Cases reported "Anemia, Hemolytic"

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1/12. Cold agglutinins in low-grade B-cell lymphoma.

    The presence of serum cold agglutinin can be the initial presentation of lymphoproliferative diseases. Conditions with persistent cold agglutinins are a spectrum of diseases that vary from benign lymphoproliferation of the "autoimmune-like chronic cold agglutinin disease" to malignant lymphoma. We report a case of a 72-year-old woman who presented with severe anaemia, hepatosplenomegaly and episodes of peripheral haemagglutination precipitated by cold exposure. The haemoglobin was 5.6 g/dL with a cold agglutinin titer of 1:256 at 4 degrees C and 1:8 at room temperature (30 degrees C). The cold agglutinin showed anti-I specificity and kappa light chain restriction. Peripheral blood showed atypical lymphoid cells with a B-cell immunophenotype. Immunoglobulin gene rearrangement study by polymerase chain reaction (PCR) showed an amplified band at 100 bp, consistent with a clonal proliferation of b-lymphocytes. We believe that our patient had cold antibody haemolytic anaemia as the initial presentation of a low-grade non-Hodgkin's lymphoma. The association of cold antibody haemolytic anaemia with low-grade B-cell lymphoma is unusual.
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2/12. Clostridial sepsis with massive intravascular hemolysis: rapid diagnosis and successful treatment.

    A 61-year-old man developed a pyrescia accompanied by a massive intravascular hemolysis after abdominal surgery (Whipple's operation) of a pancreatic adenocarcinoma. Abdominal ultrasound and the abdominal CT-scan showed marked aerobilia and multiple liver abscesses. Laboratory tests demonstrated the presence of the Thomsen-Friedenreich cryptantigen (TCA) on the membranes of the patient's erythrocytes. The enzymatic cleavage of N-acetyl-neuraminic acid usually covering the TCA may lead to a life threatening intravascular hemolysis. Since Clostridial bacteriae typically synthesize neuraminidase, the presumptive diagnosis of Clostridial sepsis complicated by massive hemolysis was made. Immediate antibiotic therapy including penicillin g and metronidazole stopped hemolysis within a few hours and the patient servived. On the following day, microbiological examination identified clostridium perfringens in the patient's blood cultures. Clostrial sepsis should be suspected in patients with underlying infections and/or malignant diseases, particularly of the gastrointestinal or genitourinary tract, who present with septic shock and acute intravascular hemolysis. Whereas microbiological specification of the organism is time consuming, the relatively simple agglutination test with anti-TCA peanut lectin can provide a rapid presumptive diagnosis. The immediate onset of an appropriate antimicrobial therapy is of central importance and might be life-saving.
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3/12. asialoglycoprotein receptor facilitates hemolysis in patients with alcoholic liver cirrhosis.

    hemolysis in patients with advanced alcoholic liver disease is a common clinical problem and indicates an unfavorable prognosis. In many cases, the etiology of the hemolysis remains unknown. We observed three patients with alcoholic liver disease, suffering from severe hemolytic anemia, requiring multiple blood transfusions. Steroid therapy was ineffective and two of the patients died. All patients had a soluble variant of the human asialoglycoprotein receptor (s-ASGP-R) in their serum, as well as high titers of autoantibodies against this receptor (anti-ASGP-R). Consecutively, examination of 60 patients with alcoholic liver disease revealed a high incidence for s-ASGP-R (36%) and anti-ASGP-R (27%) in patients with alcoholic liver cirrhosis (ALC) compared to patients with cirrhosis due to viral hepatitis. The potential etiology of hemolysis was studied in vitro on erythrocytes from patients with ALC and from healthy donors. Isolated ASGP-R but not anti-ASGP-R bound to the surface of erythrocytes preferentially of blood group A1 and caused dose-dependent agglutination and hemolysis, while this phenomenon was much lower using erythrocytes of the blood group B and almost absent with blood group O-erythrocytes. Furthermore, agglutination and hemolysis only occurred in erythrocytes from ALC-patients or after the pre-treatment of cells with neuraminidase. ASGP-R induced agglutination and hemolysis was blocked by the competitive ASGP-R inhibitor asialofetuin. In conclusion, our results indicate a new, non-immunological mechanism for hemolysis in patients with alcoholic liver disease, mediated through agglutination by a soluble variant of the human asialoglycoprotein receptor and mechanical shear stress.
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4/12. ceftriaxone causes drug-induced immune thrombocytopenia and hemolytic anemia: characterization of targets on platelets and red blood cells.

