Journal articles: 'Iron overload'

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Marfil-Rivera, L. J. "Iron overload." Medicina Universitaria 17, no. 69 (October 2015): 240–42. http://dx.doi.org/10.1016/j.rmu.2015.08.001.

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Hulihan, Mary M., Cindy A. Sayers, Scott D. Grosse, Cheryl Garrison, and Althea M. Grant. "Iron Overload." American Journal of Preventive Medicine 41, no. 6 (December 2011): S422—S427. http://dx.doi.org/10.1016/j.amepre.2011.09.020.

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Siah, Chiang W., Debbie Trinder, and John K. Olynyk. "Iron overload." Clinica Chimica Acta 358, no. 1-2 (August 2005): 24–36. http://dx.doi.org/10.1016/j.cccn.2005.02.022.

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Zhabyeyev, Pavel, Subhash K. Das, Ratnadeep Basu, Mengcheng Shen, Vaibhav B. Patel, Zamaneh Kassiri, and Gavin Y. Oudit. "TIMP3 deficiency exacerbates iron overload-mediated cardiomyopathy and liver disease." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 5 (May 1, 2018): H978—H990. http://dx.doi.org/10.1152/ajpheart.00597.2017.

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Chronic iron overload results in heart and liver diseases and is a common cause of morbidity and mortality in patients with genetic hemochromatosis and secondary iron overload. We investigated the role of tissue inhibitor of metalloproteinase 3 (TIMP3) in iron overload-mediated tissue injury by subjecting male mice lacking Timp3 ( Timp3−/−) and wild-type (WT) mice to 12 wk of chronic iron overload. Whereas WT mice with iron overload developed diastolic dysfunction, iron-overloaded Timp3−/− mice showed worsened cardiac dysfunction coupled with systolic dysfunction. In the heart, loss of Timp3 was associated with increased myocardial fibrosis, greater Timp1, matrix metalloproteinase ( Mmp) 2, and Mmp9 expression, increased active MMP-2 levels, and gelatinase activity. Iron overload in Timp3−/− mice showed twofold higher iron accumulation in the liver compared with WT mice because of constituently lower levels of ferroportin. Loss of Timp3 enhanced the hepatic inflammatory response to iron overload, leading to greater neutrophil and macrophage infiltration and increased hepatic fibrosis. Expression of inflammation-related MMPs (MMP-12 and MMP-13) and inflammatory cytokines (IL-1β and monocyte chemoattractant protein-1) was elevated to a greater extent in iron-overloaded Timp3−/− livers. Gelatin zymography demonstrated equivalent increases in MMP-2 and MMP-9 levels in WT and Timp3−/− iron-overloaded livers. Loss of Timp3 enhanced the susceptibility to iron overload-mediated heart and liver injury, suggesting that Timp3 is a key protective molecule against iron-mediated pathology. NEW & NOTEWORTHY In mice, loss of tissue inhibitor of metalloproteinase 3 ( Timp3) was associated with systolic and diastolic dysfunctions, twofold higher hepatic iron accumulation (attributable to constituently lower levels of ferroportin), and increased hepatic inflammation. Loss of Timp3 enhanced the susceptibility to iron overload-mediated injury, suggesting that Timp3 plays a key protective role against iron-mediated pathology.

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Jacobs, Allan, and A. V. Hoffbrand. "Iron deficiency and iron overload." Critical Reviews in Oncology/Hematology 3, no. 2 (January 1985): 143–86. http://dx.doi.org/10.1016/s1040-8428(85)80023-8.

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Díez-López, Carles, Josep Comín-Colet, and José González-Costello. "Iron overload cardiomyopathy." Current Opinion in Cardiology 33, no. 3 (May 2018): 334–40. http://dx.doi.org/10.1097/hco.0000000000000511.

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Camaschella, Clara. "Treating Iron Overload." New England Journal of Medicine 368, no. 24 (June 13, 2013): 2325–27. http://dx.doi.org/10.1056/nejmcibr1304338.

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Lombard, M., A. Bomford, and R. Williams. "Genetic Iron Overload." Journal of the Royal Society of Medicine 82, no. 12 (December 1989): 701–3. http://dx.doi.org/10.1177/014107688908201202.

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Kushner, James P., John P. Porter, and Nancy F. Olivieri. "Secondary Iron Overload." Hematology 2001, no. 1 (January 1, 2001): 47–61. http://dx.doi.org/10.1182/asheducation-2001.1.47.

