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Ursodeoxycholic acid inhibits eosinophil degranulation in patients with primary biliary cirrhosis
Author(s) -
Yamazaki Kiyoshi,
Suzuki Kazuyuki,
Nakamura Atsushi,
Sato Shunichi,
Lindor Keith D.,
Batts Kenneth P.,
Tarara James E.,
Kephart Gail M.,
Kita Hirohito,
Gleich Gerald J.
Publication year - 1999
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510300121
Subject(s) - ursodeoxycholic acid , primary biliary cirrhosis , eosinophilia , major basic protein , eosinophil , eosinophil cationic protein , medicine , immunology , eosinophil granule proteins , biliary cirrhosis , hypereosinophilic syndrome , eosinophil peroxidase , gastroenterology , autoimmune hepatitis , hepatitis , antibody , autoimmune disease , asthma
Eosinophilia is a distinctive feature of primary biliary cirrhosis (PBC), especially in its early stages. Intriguingly, treatment with ursodeoxycholic acid (UDCA) ameliorates eosinophilia as well as liver tests in patients with PBC. It remains unknown, however, whether eosinophils in PBC patients are functionally activated and whether UDCA inhibits eosinophil activation. In the present study, we systematically examined eosinophil dynamics in the blood and liver in patients with stage I to II PBC before and after UDCA treatment. We determined serum concentrations of eosinophil granule proteins (major basic protein [MBP] and eosinophil‐derived neurotoxin [EDN]) by radioimmunoassay and quantitated eosinophil degranulation using computer‐assisted morphometry after MBP immunohistochemistry. Before UDCA treatment, patients with PBC (n = 25) showed significantly higher circulating eosinophil counts ( P < .05) and serum concentrations of MBP ( P < .0005) and EDN ( P < .02) compared with patients with chronic viral hepatitis (n = 22), autoimmune hepatitis (n = 10), and obstructive jaundice (n = 12). Four‐week UDCA treatment significantly reduced blood eosinophil counts ( P < .0001) and serum MBP ( P < .0001) and EDN ( P < .0001) levels in PBC patients. MBP immunohistochemistry and computer‐assisted quantitative morphometry showed infiltration and degranulation of eosinophils in the portal tract in patients with PBC and significant reductions in the number of sites and the area occupied by extracellular MBP deposits after UDCA treatment for 2 years ( P < .02) but not in placebo‐treated patients. Our results suggest that eosinophils in patients with PBC are not only increased in number, but also release granule proteins, and that UDCA treatment inhibits this eosinophil activation/degranulation

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