    BACKGROUND: ceftriaxone, a third-generation cephalosporin, has been reported to occasionally cause fatal drug-induced immune hemolytic anemia (DIHA). A clinical and serologic analysis of the first two patients with severe drug-induced thrombocytopenia (DITP) due to ceftriaxone and one patient with fatal DIHA is reported. STUDY DESIGN AND methods: Sera were assessed by the IAT, EIA, glycoprotein (GP)-specific immunoassay, flow cytometry, and immunoprecipitation using transfectants expressing GPIIb/IIIa and GPIb/IX and with different cephalosporins. RESULTS: Sera from patients 1 and 2 reacted strongly with PLTs in the presence of the drug, but not with RBCs. The binding sites of the drug-dependent antibodies (DDAbs) could be localized to GPIIb/IIIa and GPIb/IX, respectively. Inhibition studies indicated that DDAbs recognized epitopes residing on the GPIIb/IIIa complex and on the GPIX subunit, respectively. No cross-reactivity was observed with other cephalosporin derivatives. serum 3 showed strong agglutination with RBCs of Rh(null) phenotype in the presence of ex-vivo metabolites of ceftriaxone, but no cross-reactivity with PLTs. CONCLUSIONS: The first two cases of severe DITP and a third patient with DIHA are reported. DDAbs from all patients showed individual reaction patterns and clear cell lineage specificity. In addition, the DDAbs were dependent on the substitution at position 3 of the ceftriaxone molecule. epitopes on GPIIb/IIIa and GPIX were involved on PLTs. The Rh protein was not the only target of DDAbs on RBCs.
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5/12. Altered glycosylation leads to Tr polyagglutination.

    BACKGROUND: Polyagglutination refers to red blood cells (RBCs) that are agglutinated by a high proportion of ABO-matched adult sera but not by cord sera. Polyagglutinable RBCs have been associated with microbial infection, myeloproliferative disorders, and myelodysplasia. lectins aid in the identification of polyagglutination. CASE STUDY: A Hispanic male infant with mild hemolytic anemia, a "Bernard-Soulier-like" syndrome, intermittent neutropenia, mitral valve regurgitation, ligament hyperlaxity, and mild mental retardation was studied. The patient's Group O RBCs were polyagglutinable; they were agglutinated by normal human sera, several lectins [including Arachis hypogea, salvia sclarea, salvia horminum, glycine max, ulex europaeus, griffonia simplicifolia I, and Gr. simplicifolia II], and some monoclonal antibodies. His RBCs were not agglutinated by cord sera, dolichos biflorus, or phaseolus lunatus. sodium dodecyl sulfate-polyacrylamide gel electrophoresis on the RBC membranes followed by staining with periodic acid-Schiff stain showed markedly reduced staining of glycophorins A and B. Staining with Coomassie brilliant blue revealed that Band 3 has a faster mobility than normal. CONCLUSIONS: Collectively, the results suggest that the patient's RBCs have a reduction in n-acetylneuraminic acid on both N- and O-glycans, exposing, respectively, beta1,4-galactosidase and beta1,3-galactosidase. The patient likely has an altered glycosyltransferase that results in defective glycosylation in RBCs and other cell lineages. This type of polyagglutination was named Tr.
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6/12. ceftriaxone-induced hemolytic anemia and hepatitis in an adolescent with hemoglobin sc disease.

    OBJECTIVES: To describe a case of a ceftriaxone-induced hemolytic anemia and hepatitis leading to multiple organ failure and death in an adolescent with hemoglobin sc disease and to review the previous cases of this rare and potentially fatal disorder in children. DESIGN: Case report and literature review. SETTING: intensive care unit. Patient: adolescent with hemoglobin SC. INTERVENTIONS: emergency treatment. MEASUREMENTS AND MAIN RESULTS: After 4 days of ceftriaxone therapy, the adolescent experienced an acute hemolytic reaction (hemoglobin decreased to 5 g/dL with hemoglobinuria) and severe hepatitis (all enzymes increasing dramatically including aminoaspartate transferase >20,000 IU/L). Renal failure and ultimately multiple organ failure ensued, and the patient died on hospital day 19. Direct antiglobulin tests on red cells obtained from the patient on hospital day 2 showed microscopic agglutination with polyspecific and anticomplement (C3) antiglobulin reagents. Plasma samples showed macroscopic agglutination reactions when incubated in the presence of ceftriaxone, many days after cessation of ceftriaxone, indicating the continued presence of ceftriaxone-dependent antibodies. CONCLUSIONS: Drug reactions leading to hemolysis are relatively uncommon, and a total of ten cases of ceftriaxone-induced hemolytic anemia have been reported in children. The present case describes an adolescent who ultimately died on hospital day 19 from multiple organ failure, although the presentation of this case seems atypical in several respects. Children with clinical syndromes that place them at risk for hemolysis and children who frequently require broad spectrum antibiotics present unique diagnostic challenges, and the possibility that hemolytic syndromes may be due to ceftriaxone must be considered.
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7/12. Serial blood donations for intrauterine transfusions of severe hemolytic disease of the newborn with the use of recombinant erythropoietin in a pregnant woman alloimmunized with anti-Ku.

