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George Garratty - One of the best experts on this subject based on the ideXlab platform.
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A severe case of cefoxitin-induced immune Hemolytic Anemia.
Acta Haematologica, 2010Co-Authors: David E. Leaf, George Garratty, Nathaniel B. Langer, Mark Markowski, David L. DiuguidAbstract:Drug-induced immune Hemolytic Anemia is a rare but underdiagnosed and potentially fatal condition. We report a case of severe Hemolytic Anemia induced by cefoxitin in a 45-year-old woman admitted with menometrorrhagia. Hemoglobin levels reached a nadir of 4.7 g/dl approximately 72 h after cefoxitin initiation, and hemolysis resolved when cefoxitin was discontinued and prednisone 1 mg/kg was initiated. A transfusion reaction workup revealed no abnormalities. Direct antiglobulin testing was weakly positive with anti-C3. The patient’s plasma and RBC eluate reacted with cefoxitin-treated RBCs but not with untreated RBCs in the presence or absence of cefoxitin.
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immune Hemolytic Anemia associated with drug therapy
Blood Reviews, 2010Co-Authors: George GarrattyAbstract:Drug-induced immune Hemolytic Anemia (DIIHA) is rare; it can be mild or associated with acute severe Hemolytic Anemia (HA) and death. About 125 drugs have been implicated as the cause. The HA can be caused by drug-independent antibodies that are indistinguishable, in vitro and in vivo, from autoantibodies causing idiopathic warm type autoimmune Hemolytic Anemia (AIHA). More commonly, the antibodies are drug-dependent (i.e., will only react in vitro in the presence of the drug). The most common drugs to cause DIIHA are anti-microbials (e.g., cefotetan, ceftriaxone and piperacillin), which are associated with drug-dependent antibodies. The most common drug to cause AIHA is fludarabine. Finding out which drug is causing the problem and stopping that drug is the first approach to therapy. It is not easy to identify the drug interactions accurately in vitro; laboratories specializing in this area can be of great help.
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a high titer high thermal amplitude autoanti b associated with acrocyanosis but no obvious Hemolytic Anemia
Transfusion, 2003Co-Authors: Patricia A Arndt, Jennifer B Do, George Garratty, Mercy A Kuriyan, Roger Strair, Akhil BaranwalAbstract:BACKGROUND: ABO autoantibodies are rare. Most reported examples have been antibodies with 4°C titers not greater than 256 in patients without apparent Hemolytic Anemia. Most high-titer, high-thermal-amplitude, complement-activating cold agglutinins are associated with Hemolytic Anemia. STUDY DESIGN AND METHODS: A 52-year-old man presented with acrocyanosis and mild small-vessel brain disease, but no evidence of obvious Hemolytic Anemia. Regular plasmapheresis treatment was helpful in relieving the clinical symptoms associated with acrocyanosis. Serologic methods were used to study the patient's RBCs and sera. RESULTS: The patient's RBCs were strongly reactive with anti-C3 and anti-IgM and weakly reactive with anti-IgA. The patient's serum contained a high-titer, high-thermal-amplitude, IgMκ autoanti-B, capable of activating complement in vitro. CONCLUSION: A patient with a powerful ABO autoantibody is described. This patient had acrocyanosis but did not appear to have an obvious Hemolytic Anemia. This case is a good example of the lack of correlation between in vitro serologic tests and in vivo reactions in individual patients.
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severe immune Hemolytic Anemia associated with prophylactic use of cefotetan in obstetric and gynecologic procedures
American Journal of Obstetrics and Gynecology, 1999Co-Authors: George Garratty, Regina M. Leger, Patricia A ArndtAbstract:Abstract Second- and third-generation cephalosporins, especially cefotetan, are increasingly associated with severe, sometimes fatal immune Hemolytic Anemia. We noticed that 10 of our 35 cases of cefotetan-induced Hemolytic Anemias were in patients who had received cefotetan prophylactically for obstetric and gynecologic procedures. Eight of these cases of severe immune Hemolytic Anemia are described. (Am J Obstet Gynecol 1999;181:103-4.)
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fatal immune Hemolytic Anemia due to cefotetan
Transfusion, 1992Co-Authors: George Garratty, Sarafina Nance, M. Lloyd, Ronald E. DomenAbstract:: In the first death associated with immune Hemolytic Anemia due to cefotetan, the patient developed Hemolytic Anemia and renal failure, dying 12 days after the beginning of 1 week's cefotetan therapy. The patient's serum contained strong antibodies reacting with cefotetan-treated red cells (RBCs) and with uncoated RBCs in the presence of cefotetan; a much weaker, drug-independent antibody was also detected. Three-days before the patient's death, the antibody reacting with cefotetan-coated RBCs rose to a titer of 262,144; the titer of the antibody to uncoated RBCs, in the presence of cefotetan, rose to 2048; the titer of the drug-independent antibody remained at 4.
Carol A. Kauffman - One of the best experts on this subject based on the ideXlab platform.
