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Lucilla Zilletti - One of the best experts on this subject based on the ideXlab platform.

  • effect of 21 aminosteroid u74500a pregna 1 4 9 11 triene 3 20 dione 21 4 5 6 bis diethylamino 2 pyridinyl 1 piperazinyl 16 methyl hcl 16α on rat brain cortex lipid peroxidation induced in vivo by Iron carbohydrate
    Biochemical Pharmacology, 1994
    Co-Authors: Mario Ciuffi, G. Gentilini, S Franchimicheli, Lucilla Zilletti
    Abstract:

    Abstract Compounds derived from glucocorticoids, 21-aminosteroids, were reported to inhibit in vitro lipid peroxidation in CNS tissue. In order to evaluate the possible scavenging and/or Iron chelating activities in vivo of the 21-aminosteroid U74500A (pregna-1,4,9(11)-triene-3,20-dione, 21-(4-(5,6-bisdiethylamino)-2-pyridinyl)-1-piperazinyl)-16-methyl-, HCl (16α)), the drug was administered for seven days to rats. These rats had been induced by Iron-Saccharate complex injection a slow process of lipid peroxidation into their right brain hemicortex. The drug was injected also to intact rats (normal rats). Seven days after the operation the extent of Iron-induced lipid peroxidation in both the hemicortices and the effect of the drug, were assessed by the evaluation of lipid-soluble fluorescence and of conjugated diene formation. The assessment was performed both in vehicle (control) and in U74500A-treated rats. In the Iron-injected rat groups the drug induced a significant dose-related reduction of fluorescence values. Formation of conjugated dienes showed a significant decrease when U74500A (48 mg/kg every 48 hr) was administered to cortico-cerebrally Iron-injected animals. The lipid peroxidation of cortices in normal rats was evaluated as thiobarbituric acid reactant substances in both the drug-treated and the control animals. In normal rats, U74500A (48 mg/kg every 48 hr) caused a significant decrease of TEARS values, as compared to those observed in the control group. The Iron content in the Iron-injected hemicortices, which was evaluated by the ferrozine method, was not modified by drug treatment. U74500A appears to have in vivo antioxidant properties and not to affect the Iron content in the neural tissue. An interaction of this drug with the metal, however, cannot be excluded.

  • D-penicillamine affects lipid peroxidation and Iron content in the rat brain cortex
    Neurochemical Research, 1992
    Co-Authors: Mario Ciuffi, G. Gentilini, Sergio Franchi-micheli, Lucilla Zilletti
    Abstract:

    d-Penicillamine, a trifunctional aminoacid known for its ability to form metal complexes and for being a radical scavenger, has been investigated “in vitro” and “in vivo” in the rat brain cortex. At 50 μM the drug facilitate lipid hydroperoxides and TBARS formation in brain cortex homogenates, while at higher concentrations a clear inhibition of the lipid peroxidative process was observed. The activity of thed-penicillamine (25 and 50 mg/Kg i.p) was evaluated “in vivo” after a 7-day treatment in rats in whose brain cortex a slow process of lipid peroxidation was induced by Iron-Saccharate injection. Lipid hydroperoxides, lipid soluble fluorescent compounds and the Iron content of both Iron-injected and contralateral hemicortices showed a significant decrease in comparison to rats untreated withd-penicillamine. The higher dose also induced in normal rats a significant decrease in basal TBARS and Iron content of the brain cortex. In the Iron-injected cortex the observed Fe2+/Fe3+ ratio was significantly different from that of normal rats. On the contrary ratios obtained formd-penicillamine treated animals were higher in comparison to both normal and Iron-injected animals. These results suggest thatd-penicillamine, acting as a reducing agent, inhibits the Iron redox system and, as a chelating agents, can remove metal from action sites where lipid peroxidation may occur.

