Successful Treatment of Hepatic Venocclusive Disease in a Bone Marrow Transplant Patient With Side-to-Side Portacaval Shunt

Murray, Jeffrey; LaBrecque, Douglas R.; Gingrich, Roger D.; Pringle, Kevin C.; Mitros, Frank A.

doi:10.1016/0016-5085(87)90985-1

Cited by 29 publications

(3 citation statements)

References 15 publications

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“…15,16 Compared to surgical porta-caval shunts, TIPS may be performed without laparotomy which is associated with the risks of infection in an immunocompromised patient and bleeding due to the coagulopathy. In addition, TIPS reduces the operative stress and the tissue trauma to a minimum.…”

Section: Discussionmentioning

confidence: 99%

Transjugular intrahepatic portosystemic shunt (TIPS) for severe veno-occlusive disease of the liver following bone marrow transplantation

Azoulay

Castaing

Lemoine

et al. 2000

Bone Marrow Transplant

113

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Summary:Severe veno-occlusive disease (VOD) of the liver is a leading cause of mortality after bone marrow transplantation (BMT). Vascular and parenchymal injuries account for acute portal hypertension and liver failure is frequently present. We describe the results of transjugular intrahepatic portosystemic shunt (TIPS) for the management of VOD after BMT. TIPS was performed in 10 patients with histologically proven severe VOD. Portal hypertension was controlled by TIPS in all patients (mean hepatic venous pressure gradient before, 20 ؎ 11 vs 6 ؎ 5 mm Hg after TIPS, P Ͻ 0.01) without technical complications. Five patients with rapidly worsening VOD died within 10 days of TIPS without any improvement. The five remaining patients with less advanced disease showed improvement in various clinical and biological parameters. Four patients subsequently died. The lone survivor continues to do well with resolution of VOD 6 months after TIPS. TIPS can be performed safely and controls portal hypertension in VOD after BMT. Arguments from the present series and from eight previously reported cases favour earlier application of TIPS to obtain improved overall survival. Bone Marrow Transplantation (2000) 25, 987-992. Keywords: veno-occlusive disease of the liver; bone marrow transplantation; transjugular intrahepatic portosystemic shunt Veno-occlusive disease (VOD) of the liver complicates bone marrow transplantation (BMT) in 1-2% to 64% of cases depending on the intensity of conditioning regimens, individual pharmacokinetic metabolism of antineoplastic drugs, indication for transplantation, type of marrow donor, and certain risk factors such as pretransplant hepatitis and fever (for review see Ref. 1). VOD post BMT is the main cause of dose-limiting toxicity in high-dose radio-chemotherapy conditioning regimens for BMT, and subsequently one of the three leading causes of transplantation-related death together with graft-versus-host disease and infections in bone marrow recipients.2 In Western countries, approxi-

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Section: Discussionmentioning

confidence: 99%

Transjugular intrahepatic portosystemic shunt (TIPS) for severe veno-occlusive disease of the liver following bone marrow transplantation

Azoulay

Castaing

Lemoine

et al. 2000

Bone Marrow Transplant

113

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“…Two patients with SOS underwent successful portosystemic shunts for persistent ascites, but liver dysfunction had resolved long before these shunts were placed. 181,182 Peritoneovenous shunts for intractable ascites have been unsuccessful. Eleven patients have received liver transplants for severe SOS, 165,[183][184][185][186][187][188][189] four of whom were midterm survivors.…”

Section: Surgical Approachesmentioning

confidence: 99%

Toxic Injury to Hepatic Sinusoids: Sinusoidal Obstruction Syndrome (Veno-Occlusive Disease)

