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Article ; Online: Recent advances in the molecular understanding of non-transfusion-dependent thalassemia.

Galanello, Renzo

2012 Volume 26 Suppl 1, Page(s) S7–S11

Abstract: Thalassemias are a group of inherited autosomal recessive hematologic disorders that occur because of defects in the alpha (α)- and beta (β)-globin genes of adult hemoglobin (Hb). An imbalance in the synthesis of one or more of the globin chains can ... ...

Abstract	Thalassemias are a group of inherited autosomal recessive hematologic disorders that occur because of defects in the alpha (α)- and beta (β)-globin genes of adult hemoglobin (Hb). An imbalance in the synthesis of one or more of the globin chains can result in a wide spectrum of phenotypes depending on the type and amount of globin synthesized and additional genetic modifiers. In patients with thalassemia intermedia, a condition known as non-transfusion-dependent thalassemia (NTDT), transfusion requirements are absent or episodic. Non-transfusion-dependent thalassemia includes β-thalassemia intermedia, HbE β-thalassemia, and α-thalassemia intermedia, also known as Hb H disease. This article focuses on the molecular features and genetic mutations specific to NTDT.
MeSH term(s)	Blood Transfusion ; Humans ; Phenotype ; Thalassemia/genetics ; Thalassemia/therapy
Language	English
Publishing date	2012-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639015-8
ISSN	1532-1681 ; 0268-960X
ISSN (online)	1532-1681
ISSN	0268-960X
DOI	10.1016/S0268-960X(12)70004-8
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Article: Deferiprone in the treatment of transfusion-dependent thalassemia: a review and perspective.

Galanello, Renzo

Therapeutics and clinical risk management

2008 Volume 3, Issue 5, Page(s) 795–805

Abstract: Deferiprone is an orally active iron chelator which has emerged from an extensive search for new treatment of iron overload. Comparative studies have shown that at comparable doses deferiprone may be as effective as deferoxamine in removing body iron. ... ...

Abstract	Deferiprone is an orally active iron chelator which has emerged from an extensive search for new treatment of iron overload. Comparative studies have shown that at comparable doses deferiprone may be as effective as deferoxamine in removing body iron. Retrospective and prospective studies have shown that deferiprone monotherapy is significantly more effective than deferoxamine in improving myocardial siderosis in thalassemia major. Agranulocytosis is the most serious side effect associated with the use of deferiprone, occurring in about 1% of the patients. More common but less serious side effects are gastrointestinal symptoms, arthralgia, zinc deficiency, and fluctuating transaminases levels. Deferiprone can be used in combination with desferrioxamine. This regimen of chelation is tolerable and attractive for patients unable to comply with standard deferoxamine infusions or with inadequate response to deferiprone alone. Combination therapy has been effectively used in the management of severe cardiac siderosis.
Language	English
Publishing date	2008-05-08
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2186560-7
ISSN	1178-203X ; 1176-6336
ISSN (online)	1178-203X
ISSN	1176-6336
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Article: Evaluation of ICL670, a once-daily oral iron chelator in a phase III clinical trial of beta-thalassemia patients with transfusional iron overload.

Galanello, Renzo

Annals of the New York Academy of Sciences

2005 Volume 1054, Page(s) 183–185

Abstract: Osteoporosis and osteopenia are frequent complications of thalassemia major (TM) and intermedia (TI). Osteoporosis was found in 23/25 patients with TI and in 115/239 patients with TM. In TM, no association was found with specific polymorphisms in ... ...

