A case of hypophosphatemic osteomalacia secondary to deferasirox therapy

Patients with β‐thalassemia major require iron‐chelation therapy to avoid the complication of iron overload. Until recently, deferoxamine (DFO) was the major iron chelator used in patients requiring chronic hypertransfusion therapy, but DFO required continuous subcutaneous therapy. The availability of deferasirox (Exjade®), an orally active iron chelator, over the past 4 years represented a necessary alternative for patients requiring chelation therapy. However, there have been increasing reports of proximal renal tubular dysfunction and Fanconi Syndrome associated with deferasirox in the literature. We report a case of hypophosphataemic osteomalacia secondary to deferasirox therapy. © 2012 American Society for Bone and Mineral Research     

Comparative study of intravenous ascorbic acid versus low-dose desferroxamine in patients on hemodialysis with hyperferritinemia

BACKGROUND: In patients on hemodialysis (HD), parenteral iron improves the response to recombinant human erythropoietin (rhuEPO) therapy, but in some subjects it produces an iron overload, increasing their morbidity and mortality rates. In these cases, iron administration must be discontinued. This study aimed to investigate the efficiency of treatment with ascorbic acid (AA) or desferroxamine (DFO) to mobilize and reduce iron stores, and to determine the effect of these compounds on erythropoiesis. METHODS: We performed a prospective and randomized trial over 6 months, which included 27 patients with serum ferritin levels >800 ng/mL, TSAT >30% and stabilized hemoglobin (Hb) and rhuEPO doses. All patients had previously received parenteral iron (Ferlecit). Nine patients received 200 mg of intravenous (i.v.) AA 3 times/week and nine patients received 1 mg/Kg/week of DFO; the remaining nine patients were the control group. RESULTS: There were no significant differences in iron loss or mobilization due to dialysis. When Ferlecit was discontinued, functional iron did not vary and the epoetin resistance index (rhuEPO dose/Hb) was reduced by 21% in the i.v. AA group. In the DFO and control groups, functional iron levels fell. In the DFO group the epoetin resistance index increased by 20%, with no modifications in the control group. There was a positive correlation between transaminases and serum ferritin. CONCLUSIONS: In HD patients with an iron overload, neither i.v. AA administration or low-dose DFO increased iron mobilization or iron loss due to dialysis. I.v. AA administration allows elimination of iron from stores without any drop in the functional iron produced by discontinuing parenteral maintenance iron; it also improves the response to rhuEPO. DFO did not elicit any positive effects on erythropoiesis.     

Short-term small-dose intravenous iron trial to detect functional iron deficiency in dialysis patients

BACKGROUND/AIM: Management of renal anemia in end-stage renal disease requires careful evaluation of the iron status before and in particular during erythropoietin treatment. However, there is no simple and practical iron index accurately predictive of functional iron deficiency in these patients till now. The purpose of this prospective study, therefore, is to evaluate whether a short course of low-dose intravenous iron challenge can detect functional iron deficiency in hemodialysis patients. METHODS: Twenty-four patients with baseline serum ferritin levels between 100 and 500 ng/ml were treated with intravenous saccharated ferric oxide, 960 mg over 24 hemodialysis treatments, and the hemoglobin level was checked every week. RESULTS: Patients whose hemoglobin value increased at least by 1 g/dl within the 8-week period were classified as having functional iron deficiency or as responders (n = 26; 81.2%). All other subjects were classified as having adequate iron levels or as nonresponders (n = 6; 18.8%). There were no significant differences in age, sex, dialysis years, Kt/V, dialyzers, hemoglobin, and basal and final transferrin saturation and ferritin between responders and nonresponders. In addition, there were no iron indices with acceptable levels of sensitivity and specificity. On the contrary, the cutoff value of increments of hemoglobin of at least 0.2 g/dl after a 2-week intravenous iron trial had a sensitivity of 96.2% and a specificity of 100% in all patients (n = 32) and a sensitivity of 100% and a specificity of 100% after patients with transferrin saturation <20% were excluded (n = 24). These values had the greatest utility of the tests studied in this work. CONCLUSION: A 240-mg intravenous iron challenge during a 2-week period may be a simple, accurate, and straightforward method to detect a functional iron deficiency status in hemodialysis patients undergoing erythropoietin therapy.     

