Ruptured Metastatic Liver Tumor from an α-fetoprotein-producing Gastric Cancer

We describe a patient with a ruptured and rapidly enlarging secondary tumor of the liver metastasized from an α-fetoprotein (AFP)-producing gastric cancer. The ruptured liver metastasis was successfully treated by transarterial embolization (TAE) followed by hepatic resection. A 65-year-old woman was admitted to our hospital with residual gastric cancer. No liver metastasis was detected by preoperative computed tomography (CT), or ultrasonography, and total gastrectomy was performed. Microscopically, the tumor was a poorly differentiated adenocarcinoma invading no deeper than the subserosa, with positive staining for AFP and positive staining for Ki67 in approximately 80% of the tumor cells. Severe venous and lymphatic involvements were evident. The serum AFP level was 100 ng/ml at 3 weeks after the total gastrectomy, but decreased to 16 ng/ml by the end of postoperative month 3. At 6 months, the patient was referred and readmitted to our hospital with sudden severe pain in the upper abdomen. She was admitted in a state of shock with laboratory findings of anemia. A liver tumor surrounded by effusion was detected in segment 8 and diagnosed as a ruptured liver metastasis. Emergency arteriography revealed a large hypervascular tumor, and a TAE performed promptly thereafter was successful in improving the blood pressure. A second TAE was performed 2 months after first TAE due to a dramatic elevation of serum AFP to 180,000 ng/ml. The second TAE decreased the patient's serum AFP to 2,200 ng/ml, but the level remained in the abnormal range. A right hepatectomy was performed after confirming the absence of other detectable metastatic tumors. The resected specimen contained a well-defined tumor, measuring 6×6 cm that appeared almost necrotic under microscope. Over the 6 years since the hepatectomy, no recurrence has appeared and serum AFP has remained within the normal range.