P1889 - Hepatic Sinusoidal Obstruction Syndrome: A Rare Occurrence After R-CHOP Therapy

Abdul Ahad Ehsan Sheikh, MD¹, Fouzia Oza, MD¹, Mladen Jecmenica, MD¹, Kalmen Feinberg, MD^2
1Wright Center for GME, Scranton, PA; ²Commonwealth Health Regional Hospital of Scranton, Scranton, PA

Introduction: Hepatic sinusoidal obstruction syndrome (HSOS) is a life-threatening disease that can cause blockage of the terminal hepatic venules. It is known to commonly occur after hematopoietic stem cell transplantation (HSCT). Herein, we present a rare case of HSOS after R-CHOP therapy.

Case Description/Methods: A 76-year-old female with a history of non-Hodgkin’s lymphoma presented with generalized weakness, jaundice, and nausea for 2 weeks. She underwent R-CHOP therapy 4 months ago. On presentation lab work showed elevated LFTs and deranged PT/INR and negative hepatitis panel. Ultrasound of the abdomen revealed a normal-sized common bile duct. MRCP revealed cholelithiasis without evidence of intrahepatic or extrahepatic biliary dilatation. A liver biopsy was done which showed portal tracts exhibiting varying degrees of fibrosis including peri hepatocytic fibrosis. It also showed Zone 3 sinusoidal dilatation and focal peri hepatocytic necrosis with congestion suggestive of HSOS.

Discussion: HSOS is caused by activation of and subsequent damage to sinusoidal endothelial cells (SECs) of the acinar zone, resulting in hepatic sinusoidal obstruction. While this complication is well known to occur with HSCT, patients undergoing chemotherapy have also been reported. Chemotherapy triggers SECs into an activated state, which then causes the following cascade of events. There is continual cytokine production which causes SEC damage and subsequent swelling of these cells. HSOS ensues when there is a progressive loss of intracellular nitric oxide and glutathione. This is followed by increased production of vascular endothelial growth factor, intrahepatic matrix metalloproteinases, and clotting factors, leading to obstruction of the sinusoids with cellular debris. Our patient received R-CHOP therapy which comprises Rituxan, cyclophosphamide (CPA), doxorubicin, vincristine, and prednisone. CPA metabolites can cause depletion of glutathione levels, initiating the cascade as described above. Doxorubicin can cause direct toxic injury from its metabolic byproducts in the liver. While there is data on certain chemotherapeutic agents such as oxaliplatin [1] causing this disorder, there is scarce data on the association of R-CHOP and HSOS making our case very unique. Hence, HSOS should be kept in the differentials as a potential complication after R-CHOP therapy.

1. Liu F et al. Oxaliplatin-induced hepatic sinusoidal obstruction syndrome in a patient with gastric cancer: A case report. Mol Clin Oncol. 2018;8(3):453-456.

Disclosures:


Abdul Ahad Ehsan Sheikh, MD¹, Fouzia Oza, MD¹, Mladen Jecmenica, MD¹, Kalmen Feinberg, MD². P1889 - Hepatic Sinusoidal Obstruction Syndrome: A Rare Occurrence After R-CHOP Therapy, ACG 2021 Annual Scientific Meeting Abstracts. Las Vegas, Nevada: American College of Gastroenterology.