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PubMed2006

Effective new treatments of iron overload in thalassaemia using the ICOC combination therapy protocol of deferiprone (L1) and deferoxamine and of new chelating drugs.

An expert group of the International Committee on Oral Chelators (ICOC) has recommended a universally effective chelation combination protocol of oral deferiprone (L1) during the day (80-110 mg/kg /day) and subcutaneous deferoxamine (40-60 mg/kg) of a minimum of three nights per week for the rapid, safe and effective depletion of excess body iron in transfused iron loaded patients. Following the clearance of excess cardiac and liver iron load, deferiprone (L1) monotherapy at doses exceeding 80 mg/kg/day has been recommended for preventing the re-accumulation of excess iron in the heart and other organs. New chelators such as deferasirox may also be used in combinations with deferiprone (L1) and deferoxamine, especially in patients not tolerating the deferiprone (L1) / deferoxamine combination.

Deferiprone↗
PubMedDate not supplied

Suppressive effect of deferoxamine on the growth of Pneumocystis carinii in vitro.

The effects of the iron chelator deferoxamine on the growth of rat-derived Pneumocystis carinii in culture with human embryonic lung fibroblasts were studied. Growth inhibition was calculated by comparison of trophozoite numbers in replicate samples of supernatant of treated and untreated samples. Deferoxamine, in concentrations safely achievable in humans (5-15 micrograms/ml, corresponding to 7.6-22.8 microM), reproducibly suppressed P. carinii growth in a dose-dependent manner. The suppressive effect was reversed by prior iron saturation of the deferoxamine. Since the utility of current therapeutic agents for P. carinii disease is limited by toxicity and incomplete efficacy, the role of iron chelation as an adjunct to anti-Pneumocystis chemotherapy merits further investigation.

Antifungal Agents↗
PubMed1990

Current status of iron chelation therapy with deferoxamine.

Long-term chelation therapy with deferoxamine is an effective and generally safe method for removing excessive iron, preventing iron-induced organ damage and improving survival of patients with transfusion-dependent disorders. The current treatment of iron overload is an important standard against which new forms of therapy, such as oral chelators, should be measured to ensure that their risks and benefits compare favorably with deferoxamine. Until new treatments are available, continuing studies of deferoxamine will help to define its long-term efficacy and toxicity for patients with thalassemia major and other hematologic disorders.

Chelation Therapy↗
PubMed1990

Deferoxamine for aluminum toxicity in dialysis patients.

Aluminum toxicity, prevalent among individuals with chronic renal failure, is associated with disabling osteomalacia, encephalopathy, and anemia. The control of aluminum intake has included standards to limit the amount of aluminum in the dialysis fluid in addition to the use of nonaluminum containing phosphate binders. Deferoxamine mesylate, a heavy metal chelating agent, is used to remove aluminum from the tissues of dialysis patients. Chelation therapy has resulted in improvements of clinical symptoms and bone histology. Ocular, auditory, and infectious adverse effects have occurred with the use of deferoxamine. Future studies are needed to determine the most effective method of removing the aluminum-deferoxamine complex.

Aluminum↗
PubMed1989

Amelioration of postischemic stunning by deferoxamine-blood cardioplegia.

Limitation of oxygen free-radical injury was assessed in canine hearts by sonomicrometrically quantifying regional stroke work (RSW) in areas of myocardium perfused by the left anterior descending (LAD) and left circumflex (LCX) arteries. Volume loading of the left ventricle was performed on modified right-heart bypass before and 30 minutes after 20 minutes of LAD occlusion followed by 60 minutes of global cardioplegic arrest with either blood cardioplegia (group 1), blood cardioplegia with adjuvant deferoxamine (500 mg/l) plus 100 mg infused into the aortic root for 5 minutes after unclamping (group 2), or blood cardioplegia with adjuvant deferoxamine (600 mg/l) with unmodified reperfusion (group 3). Surgical revascularization was modeled by reopening the LAD with the first cardioplegia reinfusion. The slope of the RSW versus preload relation (a load-independent index of contractility) was decreased by a mean amount of 44% in the LAD region of group 1 hearts but was preserved in group 2 and 3 hearts. The slope of the LCX region was preserved in all groups. The use of adjuvant deferoxamine in this model of early surgical reperfusion eliminates measurable postischemic stunning.

Animals↗
PubMed1987

Deferoxamine induced decreases of lipid peroxides in rheumatoid arthritis.

