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5,8,14 Furthermore, the grading of necroinflammatory activity to reflect the autoimmune-mediated pathogenesis of PBC is not reflected in these classical staging systems. Since publication of the latest staging method, that of Ludwig et?al. in 1978,13 much progress has been made in clinical areas, particularly ALOX15 in therapeutic fields.15�C18 There are now a number of treatments for PBC such as ursodeoxycholic acid (UDCA) and also combined UDCA and corticosteroid therapy for overlapping syndrome (hepatitic form of PBC).16,18 The effects of such therapies should be evaluated according to histological aspects, in addition to laboratory and clinical effects. We recently proposed a new histological staging and grading system of PBC, for the comprehensive analysis of the histological progression of PBC (staging) toward extensive duct loss, chronic cholestasis and cirrhosis, and also of the immune-mediated necroinflammatory activity of small bile duct (chronic cholangitis) and of hepatocytes (interface and lobular hepatitis).5 The original description, however, is very detailed and practical application seems not easy.5 Herein we have proposed a practical and convenient version of this new histological staging and grading system. First, we concisely described the convenient version of our new staging and grading system of PBC. Then, we assessed the system using interobserver agreement among a total of 28 liver pathologists, using 62 needle liver biopsy specimens. The intrahepatic biliary tree is classified into the intrahepatic large and small bile ducts according to their size and distributions C59 wnt in the liver.6,19 Intrahepatic small bile ducts, which are recognizable on microscopy, run parallel with hepatic arterial branch(es) and portal vein branch within portal tracts. They are classifiable into septal and interlobular bile ducts: the former has its own fibrous wall and its size is >80??m, while the latter's size is Alisertib (Fig.?1a) and is used for the histological staging of chronic hepatitis and non-alcoholic steatohepatitis (NASH).20�C22 Bile duct loss is characteristic of PBC and a result of immune-mediated progressive bile damage (Fig.?1b).4,6,23 Orcein-positive granules are copper-binding proteins in lysosomes and their deposition reflects chronic cholestasis.5,24 These granules are detectable in the relatively early stages of PBC, and their deposition becomes more severe and extensive with the progression of the disease (Fig.?1c). These three items constitute the basis of this staging system. The three items are scored as shown in Table?1.