Cases reported "Thrombocytopenia"

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1/10. A woman with leg cramps and rash.

    A 68-year-old woman presented with generalized weakness and a rash on her lower extremities. The weakness began one week earlier, shortly after treatment for leg cramps and two days before the rash appeared. She had also had blood-streaked sputum a few days before admission. There was no history of bleeding diathesis, nose bleeding, hematuria, vasculitis, muscle or joint aches, cinchonism, or exposure to tuberculosis. She denied fever, chills, night sweats, leg pain or swelling, chest pain, or abdominal pain.
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2/10. Reversible thrombocytopenia associated with eptifibatide.

    OBJECTIVE: To report a patient who experienced severe, reversible thrombocytopenia after receiving eptifibatide for acute coronary syndrome. CASE SUMMARY: A 61-year-old white man with a past medical history of coronary artery disease, peripheral vascular disease, insulin-dependent diabetes, hypertension, and dyslipidemia was treated with eptifibatide as an adjunct to standard antiischemic therapy for acute coronary syndrome. On administration of eptifibatide, the patient experienced chills accompanied by sharp pains that radiated throughout his body. The infusion was immediately stopped and the symptoms resolved. A platelet count obtained 11 hours later showed a decrease from a baseline of 230 to 3 x 10(3)/mm(3) (normal 160-360). Multiple platelet analyses confirmed profound thrombocytopenia. Over the course of the hospitalization, the patient's platelet count returned to normal; he experienced no other adverse hematologic sequelae. DISCUSSION: All of the glycoprotein IIb/IIIa receptor antagonists are associated with thrombocytopenia. However, the risk of thrombocytopenia has been observed to be less with eptifibatide. Because of the temporal relationship between eptifibatide administration and the patient's symptoms and laboratory analysis, we believe that the thrombocytopenia was the result of an adverse reaction. CONCLUSIONS: The temporal relationship to administration and the resolution of the adverse reaction on discontinuation of the drug support the likelihood that the severe, reversible thrombocytopenia was associated with eptifibatide.
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3/10. vancomycin-induced thrombocytopenia: a case proven with rechallenge.

    In a rare case of vancomycin-induced thrombocytopenia, a 50-year-old man with culture-negative subacute bacterial endocarditis underwent mitral valve replacement surgery and was treated with vancomycin. His platelet count dropped from 346 x 10(3)/mm3 to 13 x 10(3)/mm3 on postoperative day 4, and a differential diagnosis of heparin- versus drug-induced thrombocytopenia was considered. Antiheparin antibodies were detected in the patient's serum on day 5. He showed no signs of bleeding. His platelet count remained below 5 x 10(3)/mm3 despite two platelet transfusions on day 5. A hemorrhagic pericardial effusion with tamponade developed, requiring drainage. A trial with intravenous immunoglobulin led to fever and chills, and the infusion was not completed. vancomycin was changed to clindamycin on day 9, and methylprednisolone therapy was started on day 11. On day 12, the patient's clinical condition improved, and his platelet count increased from 3 x 10(3)/mm3 to 32 x 10(3)/mm3 with no bleeding. On day 18, his platelet count was 424 x 10(3)/mm3, and he was scheduled for discharge with vancomycin therapy for a total of 6 weeks. He received a single dose of intravenous vancomycin 1 g at the hospital; his platelet count dropped to 160 x 10(3)/mm3 1 hour after the infusion and to 58 x 10(3)/mm3 12 hours later. vancomycin was discontinued and clindamycin and prednisone were restarted. On day 20, the patient's platelet count increased to 105 x 10(3)/mm3 and he was discharged with warfarin, prednisone, and clindamycin therapy. We suspect that our patient's thrombocytopenia was due to vancomycin.
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4/10. Oxaliplatin-induced acute-onset thrombocytopenia, hemorrhage and hemolysis.

