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Intracranial Bleeding (intracranial + bleeding)

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Medical Sciences	91%

Selected Abstracts

Successful unrelated cord blood transplantation in a 7-year-old boy with Evans syndrome refractory to immunosuppression and double autologous stem cell transplantation

EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 6 2006
Christian Urban
Abstract:, Evans syndrome is an autoimmunopathy characterized by thrombocytopenia and autoimmune hemolytic anemia with poor response to immunosuppression. A 2-yr-old boy with Evans syndrome showed only short-lasting responses to immunosuppressive treatment including double autologous peripheral stem cell transplantation (SCT). Intracranial bleeding required emergency splenectomy and external ventricular drainage. Unrelated umbilical cord blood was given following conditioning with busulfan, thiotepa, etoposide and antithymocyte globulin. One year after SCT the patient shows stable blood counts without immunosuppression. This is the first child reported with Evans syndrome successfully treated by means of unrelated cord blood transplantation. [source]

Tissue-specific expression of Cre recombinase from the Tgfb3 locus

GENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 2 2008
Liang-Tung Yang
Abstract Tgfb3, a member of the TGF-, superfamily, is tightly regulated, both spatially and temporally, during embryogenesis. Previous mouse knockout studies have demonstrated that Tgfb3 is absolutely required for normal palatal fusion and pulmonary development. We have generated a novel tool to ablate genes in Tgfb3 -expressing cells by targeting the promoterless Cre-pgk-Neo cassette into exon 1 of the mouse Tgfb3 gene, which generates a functionally null Tgfb3 allele. Using the Rosa26 reporter assay, we demonstrate that Cre -induced recombination was already induced at embryonal day 10 (E10) in the ventricular myocardium, limb buds, and otic vesicles. At E14, robust recombination was detected in the prefusion palatal epithelium. Deletion of the TGF-, type I receptor Alk5 (Tgfbr1) specifically in Tgfb3 expressing cells using the Tgfb3-Cre driver line lead to a cleft palate phenotype similar to that seen in conventional Tgfb3 null mutants. In addition, Alk5/ Tgfb3-Cre mice displayed hydrocephalus, and severe intracranial bleeding due to germinal matrix hemorrhage. genesis 46:112,118, 2008. © 2008 Wiley-Liss, Inc. [source]

Central venous catheter-related thrombosis after replacement therapy for intracranial bleeding in a patient with afibrinogenaemia

HAEMOPHILIA, Issue 1 2008
T. MATSUMOTO
First page of article [source]

Tyr2105Cys mutation in exon 22 of FVIII gene is a risk factor for the development of inhibitors in patients with mild/moderate haemophilia A

HAEMOPHILIA, Issue 4 2006
M. FRANCHINI
Summary., We report the case of a patient with mild haemophilia A, due to a Tyr2105Cys mutation in exon 22 of the C1 domain, who developed a high-titre factor VIII inhibitor (maximum titre 1600 BU) with recurrent severe haemorrhages and fatal intracranial bleeding. Based on published data, it appears that although this mutation occurs rarely in patients with mild or moderate haemophilia A, it is frequently associated with the development of high-titre inhibitors. [source]

Spontaneous intracranial bleeding in two patients with congenital afibrinogenaemia and the role of replacement therapy

HAEMOPHILIA, Issue 6 2000
R. Parameswaran
Congenital afibrinogenaemia and hypofibrinogenaemia are rare disorders of haemostasis. In this case report the problems posed in the management of two patients with fibrinogen levels less than 0.1 g L,1 and who developed intracranial bleeding are considered. The value of fibrinogen concentrate and the role of prophylaxis is also discussed. [source]

Stromelysin-1 (MMP-3) is critical for intracranial bleeding after t-PA treatment of stroke in mice

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2007
Y. SUZUKI
Summary.,Background:,Tissue-type plasminogen activator (t-PA) is approved for treatment of ischemic stroke patients, but it may increase the risk of intracranial bleeding (ICB). Matrix metalloproteinases (MMPs), which can be activated through the plasminogen/plasmin system, may contribute to ICB after ischemic stroke. Objectives:,To explore the contribution of plasminogen, MMP-3 and MMP-9 to ICB associated with t-PA treatment after ischemic stroke. Methods:,Using a thrombotic middle cerebral artery occlusion (MCA-O) model, ICB was studied in mice with genetic deficiencies of plasminogen (Plg,/,), stromelysin-1 (MMP-3,/,), or gelatinase B (MMP-9,/,) and their corresponding wild-type (WT) littermates. The induction of MMP-3 and MMP-9 was also studied in C57BL/6 WT mice. Results:,ICB induced by t-PA (10 mg kg,1) was significantly less than WT in Plg,/, (P < 0.05) and MMP-3,/, (P < 0.05) but not in MMP-9,/, mice. Furthermore, administration of the broad-spectrum MMP inhibitor GM6001 after t-PA treatment reduced ICB significantly (P < 0.05) in MMP-3+/+ mice, but had no effect on MMP-3,/, mice. MMP-3 expression was significantly enhanced at the ischemic hemisphere; with placebo treatment, it was expressed only in neurons, whereas it was up-regulated in endothelial cells with t-PA treatment. Although MMP-9 expression was also significantly enhanced at the ischemic brain, the amount and the distribution were comparable in mice with and without t-PA treatment. Conclusions:,Our data with gene-deficient mice thus suggest that plasminogen and MMP-3 are relatively more important than MMP-9 for the increased ICB induced by t-PA treatment of ischemic stroke. [source]

