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PubMed1985

Do serum aluminum levels reflect underlying skeletal aluminum accumulation and bone histology before or after chelation by deferoxamine?

Patients undergoing dialysis may accumulate tissue aluminum burdens, and are at risk of developing two aluminum-associated syndromes, namely dialysis osteomalacia and encephalopathy. We address the clinical usefulness of serum aluminum levels in the diagnosis of dialysis osteomalacia. Twenty-four patients, 15 with dialysis osteomalacia and nine with clinically apparent secondary hyperparathyroidism, had serum aluminum levels measured before and after a standard infusion of a chelating agent, deferoxamine (DFO). Baseline serum aluminum levels were regarded as "high" (greater than 133 micrograms/L) if they exceeded 1 SD above the mean (74 micrograms/L) for a larger population of 152 patients undergoing routine hemodialysis. All patients had a bone biopsy for assessment of aluminum deposits by a specific histochemical stain. High serum aluminum levels had a diagnostic sensitivity of 60% in predicting those patients ultimately shown to have dialysis osteomalacia associated with histochemical evidence of aluminum accumulation in bone biopsy specimens; however, 40% of patients with histologic evidence of dialysis osteomalacia would have been missed if only serum aluminum had been used as a diagnostic test. Serum aluminum levels (+/- SEM) were 194 +/- 31 micrograms/L in patients with dialysis osteomalacia and 120 +/- 42 micrograms/L in those with secondary hyperparathyroidism (P greater than 0.05). Serum aluminum levels rose in all patients after DFO infusion to peak levels of 664 +/- 110 and 514 +/- 90 micrograms/L in patients with osteomalacia and hyperparathyroidism, respectively. However, neither the peak serum aluminum level nor its increment after DFO infusion distinguished between patients with osteomalacia and secondary hyperparathyroidism more effectively than did the baseline serum aluminum level.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Effect of two years of deferoxamine therapy on iron balance, ferritin, liver and heart in patients with thalassemia major].

The iron balance, the urinary excretion of iron between transfusions, the serum ferritin, the liver density, the size of the heart, the ECG and the echocardiogram of 14 children with thalassaemia major were assessed before and during or after 2 years of deferoxamine therapy (DF, 1 or 2 g/kg body weight/day according to age, by subcutaneous infusion on 5 days per week, 11 months per year). The mean iron balance decreased significantly (p less than 0.001) from 15.4 +/- 4 mg/kg body weight/month before DF to -7.1 +/- 9.4 mg/kg body weight/month in the first year of DF and increased to -2.5 +/- 6.5 mg/kg body weight/month during the second year of DF therapy. Despite administration of a constant dose of DF the urinary excretion of iron during the last days before transfusion was twice as high as during the first days after transfusion. The mean serum ferritin level fell from 6380 +/- 2600 ng/ml before DF to 5074 +/- 1600 ng/ml during the first and 4346 +/- 1900 ng/ml during the second year of DF therapy (p less than 0.05). There was no significant change in liver density or cardiac parameters.

Adolescent↗
PubMed1979

Effects of deferoxamine methanesulfonate on Trichophyton mentagrophytes.

Deferoxamine methanesulfonate (Desferal), an iron chelator, inhibited germ tube formation and growth of Trichophyton mentagrophytes in a microculture assay. A 50% reduction of germ tube formation required Desferal at 5 mg/ml and a 50% reduction of growth required 1.5 mg/ml. Growth was almost completely inhibited with 50 and 100 mg/ml. Also, Desferal at 100 mg/ml inhibited further elongation when added to short hyphae (II and 21 micrometer), but showed less inhibitory effects when added to long hyphae (64 micrometer). Iron (133 microgram/ml) reversed the inhibition of growth produced by incubating spores with Desferal at 5 mg/ml, providing iron was added before 72 h incubation. Desferal at 100 mg/ml decreased viability of activated spores incubated for 3 days at 30 degrees C, but did not decrease viability of spores incubated for 3 days at 4 degrees C. The growth inhibitory effect of Desferal and transferrin were compared. Transferrin was inhibitory at low molarities (0.001 to 1.0 mM), while Desferal was inhibitory only at higher molarities (greater than 1 mM). Desferal (0.05 mM) also reversed the inhibition expected with 0.05 mM transferrin. These findings indicate that Desferal and transferrin deprive T. mentagrophytes of nutritional iron and thus inhibit growth of the fungus. Low concentrations of Desferal can also promote growth in the presence of transferrin.

