196,435 research outputs found
Iron overload in β-thalassemia intermedia: An emerging concern
No full textPurpose of Review: The aim is to overview recent evidence on consequences, assessment, and management of iron overload in transfusion-independent patients with β-thalassemia intermedia. Recent Findings: Despite their transfusion-independence, β-thalassemia intermedia patients can still accumulate iron due to increased intestinal absorption. Recent observational studies show that iron burden in this group of patients can ultimately reach considerably high thresholds, and leads to a variety of serious morbidities involving the liver, endocrine glands, and arguably the vascular system. The diagnosis of iron overload in this patient population can follow established guidelines from β-thalassemia major patients, although with careful interpretation of spot serum ferritin levels. Data from a recent randomized clinical trial demonstrated the efficacy and safety of iron chelation therapy in decreasing liver iron concentration in this group of patients, which may ultimately help in reducing morbidity risk. Summary: Iron overload in transfusion-independent patients with β-thalassemia intermedia deserves careful attention, and prompt diagnosis and management are recommended. © 2013 Wolters Kluwer Health | Lippincott Williams and Wilkins.Casanovas G, 2013, HAEMATOLOGICA, V98, P444, DOI 10.3324-haematol.2012.069807; Gardenghi S, 2010, J CLIN INVEST, V120, P4466, DOI 10.1172-JCI41717; Ginzburg Y, 2011, BLOOD, V118, P4321, DOI 10.1182-blood-2011-03-283614; Karimi M, 2011, EUR J INTERN MED, V22, P607, DOI 10.1016-j.ejim.2011.05.013; Li HH, 2010, NAT MED, V16, P177, DOI 10.1038-nm.2073; Maakaron JE, 2013, ANN HEPATOL, V12, P142; Musallam KM, 2012, ANN HEMATOL, V91, P235, DOI 10.1007-s00277-011-1291-3; Musallam KM, 2011, HEMOGLOBIN, V35, P503, DOI 10.3109-03630269.2011.605499; Musallam KM, 2012, BLOOD CELL MOL DIS, V49, P136, DOI 10.1016-j.bcmd.2012.06.001; Musallam KM, 2011, HAEMATOL-HEMATOL J, V96, P1605, DOI 10.3324-haematol.2011.047852; Musallam KM, 2012, CSH PERSPECT MED, V2, DOI 10.1101-cshperspect.a013482; Musallam KM, 2012, BLOOD, V120; Musallam KM, 2012, BLOOD, V120; Musallam KM, 2012, BLOOD REV, V26, pS16, DOI 10.1016-S0268-960X(12)70006-1; Musallam KM, 2011, EUR J HAEMATOL, V87, P539, DOI 10.1111-j.1600-0609.2011.01706.x; Musallam KM, 2012, THROMB RES, V130, P695, DOI 10.1016-j.thromres.2012.07.013; Nai A, 2012, BLOOD, V119, P5021, DOI 10.1182-blood-2012-01-401885; Origa R, 2007, HAEMATOL-HEMATOL J, V92, P583, DOI 10.3324-haematol.10842; Pakbaz Z, 2007, PEDIATR BLOOD CANCER, V49, P329, DOI 10.1002-pbc.21275; Parrow NL, 2012, BLOOD, V119, P3187, DOI 10.1182-blood-2012-01-405563; Rivella S, 2012, BLOOD REV, V26, pS12, DOI 10.1016-S0268-960X(12)70005-X; Taher A, 2008, HAEMATOL-HEMATOL J, V93, P1584, DOI 10.3324-haematol.13098; Taher A, 2009, BRIT J HAEMATOL, V146, P569, DOI 10.1111-j.1365-2141.2009.07810.x; Taher A, 2012, HAEMATOLOGICA, V96, P0924; Taher A., 2012, HAEMATOLOGICA, V96; Taher AT, 2010, AM J HEMATOL, V85, P288, DOI 10.1002-ajh.21626; Taher AT, 2010, BRIT J