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炎症性肠病的肝胆表现

Authors
Gad Friedman, MD, FRCPC
Alain Bitton, MD, FRCPC
Section Editor
Paul Rutgeerts, MD, PhD, FRCP
Deputy Editor
Shilpa Grover, MD, MPH, AGAF
Translators
楚慧款, 主治医师

引言

肝脏和胆道疾病是炎症性肠病(inflammatory bowel disease, IBD)常见的肠外表现(表 1)[1-3]。原发性硬化性胆管炎(primary sclerosing cholangitis, PSC)是IBD较常见的肝胆并发症之一，尤其在溃疡性结肠炎患者中。据估计，约5%的溃疡性结肠炎患者发生PSC，而高达90%的PSC患者存在溃疡性结肠炎[4]。 (参见“原发性硬化性胆管炎：流行病学及发病机制”)

高达30%的IBD患者有肝脏生化检测异常，这些异常似乎与疾病活动度无关[5]。因此，肝脏生化检查结果持续异常的患者通常应进行评估。本专题将重点讨论IBD患者中可发生的其他肝胆表现。IBD与PSC的关联将在别处讨论。 (参见“原发性硬化性胆管炎：流行病学及发病机制”，关于‘PSC与炎症性肠病’一节)

药物诱导的肝毒性

大部分用于IBD内科治疗的药物具有肝毒性，但严重并发症的总体发生率低[6,7]。下列为可出现的反应：

●柳氮磺吡啶可引起肝细胞酶与胆淤指示酶异常，常与超敏反应有关。新型的无磺胺基对氨水杨酸制剂将更大量的柳氮磺吡啶药理活性成分[5-对氨基水杨酸(5-aminosalicylic acid, 5-ASA)，美沙拉秦]释放至活动性肠病部位，并且全身性毒性更低。5-ASA偶尔可引起胰腺炎。 (参见“柳氮磺吡啶和5-氨基水杨酸类药物治疗炎症性肠病”)

●硫唑嘌呤可引起一系列肝脏损伤，从无症状的氨基转移酶升高(约5%的患者)到胆汁淤积、肝静脉闭塞性疾病及肝紫癜病。巯嘌呤(6-Mercaptopurine, 6-MP)是硫唑嘌呤的一种代谢产物，也可引起肝细胞性和淤胆性肝炎。因此，用硫唑嘌呤或6-MP治疗的患者应定期进行肝脏生化监测。治疗停止后，肝脏异常通常可消退。 (参见“克罗恩病的免疫调节剂治疗”，关于‘毒性’一节)

         