DeLeve¹,

Shulman²,

McDonald³

2002

Semin Liver Dis

614

396

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The term veno-occlusive disease of the liver refers to a form of toxic liver injury characterized clinically by the development of hepatomegaly, ascites, and jaundice, and histologically by diffuse damage in the centrilobular zone of the liver. The cardinal histologic features of this injury are marked sinusoidal fibrosis, necrosis of pericentral hepatocytes, and narrowing and eventual fibrosis of central veins. Recent studies suggest that the primary site of the toxic injury is sinusoidal endothelial cells, followed by a series of biologic processes that lead to circulatory compromise of centrilobular hepatocytes, fibrosis, and obstruction of liver blood flow. Thus we propose a more appropriate name for this form of liver injury--sinusoidal obstruction syndrome. This review encompasses historical perspectives, clinical manifestations of sinusoidal obstruction syndrome in the setting of hematopoietic cell transplantation, histologic features of centrilobular injury, and a discussion of the pathophysiology of sinusoidal injury, based on both animal and clinical investigations.

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“…Liver transplantation, although effective in some patients, 40,41 is limited by the availability of a suitable donor liver. Surgical 42,43 or transjugular [44][45][46] venous shunting in the treatment of VOD are promising, but invasive techniques in these patients at high risk of bleeding. Earlier intervention, and perhaps combinations of effective agents with differing mechanisms of action are worthy approaches to future investigations for treating patients with hepatic RRT.…”

Section: Discussionmentioning

confidence: 99%

Does early treatment with high-dose methylprednisolone alter the course of hepatic regimen-related toxicity?

Khoury

Adkins

Brown

et al. 2000

Bone Marrow Transplant

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Summary:Hepatic regimen-related toxicity (RRT) is a serious complication of stem cell transplantation. Cytokine activation may be involved in the pathogenesis. Corticosteroids are potent inhibitors of cytokine production, and, therefore could play a role in the treatment of hepatic RRT. Between January 1994 and June 1998, 28 of 782 consecutive transplant patients (3.6%) developed hepatic RRT (20 veno-occlusive disease (VOD) and eight liver dysfunction of uncertain etiology (LDUE) as defined by Seattle criteria), and were treated with highdose methylprednisolone (MP, 500 mg/m 2 i.v. every 12 h for six doses), initiated upon increase in serum total bilirubin to у4 mg/dl. Other causes of liver dysfunction were excluded. Response to therapy with high-dose MP was defined as reduction in total bilirubin by 50% within 10 days of initiation of MP. Overall, 17 patients (61%) responded to treatment (12 patients with VOD, five patients with LDUE). The bilirubin in responding patients decreased from a mean of 8.6 mg/dl (range, 4-17.9) at the start of MP to 4.1 mg/dl (range, 0.5-17.9) 10 days later. There were no statistically significant differences between responders and non-responders in the day treatment with high-dose MP was initiated (P = 0.38), total serum bilirubin (P = 0.17) and percent weight gain at the time high-dose MP was started (P = 0.10) or the calculated probability of fatal outcome from VOD (18% for responders, 23% for non-responders; P = 0.30). A lower pre-transplant DLCOc was observed among non-responders (P = 0.04). At 100 days posttransplant, hepatic RRT resolved in all 13 survivors who responded to high-dose MP, and in one nonresponding patient. No serious toxicities due to highdose MP were observed. We conclude that resolution of hepatic RRT occurred in the majority of patients treated with high-dose MP in this study; however, randomized controlled trials are required to determine the efficacy of high-dose MP for treatment of hepatic RRT. Bone Marrow Transplantation (2000) 25, 737-743.

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Successful Treatment of Hepatic Venocclusive Disease in a Bone Marrow Transplant Patient With Side-to-Side Portacaval Shunt

Cited by 29 publications

References 15 publications

Transjugular intrahepatic portosystemic shunt (TIPS) for severe veno-occlusive disease of the liver following bone marrow transplantation

Transjugular intrahepatic portosystemic shunt (TIPS) for severe veno-occlusive disease of the liver following bone marrow transplantation

Toxic Injury to Hepatic Sinusoids: Sinusoidal Obstruction Syndrome (Veno-Occlusive Disease)

Does early treatment with high-dose methylprednisolone alter the course of hepatic regimen-related toxicity?

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