Cases reported "Anemia, Hemolytic"

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1/107. Apparent hemolysis in an AIDS patient receiving trimethoprim/sulfamethoxazole: case report and literature review.

    OBJECTIVE: To describe a case of acute hemolysis associated temporally with administration of trimethoprim/sulfamethoxazole (TMP/SMX) in a patient with AIDS, review the available literature on TMP/SMX-induced hemolytic anemia, and discuss possible drug- and disease-related factors that may have contributed to the episode of hemolysis. CASE SUMMARY: A precipitous decrease in red blood cell count, hemoglobin, and hematocrit occurred shortly after a black woman with AIDS received a single intravenous dose of TMP/SMX for pneumocystis carinii pneumonia. Following drug discontinuation and repeated transfusions, the patient's hematologic indices returned to baseline. literature SOURCES: References were obtained using medline searches, the bibliographies of articles identified during the searches, review articles, and standard textbooks. DATA SYNTHESIS: Of the two different mechanisms of TMP/SMX-induced hemolytic anemia, the reaction is most likely to occur via dose-related oxidative disruption of the erythrocyte membrane in subpopulations deficient in glucose-6-phosphate dehydrogenase (G6PD) activity. In the US, G6PD deficiency most frequently is encountered among blacks. The potential for hemolysis may be further increased in G6PD-deficient AIDS patients, who also appear to lack adequate intracellular glutathione, which is essential for protecting the erythrocyte membrane from oxidative damage. Although an assay for G6PD activity was not conducted, the case circumstances were consistent with TMP/SMX-induced hemolysis in a G6PD-deficient patient. CONCLUSIONS: Black patients with AIDS who are receiving relatively high (greater than or equal to 50 mg/kg/d) dosages of TMP/SMX should be monitored closely for signs and symptoms of hemolytic anemia.
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2/107. 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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3/107. 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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4/107. Oxaliplatin-induced haemolytic anaemia.

    A case of haemolytic anaemia after therapy with oxaliplatin, an anticancer chemotherapeutic agent, was investigated. Haemolytic anaemia has been associated with cisplatin and carboplatin, two related drugs, but not with oxaliplatin.
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5/107. Benzathine penicillin induced immune haemolytic anaemia.

    Penicillin-induced immune haemolytic anaemia is very rare. A ten year-old-female with rheumatic mitral stenosis on benzathine penicillin prophylaxis presented with features of haemolytic anaemia and investigations supported the diagnosis of immune haemolytic anaemia. Patient responded to discontinuation of the drug and therapy with oral prednisolone. This is first such case reported from india.
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6/107. Drug-induced hemolysis: cefotetan-dependent hemolytic anemia mimicking an acute intravascular immune transfusion reaction.

    Numerous cases of drug-induced hemolytic anemia have been described in patients treated with penicillin or cephalosporin. Second and third generation cephalosporins are more commonly implicated in hemolytic reactions than first generation cephalosporins. We report a case of severe cefotetan-induced hemolytic anemia in a previously healthy 46-year-old woman undergoing an elective hysterectomy. The patient received 2 g of intravenous cefotetan intraoperatively and subsequently at 12 and 24 h post-operatively. She complained of diarrhea and fever on the third post-operative day and was seen in her gynecologist's office on the fifth post-operative day (hemoglobin = 10.5 g/dL). On the seventh post-operative day, she complained of fever and soreness around the suprapubic catheter site and was given a prescription for 500 mg oral cephalexin four times a day. The next day she was seen in the gynecologist's office and reported feeling better. Ten days after the operation her fatigue worsened and her hemoglobin was 4.8 g/dL. She was transfused with 3 units of packed red blood cells (PRBC) and was given 1 g of cefotetan intravenously. During the transfusion of the second unit of PRBC nursing staff observed gross hemoglobinuria and she subsequently developed acute renal failure. Laboratory chemistry parameters were consistent with severe acute hemolysis. The patient's direct antiglobulin test was reactive and her serum reacted with cefotetan-coated red blood cells (RBCs) and serum plus soluble cefotetan reacted with untreated RBCs. The titration endpoint of the serum against cefotetan-coated RBCs was 40,960, while the serum plus soluble cefotetan against uncoated RBCs was 2,560. This case of severe cefotetan-induced hemolysis was complicated by an acute hemolytic event that occurred during the transfusion of PRBC. Clinical and transfusion service staff must consider drug-induced hemolysis in the differential diagnosis of acute anemia.
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7/107. amyl nitrite induced acute haemolytic anaemia in hiv-antibody positive man.

    Volatile nitrites (amyl and butyl) are popular recreational drugs, especially in the homosexual population. Haemolytic anaemia is a rare complication of nitrite inhalation and occurs when the reducing capacity of the red cell enzymes is overcome by the oxidizing effect of the nitrite. We describe here a patient with hiv infection who developed a profound haemolytic anaemia after repeated inhalation of large quantities of amyl nitrite.
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8/107. glucose-6-phosphate dehydrogenase deficiency-induced hemolysis in newly diagnosed diabetic monozygotic twins.

    A pair of monozygotic male twins are described who manifested hemolysis at the concurrent onset of diabetes type 1. hemolysis appeared progressively following the correction of hyperglycemia and ketoacidosis (one twin). It was found to be related to unknown glucose 6-phosphate dehydrogenase (G-6-PD) deficiency. Other causes of hemolysis such as drugs or bacterial infection were excluded. The fall in glucose availability after the correction of hyperglycemia is proposed as a possible explanation for hemolysis.
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9/107. Autoimmune thrombocytopenia: a complication of fludarabine therapy in lymphoproliferative disorders.

    We describe two cases of autoimmune thrombocytopenia precipitated by fludarabine therapy in patients with chronic lymphatic leukaemia. Both were treated with high dose steroids and initially responded with recovery of normal platelet counts. One patient developed recurrent autoimmune thrombocytopenia on two occasions following re-exposure to the drug when his disease had become refractory to all other treatments. A retrospective review of the case notes of 45 patients with lymphoproliferative disorders treated with fludarabine over the past 6 years indicated the development of autoimmune thrombocytopenia in 4.5% (two out of 45) and autoimmune haemolytic anaemia in 6.7% (three of the 45).
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10/107. Hemolytic anemia in native valve infective endocarditis: a case report and literature review.

    Hemolytic anemia is a rare manifestation of infective endocarditis. A 19-year-old man with a small ventricular septal defect developed right-sided infective endocarditis with huge vegetations involving the tricuspid valve, the ventricular septal defect, and the pulmonary valve. Intravascular hemolysis was suggested by the presence of numerous fragmented erythrocytes, giant platelets and polychromasia of the red blood cells. The direct coombs test was positive, and there were spherocytes and splenomegaly, findings that suggested an immune-mediated mechanism also played a role in the hemolysis. The hematological picture persisted despite antibiotic therapy and recovered only after surgical removal of the vegetations, tricuspid and pulmonary valvectomy, and patch closure of the ventricular septal defect.
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