused at a rate not to exceed 15 mg per kg of body weight per hour; it is preferably administered during the post-dialysis period, although administration during the last two hours of dialysis is acceptable.{43}

Usual adult prescribing limits
Up to 6 grams in twenty-four hours.{06}{24}{43}

Usual pediatric dose
Iron toxicity, acute and chronic

Children up to 3 years of age:
Iron toxicity, acute—Intravenous, 15 mg per kg of body weight per hour.{41}{55}

Iron toxicity, chronic—Subcutaneous, 10 mg per kg of body weight a day.{53}{60}

[Aluminum toxicity, diagnosis of]—Intravenous, 15 to 20 mg per kg of body weight, infused at a rate not to exceed 15 mg per kg of body weight per hour; it is preferably administered during the post-dialysis period, although administration during the last two hours of dialysis is acceptable.{43}

Children over 3 years of age:
See Usual adult and adolescent dose.

Size(s) usually available:

500 mg (Rx) [Desferal]


500 mg (Rx) [Desferal]

2 grams (Rx) [Desferal]{25}

Packaging and storage:
Store below 30 °C (86 °F).{43}{44}

Preparation of dosage form:
For intramuscular or subcutaneous use—Add 2 mL of sterile water for injection to each 500-mg vial and 8 mL of sterile water for injection to each 2-gram vial.{25}{43} The powder should be completely dissolved before administration.{43}{44}

For intravenous infusion—Add 2 mL of sterile water for injection to each 500-mg vial and 8 mL of sterile water for injection to each 2-gram vial.{25} The resulting solution should be further diluted in either 0.9% sodium chloride injection, dextrose injection, or lactated Ringer"s injection before infusion.{24}{43}

Reconstituted solutions should be used within the time period specified by the manufacturer.

Precipitation may result if the solution is reconstituted with solvents or under conditions other than those recommended.{24}