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Abstract Transfusion therapy for inherited anemias and acquired refractory anemias both improves the quality of life and prolongs survival. A consequence of chronic transfusion therapy is secondary iron overload, which adversely affects the function of the heart, the liver and other organs. This session will review the use of iron chelating agents in the management of transfusion-induced secondary iron overload. In Section I Dr. John Porter describes techniques for the administration of deferoxamine that exploit the pharmacokinetic properties of the drug and minimize potential toxic side effects. The experience with chelation therapy in patients with thalassemia and sickle cell disease will be reviewed and guidelines will be suggested for chelation therapy of chronically transfused adults with refractory anemias. In Section II Dr. Nancy Olivieri examines the clinical consequences of transfusion-induced secondary iron overload and suggests criteria useful in determining the optimal timing of the initiation of chelation therapy. Finally, Dr. Olivieri discusses the clinical trials evaluating orally administered iron chelators.

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Kasvosve, I., It Gangaidzo, Zar Gomo, and Vr Gordeuk. "African Iron Overload." Acta Clinica Belgica 55, no. 2 (January 2000): 88–93. http://dx.doi.org/10.1080/17843286.2000.11754276.

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Holding, Cathy. "Iron overload lifted." Genome Biology 4 (2003): spotlight—20031201–01. http://dx.doi.org/10.1186/gb-spotlight-20031201-01.

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Gordeuk, Victor R. "African iron overload." Seminars in Hematology 39, no. 4 (October 2002): 263–69. http://dx.doi.org/10.1053/shem.2002.35636.

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Ault, Patricia, and Karen Jones. "Understanding Iron Overload." Clinical Journal of Oncology Nursing 13, no. 5 (January 1, 2009): 511–17. http://dx.doi.org/10.1188/09.cjon.511-517.

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HALLIDAY, J. W. "Inherited Iron Overload." Acta Paediatrica 78 (October 1989): 86–95. http://dx.doi.org/10.1111/apa.1989.78.s361.86.

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Turlin, Bruno, and Yves Deugnier. "Iron overload disorders." Clinics in Liver Disease 6, no. 2 (May 2002): 481–96. http://dx.doi.org/10.1016/s1089-3261(02)00004-1.

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Bacon, Bruce R. "IRON OVERLOAD STATES." Clinics in Liver Disease 2, no. 1 (February 1998): 63–75. http://dx.doi.org/10.1016/s1089-3261(05)70364-0.

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Gujja, Pradeep, Douglas R. Rosing, Dorothy J. Tripodi, and Yukitaka Shizukuda. "Iron Overload Cardiomyopathy." Journal of the American College of Cardiology 56, no. 13 (September 2010): 1001–12. http://dx.doi.org/10.1016/j.jacc.2010.03.083.

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Izzy, Manhal, and Patrick S. Kamath. "Severe Iron Overload." Clinical Gastroenterology and Hepatology 17, no. 13 (December 2019): A28. http://dx.doi.org/10.1016/j.cgh.2018.08.032.

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Marcus, Robert E., and E. R. Huehns. "Transfusional iron overload." Clinical & Laboratory Haematology 7, no. 3 (September 1985): 195–212. http://dx.doi.org/10.1111/j.1365-2257.1985.tb00026.x.

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Munoz, Javier, Natalia Ferrari, and Philip Kuriakose. "Iron-overload myopathy." International Journal of Hematology 94, no. 6 (November 3, 2011): 503–4. http://dx.doi.org/10.1007/s12185-011-0961-1.

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Tsay, Jaime, Zheiwei Yang, F. Patrick Ross, Susanna Cunningham-Rundles, Hong Lin, Rhima Coleman, Philipp Mayer-Kuckuk, et al. "Bone loss caused by iron overload in a murine model: importance of oxidative stress." Blood 116, no. 14 (October 7, 2010): 2582–89. http://dx.doi.org/10.1182/blood-2009-12-260083.

