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Haematological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Blood film microscopy:Polychromasia caused by the presence of young red cellsDiagnostic abnormalities of red cell shape (e.g. sickle cells, elliptocytes, spherocytes)Red cell fragments (schistocytes) indicate a microangiopathic haemolytic process
Haematology
Published in Paul Bentley, Ben Lovell, Memorizing Medicine, 2019
Bloods: Reticulocytes >5% MCV: Normocytic: Most chronic haemolytic anaemiasMicrocytic: Thalassaemia, spherocytes, secondary iron loss with chronic haemolysisMacrocytic: Acute haemolysis due to reticulocytosisFilm: Polychromasia, due to immature cellsSpecific red cell forms: Spherocytes (↓ surface area/volume); target cells (↑ s.a./vol.)Bone marrow: erythroid hyperplasia
Hemolytic Anemia Associated with Red Cell Membrane Defects
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
In the evaluation of all anemia patients, especially those with suspected hemolytic anemia, examination of the peripheral blood smear is of paramount importance. The morphologic findings in HS are quite characteristic and are therefore a vital aid in diagnosis (Fig. 2). Spherocytic erythrocytes are recognized by their decreased central pallor. Prior to splenectomy, microspherocytes may abound. Polychromasia suggests reticulocytosis. Postsplenectomy, spherocytosis persists but microspherocytes decrease and polychromasia recedes. Howell-Jolly bodies and acanthocytes are typically found postsplenectomy. In mild HS, the morphology may be subtle and easily missed, even by experienced observers.
Targeted next-generation sequencing revealed a novel homozygous mutation in the LRBA gene causes severe haemolysis associated with Inborn Errors of Immunity in an Indian family.
Published in Hematology, 2022
Prabhakar Kedar, Rashmi Dongerdiye, Shanmukhaiah Chandrakala, Umair Ahmed Bargir, Manisha Madkaikar
On examination child’s general condition was fair. She was febrile and showed a mild pallor and moderate icterus. Her abdominal examination revealed splenomegaly (3 cm below costal margin); later confirmed on ultrasonography (USG). There were no palpable lymph nodes on examination. Other systemic investigations were within normal limits. Her work-up for red cell membrane disorders, enzymopathies, and inherited haematological diseases were ruled out. Peripheral blood smear showed anisocytosis, poikilocytosis, microcytosis, polychromasia, and left to shift of polymorphs. The hematological, biochemical, and molecular data are shown in Table 1. The Hb-electrophoresis of the index cases and her mother was normal. Haemoglobinopathies assays were normal in the patient and her parents. The most common red cell enzymes (PK, G6PD, GPI, and P5N) are within the normal limit, whereas LDH activity was increased to 3144 U/L (Table 1). The EMA binding assay for red cell membrane protein defect was showed normal mean channel fluorescence (MCF) . There were few nRBCs, and reticulocyte count was increased to 40%.
Molecular Characterization of β- and α-Globin Gene Mutations in Individuals with Borderline Hb A2 Levels
Published in Hemoglobin, 2020
Surada Satthakarn, Sitthichai Panyasai, Sakorn Pornprasert
The levels of MCV in Hb H disease and heterozygous α0-thal or β-thal were significantly decreased when compared with those of the uncharacterized group. The MCV levels were lower than the normal range (80.0 fL) in all individuals with Hb H disease and heterozygous α0-thal, suggesting that individuals who have borderline Hb A2 levels and decreased MCV need to be investigated for α0-thal and/or α+-thal mutations. Most β-thal subjects had MCV below the reference range; however, two had MCV within the normal value. Probably, individuals with severe anemia may also have polychromasia, which led to unusually increased MCV values. Thus, molecular analysis for detection of β-globin mutations should be performed in individuals with borderline Hb A2 levels who either have normal or low MCV values.
Anemia and transfusion requirements among Ugandan children with severe malaria treated with intravenous artesunate
Published in Pediatric Hematology and Oncology, 2020
Michael T. Hawkes, Robert O. Opoka, Andrea L. Conroy, Robyn E. Elphinstone, Heather A. Hume, Sophie Namasopo, Kevin C. Kain
Hematologic indices (Hb, hematocrit, RBC distribution width, mean corpuscular volume, mean corpuscular Hb, and mean corpuscular Hb concentration) were assessed using automated Beckman Coulter AcT 5 Diff hematology analyser (Beckman Coulter, Inc., Fullerton, CA) at a College of American Pathologists-certified research laboratory (the Makerere University–John’s Hopkins University Core Laboratory in Kampala, Uganda). LDH activity was quantified using a commercial assay according to manufacturer’s instructions (BioVision, Milpitas, CA, USA). Haptoglobin was measured by ELISA according to manufacturer’s instructions (GenWay Biotech, San Diego, CA, USA). Stained peripheral blood films were inspected by an experienced hematology technician and scored using a standardized case record form, blinded to other clinical and hematologic parameters. Grading of polychromasia (none, 1+, 2+, or 3+) was a semi-quantitative scale, but not a standardized index. Testing for ABO/RhD blood grouping and a room temperature cross-match was performed prior to all RBC transfusions. Pre-transfusion screening for irregular antibodies and 37 °C cross-match were not performed. Due to lack of availability at our resource-constrained hospital, additional hematology testing (e.g., absolute reticulocyte count, direct antiglobulin test, bilirubin, and glucose-6-phosphate dehydrogenase activity) were not performed. Furthermore, urine was not tested for hemoglobinuria.