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Literature review current through: 2017-06 . | This topic last updated: 2017-07-10.
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References
Top
  1. Raj V, Lichtenstein DR. Hepatobiliary manifestations of inflammatory bowel disease. Gastroenterol Clin North Am 1999; 28:491.
  2. Riegler G, D'Incà R, Sturniolo GC, et al. Hepatobiliary alterations in patients with inflammatory bowel disease: a multicenter study. Caprilli & Gruppo Italiano Studio Colon-Retto. Scand J Gastroenterol 1998; 33:93.
  3. Wewer V, Gluud C, Schlichting P, et al. Prevalence of hepatobiliary dysfunction in a regional group of patients with chronic inflammatory bowel disease. Scand J Gastroenterol 1991; 26:97.
  4. Lee YM, Kaplan MM. Primary sclerosing cholangitis. N Engl J Med 1995; 332:924.
  5. Mendes FD, Levy C, Enders FB, et al. Abnormal hepatic biochemistries in patients with inflammatory bowel disease. Am J Gastroenterol 2007; 102:344.
  6. Stricker BH. Drug-Induced Hepatic Injury, 2nd ed, Elsevier, New York 1992.
  7. Gisbert JP, Luna M, González-Lama Y, et al. Liver injury in inflammatory bowel disease: long-term follow-up study of 786 patients. Inflamm Bowel Dis 2007; 13:1106.
  8. Dubinsky MC, Vasiliauskas EA, Singh H, et al. 6-thioguanine can cause serious liver injury in inflammatory bowel disease patients. Gastroenterology 2003; 125:298.
  9. Ferlitsch A, Teml A, Reinisch W, et al. 6-thioguanine associated nodular regenerative hyperplasia in patients with inflammatory bowel disease may induce portal hypertension. Am J Gastroenterol 2007; 102:2495.
  10. Kremer JM. Liver toxicity does not have to follow methotrexate therapy of patients with rheumatoid arthritis. Am J Gastroenterol 1997; 92:194.
  11. Coté T. TNF Blocker Safety: Lymphoma and Liver Failure. Federal Drug Administration, March 4, 2003.
  12. Tobon GJ, Cañas C, Jaller JJ, et al. Serious liver disease induced by infliximab. Clin Rheumatol 2007; 26:578.
  13. Menghini VV, Arora AS. Infliximab-associated reversible cholestatic liver disease. Mayo Clin Proc 2001; 76:84.
  14. Ierardi E, Della Valle N, Nacchiero MC, et al. Infliximab single administration followed by acute liver injury. Inflamm Bowel Dis 2006; 12:1089.
  15. Adar T, Mizrahi M, Pappo O, et al. Adalimumab-induced autoimmune hepatitis. J Clin Gastroenterol 2010; 44:e20.
  16. Hagel S, Bruns T, Theis B, et al. Subacute liver failure induced by adalimumab. Int J Clin Pharmacol Ther 2011; 49:38.
  17. Parente F, Pastore L, Bargiggia S, et al. Incidence and risk factors for gallstones in patients with inflammatory bowel disease: a large case-control study. Hepatology 2007; 45:1267.
  18. Maurer P, Haag K, Roth M, et al. No evidence for abnormal gallbladder emptying in Crohn's disease. Hepatogastroenterology 1996; 43:807.
  19. Mibu R, Makino I, Chijiiwa K. Gallstones and their composition in patients with ileoanal anastomosis. J Gastroenterol 1995; 30:413.
  20. Greenstein AJ, Sachar DB, Panday AK, et al. Amyloidosis and inflammatory bowel disease. A 50-year experience with 25 patients. Medicine (Baltimore) 1992; 71:261.
  21. Meyers S, Janowitz HD, Gumaste VV, et al. Colchicine therapy of the renal amyloidosis of ulcerative colitis. Gastroenterology 1988; 94:1503.
  22. Vakil N, Hayne G, Sharma A, et al. Liver abscess in Crohn's disease. Am J Gastroenterol 1994; 89:1090.
  23. Mir-Madjlessi SH, McHenry MC, Farmer RG. Liver abscess in Crohn's disease. Report of four cases and review of the literature. Gastroenterology 1986; 91:987.
  24. Bermejo F, Lopez-Sanroman A, Taxonera C, et al. Acute pancreatitis in inflammatory bowel disease, with special reference to azathioprine-induced pancreatitis. Aliment Pharmacol Ther 2008; 28:623.
  25. Xiao WB, Liu YL. Primary biliary cirrhosis and ulcerative colitis: a case report and review of literature. World J Gastroenterol 2003; 9:878.
  26. Koulentaki M, Koutroubakis IE, Petinaki E, et al. Ulcerative colitis associated with primary biliary cirrhosis. Dig Dis Sci 1999; 44:1953.
  27. Arai O, Ikeda H, Mouri H, et al. Two cases of inflammatory bowel disease diagnosed in the course of primary biliary cirrhosis. Nihon Shokakibyo Gakkai Zasshi 2010; 107:900.
  28. Ohge H, Takesue Y, Yokoyama T, et al. Progression of primary biliary cirrhosis after proctocolectomy for ulcerative colitis. J Gastroenterol 2000; 35:870.
  29. Onishi S, Sakamaki T, Maeda T, et al. DNA typing of HLA class II genes; DRB1*0803 increases the susceptibility of Japanese to primary biliary cirrhosis. J Hepatol 1994; 21:1053.