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cefotetan induced immune Hemolytic Anemia
Clinical Infectious Diseases, 1992Co-Authors: Carol E Chenoweth, John W Judd, Ann E Steiner, Carol A. KauffmanAbstract:: Immune Hemolytic Anemia due to a drug-adsorption mechanism has been described primarily in patients receiving penicillins and first-generation cephalosporins. We describe a patient who developed Anemia while receiving intravenous cefotetan. Cefotetan-dependent antibodies were detected in the patient's serum and in an eluate prepared from his red blood cells. The eluate also reacted weakly with red blood cells in the absence of cefotetan, suggesting the concomitant formation of warm-reactive autoantibodies. These observations, in conjunction with clinical and laboratory evidence of extravascular hemolysis, are consistent with drug-induced Hemolytic Anemia, possibly involving both drug-adsorption and autoantibody formation mechanisms. This case emphasizes the need for increased awareness of Hemolytic reactions to all cephalosporins.
Robert A Brodsky - One of the best experts on this subject based on the ideXlab platform.
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warm autoimmune Hemolytic Anemia
The New England Journal of Medicine, 2019Co-Authors: Robert A BrodskyAbstract:Key Clinical Points Warm Autoimmune Hemolytic Anemia Warm autoimmune Hemolytic Anemia (WAHA) is a chronic, relapsing disease characterized by Anemia, reticulocytosis, other laboratory evidence of h...
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high dose cyclophosphamide for refractory autoimmune Hemolytic Anemia
Blood, 2002Co-Authors: Victor M Moyo, Douglas H Smith, Isadore Brodsky, Pamela Crilley, Richard J Jones, Robert A BrodskyAbstract:High-dose cyclophosphamide, without stem cell rescue, has been used successfully to treat aplastic Anemia and other autoimmune disorders. To determine the safety and efficacy of high-dose cyclophosphamide among patients with severe refractory autoimmune Hemolytic Anemia, we treated 9 patients with cyclophosphamide (50 mg. kg(-1). d(-1) for 4 days) who had failed a median of 3 (range, 1-7) other treatments. The median hemoglobin before treatment was 6.7 g/dL (range, 5-10 g/dL). The median time to reach an absolute neutrophil count of 500/microL or greater was 16 days (range, 12-18 days). Six patients achieved complete remission (normal untransfused hemoglobin for age and sex), and none have relapsed after a median follow-up of 15 months (range, 4-29 months). Three patients achieved and continue in partial remission (hemoglobin at least 10 g/dL without transfusion support). High-dose cyclophosphamide was well tolerated and induced durable remissions in patients with severe refractory autoimmune Hemolytic Anemia.
Patricia A Arndt - One of the best experts on this subject based on the ideXlab platform.
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a high titer high thermal amplitude autoanti b associated with acrocyanosis but no obvious Hemolytic Anemia
Transfusion, 2003Co-Authors: Patricia A Arndt, Jennifer B Do, George Garratty, Mercy A Kuriyan, Roger Strair, Akhil BaranwalAbstract:BACKGROUND: ABO autoantibodies are rare. Most reported examples have been antibodies with 4°C titers not greater than 256 in patients without apparent Hemolytic Anemia. Most high-titer, high-thermal-amplitude, complement-activating cold agglutinins are associated with Hemolytic Anemia. STUDY DESIGN AND METHODS: A 52-year-old man presented with acrocyanosis and mild small-vessel brain disease, but no evidence of obvious Hemolytic Anemia. Regular plasmapheresis treatment was helpful in relieving the clinical symptoms associated with acrocyanosis. Serologic methods were used to study the patient's RBCs and sera. RESULTS: The patient's RBCs were strongly reactive with anti-C3 and anti-IgM and weakly reactive with anti-IgA. The patient's serum contained a high-titer, high-thermal-amplitude, IgMκ autoanti-B, capable of activating complement in vitro. CONCLUSION: A patient with a powerful ABO autoantibody is described. This patient had acrocyanosis but did not appear to have an obvious Hemolytic Anemia. This case is a good example of the lack of correlation between in vitro serologic tests and in vivo reactions in individual patients.
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severe immune Hemolytic Anemia associated with prophylactic use of cefotetan in obstetric and gynecologic procedures
American Journal of Obstetrics and Gynecology, 1999Co-Authors: George Garratty, Regina M. Leger, Patricia A ArndtAbstract:Abstract Second- and third-generation cephalosporins, especially cefotetan, are increasingly associated with severe, sometimes fatal immune Hemolytic Anemia. We noticed that 10 of our 35 cases of cefotetan-induced Hemolytic Anemias were in patients who had received cefotetan prophylactically for obstetric and gynecologic procedures. Eight of these cases of severe immune Hemolytic Anemia are described. (Am J Obstet Gynecol 1999;181:103-4.)
Ilene C Weitz - One of the best experts on this subject based on the ideXlab platform.
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autoimmune Hemolytic Anemia
Medical Clinics of North America, 2017Co-Authors: Howard A Liebman, Ilene C WeitzAbstract:Autoimmune Hemolytic Anemia is an acquired autoimmune disorder resulting in the production of antibodies directed against red blood cell antigens causing shortened erythrocyte survival. The disorders can present as a primary disorder (idiopathic) or secondary to other autoimmune disorders, malignancies, or infections. Treatment involves immune modulation with corticosteroids and other agents.