Prevention of venous thromboembolism after acute ischemic stroke

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 6 2005
P. W. KAMPHUISEN
Summary., Venous thromboembolism (VTE) is a common complication after acute ischemic stroke. When screened by 125I fibrinogen scanning or venography, the incidence of deep-vein thrombosis (DVT) in stroke patients is comparable with that seen in patients undergoing hip or knee replacement. Most stroke patients have multiple risk factors for VTE, like advanced age, low Barthel Index severity score or hemiplegia. As pulmonary embolism is a major cause of death after acute stroke, the prevention of this complication is of crucial importance. Prospective trials have shown that both unfractionated heparin (UFH) and low molecular weight heparin (LMWH) are effective in reducing DVT and pulmonary embolism in stroke patients. Current guidelines recommend the use of these agents in stroke patients with risk factors for VTE. Some clinicians are concerned that the rate of intracranial bleeding associated with thromboprophylaxis may outweigh the benefit of prevention of VTE. Low-dose LMWH and UFH seem, however, safe in stroke patients. Higher doses clearly increase the risk of cerebral bleeding and should be avoided for prophylactic use. Both aspirin and mechanical prophylaxis are suboptimal to prevent VTE. Graduated compression stockings should be reserved to patients with a clear contraindication to antithrombotic agents. [source]

Prophylaxis against thromboembolism in patients with traumatic brain injury: a survey of UK practice

ANAESTHESIA, Issue 8 2001
J. M. Cupitt
Venous thromboembolism is a major complication associated with traumatic brain injury and is responsible for significant morbidity and mortality. There has been a general reluctance over the years to use anticoagulant prophylaxis for patients with head injury who have suffered intracranial bleeding or for whom intracranial surgery is needed. We conducted a postal questionnaire survey of all neurosurgical centres in the United Kingdom, enquiring about the use of thromboprophylactic methods in the management of patients with traumatic brain injury. A diversity of practice and opinion in the use of such methods was evident from the replies received. The survey highlighted concern about the failure to implement even the most simple means of prophylaxis. The evidence for the use of the various methods of prophylaxis is reviewed. [source]

Erlotinib plus bevacizumab in previously treated patients with malignant pleural mesothelioma

CANCER, Issue 4 2008
David M. Jackman MD
Abstract BACKGROUND. We conducted a phase 2, multicenter, open-label study of erlotinib plus bevacizumab in patients with malignant pleural mesothelioma who had previously received 1 prior chemotherapy regimen. These agents have activity in non,small cell lung cancer, but their role in mesothelioma is unclear. The primary endpoint is response rate. Secondary endpoints include time to progression, survival, and toxicity. METHODS. Eligible patients with mesothelioma who had previously received 1 chemotherapy regimen were treated with erlotinib 150 mg per os daily and bevacizumab 15 mg/kg administered intravenously on Day 1 of a 21-day cycle. Treatment continued until disease progression or development of significant toxicity. Tumor response was assessed after every 2 cycles using previously established mesothelioma response criteria from Byrne and Nowak. RESULTS. Twenty-four eligible patients initiated therapy with erlotinib and bevacizumab between February 2004 and October 2006. There were no complete or partial responses, although 12 patients achieved stable disease for at least 2 cycles of treatment. The median time to progression was 2.2 months (95% confidence interval [CI], 1.4 months-5.9 months). The median survival was 5.8 months (95% CI, 2.8 months-10.1 months). The most common toxicities were rash and diarrhea. There were no treatment-related deaths, intracranial bleeding, or hemoptysis. CONCLUSIONS. The combination of erlotinib and bevacizumab was tolerated reasonably well, but there was no evidence of radiographic response. This study demonstrates the feasibility of conducting trials in mesothelioma patients who have failed first-line therapy. More therapeutic studies with effective agents are needed for these patients. Cancer 2008. © 2008 American Cancer Society. [source]

Acute retrobulbar optic neuropathy due to rupture of an anterior communicating artery aneurysm

ACTA OPHTHALMOLOGICA, Issue 1 2006
Catherine Claes
Abstract. Purpose:,The vast majority of ruptured aneurysms of the anterior communicating artery typically present with subarachnoid haemorrhage. Isolated visual complaints are very uncommon in this setting. We present an unusual case of a patient with an acute retrobulbar optic neuropathy, secondary to a ruptured anterior communicating artery aneurysm. Design:,Observational case report. Methods:,A 29-year-old woman was assessed for an acute, isolated unilateral optic neuropathy of unknown origin. Although an initial encephalic MRI was believed to be normal, an underlying ruptured anterior communicating artery aneurysm was eventually diagnosed when the patient became stuporous because of intracranial bleeding. Conclusions:,Occurrence of an acute retrobulbar optic neuropathy may be the initial isolated sign related to a ruptured anterior communicating artery aneurysm, prompting an appropriate neuroradiological assessment. [source]