Autoimmune hepatitis associated with bile duct injury resembling chronic non‐suppurative destructive cholangitis
Identifieur interne : 003D81 ( Istex/Corpus ); précédent : 003D80; suivant : 003D82Autoimmune hepatitis associated with bile duct injury resembling chronic non‐suppurative destructive cholangitis
Auteurs : Yasunori Sato ; Kenichi Harada ; Yoshiko Sudo ; Kishichiro Watanabe ; Tohru Nakahama ; Hideo Morimoto ; Yasuni NakanumaSource :
- Pathology International [ 1320-5463 ] ; 2002-07.
English descriptors
- Teeft :
- Aberrant expression, Aggregate score, Alkaline phosphatase, Antimitochondrial, Antimitochondrial antibodies, Antimitochondrial antibody, Antinuclear autoantibody, Antismooth muscle antibody, Autoimmune, Autoimmune cholangitis, Autoimmune hepatitis, Autoimmune liver disease, Bile, Bile duct injuries, Bile duct injury, Bile duct lesions, Bile ducts, Biliary, Case report, Cholangitis, Chronic hepatitis, Cirrhosis, Consecutive occurrence, Destructive cholangitis, Duct, Epithelioid cells, Granuloma formation, Hepatitis, Hepatitis group, Histological, Histological features, Human pathology, Immunosuppressive therapy, Interlobular bile duct, Interlobular bile ducts, Intrahepatic bile ducts, Kanazawa, Kanazawa university graduate school, Laboratory data, Lesion, Liver biopsy, Liver disease, Liver diseases, Lobular hepatitis, National hospital, Normal limits, Normal range, Perivenular zonal necrosis, Portal tracts, Present case, Primary biliary cirrhosis, Serum levels, Syndrome, Unusual case, Ursodeoxycholic acid.
Abstract
Autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC) are representative autoimmune liver diseases in which hepatocytes and intrahepatic bile ducts, respectively, are selectively damaged by autoimmune mechanisms. Bile duct injury and loss is characteristic of PBC and chronic non‐suppurative destructive cholangitis (CNSDC), in particular, is a histological hallmark of PBC. In this report, we present an unusual case of AIH accompanied by CNSDC‐like bile duct injury in a 46‐year‐old woman. The patient's serum aminotransferase level was abnormally high. The serum levels of alkaline phosphatase, γ‐GTP and IgG were also elevated, but the IgM level was within normal limits. The titer of antismooth muscle antibody (SMA) was 1:80 , while antinuclear autoantibody (ANA) and the M2 fraction of antimitochondrial antibody (AMA) were both negative. Liver biopsy disclosed CNSDC‐like bile duct injuries and severe interface hepatitis and lobular hepatitis with perivenular zonal necrosis were observed. The aggregate score of the International Autoimmune Hepatitis Group corresponded to the category of probable AIH. Immunohistochemically, histocompatibility leukocyte antigen‐DR, which is aberrantly expressed in the damaged bile ducts of PBC, was not found in the injured bile ducts of this case. Laboratory data were much improved by treatment with prednisone, but ursodeoxycholic acid was not effective. Although the possibility of an overlapping syndrome of AIH‐ and AMA‐negative PBC could not be excluded, this case was diagnosed as AIH with CNSDC‐like bile duct lesions.
