A 63-year-old man visited our hospital because he was undergoing treatment of hepatocellular carcinoma (HCC) in 2007. Multinodular HCC had been detected, and he had been treated 8 times with transcatheter arterial chemoembolization and twice with radiofrequency ablation. In addition, he received endoscopic variceal ligation (EVL) and endoscopic injection therapy due to esophageal varices. Three years after commencing treatment, the patient represented with melena. Bleeding esophageal varices were diagnosed and EVL was performed. At this time, abdominal CT demonstrated multinodular-type HCC in both lobes of the liver, with tumor thrombi in the portal vein. Follow-up upper endoscopy revealed a post-EVL ulcer at the esophagogastric junction (Figure 1). Two months later, upper endoscopy was performed due to slight progression of anemia. Endoscopic examination showed two whitish polypoid masses at the site of EVL (Figure 2a), and a submucosal tumor-like protrusion was recognized on the oral side of the polypoid lesions (Figure 2b). Biopsy specimens obtained from the polypoid mass showed a tumor that was histologically consistent with HCC (Figure 3a) and that was focal positive staining for alphafetoprotein (Figure 3b) and glypican-3 (Figure 3c). After biopsy specimens were taken, argon plasma coagulation was performed at the biopsy site. The patient died of progressive hepatic failure one month later.

HCC is a common malignancy worldwide and extrahepatic metastasis in patients with HCC occurs frequently, in 30–75% of patients. Gastrointestinal involvement is seldom found, in only 4–12% of cases in autopsy series, whereas it has been reported that premortem-diagnosed gastrointestinal tract involvement is found in 0.5–2% of cases. The most commonly involved site was the duodenum, followed by the stomach, the colon, and the jejunum.

Portal blood flow can be reversed by increased intrahepatic resistance and arteriovenous communications in patients with liver cirrhosis associated with HCC, which may cause retrograde metastasis of HCC via the portal system. There are two different hypotheses concerning the way HCC metastasizes to the esophagus: either by direct invasion of the gastrointestinal tract via contiguation between the serosal side of a liver tumor and the esophagus, or via the hematogenous spread of tumor emboli infiltrating via the portal vein system and being disseminated by hepatofugal portal blood flow to the esophagus.

In our patient, the therapy for esophageal varices may have caused the esophageal metastasis of HCC. Tumor emboli in the portal system may have been trapped at the site where the variceal bloodstream was interrupted by EVL, and the metastatic tumor then could have grown and broken through the ulcer base due to EVL. The metastatic tumor from HCC in the esophagus showed a rapid increase in size, and it changed to the appearance of a submucosal mass. As the tumor size increased further, the shape of the esophageal metastasis appeared to change from a submucosal mass to a polypoid mass.

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