  • Lipid peroxidation induced “in vivo” by Iron-carbohydrate complex in the rat brain cortex
    Neurochemical Research, 1991
    Co-Authors: Mario Ciuffi, G. Gentilini, Sergio Franchi-micheli, Lucilla Zilletti
    Abstract:

    In view of the emerging role of metals and particularly Iron in the pathogenesis of several ischemic or degenerative CNS diseases, via a lipid peroxidative process, a model of slow Iron-induced peroxidative damage in the rat brain cortex has been carried out. Iron-carbohydrate complexes were injected in the right brain cortex, and biochemical assays were performed on ipsilateral and contralateral samples two hours or seven days after injection. Iron-sacchararate caused a significant increase in the ipsilateral cortex in TBARS, conjugated dienes and fluorescent substances seven days after injection, whereas no biochemical alteration was observed two hours after treatment. In order to prevent or to limit lipid peroxidation, some drugs known for chelating and/or scavening activity were administered to Iron-injected rats. DL-α-tocopherol, methylprednisolone, D-penicillamine significantly decreased the value of fluorescent products formed by Iron-Saccharate, whereas desferrioxamine was not effective.

Mario Ciuffi - One of the best experts on this subject based on the ideXlab platform.

  • effect of 21 aminosteroid u74500a pregna 1 4 9 11 triene 3 20 dione 21 4 5 6 bis diethylamino 2 pyridinyl 1 piperazinyl 16 methyl hcl 16α on rat brain cortex lipid peroxidation induced in vivo by Iron carbohydrate
    Biochemical Pharmacology, 1994
    Co-Authors: Mario Ciuffi, G. Gentilini, S Franchimicheli, Lucilla Zilletti
    Abstract:

    Abstract Compounds derived from glucocorticoids, 21-aminosteroids, were reported to inhibit in vitro lipid peroxidation in CNS tissue. In order to evaluate the possible scavenging and/or Iron chelating activities in vivo of the 21-aminosteroid U74500A (pregna-1,4,9(11)-triene-3,20-dione, 21-(4-(5,6-bisdiethylamino)-2-pyridinyl)-1-piperazinyl)-16-methyl-, HCl (16α)), the drug was administered for seven days to rats. These rats had been induced by Iron-Saccharate complex injection a slow process of lipid peroxidation into their right brain hemicortex. The drug was injected also to intact rats (normal rats). Seven days after the operation the extent of Iron-induced lipid peroxidation in both the hemicortices and the effect of the drug, were assessed by the evaluation of lipid-soluble fluorescence and of conjugated diene formation. The assessment was performed both in vehicle (control) and in U74500A-treated rats. In the Iron-injected rat groups the drug induced a significant dose-related reduction of fluorescence values. Formation of conjugated dienes showed a significant decrease when U74500A (48 mg/kg every 48 hr) was administered to cortico-cerebrally Iron-injected animals. The lipid peroxidation of cortices in normal rats was evaluated as thiobarbituric acid reactant substances in both the drug-treated and the control animals. In normal rats, U74500A (48 mg/kg every 48 hr) caused a significant decrease of TEARS values, as compared to those observed in the control group. The Iron content in the Iron-injected hemicortices, which was evaluated by the ferrozine method, was not modified by drug treatment. U74500A appears to have in vivo antioxidant properties and not to affect the Iron content in the neural tissue. An interaction of this drug with the metal, however, cannot be excluded.

  • D-penicillamine affects lipid peroxidation and Iron content in the rat brain cortex
    Neurochemical Research, 1992
    Co-Authors: Mario Ciuffi, G. Gentilini, Sergio Franchi-micheli, Lucilla Zilletti
    Abstract:

