Cases reported "Anemia, Hemolytic"

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1/35. ceftizoxime-induced hemolysis due to immune complexes: case report and determination of the epitope responsible for immune complex-mediated hemolysis.

    BACKGROUND: Several occurrences of immune complex-mediated, cephalosporin-induced intravascular hemolysis have been reported. This report describes the first case of hemolytic anemia caused by an immune-complex mechanism associated with ceftizoxime and delineates the epitope responsible for hemolysis. CASE REPORT: The patient's serum was tested for antibody that reacted with five penicillins and 30 cephems (all types of cephalosporins) by using protocols to detect drug-adsorption and immune-complex mechanisms. The patient's antibody that formed immune complexes with ceftizoxime reacted with 10 of 30 cephems. These 10 drugs were classified as oxime-type cephalosporins, which have a common structural formula consisting of [(Z)-2-(2-amino-4-thiazolyl)-2-methoxyiminoacetoamido] at the C7 position on 7-aminocephalosporinic acid with or without substitution at the C3 position. CONCLUSION: The patient's antibody recognized a common structure in 10 oxime-type cephalosporins, and immune complexes formed by the antibody specifically or nonspecifically bound to red cell membranes. Therefore, when intermittent antibiotic therapy is required, as in this case, care should be taken in antibiotic selection to avoid drug-induced hemolytic anemia. In addition, when this type of hemolysis is observed, tests for antibody that reacts by adsorption and immune-complex mechanisms should be performed against penicillins and cephems to select antibiotics not showing a cross-reaction.
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2/35. Acute coagulopathy following infusion of prothrombin complex concentrate.

    An acute coagulopathy developed in a 49 year old woman with severe liver disease after she received an infusion of prothrombin complex concentrate. The concentrate used in the infusion was subsequently studied by observing the effect of the concentrate on the partial thromboplastin times of various plasmas. The evidence suggests that activated coagulation factors, including activated factor X, were present in the concentrate, and probably played a role in initiating the acute change in the patient's coagulation status. Mechanisms whereby liver disease predisposes toward the development of such a coagulopathy are discussed. It would appear that prothrombin complex concentrates should be used in patients with liver disease only with utmost caution.
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3/35. ceftriaxone associated hemolysis.

    A 48-year-old immunocompetent women treated with ceftriaxone 2 g daily i.v. for late Lyme borreliosis developed severe haemolytic anaemia. The patient had previously received the same antibiotic two times without any side effects. The first clinical signs began to appear on the seventh day of treatment. The patient developed severe anaemia with a haemoglobin level of 45 mg/l on day 10; thereafter she ceased to receive the antibiotic. The outcome was favourable. The clinical course and serologic results suggest that severe anaemia was induced by ceftriaxone and that drug adsorption as well as immune complex mechanisms were involved in the pathogenesis.
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4/35. Hemolytic crisis after excessive ingestion of fava beans in a male infant with G6PD Canton.

    After ingesting fava beans, a 26-month-old Chinese-Japanese male infant showed a sickly complexion and yellowish-brownish skin and was hospitalized. Severe hemolytic anemia was observed on admission, and transfusion of 200 ml of packed red cells was required. Red cell enzyme assay revealed that the patient and the mother were deficient in glucose-6-phosphate dehydrogenase (G6PD). Subsequent molecular analysis showed that the patient had a missense mutation 1376 G to T (G6PD Canton) and his mother was a homozygote for the mutation. The patient was a son of a Chinese (Taiwanese) mother and a Japanese father. Although G6PD deficiency is rare in the original Japanese population, the number of "imported" cases could be rising rapidly. This is the first reported Japanese case of G6PD deficiency with G6PD Canton.
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5/35. Hemolytic anemia and benign pelvic tumors. A case report.

    BACKGROUND: Hemolytic anemia associated with benign pelvic neoplasms is very rare. Sixteen cases have been reported in the English-language literature. CASE: A 27-year-old woman complained of dizziness, fatigue and headache. physical examination revealed jaundice and mild tachycardia. Laboratory evaluation indicated intravascular hemolysis, and workups for hematologic and infectious disease etiologies were negative. Multiple blood transfusions and steroids failed. Computed tomography showed a large, complex pelvic mass (10 x 10 x 6 cm). Exploratory laparotomy and excision of bilateral dermoid cysts were performed, and the anemia resolved. The patient was healthy, without recurrence, seven years later. CONCLUSION: It is important to seek to identify pelvic tumors in patients presenting with hemolytic anemia because this condition is often resistant to standard medical therapy and resolves only after removal of the neoplasm.
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6/35. Runner's anemia.