Revised: 06/22/2000

  1. Ehlers K, Giardina P, Lesser M, Engle M, Hilgartner M. Prolonged survival in patients with beta-thalassemia major treated with deferoxamine. J Pediatr 1991; 118: 540-5.
  1. Warady B, Ford D, Gaston C, Sedman P, Huffer W, Lum G. Aluminum intoxication in a child: treatment with intraperitoneal desferrioxamine. Pediatr 1986; 78: 651-5.
  1. Nebeker H, Coburn J. Aluminum and renal osteodystrophy. Ann Rev Med 1986; 37: 79-95.
  1. Malluche H, Smith A, Abreo K, Faugere M. The use of deferoxamine in the management of aluminum accumulation in bone in patients with renal failure. N Engl J Med 1984; 311: 140-4.
  1. Drug evaluations subscription. Chicago: American Medical Association, Spring 1991.
  1. Gilman AG, Rall TW, Nies AS, Taylor P, editors. Goodman and Gilman"s the pharmacological basis of therapeutics. 8th ed. New York: Pergamon Press, 1990: 1611-2.
  1. Guerin A, London G, Marchais S, Metivier F, Pelisse J. Acute deafness and desferrioxamine. Lancet 1985; 2: 39-40.
  1. Olivieri N, Buncic J, Chew E, Gallant T, Harrison R, Keenan N, et al. Visual and auditory neurotoxicity in patients receiving subcutaneous deferoxamine infusions. N Engl J Med 1986; 314: 869-73.
  1. Lakhanpal V, Schocket S, Jiji R. Deferoxamine (Desferal)-induced toxic retinal pigmentary degeneration and presumed optic neuropathy. Ophthalmology 1984; 91: 443-51.
  1. Crawford D, Halliday J. Current concepts in rational therapy for haemochromatosis. Drugs 1991; 41: 875-82.
  1. Poison management manual, 1984: 195.
  1. Handbook of common poisonings in children. 2nd ed. American Academy of Pediatrics, 1986-7.
  1. Wyngaarden JB, Smith LH, editors. Cecil textbook of medicine. 18th ed. Philadelphia: W.B. Saunders Company, 1988: 932.
  1. Rowe PC, editor. The Harriet Lane handbook. A manual for pediatric house officers. 10th ed. Chicago: Year Book Medical Publishers, Inc., 1986.
  1. VanMouwerik T, Hart L. Deferoxamine in the treatment of aluminum toxicity. DICP 1984; 18: 971-2.
  1. Andreoli S, Dunn D, DeMeyer W, Sherrard D, Bergstein J. Intraperitoneal deferoxamine therapy for aluminum intoxication in a child undergoing continuous ambulatory peritoneal dialysis. J Pediatr 1985; 107: 760-3.
  1. Freundlich M, Zilleruelo G, Faugere M, Abitbol C, Strauss J, Malluche H. Treatment of aluminum toxicity in infantile uremia with deferoxamine. J Pediatr 1986; 109: 140-3.
  1. Kirking M. Treatment of chronic iron overload. Clin Pharm 1991; 10: 775-83.
  1. Schafer A, Rabinowe S, LeBoff M, Bridges K, Cheron R, Dluhy R. Long-term efficacy of deferoxamine iron chelation therapy in adults with acquired transfusional iron overload. Arch Intern Med 1985; 145: 1217-21.
  1. Engle J, Polin K, Stile I. Acute iron intoxication: treatment controversies. DICP 1987; 21: 153-9.
  1. Fleeger CA, editor. USAN 1994. USAN and the USP dictionary of drug names. Rockville, MD: The United States Pharmacopeial Convention, Inc., 1993: 192.
  1. Reynolds JEF, editor. Martindale, the extra pharmacopeia. 28th ed. London: The Pharmaceutical Press, 1982: 381.
  1. Panel comment.
  1. Desferal package insert (Ciba—US), Rev 8/87, Rec 1/89.
  1. Desferal package insert (Ciba—Canada), Rev 10/88, Rec 3/90.
  1. Hoen B, Renoult E, Jonon B, Kessler M. Septicemia due to Yersinia enterolitica in a long-term hemodialysis patient after a single desferrioxamine administration. Nephron 1988; 50: 378-9.
  1. Hughes T, Janmohamed R, Leyland M. Yersinia and iron. Lancet 1987; 1: 929.
  1. Gallant T, Freeman M, Vellend H, Francombe W. Yersinia sepsis in patients with iron overload treated with deferoxamine. N Engl J Med 1986; 314: 1643.
  1. Mofenson H, Caraccio T, Sharieff N. Iron sepsis: Yersinia enterocolitica septicemia possibly caused by an overdose of iron. N Engl J Med 1987; 317: 1092-3.
  1. Daly A, Velazquez L, Bradley S, Kauffman C. Mucormycosis: association with deferoxamine therapy. Am J Med 1989; 87: 468-71.
  1. Windus D, Stokes T, Julian B, Fenves A. Fatal rhizopus infections in hemodialysis patients receiving deferoxamine. Ann Intern Med 1987; 107: 678-80.