    d-Penicillamine, a trifunctional aminoacid known for its ability to form metal complexes and for being a radical scavenger, has been investigated “in vitro” and “in vivo” in the rat brain cortex. At 50 μM the drug facilitate lipid hydroperoxides and TBARS formation in brain cortex homogenates, while at higher concentrations a clear inhibition of the lipid peroxidative process was observed. The activity of thed-penicillamine (25 and 50 mg/Kg i.p) was evaluated “in vivo” after a 7-day treatment in rats in whose brain cortex a slow process of lipid peroxidation was induced by Iron-Saccharate injection. Lipid hydroperoxides, lipid soluble fluorescent compounds and the Iron content of both Iron-injected and contralateral hemicortices showed a significant decrease in comparison to rats untreated withd-penicillamine. The higher dose also induced in normal rats a significant decrease in basal TBARS and Iron content of the brain cortex. In the Iron-injected cortex the observed Fe2+/Fe3+ ratio was significantly different from that of normal rats. On the contrary ratios obtained formd-penicillamine treated animals were higher in comparison to both normal and Iron-injected animals. These results suggest thatd-penicillamine, acting as a reducing agent, inhibits the Iron redox system and, as a chelating agents, can remove metal from action sites where lipid peroxidation may occur.

  • Lipid peroxidation induced “in vivo” by Iron-carbohydrate complex in the rat brain cortex
    Neurochemical Research, 1991
    Co-Authors: Mario Ciuffi, G. Gentilini, Sergio Franchi-micheli, Lucilla Zilletti
    Abstract:

    In view of the emerging role of metals and particularly Iron in the pathogenesis of several ischemic or degenerative CNS diseases, via a lipid peroxidative process, a model of slow Iron-induced peroxidative damage in the rat brain cortex has been carried out. Iron-carbohydrate complexes were injected in the right brain cortex, and biochemical assays were performed on ipsilateral and contralateral samples two hours or seven days after injection. Iron-sacchararate caused a significant increase in the ipsilateral cortex in TBARS, conjugated dienes and fluorescent substances seven days after injection, whereas no biochemical alteration was observed two hours after treatment. In order to prevent or to limit lipid peroxidation, some drugs known for chelating and/or scavening activity were administered to Iron-injected rats. DL-α-tocopherol, methylprednisolone, D-penicillamine significantly decreased the value of fluorescent products formed by Iron-Saccharate, whereas desferrioxamine was not effective.

W H Horl - One of the best experts on this subject based on the ideXlab platform.

  • Anemia and carnitine supplementation in hemodialyzed patients.
    Kidney international. Supplement, 1999
    Co-Authors: J Kletzmayr, W H Horl, G Mayer, E Legenstein, G Heinz-peer, T Leitha, J Kovarik
    Abstract:

    Carnitine supplementation in hemodialyzed patients was studied in a double-blinded, randomized, controlled trial in order to elucidate the effect of intravenous carnitine on renal anemia in patients treated with recombinant human erythropoietin (rHuEPO). Twenty stable hemodialysis (HD) patients received intravenous L-carnitine after each dialysis session in a dosage of 5 (N = 15) and 25 (N = 5) mg/kg, respectively, together with intravenous Iron Saccharate (20 mg/HD session) for four months and without Iron for a further four months. Twenty patients received placebo instead of carnitine with an identical Iron regimen. After a run-in phase of six months with a stable rHuEPO requirement, the rHuEPO dose was adjusted monthly when necessary to maintain target hemoglobin levels. At study entry (T0), plasma and red blood cell carnitine levels did not correlate significantly with the rHuEPO requirement. However, plasma free and total carnitine levels showed a significant negative correlation with erythrocyte survival time at T0. After four months of coadministration of intravenous Iron and L-carnitine (T4), the rHuEPO requirement decreased in 8 of 19 evaluable HD patients. In these responders, the weekly rHuEPO dose was decreased significantly by 36.9+/-23.3% (183.7+/-131.7 at T0 vs. 126.6+/-127.9 U/kg/week at T4, P < 0.001). The rHuEPO requirement, however, was unchanged when all carnitine-treated patients were compared between T0 and T4 (T0: 172.0+/-118.0 vs. T4: 152.3+/-118.8 U/kg/week, P = 0.07, NS), but the erythropoietin resistance index decreased significantly in this group (T0: 16.0+/-11.0 vs. T4: 13.6+/-10.5 U/kg/week/g of hemoglobin, P < 0.02). The erythrocyte survival time was measured in five HD patients treated with Iron and carnitine at T0 and T4. Two out of these patients were carnitine responders and showed an increase of erythrocyte survival time of 15 and 20%, respectively. After the withdrawal of Iron supplementation, the rHuEPO requirement increased comparably in both L-carnitine- and placebo-treated patients during four more months. According to our data, L-carnitine, in addition to Iron supplementation, may have an effect on erythropoietin resistance and erythrocyte survival time in HD patients. More than half of our patients, however, showed no benefit. Further studies to identify those HD patients who might have a benefit of carnitine supplementation, as well as studies concerning the optimal dosage, duration, and way of administration of carnitine supplementation and its mechanism of action, are required.

