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Cholecystocolonic fistula: malabsorptive consequences of lost bile acids.

作者信息

Benage D, O'Connor K W

机构信息

Department of Medicine, Indiana University School of Medicine, Indianapolis.

出版信息

J Clin Gastroenterol. 1990 Apr;12(2):192-4.

PMID:2324484
Abstract

A patient with the painless onset of a cholecystocolonic fistula associated with virtually complete common bile duct obstruction due to stones provided a unique opportunity to assess the consequences of prolonged bile acid depletion on the digestion and absorption of nutrients. Over 2 years, the patient insidiously developed steatorrhea, osteomalacia with an atraumatic pelvic fracture, and congestive heart failure complicated by polymorphic ventricular tachycardia (torsade de pointes) all of which could be attributed to malabsorption of fat and fat-soluble vitamins.

摘要

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引用本文的文献

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The rare entity of cholocystocolonic fistula: a case report.罕见的胆肠瘘实体:一例报告。
Pan Afr Med J. 2021 Mar 15;38:262. doi: 10.11604/pamj.2021.38.262.27409. eCollection 2021.
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Pneumobilia, chronic diarrhea, vitamin K malabsorption: a pathognomonic triad for cholecystocolonic fistulas.气腹、慢性腹泻、维生素K吸收不良:胆囊结肠瘘的特征性三联征。
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Multiple cyclin kinase inhibitors promote bile acid-induced apoptosis and autophagy in primary hepatocytes via p53-CD95-dependent signaling.
多种细胞周期蛋白激酶抑制剂通过p53-CD95依赖性信号通路促进胆汁酸诱导的原代肝细胞凋亡和自噬。
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Bile acid regulation of C/EBPbeta, CREB, and c-Jun function, via the extracellular signal-regulated kinase and c-Jun NH2-terminal kinase pathways, modulates the apoptotic response of hepatocytes.胆汁酸通过细胞外信号调节激酶和c-Jun氨基末端激酶途径对C/EBPβ、CREB和c-Jun功能的调节,可调控肝细胞的凋亡反应。
Mol Cell Biol. 2003 May;23(9):3052-66. doi: 10.1128/MCB.23.9.3052-3066.2003.
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Deoxycholic acid (DCA) causes ligand-independent activation of epidermal growth factor receptor (EGFR) and FAS receptor in primary hepatocytes: inhibition of EGFR/mitogen-activated protein kinase-signaling module enhances DCA-induced apoptosis.脱氧胆酸(DCA)可导致原代肝细胞中表皮生长因子受体(EGFR)和FAS受体的非配体依赖性激活:抑制EGFR/丝裂原活化蛋白激酶信号模块可增强DCA诱导的细胞凋亡。
Mol Biol Cell. 2001 Sep;12(9):2629-45. doi: 10.1091/mbc.12.9.2629.