Eleven patients with rheumatoid arthritis (RA) were treated with intraarticular deferoxamine or placebo to test the hypothesis that iron chelation decreased hydroxyl radical mediated lipid peroxidation in RA. Intraarticular administration of deferoxamine 100 mg resulted in predominantly systemic effects with decreased serum ferritin and decreased serum levels of lipid peroxidation products. Similar changes were not detected in synovial fluid at this dose. Iron chelation with deferoxamine may provide a novel approach to preventing tissue injury in RA by inhibiting hydroxyl radical production and lipid peroxidation.

Adult↗
PubMed1987

Effect of deferoxamine on DNA synthesis, DNA repair, cell proliferation, and differentiation of HL-60 cells.

The ribonucleotide reductase inhibitors deferoxamine and hydroxyurea induce monocyte-macrophage cell differentiation in the leukemic cell line HL-60 as judged by the expression of cell surface antigens, nonspecific esterase activity, and morphological changes. Treatment of HL-60 cells with deferoxamine results in inhibition of DNA synthesis and irreversible loss of colony-forming ability. In addition, both deferoxamine and hydroxyurea caused an increase in the number of DNA strand breaks in HL-60 cells. A DNA methylating agent, N-methyl-N'-nitro-N-nitrosoguanidine, also caused cellular differentiation in HL-60 cells associated with DNA strand breaks. These observations are consistent with a role for DNA damage or for inhibition of DNA synthesis and repair in the differentiation process of HL-60 cells.

Antigens, Surface↗
PubMedDate not supplied

Deferoxamine for the treatment of hemosiderosis during CAPD.

The effects of chelation therapy by intravenous and intraperitoneal administration of deferoxamine were compared during maintenance continuous ambulatory peritoneal dialysis (CAPD) in a child with end stage renal disease and hemosiderosis. We demonstrate that intraperitoneally administered deferoxamine is safer, more practical and efficient than weekly intravenously administered deferoxamine for the treatment of iron overload in the pediatric patient undergoing CAPD.

Adolescent↗
PubMed1986

Deferoxamine improves left ventricular function in beta-thalassemia.

Serial echocardiographic examinations were made to study the changes in left ventricular (LV) function and wall mass in 35 patients with thalassemia followed up for 5.5 +/- 2 years (mean +/- SD). Twenty patients received deferoxamine sulfate for 2.0 +/- 0.6 years (drug group) and 15 patients did not (nondrug group). Repeated blood transfusions were used to maintain the pretransfusion hemoglobin levels at 9 g/dL (90 g/L). Deferoxamine therapy improved LV function and decreased LV wall mass. Percentage shortening of LV diameter improved in the drug group (5.0% +/- 3.9%) and deteriorated in the nondrug group (-6.8% +/- 5.6%). Similarly, the maximum velocity of LV posterior wall motion improved in the drug group (16.1 +/- 20.1 mm/s) and deteriorated in the nondrug group (-18.3 +/- 19.0 mm/s). Left ventricular wall mass decreased in the drug group when compared with the nondrug group. In a subset of the drug group, pathologic natural deterioration in LV systolic function was reversed by treatment. Correlation studies indicated that frequent blood transfusions together with chelation therapy reduced LV dilatation and wall thickness, but blood transfusions alone did not have the same effect. Thus, treatment of patients with thalassemia with modest blood transfusions and deferoxamine can prevent deterioration and may even improve their LV systolic function, associated probably with arrest and reversal of the pathologic process that increases LV wall mass.

Adolescent↗
PubMed1985

Long-term efficacy of deferoxamine iron chelation therapy in adults with acquired transfusional iron overload.

Transfusional iron overload in adult patients with acquired anemias may result in widespread organ dysfunction. Long-term deferoxamine mesylate therapy was administered by continuous subcutaneous infusion to six such patients, who have been followed up for up to 66 months of therapy while continuing to be transfusion-dependent. During deferoxamine therapy, liver density by computed tomographic scan decreased in four of five patients, liver iron content decreased in two of three patients, and liver function normalized in two patients. Plasma cortisol response to insulin-induced hypoglycemia improved in three of five patients receiving therapy. Pituitary growth hormone reserve normalized in two patients and remained normal in the other three tested. One patient, treated concurrently with ascorbic acid, died suddenly. The other five patients have had no cardiac deterioration by noninvasive testing. We conclude that long-term deferoxamine iron chelation therapy is effective not only in retarding but, in some cases, even reversing organ damage caused by transfusional iron overload.

Adult↗
PubMed1985

Ocular and auditory toxicity of long-term, high-dose subcutaneous deferoxamine therapy.

