Cases reported "Thrombocytopenia"

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1/18. Rituximab therapy in hematologic malignancy patients with circulating blood tumor cells: association with increased infusion-related side effects and rapid blood tumor clearance.

    PURPOSE: Rituximab was recently approved for use in relapsed, low-grade non-Hodgkin's lymphoma; however, few data exist regarding the safety of this agent in patients with a high number of tumor cells in the blood. methods AND RESULTS: After the observation at our institution of a rapid reduction of peripheral-blood tumor cells with associated severe pulmonary infusion-related toxicity in two patients with refractory hematologic malignancies, data on three additional cases were collected from physician-submitted reports of adverse events related to rituximab treatment. Five patients with hematologic malignancies possessing a high number of blood tumor cells were treated with rituximab and developed rapid tumor clearance. The median age was 68 years (range, 26 to 78 years). patients were diagnosed with B-cell prolymphocytic leukemia (n = 2), chronic lymphocytic leukemia (n = 2), or transformed non-Hodgkin's lymphoma (n = 1). All of these patients had bulky adenopathy or organomegaly. All five patients developed a unique syndrome of severe infusion-related reactions, thrombocytopenia, rapid decrement in circulating tumor cell load, and mild electrolyte evidence of tumor lysis, and all required hospitalization. In addition, one patient developed ascites. These events resolved, and four patients were subsequently treated with rituximab without significant complications. CONCLUSION: Rituximab administration in patients who have a high number of tumor cells in the blood may have an increased likelihood of severe initial infusion-related reactions. These data also suggest that rituximab may have activity in a variety of other lymphoid neoplasms, such as chronic lymphocytic leukemia and B-cell prolymphocytic leukemia.
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2/18. Bell's palsy during interferon therapy for chronic hepatitis c infection in patients with haemorrhagic disorders.

    Two adult patients with life-long severe haemorrhagic disorders commenced on interferon-alpha2b therapy for chronic hepatitis c infection. Both developed Bell's palsy several weeks after commencing therapy, They were started on steroids and, in addition, the first patient discontinued interferon-alpha2b therapy while the second patient elected to continue with therapy. In both cases facial paralysis improved over the ensuing weeks. Bell's palsy is often idiopathic but has been reported. in association with herpesviruses. It is not a recognised complication of chronic hepatitis b or C infection, or interferon-alpha2b therapy. However, the interferons are associated with numerous adverse reactions including various neuropsychiatric manifestations and neurological syndromes. There are several reports of nerve palsies, including optic tract neuropathy, occurring during interferon therapy, and immune-based mechanisms are thought to play a role in the aetiopathogenesis. No reports of Bell's palsy in association with interferon therapy were identified in our literature search, although one possible case has been reported to the Committee of safety in medicine. Although Bell's palsy in our patients may have occurred by chance, a neuropathic effect of interferon-alpha2b on the facial nerve cannot be excluded and we urge physicians using interferons to be aware of this potential side-effect.
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3/18. EDTA-dependent pseudothrombocytopenia in a case of liver cirrhosis.

    Pseudothrombocytopenia (PTCP) is the consequence of an EDTA-activated platelet agglutination, resulting in a spuriously low platelet count. We report the case of a 54-year-old man with EDTA-dependent PTCP associated with liver cirrhosis. He couldn't undergo endoscopic examination and dental care for two years because of a previous diagnosis of severe thrombocytopenia secondary to liver cirrhosis. Lack of PTCP recognition may lead the physician to misdiagnosis and mismanagement of the patient.
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4/18. Delayed-onset heparin-induced thrombocytopenia.