    BACKGROUND: Oxaliplatin is a novel platinum derivative with established anti-tumor activity in colorectal cancer. Acute-onset hemolytic anemia and thrombocytopenia associated with this drug have rarely been reported and some of these cases have been severe or even fatal. CASE REPORT: This case report describes a patient who developed fever, chills, abdominal and back pain as well as sudden-onset severe thrombocytopenia, upper gastrointestinal bleeding and hemolysis immediately after treatment with oxaliplatin for metastatic colorectal cancer. The reaction appeared during the 14th cycle of chemotherapy. Corticosteroids and antihistamines were administered together with platelet transfusions. Over the next 2 days platelet count improved and the syndrome abated. The patient was discharged 4 days later. Furthermore, the reaction was accompanied by a strongly positive coombs test and increased TNF-alpha and IL-10 serum levels which returned to normal following anti-inflammatory drug administration. CONCLUSION: physicians should be aware of the possibility of acute hematological emergencies following oxaliplatin administration.
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5/10. Acute thrombocytopenia after intravenous infusion of radiographic contrast medium.

    Acute thrombocytopenia due to intravenous infusion of radiographic contrast media is extremely rare. We report the first such case in japan. A 52-year-old male was admitted to hospital because of right ureteral stone. Two hours after drip infusion pyelography, the patient experienced chills and fever. It was shown that his platelet count had decreased abruptly from 233,000 to 8000/mm3. Platelet associated immunoglobulin was not detected. An in vitro test for platelet aggregation by contrast media was negative. Following infusion of hydrocortisone, the platelet count recovered to a normal level within several days.
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6/10. quinine-induced immune thrombocytopenia with hemolytic uremic syndrome: clinical and serological findings in nine patients and review of literature.

    quinine-induced immune thrombocytopenia with hemolytic uremic syndrome (HUS) is a recently defined clinical entity. In this paper we have attempted to characterize the natural history and laboratory abnormalities typical of quinine-induced immune thrombocytopenia associated with hemolytic uremic syndrome in nine patients experiencing ten episodes of the disease. In addition, review of other reported cases of probable quinine-induced HUS is presented. The disease was characterized by the onset of chills, diapheresis, nausea and vomiting, abdominal pain, decreased urine output, and petechiae following quinine exposure. All patients experience significant anemia, severe thrombocytopenia, increased lactate dehydrogenase, elevated serum creatinine, and oliguria. quinine-dependent platelet-reactive antibodies were identified in eight of nine using flow cytometry. Unexpectedly, drug-dependent antibodies reactive with red cells and granulocytes were identified in four and eight patients, respectively. All patients were treated with plasma exchange (range 1-12 procedures), and seven required hemodialysis. All survive without residual abnormality. Our experience with nine patients with quinine-induced HUS and the nine additional cases reported by others and reviewed in this paper establishes this condition as a distinct clinical entity. adult patients presenting with HUS should routinely be asked about exposure to quinine in the form of medication or beverages. The mechanism by which quinine-dependent antibodies produce renal failure is uncertain, but preliminary studies (described elsewhere) suggest that drug-induced antibodies reactive with endothelial cells and possibly margination of granulocytes in renal glomeruli may be responsible for this complication. The prognosis in quinine-induced HUS is better than in other forms of adult HUS.
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7/10. Human granulocytic ehrlichiosis in the upper Midwest united states. A new species emerging?

