S5825 Oxaliplatin-Induced Non-Cirrhotic Portal Hypertension (NCPH): A Cause of Gastric Variceal Bleeding

Introduction: Non-cirrhotic portal hypertension (NCPH) is an uncommon but clinically important form of portal hypertension occurring without underlying liver cirrhosis. Oxaliplatin-based chemotherapy, a component of the FOLFOX (leucovorin, fluorouracil, and oxaliplatin) regimen frequently used for colorectal cancer, is a detrimental cause of nodular regenerative hyperplasia (NRH) and subsequent NCPH. This case reveals diagnostic complexities and critical considerations for oxaliplatin-associated NRH presenting as gastric variceal hemorrhage. Case Description/Methods: A 68-year-old woman with a remote history of stage III colon cancer, status-post surgical intervention and 12 cycles of FOLFOX chemotherapy, presented with melena. Her hemoglobin was 6.7 g/dL with a baseline of 13 g/dL just one month prior. Labs revealed a platelet count greater than 150,000, normal coagulation parameters, and normal liver enzyme levels. Computed tomography angiography of the abdomen and pelvis revealed no active gastrointestinal bleeding, but identified a large splenorenal shunt. Duplex ultrasonography showed no evidence of thrombosis within splenic or hepatic vasculature. Prior to admission, the patient had undergone 6 endoscopic evaluations at an outside hospital. Repeat esophagogastroduodenoscopy identified 2 columns of large, isolated type 1 gastric varices with high-risk stigmata, indicating the likely source of melena and anemia. Interventional radiology subsequently performed balloon-occluded retrograde transvenous obliteration, transjugular liver biopsy, and hepatic venous pressure gradient (HVPG) measurements as the patient did not have other complications of portal hypertension. She underwent liver biopsy confirming the diagnosis of NRH without cirrhosis. The HVPG was normal, consistent with portal hypertension secondary to NRH rather than hepatic cirrhosis. Discussion: This case demonstrates deleterious complications of oxaliplatin therapy on the liver, the potential for oxaliplatin-induced NRH to be missed on initial endoscopy, and underscores the value of repeat evaluation for detection of gastric varices. Heightened clinician awareness of oxaliplatin-related liver injury is crucial for risk stratification, surveillance, and management in FOLFOX-treated colorectal cancer survivors.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001150760.11170.09
Primary Topic
Liver Disease and Transplantation
Type
article
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article

S5825 Oxaliplatin-Induced Non-Cirrhotic Portal Hypertension (NCPH): A Cause of Gastric Variceal Bleeding

Nilofar Najafian, Aida Rezaie, Ericka Charley, Sarah Salama
The American Journal of Gastroenterology
Liver Disease and Transplantation
article

S5825 Oxaliplatin-Induced Non-Cirrhotic Portal Hypertension (NCPH): A Cause of Gastric Variceal Bleeding

Nilofar Najafian, Aida Rezaie, Ericka Charley, Sarah Salama
article en

Abstract

Introduction: Non-cirrhotic portal hypertension (NCPH) is an uncommon but clinically important form of portal hypertension occurring without underlying liver cirrhosis. Oxaliplatin-based chemotherapy, a component of the FOLFOX (leucovorin, fluorouracil, and oxaliplatin) regimen frequently used for colorectal cancer, is a detrimental cause of nodular regenerative hyperplasia (NRH) and subsequent NCPH. This case reveals diagnostic complexities and critical considerations for oxaliplatin-associated NRH presenting as gastric variceal hemorrhage. Case Description/Methods: A 68-year-old woman with a remote history of stage III colon cancer, status-post surgical intervention and 12 cycles of FOLFOX chemotherapy, presented with melena. Her hemoglobin was 6.7 g/dL with a baseline of 13 g/dL just one month prior. Labs revealed a platelet count greater than 150,000, normal coagulation parameters, and normal liver enzyme levels. Computed tomography angiography of the abdomen and pelvis revealed no active gastrointestinal bleeding, but identified a large splenorenal shunt. Duplex ultrasonography showed no evidence of thrombosis within splenic or hepatic vasculature. Prior to admission, the patient had undergone 6 endoscopic evaluations at an outside hospital. Repeat esophagogastroduodenoscopy identified 2 columns of large, isolated type 1 gastric varices with high-risk stigmata, indicating the likely source of melena and anemia. Interventional radiology subsequently performed balloon-occluded retrograde transvenous obliteration, transjugular liver biopsy, and hepatic venous pressure gradient (HVPG) measurements as the patient did not have other complications of portal hypertension. She underwent liver biopsy confirming the diagnosis of NRH without cirrhosis. The HVPG was normal, consistent with portal hypertension secondary to NRH rather than hepatic cirrhosis. Discussion: This case demonstrates deleterious complications of oxaliplatin therapy on the liver, the potential for oxaliplatin-induced NRH to be missed on initial endoscopy, and underscores the value of repeat evaluation for detection of gastric varices. Heightened clinician awareness of oxaliplatin-related liver injury is crucial for risk stratification, surveillance, and management in FOLFOX-treated colorectal cancer survivors.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 48%
Liver Disease and Transplantation
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