    BACKGROUND: heparin-induced thrombocytopenia presents 5 to 12 days after heparin exposure, with or without arterial or venous thromboemboli. Delayed recognition and treatment of heparin-induced thrombocytopenia contribute to poor patient outcomes. OBJECTIVE: To describe and increase awareness of a clinical scenario in which the onset or manifestations of heparin-induced thrombocytopenia are delayed. DESIGN: Retrospective case series. SETTING: Three large urban hospitals (with active cardiovascular surgery programs). patients: 14 patients seen over a 3-year period in whom heparin-induced thrombocytopenia became apparent on delayed presentation with thromboembolic complications. MEASUREMENTS: Platelet counts, onset of objectively determined thromboembolism, results of heparin-induced platelet factor 4 antibody tests, and outcomes. RESULTS: patients went home after hospitalizations that had included heparin exposure--in most cases, with no thrombocytopenia recognized--only to return to the hospital (median, day 14) with thromboembolic complications. Thromboemboli were venous (12 patients, 7 with pulmonary emboli) or arterial (4 patients) or both. Platelet counts were mildly decreased in all but 2 patients on second presentation. On readmission, 11 patients received therapeutic heparin, which worsened the patients' clinical condition and, in all 11 cases, decreased the platelet count (mean at readmission, 143 x 10(9) cells/L; mean nadir after heparin re-exposure, 39 x 10(9) cells/L). Results of serologic tests for heparin-induced antibodies were positive in all patients. Subsequent treatments included alternative anticoagulants (11 patients), thrombolytic drugs (3 patients), inferior vena cava filters (3 patients) and, eventually, warfarin (11 patients). Three patients died. CONCLUSIONS: Delayed-onset heparin-induced thrombocytopenia is increasingly being recognized. To avoid disastrous outcomes, physicians must consider heparin-induced thrombocytopenia whenever a recently hospitalized patient returns with thromboembolism; therapy with alternative anticoagulants, not heparin, should be initiated.
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5/18. Cases from the Osler Medical Service at Johns Hopkins University.

    PRESENTING FEATURES: An 18-year-old white man was admitted to the Osler Medical Service with the chief complaint of back pain. Two weeks prior to admission, the patient developed diffuse and aching upper back pain. Over the next couple of days, he also developed severe anterior chest pain that was somewhat pleuritic in nature but diffuse and extending bilaterally into the shoulders. One week prior to admission, he developed intermittent fevers and night sweats. The patient denied any lymphadenopathy, pharyngitis, sick contacts, shortness of breath, rash, or bleeding. He was seen by a physician and told that he had thrombocytopenia. There was no history of recent or remote unusual bleeding episodes. His medical history was unremarkable except for a childhood diagnosis of attention deficit/hyperactivity disorder. He was not taking any medications and had no history of tobacco, alcohol, or illicit drug use. He had no risk factors for human immunodeficiency virus infection. physical examination showed that he was afebrile and had normal vital signs. He was a well-appearing man who was lying still because of pain. HEENT examination was unremarkable. There was no pharyngeal erythema or exudates. His lungs were clear. His neck was supple and without lymphadenopathy. Examination of his back and chest revealed no focal tenderness. There was no hepatosplenomegaly, and his skin was without petechiae or rashes. Examination of the patient's joints showed pain on passive and active movement of his shoulders bilaterally, but no frank arthritis. There was no rash, petechiae, or echymoses. Chest radiograph and electrocardiogram were unremarkable. On admission, the laboratory examination was notable for a hematocrit level of 32.5%, with a mean corpuscular volume of 79 fL, and white blood cell count of 2.8 x 10(3)/microL. platelet count was 75 x 10(3)/microL. A white blood cell differential revealed 7% bands, 53% polys, 34% lymphs, 5% atypical lymphocytes, 2% nucleated red cells, and a few young unidentified cells. His chemistry studies were unremarkable. What is the diagnosis?
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6/18. heparin-induced thrombocytopenia in the emergency department.