Url:
DOI: 10.1046/j.1440-1827.2002.01377.x
Links to Exploration step
ISTEX:ED8943BE61D1A3D7CFA59BE2EA94D72D61EDF030Le document en format XML
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first="Kishichiro" last="Watanabe">Kishichiro Watanabe</name><affiliation><mods:affiliation>Department of Pathology, National Hospital of Kanazawa, Kanazawa, Japan,</mods:affiliation></affiliation></author><author><name sortKey="Nakahama, Tohru" sort="Nakahama, Tohru" uniqKey="Nakahama T" first="Tohru" last="Nakahama">Tohru Nakahama</name><affiliation><mods:affiliation>Department of Internal Medicine, National Hospital of Kanazawa, Kanazawa, Japan</mods:affiliation></affiliation></author><author><name sortKey="Morimoto, Hideo" sort="Morimoto, Hideo" uniqKey="Morimoto H" first="Hideo" last="Morimoto">Hideo Morimoto</name><affiliation><mods:affiliation>Department of Internal Medicine, National Hospital of Kanazawa, Kanazawa, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nakanuma, Yasuni" sort="Nakanuma, Yasuni" uniqKey="Nakanuma Y" first="Yasuni" last="Nakanuma">Yasuni Nakanuma</name><affiliation><mods:affiliation>Department of Human Pathology, Kanazawa University 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duct</term><term>Interlobular bile ducts</term><term>Intrahepatic bile ducts</term><term>Kanazawa</term><term>Kanazawa university graduate school</term><term>Laboratory data</term><term>Lesion</term><term>Liver biopsy</term><term>Liver disease</term><term>Liver diseases</term><term>Lobular hepatitis</term><term>National hospital</term><term>Normal limits</term><term>Normal range</term><term>Perivenular zonal necrosis</term><term>Portal tracts</term><term>Present case</term><term>Primary biliary cirrhosis</term><term>Serum levels</term><term>Syndrome</term><term>Unusual case</term><term>Ursodeoxycholic acid</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC) are representative autoimmune liver diseases in which hepatocytes and intrahepatic bile ducts, respectively, are selectively damaged by autoimmune mechanisms. Bile duct injury and loss is characteristic of PBC and chronic non‐suppurative destructive cholangitis (CNSDC), in particular, is a histological hallmark of PBC. In this report, we present an unusual case of AIH accompanied by CNSDC‐like bile duct injury in a 46‐year‐old woman. The patient's serum aminotransferase level was abnormally high. The serum levels of alkaline phosphatase, γ‐GTP and IgG were also elevated, but the IgM level was within normal limits. The titer of antismooth muscle antibody (SMA) was 1:80 , while antinuclear autoantibody (ANA) and the M2 fraction of antimitochondrial antibody (AMA) were both negative. Liver biopsy disclosed CNSDC‐like bile duct injuries and severe interface hepatitis and lobular hepatitis with perivenular zonal necrosis were observed. The aggregate score of the International Autoimmune Hepatitis Group corresponded to the category of probable AIH. Immunohistochemically, histocompatibility leukocyte antigen‐DR, which is aberrantly expressed in the damaged bile ducts of PBC, was not found in the injured bile ducts of this case. Laboratory data were much improved by treatment with prednisone, but ursodeoxycholic acid was not effective. Although the possibility of an overlapping syndrome of AIH‐ and AMA‐negative PBC could not be excluded, this case was diagnosed as AIH with CNSDC‐like bile duct lesions.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>autoimmune</json:string><json:string>duct</json:string><json:string>biliary</json:string><json:string>cholangitis</json:string><json:string>cirrhosis</json:string><json:string>primary biliary cirrhosis</json:string><json:string>bile duct injury</json:string><json:string>autoimmune hepatitis</json:string><json:string>kanazawa</json:string><json:string>histological</json:string><json:string>antimitochondrial</json:string><json:string>bile duct lesions</json:string><json:string>bile</json:string><json:string>present case</json:string><json:string>destructive cholangitis</json:string><json:string>normal range</json:string><json:string>hepatitis</json:string><json:string>normal limits</json:string><json:string>ursodeoxycholic acid</json:string><json:string>portal tracts</json:string><json:string>bile ducts</json:string><json:string>epithelioid cells</json:string><json:string>serum levels</json:string><json:string>intrahepatic bile ducts</json:string><json:string>lesion</json:string><json:string>antimitochondrial antibody</json:string><json:string>interlobular bile duct</json:string><json:string>autoimmune cholangitis</json:string><json:string>aggregate score</json:string><json:string>granuloma formation</json:string><json:string>autoimmune liver disease</json:string><json:string>syndrome</json:string><json:string>unusual case</json:string><json:string>laboratory data</json:string><json:string>antimitochondrial antibodies</json:string><json:string>alkaline phosphatase</json:string><json:string>human pathology</json:string><json:string>antismooth muscle antibody</json:string><json:string>antinuclear