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AbstractOsteoporosis is a frequent problem in disorders characterized by iron overload, such as the thalassemias and hereditary hemochromatosis. The exact role of iron in the development of osteoporosis in these disorders is not established. To define the effect of iron excess in bone, we generated an iron-overloaded mouse by injecting iron dextran at 2 doses into C57/BL6 mice for 2 months. Compared with the placebo group, iron-overloaded mice exhibited dose-dependent increased tissue iron content, changes in bone composition, and trabecular and cortical thinning of bone accompanied by increased bone resorption. Iron-overloaded mice had increased reactive oxygen species and elevated serum tumor necrosis factor-α and interleukin-6 concentrations that correlated with severity of iron overload. Treatment of iron-overloaded mice with the antioxidant N-acetyl-L-cysteine prevented the development of trabecular but not cortical bone abnormalities. This is the first study to demonstrate that iron overload in mice results in increased bone resorption and oxidative stress, leading to changes in bone microarchitecture and material properties and thus bone loss.

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Mangaonkar, Abhishek, Niren Patel, Hongyan Xu, Kavita Natrajan, Betsy Clair, Leigh G. Wells, Latanya Bowman, Nadine Barret, and Abdullah Kutlar. "Plasma Biomarkers of Iron Regulation, Overload, and Inflammation in Sickle Cell Disease." Blood 124, no. 21 (December 6, 2014): 1380. http://dx.doi.org/10.1182/blood.v124.21.1380.1380.

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Abstract Transfusional iron overload has been increasingly recognized among patients with sickle cell disease (SCD) over the past two decades. We recently reported on the prevalence of iron overload among 635 adult SCD patients followed at our center and found that 80 patients (12%) had developed iron overload as a result of repeated blood transfusions. Fifty six (70%) of these subjects developed iron overload as a result of episodic, mostly unnecessary transfusions at outlying hospitals. There have been reports of association of increased morbidity and mortality among iron overloaded SCD patients; it has also been hypothesized that SCD patients tend to develop fewer complications of iron overload, compared to transfusion dependent beta thalassemia, primarily due to the chronic inflammatory state with resultant upregulation of hepcidin, and lower extra-hepatic iron loading. We studied biomarkers of iron metabolism, iron regulation, and inflammatory markers in 22 patients with SCD (SS) and iron overload (two consecutive ferritin levels of >1000 ng/ml and significant transfusion history) and compared these with 14 SCD patients without iron overload (ferritin <1000 ng/ml, and no significant transfusion history). Serum Fe, ferritin, %transferrin saturation (Tf) and total iron binding capacity, as well as high sensitivity C reactive protein (hsCRP) were performed by routine laboratory methods. Plasma concentrations of soluble transferrin receptor (sTfR), interleukin-6 (IL-6), Growth Differentiation Factor-15 (GDF-15) were measured using commercially available ELISA kits (R&D Systems, Minneapolis, USA). Plasma hepcidin was measured using a commercially available kit from DRG Diagnostics (Marburg, Germany). The results are summarized below: Abstract 1380. TableAgeyearsFerritin ng/ml% sathsCRPmg/dLHepcidinng/mlsTfRnmol/LGDF-15pg/mlIL-6pg/mlCases (n=22)33.42083.560.40.8829.872.21201.55.2Controls (n=14)29.0401.840.40.9512.477.11115.34.1p-value0.236.14E-050.020.80.0020.20.550.24 As expected, ferritin and % Tf saturation were significantly higher in the iron overloaded group. Hepcidin levels were also significantly higher in cases vs. controls, indicative of appropriate upregulation of hepcidin in Fe overload. sTfR and GDF-15 levels, as well as the inflammatory markers (hsCRP and IL-6) did not differ significantly between Fe overloaded and non-iron overloaded SCD patients. The two groups did not differ significantly in terms of the measures of disease severity (number of pain crises/year and number of hospitalizations/year). We further looked at the ratio of hepcidin/ferritin, sTfR/log ferritin, GDF-15/hepcidin, and tested the correlation between GDF-15 and hepcidin levels and ferritin and hepcidin levels; the ratio of hepcidin to ferritin was not different between cases and controls (0.019 and 0.021, respectively, p=0.73). sTfR to log ferritin ratio was significantly lower in cases compared to controls (22.3 vs 33.24, p=0.0004). GDF-15/hepcidin ratio was also found to be significantly lower in cases (262.1 vs 1896.7, p=0.01). Additionally, GDF-15 and hepcidin levels correlated significantly in controls but not iron overloaded SCD patients (p=0.04 vs p=0.7). Similarly, hepcidin and ferritin levels were significantly correlated in controls (p=0.03) but not in cases (p=0.8). Our results suggest that i) hepcidin levels are appropriately upregulated in iron overloaded SCD patients, ii) inflammatory markers (hsCRP and IL-6) were not significantly different between iron overloaded and non-iron overloaded patients, suggesting that systemic inflammation is not the driving factor behind hepcidin upregulation in iron overloaded SCD patients; however, a local/paracrine effect of IL-6 on hepatocytes secondary to Fe related inflammation in the liver cannot be excluded; and iii) GDF-15 and sTfR levels are not different between cases and controls, indicating that erythropoiesis does not differ between Fe overloaded and non-iron overloaded SCD patients. The observation that the correlation between GDF-15 and hepcidin levels is lost in iron overloaded SCD patients suggests that erythropoiesis does not contribute to hepcidin regulation in these subjects. This can further be clarified by studying the role of the newly described erythroid regulator of hepcidin, erythroferrone in SCD with and without iron overload. Disclosures No relevant conflicts of interest to declare.

