42,918 research outputs found
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
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
Magnetic resonance evaluation of hepatic and myocardial iron deposition in transfusion-independent thalassemia intermedia compared to regularly transfused thalassemia major patients
No full textExtremely diverse phenotypes exist within the homozygous and compound heterozygote states for β-thalassemia. The terms thalassemia major (TM) and intermedia (TI) lack specific molecular correlates, but encompass a wide spectrum of clinical and laboratory abnormalities [1]. At the severe end of the spectrum are patients whose clinical course is characterized by profound anemia, who present to medical attention in the first year of life, and who subsequently require regular transfusions for survival, the condition known as TM. But many patients with inheritance of two mutant beta alleles have a milder illness, with a broad range of severity including, at least in early childhood, a virtually asymptomatic state. Patients in this group who present to medical attention in later childhood and remain largely transfusion free are said to have TI [1]. The pathophysiology, clinical consequences, and treatment of iron overload in regularly transfused patients with TM have been extensively studied; however, in transfusion-independent patients with TI data remain limited. Recent advances in the assessment of organ-specific iron deposition using magnetic resonance imaging (MRI) are promising and could potentially aid understanding the pathophysiology of iron in patients with TI
Optimal management of ß thalassaemia intermedia
No full textOur understanding of the molecular and pathophysiological mechanisms underlying the disease process in patients with β thalassaemia intermedia (TI) has substantially increased over the past decade. The hallmark of disease process in patients with TI includes ineffective erythropoiesis, chronic haemolytic anaemia, and iron overload. There are a number of options currently available for managing patients with TI including splenectomy, transfusion therapy, iron chelation therapy, modulation of fetal haemoglobin production, and several other agents targeting specific clinical complications. Limited studies assessed the efficacy and safety of these modalities; hence, there are currently no clear guidelines for managing patients with TI. Until solid evidence-based guidelines are available, individualised treatment should be entertained
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
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
Measurement of the ratio of branching fractions B(B0→K∗0γ )/B(B0s→φγ ) and the directCP asymmetry inB 0→K∗0γ
No full textThe ratio of branching fractions of the radiative B decays B0→K⁎0γ and B0s→ϕγ has been measured using an integrated luminosity of 1.0 fb−1 of pp collision data collected by the LHCb experiment at a centre-of-mass energy of s√=7TeV. The value obtained is
B(B0→K⁎0γ)B(B0s→ϕγ)=1.23±0.06(stat.)±0.04(syst.)±0.10(fs/fd),
where the first uncertainty is statistical, the second is the experimental systematic uncertainty and the third is associated with the ratio of fragmentation fractions fs/fd. Using the world average value for B(B0→K⁎0γ), the branching fraction B(B0s→ϕγ) is measured to be (3.5±0.4)×10−5.
The direct CP asymmetry in B0→K⁎0γ decays has also been measured with the same data and found to be
ACP(B0→K⁎0γ)=(0.8±1.7(stat.)±0.9(syst.))%.
Both measurements are the most precise to date and are in agreement with the previous experimental results and theoretical expectations
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 therap
Splenectomy and thrombosis : the case of thalassemia intermedia
No full textBackground: Hypercoagulability in splenectomized patients with thalassemia intermedia (TI) has been extensively evaluated. However, clinical and laboratory characteristics of patients who eventually develop overt thromboembolic events (TEE) are poorly studied. Patients/Methods: Three Groups of TI patients (n = 73 each) were retrospectively identified from a registry involving six centers across the Middle East and Italy: Group I, all splenectomized patients with a documented TEE; Group II, age- and sex-matched splenectomized patients without TEE; and Group III, age- and sex-matched nonsplenectomized patients without TEE. Retrieved data included demographics, laboratory parameters, clinical complications, and received treatments that may influence TEE development, and reflected the period prior to TEE occurrence in Group I. Results: The mean age of Group I patients at development of TEE was 33.1 ± 11.7 years, with a male to female ratio of 33:40. TEE were predominantly venous (95%) while four patients (5%) had documented stroke. Among studied parameters, Group I patients weremore likely to have a nucleated red blood cell (NRBC) count ≥ 300 × 106 L-1, a platelet count ≥ 500 × 109 L-1 and evidence of pulmonary hypertension (PHT), or be transfusion nai{dotless}̈ve. The median time to thrombosis following splenectomy was 8 years. Patients with an NRBC count ≥ 300 × 106 L-1, a platelet count ≥ 500 × 109 L-1, or who were transfusion naive also had a shorter time to thrombosis following splenectomy. Conclusion: Splenectomized TI patients who will develop TEE may be identified early on by high NRBC and platelet counts, evidence of PHT, and transfusion naivety
Potential mechanisms for renal damage in beta-thalassemia
No full textImprovement of survival in patients with β-thalassemia has allowed several clinical morbidities to manifest, including renal complications. Patients may experience proximal tubular dysfunctions and abnormalities in glomerular filtration rate. Several risk factors have been proposed. Hypoxia may lead to renal damage with resulting proximal tubular epithelial cell dysfunction and interstitial fibrosis, while anemia induces renal hemodynamic changes. Iron overload secondary to regular transfusion therapy can also result in an increase in oxidative stress and direct cytotoxicity to the kidney. Moreover, the use of certain iron-chelating agents is associated with a transient, nonprogressive increase in serum creatinine levels. However, most available evidence comes from small, cross-sectional studies. 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