    We describe 3 patients who presented to the emergency department (ED) with stroke, deep venous thrombosis, or pulmonary embolism and renal failure after undergoing cardiac surgery 7 to 17 days earlier. Their onset of thrombosis after previous heparin exposure was temporally plausible for complications of heparin-induced thrombocytopenia, an immune-mediated thrombotic disorder triggered by heparin. The patients had normal platelet counts at presentation, yet each had circulating heparin-induced thrombocytopenia antibodies that were ultimately confirmed. Two patients had heparin reexposure in the ED, 1 of whom developed thrombocytopenia with new thrombosis and died. Alternative parenteral anticoagulation prevented further thrombosis in 2 patients. Because heparin use can be catastrophic in patients with heparin-induced thrombocytopenia, physicians should be vigilant in suspecting heparin-induced thrombocytopenia in patients with thrombosis after recent hospitalization or heparin exposure. Alternative anticoagulants are available for these at-risk patients.
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7/18. Multifocal lymphangioendotheliomatosis with thrombocytopenia: a rare cause of gastrointestinal bleeding in the newborn period.

    Severe gastrointestinal bleeding in the newborn period is a serious but uncommon phenomenon that has a broad differential diagnosis. In the following case report we describe a rare phenomenon in which a newborn presents with severe hematemesis, hematochezia, and thrombocytopenia that are resistant to repeated platelet and packed red blood cell transfusions. Previous cases have been reported, but none of the patients described presented within the first 8 days of life. The early age of presentation and refractory nature of this disease entity to multiple therapies make it a diagnostic and therapeutic dilemma for all physicians involved in the care of newborns.
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8/18. Anticoagulant-induced pseudothrombocytopenia occurring after transcatheter arterial embolization for hepatocellular carcinoma.

    Pseudothrombocytopenia (PTCP) is the in vitro phenomenon of anticoagulant-activated platelet agglutination that results in spuriously low platelet counts. We report the case of a 65-year-old man with EDTA- and sodium citrate-dependent PTCP occurring after transcatheter arterial embolization (TAE) for hepatocellular carcinoma (HCC) due to hepatitis c cirrhosis. Invasion of the portal and hepatic veins by HCC formed severe trans-tumoral arterio-venous shunts that were effectively treated by TAE. Two days after the therapy, PTCP was seen on blood count and continued for 4 months. The patient received unnecessary treatment for disseminated intravascular coagulation (DIC) until the diagnosis of PTCP was established. PTCP is a rare complication but should be considered after TAE for HCC; lack of recognition may lead the physician to misdiagnosis and patient mismanagement.
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9/18. Persistent thrombocytopenia during melanoma treatment with fotemustine.

    Haematological toxicity characterized by delayed and reversible neutropenia and/or thrombocytopenia is an adverse effect observed in 40% of patients receiving fotemustine. We report the case of a 66-year-old man with metastatic malignant melanoma treated with fotemustine as monotherapy. A severe persistent and prolonged thrombocytopenia occurred, so that chemotherapy was discontinued. bone marrow involvement was excluded. The physician should be aware of this prolonged thrombocytopenia secondary to fotemustine, so that it may be recognized early and not attributed erroneously to tumour evolution. This observation could be substantial for the design of combination regimens with fotemustine and other myelotoxic drugs in pretreated melanoma patients.
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10/18. A review of carbamazepine's hematologic reactions and monitoring recommendations.

    Early case reports of fatal hematologic effects attributed to carbamazepine (CBZ) resulted in extensive monitoring recommendations by the manufacturer. The rarity of blood dyscrasias led many authors to question the manufacturer's guidelines. Thus the manufacturer removed specific monitoring guidelines, allowing physicians to monitor CBZ using their clinical judgment. This article reviews case reports and studies of CBZ's hematologic effects. Due to their rapid onset, daily laboratory checks would be necessary to monitor for aplastic anemia, agranulocytosis, and thrombocytopenia. These adverse effects are best monitored by informing patients and physicians to carefully watch for signs and symptoms. leukopenia develops more slowly, occurring in approximately 12 percent of children and 7 percent of adults. Its onset is typically within the first three months of treatment, with patients at risk having a low or low-normal pretreatment white blood cell (WBC) count. leukopenia often reverses, even if CBZ is continued. Based upon our review of the literature, we recommend monitoring of those high-risk patients during the first three months of treatment with the frequency being determined by results of each laboratory value. WBC counts less than 3000/mm3 or neutrophil counts below 1000/mm3 warrant a decrease in dose with frequent monitoring or CBZ discontinuation, if necessary.
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