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1 parenteral nutrition (TPN) with TPN-related cholestatic liver disease.
2 cid synthesis as a metabolic cause of severe cholestatic liver disease.
3 thanol (20% ethanol alone), and only 12% had cholestatic liver disease.
4 ents with primary biliary cirrhosis, another cholestatic liver disease.
5 ted here suggest that PHB1 is also linked to cholestatic liver disease.
6 which is frequently used in the treatment of cholestatic liver disease.
7 neficial use of fenofibrate therapy in human cholestatic liver disease.
8 itochondrial morphology has been observed in cholestatic liver disease.
9 tight-junction structure, leading to severe cholestatic liver disease.
10 ochondrial morphology to the pathogenesis of cholestatic liver disease.
11 , MDR3 is a potential therapeutic target for cholestatic liver disease.
12 d (TUDC), is a mainstay for the treatment of cholestatic liver disease.
13 ndings from genetic studies of patients with cholestatic liver disease.
14 the formation of bile and the prevention of cholestatic liver disease.
15 were increased in livers from patients with cholestatic liver disease.
16 n the liver and prevent hepatocyte injury in cholestatic liver disease.
17 g colon cancer formation and progression and cholestatic liver disease.
18 fusion (IR) injury is frequently followed by cholestatic liver disease.
19 rine when hepatic elimination is impaired by cholestatic liver disease.
20 vitamins is a major complication of chronic cholestatic liver disease.
21 latively common in children who have chronic cholestatic liver disease.
22 R agonists may be useful in the treatment of cholestatic liver disease.
23 s may prove useful in the treatment of human cholestatic liver disease.
24 cific instrument in ambulatory patients with cholestatic liver disease.
25 aling may be important for the management of cholestatic liver diseases.
26 rters and are natural targets for therapy of cholestatic liver diseases.
27 e for the maintenance of biliary mass during cholestatic liver diseases.
28 itus and painless jaundice that occur during cholestatic liver diseases.
29 r (FXR) and its potential therapeutic use in cholestatic liver diseases.
30 beticholic acid for the treatment of chronic cholestatic liver diseases.
31 ial targets for pharmacological therapies of cholestatic liver diseases.
32 DHEA-S levels was not seen in patients with cholestatic liver diseases.
33 gies targeting BA transport and signaling in cholestatic liver diseases.
34 et to modulate bile flow in the treatment of cholestatic liver diseases.
35 his review focuses on the recent advances in cholestatic liver diseases.
36 frequently the most debilitating symptom of cholestatic liver diseases.
37 dvance our understanding of the treatment of cholestatic liver diseases.
38 better understanding of the pathogenesis of cholestatic liver diseases.
39 better understanding of the pathogenesis of cholestatic liver diseases.
40 ary cholangitis (PBC) pathogenesis and other cholestatic liver diseases.
41 biting PAI-1 might attenuate liver injury in cholestatic liver diseases.
42 be a therapeutic antifibrogenic strategy in cholestatic liver diseases.
43 ur cohort of 28 MVID patients, 8 developed a cholestatic liver disease akin to progressive familial i
44 for cryptogenic, autoimmune, hepatitis B, or cholestatic liver disease and 91 non-liver transplantati
45 -alcoholic steatohepatitis, viral hepatitis, cholestatic liver disease and autoimmune liver diseases.
