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Cholecystectomy Causes Ultrasound Evidence of Increased Hepatic Steatosis

Authors
Yun, SangchulChoi, DonghoLee, Kyeong GeunKim, Han JoonKang, Bo-KyeongKim, HyunsungPaik, Seung Sam
Issue Date
Jun-2016
Publisher
Springer Verlag
Keywords
cholecystectomy; hepatic steatosis
Citation
World Journal of Surgery, v.40, no.6, pp 1412 - 1421
Pages
10
Journal Title
World Journal of Surgery
Volume
40
Number
6
Start Page
1412
End Page
1421
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/9089
DOI
10.1007/s00268-015-3396-7
ISSN
0364-2313
1432-2323
Abstract
Cholecystectomy might contribute to the development of hepatic steatosis through metabolic changes. The biologic alteration of the enterohepatic circulation of bile acids and the alteration of the metabolic activity of bile acid that follows cholecystectomy may contribute to hepatic steatosis. This prospective study was conducted to clarify the possibility of steatosis development after cholecystectomy. From October 2013 to July 2014, 82 consecutive patients with a presumptive diagnosis of gallbladder disease were cholecystectomized. Liver parenchymal steatosis was measured using ultrasound and the hepatic steatosis index. In all 82 patients, the hepatic steatosis index was found to be significantly correlated with the US fatty liver grade (Spearman's correlation r (2) = 0.331, P < 0.001). A total of 62 patients were followed up for 3 months. Comparison with the initial grade showed that 12 (18.5 %) patients had worsened from normal to mild (n = 10), from mild to moderate (n = 1), and from mild to severe (n = 1). The other patients stayed at their initial grade except one patient who improved (from moderated to mild). Analysis of laboratory findings showed that white blood cell count, aspartate transaminase, alanine transaminase level, and total bilirubin level were decreased. However, serum albumin and high-density lipoprotein cholesterol levels significantly increased. Hepatic steatosis significantly developed 3 months after cholecystectomy. Therefore, cholecystectomy might be considered a risk factor for hepatic steatosis, but the relationship should be confirmed with long-term follow-up from a large group of patients.
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