    Macrocytic anemia occurring in patients with fatigue suggests numerous diagnoses, ranging from nutritional deficiencies to a myelodysplastic syndrome. A careful history-taking is critically important for recognition of runner's anemia, which is due to plasma volume expansion, with hemolysis from the pounding of feet on pavement, and hemoglobinuria. Gastrointestinal blood loss may also contribute to anemia in long-distance runners. Early recognition of runner's anemia in patients with a complex presentation of anemia is important in circumventing many diagnostic tests. Runner's anemia should be considered when, amidst a constellation of signs and symptoms, mild anemia is well tolerated by an avid runner.
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7/35. ceftriaxone-induced haemolytic anaemia in a child with no immune deficiency or haematological disease.

    A 5-year-old girl, with no underlying immune deficiency or haematologic disease, was treated with ceftriaxone for a urinary tract infection. After receiving ceftriaxone intramuscularly, massive haemolytic anaemia developed. Laboratory studies showed the presence of an antibody against ceftriaxone, and the findings reflected immune complex type haemolysis. High-dose corticosteroids appeared to be effective therapeutically.
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8/35. Two cases of immune haemolytic anaemia, associated with anti-piperacillin, detected by the 'immune complex' method.

    BACKGROUND AND OBJECTIVES: Sera containing antibodies to penicillin and penicillin-related drugs are typically thought to react with drug-coated red blood cells (RBCs) (drug adsorption method), but not when the sera are added to drug and RBCs in the same tube ('immune complex' method). Two cases of immune haemolytic anaemia caused by anti-piperacillin have been previously described. Serological details were given in only one patient. In that subject, the antibody was immunoglobulin (Ig)M IgG and reacted by both the drug adsorption and 'immune complex' methods. MATERIALS AND methods: Two patients with cystic fibrosis developed positive direct antiglobulin tests (DATs) and haemolytic anaemia after 11-12 days of piperacillin therapy. Serological studies were performed with piperacillin, Zosyn (piperacillin tazobactam) and penicillin by using the drug adsorption and 'immune complex' methods. RESULTS: The first patient's serum contained an IgG, complement-activating anti-piperacillin that reacted by the 'immune complex' method only. The second patient's IgM IgG, complement-activating anti-piperacillin reacted by the 'immune complex' method and agglutinated piperacillin-treated RBCs. An eluate from the patient's RBCs reacted weakly with all RBCs tested without the presence of drug. This patient had evidence of intravascular haemolysis and died. CONCLUSIONS: We describe the third and fourth examples of immune haemolytic anaemia caused by anti-piperacillin; one was associated with fatal haemolytic anaemia. As piperacillin is commonly used in the treatment of cystic fibrosis, anti-piperacillin should be considered whenever patients with cystic fibrosis develop haemolytic anaemia and/or positive DATs.
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9/35. Colonic perforations in systemic lupus erythematosus.

    Five patients with systemic lupus erythematosus (SLE), four of whom died with colonic perforations, are reported. Perforation of the colon constituted the most frequent cause of death among 107 patients with SLE admitted to the Rheumatic disease Unit during a three year period. All five patients with colonic perforation had clinical and laboratory manifestations of active SLE in addition to the abdominal syndrome. Most striking was evidence of active arteritis in all patients with either central nervous system involvement and/or peripheral arteritis, in addition to that found in the gastrointestinal tract. Hyperglobulinemia and rheumatoid factor as well as antinuclear antibodies were present at some time in all patients. The abdominal syndrome was characterized by the insidious onset of lower quadrant pain which was intermittent and colicky. Although direct abdominal tenderness was eventually present in all patients, rebound tenderness and hypoactive bowel sounds were variable and abdominal rigidity occurred only in one patient and late in the course. The differential diagnosis of abdominal pain in SLE is reviewed and possible mechanisms for the production of colonic perforations are discussed. It is suggested that the presence of rheumatoid factors in conjunction with circulating immune complexes may be the pathogenetic mechanism via the production of a mesenteric arteritis.
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10/35. Penicillin-induced immunohemolytic anemia associated with circulating immune complexes.

    Eleven days after administration of multiple penicillin analogs, a 55-year-old female developed a Coombs-positive hemolytic anemia. The patient's erythrocytes were coated with IgG, complement components (C4/C3) and her serum contained elevated 125I-Clq binding activity (a measure of the presence of immune complexes). Her serum, in the presence of fresh complement and penicillin, induced complement sensitization of normal erythrocytes. Immune complex-mediated complement activation and the haptene type of erythrocyte sensitization accounted for accelerated red blood cell destruction in this patient.
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