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Kohgo, Yutaka. "2. Iron Metabolism and Iron Overload." Nihon Naika Gakkai Zasshi 100, no. 9 (2011): 2412–24. http://dx.doi.org/10.2169/naika.100.2412.

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Kohgo, Yutaka. "2. Iron Metabolism and Iron Overload." Nihon Naika Gakkai Zasshi 100, Suppl (2011): 46a—50a. http://dx.doi.org/10.2169/naika.100.46a.

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25

Andrews, Nancy C. "IRONMETABOLISM: Iron Deficiency and Iron Overload." Annual Review of Genomics and Human Genetics 1, no. 1 (September 2000): 75–98. http://dx.doi.org/10.1146/annurev.genom.1.1.75.

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26

Pietrangelo, Antonello. "Iron chelation beyond transfusion iron overload." American Journal of Hematology 82, S12 (December 2007): 1142–46. http://dx.doi.org/10.1002/ajh.21101.

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Beutler, Ernest, A. Victor Hoffbrand, and James D. Cook. "Iron Deficiency and Overload." Hematology 2003, no. 1 (January 1, 2003): 40–61. http://dx.doi.org/10.1182/asheducation-2003.1.40.

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Abstract In the past seven years numerous genes that influence iron homeostasis have been discovered. Dr. Beutler provides a brief overview of these genes, genes that encode HFE, DMT-1, ferroportin, transferrin receptor 2, hephaestin, and hepcidin to lay the groundwork for a discussion of the various clinical forms of iron storage disease and how they differ from one another. In Section I, Dr. Beutler also discusses the types of hemochromatosis that exist as acquired and as hereditary forms. Acquired hemochromatosis occurs in patients with marrow failure, particularly when there is active ineffective erythropoiesis. Hereditary hemochromatosis is most commonly due to mutations in the HLA-linked HFE gene, and hemochromatosis clinically indistinguishable from HFE hemochromatosis is the consequence of mutations in three transferrin receptor-2 gene. A more severe, juvenile form of iron storage disease results from mutations of the gene encoding hepcidin or of a not-yet-identified gene on chromosome 1q. Autosomal dominant iron storage disease is a consequence of ferroportin mutations, and a polymorphism in the ferroportin gene appears to be involved in the African iron overload syndrome. Evidence regarding the biochemical and clinical penetrance of hemochromatosis due to mutations of the HFE gene is rapidly accumulating. These studies, emanating from several centers in Europe and the United States, all agree that the penetrance of hemochromatosis is much lower than had previously been thought. Probably only 1% of homozygotes develop clinical findings. The implications of these new findings for the management of hemochromatosis will be discussed. In Section II, Dr. Victor Hoffbrand discusses the management of iron storage disease by chelation therapy, treatment that is usually reserved for patients with secondary hemochromatosis such as occurs in the thalassemias and in patients with transfusion requirements due to myelodysplasia and other marrow failure states. Tissue iron can be estimated by determining serum ferritin levels, measuring liver iron, and by measuring cardiac iron using the MRI-T2* technique. The standard form of chelation therapy is the slow intravenous or subcutaneous infusion of desferoxamine. An orally active bidentate iron chelator, deferiprone, is now licensed in 25 countries for treatment of patients with thalassemia major. Possibly because of the ability of this compound to cross membranes, it appears to have superior cardioprotective properties. Agranulocytosis is the most serious complication of deferiprone therapy and occurs in about 1% of treated patients. Deferiprone and desferoxamine can be given together or on alternating schedules. A new orally active chelating agent ICL 670 seems promising in early clinical studies. In Section III, Dr. James Cook discusses the most common disorder of iron homeostasis, iron deficiency. He will compare some of the standard methods for identifying iron deficiency, the hemoglobin level, transferrin saturation, and mean corpuscular hemoglobin and compare these with some of the newer methods that have been introduced, specifically the percentage of hypochromic erythrocytes and reticulocyte hemoglobin content. The measurement of storage iron is achieved by measuring serum ferritin levels. The soluble transferrin receptor is a truncated form of the cellular transferrin receptor and the possible value of this measurement in the diagnosis of iron deficiency will be discussed. Until recently iron dextran was the only parental iron preparation available in the US. Sodium ferric gluconate, which has been used extensively in Europe for many years, is now available in the United States. It seems to have a distinct advantage over iron dextran in that anaphylactic reactions are much less common with the latter preparation.