There have been few reported ocular side effects of parenterally administered deferoxamine when used for the treatment of transfusional iron overload or acute iron poisoning. No auditory side effects have previously been reported. We describe two siblings with beta-thalassemia major who, while receiving daily subcutaneous infusions of deferoxamine, experienced visual loss secondary to optic neuropathy and sensorineural hearing loss. After discontinuation of the drug one sibling showed almost complete reversal of the optic neuropathy, but the other had a permanent unilateral visual loss. Both had a permanent hearing loss but benefited from hearing aids. The mechanism of these complications is presently unknown. Patients receiving deferoxamine should be closely monitored for ocular and auditory side effects. When such effects are detected the drug should be discontinued and the patient observed for improvement. When improvement has stabilized, therapy should be restarted at a reduced dosage.

Child, Preschool↗
PubMed1985

Improvement of anemia with deferoxamine in hemodialysis patients with aluminum-induced bone disease.

As microcytic anemia is a feature of aluminium intoxication, we prospectively studied the hematologic effects of deferoxamine in 10 hemodialysis patients with aluminum-induced bone disease. Comparing the mean monthly results of a 4 month period before and during deferoxamine therapy, we observed an important decrease of the transfusion needs (alpha less than 0.025) and an increase of hematocrit (p less than 0.02), hemoglobin (p less than 0.02), MCV (p less than 0.02) and MCH (p less than 0.05); the number of red blood cells remained unchanged. Our results show that deferoxamine treatment of dialysis patients with aluminum bone disease can markedly improve their anemia, even in the absence of recent aggravation, microcytosis and hypochromia. They also suggest that aluminum could participate in the anemia of dialysis patients even if it is normocytic.

Adult↗
PubMed1979

Pharmacist involvement in a deferoxamine education program for patients with Cooley's anemia.

A program to train patients with Cooley's anemia to self-administer deferoxamine via an intermittent infusion pump is described. A pharmacist provides the patient and his family with indepth information on the disease and on deferoxamine dosage, preparation, subcutaneous administration, stability, storage, side effects and precautions. Patients are trained by the pharmacist in aseptic technique and in use and maintenance of the intermittent infusion pump. The patient education program allows patients with Cooley's anemia to receive their daily deferoxamine therapy without the neef for frequent hospitalization.

Ascorbic Acid↗
PubMed1978

Continuous intravenous deferoxamine infusion. Treatment of secondary hemochromatosis in adults.

Adult patients with chronic iron overload were given oral ascorbic acid and continuous intravenous infusions of deferoxamine mesylate. The dosage of deferoxamine mesylate was altered every 48 hours from 1 g/sq m/24 hr to 2 or 4 g/sq m/24 hr. The average iron mobilization was 55.6 mg per day at the 1 g/sq m/24 hr dosage level, 78.6 mg every 24 hours at the 2 g/sq m/24 hr dosage level, and 90.1 mg every 24 hours at the 4 g/sq m/24 hr dosage level. Iron mobilization was undiminished when successive 14-day courses of deferoxamine separated by six-week intervals were administered.

Administration, Oral↗
PubMed1982

Hemosiderosis in a dialysis patient: treatment with hemofiltration and deferoxamine chelation therapy.

Although the highly permeable membranes utilized in hemofiltration are theoretically more permeable to deferoxamine-chelated iron than the standard cuprophan membranes used in conventional hemodialysis, no clinical data support this contention. Ours are the first published results of a preliminary short-term trial of combined therapy with deferoxamine and hemofiltration in a dialysis patient with hemosiderosis. An average of 15.3 mg of iron was mobilized with a 19.5-liter exchange over only 4 1/2 hours of postdilution hemofiltration. This compares favorable with previous reports in which 8 to 12 hours of dialysis were performed with Kiil dialyzers, and also with the 24-hour urinary excretion of chelated iron in iron-overloaded patients with normal renal function. We conclude that combined therapy with deferoxamine and hemofiltration offers promises as an effective means of iron mobilization in dialysis patients with hemosiderosis.

Aged↗
PubMedDate not supplied

Left ventricular function in thalassemia major: protective effect of deferoxamine.