Deferoxamine↗
PubMed1984

[Manual method of assaying plasma hemoglobin by tetramethylbenzidine and deferoxamine].

We describe a manual method to determine very low concentrations of hemoglobin in plasma (0,25 to 37,3 mumol/l). We use peroxidase properties of hemoglobin which decomposes hydrogen peroxide releasing oxygen. This released oxygen will oxidize tetramethylbenzidine. The original feature of the proposed method lies in the stabilization of the obtained colour by a complexing agent, the deferoxamine. The technique is quick, reliable, cheap and does not need specialized equipment. It is possible to use the method for urines.

Benzidines↗
PubMed1984

Different actions of deferoxamine and iron on Ga-67 abscess detection in rats.

The contrast-enhancing properties of iron (Fe) and deferoxamine (DFO) in abscess imaging with Ga-67 citrate were compared in rats bearing turpentine-induced abscesses. Iron administration shifted Ga-67 from plasma into tissues such as muscle and fat. As a result, the abscess-to-plasma ratio increased whereas the abscess-to-muscle ratio decreased. DFO enhanced the abscess-to-muscle and abscess-to-plasma ratios by increasing urinary Ga-67 excretion. In contrast to Fe, DFO removed abscess-bound Ga-67, thus representing a disadvantage of DFO compared with Fe. As a result, the abscess-to-plasma ratio was more effectively enhanced by Fe than by DFO. We conclude that abscess imaging with Ga-67 citrate may be improved by administration of Fe for detection of abscesses masked by blood activity, or DFO for detection of abscesses surrounded by muscle tissue.

Abscess↗
PubMed1982

Use of subcutaneous deferoxamine in a child with hemochromatosis associated with congenital dyserythropoietic anemia, type I.

A 12-year-old girl with congenital dyserythropoietic anemia, type I, was diagnosed as having hemochromatosis. Deferoxamine was given subcutaneously for 14 months. Iron overload, as measured by liver iron and serum ferritin levels, was reduced substantially, liver function tests improved, and hepatomegaly decreased. Toxicity was negligible.

Anemia, Dyserythropoietic, Congenital↗
PubMed1982

Effect of subcutaneous deferoxamine and oral vitamin C on iron excretion in congenital hypoplastic anemia and refractory anemia associated with the 5q-syndrome.

Chronic refractory anemia associated with congenital hypoplastic anemia (CHA, Blackfan-Diamond syndrome) and with the 5q-syndrome may require chronic transfusion therapy to sustain life. Hemosiderosis and death from chronic iron overload may result from such a program. The effect of subcutaneous (SC) deferoxamine (DF) and supplemental oral vitamin C (vit. C) on urinary iron excretion was studied in two patients with congenital hypoplastic anemia and one patient with 5q-syndrome. In the two patients with CHA, urinary iron excretion in response to DF given SC over 24 hours was comparable to the results following intravenous (I.V.) administration. Both of these cases had low levels of plasma ascorbate on initial evaluation and excreted more iron in response to two different doses of DF after they had received supplemental vit C and their stores were repleted. Significant iron excretion occurred in all three patients for 12 hours during the SC infusion of DF and for 12 hours after the end of the infusion. In all three patients, increasing the dose of DF up to 3-4 g given SC over 12 hours resulted in a linear increase in iron excretion. Once normal body stores of ascorbate were achieved by oral supplementation, increasing doses of vit C did not appear to cause a further increment in iron excretion. DF administered by a slow SC infusion appears to be an effective approach to iron overload in patients with refractory anemia and hemosiderosis secondary to chronic transfusions. Only small amounts of supplemental vit. C necessary to sustain adequate body stores are required for optimal iron excretion.

Administration, Oral↗
PubMed1982

Deferoxamine, a promising bifunctional chelating agent for labeling proteins with gallium: Ga-67 DF-HSA: concise communication.

A new efficient method has been developed for the labeling of various biologically important proteins with radiogallium, using deferoxamine (DF) as a bifunctional chelating agent. Human serum albumin (HSA) was chosen for studying the DF coupling reaction by a glutaraldehyde two-step method. The DF-HSA conjugate obtained was then easily labeled with Ga-67 with high efficiency and reproducibility. High stability of the Ga-67 DF-HSA was observed both in vitro and in vivo. In rats the half-time of blood clearance at the first phase was 234 min for the Ga-67 DF-HSA, whereas most conventional I-131 HSA gives 121 min. The excellent pharmacological and physiological properties were assessed by plasma clearance and plasma volume measurements in normal volunteers. Even at 2 hr after injection, (90.0 +/- 3.0)% of Ga-67 DF-HSA was retained within the vascular space. The mean plasma volume per kilogram of body weight, measured with Ga-67 DF-HSA, was 46.6 +/- 3.4 ml/kg, compared with 52.2 +/- 2.4 ml/kg as determined with I-131 HSA in the same men.

