Objective To investigate the clinical features of cholestatic liver disease ( CLD) , and to provide a reference for strengthening the diagnosis and treatment of this disease. Methods A retrospective analysis was performed for the clinical data of 107 patients who were admitted to Chenggong Hospital Affiliated to Xiamen University from January 2015 to December 2017 and were diagnosed with CLD. The t-test was used for comparison of continuous data between groups. Results Most patients had the clinical symptoms of weakness, loss of appetite, nausea, abdominal distension, pruritus, and jaundice. According to the site of cholestasis, there were 64 patients ( 59. 8%) with intrahepatic cholestasis and 43 ( 40. 2%) with extrahepatic cholestasis. The cause of the disease was common bile duct stones in 21 patients ( 19. 6%) , bile duct parasites in 1 patient ( 0. 9%) , primary sclerosing cholangitis in 2 patients ( 1. 9%) , primary biliary cirrhosis in 3 patients ( 2. 8%) , liver cancer in 8 patients ( 7. 5%) , bile duct carcinoma in 5 patients ( 4. 7%) , pancreatic cancer in 4 patients ( 3. 7%) , pancreatitis in 12 patients ( 11. 2%) , viral hepatitis in 28 patients ( 26. 2%) , drug-induced liver injury in 11 patients ( 10. 3%) , alcoholic hepatitis in 6 patients ( 5. 6%) , nonalcoholic fatty liver disease in 4 patients ( 3. 7%) , and autoimmune hepatitis in 2 patients ( 1. 9%) . The CLD patients with underlying diseases had a significantly poorer liver function ( alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transpeptidase, alkaline phosphatase, bile acid, and total bilirubin) than those with CLD alone ( t =-3. 44, -2. 99, -2. 42, -4. 39, -3. 34, and-2. 49, all P < 0. 05) . Most of the patients achieved good recovery after liver-protecting, transaminase-lowering, and jaundice clearance treatment. The patients with tumors had poor prognosis. Conclusion CLD has various causes, and its clinical features lack specificity. Clinicians should pay enough attention to this disease.
[1] ZHU JY, HAN Y. Something should be clear in diagnosis of patients with cholestasis liver diseases[J]. J Pract Hepatol, 2016, 19 (6) :647-649. (in Chinese) 朱疆依, 韩英.关于胆汁淤积性肝病诊断的几点探讨[J].实用肝脏病杂志, 2016, 19 (6) :647-649.
|
[2] KUNTZ K, KUNTZ HD. Cholestasic[M]//Hepatology:Principles and practice. 2nd ed. Springer Medizin Verlag Heidelberg, 2006:227-242.
|
[3] Chinese Society of Hepatology, Chinese Medical Association; Chinese Society of Gastroenterology, Chinese Medical Association; Chinese Society of Infectious Diseases, Chinese Medical Association. Consensus on the diagnosis and treatment of cholestasis liver diseases (2015) [J]. J Clin Hepatol, 2015, 31 (12) :1989-1999. (in Chinese) 中华医学会肝病学分会, 中华医学会消化病学分会, 中华医学会感染病学分会.胆汁淤积性肝病诊断和治疗共识 (2015) [J].临床肝胆病杂志, 2015, 31 (12) :1989-1999.
|
[4] European Association for the Study of the Liver. EASL clinical practice guidelines:Management of cholestatic liver diseases[J]. J Hepatol, 2009, 51 (2) :237-267.
|
[5] BEUERS U, TRAUNER M, JANSEN P, et al. New paradigms in the treatment of hepatic cholestasis:From UDCA to FXR, PXR and beyond[J]. J Hepatol, 2015, 62 (1) :s25-s37.
|
[6] SHEN FF, LU LG. Etiology of cholestatic liver diseases[J]. J Pract Hepatol, 2016, 19 (6) :644-646. (in Chinese) 沈斐斐, 陆伦根.胆汁淤积性肝病的病因[J].实用肝脏病杂志, 2016, 19 (6) :644-646.
|
[7] WANG K. Molecular mechanisms of liver injury:Apoptosis or necrosis[J]. Exp Toxicol Pathol, 2014, 66 (8) :351-356.
|
[8] KAIS Z, ANILGA T, KEITH D, et al. Symptoms, quality of life and pregnancy in cholestatic liver disease[J]. Liver Int, 2018, 38 (3) :399-411.
|
[9] STEPHENS C, ANDRADE RJ, LUCENA MI. Mechanisms of drug-induced liver injury[J]. Curr Opin Allergy Clin Immunol, 2014, 14 (4) :286-292.
|
[10] CHEN CW. Research advance in drug-induced liver injury and existing problem in China[J]. J Clin Hepatol, 2018, 34 (6) :1147-1151. (in Chinese) 陈成伟.药物性肝损伤的研究进展及我国存在的问题[J].临床肝胆病杂志, 2018, 34 (6) :1147-1151.
|
[11] HU Q, LIU W, SHAO H. Research progress of pharmacotherapy druginduced liver injury[J]. Chin J Clin Pharmacol Ther, 2016, 21 (2) :231-236. (in Chinese) 胡琴, 刘维, 邵宏.药物性肝损伤的药物治疗研究进展[J].中国临床药理学与治疗学, 2016, 21 (2) :231-236.
|
[12] VINKEN M, MAES M, VANHAECKE T, et al. Drug-induced liver injury:Mechanisms, types and biomarkers[J]. Curr Med Chem, 2013, 20 (24) :3011-3021.
|
[13] BHOGAL HK, SANYAL AJ. The molecular pathogenesis of cholestasis in sepsis[J]. Front Biosci (Elite Ed) , 2013, 5:87-96.
|
[14] TUNG BY, CARITHERS RL. Cholestasis and alcoholic liver disease[J]. Clin Liver Dis, 1999, 3 (3) :585-601.
|
[15] SUO YH, LIU JC. Research advances in the treatment of nonalcoholic fatty liver disease[J]. J Clin Hepatol, 2018, 34 (10) :2232-2236. (in Chinese) 索宇鸿, 刘近春.非酒精性脂肪性肝病的治疗进展[J].临床肝胆病杂志, 2018, 34 (10) :2232-2236.
|
[16] SORRENTINO P, TARANTINO G, PERRELLA A, et al. A clinical morphological study on cholestatic presentation of nonalcoholic fatty liver disease[J]. Dig Dis Sci, 2005, 50 (6) :1130-1135.
|
[17] FORSMARK CE, VEGE SS, WILCOX CM. Acute pancreatitis[J]. N Engl J Med, 2016, 375 (20) :1972-1981.
|
[18] WEI S, HUANG Q, LI J, et al. Taurine attenuates liver injury by downregulating phosphorylated p38 MAPK of Kupffer cells in rats with severe acute pancreatitis[J]. Inflammation, 2012, 35 (2) :690-701.
|
[19] HOQUE R, FAROOQ A, GHANI A, et al. Lactate reduces liver and pancreatic injury in Toll-like receptor and inflammasome-mediated inflammation via GPR81-mediated suppression of innate immunity[J]. Gastroenterology, 2014, 146 (7) :1763-1774.
|
[20] FEOKITSTOVA M, LEVERKUS M. Programmed necrosis and necroptosis signaling[J]. FEBS J, 2015, 282 (1) :19-31.
|