A surgical resection of metastatic liver lesions from colorectal cancer contributes to an improved prognosis. However, the postoperative recurrence rate remains high, particularly in the residual liver. This is probably the result of the failure to detect small lesions. In the present study, we histologically examined the presence of intrahepatic micrometastases, which are considered to be related to recurrence in the residual liver. Intrahepatic micrometastases were histologically examined in 31 resected specimens of 25 patients undergoing a hepatic resection because of metastasis to the liver from colorectal cancer. Micrometastases were found in 14 of 25 cases (56.0%). They were located in the portal veins, central veins, sinusoid, and bile ducts. The longest distance from the main metastasis was 38.2 (mean 7.5 +/- 8.0) mm. The size of the macrometastases became larger, and the frequency of micrometastases and the distance of micrometastases from macrometastases had a tendency to increase. Continuous invasion of the macrometastases into the micrometastases through the vasculature or bile duct was also observed. These results suggested that some micrometastases observed in the metastatic liver from colorectal cancer were thus seeded from the primary lesions, while other micrometastases originated from the macrometastatic lesions as satellite lesions.
Hepatic micrometastases of the parenchyma adjacent to a macroscopic lesion were detected in 17 of 31 resected liver metastases. Fifty-nine micrometastatic lesions were detected in total; 26 lesions were situated in the portal vein (PV), 22 in the central vein (CV), 5 in the bile duct (BD), and 6 in the sinusoid (SS). A histological study confirmed the direct invasion of the macrometastatic cancer cells into the adjacent PV, CV, BD, and SS. According to the tumor doubling time, the mean diameter of the macrometastases in 19 remnant livers was calculated to have been 0.57 _+ 0.87cm at the time of the primary resection. The 9 calculated diameter of 3 of these 19 macrometastases was found to be less than 0.01cm, the minimum implantable size, indicating that the cancer recurrence in these specimens may have developed from macroscopic metastatic lesions as a satellite, and not from the primary tumor. In 13 patients who received doses of 5250mg or more of 5 fluorouracil (FU) via the hepatic artery, the cumulative disease-free rate 2 years postoperatively was 100%; this value was 47.6% in 11 patients who received less than 5250mg of 5 FU via the hepatic artery, and 0% in 39 patients who received no chemotherapy (P < 0.005). These results suggest that anatomical hepatic resection for satellite lesions, combined with prophylactic hepatic arterial chemotherapy for micrometastases, decreases the recurrence rate of hepatic metastases in the remnant liver.
A surgical resection of metastatic liver lesions from colorectal cancer contributes to an improved prognosis. However, the postoperative recurrence rate remains high, particularly in the residual liver. This is probably the result of the failure to detect small lesions. In the present study, we histologically examined the presence of intrahepatic micrometastases, which are considered to be related to recurrence in the residual liver. Intrahepatic micrometastases were histologically examined in 31 resected specimens of 25 patients undergoing a hepatic resection because of metastasis to the liver from colorectal cancer. Micrometastases were found in 14 of 25 cases (56.0%). They were located in the portal veins, central veins, sinusoid, and bile ducts. The longest distance from the main metastasis was 38.2 (mean 7.5 +/- 8.0) mm. The size of the macrometastases became larger, and the frequency of micrometastases and the distance of micrometastases from macrometastases had a tendency to increase. Continuous invasion of the macrometastases into the micrometastases through the vasculature or bile duct was also observed. These results suggested that some micrometastases observed in the metastatic liver from colorectal cancer were thus seeded from the primary lesions, while other micrometastases originated from the macrometastatic lesions as satellite lesions.
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