Decreased parathyroid hormone secretion in chronic hemodialysis patients without active vitamin D treatment

Abrstact Sixty-eight out of 149 chronic hemodialysis patients without recent administration of the active vitamin D did not actually show the secondary hyperparathyroidism evaluating by the intact PTH levels. High incidence of diabetes mellitus was recognized in the patients with the normal or low intact PTH level. The 33 patients could be divided into two groups, the responders and nonresponders, in accordance with the intact PTH response to calcium-free hemodialysis technique. The basal C-PTH and intact PTH of the responders were higher than those of the nonresponders, however the levels of plasma ferritin and aluminium, and desferrioxamine loading tests did not show any difference between them. Number of Diabetic patient also distributed evenly between two groups. Diabetes mellitus, aluminium intoxication and iron overload were not fully responsible for the poor secretion of intact PTH in the chronic hemodialysis patients.     

去铁胺对输血相关性铁过载患者骨密度的影响

目的观察输血相关铁过载患者在使用去铁胺(DFO)降铁治疗后骨密度的变化,探讨去铁胺对铁过载骨质疏松患者辅助治疗的应用前景。方法回顾性研究22例输血相关铁过载患者临床资料,检测患者DFO降铁治疗前后的骨密度和血清生化指标。采用配对样本t检验、Wilcoxon非参数检验分析研究患者DFO降铁治疗前后骨密度以及血清生化指标的变化。结果进行DFO有效的铁螯合治疗后,患者血清铁蛋白(Fer)明显下降,由基线水平的2019.95±630.77 ng/m L降至843.61±91.01 ng/m L(P0.05);股骨颈和腰椎的骨密度明显增加,分别由基线水平的0.73±0.12 g/cm2、0.92±0.14 g/cm2增加至0.77±0.09 g/cm2、0.94±0.14 g/cm2(P0.05);骨量正常、骨量减少和骨质疏松患者分别由治疗前的4、12、6例变为治疗后的10、11、1例(P0.05)。结论 DFO降铁治疗可改善输血相关铁过载患者的低骨量状态。本研究为DFO可能用于伴有铁过载的骨质疏松症的辅助治疗提供了有意义的支撑。     

Successful treatment of dialysis osteomalacia and dementia, using desferrioxamine infusions and oral 1-alpha hydroxycholecalciferol

A 54-year-old patient with fracturing dialysis osteomalacia and dementia demonstrated rapid deterioration following parathyroidectomy which was performed for sustained hypercalcemia. Reduction of the total body aluminum burden was attempted using desferrioxamine (DFO) as a chelating agent. After 6 months, DFO infusion resulted in sustained clinical remission of both neurological and skeletal symptoms, associated with an improvement in the EEG and improved mineralization of bone. A reduction in total body aluminum burden was reflected by reduced skeletal aluminum content, quantitated histochemically in iliac crest bone biopsies before and after DFO therapy. Dramatic increases in serum aluminum levels were documented in the initial weeks of DFO therapy leading to increased removal of aluminum during dialysis; in vitro studies indicated that the ultrafiltrable fraction of serum aluminum increased from 17 to more than 60% after initiating DFO treatment. However, after 6 months of therapy, serum aluminum levels remained unchanged after DFO infusion. These findings suggest that the serum aluminum response to DFO infusion might be a useful reflection of the total-body aluminum burden and also a reflection of the adequacy of a chelation program designed to reduce whole-body aluminum content.     

Low dose desferrioxamine can improve erythropoiesis in iron-overload hemodialysis patients without side effects

OBJECTIVE: Multiple blood transfusions were often required to treat anemia in uremia patients before the era of recombinant human erythropoietin (r-HuEPO). Iron overload thus frequently occurred in chronic hemodialysis patients. Desferrioxamine (DFO) is an effective chelating agent, which can remove excessive iron and can enhance erythropoiesis. Large dose DFO treatment is a therapy associated with the development of severe complications. In this study, a low dose DFO regime was used to treat iron overloaded hemodialysis patients. The efficacy and side effects of this regiment were evaluated. MATERIALS AND METHODS: Eight iron overloaded chronic hemodialysis patients were enrolled in this study. All patients received DFO 500 mg intravenously twice-a-week for eight months. Serum aluminum, transferrin saturation (TFS) and r-HuEPO requirement were recorded before and after DFO treatment. Serum ferritin and hematocrit (Hct) were measured before, during, and after the DFO withdrawal period. All patients were evaluated and followed closely during treatment. RESULTS: Changes in aluminum, TFS and r-HuEPO dosage were unremarkable (p > 0.05). Hct increased significantly after eight months of DFO treatment (from 25.3% to 27.0%, p < 0.05). Ferritin level was reduced by 43.2% at the end of treatment and an evident decline of ferritin was achieved after four months of treatment (2102 ng/mL to 1166 ng/mL, p < 0.05). All patients tolerated the treatment well and no complications were found. CONCLUSION: Low dose DFO can chelate iron effectively in chronic hemodialysis patients. This treatment can enhance erythropoiesis without adverse effects.     