Abstract	Osteoporosis and osteopenia are frequent complications of thalassemia major (TM) and intermedia (TI). Osteoporosis was found in 23/25 patients with TI and in 115/239 patients with TM. In TM, no association was found with specific polymorphisms in candidate genes (vitamin D receptor, estrogen receptor, calcitonin receptor, and collagen type 1 alpha 1). Osteoporosis in TM female was strongly associated with primary amenorrhea (P < .0001), while in male patients with TM hypogonadism was not significantly related to BMD (P = .0001). Low BMD was also associated with cardiomiopathy (P = .01), diabetes mellitus (P = .0001), chronic hepatitis (P = .0029), and increased ALT (P = .01).
MeSH term(s)	Administration, Oral ; Adult ; Benzoates/administration & dosage ; Benzoates/adverse effects ; Benzoates/therapeutic use ; Chelation Therapy ; Child ; Dose-Response Relationship, Drug ; Hemosiderosis/drug therapy ; Hemosiderosis/etiology ; Humans ; Iron/analysis ; Iron Chelating Agents/administration & dosage ; Iron Chelating Agents/adverse effects ; Iron Chelating Agents/therapeutic use ; Iron Overload/drug therapy ; Iron Overload/etiology ; Liver/chemistry ; Transfusion Reaction ; Treatment Outcome ; Triazoles/administration & dosage ; Triazoles/adverse effects ; Triazoles/therapeutic use ; beta-Thalassemia/complications ; beta-Thalassemia/drug therapy ; beta-Thalassemia/therapy
Chemical Substances	Benzoates ; Iron Chelating Agents ; Triazoles ; Iron (E1UOL152H7) ; deferasirox (V8G4MOF2V9)
Language	English
Publishing date	2005
Publishing country	United States
Document type	Clinical Trial, Phase III ; Comparative Study ; Journal Article ; Multicenter Study ; Randomized Controlled Trial
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1196/annals.1345.021
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Article: A thalassemic child becomes adult.

Galanello, Renzo

Reviews in clinical and experimental hematology

2003 Volume 7, Issue 1, Page(s) 4–21

Abstract: In the last decades, treatment of patients with beta-thalassemia has changed considerably, with advances in red cell transfusion and the introduction of iron chelation therapy. This progress has greatly increased the probability for a thalassemic child ... ...

Abstract	In the last decades, treatment of patients with beta-thalassemia has changed considerably, with advances in red cell transfusion and the introduction of iron chelation therapy. This progress has greatly increased the probability for a thalassemic child to reach adult age with a good quality of life. At present, the prognosis for thalassemia major patients is "open-ended". Compliance with the conventional treatment and psychological support are critical to obtain good results. The expectancy of a long survival of good quality encourages the patients to plan their future life, having a job, a family and often children. Optimal treatment of thalassemia major is expensive and for this reason, unfortunately, available only for a minority of patients in the world. Despite the significant advances, other progresses are expected to further improve survival and quality of life. The major aim is the cure of the disease, increasing the possibility of bone marrow transplantation using HLA-matched unrelated donors, and hopefully, in the future, gene therapy. However, even the conventional treatment and in particular iron chelation is expected to improve. Efforts should be made by the Western countries, and by the international health and economic organizations to provide continuous and concrete support for achieving a high standard of management for thalassemia in all places of the world.
MeSH term(s)	Adult ; Age Distribution ; Child ; Disease Management ; Humans ; Prognosis ; Survivors ; Thalassemia/complications ; Thalassemia/mortality ; Thalassemia/therapy
Language	English
Publishing date	2003-03
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2086903-4
ISSN	1825-151X ; 1127-0020
ISSN (online)	1825-151X
ISSN	1127-0020
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Article ; Online: Renal aspects of thalassaemia a changing paradigm.

Bhandari, Sunil / Galanello, Renzo

European journal of haematology

2012 Volume 89, Issue 3, Page(s) 187–197

Abstract: Beta-thalassaemia is characterised by progressive anaemia necessitating regular blood transfusions to sustain life. With the advent of effective chelating agents that can reduce the iron burden and extend patients' survival, renal disease, as in other ... ...