HAEMATOL, V150, P486, DOI 10.1111-j.1365-2141.2010.08220.x; Taher AT, 2012, BLOOD, V120, P970, DOI 10.1182-blood-2012-02-412692; Taher AT, 2011, BRIT J HAEMATOL, V152, P512, DOI 10.1111-j.1365-2141.2010.08486.x; Taher AT, 2012, BLOOD, V120, P3258; Taher AT, 2010, BLOOD, V115, P1886, DOI 10.1182-blood-2009-09-243154; Wood John C, 2011, Hematology Am Soc Hematol Educ Program, V2011, P443, DOI 10.1182-asheducation-2011.1.443; Ziyadeh FN, 2012, NEPHRON CLIN PRACT, V121, pC136, DOI 10.1159-00033978789
Cerebral infarction in β-thalassemia intermedia: Breaking the silence
No full textDespite remarkable advances in understanding cerebrovascular disease attributed to sickle cell anemia, data from other hemoglobinopathies have only recently started to emerge. Several brain magnetic resonance imaging studies confirm a high prevalence of silent ischemic lesions in patients with β-thalassemia intermedia, especially in splenectomized adults who are transfusion-independent and those with elevated platelet counts. Large-vessel disease is also common in this patient population but without apparent association with silent white matter infarcts, leaving smaller arteriolar involvement as a potential explanation. The hypothesized pathophysiology is multifactorial with hypercoagulability and toxicity from free iron species playing major roles. The long-term sequelae of such covert findings is unknown, although experience from patients with sickle cell anemia confirms their association with subsequent overt stroke and neurocognitive deficits. The roles of transfusion and antiplatelet therapy to prevent the occurrence and progression of silent ischemic lesions in patients with β-thalassemia intermedia should be the focus of future trials. © 2012 Elsevier Ltd.Abboud MR, 2004, BLOOD, V103, P2822, DOI 10.1182-blood-2003-06-1972; Aessopos A, 2009, Hemoglobin, V33 Suppl 1, pS170, DOI 10.3109-03630260903351676; Aessopos A, 1997, STROKE, V28, P2421; Akhlaghpoor S, 2011, CLIN NEURORADIOL; Arkuszewski M, 2010, ADV MED SCI-POLAND, V55, P115, DOI 10.2478-v10039-010-0045-0; Armstrong FD, 2005, ANN NY ACAD SCI, V1054, P283, DOI 10.1196-annals.1345.036; Ashjazadeh N, 2012, ANEMIA, V2012; Ataga KI, 2007, BRIT J HAEMATOL, V139, P3, DOI 10.1111-j.1365-2141.2007.06740.x; Atichartakarn V, 2002, BRIT J HAEMATOL, V118, P893, DOI 10.1046-j.1365-2141.2002.03711.x; Atichartakarn V, 2003, INT J HEMATOL, V77, P299, DOI 10.1007-BF02983790; Auer JW, 2002, CIRCULATION, V106, pE7, DOI 10.1161-01.CIR.0000019984.69119.4F; Bernaudin F, 2011, BLOOD, V117, P1130, DOI 10.1182-blood-2010-06-293514; 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Iron chelation therapy for non-transfusion-dependent thalassemia (NTDT): A status quo