autoantibody</json:string><json:string>liver disease</json:string><json:string>case report</json:string><json:string>liver diseases</json:string><json:string>liver biopsy</json:string><json:string>interlobular bile ducts</json:string><json:string>aberrant expression</json:string><json:string>kanazawa university graduate school</json:string><json:string>lobular hepatitis</json:string><json:string>histological features</json:string><json:string>immunosuppressive therapy</json:string><json:string>chronic hepatitis</json:string><json:string>perivenular zonal necrosis</json:string><json:string>consecutive occurrence</json:string><json:string>national hospital</json:string><json:string>hepatitis group</json:string><json:string>bile duct injuries</json:string></teeft></keywords><author><json:item><name>Yasunori Sato</name><affiliations><json:string>Department of Human Pathology, Kanazawa University Graduate School of Medicine, Japan,</json:string></affiliations></json:item><json:item><name>Kenichi Harada</name><affiliations><json:string>Department of Human Pathology, Kanazawa University Graduate School of Medicine, Japan,</json:string></affiliations></json:item><json:item><name>Yoshiko Sudo</name><affiliations><json:string>Department of Human Pathology, Kanazawa University Graduate School of Medicine, Japan,</json:string></affiliations></json:item><json:item><name>Kishichiro Watanabe</name><affiliations><json:string>Department of Pathology, National Hospital of Kanazawa, Kanazawa, Japan,</json:string></affiliations></json:item><json:item><name>Tohru Nakahama</name><affiliations><json:string>Department of Internal Medicine, National Hospital of Kanazawa, Kanazawa, Japan</json:string></affiliations></json:item><json:item><name>Hideo Morimoto</name><affiliations><json:string>Department of Internal Medicine, National Hospital of Kanazawa, Kanazawa, Japan</json:string></affiliations></json:item><json:item><name>Yasuni Nakanuma</name><affiliations><json:string>Department of Human Pathology, Kanazawa University Graduate School of Medicine, Japan,</json:string><json:string>E-mail: pbcpsc@kenroku.kanazawa‐u.ac.jp</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>autoimmune hepatitis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>bile duct injury</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>chronic non‐suppurative destructive cholangitis</value></json:item></subject><articleId><json:string>PIN1377</json:string></articleId><arkIstex>ark:/67375/WNG-FJHGHC12-2</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC) are representative autoimmune liver diseases in which hepatocytes and intrahepatic bile ducts, respectively, are selectively damaged by autoimmune mechanisms. Bile duct injury and loss is characteristic of PBC and chronic non‐suppurative destructive cholangitis (CNSDC), in particular, is a histological hallmark of PBC. In this report, we present an unusual case of AIH accompanied by CNSDC‐like bile duct injury in a 46‐year‐old woman. The patient's serum aminotransferase level was abnormally high. The serum levels of alkaline phosphatase, γ‐GTP and IgG were also elevated, but the IgM level was within normal limits. The titer of antismooth muscle antibody (SMA) was 1:80 , while antinuclear autoantibody (ANA) and the M2 fraction of antimitochondrial antibody (AMA) were both negative. Liver biopsy disclosed CNSDC‐like bile duct injuries and severe interface hepatitis and lobular hepatitis with perivenular zonal necrosis were observed. The aggregate score of the International Autoimmune Hepatitis Group corresponded to the category of probable AIH. Immunohistochemically, histocompatibility leukocyte antigen‐DR, which is aberrantly expressed in the damaged bile ducts of PBC, was not found in the injured bile ducts of this case. Laboratory data were much improved by treatment with prednisone, but ursodeoxycholic acid was not effective. Although the possibility of an overlapping syndrome of AIH‐ and AMA‐negative PBC could not be excluded, this case was diagnosed as AIH with CNSDC‐like bile duct lesions.</abstract><qualityIndicators><score>7.325</score><pdfWordCount>2601</pdfWordCount><pdfCharCount>17099</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>5</pdfPageCount><pdfPageSize>595 x 842 pts (A4)</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>227</abstractWordCount><abstractCharCount>1582</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>Autoimmune hepatitis associated with bile duct injury resembling chronic non‐suppurative destructive cholangitis</title><pmid><json:string>12167107</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Pathology 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Pty</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2002-07"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Autoimmune hepatitis associated with bile duct injury resembling chronic non‐suppurative destructive cholangitis</title><title level="a" type="short">Autoimmune hepatitis with bile duct injury</title><author xml:id="author-0000"><persName><forename type="first">Yasunori</forename><surname>Sato</surname></persName><affiliation><orgName