  • Neutrophil impairment associated with Iron therapy in hemodialysis patients with functional Iron deficiency.
    Journal of the American Society of Nephrology, 1998
    Co-Authors: S I Patruta, R Edlinger, G Sunder-plassmann, W H Horl
    Abstract:

    Hemodialysis patients treated with recombinant human erythropoietin (rhEPO) need adequate Iron supplementation to avoid rhEPO hyporesponsiveness due to Iron deficiency. Low serum ferritin reflects absolute Iron deficiency, whereas normal or high ferritin values in combination with low transferrin saturation (< 20%) indicate functional Iron deficiency. In this study, healthy subjects (group I) were compared with intravenous (i.v.) rhEPO-treated and i.v. Iron-Saccharate-treated regular hemodialysis patients that were subdivided into three groups as follows: patients with serum ferritin > 100 and < 350 micrograms/L (group II), patients with ferritin < 60 micrograms/L (group III), and patients with ferritin > 650 micrograms/L but transferrin saturation < 20% (group IV). Polymorphonuclear leukocyte (PMNL) parameters (phagocytosis, intracellular killing of bacteria, oxidative metabolism, glucose uptake, intracellular calcium) for each group were compared with those of multitransfused, Iron-overloaded primary hematologic patients (group V) and those of patients suffering from hereditary hemochromatosis (group VI). Compared with PMNL obtained from healthy subjects (group I), group II hemodialysis patients showed mild inhibition of phagocytosis but significant inhibition of intracellular killing of bacteria. Oxidative burst of PMNL from group II patients was also significantly reduced after stimulation in vitro. These dysfunctions were not affected by absolute Iron deficiency (comparable data in group III patients). However, impairment of PMNL was markedly aggravated in group IV patients. Intracellular calcium concentration under basal conditions and after stimulation was not different. These data suggest that Iron is responsible for the PMNL dysfunctions observed in group IV patients. The PMNL defect of group IV patients was comparable to group V and group VI patients with normal renal function, suggesting again a direct inhibitory effect of Iron. It is concluded that hemodialysis patients with high ferritin but low serum Iron and low transferrin saturation ("functional Iron deficiency") display a significant impairment of fundamental PMNL functions during i.v. Iron and rhEPO therapy. This may result in increased risk of infectious complications. Therefore, overtreatment of hemodialysis patients with i.v. Iron should be avoided.

  • safety of intravenous injection of Iron Saccharate in haemodialysis patients
    Nephrology Dialysis Transplantation, 1996
    Co-Authors: Gere Sunderplassmann, W H Horl
    Abstract:

    Background. The most frequent i.v. Iron preparations used for haemodialysis patients are Iron dextran, Iron gluconate and Iron Saccharate. Possible side effects include anaphylactic reactions due to preformed antibodies to dextran or vascular reactions due to unbound Iron during treatment with Iron gluconate or Iron Saccharate. Methods. Four dosage regimens of i.v. Iron Saccharate therapy were studied : 10, 20, 40 and 100 mg, which were given over a time period of 1 min after the end of the dialysis session. Iron metabolism parameters (serum Iron concentration, transferrin saturation and serum ferritin levels) were measured at 0, 1, 5, 15 and 30 min after application and immediately prior to the next dialysis session. All 18 regular haemodialysis patients studied received recombinant human erythropoietin (rHuEpo). Results. Serum Iron levels and transferrin saturation increased significantly following i.v. injection of all doses of Iron Saccharate. Iron 'oversaturation' of transferrin Iron binding did not occur in patients with transferrin levels >180 mg/dl. However, in patients with transferrin levels 180 mg/dl (high-risk patients : transferrin <100 mg/dl). This may explain, at least in part, the minimal side effects observed during the i.v. application of Iron Saccharate. Low-dose i.v. Iron Saccharate (10-40 mg) is recommended for Iron supplementation of haemodialysis patients. If injection of 100 mg is necessary, serum transferrin level should exceed 180 mg/dl. There is, however, no need for fast i.v. injection during routine Iron supplementation.

