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1 vel advance for the treatment of pruritus in primary biliary cholangitis.
2 nd autoimmune T lymphocytes similar to human primary biliary cholangitis.
3 the human biliary tree, is down-regulated in primary biliary cholangitis.
4 ng the 0 to 10 numerical rating scale (NRS), primary biliary cholangitis-40 (PBC-40) itch domain scor
5 acid receptor FXR, is effective in treating primary biliary cholangitis, an autoimmune liver disease
6 hat cholestatic liver diseases, particularly primary biliary cholangitis and primary sclerosing chola
7 propose a new view on the pathophysiology of primary biliary cholangitis and PSC in the hope that the
12 acid, the standard first-line treatment for primary biliary cholangitis, is largely ineffective for
13 icity are effective in only about 50%-60% of primary biliary cholangitis patients, with no effective
14 Primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) are human primary chol
19 ophage activation is an important feature of primary biliary cholangitis (PBC) pathogenesis and other
20 tibodies (AMAs), but no clinical evidence of primary biliary cholangitis (PBC), are largely unknown.
21 ls (BECs) is critical to the pathogenesis of Primary Biliary Cholangitis (PBC), we have analyzed the
25 ents with cholestatic liver diseases such as primary biliary cholangitis (PBC, previously referred to
26 uman cholangiopathies (biliary atresia [BA], primary biliary cholangitis [PBC], and primary sclerosin
27 s monotherapy for 12 months in patients with primary biliary cholangitis resulted in decreases from b
28 apoptotic pathway; down-regulation of AE2 in primary biliary cholangitis sensitizes cholangiocytes to
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