Acute cellular rejection resulting in sinusoidal obstruction syndrome and ascites postliver transplantation. Academic Article uri icon

Overview

abstract

  • BACKGROUND: The cause of ascites formation postliver transplantation (LT) is multifactorial. Sinusoidal obstruction syndrome (SOS) is a rare cause of ascites post-LT and has been reported to occur as a sequela of acute cellular rejection (ACR). We sought to examine the histologic features of patients developing ascites in the setting of ACR. METHODS: By using the pathology database, we identified five patients with ACR who had ascites and 10 control patients with severe ACR without ascites. Features of SOS such as congestion, central venulitis, and hepatocyte necrosis were scored (zero absent, one mild, two moderate, and three severe) and perivenular fibrosis (zero absent, one mild, two fibrous septa present, three bridging fibrous septa, and four numerous septa with architectural distortion). Rejection activity index (Banff criteria) was determined. Clinical, biochemical and outcome information were obtained from chart review. RESULTS: All five ascites patient had histologic evidence of SOS. Statistical significance was noted between the ascites and control groups for perivenular fibrosis score (3.6 vs. 0.8, P=0.0004), congestion (3 vs. 1.2, P=0.000005), and central venulitis (3 vs. 1.7, P=0.002). All patients in the ascites group required re-LT or died whereas all control patients remain alive. No significant statistical difference was noted with donor age despite the mean being older in the ascites group (52.8 vs. 35.8 years). CONCLUSIONS: ACR resulting in SOS and associated with significant perivenular fibrosis, central venulitis and congestion may be the cause of ascites post-LT and may portend a poor prognosis for recovery.

publication date

  • November 27, 2011

Research

keywords

  • Ascites
  • Graft Rejection
  • Hepatic Veno-Occlusive Disease
  • Liver Transplantation

Identity

Scopus Document Identifier

  • 80855156615

Digital Object Identifier (DOI)

  • 10.1097/TP.0b013e318234119d

PubMed ID

  • 21993182

Additional Document Info

volume

  • 92

issue

  • 10