  • Safety of intravenous injection of Iron Saccharate in haemodialysis patients
    Nephrology dialysis transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 1996
    Co-Authors: Gere Sunder-plassmann, W H Horl
    Abstract:

    Background. The most frequent i.v. Iron preparations used for haemodialysis patients are Iron dextran, Iron gluconate and Iron Saccharate. Possible side effects include anaphylactic reactions due to preformed antibodies to dextran or vascular reactions due to unbound Iron during treatment with Iron gluconate or Iron Saccharate. Methods. Four dosage regimens of i.v. Iron Saccharate therapy were studied : 10, 20, 40 and 100 mg, which were given over a time period of 1 min after the end of the dialysis session. Iron metabolism parameters (serum Iron concentration, transferrin saturation and serum ferritin levels) were measured at 0, 1, 5, 15 and 30 min after application and immediately prior to the next dialysis session. All 18 regular haemodialysis patients studied received recombinant human erythropoietin (rHuEpo). Results. Serum Iron levels and transferrin saturation increased significantly following i.v. injection of all doses of Iron Saccharate. Iron 'oversaturation' of transferrin Iron binding did not occur in patients with transferrin levels >180 mg/dl. However, in patients with transferrin levels 180 mg/dl (high-risk patients : transferrin

  • Importance of Iron supply for erythropoietin therapy
    Nephrology dialysis transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 1995
    Co-Authors: Gere Sunder-plassmann, W H Horl
    Abstract:

    BACKGROUND rHuEpo and Iron therapy corrects renal anaemia. However, dosage, route of administration, and monitoring of Iron and rHuEpo therapy in uraemic patients remains controversial. METHODS Therefore a 22-month i.v. Iron substitution trial, subdivided into four study periods, was initiated in 64 Iron-depleted chronic haemodialysis (HD) patients receiving i.v. rHuEpo therapy. Within the first period (6 months) patients were treated with high-dose Iron (100 mg at the end of HD treatment, mean cumulative i.v. Iron Saccharate dosage was 2538 +/- 810 mg per patient) in order to replete the Iron stores. During the 2nd period (6 months) the available Iron pool was maintained with low-dose Iron by administration of 10, 20, or 40 mg Iron at each HD, depending on haemoglobin, serum ferritin and transferrin saturation levels. During the 3rd period (4 months), the Iron-replete patients were randomized to i.v. or s.c. route of rHuEpo administration. During the 4th period (3 months) Iron substitution was omitted to exclude severe Iron overload. RESULTS In the first study period, high-dose Iron therapy dramatically reduced the weekly rHuEpo requirement by 70% of the initial dose (from 217 +/- 179 to 62.6 +/- 70.2 U/kg/week). In the 2nd period Iron storage pools were easily maintained. Serum ferritin and transferrin saturation levels remained stable during this study period. Randomization for thrice-weekly i.v. or s.c. administration of rHuEpo in the 3rd study period revealed comparable efficacy for both administration routes in Iron-replete patients. In well-nourished patients (serum albumin > 40 g/l) without hyperparathyroidism (parathyroid hormone levels 100 U/kg/week in patients with hyperparathyroidism. In the 4th study period, withdrawal of Iron administration led to a rapid decrease of serum ferritin and transferrin saturation levels, indicating the absence of severe Iron overload. CONCLUSIONS Long-term thrice-weekly i.v. low-dose Iron therapy (10-20 mg per HD treatment) proved to be a very effective, economical and safe treatment schedule for Iron-replete HD patients. Intravenous and s.c. rHuEpo therapy was equally efficacious in Iron-replete, well-nourished patients. HD patients with increased parathyroid hormone levels require significantly more rHuEpo than HD patients with parathyroid hormone levels values < 100 pg/ml).