Animals↗
PubMed1980

The effects of deferoxamine mesylate on gallium-67 distribution in normal and abscess-bearing animals: concise communication.

Deferoxamine mesylate (DFO), given to rabbits 20 min after gallium-67 citrate, induces prompt and rapid urinary excretion of Ga-67 activity with concommitant decrease in blood and muscle activity. When DFO is given after 2 hr or later, the effect is smaller (15% decrease in blood activity compared with 50%). In abscess-bearing rats the same effect was observed: DFO accelerated the Ga-67 blood clearance by increasing urinary excretion. Tissue-distribution studies and direct counting of abscesses showed that DFO lowers Ga-67 activity in all organs as well as in the abscess if given 2 or 4 hr after Ga-67 citrate, but the abscess-to-blood ratio increases. At 24 hr after Ga-67 citrate, DFO administration causes an improvement in the ratios of abscess-to-blood and abscess-to-normal tissue. Thus, DFO could be used to decrease the radiation burden from Ga-67 citrate after imaging has been performed, and also to increase the target-to-nontarget ratio.

Abscess↗
PubMed1980

Modified aca method for determination of iron chelated by deferoxamine and other chelators.

Iron in serum and urine specimens containing deferoxamine (a chelator used in treating acute iron intoxication) can be measured by the DuPont aca discrete-analyzer method for iron if 0.5 mL of a 100 mL/L solution of thioglycolic acid (mercaptoacetic acid) is added to the IRN-1 and IRN-2 test packs before their use. This reagent releases the unreactive chelated iron, allowing reliable colorimetry. Because about 50% of hemoglobin iron is measured by the modified method, hemolysed samples should not be used (or results should be corrected for hemoglobin iron). The modification allows emergency determination to total serum iron and assessment of urinary iron during chelation therapy, as well as measurement of plasma iron in samples treated with sodium citrate or oxalate plus fluoride (the unmodified aca iron method gives falsely low iron values in the presence of these chelators). About 60% of iron present as the dextran complex (Imferon) is measured by the modified aca method, as compared with <5% by the unmodified aca technique.

Anticoagulants↗
PubMed1980

[Role and therapeutic use of deferoxamine in iron overload due to thalassemia (author's transl)].

Eight children aged between 4 and 16 years with thalassemia major were treated for 30 months with repeated transfusions and a chelating agent. Deferoxamine was given intravenously for 12 months and subcutaneously in the next 18 months. The results of urine iron concentrations, the practical difficulties of both routes of administration and the clinical results are presented. The therapeutic regime proposed is capable or reducing the iron overload.

Adolescent↗
PubMed1994

Enhancement of retinal recovery by conjugated deferoxamine after ischemia-reperfusion.

PURPOSE: Although toxic to the retina in its native form, the iron chelator deferoxamine (DFO) shows no apparent retinal toxicity when bound to hydroxyethyl-starch (HES). Conjugation of DFO does not alter its iron binding properties. Once bound, iron is no longer active in the production of toxic oxygen intermediates. This investigation seeks to determine whether HES-conjugated DFO (HES-DFO) protects against ischemia-reperfusion injury in the retina. METHODS: Retinal ischemia was induced in cats, pretreated with HES-DFO, using both the vascular ligation and the increased intraocular pressure models. Retinal recovery was monitored by electroretinography. Fundal fluorescein angiography was performed in treated and untreated animals after ischemia-reperfusion. RESULTS: Our results indicate that pretreatment with an intravenous bolus of HES-DFO, significantly enhances recovery of the postischemic b-wave and decreases fluorescein leakage after ischemia-reperfusion. CONCLUSIONS: HES-DFO improves recovery of the neural retina after ischemia-reperfusion. It also maintains the integrity of the blood-retinal barrier. The protective effect of HES-DFO on the blood-retinal barrier is consistent with its intravascular confinement. That HES-DFO results in protection of the neural retina underscores the importance of the blood-retinal barrier as a mediator of ischemia-reperfusion injury. HES-DFO may have a role in the early management of ischemic retinal disease both as an iron chelator and as a blood-retinal barrier protector.

