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      A case of extravascular hemolysis with Tk-activation

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          Abstract

          Key Clinical Message

          A 50-year-old female with ovarian cancer for 4 years presented with abdominal pain. She started antibiotics for possible infection, and developed extravascular hemolysis. All antigen detection tests were negative, but lectin panel suggested Tk-activation. Additional laboratory testing in conjunction with blood bank is essential to investigate rare cause of hemolysis.

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          Most cited references31

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          Pathology consultation on drug-induced hemolytic anemia.

          Andrew A. Pierce, Theresa Nester, (2011)
          Drug-induced immune hemolytic anemia is considered to be rare but is likely underrecognized. The consulting pathologist plays a critical role in integrating serologic findings with the clinical history, as drug-induced antibodies should be distinguished as either drug-dependent or drug-independent for appropriate clinical management. Drug-dependent antibodies (DDABs) are most commonly associated with cefotetan, ceftriaxone, and piperacillin, whereas fludarabine, methyldopa, β-lactamase inhibitors, and platinum-based chemotherapeutics are frequent causes of drug-independent antibodies (DIABs). DDABs usually demonstrate a positive direct antiglobulin test and a negative elution, while DIABs are serologically indistinguishable from warm autoantibodies and are similarly steroid-responsive. Drug cessation is always recommended.
          Article 0 comments Cited 18 times – based on 0 reviews     Review now
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            Role of sialic acid in survival of erythrocytes in the circulation: interaction of neuraminidase-treated and untreated erythrocytes with spleen and liver at the cellular level.

            Ashley R. Williams, W. H. Bell, W Bruegge … (1977)
            Sialidase (neuraminidase; acylneuraminyl hydrolase; EC 3.2.1.18)-treated erythrocytes obtained from different species are susceptible to rapid elimination from the circulation and are sequestered in the liver and spleen. The present studies were concerned with the mechanism of this clearance and how it may relate to the normal physiological process of removing senescent erythrocytes from the circulation. The results obtained indicate a preferential recognition of sialidase-treated as compared to normal erythrocytes by mono-nuclear spleen cells and Kupffer cells of the liver. This recognition manifests itself in both autologous and homologous systems by adhesion of the complementary cells in the form of rosettes, and as such could explain the removal of enzyme-treated erythrocytes from the circulation with their accumulation in liver and spleen. This phenomenon may represent a normal physiological mechanism for removal of senescent erythrocytes containing decreased sialic acid.
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              Role of sialic acid in erythrocyte survival.

              Agatha M Conrad, Warren R. Payne, J Durocher (1974)
              The role of membrane sialic acid in erythrocyte survival is unclear, although there is evidence for a reduction in sialic acid and surface charge in older erythrocytes. We reduced the surface charge of human, rat, and rabbit erythrocytes by removing sialic acid with neuraminidase. Reduction in sialic acid correlated with decreases in electrophoretic mobility and loss of PAS staining of membrane glycoproteins on polyacrylamide gels. No changes in ATP levels or deformability were found. 51Cr erythrocyte survivals in rats and rabbits showed rapid clearance of desialylated erythrocytes with sequestration by the liver. These results suggest that reduction in erythrocyte sialic acid is a mechanism of erythrocyte destruction and may be important in erythrocyte senescence.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Case Rep
                Journal ID (iso-abbrev): Clin Case Rep
                Journal ID (publisher-id): ccr3
                Title: Clinical Case Reports
                Publisher: Blackwell Publishing Ltd (Oxford, UK )
                ISSN (Print): 2050-0904
                ISSN (Electronic): 2050-0904
                Publication date (Print): August 2014
                Publication date (Electronic): 03 June 2014
                Volume: 2
                Issue: 4
                Pages: 137-142
                Affiliations
                Transfusion Medicine Division, Department of Pathology, University of Michigan Ann Arbor, Michigan
                Author notes
                Chisa Yamada, University of Michigan, Blood Bank/Transfusion Medicine, Department of Pathology, 1500 E. Medical Center Dr. SPC 5054, 2F225 UH, Ann Arbor, MI 48109-5054. Tel: (734) 936-6776; Fax: (734) 936-6888; E-mail: yamadac@ 123456med.umich.edu

                Funding Information No funding information provided.

                Article
                DOI: 10.1002/ccr3.80
                PMC ID: 4184649
                SO-VID: 61afdda9-ae8c-4b08-8209-b1ec2dcd283b
                Copyright © © 2014 The Authors. Clinical Case Reports published by John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 28 January 2014
                Date revision received : 26 February 2014
                Date accepted : 15 April 2014
                Categories
                Subject: Case Reports

                Keywords: extravascular hemolysis,polyagglutination,tk-activation
                Data availability:
                Keywords: extravascular hemolysis, polyagglutination, tk-activation

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