    BACKGROUND: The management of a pregnant woman with the rare Ko phenotype and anti-Ku is a special challenge, because matched blood is extremely rare and the possibility of severe hemolytic disease of the newborn is high. CASE REPORT: A 30-year-old woman with rare Ko (Knull) phenotype presented at 18 weeks of gestation with positive indirect agglutination test results. She had anti-Ku due to previous blood transfusion, one pregnancy, and two abortions. STUDY DESIGN AND methods: During this pregnancy, anti-Ku titers ranged from 1024 to 4096. At the 26th week of gestation ultrasound showed a hydropic fetus and urgent intrauterine exchange transfusion was performed with the maternal red blood cells (RBCs). Recombinant human erythropoietin (rHu-EPO) and intravenous (IV) iron were administered to the mother to ensure an adequate supply of matched RBCs for intrauterine transfusions and possible perinatal hemorrhage. RESULTS: Intrauterine transfusions were repeated every 1 to 3 weeks. By 35 weeks 2 days of gestation, the mother had donated 4 units of blood, and four intrauterine transfusions had been performed. cesarean section was then decided and a healthy male newborn was born. He was treated with phototherapy but without exchange transfusions. By the 15th day of life rHu-EPO was administrated to the newborn because of anemia. The maternal RBCs completely disappeared from the child's blood by Day 100. CONCLUSIONS: As shown in this case, treatment with rHu-EPO and IV Fe has effectively increased the mother's capacity to donate RBCs for autologous use and intrauterine transfusions, with no adverse effects to the mother or the child.
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8/12. A pesticide (dieldrin)-induced immunohemolytic anemia.

    The unusual presentation of a factory worker with severe hemolytic anemia which remitted following splenectomy prompted a search for an environmental cause for red cell injury. The investigation showed the presence of an immunoglobulin in the patient's serum and on the red cells and small amounts of complement on red cells. The patient's serum caused agglutination of a normal person's red cells only when dieldrin-coated, a reaction blocked by first reacting the serum with dieldrin. The spleen of the patient had a greater than normal concentration of dieldrin, the source of dieldrin being dietary. It is concluded that dieldrin became immunogenic and provoked a chemical immunohemolytic anemia. The spleen played a major role in destruction of red cells injured by the immunopathic process and in accumulation of the antigenic substance dieldrin.
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9/12. Intravascular [correction of intracellular] hemolysis and renal failure in a patient with T polyagglutination.

    A patient with postoperative intravascular hemolysis aggravated by transfusion with fresh whole blood and fresh plasma products had acute renal failure. Screening with arachis hypogaea and glycine soja lectins showed that his red cells were T-transformed. Only washed red cells were transfused subsequently, and no further fresh plasma products were given. All hemolysis ceased, the renal function returned to normal, and the T-polyagglutination as measured by lectin tests disappeared 4 months after surgery. early diagnosis of polyagglutination using lectin screening tests is simple to perform, and will facilitate the immediate choice of the correct transfusion therapy, which in this case may have been life-saving.
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10/12. Severe delayed hemolytic transfusion reaction complicating an ABO-incompatible bone marrow transplantation.

    A 26-year-old, blood group O bone marrow transplant recipient experienced a severe, delayed hemolytic transfusion reaction 6 days following transplantation of marrow from his HLA-mixed lymphocyte culture - identical, blood group AB sister. The patient's pretransplant serum contained both anti-A (IgG titer = 1:128; IgM = 1:32) and anti-B (IgG = 1:16; IgM = 1:64) which was reduced by a two-plasma volume plasma exchange followed by transfusion of four units of incompatible, donor type red cells. The patient experienced no immediate adverse reaction. On the 6th posttransplant day, he became acutely dyspneic. His hematocrit dropped to 18%; the direct antiglobulin test was positive for IgG and complement; anti-A and anti-B were eluted from his red cells. His peripheral blood smear demonstrated extensive agglutination resembling a mixed field reaction. This case demonstrates that significant morbidity may be associated with major ABO-incompatible bone marrow transplantation, that the transfusion of incompatible red cells should be undertaken with extreme caution, and that efforts should be continued to develop methods of pretransplant in vitro red cell removal from the infused bone marrow.
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