Animals↗
PubMed1995

Iron metabolism and oxidative stress during acute and chronic phases of experimental inflammation: effect of iron-dextran and deferoxamine.

Iron overload induces a rise in lipid peroxidation, but there are no data on the effects of iron administered in vivo on the production of free radicals by inflammatory cells. Further, there is lack of agreement about the benefits of deferoxamine (Dfx) in the treatment of anemia and oxidative stress during inflammation and chronic diseases. In this study, iron-dextran (Fe-dextran) or Dfx was administered subcutaneously during the acute and chronic phases of carrageenan-induced granuloma. Several parameters related to iron metabolism, inflammatory cell activity, and lipid peroxidation were measured in liver, plasma, and the inflammatory exudate. Treatment with Fe-dextran increased iron content in plasma and in stores, increased production of superoxide anion (O2-) by inflammatory cells and lipid peroxidation, and also altered the inflammatory process. Dfx mobilized iron from stores without modifying essential parameters related to anemia or to the level of lipid peroxidation induced by inflammation. We conclude that treatment with Fe-dextran had a beneficial effect on recovery from the anemia of inflammation. Nevertheless, the high levels of loosely-bound iron found after Fe-dextran treatment in plasma and in exudate contribute to the increase in oxidative stress. Dfx treatment had no effect on anemia or on lipid peroxidation.

Acute Disease↗
PubMed1993

Effect of deferoxamine-hydroxyethyl pentafraction starch on free, autogenous full-thickness skin grafts in dogs.

Free, autogenous, full-thickness skin grafting was performed on 10 dogs; 5 dogs were given an iron chelator, deferoxamine-10% hydroxyethyl pentafraction starch (DEF-HES; 50 mg/kg of body weight, IV), and 5 dogs were given 10% hydroxyethyl pentafraction starch (HES) in 0.9% saline solution (5 ml/kg, IV). The percentage of viable graft on day 10 was higher, but not significantly so, in DEF-HES-treated dogs (mean +/- SD, 72.6 +/- 24.8%; median 76.5%) than in HES-treated dogs (mean +/- SD, 46.7 +/- 34.3%; median, 48.8%). A trend for a positive correlation between the percentage of viable graft (on day 10) and the percentage of original graft area (on day 28) was observed in HES- and DEF-HES-treated dogs; this trend was significant in HES-treated dogs (P = 0.012). Both groups had significant positive correlation between percentage of viable graft on day 10 and percentage of haired skin on day 28 (HES, P = 0.000002; DEF-HES, P = 0.0148). A unique finding in DEF-HES treated dogs was the consistent observation of foamy macrophages in the dermis adjacent to the grafts, in deep subcutaneous tissue below the grafts, and in normal dermis.

Animals↗
PubMedDate not supplied

Deferoxamine in children with recurrent neuroblastoma.

We examined the short-term efficacy and toxicity of high doses of intravenous deferoxamine (DFO) in children with recurrent neuroblastoma. Ten children (3 2/12-20 years, median 6 5/12 years) had measurable recurrent disease following 1-3 prior treatment regimens. DFO (120-240 mg/kg/d) was planned as a continuous i.v. infusion for five days every other week. Serum ferritins at the start of this therapy ranged from 133-->5000 ng/ml (median 611 ng/ml). Of eight patients begun at a dose of 120-150 mg/kg/d, a single patient experienced visual disturbances which resolved after DFO was discontinued. Two patients begun at 240 mg/kg/d (with serum ferritins levels of 505 and 717 ng/ml) both experienced dose-limiting toxicity including lethargy, dizziness, blurred vision and leg cramps. Although decreases in serum ferritin levels of a least 10% were noted in 4 patients, there were no partial or complete response. DFO given at a dose of 150 mg/kg/d i.v. according to this schedule appears to be ineffective as a single agent against neuroblastoma. Starting doses of 240 mg/kg/d have unacceptable short-term toxicity.

Adolescent↗
PubMed1994

[Evaluation of the efficacy of chelation therapy with deferoxamine in patients with thalassemia major].