OBJECTIVE: To test the hypothesis that chelation therapy with deferoxamine would prevent alterations in left ventricular systolic and diastolic function due to transfusional iron overload in patients with thalassemia major. DESIGN: A consecutive series of patients receiving chronic transfusional and chelation therapy were studied by two-dimensional and Doppler echocardiography. SETTING: Primary clinic. PATIENTS: Eight thalassemic patients (four men and four women), mean age 22 years (range 14 to 28) and seven age and sex matched control subjects. INTERVENTIONS: All patients had received transfusional therapy since birth, with mean annual load of red blood cells of 200 mL/kg. Iron chelation therapy with deferoxamine, using a subcutaneous infusion pump, was administered from age two years in the younger patients and from age 16 years in the two older cases. Doses were 25 mg/kg/day in children and 1.5 to 4 g per 12 h in adults to maintain ferritin blood levels at 1000 to 1500 ng/L. MAIN RESULTS: No significant differences were found in the following Doppler diastolic indexes: isovolumic relaxation time, early flow velocity (E wave), late flow velocity (A wave), E:A ratio, rate of deceleration of flow velocity in early diastole (EF slope), flow velocity deceleration time and end-diastolic volume. Ejection fraction was similar in the two groups (59 +/- 7 versus 64 +/- 5%), but contractility, expressed as end-systolic pressure/end-systolic volume index, appeared slightly depressed (4.6 +/- 1 versus 6.7 +/- 0.8) in the thalassemic group. CONCLUSIONS: Deferoxamine prevents alteration of left ventricular diastolic function in chronic transfusional therapy for thalassemia major. Depression of contractility, in spite of a normal ejection fraction, may be an early sign of worsening systolic performance, unavoidable even with chelation therapy.

Adolescent↗
PubMed1994

Additive effect of allopurinol and deferoxamine in the prevention of spinal cord injury caused by aortic crossclamping.

Fourteen domestic swine were divided into two groups. Group A (n = 7) was the control group, in which no pharmacologic intervention was applied. In group B (n = 7), the ischemic-reperfused spinal cord was treated with the combination of allopurinol (50 mg/kg/day for 3 days before the day of operation) and deferoxamine (Desferal, 50 mg/kg administered intravenously over 3 to 4 hours). The administration of deferoxamine was completed 1 hour before crossclamping. The crossclamp was placed on the descending aorta just distal to the left subclavian artery for 30 minutes. Proximal hypertension was controlled with sodium nitroprusside and volume depletion. Methods of assessment included an evaluation of the neurologic status of the animals by quantitative Tarlov criteria, blood flow by radiolabeled microspheres, and histologic examination of the spinal cord. All animals in the control group, group A, were completely paraplegic with 0% recovery by Tarlov criteria at 24 hours after the removal of the crossclamp. In contrast, all animals in group B, in which the combination of allopurinol and deferoxamine was used, completely recovered (100% recovery by Tarlov criteria), and at 24 hours after the ischemic episode they were able to walk with no difficulty and had intact sensation. Functional parameters of these animals fully correlated with the morphologic findings. Widespread acute neuronal injury and vacuolation of neuropil were observed in the control group of animals. In contrast, animals in group B showed much less pronounced morphologic changes after the same period of ischemia. In summary, the combined use of these agents significantly (p < 0.001) reduced the incidence of paraplegia induced by aortic crossclamping with 82% additivity.

Allopurinol↗
PubMed1993

Coronary vascular injury following transient coronary artery occlusion: prevention by pretreatment with deferoxamine, dimethylthiourea and N-2-mercaptoproprionyl glycine.

The role of oxygen-derived free radicals as initiators of vascular dysfunction observed 24 hr after transient coronary artery occlusion (15 or 30 min) was examined in the anesthetized dog. A 15-min occlusion increased human serum (HSA) albumin extravasation within anterior myocardium without producing myocardial necrosis or edema. Minimal leukocyte uptake and free radical formation were present at 24 hr. 2-Mercaptoproprionyl glycine (MPG) (a free radical scavenger), deferoxamine (a chelator of ferrous ions) and dimethylthiourea (a hydroxyl ion scavenger), administered 15 min before coronary artery occlusion and extending 1.5 hr into reperfusion, reduced HSA uptake within anterior myocardium. A different pattern of injury was present after a 30-min occlusion. Subendocardial necrosis (1.2 +/- 0.8 g), edema, HSA extravasation and leukocyte uptake were observed at 24 hr. MPG failed to reduce the extent of necrosis, HSA extravasation, edema, leukocyte uptake or free radical formation. HSA extravasation, leukocyte uptake, tissue edema and free radical formation present 24 hr after a 30-min occlusion were reduced by acute deferoxamine and dimethylthiourea, but not by acute MPG administration. The failure of MPG to reduce HSA extravasation observed 24 hr after a 30-min coronary artery occlusion was associated with both leukocyte uptake and continued free radical formation, whereas dimethylthiourea and deferoxamine reduced leukocyte uptake, free radical formation and HSA extravasation.

Animals↗