Diagnosis and treatment of iron overload in paediatric patients on chronic haemodialysis

In this study the incidence and contributing factors of iron overload in paediatric patients treated with intermittent haemodialysis were evaluated. Particular attention was given to the diagnostic value of serum ferritin in the assessment of body iron stores in patients with hepatocellular damage. The results of treatment of secondary haemosiderosis with desferrioxamine (DFO) are reported. Serum ferritin levels were measured in 18 children and adolescents undergoing long-term haemodialysis; 8 of these had biochemical evidence of hepatocellular damage. In all patients a good correlation was found between serum ferritin levels and the amount of iron stored in the reticuloendothelial system. Six patients developed iron overload. Patients with secondary haemosiderosis were younger at the start of haemodialysis and received significantly more blood. Although not significant, more patients with haemochromatosis-associated alleles and bilateral nephrectomy had iron overload, and the duration of dialysis was obviously longer for overloaded patients (40 months versus 26 months). The patients with iron overload were treated with DFO. The data from all patients showed that DFO was ineffective when administered at a dose of 25 mg/kg during dialysis and that in individual patients changes in serum ferritin correlated with changes in the amount of blood transfusions administered.     

Intravenous ascorbic acid administration for erythropoietin-hyporesponsive anemia in iron loaded hemodialysis patients

Intravenous ascorbic acid administration (IVAA) could override recombinant human erythropoietin (rHuEPO) resistance in hemodialysis patients with iron overload. We investigated the hematopoietic response to IVAA in iron-overloaded hemodialysis patients. We included 36 patients whose ferritin levels were higher than 500 microg/L and who needed more than 100 U/kg/week of rHuEPO. The study included an initial phase (500 mg IVAA twice weekly was administered to all of the patients for 8 weeks) and a maintenance phase (patient groups were formed; Group 1 received IVAA 500 mg/week for 8 weeks and Group 2 received no therapy). We observed a significant increase in hematocrit and transferrin saturation and a decrease in the percentage of hypochromic red cells and ferritin levels at the end of the initial phase. The total weekly-required rHuEpo dose and rHuEpo/hemoglobin also fell significantly after the initial phase. The response remained stable in patient groups during the maintenance phase. In 6 nonresponders, the hypochromic red cells were <10%. In conclusion, IVAA effectively overrides rHuEPO resistance in iron-overloaded hemodialysis patients.     

Fatal fungal peritonitis in an adolescent on continuous ambulatory peritoneal dialysis: association with deferoxamine

An unusual case ofRhizopus microsporus (mucormycosis) fungal infection in a teenage boy on continuous ambulatory peritoneal dialysis is presented. Premortem cultures were negative and the patient developed a rapidly disseminated fatal infection. The patient was being treated with deferoxamine (DFO) for iron and aluminum overload. An argument is made for a probable association between DFO and this fatal fungal infection in patients with end-stage renal disease.     

The effect of an iron supplement on serum aluminum level and desferrioxamine mobilization test in hemodialysis patients.

BACKGROUND: The serum aluminum (Al) measurement with desferrioxamine (DFO) mobilization is a screening test for uremic patients with an Al overload. In these patients, body iron status is one of the factors affecting the serum Al level. This study is designed to elucidate the effects of iron supplements on the serum Al and the DFO mobilization test. METHODS: Our study featured ten hemodialysis patients with iron deficiency anemia. The iron supplement was given intravenously with saccharated ferric oxide, 40 mg three times weekly, at the end of each hemodialysis. The total amount of iron supplement was 1,000 mg. All the patients underwent a DFO test at a dose of 5 mg/kg. The same test was repeated two weeks after completion of the iron supplement. RESULTS: After the iron supplement, patients' iron deficiency anemia improved with a serum ferritin elevation from 312.4 +/- 589.5 to 748.2 +/- 566.2 microg/L (p < 0.01), and iron saturation from 21.6 +/- 20.3 to 41.1 +/- 21.7% (p = 0.06). The basal serum Al level decreased from 34.3 +/- 13.8 to 21.8 +/- 8.5 microg/L (p = 0.01). In the DFO mobilization test, the peak serum Al level decreased from 63.4 +/- 19.3 to 50.7 +/- 20.5 microg/L (p < 0.01). The amount of Al increment (deltaAl) in DFO test was not changed (29.1 +/- 12.0 vs. 28.9 +/- 15.9 microg/L, p = 0.86). The change in basal Al level tended to negatively correlate with the percentage of increment in iron saturation (r = -0.628, p = 0.05). CONCLUSION: Results in this study suggest that iron supplements may significantly reduce the basal serum Al and peak Al in DFO mobilization test, without significant change of the mean deltaAl. The data presented indicate that in the interpretation of serum aluminum levels the iron status should be taken into account.     