No full text[No abstract available]Alkrawinthawong K., 2011, HEMATOLOGY, V16, P113; Chan JCW, 2006, BRIT J HAEMATOL, V133, P198, DOI 10.1111-j.1365-2141.2006.05984.x; COSSU P, 1981, EUR J PEDIATR, V137, P267, DOI 10.1007-BF00443255; Ladis V, 2010, BRIT J HAEMATOL, V151, P504, DOI 10.1111-j.1365-2141.2010.08346.x; Musallam K., 2013, HAEMATOLOGICA, V98, P486; Musallam KM, 2013, CURR OPIN HEMATOL, V20, P187, DOI 10.1097-MOH.0b013e32835f5a5c; Musallam KM, 2013, BLOOD CELL MOL DIS, V51, P35, DOI 10.1016-j.bcmd.2013.01.015; Musallam KM, 2011, HAEMATOL-HEMATOL J, V96, P1605, DOI 10.3324-haematol.2011.047852; Musallam KM, 2012, BLOOD REV, V26, pS16, DOI 10.1016-S0268-960X(12)70006-1; Musallam KM, 2013, HAEMATOLOGICA, V98, P833, DOI 10.3324-haematol.2012.066845; OLIVIERI NF, 1992, BLOOD, V79, P2741; Pippard M J, 1988, Birth Defects Orig Artic Ser, V23, P29; Pootrakul P, 2003, BRIT J HAEMATOL, V122, P305, DOI 10.1046-j.1365-2141.2003.04412.x; Rombos Y, 2000, HAEMATOLOGICA, V85, P115; Taher A., 2013, HAEMATOLOGICA, V98, P165; Taher A., 2012, HAEMATOLOGICA, V96; Taher A, 2013, HAEMATOLOGICA, V98, P486; Taher A. T., 2013, GUIDELINES MANAGEMEN; Taher AT, 2013, ANN HEMATOL, V92, P1485, DOI 10.1007-s00277-013-1808-z; Taher AT, 2010, BRIT J HAEMATOL, V150, P486, DOI 10.1111-j.1365-2141.2010.08220.x; Taher AT, 2012, BLOOD, V120, P970, DOI 10.1182-blood-2012-02-412692; Taher AT, 2013, AM J HEMATOL, V88, P409, DOI 10.1002-ajh.23405; Taher AT, 2013, AM J HEMATOL, V88, P503, DOI 10.1002-ajh.23445; Voskaridou E, 2010, BRIT J HAEMATOL, V148, P332, DOI 10.1111-j.1365-2141.2009.07930.x11
A killer revealed: 10-year experience with beta-thalassemia intermedia
No full textObjectives: Patients with beta-thalassemia intermedia tend to present later in life with milder anemia than beta-thalassemia major patients. The incidence of mortality and its causes in this patient population remains unknown. We aim to reveal the incidence and most common causes of death in this population. Methods and results: We reviewed the charts of all of the beta-thalassemia intermedia patients who had been followed at the Chronic Care Center in Hazmieh, Lebanon during a 10-year period. A total of 18 patients out of 127 had died during the follow-up period giving a cumulative 10-year mortality incidence of 14percent. The most common causes of cardiac deaths were due to renal and cardiac causes. Discussion: Most causes of death have been linked to the high levels of iron coupled with anemia present in this patient population. Many of deaths could be prevented by adequate treatment. Conclusion: Larger studies with more comprehensive data capture on risk factors of mortality in this patient population are called for. © W. S. Maney and Son Ltd 2014.Maakaron JE, 2013, ANN HEPATOL, V12, P142; Musallam KM, 2012, BLOOD CELL MOL DIS, V49, P136, DOI 10.1016-j.bcmd.2012.06.001; Musallam KM, 2011, HAEMATOL-HEMATOL J, V96, P1605, DOI 10.3324-haematol.2011.047852; Musallam KM, 2012, CSH PERSPECT MED, V2, DOI 10.1101-cshperspect.a013482; Musallam KM, 2012, BLOOD REV, V26, pS16, DOI 10.1016-S0268-960X(12)70006-1; Musallam KM, 2012, J AM SOC NEPHROL, V23, P1299, DOI 10.1681-ASN.2011111070; Poggi M, 2011, HEMOGLOBIN, V35, P439, DOI 10.3109-03630269.2011.588355; Taher A, 2006, BLOOD CELL MOL DIS, V37, P12, DOI 10.1016-j.bcmd.2006.04.005; Taher AT, 2010, AM J HEMATOL, V85, P288, DOI 10.1002-ajh.21626; Ziyadeh FN, 2012, NEPHRON CLIN PRACT, V121, pC136, DOI 10.1159-0003397871
β-thalassemia intermedia: A clinical perspective