    OBJECTIVE--To characterize the clinical presentation and course, laboratory findings, and treatment outcome of 12 patients with human granulocytic ehrlichiosis. SETTING--The 12 patients were male, ranged in age from 29 to 91 years, and contracted their illness in wisconsin or minnesota. methods--Cases were recognized by the presence of intracytoplasmic inclusions (morulae) in peripheral neutrophils of patients presenting with temperature of 38.5 degrees C or higher, chills, severe headache, and myalgias. All patients had a complete blood cell count and blood chemistry profile. Blood smears were examined by light microscopy. All available paired serum samples were analyzed for presence of indirect fluorescent antibodies against ehrlichia chaffeensis, Ehrlichia phagocytophila, and Ehrlichia equi. Blood samples from 12 patients were subjected to polymerase chain reaction analysis using primers specific for the E phagocytophila/E equi group, primers that include the agent identified in our patients, as well as E chaffeensis. RESULTS--Varying combinations of leukopenia, anemia, and thrombocytopenia were found in all but one patient. All 12 patients demonstrated morulae in the cytoplasm of neutrophils, but not in mononuclear white blood cells. serum assays failed to detect antibodies against E chaffeensis, but eight of 10 patients and seven of 10 patients tested had antibody titers of 1:80 or more for E phagocytophila and E equi, respectively. polymerase chain reaction products obtained with primers for E phagocytophila, E equi, and the granulocytotropic Ehrlichia revealed that seven patients were infected with the same agent. The results of serological assays or polymerase chain reaction strongly suggest that all 12 patients were infected by E phagocytophila, E equi, or a closely related Ehrlichia species. Two of the 12 patients died. The other 10 patients improved rapidly with oral doxycycline treatment. CONCLUSIONS--We believe that all 12 patients have been infected with a granulocytic Ehrlichia species, reflecting a recently described new disease entity. The infective organism appears to be closely related to E phagocytophila and E equi. The geographic domain of human granulocytic ehrlichiosis is currently unknown. This novel granulocytic Ehrlichia species is capable of causing fatal infections in humans. Early detection and treatment with tetracycline drugs appear to offer the best chance for complete recovery.
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8/10. ATGAM associated coagulopathy in renal transplant patients: a report of two unusual cases.

    Polyclonal antibodies, used for both induction and rejection therapy in renal transplant recipients, are associated with such side effects as chills and fever. We describe two patients who developed a coagulopathy during antithymocyte globulin (ATGAM) therapy, a previously unknown complication. The laboratory tests revealed prolonged prothrombin and partial thromboplastin times and thrombocytopenia. Discontinuation of ATGAM therapy resulted in correction of these abnormalities.
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9/10. Severe thrombocytopenia and response to corticosteroids in a case of nephropathia epidemica.

    Nine days after working in the woods, a previously healthy 32-year-old man fell seriously ill. His symptoms included high fever, chills, diffuse myalgia, severe headache, and back pain. On the fifth day of onset of symptoms, blood tests showed creatinine levels of 5.4 mg/dL accompanied by marked proteinuria. After admission to the hospital, a diagnosis of nephropathia epidemica (NE) caused by puumala virus was made using solid-phase enzyme-linked immunosorbent assay (ELISA). The patient gradually recovered renal function without requiring dialysis. However, he surprisingly experienced a sharp decline in platelet count to a minimum of 2,000/microL with concomitant occurrence of petechiae and conjunctival hemorrhage. Prednisolone was initiated, resulting in a swift rise in platelets. Six days later, when the medication was withdrawn, a sharp decrease in platelets recurred. The steroids were then readministered for the next 3 months, thus reestablishing a stable platelet count. The immediate rise of platelets after administration of prednisolone supports the pathophysiological view of hantavirus infection as an immunologically mediated disease. Corticosteroids in the treatment of hantavirus-associated thrombocytopenia might need further systematic evaluation.
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10/10. Recombinant interleukin-6 in the treatment of congenital thrombocytopenia associated with absent radii.

    PURPOSE: The role interleukin-6 (IL-6) in the treatment of congenital thrombocytopenias is unknown. The purpose of this case report is to describe the efficacy of IL-6 in a child with thrombocytopenia with absent radii (TAR) syndrome. methods: A 23-month-old girl with TAR syndrome was treated with recombinant IL-6 (Sigosix; Serono laboratories, Norwell, MA) at a dose of 7 micrograms/kg subcutaneously daily. Complete blood counts were monitored weekly. The child was closely monitored for any toxicity. RESULTS: After 3 weeks of therapy, the patient had an increase in platelet count from a baseline of 5,000 to 8,000/microliter to a maximal level of 33,000/microliter. She was platelet transfusion-independent during IL-6 therapy. Fevers and chills, the main toxicities encountered, were controlled with acetaminophen and ibuprofen. An increase in the IL-6 dose caused anemia with no further increase in platelet count. After discontinuation of the drug, her hemoglobin rose to baseline and the platelet count returned to pretreatment levels. CONCLUSIONS: We conclude that IL-6 may benefit some children with TAR syndrome. The role of IL-6 and other thrombopoietic agents in the treatment of TAR and other congenital thrombocytopenias deserves further clinical study.
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