1 tomegaly, 15 (30%) cholelithiasis and 3 (6%) biliary sludge.

2 ses of unexplained AP showed 6 patients with biliary sludge, 4 microlithiasis, 4 sphincter of Oddi dy

3 wever, the impact of nutritional strategy on biliary sludge and CLD has not been fully characterized.

4 leads to the development of cholestasis; and biliary sludge and gallstones, which exacerbate hepatic

5 asma bilirubin but reduced the occurrence of biliary sludge and lowered GGT, ALP, and ALT.

6 dence, natural history, and risk factors for biliary sludge and stones during pregnancy and the postp

7 er motility and promoting the development of biliary sludge in the early stage of gallstone formation

8  and events associated with the formation of biliary sludge include rapid weight loss, pregnancy, cef

9                                              Biliary sludge may cause complications, including biliar

10      Cholestatic liver dysfunction (CLD) and biliary sludge often occur during critical illness and a

11 late PN than in the early PN group developed biliary sludge on day 5 (37% versus 45%; P = 0.04).

12 one (2%) person had cholelithiasis, one (2%) biliary sludge, one (2%) fatty liver and none hepatomega

13                       The clinical course of biliary sludge varies, and complete resolution, a waxing

14                                              Biliary sludge was first described with the advent of ul

15                                              Biliary sludge was ultrasonographically evaluated on ICU

16 this study, hepatomegaly, cholelithiasis and biliary sludge were the most common hepatobiliary ultras

17 atural history, and clinical associations of biliary sludge will be essential to our understanding of