type="department">Department of Human Pathology</orgName><orgName type="institution">Kanazawa University Graduate School of Medicine</orgName><address><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Kenichi</forename><surname>Harada</surname></persName><affiliation><orgName type="department">Department of Human Pathology</orgName><orgName type="institution">Kanazawa University Graduate School of Medicine</orgName><address><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Yoshiko</forename><surname>Sudo</surname></persName><affiliation><orgName type="department">Department of Human Pathology</orgName><orgName type="institution">Kanazawa University Graduate School of Medicine</orgName><address><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Kishichiro</forename><surname>Watanabe</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><address><addrLine>National Hospital of Kanazawa</addrLine><addrLine>Kanazawa</addrLine><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Tohru</forename><surname>Nakahama</surname></persName><affiliation><orgName type="department">Department of Internal Medicine</orgName><address><addrLine>National Hospital of Kanazawa</addrLine><addrLine>Kanazawa</addrLine><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first"> Hideo</forename><surname>Morimoto</surname></persName><affiliation><orgName type="department">Department of Internal Medicine</orgName><address><addrLine>National Hospital of Kanazawa</addrLine><addrLine>Kanazawa</addrLine><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0006" role="corresp"><persName><forename type="first">Yasuni</forename><surname>Nakanuma</surname></persName><affiliation><orgName type="department">Department of Human Pathology</orgName><orgName type="institution">Kanazawa University Graduate School of Medicine</orgName><address><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation><affiliation>Yasuni Nakanuma, MD, PhD, Department of Human Pathology, Kanazawa University Graduate School of Medicine , 13‐1 Takara‐machi, Kanazawa 920‐8640, Japan. Email: pbcpsc@kenroku.kanazawa‐u.ac.jp</affiliation></author><idno type="istex">ED8943BE61D1A3D7CFA59BE2EA94D72D61EDF030</idno><idno type="ark">ark:/67375/WNG-FJHGHC12-2</idno><idno type="DOI">10.1046/j.1440-1827.2002.01377.x</idno><idno type="unit">PIN1377</idno><idno type="toTypesetVersion">file:PIN.PIN1377.pdf</idno></analytic><monogr><title level="j" type="main">Pathology International</title><title level="j" type="alt">PATHOLOGY INTERNATIONAL</title><idno type="pISSN">1320-5463</idno><idno type="eISSN">1440-1827</idno><idno type="book-DOI">10.1111/(ISSN)1440-1827</idno><idno type="book-part-DOI">10.1111/pin.2002.52.issue-7</idno><idno type="product">PIN</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">52</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="478">478</biblScope><biblScope unit="page" to="482">482</biblScope><biblScope unit="page-count">5</biblScope><publisher>Blackwell Science Pty</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2002-07"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p>Autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC) are representative autoimmune liver diseases in which hepatocytes and intrahepatic bile ducts, respectively, are selectively damaged by autoimmune mechanisms. Bile duct injury and loss is characteristic of PBC and chronic non‐suppurative destructive cholangitis (CNSDC), in particular, is a histological hallmark of PBC. In this report, we present an unusual case of AIH accompanied by CNSDC‐like bile duct injury in a 46‐year‐old woman. The patient's serum aminotransferase level was abnormally high. The serum levels of alkaline phosphatase, γ‐GTP and IgG were also elevated, but the IgM level was within normal limits. The titer of antismooth muscle antibody (SMA) was 1:80 , while antinuclear autoantibody (ANA) and the M2 fraction of antimitochondrial antibody (AMA) were both negative. Liver biopsy disclosed CNSDC‐like bile duct injuries and severe interface hepatitis and lobular hepatitis with perivenular zonal necrosis were observed. The aggregate score of the International Autoimmune Hepatitis Group corresponded to the category of probable AIH. Immunohistochemically, histocompatibility leukocyte antigen‐DR, which is aberrantly expressed in the damaged bile ducts of PBC, was not found in the injured bile ducts of this case. Laboratory data were much improved by treatment with prednisone, but ursodeoxycholic acid was not effective. Although the possibility of an overlapping syndrome of AIH‐ and AMA‐negative PBC could not be excluded, this case was diagnosed as AIH with CNSDC‐like bile duct lesions.