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      Cancer-associated thrombotic microangiopathy

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          Abstract

          Cancer-associated thrombotic microangiopathy refers to a group of disorders characterised by microvascular thrombosis, thrombocytopenia, and ischaemic end-organ damage. Haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura are the two major subtypes. It can be a manifestation of the malignancy itself or a complication of its therapy. The addition of several new drugs to the therapeutic armamentarium of cancer has brought to light several novel causative factors of this hitherto uncommon complication. This review covers the aetiology, pathogenesis, clinical manifestations, complications, and the management of cancer-associated thrombotic microangiopathy. Careful review of the patient’s medical records coupled with the correlation of clinical findings and laboratory reports can help clinch the diagnosis and institute appropriate treatment on time.

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          Biochemistry and genetics of von Willebrand factor.

          J Sadler (1998)
          Von Willebrand factor (VWF) is a blood glycoprotein that is required for normal hemostasis, and deficiency of VWF, or von Willebrand disease (VWD), is the most common inherited bleeding disorder. VWF mediates the adhesion of platelets to sites of vascular damage by binding to specific platelet membrane glycoproteins and to constituents of exposed connective tissue. These activities appear to be regulated by allosteric mechanisms and possibly by hydrodynamic shear forces. VWF also is a carrier protein for blood clotting factor VIII, and this interaction is required for normal factor VIII survival in the circulation. VWF is assembled from identical approximately 250 kDa subunits into disulfide-linked multimers that may be > 20,000 kDa. Mutations in VWD can disrupt this complex biosynthetic process at several steps to impair the assembly, intracellular targeting, or secretion of VWF multimers. Other VWD mutations impair the survival of VWF in plasma or the function of specific ligand binding sites. This growing body of information about VWF synthesis, structure, and function has allowed the reclassification of VWD based upon distinct pathophysiologic mechanisms that appear to correlate with clinical symptoms and the response to therapy.
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            Thrombotic microangiopathies.

            Joel L. Moake (2002)
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              Phase II trial of recombinant immunotoxin RFB4(dsFv)-PE38 (BL22) in patients with hairy cell leukemia.

              Inger Margulies, David J P Fitzgerald, R J Kreitman … (2009)
              To conduct a phase II trial in chemoresistant hairy cell leukemia (HCL) with BL22, a recombinant anti-CD22 immunotoxin which showed phase I activity in HCL. Eligible patients had relapsed/refractory HCL and needed treatment based on blood counts. Patients were stratified into three groups: response to cladribine less than 1 year, those with a response lasting 1 to 4 years, or no response and uncontrolled infection. Patients received BL22 40 microg/kg every other day for three doses on cycle 1. Those achieving hematologic remission (HR), defined as neutrophils > or = 1,500/mm(3), hemoglobin > or = 11 g/dL, and platelets > or = 100,000/mm(3), were observed. Patients without HR were re-treated at 30 microg/kg every other day for three doses every 4 weeks beginning at least 8 weeks after cycle 1. Thirty-six patients were enrolled including 26, nine, and one in groups 1 to 3. The response after one cycle (CR, 25%; PR, 25%) improved when 56% were re-treated (CR, 47%; PR, 25%). CR rate was similar in groups 1 and 2 (P = .7). Twenty-two with baseline spleen height lower than 200 mm had higher CR (64% v 21%; P = .019) and OR rates (95% v 36%; P = .0002) compared to 14 with spleens either absent or higher than 200 mm. The only serious toxicity was reversible grade 3 hemolytic uremic syndrome, not requiring plasmapheresis, in two patients (6%). High neutralizing antibodies were observed in four patients (11%) and prevented re-treatment. BL22 activity in HCL is confirmed. Best responses to BL22 after cladribine failure are achieved before the patients develop massive splenomegaly or undergo splenectomy.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ecancermedicalscience
                Journal ID (iso-abbrev): Ecancermedicalscience
                Journal ID (publisher-id): ecancermedicalscience
                Title: ecancermedicalscience
                Publisher: Cancer Intelligence
                ISSN (Electronic): 1754-6605
                Publication date Collection: 2016
                Publication date (Electronic): 28 June 2016
                Volume: 10
                Electronic Location Identifier: 649
                Affiliations
                Department of Medical Oncology, Kidwai Memorial Institute of Oncology, Dr MH Marigowda road, Hombegowdanagar, Bangalore-560029, India
                Author notes
                Correspondence to: Gita R Bhat. livewire841@ 123456gmail.com
                Article
                Publisher ID: can-10-649
                DOI: 10.3332/ecancer.2016.649
                PMC ID: 4929977
                PubMed ID: 27433282
                SO-VID: 768682b5-08a5-401d-857b-659c97726a46
                Copyright © © the authors; licensee ecancermedicalscience.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 03 May 2016
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: thrombotic microangiopathy,haemolytic uraemic syndrome,thrombotic thrombocytopenic purpura,gemcitabine,mitomycin-c,haematopoietic stem cell transplant,immunotoxins,anti-vegf,plasmapheresis
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: thrombotic microangiopathy, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura, gemcitabine, mitomycin-c, haematopoietic stem cell transplant, immunotoxins, anti-vegf, plasmapheresis

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