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Waldenström Macroglobulinemia
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
IgM paraprotein directed to erythrocyte antigens can lead to autoimmune hemolytic anemia. While 10% of patients may have a positive Coombs test, only 3% will develop significant hemolysis [57]. Immune thrombocytopenic purpura and acquired von Willebrand disease are rare but well-described manifestations in WM [65]. Cryoglobulinemia, manifested by Raynaud phenomenon, acrocyanosis, peripheral neuropathy, vasculitis, or renal failure, is the result of IgM immune-complex precipitation [66]. Cold agglutinin disease, manifested by extravascular hemolytic anemia after cold exposure, is the result of IgM binding to RBC surface antigens [67]. Both manifestations have been described in approximately 10% of patients with WM [57].
Immunohematology
Published in Gabriel Virella, Medical Immunology, 2019
Gabriel Virella, Armand Glassman
Laboratory diagnosis. Testing for cold agglutinins is usually done by incubating a series of dilutions of the patient's serum (obtained by clotting and centrifuging the blood at 37°C immediately after drawing) with normal group O RBC at 4°C. Titers up to the hundreds of thousands can be observed in patients with cold agglutinin disease. Intermediate titers (below 1000) are when the cold agglutinins are associated with an infectious disease.
Bronchiolitis obliterans organizing pneumonia induced by drugs or radiotherapy
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
A 40-year-old man began taking phenytoin 300 mg daily after a craniotomy, and in 4 weeks developed fever, rash, unproductive cough, shortness of breath and bilateral crackles.51 The chest radiograph showed bilateral patchy infiltrates, and the open lung biopsy showed myxoid granulation tissue in the bronchioles extending to alveolar ducts and alveoli consistent with BOOP. The patient had also developed new-onset cold agglutinin disease. Corticosteroid therapy was given for 1 year. The chest radiograph, liver function and haematological abnormalities resolved.
Monoclonal antibodies for treatment of cold agglutinin disease
Published in Expert Opinion on Biological Therapy, 2023
Georg Gelbenegger, Sigbjørn Berentsen, Bernd Jilma
The safety and efficacy of eculizumab in patients with CAD was evaluated in a prospective, open-label, bicentric, nonrandomized phase II trial [21] (Table 3, Supplementary Table S2). Patients were eligible for inclusion if they were 18 years of age or older, required treatment because of CAD-related symptoms or had transfusion dependency, and had LDH levels that were at least double the upper limit of normal. Cold agglutinin disease was defined as chronic hemolysis, a cold agglutinin titer of 64 or more at 4°C, and a DAT strongly positive for C3d but negative or only weakly positive for IgG. Key exclusion criteria were treatment with rituximab, alkylating agents, human immunoglobulins, or plasmapheresis at least four weeks before screening. Patients were vaccinated for Neisseria meningitidis before receiving complement inhibition treatment. Included patients received treatment with eculizumab 600 mg weekly for four weeks, followed one week later by eculizumab 900 mg every other week through week 26. The primary endpoint was the difference in LDH level between the first and the last day of eculizumab treatment. The trial included 13 CAD patients. Eleven patients completed the 26-week treatment phase and received all 16 scheduled eculizumab infusions. Eculizumab significantly reduced LDH levels from 572 U/L to 334 U/L (p = 0.0215) but did not significantly increase hemoglobin levels. Despite failure to increase hemoglobin levels, eight patients achieved transfusion independency. Eculizumab was well tolerated, and no meningococcal infections occurred.
Healthcare resource utilization among patients with cold agglutinin disease in Denmark
Published in Current Medical Research and Opinion, 2021
Emese K. Vágó, Gina Nicholson, Erzsébet Horváth-Puhó, Naushin Hooda, Jon P. Fryzek, Jun Su
Cold agglutinin disease (CAD), a rare subtype of autoimmune hemolytic anemia, affects an estimated 16 per 1 million individuals, with a median survival of 8.5–12.5 years after disease onset in European cohorts1,2. CAD is mediated by monoclonal immunoglobulin M autoantibodies, called cold agglutinins, which bind to the I antigen on the surface of red blood cells3. Cold agglutinins are most pathogenic when their thermal amplitude (the highest temperature at which they bind to red blood cell antigens) overlaps with vascular temperatures at the lower limit of normal4. When bound to red blood cells, cold agglutinins activate complement component 1 (C1 complex) and trigger the classical complement pathway, resulting in extravascular hemolysis and, to a lesser extent, intravascular hemolysis3,5,6.
Transitioning Select Chemotherapeutics to the Outpatient Setting Improves Care and Reduces Costs
Published in Oncology Issues, 2021
Since 2015 when we transitioned certain rituximab administrations to the outpatient setting, we decreased our inpatient bed stays, reduced our inpatient chemotherapy costs, and increased the use of our own specialty pharmacy for patients receiving intravenous rituximab combination regimens, as well as an increased use of this model post-implementation for standard order sets. However, not every patient receiving rituximab can be treated in the outpatient setting. Accordingly, we have developed patient restrictions for rituximab in the outpatient setting, including:Immune thrombocytopenic purpura—dose-reduced rituximab, 100 mg9.Cold agglutinin disease.Post-transplant lymphoproliferative disease.Autoimmune hemolytic anemia.Prolonged chemotherapy inpatient stays requiring continued treatment.Infusion reaction or need for rituximab desensitization.