Cases reported "Thrombocytopenia"

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1/239. ticlopidine-induced thrombocytopenia.

    A case is presented of a 58-year-old woman developing profound thrombocytopenia within one week after starting treatment with ticlopidine. ticlopidine was prescribed following coronary artery stenting. The patient recovered rapidly after discontinuation of the drug, suggesting a possible relationship between ticlopidine and thrombocytopenia. Haematological disorders associated with ticlopidine, such as neutropenia, thrombocytopenia and bone marrow aplasia, are rare and usually seen within the first three months of therapy. As the use of ticlopidine increases, clinicians should be aware of haematological complications associated with its use and inform their patients appropriately.
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2/239. Elevated reticulocyte count--a clue to the diagnosis of haemolytic-uraemic syndrome (HUS) associated with gemcitabine therapy for metastatic duodenal papillary carcinoma: a case report.

    In adults, the haemolytic-uraemic syndrome (HUS) is associated with probable causative factors in the minority of all cases. Cytotoxic drugs are one of these potential causative agents. Although metastatic cancer by itself is a recognized risk-factor for the development of HUS, therapy with mitomycin-C, with cis-platinum, and with bleomycin carries a significant, albeit extremely small, risk for the development of HUS, compared with all other cytotoxic drugs. Gemcitabine is a novel cytotoxic drug with promising activity against pancreatic adenocarcinoma. We are reporting on one patient with metastatic duodenal papillary carcinoma developing HUS while on weekly gemcitabine therapy. The presenting features in this patient were non-cardiac pulmonary oedema, renal failure, thrombocytopenia and haemolytic anaemia. The diagnosis of HUS was made on the day of admission of the patient to this institution. Upon aggressive therapy, including one single haemodialysis and five plasmaphereses, the patient recovered uneventfully, with modestly elevated creatinine-values as a remnant of the acute illness. Re-exposure to gemcitabine 6 months after the episode of HUS instituted for progressive carcinoma, thus far has not caused another episode of HUS.
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3/239. plasma exchange for thrombocytopenia in antiphospholipid syndrome: a case report.

    The remarkable effect of plasma exchange (PE) was observed on thrombocytopenia in a patient with antiphospholipid syndrome (APS) associated with systemic lupus erythematosus. Three times PE led to recovery from severe thrombocytopenia refractory to treatment with corticosteroid, anticoagulant, and antiplatelet drugs accompanied by a decrease in the serum cardiolipin beta2 glycoprotein I antibody level. This result suggests that PE is a valuable therapeutic tool for refractory thrombocytopenia in APS.
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4/239. Clinical experience with combined treatment of thrombin inhibitors and GPIIb/IIIa inhibitors in patients with HIT.

    Despite the use of potent anticoagulants such as r-hirudin and argatroban, the morbidity/mortality of heparin-induced thrombocytopenia (HIT) patients remains high. In the last several months, we have treated three HIT-positive patients with a combined therapy of thrombin inhibitor and GPIIb/IIIa inhibitor when treatment with thrombin inhibitor alone failed to alleviate acute thrombosis. Combination therapies included r-hirudin (Refludan) with tirofiban (Aggrastat) or argatroban (Novastan) with ReoPro. A reduced dose of the thrombin inhibitor with the standard dose of the antiplatelet drug was the dosing regimen used. In all cases, there was no overt bleeding that required intervention and all patients had improved or fully recovered. This first report of the use of GPIIb/IIIa inhibitors with thrombin inhibitors in HIT patients with active thrombosis suggests that this combined therapy may be more effective than thrombin inhibitor treatment alone. The data from these three cases warrant testing of this therapeutic regimen in larger studies to determine optimal dosing strategies.
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5/239. Immediate vein graft thrombectomy for acute occlusion after coronary artery bypass grafting.

    A 76-year-old man underwent coronary bypass grafting 3 days after exposure to heparin. Immediately after chest closure, he developed acute graft thrombosis and cardiac arrest in the setting of thrombocytopenia. Immediate graft thrombectomies were performed. Postoperative tests for heparin-induced thrombocytopenia and thrombosis (HITT) were positive. This case represents a dramatic example of HITT after coronary revascularization.
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6/239. Acute profound thrombocytopenia following C7E3 Fab (Abciximab) therapy: case reports, review of the literature and implications for therapy.