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">autoimmune hepatitis</term><term xml:id="k2">bile duct injury</term><term xml:id="k3">chronic non‐suppurative destructive cholangitis </term></keywords><keywords rend="tocHeading1"><term>CASE REPORTS</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-FJHGHC12-2/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Science Pty</publisherName><publisherLoc>Melbourne, Australia</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1440-1827</doi><issn type="print">1320-5463</issn><issn type="electronic">1440-1827</issn><idGroup><id type="product" value="PIN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="PATHOLOGY INTERNATIONAL">Pathology International</title></titleGroup></publicationMeta><publicationMeta level="part" position="07007"><doi origin="wiley">10.1111/pin.2002.52.issue-7</doi><numberingGroup><numbering type="journalVolume" number="52">52</numbering><numbering type="journalIssue" number="7">7</numbering></numberingGroup><coverDate startDate="2002-07">July 2002</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0047800" status="forIssue"><doi origin="wiley">10.1046/j.1440-1827.2002.01377.x</doi><idGroup><id type="unit" value="PIN1377"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="tocHeading1">CASE REPORTS</title></titleGroup><eventGroup><event type="firstOnline" date="2002-08-21"></event><event type="publishedOnlineFinalForm" date="2002-08-21"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-02"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-06"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="478">478</numbering><numbering type="pageLast" number="482">482</numbering></numberingGroup><correspondenceTo> Yasuni Nakanuma, MD, PhD, Department of Human Pathology, Kanazawa University Graduate School of Medicine , 13‐1 Takara‐machi, Kanazawa 920‐8640, Japan. Email: <email normalForm="pbcpsc@kenroku.kanazawa-u.ac.jp">pbcpsc@kenroku.kanazawa‐u.ac.jp</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PIN.PIN1377.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="22"></count><count type="wordTotal" number="2262"></count><count type="linksPubMed" number="11"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Autoimmune hepatitis associated with bile duct injury resembling chronic non‐suppurative destructive cholangitis</title><title type="shortAuthors">Y. Sato</title><title type="short">Autoimmune hepatitis with bile duct injury</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Yasunori</givenNames><familyName>Sato</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Kenichi</givenNames><familyName>Harada</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Yoshiko</givenNames><familyName>Sudo</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>Kishichiro</givenNames><familyName>Watanabe</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a3"><personName><givenNames>Tohru</givenNames><familyName>Nakahama</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a3"><personName><givenNames> Hideo</givenNames><familyName>Morimoto</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1" corresponding="yes"><personName><givenNames>Yasuni</givenNames><familyName>Nakanuma</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="JP"><unparsedAffiliation>Department of Human Pathology, Kanazawa University Graduate School of Medicine, Japan,</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="JP"><unparsedAffiliation>Department of Pathology, National Hospital of Kanazawa, Kanazawa, Japan,</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="JP"><unparsedAffiliation>Department of Internal Medicine, National Hospital of Kanazawa, Kanazawa, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">autoimmune hepatitis</keyword><keyword xml:id="k2">bile duct injury</keyword><keyword xml:id="k3">chronic non‐suppurative destructive cholangitis </keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC) are representative autoimmune liver diseases in which hepatocytes and intrahepatic bile ducts, respectively, are selectively damaged by autoimmune mechanisms. Bile duct injury and loss is characteristic of PBC and chronic non‐suppurative destructive cholangitis (CNSDC), in particular, is a histological hallmark of PBC. In this report, we present an unusual case of AIH accompanied by CNSDC‐like bile duct injury in a 46‐year‐old woman. The patient's serum aminotransferase level was abnormally high. The serum levels of alkaline phosphatase, γ‐GTP and IgG were also elevated, but the IgM level was within normal limits. The titer of antismooth muscle antibody (SMA) was 1:80 , while antinuclear autoantibody (ANA) and the M2 fraction of antimitochondrial antibody (AMA) were both negative. Liver biopsy disclosed CNSDC‐like bile duct injuries and severe interface hepatitis and lobular hepatitis with perivenular zonal necrosis were observed. The aggregate score of the International Autoimmune Hepatitis Group corresponded to the category of probable AIH. Immunohistochemically, histocompatibility leukocyte antigen‐DR, which is aberrantly expressed in the damaged bile ducts of PBC, was not found in the injured bile ducts of this case. Laboratory data were much improved by treatment with prednisone, but ursodeoxycholic acid was not effective. Although the possibility of an overlapping syndrome of AIH‐ and AMA‐negative PBC could not be excluded, this case was diagnosed as AIH with CNSDC‐like bile duct lesions.