  1. Goodill J, Absielo J. Mucormycosis—a new risk of deferoxamine therapy in dialysis patients with aluminum or iron overload. N Engl J Med 1987 Jul 2: 54.
  1. Veis J, Contiguglia R, Klein M, Mishell J, Alfrey A, Shapiro J. Mucormycosis in deferoxamine-treated patients on dialysis. Ann Intern Med 1987; 107: 258.
  1. Panel comment, 1990.
  1. Panel comment, 1990.
  1. Manufacturer comment, 1991.
  1. Desferrioxamine indication. Pharm J; 245(6615): 798.
  1. Panel comment, 1991.
  1. Panel comment, 1991.
  1. Pengloan J, Dantal J, Rossozza C, Abazza M, Nivet H. Ocular toxicity after a single intravenous dose of desferrioxamine in 2 hemodialyzed patients. Nephron 1987; 46: 211-2.
  1. Felsenfeld A, Rodriquez M, Coleman M, Ross D, Llach F. Desferrioxamine therapy in hemodialyzed patients with aluminum-associated bone disease. Kidney Int 1989; 35: 1377-8.
  1. Mann K, Picciotti M, Spevack T, Durbin D. Management of acute iron overdose. Clin Pharm 1989; 8: 428-40.
  1. Desferal package insert (Ciba—Canada), Rec 7/19/93.
  1. Desferal (Ciba). In: PDR Physicians" desk reference. 48th ed. 1994. Montvale, NJ: Medical Economics Data, 1994: 818.
  1. Thompson DF. Reassessment of measuring total iron binding capacity in acute iron overdose. Ann Pharmacother 1994; 28: 63-6.
  1. Panel comment, 3/94.
  1. Panel comment, 1991.
  1. Bentur Y, St Louis P, Klein J, Koren G. Misinterpretation of iron-binding capacity in the presence of deferoxamine. J Pediatr 1991; 118: 139-42.
  1. Milliner D, Nebeker H, Ott S, Andress D, Sherrard D, Alfrey A, et al. Use of deferoxamine infusion test in the diagnosis of aluminum-related osteodystrophy. Ann Intern Med 1984; 101: 755-80.
  1. Panel comment, 1991.
  1. Panel comment, 1991.
  1. Ellenhorn MJ, Barceloux DG. Medical toxicology. Diagnosis and treatment of human poisoning. New York: Elsevier, 1988: 1027-9.
  1. Panel comment, 1991.
  1. Panel comment, 3/94.
  1. Consensus on review of evidence table, 12/23/99.
  1. Boelaert J, Fenves A, Coburn J. Deferoxamine therapy and mucormycosis: report of an international registry. Brugge, Belgium.
  1. Panel comment, 1991.
  1. Leikin S, Vossough P, Mochir-Fatemi F. Chelation therapy in acute iron poisoning. Pediatrics 1967; 71: 425-30.
  1. Poisonindex.
  1. Allain P, Mauras Y, Chaleh D, Simon P, Ang K, Cam G, et al. Pharmacokinetics and renal elimination of desferrioxamine and ferrioxamine in healthy subjects and patients with haemochromatosis. Br J Clin Pharmacol 1987; 24: 207-12.
  1. Panel comment, 1991.
  1. Klein G, Snodgrass W, Griffin M, Miller N, Alfrey A. Hypocalcemia complicating deferoxamine therapy in an infant with parenteral nutrition–associated aluminum overload: evidence for a role of aluminum in the bone disease of infants. J Pediatr Gastroenterol Nutr 1989; 9: 400-3.
  1. Ott, et al. Kidney Int 1986; 29(Suppl 18): S108-S113.
  1. Panel comment, 1991.
  1. Reviewers" consensus on monograph revision of 1991.
  1. Reviewer comment, 4/94.
  1. McEnery JT, Greengard J. Treatment of acute iron ingestion with deferoxamine in 20 children. Pediatrics 1966; 68: 773-9.
  1. Westlin WF. Deferoxamine in the treatment of acute iron poisoning: clinical experiences with 172 children. Clin Pediatr 1966; 5: 531-5.
  1. Cheney K, Gumbiner C, Benson B, et al. Survival after a severe iron poisoning treated with intermittent infusions of deferoxamine. Clin Toxicol 1995; 33: 61-6.
  1. Segal G. Iron ingestion in an 11-month-old child. Emerg Off Pediatr 1995; 8: 26-9.
  1. Mann KV, Picciotti MA, Spevack TA, et al. Management of acute iron overdose. Clin Pharm 1989; 8: 428-40.
  1. Henretig FM, Karl SR, Weintraub WH. Severe iron poisoning treated with enteral and intravenous deferoxamine. Ann Emerg Med 1983; 12: 306-9.
  1. Snyder R, Mofenson HC, Greensher J. Acute iron poisoning in infancy: guide to treatment. N York State J Med 1974 Nov: 2215-7.
  1. Greenberg MS, Rosen B. Iron toxicity treated with deferoxamine. Clin Pediatr 1966; 5: 485-92.
  1. Jacobs J, Greene H, Gendel BR. Acute iron intoxication. N Engl J Med 1965; 273: 1124-7.
  1. Santos AS, Pisciotta AV. Acute iron intoxication: treatment with desferrioxamine (Ba-29837). Am J Dis Child 1964; 107: 424-7.