S5916 Hepatic Sinusoidal Obstruction Syndrome Induced by FOLFOX Chemotherapy in a Lynch Syndrome Patient With Rectal Cancer Presenting With Anemia

Introduction: Hepatic Sinusoidal Obstruction Syndrome (HSOS) is a rare condition where sinusoidal endothelial cell damage causes obstruction of veins in the liver leading to congestion, cell damage, and liver dysfunction. HSOS is commonly seen as a complication of chemotherapy, particularly with agents like oxaliplatin (OXA). The pathogenesis of OXA-induced HSOS is likely due to oxidative stress, inflammation, and fibrosis. We present a case of HSOS in a patient with stage III rectal cancer with underlying Lynch syndrome highlighting diagnostic challenges and implications for surveillance. Case Description/Methods: A 25-year-old woman with stage III rectal adenocarcinoma who completed neoadjuvant chemoradiation with 6 cycles of 5-fluorouracil prior to 12 rounds of folinic acid, fluorouracil, and oxaliplatin. Biopsy with genetic testing later showed MLH1 and PMS2 gene mutations, confirming Lynch syndrome. She subsequently underwent colectomy with low colorectal anastomoses along with prophylactic hysterectomy, salpingo-oophorectomy and posterior vaginal wall removal. Patient later presented with anemia with hemoglobin level of 4.9. Subsequent esophagogastroduodenoscopy demonstrated bleeding esophageal varices. Liver biopsy was done due to suspected cirrhosis and showed sinusoidal dilation and periportal hepatocyte necrosis, suggestive of sinusoidal obstructive syndrome. Although no evidence of shrunken central veins or congested sinusoids, which would provide stronger evidence of OXA-induced HSOS, patient continues to undergo surveillance for her esophageal varices with repeated need for banding secondary to portal hypertension in the setting of HSOS. Discussion: Patients with HSOS often present with symptoms of liver failure such as jaundice, hepatomegaly, and ascites. Diagnosis is made using clinical criteria such as the modified Seattle criteria. Treatment involves cessation of the causative drug and treatment of complications related to portal hypertension. This case highlights a serious adverse drug reaction (ADR) associated with OXA. OXA-induced HSOS is a potentially fatal complication of chemotherapy in obstruction of venous outflow, hepatic congestion, and liver dysfunction. Early recognition is crucial for management. Gastroenterologists must be cognizant of this ADR as timely intervention is critical to preventing irreversible hepatic damage and avoid complications related to portal hypertension that may require long-term surveillance.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001151124.67982.a9
Primary Topic
Hematopoietic Stem Cell Transplantation
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article
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article

S5916 Hepatic Sinusoidal Obstruction Syndrome Induced by FOLFOX Chemotherapy in a Lynch Syndrome Patient With Rectal Cancer Presenting With Anemia

The American Journal of Gastroenterology
Hematopoietic Stem Cell Transplantation
article

S5916 Hepatic Sinusoidal Obstruction Syndrome Induced by FOLFOX Chemotherapy in a Lynch Syndrome Patient With Rectal Cancer Presenting With Anemia

article en

Abstract

Introduction: Hepatic Sinusoidal Obstruction Syndrome (HSOS) is a rare condition where sinusoidal endothelial cell damage causes obstruction of veins in the liver leading to congestion, cell damage, and liver dysfunction. HSOS is commonly seen as a complication of chemotherapy, particularly with agents like oxaliplatin (OXA). The pathogenesis of OXA-induced HSOS is likely due to oxidative stress, inflammation, and fibrosis. We present a case of HSOS in a patient with stage III rectal cancer with underlying Lynch syndrome highlighting diagnostic challenges and implications for surveillance. Case Description/Methods: A 25-year-old woman with stage III rectal adenocarcinoma who completed neoadjuvant chemoradiation with 6 cycles of 5-fluorouracil prior to 12 rounds of folinic acid, fluorouracil, and oxaliplatin. Biopsy with genetic testing later showed MLH1 and PMS2 gene mutations, confirming Lynch syndrome. She subsequently underwent colectomy with low colorectal anastomoses along with prophylactic hysterectomy, salpingo-oophorectomy and posterior vaginal wall removal. Patient later presented with anemia with hemoglobin level of 4.9. Subsequent esophagogastroduodenoscopy demonstrated bleeding esophageal varices. Liver biopsy was done due to suspected cirrhosis and showed sinusoidal dilation and periportal hepatocyte necrosis, suggestive of sinusoidal obstructive syndrome. Although no evidence of shrunken central veins or congested sinusoids, which would provide stronger evidence of OXA-induced HSOS, patient continues to undergo surveillance for her esophageal varices with repeated need for banding secondary to portal hypertension in the setting of HSOS. Discussion: Patients with HSOS often present with symptoms of liver failure such as jaundice, hepatomegaly, and ascites. Diagnosis is made using clinical criteria such as the modified Seattle criteria. Treatment involves cessation of the causative drug and treatment of complications related to portal hypertension. This case highlights a serious adverse drug reaction (ADR) associated with OXA. OXA-induced HSOS is a potentially fatal complication of chemotherapy in obstruction of venous outflow, hepatic congestion, and liver dysfunction. Early recognition is crucial for management. Gastroenterologists must be cognizant of this ADR as timely intervention is critical to preventing irreversible hepatic damage and avoid complications related to portal hypertension that may require long-term surveillance.

The American Journal of GastroenterologyVol. 120(10S2)
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Hematopoietic Stem Cell Transplantation
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