Abstract	Beta-thalassaemia is characterised by progressive anaemia necessitating regular blood transfusions to sustain life. With the advent of effective chelating agents that can reduce the iron burden and extend patients' survival, renal disease, as in other ageing populations, has become more prevalent. In recent years, chronic kidney disease (CKD) has become overwhelming; indeed, approximately 8% or 6 million people of the UK population has evidence of CKD. Several factors, which occur in patients with thalassaemia, account for the relative explosion of renal disease in the general population including increasing age, diabetes, hypertension and the advent of novel measures of renal function facilitating early detection of kidney disease. In addition, some patients with thalassaemia develop renal tubular dysfunction related to the disease itself, the effects of iron overload and the effects of chelator therapy, while other patients have an increased creatinine clearance leading to hyperfiltration. More recently, there is a noticeable increasing prevalence of impaired renal function and proteinuria because of several putative factors including chelators. We review current data on the potential mechanisms leading to renal abnormalities seen in patients with thalassaemia, the potential effects of iron loading within the kidney and the potential renal effects of chelator therapy. This article gives a speculative account of possible mechanisms and theories to consider providing pause for thought and direct future research in this area.
MeSH term(s)	Chelating Agents/therapeutic use ; Humans ; Kidney Failure, Chronic/complications ; Kidney Failure, Chronic/drug therapy ; Kidney Failure, Chronic/physiopathology ; United Kingdom ; beta-Thalassemia/complications
Chemical Substances	Chelating Agents
Language	English
Publishing date	2012-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	392482-8
ISSN	1600-0609 ; 0902-4441
ISSN (online)	1600-0609
ISSN	0902-4441
DOI	10.1111/j.1600-0609.2012.01819.x
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Article ; Online: Gene test review. Alpha-thalassemia.

Galanello, Renzo / Cao, Antonio

Genetics in medicine : official journal of the American College of Medical Genetics

2011 Volume 13, Issue 2, Page(s) 83–88

MeSH term(s)	Drug Substitution ; Female ; Gene Deletion ; Genetic Association Studies ; Genetic Counseling ; Genetic Testing ; Hemoglobins, Abnormal/genetics ; Heterozygote ; Humans ; Male ; alpha-Globins/genetics ; alpha-Thalassemia/diagnosis ; alpha-Thalassemia/genetics
Chemical Substances	Hemoglobins, Abnormal ; alpha-Globins ; hemoglobin Agrinio ; hemoglobin Heraklion ; hemoglobin Quong Sze (137085-32-6) ; hemoglobin Bart's (9056-09-1)
Language	English
Publishing date	2011-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1455352-1
ISSN	1530-0366 ; 1098-3600
ISSN (online)	1530-0366
ISSN	1098-3600
DOI	10.1097/GIM.0b013e3181fcb468
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Article: Pathophysiology of beta thalassaemia.

Origa, Raffaella / Galanello, Renzo

Pediatric endocrinology reviews : PER

2011 Volume 8 Suppl 2, Page(s) 263–270

Abstract: In beta thalassemia, unbalanced alpha globin chain synthesis results in severely rheologically compromised erythrocytes with premature destruction in the peripheral circulation and ineffective erythropoiesis within the bone marrow and in extramedullary ... ...

Abstract	In beta thalassemia, unbalanced alpha globin chain synthesis results in severely rheologically compromised erythrocytes with premature destruction in the peripheral circulation and ineffective erythropoiesis within the bone marrow and in extramedullary sites. In nontransfused beta thalassemia patients, erythropoiesis,anemia and hypoxia down-regulate hepcidin, the master regulator of iron homeostasis. Hepcidin deficiency in turn allows excessive duodenal iron absorption and development of systemic iron overload. In regularly transfused patients iron overload is mostly due to red cell breakdown. When the iron binding capacity of transferrin is saturated, iron can appear in the serum in a free form, called Non-Transferrin-Bound Iron, a powerful catalyst for the formation of free radicals, capable of causing oxidative stress and damage to mitochondria, lysosomes, lipid membranes, proteins, and DNA. Apart from the iron overload-related complications, other pathological conditions such as bone disease, gallstones and thromboembolic events occur in a relevant proportion of subjects with thalassemia.
MeSH term(s)	Anemia/physiopathology ; Bone Diseases/physiopathology ; Cardiovascular Diseases/physiopathology ; Child ; Gallstones/physiopathology ; Humans ; Iron Overload/physiopathology ; beta-Thalassemia/physiopathology
Language	English
Publishing date	2011-03
Publishing country	Israel
Document type	Journal Article ; Review
ZDB-ID	2434390-0
ISSN	1565-4753
ISSN	1565-4753
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Article ; Online: Beta-thalassemia.

