Shimomura Takahito, Nakajima Tomoki, Nakashima Toshiaki, Morimoto Yasutaka, Yamaoka Junko, Shibuya Akiko, Ohno Tomoyuki, Yoshida Norimasa, Kishimoto Mitsuo, Konishi Eiichi, Tanaka Hideo, Moriguchi Michihisa, Itoh Yoshito
Department of Internal Medicine, Saiseikai Kyoto Hospital, Nagaoka-Kyo, Japan.
Department of Pathology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Case Rep Gastroenterol. 2021 Feb 18;15(1):232-243. doi: 10.1159/000512420. eCollection 2021 Jan-Apr.
A 79-year-old man presented with high fever, marked eosinophilia, altered biochemical liver function tests (LFT) with predominance of biliary enzymes, and severe wall thickening of the gallbladder. Magnetic resonance cholangiopancreatography (MRCP) suggested cholecystitis, without signs of biliary strictures. Laparoscopic cholecystectomy and exploratory liver excision revealed eosinophilic cholangitis and cholecystitis, complicated with hepatitis and portal phlebitis. Prednisolone monotherapy rapidly improved peripheral eosinophilia, but not LFT. Liver biopsy showed that infiltrating eosinophils were replaced by lymphocytes and plasma cells. Treatment with ursodeoxycholic acid improved LFT abnormalities. Nevertheless, after 2 months, transaminase-dominant LFT abnormalities appeared. Transient prednisolone dose increase improved LFT, but biliary enzymes' levels re-elevated and jaundice progressed. The second and third MRCP within a 7-month interval showed rapid progression of biliary stricture. The repeated liver biopsy showed lymphocytic, not eosinophilic, peribiliary infiltration and hepatocellular reaction to cholestasis. Eighteen months after the first visit, the patient died of hepatic failure. Autopsy specimen of the liver showed lymphocyte-dominant peribiliary infiltration and bridging fibrosis due to cholestasis. Though eosinophil-induced biliary damage was an initial trigger, repeated biopsy suggested that lymphocytes played a key role in progression of the disease. Further studies are needed to elucidate the relationship between eosinophils and lymphocytes in eosinophilic cholangitis.
一名79岁男性,表现为高热、明显嗜酸性粒细胞增多、以胆汁酶为主的生化肝功能检查(LFT)异常,以及胆囊壁严重增厚。磁共振胰胆管造影(MRCP)提示胆囊炎,无胆管狭窄迹象。腹腔镜胆囊切除术及 exploratory liver excision(此处“exploratory liver excision”可能有误,推测可能是“肝脏探查性切除术”之类的表述,暂按此翻译)显示嗜酸性胆管炎和胆囊炎,并伴有肝炎和门静脉炎。泼尼松龙单药治疗迅速改善了外周嗜酸性粒细胞增多,但未改善肝功能。肝脏活检显示浸润的嗜酸性粒细胞被淋巴细胞和浆细胞取代。熊去氧胆酸治疗改善了肝功能异常。然而,2个月后,以转氨酶为主的肝功能异常出现。短暂增加泼尼松龙剂量改善了肝功能,但胆汁酶水平再次升高且黄疸进展。在7个月内进行的第二次和第三次MRCP显示胆管狭窄迅速进展。重复肝脏活检显示胆管周围淋巴细胞浸润而非嗜酸性粒细胞浸润,以及肝细胞对胆汁淤积的反应。首次就诊18个月后,患者死于肝衰竭。肝脏尸检标本显示胆管周围以淋巴细胞为主的浸润以及胆汁淤积导致的桥接纤维化。尽管嗜酸性粒细胞诱导的胆管损伤是初始触发因素,但重复活检表明淋巴细胞在疾病进展中起关键作用。需要进一步研究以阐明嗜酸性胆管炎中嗜酸性粒细胞与淋巴细胞之间的关系。