BACKGROUND: The current treatment of thalassaemia maior (TM) is based on a hypertransfusion regimen, with deferoxamine (DFO) chelation therapy to minimize the consequences of iron overload. To evaluate the long-term efficacy of chelation therapy, a group of 9 patients treated for a period of 9 years was studied. METHODS: The mean age of patients at the beginning of chelation therapy was 7 years. The age range at the moment of the study was 11 to 21 years. Pre-transfusion haemoglobin values were maintained above 10 gr/dl. DFO was administered by 10-hour sub-cutaneous infusion, 5 or 6 days a week at a dose of 40 mg/kg. Different iron overload parameters were considered, with special attention to cardiac function, growth and endocrinologic development. Signs of DFO toxicity were also studied. RESULTS: The final mean iron elimination rate was 72.6%. One patient died from cardiac haemosiderosis. Eight of the 9 patients showed significant growth impairment and 7, who have attained puberal or post-puberal age, suffer from one or more endocrinologic disorders (6 hypogonadism, 2 diabetes mellitus, 2 hypothyroidism and 1 hypoparathyroidism). The only toxic effect observed was transient crystalline opacity in 2 patients. CONCLUSIONS: Despite the early initiation of chelation therapy, TM patients receiving hypertransfusion regimen showed iron overload, with myocardiopathy, growth retardation and several endocrinologic disorders, mainly secondary hypogonadism, glucose metabolism disfunction and primary hypothyroidism.

Child↗
PubMed1994

Long-term intravenous deferoxamine treatment for noncompliant transfusion-dependent beta-thalassemia patients.

With the introduction of long-term subcutaneous administration of deferoxamine (DFO), there has been a decline in the morbidity and mortality of transfusion-dependent beta-thalassemia patients. However, since the use of subcutaneous DFO is hindered by poor compliance, long-term i.v. DFO therapy has been attempted in order to improve compliance, prevent excessive iron accumulation and extend survival. Thirteen patients (aged 5.4-18.4 years) were started on i.v. home administration of DFO (100 mg/kg per day) via an exteriorized, tunneled right atrial catheter (Hickman type). After a median follow-up of 36 months, the mean ferritin levels had dropped significantly (5,117 +/- 1,737 to 1,816 +/- 1,062 micrograms/l. P = 0.0001). None of the patients developed new endocrine or cardiac diseases due to iron overload. Patients beginning therapy at an early age (< or = 11 years) showed a tendency for improved growth parameters at the end of the treatment period. Two patients developed moderately high frequency sensorineural hearing loss. One patient developed a right atrial thrombus. The line infection rate was low (1.7 episodes per 1,000 patients days). In view of the grave prognosis for iron overloaded patients and the fact that oral chelators are not yet readily available, we recommend this form of therapy for the young, noncompliant beta-thalassemia patient, despite the occasional complications observed.

Adolescent↗
PubMed1994

Ability of the orally effective iron chelators dimethyl- and diethyl-hydroxypyrid-4-one and of deferoxamine to restore sarcolemmal thiolic enzyme activity in iron-loaded heart cells.

In view of the profound functional and structural abnormalities shown in our previous studies in cultured, iron-loaded rat heart cells, we have examined the ability of the orally effective iron chelators dimethyl-3-hydroxypyrid-4-one (DMHP or L1) and diethyl-3-hydroxy-pyrid-4-one (DEHP or CP94) and of deferoxamine (DF) to reverse the damage caused by iron loading to heart cell organelles. At a concentration of 1.0 mmol/L, all three iron chelators were equally efficient in removing iron and restoring the activity of the thiolic sarcolemmal enzymes 5'-nucleotidase and Na,K,ATPase. However, at 0.1 mmol/L DMHP and DEHP were less effective than DF both in their iron-mobilizing effect and in promoting thiolic enzyme recovery. The superior efficiency of DF at low concentrations illustrates the advantage of the hexadentate chelating action of DF as compared with bidentate chelators such as DMHP and DEHP requiring a 3 to 1 molar ratio to iron for optimal effect. In contrast to its beneficial effect on sarcolemmal enzyme activity, iron chelation was unable to reverse the increase in beta-hexosaminidase activity caused by abnormal lysosomal fragility. Our study demonstrates for the first time that iron-induced peroxidative damage to the myocardial cell is associated with a marked loss of Na,K,ATPase activity, an enzyme with a major role in the maintenance of cellular resting potential. The timing of this damage and the restoration of Na,K,ATPase function by iron-chelating treatment suggest a cause-and-effect relationship between the observed injury to the sarcolemmal enzyme and the reversible electrophysiologic abnormalities observed in the same heart culture system in our previous studies.

5'-Nucleotidase↗