The role of aluminum in the pathogenesis of anemia in an outpatient hemodialysis population

Anemia is a well-defined complication of aluminum overload in chronic dialysis patients which may be present before other manifestations of aluminum toxicity are obvious. Causes of anemia in chronic renal failure are multiple, and at the present time there is no marker for aluminum-induced anemia. Deferoxamine (DFO) treatment can correct aluminum-related anemia and microcytosis, but may be associated with side effects. Because of the possible role of aluminum in red blood cells in causing the anemia associated with aluminum overload, we attempted to test red blood cell (RBC) aluminum as a marker for aluminum-associated anemia and to assess the prevalence of aluminum-associated anemia in an outpatient dialysis population. Both random plasma aluminum and RBC aluminum correlated well with the increase in plasma aluminum seen following DFO challenge. However, RBC aluminum was affected less by changes in oral aluminum intake than plasma aluminum. There were strong correlations of RBC and plasma aluminum to corpuscular volume (MCV) in our patients. Moreover, patients within the highest quartile of RBC aluminum had a lower mean MCV (82.1 +/- 1.7 vs 89.6 +/- 1.7, p less than .01) and hematocrit (HCT) (24.3 +/- 4 vs 28.2 +/- 1.5, p less than .05) than those within the lowest quartile. These data suggest that aluminum toxicity is an important cause of microcytic anemia in outpatient hemodialysis patients. Prospective long-term studies are needed to further define the usefulness of RBC aluminum in diagnosing and following hemodialysis patients with aluminum-induced anemia.     

Sirolimus interferes with iron homeostasis in renal transplant recipients

BACKGROUND: Sirolimus is an immunosuppressive drug whose use is frequently associated with anemia. A pathogenic link between sirolimus-induced anemia and the appearance of an inflammatory state was recently suggested. Because inflammation-related anemia is characterized by a functional iron deficiency, we investigated whether sirolimus may influence iron homeostasis and serum levels of hepcidin, a key mediator of inflammation-related anemia. METHODS: To this purpose, 42 consecutive transplanted patients with biopsy-proven chronic allograft nephropathy were randomized (2:1 ratio) to receive either a 40% cyclosporine reduction (group A, 14 patients) or immediate cyclosporine withdrawal and sirolimus introduction (group B, 28 patients). Hemoglobin levels and iron status were evaluated 6 months before and after randomization. RESULTS: The two groups had similar hemoglobin levels and iron status at baseline. We did not observe any significant change in hemoglobin and iron status in group A patients after randomization. On the contrary, we observed a significant reduction of hemoglobin without any change of red blood cell count after sirolimus introduction, with a significant reduction of mean corpuscular volume and mean corpuscular hemoglobin. Serum iron and transferrin saturation (TSAT) levels were markedly reduced after the switch, while ferritin serum concentrations remained stable. Although sirolimus-induced anemia was recently suggested to resemble inflammation-related anemia, hepcidin serum levels were similar in the two groups after randomization. None of group A and eight of group B patients presented a TSAT <20 and were given iron supplementation after randomization, in all of them oral iron therapy did not influence either hemoglobin or serum iron levels. CONCLUSION: We demonstrated that sirolimus-induced anemia is independent of the drug antiproliferative effect and does not present the features of inflammation-related anemia. This event may be due to the direct influence of sirolimus on iron homeostasis.     

Beta-thalassaemia--the Johannesburg experience

Twenty-nine patients with beta-thalassaemia major were treated in two Johannesburg hospitals between 1979 and 1984. They belonged to two ethnic groups--Mediterranean and Asian--and 53% were under the age of 6 years, the oldest being 20 years. Eight patients underwent splenectomy. All were regularly transfused and their quality of life greatly improved. The complication of regular transfusions is iron overload, which contributes to morbidity and mortality. Despite adequate iron excretion as a result of subcutaneous desferrioxamine (DFO) infusions, the patients showed significant iron overload, which suggested poor compliance in the home use of DFO and was the main long-term problem in the treatment of beta-thalassaemia major. Education needs to be directed at communities at risk and their doctors so that new cases can be prevented and the financial and emotional cost eased. If patients are given full support in complying with therapy, their life expectancy should be greatly increased.     

