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Haematological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Tissue oxygen concentration governs the rate of erythropoiesis via erythropoietin (Epo), which drives proliferation of red cells. Epo is mainly secreted in the kidney by tubular and interstitial cells that sense tissue hypoxia (low oxygen tension). In chronic renal failure, anaemia results from suppressed erythropoiesis because of failure of this mechanism.
Paper 2
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Iron deficiency anaemia, severe enough that it is not able to support erythropoiesis, may occur for various reasons; some include deficient diet, impaired absorption in the GI tract and polycythaemia vera. The radiological findings in this condition include widening of the diploic spaces and thinning of the tables, as well as osteoporosis and hair-on-end appearance of the skull. They occur due to marrow expansion/marrow hyperplasia. Hair-on-end appearance represents marrow expansion through the outer cortex. The occiput is spared due to absence of red marrow at this site. Unlike in thalassaemia major, in iron deficiency anaemia the facial bones are usually not involved. Rodent facies refers to ventral displacement of the incisors due to marrow overgrowth in the maxillary sinus and causes dental malocclusion.
Surgical transfusions: Non-cardiac
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
Lawrence Tim Goodnough, Terri G Monk
For patients subjected to more aggressive (up to 2 units weekly) phlebotomy, the endogenous erythropoietin response is more substantial.51–53 In one clinical trial,52 a linear-logarithmic relationship was demonstrated between change in hemoglobin level and the endogenous erythropoietin response.53 Erythropoietin-mediated erythropoiesis in this setting is 397–568 ml (19–26% RBC expansion,51–54 or the equivalent of 2–3 blood units).
A deep dive into future therapies for microcytic anemias and clinical considerations
Published in Expert Review of Hematology, 2023
François Rodrigues, Tereza Coman, Guillemette Fouquet, Francine Côté, Geneviève Courtois, Thiago Trovati Maciel, Olivier Hermine
Approximately 70% of the total body iron (3–5 g in adult humans) is bound to heme in red blood cells [2]. Significant fractions are distributed within the liver hepatocytes (20%) and macrophages (5%). On a daily basis, erythropoiesis requires up to 30 mg of iron, while non-erythroid cell requirements are about 5 mg. The plasma iron pool is only 3–4 mg and thus turns over more than ten times per day to satisfy the daily iron requirements. The iron carrier transferrin is central to iron trafficking. Transferrin not only serves as an iron carrier but also keeps circulating iron in a redox-inactive state. Under physiological conditions, only 30% of transferrin molecules are saturated with Fe3+. A rare genetic cause of microcytic anemia, congenital atransferrinemia, highlights the central role of transferrin as a regulated distributor of iron to erythroid and non-erythroid tissues [3]. Children affected by this condition present microcytic anemia due to inefficient iron delivery to erythroblasts, associated with iron overload in non-erythroid tissues, such as the myocardium, liver, or central nervous system because of free iron toxicity.
A systemic review and meta-analysis on the efficacy and safety of ferumoxytol for anemia in chronic kidney disease patients
Published in Renal Failure, 2022
Qianwei Zuo, Taizhong Wang, Lirong Zhu, Xiao Li, Qi Luo
Researchers have linked the presence of anemia in chronic kidney disease with worse prognostic outcomes in terms of mortality and long-term quality of life [5,6]. Erythrocytes are produced through erythropoiesis, a process typically reliant on sufficient levels of a glycoprotein-cytokine such as kidney-produced erythropoietin [7]. However, the extensive damage to nephrotic structures caused by chronic kidney disease, especially within the cortex and medulla, hinders erythropoietin manufacturing [8] and subsequent red blood cell production [9]. In addition, elevated hepcidin levels due to nephrotic inflammation can also instigate anemia by disrupting iron transport and metabolism, as well as by inhibiting erythropoiesis stimulators [10,11]. Finally, increased blood loss due to hemodialysis, increased uremic-inhibitor levels, and reduced erythrocyte lifespan have all been identified as additional factors that cause or aggravate anemia [12–14].
Decreased expression of HBA1 and HBB genes in acute myeloid leukemia patients and their inhibitory effects on growth of K562 cells
Published in Hematology, 2022
Ping Luo, Xiaoyan Liu, Zehai Tang, Bei Xiong
Erythropoiesis is a process that hematopoietic stem cells (HSCs) differentiate into erythrocytes, including early erythropoiesis and terminal erythroid differentiation [2]. Primitive erythroblasts enucleate to become reticulocytes, which subsequently mature into red blood cells [3,4]. Adult red blood cells, as the terminal differential cells, with no nucleus and rather simple structure, have ceased dividing and have no proliferation capacity [5]. The main feature of red blood cells is a high level of adult hemoglobin, with hemoglobin A (HbA) accounting for 97% of its weight, which indicates that high expression of HbA may be accompanied by the cessation of cell proliferation. Human erythroleukemia K562 cells can proliferate indefinitely, but don’t express HbA. Does this mean that no expression of HbA may be accompanied by unlimited proliferation? HBB and HBA1 are genes that encode the normal adult hemoglobin tetramer (Hb) [6]. Adult hemoglobin (HbA) is the most popular form of hemoglobin including two β-globin molecules and two α-globin molecules [7]. Therefore, we hypothesized that HBB and HBA1 may be associated with differentiation degree and proliferation ability of blood cells.