Sinus Venous Thrombosis

Bertz, Hartmut; Laubenberger, J; Steinfurth, G; Finke, Jürgen

doi:10.1097/00007890-199807270-00018

Cited by 16 publications

(5 citation statements)

References 23 publications

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“…Thrombocytopenia and micro-angiopathic haemolytic anaemia, which are the essential diagnostic criteria in classical HUS-TTP, may be absent in cyclosporine induced HUS-TTP, and acute renal failure is the principal manifestation [13,14]. Sinus venous thrombosis has been reported in patients after bone marrow transplantation who were on cyclosporine, although TTP was not demonstrated in these patients [15]. Although mild thrombocytopenia was present, our patient had no evidence of microangiopathic haemolytic anaemia, nor was there any evidence of renal involvement resulting from micro-angiopathy, and cyclosporine induced HUS-TTP was hence unlikely.…”

Section: Discussionmentioning

confidence: 99%

A kidney transplant patient on cyclosporine therapy presenting with dural venous sinus thrombosis: a case report

et al. 2009

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Section: Discussionmentioning

confidence: 99%

A kidney transplant patient on cyclosporine therapy presenting with dural venous sinus thrombosis: a case report

et al. 2009

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“…Complications that affect the central nervous system (CNS) can include infection in immunocompromised hosts, cerebrovascular events such as subdural hematoma or stroke, calcineurin-induced CNS neuropathy, and leukoencephalopathy resulting from intrathecal chemotherapy or cranial irradiation [2]. Cerebral venous sinus thrombosis (CVST) is a relatively rare complication after allogeneic HSCT [3,4] and its pathogenesis is still unclear. Here, we describe a patient who developed CVST during immunosuppressive therapy for chronic graft-versus-host disease (GVHD) after allogeneic HCST.…”

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confidence: 99%

“…There was no sinusitis/mastoiditis, oral contraceptive use, or systemic infection in the present patient. The occurrence of CVST following allogeneic HSCT is rare and only six such patients have been described [3,4]. CsA was used in the previous patients as GVHD prophylaxis and was continued after the diagnosis of CVST for a median of 43.5 days (range 25-208 days).…”

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confidence: 99%

“…MR angiography was also useful for diagnosing this complication following allogeneic HSCT in previous reports [3,4]. The consensus treatment for CVST is administration of either intravenous heparin or subcutaneous low molecular weight heparin during the acute phase and an oral vitamin K antagonist (warfarin) during the chronic phase to prevent recurrence [5,6].…”

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Cerebral venous sinus thrombosis after allogeneic stem cell transplantation