No full textOur understanding of the molecular and pathophysiological mechanisms underlying the disease process in patients with β-thalassemia intermedia has substantially increased over the past decade. Earlier studies observed that patients with β-thalassemia intermedia experience a clinical-complications profile that is different from that in patients with β-thalassemia major. In this article, a variety of clinical morbidities are explored, and their associations with the underlying disease pathophysiology and risk factors are examined. These involve several organs and organ systems including the vasculature, heart, liver, endocrine glands, bone, and the extramedullary hematopoietic system. 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Contemporary approaches to treatment of beta-thalassemia intermedia
No full textBeta-thalassemia intermedia (TI) is associated with a variety of serious clinical complications that require proactive and comprehensive management. These include skeletal deformities and osteopenia, compensatory extramedullary hematopoiesis and tumor formation, progressive splenomegaly, a hypercoagulable state resulting in thromboembolic events and pulmonary hypertension, and increased gastrointestinal iron absorption that often results in nontransfusional iron overload and liver damage. Although TI is generally considered a non-transfusion-dependent thalassemia, transfusion therapy may be an important part of the comprehensive management of this disease. This review describes the current state of the art for medical management of TI, with particular focus on the roles of splenectomy, transfusion, and iron chelation therapy. © 2012 Elsevier Ltd.Aessopos A, 2005, ANN NY ACAD SCI, V1054, P342, DOI 10.1196-annals.1345.041; Aessopos A, 2007, HAEMATOL-HEMATOL J, V92, P658, DOI 10.3324-haematol.10915; Aessopos A, 2001, BLOOD, V97, P3411, DOI 10.1182-blood.V97.11.3411; Amoozgar H, 2011, EUR J HAEMATOL, V87, P61, DOI 10.1111-j.1600-0609.2011.01620.x; [Anonymous], FERR SUMM PROD CHAR; [Anonymous], 2010, EXJADE PACK INS; [Anonymous], EXJADE SUMM PROD CHA; Ataga KI, 2007, BRIT J HAEMATOL, V139, P3, DOI 10.1111-j.1365-2141.2007.06740.x; Atichartakarn V, 2003, INT J HEMATOL, V78, P139, DOI 10.1007-BF02983382; Bisharat N, 2001, J INFECTION, V43, P182, DOI 10.1053-jinf.2001.0904; Borgna-Pignatti C, 2010, ANN NY ACAD SCI, V1202, P214, DOI 10.1111-j.1749-6632.2010.05550.x; Borgna-Pignatti C, 2007, BRIT J HAEMATOL, V138, P291, DOI 10.1111-j.1365-2141.2007.06654.x; Cappellini MD, 2005, SEMIN HEMATOL, V42, pS19, DOI 10.1053-j.seminhematol.2005.01.001; Cappellini MD, 2000, BRIT J HAEMATOL, V111, P467, DOI 10.1046-j.1365-2141.2000.02376.x; COSSU P, 1981, EUR J PEDIATR, V137, P267, DOI 10.1007-BF00443255; Davies JM, 2011, BRIT J HAEMATOL, V155, P308, DOI 10.1111-j.1365-2141.2011.08843.x; Eder AF, 2007, ARCH PATHOL LAB MED, V131, P708; Gardenghi S, 2010, J CLIN INVEST, V120, P4466, DOI 10.1172-JCI41717; Haidar R, 2010, EUR SPINE J, V19, P871, DOI 10.1007-s00586-010-1357-2; Karimi M, 2010, EUR J HAEMATOL, V84, P52, DOI 10.1111-j.1600-0609.2009.01356.x; Karimi M, 2011, EUR J INTERN MED, V22, P607, DOI 