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El-Sheikh, Arwa A., Shimaa Hamed Ameen, and Samaa Salah AbdEl-Fatah. "Ameliorating Iron Overload in Intestinal Tissue of Adult Male Rats: Quercetin vs Deferoxamine." Journal of Toxicology 2018 (November 21, 2018): 1–13. http://dx.doi.org/10.1155/2018/8023840.

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Objective. The aim of our study is to compare the role of the new natural alternative (Quercetin) with the current iron-chelation therapy (Deferoxamine (DFO)) in the effect of iron overload on small intestinal tissues and to investigate the possible underlying molecular mechanisms of such toxicity. Methods. Forty-two adult male albino rats were divided into six groups: control groups, DFO, Quercetin, iron overload, iron overload+DFO, and iron overload+Quercetin groups. Animals received daily intraperitoneal injection of Deferoxamine (125 mg /kg), Quercetin (10 mg/kg), and ferric dextran (200 mg/kg) for 2 weeks. Results. Iron overloaded group showed significant increase in serum iron, total iron binding capacity (TIBC), transferrin saturation percentage (TS %) hepcidin (HEPC), serum ferritin, nontransferrin bound iron (NTBI), and small intestinal tissues iron levels. Iron overload significantly increased the serum oxidative stress indicator (MDA) and reduced serum total antioxidant capacity (TAC). On the other hand, iron overload increased IL6 and reduced IL10 in small intestinal tissues reflecting inflammatory condition and increased caspase 3 reactivity indicating apoptosis and increased iNOs expressing cell indicting oxidative stress especially in ileum. In addition, it induced small intestinal tissues pathological alterations. The treatment with Quercetin showed nonsignificant differences as compared to treatment with DFO that chelated the serum and tissue iron and improved the oxidative stress and reduced tissue IL6 and increased IL10 and decreased caspase 3 and iNOs expressing cells in small intestinal tissues. Moreover, it ameliorated the iron overload induced pathological alterations. Conclusion. Our study showed the potential role of Quercetin as iron chelator like DFO in case of iron overload induced small intestinal toxicity in adult rats because of its serum and tissue iron chelation, improvement of serum, and small intestinal oxidative stress, ameliorating iron induced intestinal inflammation, apoptosis, and histopathological alterations.

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AL-Rousan, Rabaa, Anjaiah Katta, Satyanarayana Paturi, Brent Kidd, Kamran Manzoor, Ernest Walker, and Eric Blough. "Chronic Deferasirox Administration Decreases Hepatic Oxidative Stress and Apoptosis in the Iron Overloaded Gerbil." Blood 114, no. 22 (November 20, 2009): 1996. http://dx.doi.org/10.1182/blood.v114.22.1996.1996.