G. Gentilini - One of the best experts on this subject based on the ideXlab platform.

  • effect of 21 aminosteroid u74500a pregna 1 4 9 11 triene 3 20 dione 21 4 5 6 bis diethylamino 2 pyridinyl 1 piperazinyl 16 methyl hcl 16α on rat brain cortex lipid peroxidation induced in vivo by Iron carbohydrate
    Biochemical Pharmacology, 1994
    Co-Authors: Mario Ciuffi, G. Gentilini, S Franchimicheli, Lucilla Zilletti
    Abstract:

    Abstract Compounds derived from glucocorticoids, 21-aminosteroids, were reported to inhibit in vitro lipid peroxidation in CNS tissue. In order to evaluate the possible scavenging and/or Iron chelating activities in vivo of the 21-aminosteroid U74500A (pregna-1,4,9(11)-triene-3,20-dione, 21-(4-(5,6-bisdiethylamino)-2-pyridinyl)-1-piperazinyl)-16-methyl-, HCl (16α)), the drug was administered for seven days to rats. These rats had been induced by Iron-Saccharate complex injection a slow process of lipid peroxidation into their right brain hemicortex. The drug was injected also to intact rats (normal rats). Seven days after the operation the extent of Iron-induced lipid peroxidation in both the hemicortices and the effect of the drug, were assessed by the evaluation of lipid-soluble fluorescence and of conjugated diene formation. The assessment was performed both in vehicle (control) and in U74500A-treated rats. In the Iron-injected rat groups the drug induced a significant dose-related reduction of fluorescence values. Formation of conjugated dienes showed a significant decrease when U74500A (48 mg/kg every 48 hr) was administered to cortico-cerebrally Iron-injected animals. The lipid peroxidation of cortices in normal rats was evaluated as thiobarbituric acid reactant substances in both the drug-treated and the control animals. In normal rats, U74500A (48 mg/kg every 48 hr) caused a significant decrease of TEARS values, as compared to those observed in the control group. The Iron content in the Iron-injected hemicortices, which was evaluated by the ferrozine method, was not modified by drug treatment. U74500A appears to have in vivo antioxidant properties and not to affect the Iron content in the neural tissue. An interaction of this drug with the metal, however, cannot be excluded.

  • D-penicillamine affects lipid peroxidation and Iron content in the rat brain cortex
    Neurochemical Research, 1992
    Co-Authors: Mario Ciuffi, G. Gentilini, Sergio Franchi-micheli, Lucilla Zilletti
    Abstract:

    d-Penicillamine, a trifunctional aminoacid known for its ability to form metal complexes and for being a radical scavenger, has been investigated “in vitro” and “in vivo” in the rat brain cortex. At 50 μM the drug facilitate lipid hydroperoxides and TBARS formation in brain cortex homogenates, while at higher concentrations a clear inhibition of the lipid peroxidative process was observed. The activity of thed-penicillamine (25 and 50 mg/Kg i.p) was evaluated “in vivo” after a 7-day treatment in rats in whose brain cortex a slow process of lipid peroxidation was induced by Iron-Saccharate injection. Lipid hydroperoxides, lipid soluble fluorescent compounds and the Iron content of both Iron-injected and contralateral hemicortices showed a significant decrease in comparison to rats untreated withd-penicillamine. The higher dose also induced in normal rats a significant decrease in basal TBARS and Iron content of the brain cortex. In the Iron-injected cortex the observed Fe2+/Fe3+ ratio was significantly different from that of normal rats. On the contrary ratios obtained formd-penicillamine treated animals were higher in comparison to both normal and Iron-injected animals. These results suggest thatd-penicillamine, acting as a reducing agent, inhibits the Iron redox system and, as a chelating agents, can remove metal from action sites where lipid peroxidation may occur.