10.1016-j.ejim.2011.05.013; Karimi M, 2010, PEDIATR HEMAT ONCOL, V27, P205, DOI 10.3109-08880011003639952; Kontoghiorghes GJ, 2010, HEMOGLOBIN, V34, P251, DOI 10.3109-03630269.2010.486335; Ladis V, 2010, BRIT J HAEMATOL, V151, P504, DOI 10.1111-j.1365-2141.2010.08346.x; Li HH, 2010, NAT MED, V16, P177, DOI 10.1038-nm.2073; Musallam KM, 2011, EUR J HAEMATOL, V87, P73, DOI 10.1111-j.1600-0609.2011.01623.x; Musallam KM, 2011, HAEMATOL-HEMATOL J, V96, P1605, DOI 10.3324-haematol.2011.047852; Novartis Pharmaceutical Corporation, 2010, DESF PACK INS; Porter J, 2011, 16 C EUR HEM ASS JUN; Porter JB, 2001, SEMIN HEMATOL, V38, P63, DOI 10.1053-shem.2001.20145; Rigano P, 2010, BRIT J HAEMATOL, V151, P509, DOI 10.1111-j.1365-2141.2010.08397.x; Sankaran VG, 2010, NEW ENGL J MED, V363, P2258, DOI 10.1056-NEJMcibr1010767; STURGEON P, 1955, BRIT J HAEMATOL, V1, P264, DOI 10.1111-j.1365-2141.1955.tb05509.x; Taher A, 2008, HAEMATOL-HEMATOL J, V93, P1584, DOI 10.3324-haematol.13098; Taher A, 2006, THROMB HAEMOSTASIS, V96, P488, DOI 10.1160-TH06-05-0267; Taher A, 2006, BLOOD CELL MOL DIS, V37, P12, DOI 10.1016-j.bcmd.2006.04.005; Taher A, 2009, BRIT J HAEMATOL, V147, P634, DOI 10.1111-j.1365-2141.2009.07848.x; Taher A, 2002, HEMOGLOBIN, V26, P107, DOI 10.1081-HEM-120005447; Taher AT, 2008, BLOOD REV, V22, P283, DOI 10.1016-j.blre.2008.04.001; Taher AT, 2010, BRIT J HAEMATOL, V150, P486, DOI 10.1111-j.1365-2141.2010.08220.x; Taher AT, 2011, BRIT J HAEMATOL, V152, P512, DOI 10.1111-j.1365-2141.2010.08486.x; Taher AT, 2010, J THROMB HAEMOST, V8, P54, DOI 10.1111-j.1538-7836.2009.03651.x; Taher AT, 2010, BLOOD, V115, P1886, DOI 10.1182-blood-2009-09-243154; Taher ATPJ, 2011, 53 AM SOC HEM ANN M; Treadwell MJ, 2001, SEMIN HEMATOL S1, V38, P77; Voskaridou E, 2010, BRIT J HAEMATOL, V148, P332, DOI 10.1111-j.1365-2141.2009.07930.x9151
Iron chelation therapy for transfusional iron overload: A swift evolution
No full textChronic transfusional iron overload leads to significant morbidity and mortality. While deferoxamine (DFO) is an effective iron chelator with over four decades of experience, it requires tedious subcutaneous infusions that reflect negatively on patient compliance. The novel oral iron chelators deferiprone (L1) and deferasirox (DFRA) opened new horizons for the management of transfusional siderosis. A large body of evidence is now available regarding their efficacy and safety in various populations and settings. Nevertheless, experience with both drugs witnessed some drawbacks, and the search for an ideal and cost-effective iron chelator continues. © 2011 Informa Healthcare USA, Inc.Anderson LJ, 2002, LANCET, V360, P516, DOI 10.1016-S0140-6736(02)09740-4; Borgna-Pignatti C, 2004, HAEMATOLOGICA, V89, P1187; Borgna-Pignatti C, 2006, BLOOD, V107, P3733, DOI 10.1182-blood-2005-07-2933; Brittenham GM, 2011, NEW ENGL J MED, V364, P146, DOI 10.1056-NEJMct1004810; Cappellini Maria D, 2009, Hemoglobin, V33 Suppl 1, pS58, DOI 10.3109-03630260903346924; Cappellini MD, 2007, CLIN THER, V29, P909, DOI 10.1016-j.clinthera.2007.05.007; Cappellini MD, 2010, HAEMATOL-HEMATOL J, V95, P557, DOI 