    Platelets play a crucial role in the ischemic complications of percutaneous coronary procedures. The recent availability of C7E3 Fab (Abxiximab or ReoProtrade mark), a chimeric monoclonal antibody Fab fragment directed against the platelet glycoprotein IIb/IIIa receptor, has reduced abrupt closure and other adverse events and lessened the need for revascularization procedures. As the use for this drug has increased, rare cases of severe thrombocytopenia have been revealed. From August 1995 to June 1997, 452 patients at Charleston Area Medical Center who underwent percutaneous coronary revascularization procedures and were treated with abciximab were evaluated for the development of severe thrombocytopenia (i.e., platelet count less than 20,000 within 48 hr of treatment). A review of published reports of severe thrombocytopenia was also reviewed. A review of published reports of abciximab-induced severe thrombocytopenia, as well as our three cases, reveals that: 1) the incidence is less than 0.7%; 2) the nadir platelet count (range 1, 000-16,000) was noted within 2-31 hr after abciximab infusion; 3) the platelet count increases to greater than 100,000 within 12 days in all patients; 4) bleeding episodes were treated with platelet transfusion with an improvement in platelet count within 24 hr in all patients in whom they were given; and 5) in the one patient treated with gamma globulin alone, no significant rise in platelet count was noted. Acute severe thrombocytopenia can occur after ReoProtrade mark administration. Its development is not predictable and may occur within 2 hr of administration. thrombocytopenia, therefore, requires consideration in every patient treated with this drug. It appears prudent to obtain a platelet count 2 hr after initiating ReoProtrade mark. If thrombocytopenia develops, then the drug can be stopped in a timely manner and platelet transfusion can be given.
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7/239. thrombocytopenia induced by Jui, a traditional Chinese herbal medicine.

    Jui is a traditional Chinese herbal medicine. The causal relation between the drug and thrombocytopenia was proved by a rechallenge test.
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8/239. mesalamine-associated thrombocytopenia.

    We describe a case of a 25-yr-old woman with ulcerative colitis who developed marked thrombocytopenia during treatment and upon rechallenge with oral mesalamine. In contrast to its parent drug, sulfasalazine, which has often been reported to cause serious blood disorders, particularly agranulocytosis, mesalamine has rately been implicated as a cause of serious blood disorders. Although previous cases of hematological toxicity have been described in patients taking mesalamine, none of these patients were rechallenged in an effort to prove causality between 5-aminosalicyclic acid and the hematological abnormality as well as outrule the possible "autoimmune" contribution of inflammatory bowel disease to the hematological toxicity of these agents. This report demonstrates that mesalamine has the potential, like sulphasalazine, to cause marked thrombocytopenia in an idiosyncratic fashion. All patients receiving mesalamine therapy, either orally or topically should have regular, complete blood profiles.
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9/239. Anticoagulative management of patients requiring left ventricular assist device implantation and suffering from heparin-induced thrombocytopenia type II.

    BACKGROUND: heparin-induced thrombocytopenia type II (HIT II) is a rare but life-threatening side effect of heparin therapy. We describe the perioperative anticoagulative management of patients tested positive for HIT II and requiring implantation of a left ventricular assist device (LVAD). methods: We report on 3 patients with a different perioperative anticoagulative management (preoperative, intraoperative, and postoperative anticoagulation with danaparoid-sodium; preoperative anticoagulation with recombinant hirudin, anticoagulation with danaparoid-sodium intraoperatively and postoperatively; preoperative anticoagulation with recombinant hirudin, intraoperative anticoagulation with heparin, and postoperative anticoagulation with danaparoid-sodium) and discuss the difficulties of the treatment. RESULTS: Anticoagulation with alternative drugs such as recombinant hirudin and danaparoid-sodium led to serious and life-threatening bleeding complications as well as to thromboembolic events in the first 2 patients. Therefore the third patient underwent LVAD implantation using heparin for intraoperative anticoagulation to avoid administration of high doses of recombinant hirudin or danaparoid-sodium. Despite very low anti-factor xa activities, when using danaparoid-sodium postoperatively, the patient suffered from a bleeding complication on the 4th day after LVAD implantation requiring reexploration. CONCLUSIONS: In selected cases (negative heparin-induced platelet aggregation (HIPA) test at the time of LVAD implantation and continuation of postoperative anticoagulation with recombinant hirudin or danaparoid-sodium), heparin may be used for LVAD implantation in HIT II patients to reduce bleeding complications.
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10/239. Treatment of an acute flush reaction caused by subcutaneous r-hirudin with pegylated hirudin.

    We report a patient who was treated with recombinant (r)-hirudin for heparin-induced thrombocytopenia and developed a flush reaction twice upon re-exposure to 25 mg of subcutaneous r-hirudin. Antihirudin IgG antibodies developed. The patient received 50 mg of PEG-hirudin subcutaneously over 2 days. No side-effects occurred. The level of IgG antihirudin antibodies increased. Ecarin clotting time and thrombin inhibition S2238 assay were not influenced by the patient's IgG antihirudin antibody. PEG-hirudin may be used in patients with intolerance to r-hirudin because of a dissociation of the allergenic and immunogenic properties of the pegylated drug.
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