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Hematology. 2012 Apr;17 Suppl 1:S159-62. doi: 10.1179/102453312X13336169156735.

Thrombosis in stem cell transplantation.

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1
Hacettepe University Institute of Oncology, Hematopoietic Stem Cell Transplantation Unit, Ankara, Turkey. eminkansu47@gmail.com

Abstract

Hemostatic changes and thrombotic events are frequent in patients undergoing stem cell transplantation. Arterial and venous thromboses are major causes of morbidity and mortality. Thrombotic complications can be classified into four groups including: catheter-related thrombosis, venous thromboembolic (VTE) events, sinusoidal obstructive syndrome (SOS)/veno-occlusive disease, and transplant-associated thrombotic microangiopathy (TAM). The incidence of catheter-related thrombosis is 8-20% in patients undergoing autologous hematopoietic stem cell transplantation (HSCT), and the incidence is low in syngeneic and allogeneic transplant patients. Venous duplex Doppler ultrasound, venogram, and computed tomography scan are required to visualize the venous thrombus. The treatment should be aimed at the prevention of pulmonary embolism, the avoidance of thrombus extension, and the preservation of catheter patency. Patients undergoing HSCT may have risk factors for VTE including underlying malignancy, traumatic brain injury, prolonged hospitalization, administration of conditioning regimens, and central venous catheters. Important risk factors are presence of history of VTE and graft-versus-host disease. One-year incidence of symptomatic VTE is 3.7%. SOS, also known as veno-occlusive disease, is a serious liver disease, seen in approximately 50-60% of HSCT patients. The mortality rate from the severe form of SOS is 84.3% and majority of the patients have multi-organ failure. The frequency is quite low after autologous transplantation. Risk factors for SOS include pre-existing hepatic damage, previous high-dose chemotherapy and abdominal irradiation, female gender and donor-recipient human leukocyte antigen disparity. Cyclophosphamide and busulphan are the most common agents with the highest incidence and fatal SOS. Histopathologic features of SOS include dilatation of sinusoids, necrosis of perivenular hepatocytes, and obstruction of small intrahepatic central venules by microthrombi and fibrin deposition. Signs of SOS usually occur within first 30 days after HSCT including hyperbilirubinemia, hepatomegaly, ascites, and weight gain. Symptoms of liver failure, including encephalopathy, coagulopathy, and renal failure will appear in severe form. A hepatic venous pressure gradient above 10 mmHg is highly specific for SOS. Early use of defibrotide has been shown to be effective in the treatment of high-risk SOS. TAM is a distinct, infrequent, and significant life-threatening complication of HSCT. TAM is seen in the range of 0ยท5-76% and was reported to be 10-25% in patients undergoing allogeneic HSCT with a mortality rate around 50%. It can also be seen after autologous HSCT and mainly affects the glomerular capillaries. There has been no standard therapy for TAM. Few case series reported good response to rituximab and high-dose corticosteroids were used with limited success. Trials with complement inhibitors such as eculizumab are currently underway.

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