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Acute Cellular Rejection Resulting in Sinusoidal Obstruction Syndrome and Ascites Postliver Transplantation Publisher Pubmed



Sanei MH1 ; Schiano TD2 ; Sempoux C3 ; Fan C4 ; Fiel MI5
Authors
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Authors Affiliations
  1. 1. Department of Pathology, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY, United States
  3. 3. Department of Pathology, Cliniques Universitaires Saint-Luc, Louvain Medical School, Brussels, Belgium
  4. 4. Department of Pathology, North-Shore Long Island Jewish Health System, New Hyde Park, NY, United States
  5. 5. Department of Pathology, Mount Sinai Medical Center, Box 1194, New York, NY 10029, 1468 Madison Avenue, United States

Source: Transplantation Published:2011


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. © 2011 Lippincott Williams & Wilkins.
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