  • Lipid peroxidation induced “in vivo” by Iron-carbohydrate complex in the rat brain cortex
    Neurochemical Research, 1991
    Co-Authors: Mario Ciuffi, G. Gentilini, Sergio Franchi-micheli, Lucilla Zilletti
    Abstract:

    In view of the emerging role of metals and particularly Iron in the pathogenesis of several ischemic or degenerative CNS diseases, via a lipid peroxidative process, a model of slow Iron-induced peroxidative damage in the rat brain cortex has been carried out. Iron-carbohydrate complexes were injected in the right brain cortex, and biochemical assays were performed on ipsilateral and contralateral samples two hours or seven days after injection. Iron-sacchararate caused a significant increase in the ipsilateral cortex in TBARS, conjugated dienes and fluorescent substances seven days after injection, whereas no biochemical alteration was observed two hours after treatment. In order to prevent or to limit lipid peroxidation, some drugs known for chelating and/or scavening activity were administered to Iron-injected rats. DL-α-tocopherol, methylprednisolone, D-penicillamine significantly decreased the value of fluorescent products formed by Iron-Saccharate, whereas desferrioxamine was not effective.

Saj Naqvi - One of the best experts on this subject based on the ideXlab platform.

  • experience of Iron Saccharate supplementation in haemodialysis patients treated with erythropoietin
    Nephrology, 1998
    Co-Authors: R. Hussain, Sh Chishti, Saj Naqvi
    Abstract:

    SUMMARY: We assessed the efficacy of intravenous (i.v.) Iron Saccharate (VENOFER) vs oral Iron supplementation in haemodialysis patients treated with low-dose erythropoietin (EPO). Twenty haemodialysis patients with serum ferritin >200 ng/mL and transferrin saturation >30% were assigned to one of the two groups. In Group 1, 10 were given i.v. Iron Saccharate (100 mg i.v. twice weekly) post dialysis. In Group 2, oral ferrous sulphate 200 mg was given thrice daily. In both groups, subcutaneous EPO 25 units/kg body weight (BW) was started simultaneously, twice weekly. After 3 months (study completion) the mean haemoglobin and haematocrit was significantly increased in Group 1 than in Group 2 (Hb 11.60 ± 0.64 G/ dL vs 10.5 G/dL ± 1.14 P<0.01). the final mean EPO dose was 25% lower in Group 1 than in Group 2 (3400 ± 1356 U/week vs 4600 ± 1356 U/week P=0.10) and the mean serum ferritin was higher in the i.v. Iron group than the oral group (671 ng/mL ± 388 vs 367 ng/mL ± 238 P=NS). the same was also observed with transferrin saturation (44.6%± 19.8 in Group 1 vs. 29%± 11.0 in Group 2 P=NS). No adverse effects were seen during the study. In conclusion, we observed that regular use of i.v. Iron had a significantly enhanced haemoglobin response, better maintained serum ferritin and lower EPO dosage requirement than the oral Iron group.

  • Experience of Iron Saccharate supplementation in haemodialysis patients treated with erythropoietin
    Nephrology, 1998
    Co-Authors: R. Hussain, Sh Chishti, Saj Naqvi
    Abstract:

    SUMMARY: We assessed the efficacy of intravenous (i.v.) Iron Saccharate (VENOFER) vs oral Iron supplementation in haemodialysis patients treated with low-dose erythropoietin (EPO). Twenty haemodialysis patients with serum ferritin >200 ng/mL and transferrin saturation >30% were assigned to one of the two groups. In Group 1, 10 were given i.v. Iron Saccharate (100 mg i.v. twice weekly) post dialysis. In Group 2, oral ferrous sulphate 200 mg was given thrice daily. In both groups, subcutaneous EPO 25 units/kg body weight (BW) was started simultaneously, twice weekly. After 3 months (study completion) the mean haemoglobin and haematocrit was significantly increased in Group 1 than in Group 2 (Hb 11.60 ± 0.64 G/ dL vs 10.5 G/dL ± 1.14 P