Galanello, Renzo / Origa, Raffaella

Orphanet journal of rare diseases

2010 Volume 5, Page(s) 11

Abstract: Beta-thalassemias are a group of hereditary blood disorders characterized by anomalies in the synthesis of the beta chains of hemoglobin resulting in variable phenotypes ranging from severe anemia to clinically asymptomatic individuals. The total annual ... ...

Abstract	Beta-thalassemias are a group of hereditary blood disorders characterized by anomalies in the synthesis of the beta chains of hemoglobin resulting in variable phenotypes ranging from severe anemia to clinically asymptomatic individuals. The total annual incidence of symptomatic individuals is estimated at 1 in 100,000 throughout the world and 1 in 10,000 people in the European Union. Three main forms have been described: thalassemia major, thalassemia intermedia and thalassemia minor. Individuals with thalassemia major usually present within the first two years of life with severe anemia, requiring regular red blood cell (RBC) transfusions. Findings in untreated or poorly transfused individuals with thalassemia major, as seen in some developing countries, are growth retardation, pallor, jaundice, poor musculature, hepatosplenomegaly, leg ulcers, development of masses from extramedullary hematopoiesis, and skeletal changes that result from expansion of the bone marrow. Regular transfusion therapy leads to iron overload-related complications including endocrine complication (growth retardation, failure of sexual maturation, diabetes mellitus, and insufficiency of the parathyroid, thyroid, pituitary, and less commonly, adrenal glands), dilated myocardiopathy, liver fibrosis and cirrhosis). Patients with thalassemia intermedia present later in life with moderate anemia and do not require regular transfusions. Main clinical features in these patients are hypertrophy of erythroid marrow with medullary and extramedullary hematopoiesis and its complications (osteoporosis, masses of erythropoietic tissue that primarily affect the spleen, liver, lymph nodes, chest and spine, and bone deformities and typical facial changes), gallstones, painful leg ulcers and increased predisposition to thrombosis. Thalassemia minor is clinically asymptomatic but some subjects may have moderate anemia. Beta-thalassemias are caused by point mutations or, more rarely, deletions in the beta globin gene on chromosome 11, leading to reduced (beta+) or absent (beta0) synthesis of the beta chains of hemoglobin (Hb). Transmission is autosomal recessive; however, dominant mutations have also been reported. Diagnosis of thalassemia is based on hematologic and molecular genetic testing. Differential diagnosis is usually straightforward but may include genetic sideroblastic anemias, congenital dyserythropoietic anemias, and other conditions with high levels of HbF (such as juvenile myelomonocytic leukemia and aplastic anemia). Genetic counseling is recommended and prenatal diagnosis may be offered. Treatment of thalassemia major includes regular RBC transfusions, iron chelation and management of secondary complications of iron overload. In some circumstances, spleen removal may be required. Bone marrow transplantation remains the only definitive cure currently available. Individuals with thalassemia intermedia may require splenectomy, folic acid supplementation, treatment of extramedullary erythropoietic masses and leg ulcers, prevention and therapy of thromboembolic events. Prognosis for individuals with beta-thalassemia has improved substantially in the last 20 years following recent medical advances in transfusion, iron chelation and bone marrow transplantation therapy. However, cardiac disease remains the main cause of death in patients with iron overload.
MeSH term(s)	Genetic Counseling ; Humans ; Prenatal Diagnosis ; beta-Thalassemia/diagnosis ; beta-Thalassemia/epidemiology ; beta-Thalassemia/genetics ; beta-Thalassemia/therapy
Language	English
Publishing date	2010-05-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1750-1172
ISSN (online)	1750-1172
DOI	10.1186/1750-1172-5-11
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Article ; Online: Beta-thalassemia.

