Clinica Medica "A. Murri", Department of Precision and Regenerative Medicine and Ionian Area (DiMePre-J), University of Bari "Aldo Moro", Medical School, Bari, Italy.
Division of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Section of Gastroenterology, Department of Medicine, VA Boston Healthcare System, Boston, MA, USA.
Eur J Intern Med. 2024 Oct;128:10-19. doi: 10.1016/j.ejim.2024.07.008. Epub 2024 Jul 27.
Bile acid malabsorption (BAM) is an important disorder of digestive pathophysiology as it generates chronic diarrhoea. This condition originates from intricate pathways involving bile acid synthesis and metabolism in the liver and gut, the composition of gut microbiota, enterohepatic circulation and key receptors as farnesoid X receptor (FXR), fibroblast growth factor receptor 4 (FGFR4), and the G-protein bile acid receptor-1 (GPBAR-1). Although symptoms can resemble those related to disorders of gut brain interaction, accurate diagnosis of BAM may greatly benefit the patient. The empiric diagnosis of BAM is primarily based on the clinical response to bile acid sequestrants. Specific tests including the 48-hour fecal bile acid test, serum levels of 7α-hydroxy-4-cholesten-3-one (C4) and fibroblast growth factor 19 (FGF19), and the Selenium HomotauroCholic Acid Test (SeHCAT) are not widely available. Nevertheless, lack of diagnostic standardization of BAM may account for poor recognition and delayed management. Beyond bile acid sequestrants, therapeutic approaches include the use of FXR agonists, FGF19 analogues, glucagon-like peptide-1 (GLP-1) receptor agonists, and microbiota modulation. These novel agents can best make their foray into the therapeutic armamentarium if BAM does not remain a diagnosis of exclusion. Ignoring BAM as a specific condition may continue to contribute to increased healthcare costs and reduced quality of life. Here, we aim to provide a comprehensive review of the pathophysiology, diagnosis, and management of BAM.
胆汁酸吸收不良（BAM）是一种重要的消化系统病理生理学紊乱，因为它会导致慢性腹泻。这种情况源于涉及肝脏和肠道中胆汁酸合成和代谢、肠道微生物群的组成、肠肝循环以及法尼醇 X 受体（FXR）、成纤维细胞生长因子受体 4（FGFR4）和 G 蛋白胆汁酸受体-1（GPBAR-1）等关键受体的复杂途径。尽管症状可能与肠道-大脑相互作用紊乱相关，但 BAM 的准确诊断可能会极大地使患者受益。BAM 的经验诊断主要基于胆汁酸螯合剂的临床反应。包括 48 小时粪便胆汁酸测试、血清 7α-羟基-4-胆甾烷-3-酮（C4）和成纤维细胞生长因子 19（FGF19）水平以及硒同型牛磺酸试验（SeHCAT）在内的特定测试并不广泛可用。然而，BAM 的诊断标准化缺乏可能导致认识不足和治疗延迟。除了胆汁酸螯合剂之外，治疗方法还包括使用 FXR 激动剂、FGF19 类似物、胰高血糖素样肽-1（GLP-1）受体激动剂和微生物群调节。如果 BAM 不再是排他性诊断，这些新型药物可以最好地应用于治疗武器库。忽略 BAM 作为一种特定疾病可能会继续导致医疗保健成本增加和生活质量下降。在这里，我们旨在全面综述 BAM 的病理生理学、诊断和管理。