47 ulation of bile acid homeostasis can lead to cholestatic liver disease and endoplasmic reticulum (ER)
48 e composition with important applications in cholestatic liver disease and gallstone disease, two ser
49 ry sclerosing cholangitis (PSC) is a chronic cholestatic liver disease and one of the most common ind
50 fects in patients with pruritus secondary to cholestatic liver disease and to assess the safety of lo
51 ligation (BDL) in the rat and in some human cholestatic liver diseases and is believed to ameliorate
52 langiocytes occurs during the progression of cholestatic liver diseases and is critical for the maint
53 igands may ameliorate human diseases such as cholestatic liver diseases and the associating acute ren
54 epidemiology, and treatment of a variety of cholestatic liver diseases and their associated complica
56 infants transplanted for reasons other than cholestatic liver disease, and patients transplanted bet
57 peutic indications in constipation, dry eye, cholestatic liver diseases, and inflammatory lung disord
58 malabsorption syndromes (especially owing to cholestatic liver disease), antibiotic therapy, and rena
62 ression of many of these genes is altered in cholestatic liver diseases, but few have been extensivel
65 Primary sclerosing cholangitis is a chronic cholestatic liver disease characterized by strictures of
66 Primary sclerosing cholangitis is a chronic cholestatic liver disease characterized by strictures of
67 Primary sclerosing cholangitis is a chronic cholestatic liver disease characterized by strictures of
68 Primary sclerosing cholangitis is a chronic cholestatic liver disease characterized by strictures of
69 target of cholangiopathies that are chronic cholestatic liver diseases characterized by loss of prol
70 dents is often studied as an animal model of cholestatic liver disease, characterized by obstruction
71 heimer's disease (AD), Down's syndrome (DS), cholestatic liver disease (CLD) and abetalipoproteinemia
72 ary biliary cirrhosis (PBC) is a progressive cholestatic liver disease frequently leading to developm
75 centers with either autoimmune hepatitis or cholestatic liver disease had significantly lower risks
76 UDCA, a bile acid used in the treatment of cholestatic liver disease, has anti-inflammatory and cyt
78 alidity of risk stratification in autoimmune cholestatic liver disease, highlighting strengths and we
79 ocrine phenotypes of cholangiocytes in human cholestatic liver diseases (ie, cholangiopathies) that a
81 r plasminogen activator inhibitor (PAI)-1 in cholestatic liver disease in mice suggested that tissue-
84 lic acid (UDCA) is used for the treatment of cholestatic liver diseases including primary biliary cir
85 advances have been made in the treatment of cholestatic liver diseases, including primary biliary ci
86 eased awareness of PBC as a cause of chronic cholestatic liver disease is critical in evaluating non-
87 e, inflammatory bowel diseases, gastrectomy, cholestatic liver diseases, liver transplantation, and h
91 In the assessment of QOL in patients with cholestatic liver disease, NIDDK-QA is found reliable an
94 Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease of presumed autoimmune etiolog
96 Primary sclerosing cholangitis is a chronic cholestatic liver disease of unknown origin that occurs
99 with HCV-negative patients, suggesting that cholestatic liver disease (particularly graft-versus-hos
100 In this review we develop the argument that cholestatic liver diseases, particularly primary biliary
103 urthermore, nicotine may act as a mitogen in cholestatic liver disease processes, thereby facilitatin
104 rd to the pathologic relevance of this work, cholestatic liver diseases represent a broad group of he
105 1950s as a clinical syndrome of progressive cholestatic liver disease resulting from chronic inflamm
106 tion, PCN risk was higher in recipients with cholestatic liver disease (SIR 2.78); five of these case
107 , 25% of patients undergoing OLT for chronic cholestatic liver disease still develop de novo fracture
109 ymptom commonly experienced by patients with cholestatic liver diseases such as primary biliary chola
110 ruritus is a common symptom in patients with cholestatic liver diseases such as primary biliary cirrh
111 but is believed to play an important role in cholestatic liver diseases such as primary familial intr
113 liary cirrhosis (PBC) is an uncommon chronic cholestatic liver disease that primarily afflicts young
114 ry sclerosing cholangitis (PSC) is a chronic cholestatic liver disease that progresses to death as a
115 cholangitis (PSC) are infrequent autoimmune cholestatic liver diseases, that disproportionate to the
118 an age at LTx was 9 months, the majority had cholestatic liver disease, were hospitalized pre-LTx, an
119 t-gut syndrome caused by volvulus and severe cholestatic liver disease who underwent simultaneous int
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