10.3324-haematol.2009.014696; Cappellini MD, 2011, BLOOD, V118, P884, DOI 10.1182-blood-2010-11-316646; Cappellini MD, 2009, ACTA HAEMATOL-BASEL, V122, P165, DOI 10.1159-000243801; Cappellini MD, 2008, EXPERT OPIN PHARMACO, V9, P2391, DOI [10.1517-14656566.9.13.2391 , 10.1517-14656560802335333]; Cappellini MD, 2006, BLOOD, V107, P3455, DOI 10.1182-blood-2005-08-3430; Delea TE, 2007, TRANSFUSION, V47, P1919, DOI 10.1111-j.1537-2995.2007.01416.x; Gabutti V, 1996, ACTA HAEMATOL-BASEL, V95, P26; Galanello R, 2010, ANN NY ACAD SCI, V1202, P79, DOI 10.1111-j.1749-6632.2010.05591.x; KONTOGHIORGHES GJ, 1987, LANCET, V1, P1294; Lai ME, 2010, BLOOD CELL MOL DIS, V45, P136, DOI 10.1016-j.bcmd.2010.05.005; Maggio A, 2009, BLOOD CELL MOL DIS, V42, P247, DOI 10.1016-j.bcmd.2009.01.002; Modell B, 2008, J CARDIOVASC MAGN R, V10, DOI 10.1186-1532-429X-10-42; Musallam K, 2008, PEDIATRICS, V121, pE1426, DOI 10.1542-peds.2007-1944; Musallam Khaled M, 2011, Haematologica, V96, pe5, DOI 10.3324-haematol.2010.036061; OLIVIERI NF, 1994, NEW ENGL J MED, V331, P574, DOI 10.1056-NEJM199409013310903; Pennell DJ, 2006, BLOOD, V107, P3738, DOI 10.1182-blood-2005-07-2948; Pennell DJ, 2010, BLOOD, V115, P2364, DOI 10.1182-blood-2009-04-217455; Pennell DJ, 2011, HAEMATOL-HEMATOL J, V96, P48, DOI 10.3324-haematol.2010.031468; PENNELL DJ, 2010, BLOOD, V116, P4276; Pepe A, 2011, HAEMATOL-HEMATOL J, V96, P41, DOI 10.3324-haematol.2009.019042; Piga A, 2003, HAEMATOLOGICA, V88, P489; Piga A, 2010, ANN NY ACAD SCI, V1202, P75, DOI 10.1111-j.1749-6632.2010.05586.x; Ponticelli C, 2010, BLOOD REV, V24, P239, DOI 10.1016-j.blre.2010.08.004; Porter JB, 2008, BLOOD, V112, P5423; Porter J, 2008, EUR J HAEMATOL, V80, P168, DOI 10.1111-j.1600-0609.2007.00985.x; Rienhoff HY, 2011, HAEMATOL-HEMATOL J, V96, P521, DOI 10.3324-haematol.2010.034405; Taher A, 2010, ACTA HAEMATOL-BASEL, V123, P220, DOI 10.1159-000313447; Taher A, 2009, EUR J HAEMATOL, V82, P458, DOI 10.1111-j.1600-0609.2009.01228.x; Taher A, 2009, BRIT J HAEMATOL, V147, P752, DOI 10.1111-j.1365-2141.2009.07908.x; Taher Ali T, 2009, Hemoglobin, V33 Suppl 1, pS46, DOI 10.3109-03630260903346676; Tanner MA, 2007, CIRCULATION, V115, P1876, DOI 10.1161-CIRCULATIONAHA.106.648790; Telfer PT, 2009, HAEMATOL-HEMATOL J, V94, P1777, DOI 10.3324-haematol.2009.009118; Vichinsky E, 2007, BRIT J HAEMATOL, V136, P501, DOI 10.1111-j.1365-2141.2006.06455.x; Wonke B, 1998, BRIT J HAEMATOL, V103, P361; Wood JC, 2010, BLOOD, V116, P537, DOI 10.1182-blood-2009-11-25030856
Renal complications in transfusion-dependent beta thalassaemia
No full textIncreased survival in patients with β thalassaemia major (TM) allowed for several morbidities to manifest. Renal manifestations of the disease and its treatment have been poorly evaluated. There is evidence, mainly from studies in the paediatric population, of tubular dysfunction and glomerular filtration rate abnormalities in this patient population. Long-term outcomes of these changes, however, have not been prospectively investigated. The pathogenesis of these abnormalities could be attributed to iron overload, too aggressive iron removal, and/or the underlying