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Toxic Responses of the Blood
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
Hemolytic anemia is due to an increased rate of red blood cell destruction. Frequently, there is shortened life span or an increased fragility of red blood cells. Chemicals cause hemolytic anemia by at least three mechanisms: those that produce hemolysis directly in all persons if a sufficient dose is given (e.g., arsine, benzene, lead, methyl chloride, phenylhydrazine, and trinitrotoluene); those that produce hemolysis by an immune mechanism (e.g., quinine and quinidine); and those that affect people with certain genetic defects such as glucose–6-phosphate dehydrogenase deficiency (e.g., acetanilide, naphthalene, phenylhydrazine, potassium perchlorate, and sulfanilamide). Clinical tests that are available for the determination of hemolytic anemia are blood smears, cell counts, cell morphology, Heinz body accumulation, and urinary levels of erythrocyte breakdown products.
Toxicology
Published in Martin B., S.Z., of Industrial Hygiene, 2018
Hemolytic anemia is due to an increased rate of red blood cell destruction. Frequently, there is shortened life span or an increased fragility of these red blood cells. Chemicals cause hemolytic anemia by at least three mechanisms: those that produce hemolysis directly in all persons if a sufficient dose is given (e.g., arsine, benzene, lead, methyl chloride, phenylhydrazine, and trinitrotoluene); those that produce hemolysis by an immune mechanism (e.g., quinine and quinidine); and those that affect people with certain genetic defects such as glucose-6-phosphate dehydrogenase deficiency (e.g., acetanilide, naphthalene, phenylhydrazine, potassium perchlorate, and sulfanilamide). Clinical tests that are available for the determination of hemolytic anemia are blood smears, cell counts, cell morphology, Heinz body accumulation, and urinary levels of erythrocyte breakdown products.
Hemolysis during short-term mechanical circulatory support: from pathophysiology to diagnosis and treatment
Published in Expert Review of Medical Devices, 2022
Tim Balthazar, Johan Bennett, Tom Adriaenssens
Hemolysis is the consequence of degradation of the RBCs. The normal life span of a RBC is around 120 days. Older erythrocytes become less elastic and are more easily destroyed by mechanical stress. This occurs at a rate of around 1% of RBCs daily. The hemoglobin (Hb) content of these cells is released into the blood plasma and further degraded in the liver, where the iron atoms are recycled. In a healthy person, this normal process of destruction of older RBCs (natural hemolysis) is balanced by a compensatory release of newly formed RBCs by the bone marrow, via increased erythropoietin (EPO) secretion by the kidney. In case of intravascular hemolysis, these compensatory mechanisms are overwhelmed and a decrease of the Hb level below the normal range can ensue, termed hemolytic anemia. Furthermore, other laboratory and clinical findings (such as jaundice and dark-colored urine) can be observed [23].