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Hemoglobinopathies and Thalassemias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
The hemoglobin phenotype by alkaline electrophoresis (CAE) is identical to that of SCA (Fig. 5). By CAGE the hemoglobin D comigrates with Hb A (Fig. 5). Therefore, Hb D trait has the phenotype of A/A and sickle cell hemoglobin D appears like sickle cell trait. Every ostensibly S/S blood by CAE should have one CAGE to ascertain those that have Hb S/D. By HPLC the Hb D usually elutes differently from Hb S. Sickle cell Hb D Los Angeles is accompanied by somewhat lower hemoglobin concentrations than SCA, with values that can be as low as 6 g/dL.
Oxysterol concentrations are associated with cholesterol concentrations and anemia in pediatric patients with sickle cell disease
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2019
Ahmet Yalcinkaya, Afshin Samadi, Incilay Lay, Selma Unal, Suna Sabuncuoglu, Yesim Oztas
Sickle cell disease (SCD) identifies a group of hemoglobinopathies in which a single nucleotide mutation in the beta globin gene results in the production of hemoglobin S, a type of hemoglobin that forms polymers in hypoxic conditions which distort the characteristic shape of the erythrocyte [1]. These sickle-shaped erythrocytes are prone to hemolysis which manifests as severe anemia, especially in patients who have inherited two defective beta-globin genes from their parents – a homozygote condition (HbSS) conveniently named as sickle cell anemia (SCA) [2]. Patients who have inherited one copy of the defective gene may also have other beta-globin variants which cause compound hemoglobinopathies such as ß-thalassemia (HbSß), hemoglobin C (HbSC), hemoglobin D disease (HbSD), among others [3]. The most common types of SCD in Turkey are the HbSS and HbSß+ genotypes.
Current perspectives of sickle cell disease in Nigeria: changing the narratives
Published in Expert Review of Hematology, 2019
Oyesola O. Ojewunmi, Titilope A. Adeyemo, Oluseyi C. Ayinde, Bamidele Iwalokun, Adekunle Adekile
Sickle cell disease (SCD) is an autosomal recessive blood disorder characterized by clinical heterogeneity that may be influenced by environmental factors, ethnicity, race, social and economic factors as well as genetic and epigenetic factors [1]. A number of genotypes produced SCD characterized by the presence of one βs gene and one of the following genes: another βs (homozygous disease known as sickle cell anemia), a hemoglobin C gene, a gene for β+ or β°-thalassemia or a hemoglobin D or hemoglobin E gene. Sickle cell anemia (SCA) is the most common genetic variant of SCD, accounting for 70% of cases worldwide [2]. In the last two decades, an improved understanding of the pathophysiology of SCD has resulted in the development of evidence-based treatment algorithm of SCD for improved quality of life and prevention of SCD complications such as stroke and acute chest syndrome coupled with significant reduction in the need for transfusion and hospitalisation and intensive care of SCD patients in the developed countries [3]. However, gaps in the management of SCD still exist in low-medium income countries such as Nigeria due to poor pooling of evidence to inform better treatment algorithms and provision of infrastructures and human resources to address the huge burden of SCD in the country. The present review was carried out to provide a comprehensive nationally represented data on the current burden, pathophysiology and treatment of SCD in Nigeria with the aim of creating a better treatment, crisis prevention measures for SCD patients and set an agenda for SCD research in the country.
Is the use of ACE inb/ARBs associated with higher in-hospital mortality in Covid-19 pneumonia patients?
Published in Clinical and Experimental Hypertension, 2020
Murat Selçuk, Tufan Çınar, Muhammed Keskin, Vedat Çiçek, Şahhan Kılıç, Behruz Kenan, Selami Doğan, Süha Asal, Nuran Günay, Ersin Yıldırım, Ümran Keskin, Ahmet Lütfullah Orhan
The blood samples, including creatinine, hemoglobin, D-dimer, C-reactive protein (CRP), fibrinogen, etc., were measured in all patients following admission to hospital. A Beckman Coulter LH 780 hematology analyzer (Beckman Coulter, FL, USA) was used for the complete blood count analysis of the samples and Beckman Coulter LH 780 device (Beckman Coulter Ireland Inc., Mervue, Galway, Ireland) was used to analyze the standard biochemical parameters.