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Abstract Abstract 1996 Poster Board I-1018 Background: Iron overload occurs under conditions such as primary (hereditary) hemochromatosis and secondary iron overload (hemosiderosis) and is associated with an increased risk of developing liver fibrosis, cirrhosis, and hepatocellular carcinoma. Deferasirox is a novel oral chelator with high iron-binding potency and selectivity. Here we investigate the ability of deferasirox to remove excessive hepatic iron and prevent or reverse iron induced hepatic injury. Methods: Adult male Mongolian Gerbils were randomly divided into three groups: control, iron overload, and iron overload + deferasirox treatment (n = 8 / group). Iron overload animals received iron dextran 100mg/kg i.p /5d for 10 wks while deferasirox was given 100mg/kg/d p.o for 1-,3-, or 9- months. Hepatic iron levels were determined by inductively coupled plasma atomic emission spectrometry and Prussian blue staining was performed to examine iron deposition in the corresponding tissues. Immunoblot and immunohistochemical analyses for markers of oxidative stress were employed to assess effects of deferasirox treatment on hepatic protein oxidation and superoxide levels. TUNEL assay was employed to examine the extent of hepatic apoptosis. Results: Compared to the non-treated iron overload group, deferasirox treatment reduced hepatic iron levels by 21.3%, 43.5%, and 47.4% after 1, 3, and 9 months of treatment, respectively (p<0.05). Prussian blue staining and histological analysis detected frequent iron deposition, evidence of hepatic damage, and lipid accumulation in hepatic tissue of the iron overloaded group. Iron deposition was significantly diminished with deferasirox treatment and no evidence of lipid accumulation was observed. Immunoblotting demonstrated that iron overload caused 2- fold increase in hepatic ferritin expression (p< 0.05) which was reduced by 47.5% following three months of deferasirox treatment (p< 0.05). In addition, deferasirox significantly reduced hepatic protein oxidation and superoxide abundance. The percentage of TUNEL-positive nuclei in the deferasirox treated livers was 41.0% lower than that of iron overloaded group (p<0.05). Conclusions: These findings suggest that chronic deferasirox treatment may decrease iron-induced hepatic oxidative stress and apoptosis. Decrease in ROS accumulation in the liver may be the possible mechanism of this protective effect. Further studies are underway to delineate specific mechanisms. Disclosures: No relevant conflicts of interest to declare.

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Naeem, Uzma, Rabia Azhar, Wajiha Shadab, Nazir Awan, Maryam Naeem, and Jawairia Iftikhar. "Comparative Effects of Nigella Sativa and Cassia Senna in Iron Overloaded Mice." Pakistan Journal of Medical and Health Sciences 16, no. 4 (April 29, 2022): 1222–24. http://dx.doi.org/10.53350/pjmhs221641222.

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Background: Iron overload-related complications are the main concern in patients who must often receive blood transfusions. The only way to treat iron overload in these patients is by chelating agents. Owing to the high cost and adverse effects of chelating agents use of naturally present chelators is under study. Aim: To compare the protective effects of two commonly used herbs Nigella Sativa and Cassia Senna in iron-overloaded mice. Study Design: Experimental randomized controlled trial. Setting: Zoology department of Govt College University Lahore during six months period. Method: A total of forty-eight mice were divided into four groups (n = 12). Group one was normal to control while group 2, 3, and 4 were overloaded with iron by intravenous injection of iron dextran (0.1 ml/kg body weight) daily for fifteen days. After 15 days iron overload was confirmed by blood testing. For additional 15 days, group three mice were provided with Cassia Senna (100 mg/Kg body weight) while group four mice were permitted to feed on Nigella sativa (200 mg/Kg body weight). Animals were sacrificed on day 32 and organs were preserved to check the iron levels. Blood sampling was done on days 0, 15, and 31 to analyze serum iron levels. Results: The protective effect of Nigella Sativa was more marked than cassia senna in iron 0verloaded mice. Conclusion: The addition of Nigella Sativa instead of cassia senna in iron-laden patients as an adjunct therapy can be more beneficial in preventing the damaging effects of iron overload. Keywords: iron overload, Nigella Sativa, Cassia Senna

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Boga, Salih, Huseyin Alkim, Canan Alkim, Ali Riza Koksal, Mehmet Bayram, Muveddet Banu Yilmaz Ozguven, and Sebnem Tekin Neijmann. "The Relationship of Serum Hemojuvelin and Hepcidin Levels with Iron Overload in Nonalcoholic Fatty Liver Disease." Journal of Gastrointestinal and Liver Diseases 24, no. 3 (September 1, 2015): 293–300. http://dx.doi.org/10.15403/jgld.2014.1121.243.hak.

