Nakao Kentaro, Tsunoda Akira, Shimizu Yoshinori, Takenaka Koji, Morohara Koji, Suzuki Naoto, Yamazaki Katsuo, Aoki Takeshi, Hoshino Mitsunori, Kusano Mitsuo, Kitadai Eri, Kurihara Toshikazu, Takeuchi Yoshiaki, Imawari Michio
Second Department of Surgery, Showa University School of Medicine, 1-5-8 Hatanodai, Tokyo 146-8666, Japan.
Int J Clin Oncol. 2005 Aug;10(4):281-4. doi: 10.1007/s10147-005-0484-y.
In a 64-year-old man who had been treated with prednisolone (PSL) and 6-mercaptopurine (6MP) for a long period, for ulcerative colitis (UC), hepatocellular carcinoma (HCC) was detected incidentally. The UC was in remission with these medications. After he had been taking these medications for about 8 years, HCC was detected by computed tomography (CT), done for the evaluation of an other disease. Blood chemistry examination results were normal, except that the protein induced by vitamin K antagonist (PIVKA)-II level was 7940 AU/ml. We performed resection of liver segment V. With comparative genomic hybridization, chromosomal aberrations were recognized; these were gains of 1q, 3ptel-21, 8p12, and 22q11.23-22q13.1. Generally, HCC is associated with hepatitis virus infection in most cases, but in this patient, the HCC was not related to hepatitis C virus (HCV) or HBV. It is presumed that this case was related to the immunosuppressive therapy for UC and was associated with the gains of 1q, 3p, and 8p.
一名64岁男性长期接受泼尼松龙(PSL)和6-巯基嘌呤(6MP)治疗溃疡性结肠炎(UC),期间偶然发现肝细胞癌(HCC)。使用这些药物后UC处于缓解期。在服用这些药物约8年后,因评估其他疾病进行计算机断层扫描(CT)时发现了HCC。血液化学检查结果正常,只是维生素K拮抗剂诱导蛋白(PIVKA)-II水平为7940 AU/ml。我们对肝段V进行了切除。通过比较基因组杂交,识别出染色体畸变;这些畸变包括1q、3ptel - 21、8p12和22q11.23 - 22q13.1的增益。一般来说,大多数情况下HCC与肝炎病毒感染有关,但在该患者中,HCC与丙型肝炎病毒(HCV)或乙型肝炎病毒(HBV)无关。推测该病例与UC的免疫抑制治疗有关,并与1q、3p和8p的增益有关。