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Autoimmune hepatitis associated with bile duct injury resembling chronic non‐suppurative destructive cholangitis</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Autoimmune hepatitis with bile duct injury</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Autoimmune hepatitis associated with bile duct injury resembling chronic non‐suppurative destructive cholangitis</title></titleInfo><name type="personal"><namePart type="given">Yasunori</namePart><namePart type="family">Sato</namePart><affiliation>Department of Human Pathology, Kanazawa University Graduate School of Medicine, Japan,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kenichi</namePart><namePart type="family">Harada</namePart><affiliation>Department of Human Pathology, Kanazawa University Graduate School of Medicine, Japan,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yoshiko</namePart><namePart type="family">Sudo</namePart><affiliation>Department of Human Pathology, Kanazawa University Graduate School of Medicine, Japan,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kishichiro</namePart><namePart type="family">Watanabe</namePart><affiliation>Department of Pathology, National Hospital of Kanazawa, Kanazawa, Japan,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tohru</namePart><namePart type="family">Nakahama</namePart><affiliation>Department of Internal Medicine, National Hospital of Kanazawa, Kanazawa, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hideo</namePart><namePart type="family">Morimoto</namePart><affiliation>Department of Internal Medicine, National Hospital of Kanazawa, Kanazawa, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yasuni</namePart><namePart type="family">Nakanuma</namePart><affiliation>Department of Human Pathology, Kanazawa University Graduate School of Medicine, Japan,</affiliation><affiliation>E-mail: pbcpsc@kenroku.kanazawa‐u.ac.jp</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Science Pty</publisher><place><placeTerm type="text">Melbourne, Australia</placeTerm></place><dateIssued encoding="w3cdtf">2002-07</dateIssued><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">0</extent><extent unit="tables">0</extent><extent unit="formulas">0</extent><extent unit="references">22</extent><extent unit="linksCrossRef">0</extent><extent unit="words">2262</extent></physicalDescription><abstract lang="en">Autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC) are representative autoimmune liver diseases in which hepatocytes and intrahepatic bile ducts, respectively, are selectively damaged by autoimmune mechanisms. Bile duct injury and loss is characteristic of PBC and chronic non‐suppurative destructive cholangitis (CNSDC), in particular, is a histological hallmark of PBC. In this report, we present an unusual case of AIH accompanied by CNSDC‐like bile duct injury in a 46‐year‐old woman. The patient's serum aminotransferase level was abnormally high. The serum levels of alkaline phosphatase, γ‐GTP and IgG were also elevated, but the IgM level was within normal limits. The titer of antismooth muscle antibody (SMA) was 1:80 , while antinuclear autoantibody (ANA) and the M2 fraction of antimitochondrial antibody (AMA) were both negative. Liver biopsy disclosed CNSDC‐like bile duct injuries and severe interface hepatitis and lobular hepatitis with perivenular zonal necrosis were observed. The aggregate score of the International Autoimmune Hepatitis Group corresponded to the category of probable AIH. Immunohistochemically, histocompatibility leukocyte antigen‐DR, which is aberrantly expressed in the damaged bile ducts of PBC, was not found in the injured bile ducts of this case. Laboratory data were much improved by treatment with prednisone, but ursodeoxycholic acid was not effective. Although the possibility of an overlapping syndrome of AIH‐ and AMA‐negative PBC could not be excluded, this case was diagnosed as AIH with CNSDC‐like bile duct lesions.</abstract><subject lang="en"><genre>keywords</genre><topic>autoimmune hepatitis</topic><topic>bile duct injury</topic><topic>chronic non‐suppurative destructive cholangitis</topic></subject><relatedItem type="host"><titleInfo><title>Pathology International</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">1320-5463</identifier><identifier type="eISSN">1440-1827</identifier><identifier type="DOI">10.1111/(ISSN)1440-1827</identifier><identifier type="PublisherID">PIN</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>52</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>478</start><end>482</end><total>5</total></extent></part></relatedItem><identifier type="istex">ED8943BE61D1A3D7CFA59BE2EA94D72D61EDF030</identifier><identifier type="ark">ark:/67375/WNG-FJHGHC12-2</identifier><identifier type="DOI">10.1046/j.1440-1827.2002.01377.x</identifier><identifier type="ArticleID">PIN1377</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Science Pty</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-FJHGHC12-2/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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