beta-thalassemia/hypoxia

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Significance of blood coagulation and platelet profiles in relation to pulmonary thrombosis in beta-thalassemia/Hb E.

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In beta-Thalassemia hemoglobin E (beta-thal Hb E), hypoxemia with abnormal lung function was described and postmortem examination in these patients showed organized pulmonary trombi with thickened arterial wall, particularly in post-splenectomized cases. Coagulation and platelet profiles were

Thyroid Function in Chronically Transfused Children with Beta Thalassemia Major: A Cross-Sectional Hospital Based Study.

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UNASSIGNED Thalassemia is the most common genetic disorder worldwide. Use of iron chelators has improved survival but endocrine complications have become more frequent. The frequency of hypothyroidism in Beta Thalassemia Major (BTM) children ranges from 6 to 30 %. Thyroid dysfunction mainly occurs

Methemoglobinemia and ascorbate deficiency in hemoglobin E β thalassemia: metabolic and clinical implications.

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During investigations of the phenotypic diversity of hemoglobin (Hb) E β thalassemia, a patient was encountered with persistently high levels of methemoglobin associated with a left-shift in the oxygen dissociation curve, profound ascorbate deficiency, and clinical features of scurvy; these

Hypoxia biomarkers, oxidative stress, and circulating microparticles in pediatric patients with thalassemia in Upper Egypt.

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This study aimed to investigate the oxidative stress, hypoxia biomarkers, and circulating microparticles (MPs) in β thalassemia major. The study included 56 children with thalassemia and 46 healthy controls. Hypoxia biomarkers, oxidative stress biomarkers, and total plasma fragmented DNA (fDNA) were

Pulmonary hypertension in beta-thalassemia.

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Cardiac involvement represents the leading cause of mortality in both forms of beta-thalassemia, namely, thalassemia major (TM) and thalassemia intermedia (TI), and pulmonary hypertension (PHT) is part of the cardiopulmonary complications of the disease. PHT was initially documented in a small group

Effects of teriparatide retreatment in a patient with β-thalassemia major.

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BACKGROUND Bone disease is a frequent complication of β-thalassemia major (β-ΤΜ) and its etiology is multifactorial. Marrow expansion, chronic hypoxia, endocrine complications, and iron overload caused chiefly by chronic transfusion treatment are significant factors affecting skeletal health. Bone

Iron metabolism under conditions of ineffective erythropoiesis in beta-thalassemia.

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Beta-thalassemia is inherited genetic disorder characterized by ineffective erythropoiesis (IE), leading to anemia and abnormal iron metabolism. IE is as an abnormal expansion of the number of erythroid progenitor cells with unproductive synthesis of enucleated erythrocytes, leading to anemia and

[Pulmonary hypertension in patient with beta-thalassemia major].

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We report a case of pulmonary hypertension (PH) in a 35-year old patient with beta-thalassemia major; he had commenced blood transfusions after the age of 4 years and had been splenectomised at the age of 6 years. PH clinical presentation was not uncommon. Hemodynamic study revealed precapillary PH

Potential mechanisms for renal damage in beta-thalassemia.

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Improvement 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

Extramedullary hematopoiesis-related pleural effusion: the case of beta-thalassemia.

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BACKGROUND Thalassemia intermedia has a later clinical onset and a milder anemia than thalassemia major, characterized by high output state, left ventricle remodeling, and age-related pulmonary hypertension. Bone deformities, extramedullary hematopoiesis (EMH), and spleen and liver enlargement are

Detection of hemoglobin alterations in a sample population in northwest Mexico. Preliminary report.

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Blood samples from 1,000 individuals seen at the Instituto Mexicano del Seguro Social in northwestern Mexico were assayed by multiple systems (acid, alkaline and neutral electrophoresis, heat, freeze and isopropanol stability and erythrocytic morphology under hypoxia) to detect hemoglobin (Hb)

Development of severe anemia during fever episodes in patients with hemoglobin E trait and hemoglobin H disease combinations.

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Globin chain imbalance and tissue hypoxia are important determinants of the clinical severity of thalassemias. Phenotypic expression may be further modified by interactions between alpha- and beta-thalassemia defects. We retrospectively and prospectively studied the clinical and hematologic features

Gene therapy on demand: site specific regulation of gene therapy.

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Since 1990 when the first clinical gene therapy trial was conducted, much attention and considerable promise have been given to this form of treatment. Gene therapy has been used with success in patients suffering from severe combined immunodeficiency syndromes (X-SCID and ADA-deficiency), Leber's

Deferoxamine produces nitric oxide under ferricyanide oxidation, blood incubation, and UV-irradiation

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Deferoxamine (DFO), an iron chelator, is used therapeutically for the removal of excess iron in multiple clinical conditions such as beta thalassemia and intracerebral hemorrhage. DFO is also used as an iron chelator and hypoxia-mimetic agent in in vivo and in vitro basic research. Here we

Hematopoietic cell transplantation for thalassemia and sickle cell disease: past, present and future.

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beta-Thalassemia major and sickle cell disease (SCD) are among the most common hereditary disorders worldwide. The supportive treatment of beta-thalassemia major requires chronic, life-long RBC transfusions, which cause progressive iron overload and the potential for impaired endocrine, cardiac and

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