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Background & Aims: Mild iron overload is frequently reported in patients with nonalcoholic fatty liver disease (NAFLD). Hepcidin is the master iron-regulatory peptide and hemojuvelin (HJV) is the key regulator of iron-dependent secretion of hepcidin. The aims of this study were to evaluate serum HJV and hepcidin levels in patients with biopsy-proven NAFLD with and without hepatic iron overload, and to identify potential associations of HJV and hepcidin with the clinical characteristics of the patients enrolled. Methods: Serum levels of HJV and hepcidin were measured in 66 NAFLD patients with (n=12) and without (n=54) iron overload, and controls (n=35) by enzyme-linked immunosorbent assay. Hemojuvelin and hepcidin levels were assessed in relation to clinical characteristics and liver histologic evaluation of the participants. Results: Significantly lower serum HJV (281.1 [239.2-353.6] vs. 584.8 [440.3-661] ng/ml, p<0.001) and similar serum hepcidin levels (60.5±31.1 vs. 55.8±11.9 ng/ml, p=0.285) were found in NAFLD patients when compared to controls. İron-overloaded NAFLD patients had significantly lower HJV (249.9 [187.6-296.3] vs. 292.9 [243-435] ng/ml, p=0.032) and significantly higher hepcidin (78.4±35.5 vs. 56.5±28.9ng/ml, p=0.027) levels than NAFLD patients without iron overload. Fibrosis stage was significantly higher in iron overloaded NAFLD group (p<0.001). Ferritin levels correlated significantly both with HOMA-IR (r=0.368, p=0.002) and fibrosis stage (r=0.571, p<0.001). Conclusions: Our findings suggest that HJV levels are low in NAFLD and even lower in iron overloaded NAFLD, while hepcidin levels are higher in NAFLD with iron overload. The gradually decreased HJV and increased hepcidin concentrations in our patients most likely reflect the physiological response to iron accumulation in the liver.

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Carradice, Duncan, Peter Shuttleworth, Jeffrey Szer, Andrew Roberts, and Andrew Grigg. "Tissue Iron Overload Is Common Post Transplantation (Allo BMT) and Is Associated with Red Cell Transfusion Load and HFE Genotype." Blood 104, no. 11 (November 16, 2004): 2262. http://dx.doi.org/10.1182/blood.v104.11.2262.2262.

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Abstract In order to analyse the incidence of iron overload after allo BMT and assess the role of venesection in preventing complications, we retrospectively analysed 168 consecutive patients undergoing allo BMT at our institution from 1998–2003 surviving at least one year. Iron studies were performed routinely pre-BMT, at D100, one & two years post BMT. Iron overload was defined by at least one of the following criteria i)liver biopsy (n=24), one of : a) dry weight iron concentration >80μmol/g; b) iron index >1.9; c) Perl’s stain grade 3 or 4, ii) CT liver iron >1.0mg/ml (n=13) iii) raised ferritin >1000 μg/L and transferrin saturation >55% on 2 occasions, persisting >6/12 post BMT (n=11), iv) venesection >5g iron (n=1). Using these criteria, iron overload occurred in 49/168 (29%) pts. 12/119 in the non-overloaded group had further investigation but did not meet the criteria; liver biopsy (n=10) or CT (n=2). Elevated ferritin, particularly early post-transplant, did not reliably predict for iron overload, with 55/91 evaluable patients having values >1000μg/L at D100 not fulfilling the criteria for iron overload. There was no difference between overloaded and non-overloaded patients with respect to age or sex. Acute (15/49 vs. 26/113) or chronic liver GVHD (25/46 vs. 47/105) was not different between the two groups (both p>0.05). Only 3 patients were hepatitis B sAg+ or hepatitis C Ab+. The iron overloaded group was more likely to i) have been transplanted for acute leukaemia (29/49 vs. 33/119; p 0.0002) ii) be C282Y heterozygotes (11/46 vs. 10/110, p 0.02) (iii) been transfused more units of red cells (mean 42 vs. 19; p<0.0001) and iv) have persistently abnormal liver function post-transplant, ALT (IU/ml; normal <55) at 1 year 77 vs. 52 and at 2 years 67 vs. 37 (all p<0.05). There was no effect of hetero- or homozygosity for H63D. 63 patients were analysed for the S65C, V59M and Q283P mutations. One patient was heterozygous for the S65C mutation (non-overloaded group). A mean of 12.3 units were venesected in 22 patients (range 2–46), all of whom had received >25 units of red cells. ALT fell significantly (mean pre venesection 189 IU/ml, post 36, p<0.05), as did transferrin saturation (mean pre venesection 68%, post 29%, p<0.05). We conclude that tissue iron overload is common after BMT, that biochemical measures of iron stores (ferritin and transferrin saturation) may be unreliable in this context, particularly in the early post BMT period and that radiological or histological assessment to distinguish hyperferritinaemia due to inflammation from true tissue iron overload may be required. Patients at risk of iron overload (transfusions >25 units, C282Y heterozygotes) should be closely monitored and early venesection therapy instituted to minimise organ damage.

