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      Clinical Usefulness of Haptoglobin Levels to Evaluate Hemolysis in Recently Transfused Patients

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          Abstract

          Introduction. Haptoglobin binds the globin portion of free hemoglobin. Serum haptoglobin measurement is used as a laboratory marker for the diagnosis of hemolytic anemia. Since stored blood contains free hemoglobin, transfusion may affect haptoglobin levels. Study Objectives. The aim of the study was to evaluate whether serum haptoglobin could be measured to assess hemolysis in recently transfused patients. Patients and Methods. Twenty-one patients, receiving more than one unit of packed red blood cells (PRBCs) for presumed nonhemolytic indications, were enrolled. Serum haptoglobin levels were recorded before, immediately after, and 24 and 48 hours after transfusion. Observations and Results. Analysis of variance with a repeated measures was used to examine the serum haptoglobin levels at different time periods and no significant difference was found ( P = .28). Conclusion. The results suggest that serum haptoglobin can be used in the diagnosis of hemolysis in patients receiving multiple units of PRBC.

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          The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease.

          The efficient sequestration of hemoglobin by the red blood cell membrane and the presence of multiple hemoglobin clearance mechanisms suggest a critical need to prevent the buildup of this molecule in the plasma. A growing list of clinical manifestations attributed to hemoglobin release in a variety of acquired and iatrogenic hemolytic disorders suggests that hemolysis and hemoglobinemia should be considered as a novel mechanism of human disease. Pertinent scientific literature databases and references were searched through October 2004 using terms that encompassed various aspects of hemolysis, hemoglobin preparations, clinical symptoms associated with plasma hemoglobin, nitric oxide in hemolysis, anemia, pulmonary hypertension, paroxysmal nocturnal hemoglobinuria, and sickle-cell disease. Hemoglobin is released into the plasma from the erythrocyte during intravascular hemolysis in hereditary, acquired, and iatrogenic hemolytic conditions. When the capacity of protective hemoglobin-scavenging mechanisms has been saturated, levels of cell-free hemoglobin increase in the plasma, resulting in the consumption of nitric oxide and clinical sequelae. Nitric oxide plays a major role in vascular homeostasis and has been shown to be a critical regulator of basal and stress-mediated smooth muscle relaxation and vasomotor tone, endothelial adhesion molecule expression, and platelet activation and aggregation. Thus, clinical consequences of excessive cell-free plasma hemoglobin levels during intravascular hemolysis or the administration of hemoglobin preparations include dystonias involving the gastrointestinal, cardiovascular, pulmonary, and urogenital systems, as well as clotting disorders. Many of the clinical sequelae of intravascular hemolysis in a prototypic hemolytic disease, paroxysmal nocturnal hemoglobinuria, are readily explained by hemoglobin-mediated nitric oxide scavenging. A growing body of evidence supports the existence of a novel mechanism of human disease, namely, hemolysis-associated smooth muscle dystonia, vasculopathy, and endothelial dysfunction.
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            Studies on the serum haptoglobin level in hemoglobinemia and its influence on renal excretion of hemoglobin.

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              The Binding of Haemoglobin by Plasma Proteins (Haptoglobins)

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                Author and article information

                Journal
                Adv Hematol
                AH
                Advances in Hematology
                Hindawi Publishing Corporation
                1687-9104
                1687-9112
                2011
                26 June 2011
                : 2011
                : 389854
                Affiliations
                Department of Hematology and Oncology, Sanford R Nalitt Institute for Cancer and Blood Related Diseases, Staten Island University Hospital, 256 C, Mason Avenue, Staten Island, New York-10305, USA
                Author notes

                Academic Editor: Thomas G. Gross

                Article
                10.1155/2011/389854
                3153881
                21860624
                0032f8ae-343e-4f40-9ce0-7d74d0ea0c47
                Copyright © 2011 Shilpi Gupta et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 March 2011
                : 24 April 2011
                Categories
                Clinical Study

                Hematology
                Hematology

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