Kinetics and efficacy of deferoxamine in iron-overloaded hemodialysis patients

We evaluated the kinetics and efficacy of deferoxamine (DFO) therapy in iron-overloaded hemodialysis patients. Concentrations of DFO and its chelated product, feroxamine (Fx), were assessed following single-dose DFO administration in twelve patients, and during chronic therapy over one year's time in eight, similarly iron-overloaded dialysis patients. A functional assay which relies on measurements of iron and iron binding capacity for the determination of Fx and DFO, respectively, was corroborated with liquid chromatographic techniques. Half-life measurements were also corroborated with tracer doses of 14C-DFO and 59Fe-feroxamine. Intradialytic DFO half-life (2.3 +/- 1.1 h) was considerably less than interdialytic half-life (26 +/- 1 hr). Unbound DFO was found to persist throughout the interdialytic period. Calculation of the percent saturation of the DFO dose indicated that only 30% of a given dose is chelated. The amount of iron removed dialytically was approximately 13.1 +/- 2.7 mg per dialysis session. Chronic DFO administration was also shown to enhance gastrointestinal iron excretion threefold. However, ferritin levels decreased by only 25% after one year of thrice-weekly DFO therapy. We conclude that DFO therapy for iron-overloaded hemodialysis patients is optimized by its administration interdialytically, and results in slow removal of iron, via both dialytic and gastrointestinal routes.     

L-carnitine substitution in patients on chronic hemodialysis

Patients on chronic hemodialysis with hyperlipidemia were found to respond either with decreased levels (responders) or with a further increase of the plasma triglyceride levels (nonresponders) to a carnitine substitution therapy. The aim of the present study was to find possible predictors to distinguish between responders and nonresponders prior to the initiation of therapy. Since it is suggested that erythrocytes are involved in carnitine transport to tissues, it was of interest to determine plasma and erythrocyte carnitine concentrations in the hemodialyzed patients before and during carnitine substitution therapy and to compare the results with those of healthy controls. Before therapy, comparatively lower plasma levels of both free and total carnitine, but higher portions of short-chain acylcarnitine on total carnitine were found in all patients. In erythrocytes, the nonresponders showed significantly higher total carnitine levels, compared to responders and controls. After the start of carnitine substitution, the increase of total plasma carnitine during the substitution period corresponded with the carnitine dose administered in responders, in nonresponders the highest carnitine values were found in the second week when the lower carnitine dose was administered. The changes of the plasma short-chain acylcarnitine levels with time were very similar to those of plasma triglycerides. All patients showed a time-delayed accumulation of carnitine in erythrocytes and, interestingly, markedly higher concentrations in the second week when the lower carnitine dose was administered. The results of the present study demonstrate that the erythrocyte carnitine content is a reliable predictor to distinguish between responders and nonresponders prior to the start of a carnitine substitution therapy.     

Significance of circulating matrix metalloproteinase-9 to tissue inhibitor of metalloproteinases-2 ratio as a predictor of disease progression in patients with metastatic renal cell carcinoma receiving sunitinib

ObjectivesTo assess the significance of circulating matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) as predictors of disease progression in patients with metastatic renal cell carcinoma (mRCC) receiving sunitinib.Materials and methodsCirculating levels of MMP-2, MMP-9, TIMP-1, and TIMP-2 in sera from 52 patients with mRCC treated with sunitinib were measured at the baseline and on the first day of each treatment cycle until progression using enzyme-linked immunosorbent assays.ResultsThe baseline level of MMP-9 in nonresponders to sunitinib was significantly higher than that in responders, whereas the baseline level of TIMP-2 in nonresponders was significantly lower than that in responders. However, there were no significant differences in the serum levels of MMP-2 and TIMP-1 between responders and nonresponders. The serum MMP-9/TIMP-2 ratio at the baseline in nonresponders was also significantly higher than that in responders. Univariate analysis showed that the MMP-9/TIMP-2 ratio, but not MMP-9 and TIMP-2 levels, was significantly correlated with progression-free survival, and the MMP-9/TIMP-2 ratio, in addition to the Memorial Sloan-Kettering Cancer Center classification and C-reactive protein level, appeared to be independently associated with progression-free survival on multivariate analysis. Furthermore, despite the lack of significant differences in the serum levels of MMP-9 and TIMP-2 between the baseline and the time of progression, the MMP-9/TIMP-2 ratio at the time of progression was significantly elevated compared with the baseline ratio.ConclusionsAn imbalance between the serum MMP-9 and TIMP-2 levels could be a novel biomarker to predict disease progression in patients with mRCC under treatment with sunitinib.     

