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1 acid is the preferred first-line therapy for primary biliary cholangitis.
2 ary damage and liver fibrosis in early-stage primary biliary cholangitis.
3 centrations of liver enzymes associated with primary biliary cholangitis.
4 vel advance for the treatment of pruritus in primary biliary cholangitis.
5 nd autoimmune T lymphocytes similar to human primary biliary cholangitis.
6 the human biliary tree, is down-regulated in primary biliary cholangitis.
7 ates of obeticholic acid in the treatment of primary biliary cholangitis.
8 microbiome is diminished in individuals with primary biliary cholangitis.
9 ot on any medication for management of their primary biliary cholangitis.
10 ists are effective second-line therapies for primary biliary cholangitis.
11 ng the 0 to 10 numerical rating scale (NRS), primary biliary cholangitis-40 (PBC-40) itch domain scor
12 acid receptor FXR, is effective in treating primary biliary cholangitis, an autoimmune liver disease
13 ds was performed to confirm the diagnosis of primary biliary cholangitis and determine which medicati
14 ould enable diagnosis at an earlier stage of primary biliary cholangitis and ensure access to treatme
16 n of this pool are a target of therapies for primary biliary cholangitis and nonalcoholic steatohepat
17 hosphorylation in the liver of patients with primary biliary cholangitis and primary sclerosing chola
18 breach which leads to autoimmune hepatitis, primary biliary cholangitis and primary sclerosing chola
19 hat cholestatic liver diseases, particularly primary biliary cholangitis and primary sclerosing chola
20 increased ZBP1 in the liver of patients with primary biliary cholangitis and primary sclerosing chola
21 propose a new view on the pathophysiology of primary biliary cholangitis and PSC in the hope that the
22 on of NAFLD, primary sclerosing cholangitis, primary biliary cholangitis, and alcoholic hepatitis, su
23 volved in the development and progression of primary biliary cholangitis, and extensive research has
24 ses comprise primary sclerosing cholangitis, primary biliary cholangitis, and IgG4-related cholangiti
25 ic burden of primary sclerosing cholangitis, primary biliary cholangitis, and IgG4-related cholangiti
26 iver diseases, such as autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing chol
27 diagnosis with IgG4-associated cholangitis, primary biliary cholangitis, and secondary cholangitides
28 luding NASH, primary sclerosing cholangitis, primary biliary cholangitis, and severe alcoholic hepati
29 derlying the pathogenesis and progression of primary biliary cholangitis are further clarified, speci
31 lestatic liver disease, including those with primary biliary cholangitis, can experience symptoms of
32 atients with primary sclerosing cholangitis, primary biliary cholangitis, chronic infection with hepa
37 Autoimmune hepatitis (five [4%] patients), primary biliary cholangitis (four [3%] patients), and he
40 ight modulate immunological abnormalities in primary biliary cholangitis have been studied but their
41 atients with primary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or C virus infe
42 enzyme abnormalities, autoimmune hepatitis, primary biliary cholangitis, hyposplenism or functional
43 elerated approval for treating patients with primary biliary cholangitis in whom ursodeoxycholic acid
52 acid, the standard first-line treatment for primary biliary cholangitis, is largely ineffective for
54 ggested that as many as 30% of patients with primary biliary cholangitis may have never received trea
55 ve suggested that up to 30% of patients with primary biliary cholangitis may never have received trea
57 Liver samples from alcoholic hepatitis and primary biliary cholangitis patients were used for compa
58 icity are effective in only about 50%-60% of primary biliary cholangitis patients, with no effective
59 e serum levels of itaconate in PSC (n = 64), primary biliary cholangitis (PBC) (n = 60), autoimmune h
60 evaluation of the cholestatic liver diseases primary biliary cholangitis (PBC) and primary sclerosing
62 sed AREG levels in livers from patients with primary biliary cholangitis (PBC) and primary sclerosing
63 Chronic cholestatic liver diseases, such as primary biliary cholangitis (PBC) and primary sclerosing
65 of urinary tract infections in patients with primary biliary cholangitis (PBC) and the cross-reactivi
66 eoxycholic acid (UDCA)-treated patients with primary biliary cholangitis (PBC) are associated with be
67 Primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) are human primary chol
71 t of sex on the postcirrhosis progression of primary biliary cholangitis (PBC) has not been well defi
89 ophage activation is an important feature of primary biliary cholangitis (PBC) pathogenesis and other
90 d with compete biochemical response (CBR) in primary biliary cholangitis (PBC) patients treated with
93 nosis, 43 healthy controls, 72 patients with primary biliary cholangitis (PBC), 26 patients with meta
95 tibodies (AMAs), but no clinical evidence of primary biliary cholangitis (PBC), are largely unknown.
96 st currently in clinical trials for NASH and primary biliary cholangitis (PBC), indicating that ameli
97 ients with AILD [Autoimmune Hepatitis (AIH), Primary Biliary Cholangitis (PBC), Primary Sclerosing Ch
99 ls (BECs) is critical to the pathogenesis of Primary Biliary Cholangitis (PBC), we have analyzed the
100 ied therapy has entered clinical practice in primary biliary cholangitis (PBC), with routine use of s
112 ents with cholestatic liver diseases such as primary biliary cholangitis (PBC, previously referred to
113 uman cholangiopathies (biliary atresia [BA], primary biliary cholangitis [PBC], and primary sclerosin
114 here are few effective medical therapies for primary biliary cholangitis, primary sclerosing cholangi
115 These data have particular significance in primary biliary cholangitis, primary sclerosing cholangi
117 320 with viral hepatitis, and 11 of 339 with primary biliary cholangitis/primary sclerosing cholangit
118 a confirmed single etiology of cholestatic (primary biliary cholangitis/primary sclerosing cholangit
119 s monotherapy for 12 months in patients with primary biliary cholangitis resulted in decreases from b
121 apoptotic pathway; down-regulation of AE2 in primary biliary cholangitis sensitizes cholangiocytes to
122 effectiveness and safety of PPAR agonists in primary biliary cholangitis through a systematic review
123 safety of obeticholic acid for patients with primary biliary cholangitis using 3-year interim data fr
124 hout liver disease and 13 patients with mild primary biliary cholangitis were included in the analysi
126 safety of obeticholic acid in patients with primary biliary cholangitis who are intolerant to or ina
127 as a second-line treatment for patients with primary biliary cholangitis who are unresponsive to urso
128 All patients with an ICD-10 diagnosis of primary biliary cholangitis who had any records within t
129 omly assigned (in a 2:1 ratio) patients with primary biliary cholangitis who had had an inadequate re
130 r, a significant proportion of patients with primary biliary cholangitis will qualify for second line
131 uble-blind phase of POISE, 217 patients with primary biliary cholangitis with inadequate response to
132 were both elevated in sera of patients with primary biliary cholangitis with itch and correlated wit
135 ursodeoxycholic acid for treatment of their primary biliary cholangitis, with 67% of patients having