S5669 Delayed FOLFOX-Associated Sinusoidal Obstruction Syndrome (SOS) in a Patient With Non-Metastatic Stage IIC Colorectal Adenocarcinoma: A Case Report

Introduction: Oxaliplatin is causally linked to the development and exacerbation of sinusoidal obstruction syndrome, which can precipitate or worsen portal hypertension. In this case, we report a delayed SOS secondary to oxaliplatin based chemotherapy in a patient with non-metastatic colorectal cancer. Case Description/Methods: A 48-year-old woman with stage IIC (T4bN0M0) colorectal adenocarcinoma underwent proctosigmoidectomy followed by 12 cycles of adjuvant FOLFOX. She had no hepatic metastases at diagnosis. After treatment, she reported weight gain, reflux symptoms, and joint pain. Surveillance imaging showed mild hepatic steatosis and borderline splenomegaly. One year later, labs showed mild transaminase elevation (AST: 37, ALT: 53) and normal bilirubin. Repeat computed tomography (CT) scan showed new recanalization of the umbilical vein, raising concern for portal hypertension. Magnetic resonance imaging confirmed a recanalized paraumbilical vein without other signs of portal hypertension or metastasis. EGD was unremarkable except for mild gastritis. On endoscopic ultrasound, the mean hepatic vein pressure was elevated (14 mmHg), the mean portal vein pressure was mildly elevated (12 mmHg) and there was a normal portal-systemic pressure gradient (-2 mmHg). Eventually, liver biopsy showed centrilobular congestion, hepatocellular collapse and prominent portal veins suggestive of a vascular pattern of injury. Even though complete obliteration of central veins was not seen, findings were consistent with SOS due to the patient's clinical history and chemotherapy. Discussion: This case highlights the delayed onset of oxaliplatin-associated SOS in a patient without liver metastases. SOS typically presents with hepatomegaly, transaminase elevation, and features of portal hypertension, but radiologic and histologic findings may precede clinical signs. In this case, imaging revealed a spontaneous portosystemic shunt (SPSS) and sinusoidal changes prior to overt portal hypertension. The absence of portal systemic gradient elevation is mostly due to decompression through the SPSS. This case underscores the importance of long-term hepatic surveillance in colorectal cancer patients treated with oxaliplatin, even in the absence of metastatic disease. The absence of liver metastases in our patient suggests that direct oxaliplatin-induced endothelial toxicity was the primary driver of SOS, rather than tumor-related hepatic remodeling.