et al. 2010

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Neurological complications are an important cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (HSCT) [1]. Complications that affect the central nervous system (CNS) can include infection in immunocompromised hosts, cerebrovascular events such as subdural hematoma or stroke, calcineurin-induced CNS neuropathy, and leukoencephalopathy resulting from intrathecal chemotherapy or cranial irradiation [2]. Cerebral venous sinus thrombosis (CVST) is a relatively rare complication after allogeneic HSCT [3, 4] and its pathogenesis is still unclear. Here, we describe a patient who developed CVST during immunosuppressive therapy for chronic graft-versus-host disease (GVHD) after allogeneic HCST.In August 2007, a 42-year-old Japanese woman was diagnosed as having acute myeloid leukemia. She was transferred to our hospital for allogeneic HSCT in January 2008, after achieving complete remission with combination chemotherapy. In March 2008, the patient underwent allogeneic HSCT from her HLA-identical brother. The pretransplant conditioning regimen consisted of intravenous busulfan (0.8 mg/m 2 9 4/day on days -7, -6, -5, and -4) and cyclophosphamide (60 mg/kg/day on days -3 and -2).She received GVHD prophylaxis with short-term methotrexate (15 mg/m 2 on day 1; and 10 mg/m 2 on days 3 and 6) plus cyclosporin A (CsA) as a continuous infusion at a dose of 3 mg/kg/day. She also received 250 lg/day of granulocyte colony-stimulating factor by continuous infusion from day 1 to promote granulocyte recovery. Her granulocyte count was more than 0.5 9 10 9 /L on day 19 and the platelet count exceeded 20 9 10 9 /L on day 26. Complete engraftment was confirmed on day 22 by fluorescence in situ hybridization analysis using X-and Y-chromosome probes. She developed acute GVHD (grade II) involving the skin on day 26 and was treated with a topical corticosteroid preparation. She was discharged on day 87 without any evidence of GVHD. However, she was re-admitted on day 120 after HSCT because of skin lesions and a decrease of the platelet count. A diagnosis of chronic GVHD with skin lesions (maculopapular rash, sclerotic changes, and abnormal pigmentation) and thrombocytopenia (21 9 10 9 /L) was made, and prednisolone (PSL) was started at a dose of 0.5 mg/kg daily from day 126. Although her skin lesions improved, recovery of the platelet count was not obtained. Bone marrow smear on day 135 revealed hypocellular marrow and a few megakaryocytes. Examination of the clotting profile on day 141 showed the following: her prothrombin time was 65% (normal range 70-130%), the fibrinogen level was 85 mg/dL (normal range 150-450 mg/dL), the FDP level was 31.1 lg/dL (normal range 0-5.0 lg/dL), the D-dimer level was 11.1 lg/dL (normal range 0-1.0 lg/dL), and the thrombomodulin level was 4.0 FU/mL (normal range 0-1.0 FU/mL). Lactate dehydrogenase level was within normal limits and fragmented red cells were not observed. Thrombosis was suspected from the laboratory findings, but deep vein thrombosis was not detected by scree...

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“…For example, patients with hepatic VOD often develop deposition of fibrin in the walls of terminal hepatic venules. 8 In hematopoietic cell transplant patients, large vein thrombosis is an unusual complication 9 and only sporadic cases of portal vein thrombosis, 10 sinus vein thrombosis 11 and superior vena cava thrombosis 12 have been reported. Thrombosis at the site of venous access catheters is more common.…”

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Portal vein thrombosis after hematopoietic cell transplantation: frequency, treatment and outcome

Kikuchi

Rudolph

Murakami

et al. 2002

Bone Marrow Transplant

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Summary:Patients who develop veno-occlusive disease (VOD) of the liver may have low plasma levels of the natural anticoagulants protein C and antithrombin III, but large vessel thromboses are not commonly reported in these patients. We reviewed the records of 1847 consecutive patients for evidence of portal vein thrombosis. Eight patients (0.4%) developed portal vein thrombosis (PVT) at a median of day +28 (range 3-58). All patients had clinical evidence of VOD with ascites, a median total serum bilirubin 11.9 mg/dl, and median weight gain from baseline of 7.9%. Median plasma levels of antithrombin III and protein C were low (36% and 21%, respectively). Four patients with PVT died of severe VOD and multi-organ failure, but PVT did not contribute to death. We conclude that PVT is a rare complication of hematopoietic cell transplant and is associated with hepatic VOD. We speculate that PVT resulted from diminished portal venous flow (related to hepatic sinusoidal obstruction to blood flow) and a hypercoagulable state (related to low circulating antithrombin III and protein C levels). Prognosis depended on the severity of the underlying VOD and not PVT per se, suggesting that treatments directed solely toward dissolution of portal vein thrombi should be used with caution in this setting.

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Sinus Venous Thrombosis

Cited by 16 publications

References 23 publications

A kidney transplant patient on cyclosporine therapy presenting with dural venous sinus thrombosis: a case report

A kidney transplant patient on cyclosporine therapy presenting with dural venous sinus thrombosis: a case report

Cerebral venous sinus thrombosis after allogeneic stem cell transplantation

Portal vein thrombosis after hematopoietic cell transplantation: frequency, treatment and outcome

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