THE EFFECT OF AN IRON SUPPLEMENT ON SERUM ALUMINUM LEVEL AND DESFERRIOXAMINE MOBILIZATION TEST IN HEMODIALYSIS PATIENTS

Background. The serum aluminum (Al) measurement with desferrioxamine (DFO) mobilization is a screening test for uremic patients with an Al overload. In these patients, body iron status is one of the factors affecting the serum Al level. This study is designed to elucidate the effects of iron supplements on the serum Al and the DFO mobilization test. Methods. Our study featured ten hemodialysis patients with iron deficiency anemia. The iron supplement was given intravenously with saccharated ferric oxide, 40 mg three times weekly, at the end of each hemodialysis. The total amount of iron supplement was 1,000 mg. All the patients underwent a DFO test at a dose of 5 mg/kg. The same test was repeated two weeks after completion of the iron supplement. Results. After the iron supplement, patients' iron deficiency anemia improved with a serum ferritin elevation from 312.4 ± 589.5 to 748.2 ± 566.2 μg/L (p < 0.01), and iron saturation from 21.6 ± 20.3 to 41.1 ± 21.7% (p = 0.06). The basal serum Al level decreased from 34.3 ± 13.8 to 21.8 ± 8.5 μg/L (p = 0.01). In the DFO mobilization test, the peak serum Al level decreased from 63.4 ± 19.3 to 50.7 ± 20.5 μg/L (p < 0.01). The amount of Al increment (ΔAl) in DFO test was not changed (29.1 ± 12.0 vs. 28.9 ± 15.9 μg/L, p = 0.86). The change in basal Al level tended to negatively correlate with the percentage of increment in iron saturation (r = ? 0.628, p = 0.05). Conclusion. Results in this study suggest that iron supplements may significantly reduce the basal serum Al and peak Al in DFO mobilization test, without significant change of the mean ΔAl. The data presented indicate that in the interpretation of serum aluminum levels the iron status should be taken into account.     

Erythrocyte ferritin in patients on chronic hemodialysis treatment

Serum ferritin (SF) and erythrocyte ferritin (EF) were evaluated in 35 patients on chronic hemodialysis treatment (CHD), in 45 healthy subjects and in 22 nonnephropathic females with iron deficiency anemia. Twenty-five CHD patients with basal SF less than 500 micrograms/l were treated orally with 200 mg of Fe2+ for 2 months and the positive (hemoglobin increase greater than 1 g/dl) or negative response to the therapy was correlated to the basal levels of SF and EF. Three groups of CHD patients could be defined on the basis of their basal SF levels (hypo-, normo- or hyperferritinemic). Nine patients with increased SF levels had also EF levels significantly higher than the other CHD patients and controls since they were probably iron-overloaded. In the other 2 groups of CHD patients, EF levels were significantly higher than in controls for each level of SF probably because of the reduced utilization of iron by uremic bone marrow. Among the 25 treated CHD patients, only 5 responded to the therapy: 3 were hypoferritinemic while the other 2 responders had basal SF within the normal range. Four hypoferritinemic patients did not respond to the therapy. Four out of five responders had the lowest EF levels among CHD patients. EF measurement could be an important and useful test in detecting the presence of an iron deficiency erythropoiesis in CHD patients.     

The role of desferrioxamine in dialysis-associated mucormycosis: report of three cases and review of the literature

We report 3 patients on maintenance hemodialysis who developed a fulminant, disseminated and fatal form of mucormycosis. The diagnosis was made by microscopy and culture in 1 case, yielding Rhizopus rhizopodiformis, and by post-mortem microscopy in the two other cases. These patients were receiving desferrioxamine (DFO) for aluminum overload and had no iron-overload. Ten similar patients, all (with only one possible exception) receiving DFO, have been reported from American centers. The mechanism by which DFO could precipitate mucormycosis is unsettled. The explanation might be that DFO acts as a siderophore to the Mucorales fungi. High serum levels of DFO in renal failure could enhance this mechanism. Epidemiological data, provided from an inquiry in 25 Flemish dialysis centers, support the association between DFO treatment and dialysis-associated mucormycosis.