anaemia. These changes seem to be nonprogressive, resolve spontaneously in most part, or may require iron chelator dose modifications. Relative iron depletion may explain renal function changes attributed to chelation therapy; thus, sudden removal of iron or overchelation should be avoided. Future studies should aim to evaluate the natural history of kidney function in TM patients to help understand the mechanisms and long-term sequelae of the observed renal changes
Managing unresponsiveness or intolerance to deferasirox therapy: a tale of two doses
No full textEvaluation of: Chang HH, Lu MY, Liao YM et al. Improved efficacy and tolerability of oral deferasirox by twice-daily dosing for patients with transfusion-dependent β-thalassemia. Pediatr. Blood Cancer 56(3), 420-424 (2011). Chronic transfusional iron overload leads to significant morbidity and mortality in patients with β-thalassemia major. The once-daily oral iron chelator, deferasirox, opened new horizons for the management of transfusional siderosis. A large body of evidence is now available regarding its efficacy and safety. Nevertheless, some patients remain unresponsive or intolerant to the adverse events of the drug. Chang et al. evaluated the benefit of twice-daily dosing in this setting. The authors concluded that twice-daily deferasirox improves responsiveness and tolerability. Even though the study included only a small number of patients, it offers promising insights that should be interpreted with caution. © 2011 Expert Reviews Ltd.Angelucci E, 2000, NEW ENGL J MED, V343, P327, DOI 10.1056-NEJM200008033430503; Berdoukas V, 2010, ANN HEMATOL, V89, P1177, DOI 10.1007-s00277-010-0933-1; Cappellini MD, 2007, CLIN THER, V29, P909, DOI 10.1016-j.clinthera.2007.05.007; Cappellini MD, 2010, HAEMATOL-HEMATOL J, V95, P557, DOI 10.3324-haematol.2009.014696; Cappellini MD, 2008, EXPERT OPIN PHARMACO, V9, P2391, DOI [10.1517-14656566.9.13.2391 , 10.1517-14656560802335333]; CAPPELLINI MD, 2009, BLOOD, V114, P4063; Cappellini MD, 2006, BLOOD, V107, P3455, DOI 10.1182-blood-2005-08-3430; Chang HH, 2011, PEDIATR BLOOD CANCER, V56, P420, DOI 10.1002-pbc.22826; Chirnomas D, 2009, BLOOD, V114, P4009, DOI 10.1182-blood-2009-05-222729; Farmaki K, 2011, BLOOD CELL MOL DIS, V47, P33, DOI 10.1016-j.bcmd.2011.03.007; Galanello R, 2010, ANN NY ACAD SCI, V1202, P79, DOI 10.1111-j.1749-6632.2010.05591.x; Pennell DJ, 2011, HAEMATOL-HEMATOL J, V96, P48, DOI 10.3324-haematol.2010.031468; Ponticelli C, 2010, BLOOD REV, V24, P239, DOI 10.1016-j.blre.2010.08.004; Rienhoff HY, 2011, HAEMATOL-HEMATOL J, V96, P521, DOI 10.3324-haematol.2010.034405; Taher A, 2010, ACTA HAEMATOL-BASEL, V123, P220, DOI 10.1159-000313447; Taher A, 2009, BRIT J HAEMATOL, V147, P752, DOI 10.1111-j.1365-2141.2009.07908.x; Telfer PT, 2000, BRIT J HAEMATOL, V110, P971, DOI 10.1046-j.1365-2141.2000.02298.x; Trachtenberg F, 2011, AM J HEMATOL, V86, P433, DOI 10.1002-ajh.21993; Vichinsky E, 2008, AM J HEMATOL, V83, P398, DOI 10.1002-ajh.21119; Wood JC, 2008, BLOOD REV, V22, pS14, DOI 10.1016-S0268-960X(08)70004-30
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