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Altitude, temperature, circadian rhythms and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Henning Wackerhage, Kenneth A. Dyar, Martin Schönfelder
The haematocrit and total haemoglobin mass are not static but can increase due to the production of erythrocytes, termed erythropoiesis. A high haematocrit is beneficial for endurance sports as it increases oxygen transport, and therefore VO2max. This explains the abuse of “blood doping” with erythropoietin in endurance sports where a high VO2max is desired. However, while a high haematocrit may increase endurance performance, high haematocrits are also associated with a greater risk of venous thromboembolism in the general population (12). Thus, a too high haematocrit is a health risk, and because of this in 1997, the Union Cycliste International (UCI) decided to set a 50% haematocrit as a limit for health reasons. This seems sensible because while it is possible to identify EPO in a urine sample (13) this does not seem to be a reliable test due to issues in detection at differing times of sampling, which might have been responsible for the negative anti-doping test outcomes for Lance Armstrong.
Blood Salvage
Published in T.M. Craft, P.M. Upton, Key Topics In Anaesthesia, 2021
Recombinant human erythropoietin accelerates erythropoiesis resulting in an increased red blood cell production, haematocrit level and haemoglobin concentration. The efficacy of recombinant erythropoietin is undeniable but its cost-effectiveness is debatable.
Erythropoietin, Atrial Natriuretic Peptide and Sex Hormones
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Erythropoietin stimulates mitosis in BFU-E cells, thereby increasing the number of red cell precursors. However, erythropoietin appears to exert its major effect on the next stage of red cell production by preventing DNA breakdown so that proerythroblasts are formed. Erythropoietin is also important for regulating the rate of maturation of red blood cells (Figure 64.1). Erythropoietin shortens the time between recruitment of precursor stem cells and release of reticulocytes.
Sustained-release of erythropoietin using a novel injectable thermosensitive hydrogel: in vitro studies, biological activity, and efficacy in rats
Published in Pharmaceutical Development and Technology, 2021
Mahboubeh Rezazadeh, Vajihe Akbari, Jaleh Varshosaz, Parisa Karbasizadeh, Mohsen Minaiyan
Erythropoietin (EPO) is a hormone mainly produced by kidney cells to regulate the production of red blood cells in mammalians. Recombinant EPO has been widely used to treat different types of anemia due to bone marrow transplantation, renal failure, and cancer chemotherapy (Eschbach et al. 1989; Cazzola et al. 1992). Commercial available recombinant human EPO is currently administered via two or three intravenous or subcutaneous injections per weeks for years, and there is no other patient-friendly administration routs. Thus, to improve patient compliance and also therapeutic efficacy, a sustained-release delivery system that allows EPO administration once or twice a month is desirable. To achieve sustained delivery of EPO, various formulations such as fusion of stabilizing peptide (Lee et al. 2006), PEGylation (Wang et al. 2010), and loading to microsphere (Geng et al. 2008; He et al. 2011; Hariyadi et al. 2018), nanoparticles (Bulmer et al. 2012; Fayed et al. 2012), or hydrogel (Hahn et al. 2006; Kobayashi et al. 2008; Wang et al. 2012) have been evaluated.
Epoetin alfa-epbx: a new entrant into a crowded market. a historical review of the role of erythropoietin stimulating agents and the development of the first epoetin biosimilar in the United States
Published in Expert Review of Clinical Pharmacology, 2021
Sid Anand, Jafar Al-Mondhiry, Katrina Fischer, John Glaspy
Oxygen delivery and the response to tissue hypoxia is a critically important and relatively well-understood biological process. Endogenous erythropoietin is produced by the kidney, with inadequate production in chronic kidney disease resulting in anemia. The initial use of erythropoietin was therefore in chronic renal failure, where it was found that an exogenous source of erythropoietin could ameliorate the associated anemia [1]. Subsequently, it was discovered that erythropoietin was also stimulated in low oxygen states through stabilization of the hypoxia-inducible factor (HIF) transcription factor pathway, which leads to an increase in endogenous erythropoietin production in the kidney. Further studies would go on a show that erythropoietin also leads to increased survival of red cell precursors in the marrow, thereby causing expansion and differentiation of committed erythroid progenitor cells in an iron-dependent manner [2]. To aid the action of erythropoietin, hypoxia induces HIF-dependent activation of transferrin and downregulation of hepcidin to support the transfer of iron stores from the liver and intestinal mucosal cells for use by the body [3]. These insights have driven drug developers to targeting of the HIF pathway outside of the context of exogenous erythropoietin, with oral inhibitors of HIF prolyl hydroxylase that allow for accumulation of HIF-alpha subunits and increased HIF transcriptional activity [4].
JAK2 mutation–positive polycythaemia vera associated with IgA vasculitis and nephrotic syndrome: a case report
Published in Modern Rheumatology Case Reports, 2020
Hinako Kondo, Ryu Watanabe, Soshi Okazaki, Kaori Kuriyama, Tetsuro Ochi, Gen Yamada, Akira Sugiura, Hiromu Chiba, Akira Tsukada, Shinji Taniuchi, Takehiko Igarashi, Masataka Kudo, Hideo Harigae, Hiroshi Fujii
We initially believed that this patient had ET because of high platelet counts (83.3 × 104/µL) and the results of a bone marrow biopsy, which showed a particular increase in megakaryocytes (Figure 4). However, if the patient fulfils the criteria for PV, they cannot be diagnosed with ET according to the WHO classification (17). The WHO classification for PV includes three major criteria; (1) haemoglobin level > 16.5 g/dL, (2) hypercellular bone marrow associated with triple linage expansion, and (3) JAK2 V617F mutation or JAK2 exon 12 mutation. One minor criterion is low serum erythropoietin level [17]. In our patient, serum erythropoietin level was 2.0 mIL/mL (where the normal range is from 4.2 to 23.7 mIU/mL). Therefore, our patient fulfilled the criteria for PV, excluding the diagnosis of ET. It is known that patients with JAK2 mutation–positive ET have multiple features that resemble PV, such as high haematocrit [23]. However, after immunosuppressive therapy, the platelet count normalised, but the haemoglobin level remained slightly elevated (Figure 5); this also supported our diagnosis.