Cao, Antonio / Galanello, Renzo

Genetics in medicine : official journal of the American College of Medical Genetics

2009 Volume 12, Issue 2, Page(s) 61–76

Abstract: Beta-thalassemia is caused by the reduced (beta) or absent (beta) synthesis of the beta globin chains of the hemoglobin tetramer. Three clinical and hematological conditions of increasing severity are recognized, i.e., the beta-thalassemia carrier state, ...

Abstract	Beta-thalassemia is caused by the reduced (beta) or absent (beta) synthesis of the beta globin chains of the hemoglobin tetramer. Three clinical and hematological conditions of increasing severity are recognized, i.e., the beta-thalassemia carrier state, thalassemia intermedia, and thalassemia major. The beta-thalassemia carrier state, which results from heterozygosity for beta-thalassemia, is clinically asymptomatic and is defined by specific hematological features. Thalassemia major is a severe transfusion-dependent anemia. Thalassemia intermedia comprehend a clinically and genotypically very heterogeneous group of thalassemia-like disorders, ranging in severity from the asymptomatic carrier state to the severe transfusion-dependent type. The clinical severity of beta-thalassemia is related to the extent of imbalance between the alpha and nonalpha globin chains. The beta globin (HBB) gene maps in the short arm of chromosome 11, in a region containing also the delta globin gene, the embryonic epsilon gene, the fetal A-gamma and G-gamma genes, and a pseudogene (psiB1). Beta-thalassemias are heterogeneous at the molecular level. More than 200 disease-causing mutations have been so far identified. The majority of mutations are single nucleotide substitutions, deletions, or insertions of oligonucleotides leading to frameshift. Rarely, beta-thalassemia results from gross gene deletion. In addition to the variation of the phenotype resulting from allelic heterogeneity at the beta globin locus, the phenotype of beta-thalassemia could also be modified by the action of genetic factors mapping outside the globin gene cluster and not influencing the fetal hemoglobin. Among these factors, the ones best delineated so far are those affecting bilirubin, iron, and bone metabolisms. Because of the high carrier rate for HBB mutations in certain populations and the availability of genetic counseling and prenatal diagnosis, population screening is ongoing in several at-risk populations in the Mediterranean. Population screening associated with genetic counseling was extremely useful by allowing couples at risk to make informed decision on their reproductive choices. Clinical management of thalassemia major consists in regular long-life red blood cell transfusions and iron chelation therapy to remove iron introduced in excess with transfusions. At present, the only definitive cure is bone marrow transplantation. Therapies under investigation are the induction of fetal hemoglobin with pharmacologic compounds and stem cell gene therapy.
MeSH term(s)	Bone Marrow Transplantation ; Female ; Genetic Carrier Screening ; Genetic Testing ; Globins/genetics ; Humans ; Multigene Family ; Pregnancy ; Prenatal Diagnosis ; beta-Thalassemia/diagnosis ; beta-Thalassemia/genetics ; beta-Thalassemia/therapy
Chemical Substances	Globins (9004-22-2)
Language	English
Publishing date	2009-08-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1455352-1
ISSN	1530-0366 ; 1098-3600
ISSN (online)	1530-0366
ISSN	1098-3600
DOI	10.1097/GIM.0b013e3181cd68ed
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Article ; Online: Beta-thalassemia: from genotype to phenotype.

Danjou, Fabrice / Anni, Franco / Galanello, Renzo

Haematologica

2011 Volume 96, Issue 11, Page(s) 1573–1575

MeSH term(s)	Carrier Proteins/genetics ; Female ; Humans ; Male ; Mutation ; Nuclear Proteins/genetics ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins c-myb/genetics ; Registries ; Repressor Proteins ; beta-Thalassemia/classification ; beta-Thalassemia/genetics
Chemical Substances	BCL11A protein, human ; Carrier Proteins ; Nuclear Proteins ; Proto-Oncogene Proteins c-myb ; Repressor Proteins
Language	English
Publishing date	2011-11-04
Publishing country	Italy
Document type	Editorial ; Comment
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2011.055962
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