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33

Porto, Graça. "Iron overload and immunity." World Journal of Gastroenterology 13, no. 35 (2007): 4707. http://dx.doi.org/10.3748/wjg.v13.i35.4707.

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Piperno, Alberto, Sara Pelucchi, and Raffaella Mariani. "Inherited iron overload disorders." Translational Gastroenterology and Hepatology 5 (April 2020): 25. http://dx.doi.org/10.21037/tgh.2019.11.15.

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35

Sawada, Kenichi. "Iron Deficiency and Overload." Nihon Naika Gakkai Zasshi 99, no. 6 (2010): 1171–72. http://dx.doi.org/10.2169/naika.99.1171.

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36

Fondu, P., and B. Cantinieaux. "Infections And Iron Overload." Acta Clinica Belgica 41, no. 1 (January 1986): 1–9. http://dx.doi.org/10.1080/22953337.1986.11719117.

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Ombiga, John, Leon A. Adams, Kevin Tang, Debbie Trinder, and John K. Olynyk. "Screening forHFEand Iron Overload." Seminars in Liver Disease 25, no. 04 (2005): 402–10. http://dx.doi.org/10.1055/s-2005-923312.

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38

Jensen, Peter-D. "Evaluation of iron overload." British Journal of Haematology 124, no. 6 (February 2, 2004): 697–711. http://dx.doi.org/10.1111/j.1365-2141.2004.04838.x.

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39

Sevtsuk, O., and V. Gordeuk. "Iron overload in Estonia." European Journal of Haematology 53, no. 2 (April 24, 2009): 121–22. http://dx.doi.org/10.1111/j.1600-0609.1994.tb01876.x.

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40

Andrews, Nancy C. "Inherited iron overload disorders." Current Opinion in Pediatrics 12, no. 6 (December 2000): 596–602. http://dx.doi.org/10.1097/00008480-200012000-00015.

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ADAMS, P. C. "Iron overload in Montpelier." Gut 48, no. 6 (June 1, 2001): 755–56. http://dx.doi.org/10.1136/gut.48.6.755.

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Hershko, Chaim, Gabriela Link, Abraham Konijn, and Z. Ioav Cabantchik. "Iron overload and chelation." Hematology 10, sup1 (September 2005): 171–73. http://dx.doi.org/10.1080/10245330512331390294.

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Pietrangelo, Antonello, Angela Caleffi, and Elena Corradini. "Non-HFEHepatic Iron Overload." Seminars in Liver Disease 31, no. 03 (August 2011): 302–18. http://dx.doi.org/10.1055/s-0031-1286061.

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Niederau, Claus. "Iron Overload and Atherosclerosis." Hepatology 32, no. 3 (September 2000): 672–74. http://dx.doi.org/10.1053/jhep.2000.17921.

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Richter, Goetz W. "Studies of Iron Overload." Pathology - Research and Practice 181, no. 2 (May 1986): 159–67. http://dx.doi.org/10.1016/s0344-0338(86)80005-x.

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Hoffbrand, A. "Diagnosing myocardial iron overload." European Heart Journal 22, no. 23 (December 1, 2001): 2140–41. http://dx.doi.org/10.1053/euhj.2001.2951.

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Corradini, Elena, Elena Buzzetti, and Antonello Pietrangelo. "Genetic iron overload disorders." Molecular Aspects of Medicine 75 (October 2020): 100896. http://dx.doi.org/10.1016/j.mam.2020.100896.

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Pippard, Martin J. "Detection of iron overload." Lancet 349, no. 9045 (January 1997): 73–74. http://dx.doi.org/10.1016/s0140-6736(05)60880-x.

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Hollán, Susan R. "Transfusion-associated iron overload." Current Opinion in Hematology 4, no. 6 (1997): 436–41. http://dx.doi.org/10.1097/00062752-199704060-00014.

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Gordeuk, Victor, Joshua Mukiibi, Sandra J. Hasstedt, Wade Samowitz, Corwin Q. Edwards, George West, Solomon Ndambire, et al. "Iron Overload in Africa." New England Journal of Medicine 326, no. 2 (January 9, 1992): 95–100. http://dx.doi.org/10.1056/nejm199201093260204.

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Journal articles on the topic 'Iron overload'

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