Toshihisa Kimura1,2, Takanori Goi3, Shigehiro Yokoi3, Kenji Ohnishi4, Tamotsu Togawa4, Atsushi Iida4, Makoto Ishida5, Yasunori Sato6. 1. Department of Surgery, National Hospital Organization, Tsuruga Medical Center, 33-1, Sakuragaoka, Tsuruga, Fukui, 914-0195, Japan. kimtoshi23@yahoo.co.jp. 2. First Department of Surgery, Faculty of Medicine, University of Fukui, 23-3, Matsuoka Shimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan. kimtoshi23@yahoo.co.jp. 3. First Department of Surgery, Faculty of Medicine, University of Fukui, 23-3, Matsuoka Shimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan. 4. Department of Surgery, National Hospital Organization, Tsuruga Medical Center, 33-1, Sakuragaoka, Tsuruga, Fukui, 914-0195, Japan. 5. Department of Surgery, Tannan Regional Medical Center, 1-2-31, Saburoku-cho, Sabae, Fukui, 916-8515, Japan. 6. Department of Human Pathology, Kanazawa University Graduate School of Medicine, 13-1, Takara-machi, Kanazawa, Ishikawa, 920-8640, Japan.
Abstract
BACKGROUND: Spontaneous regression of hepatocellular carcinoma (HCC) is a rare event, and its clinicopathological features and underlying mechanism are not fully understood. CASE PRESENTATION: An 84-year-old female with hepatitis C virus infection and diabetes mellitus was referred to our hospital for further examination. Abdominal ultrasonography showed a 3.4-cm solid tumor with a heterogeneous irregular center and no fibrous capsule in liver segment 8 (S8). An enhanced computed tomography (CT) scan revealed a tumor in S8 with heterogeneous enhancement in the arterial phase and washed out insufficiently in the portal and equilibrium phase. The enhanced pattern on magnetic resonance imaging was similar to that of CT. Although the imaging findings were not typical for HCC, liver resection (S8) was performed with HCC as the most probable diagnosis. Histopathological examination of the resected specimen showed that the tumor was well to moderately differentiated HCC with unique features. Approximately half of the tumor was composed of well-differentiated HCC that was focally accompanied by dense lymphocyte infiltration. The other half of the tumor was fibrotic tissue that resembled an inflammatory pseudotumor. Several foci of moderately differentiated HCC were scattered within the tumor with a nodule-in-nodule appearance, and the foci totally showed coagulative necrosis. On immunostaining, lymphocytes in the tumor stroma were positive for CD8 and programmed death 1. The expression of programmed death-ligand 1 was observed in carcinoma cells and macrophages specifically within the lymphocyte-rich area of HCC. CONCLUSIONS: We consider this case representative of spontaneous regression of HCC, and the immune response against HCC might contribute to tumor regression, leading to complex histopathological appearances. This case may provide insight into the mechanism of spontaneous regression of HCC.
BACKGROUND: Spontaneous regression of hepatocellular carcinoma (HCC) is a rare event, and its clinicopathological features and underlying mechanism are not fully understood. CASE PRESENTATION: An 84-year-old female with hepatitis C virus infection and diabetes mellitus was referred to our hospital for further examination. Abdominal ultrasonography showed a 3.4-cm solid tumor with a heterogeneous irregular center and no fibrous capsule in liver segment 8 (S8). An enhanced computed tomography (CT) scan revealed a tumor in S8 with heterogeneous enhancement in the arterial phase and washed out insufficiently in the portal and equilibrium phase. The enhanced pattern on magnetic resonance imaging was similar to that of CT. Although the imaging findings were not typical for HCC, liver resection (S8) was performed with HCC as the most probable diagnosis. Histopathological examination of the resected specimen showed that the tumor was well to moderately differentiated HCC with unique features. Approximately half of the tumor was composed of well-differentiated HCC that was focally accompanied by dense lymphocyte infiltration. The other half of the tumor was fibrotic tissue that resembled an inflammatory pseudotumor. Several foci of moderately differentiated HCC were scattered within the tumor with a nodule-in-nodule appearance, and the foci totally showed coagulative necrosis. On immunostaining, lymphocytes in the tumor stroma were positive for CD8 and programmed death 1. The expression of programmed death-ligand 1 was observed in carcinoma cells and macrophages specifically within the lymphocyte-rich area of HCC. CONCLUSIONS: We consider this case representative of spontaneous regression of HCC, and the immune response against HCC might contribute to tumor regression, leading to complex histopathological appearances. This case may provide insight into the mechanism of spontaneous regression of HCC.
Authors: K Takayasu; Y Muramatsu; Y Shima; N Moriyama; T Yamada; T Yoshida; M Makuuchi; K Kishi Journal: Am J Gastroenterol Date: 1986-10 Impact factor: 10.864