Literature DB >> 7503362

Chronic hepatitis. An update on terminology and reporting.

K P Batts1, J Ludwig.   

Abstract

The terms chronic active hepatitis (CAH), chronic persistent hepatitis (CpH), and chronic lobular hepatitis (CLH) have become obsolete, and their use without further specifications should be discontinued. This recommendation has become necessary because these names have changed from descriptive terms, intended for grading, to terms that are used either as morphologic diagnoses or disease designations or both, depending on individual preferences. Because this practice has caused serious misunderstandings, many authors and two international groups have recommended the use of a clear etiologic terminology. For the reporting practice of pathologists, we recommend that the pathologist routinely sign out biopsy samples with features of chronic hepatitis by indicating etiology, grade, and stage. An example would be autoimmune hepatitis, severe, stage 3. The stage in this case would indicate the presence of well-developed septal fibrosis but no nodular regeneration. Obviously, for the etiologic diagnosis, morphologic findings must be integrated with clinical and laboratory data. If this information is not available, clear morphologic diagnoses should be reported. Thus, instead of CPH, the diagnosis should be portal hepatitis, cause undetermined. This reporting practice eliminates ambiguous terminology and avoids the risk of inappropriate treatment as might occur, for example, when a term such as CAH is used to describe Wilson's disease and is misunderstood to mean autoimmune hepatitis. For a transitional period and to facilitate relearning, the terms CAH, CPH, and CLH can be reported in parentheses behind the etiologic diagnosis.

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Year:  1995        PMID: 7503362     DOI: 10.1097/00000478-199512000-00007

Source DB:  PubMed          Journal:  Am J Surg Pathol        ISSN: 0147-5185            Impact factor:   6.394


  266 in total

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Journal:  Pathologe       Date:  2004-09       Impact factor: 1.011

4.  Influence of liver histopathology on transaminitis following total pancreatectomy and autologous islet transplantation.

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5.  Autoimmune hepatitis induced by syngeneic liver cytosolic proteins biotransformed by alcohol metabolites.

Authors:  Geoffrey M Thiele; Michael J Duryee; Monte S Willis; Dean J Tuma; Stanley J Radio; Carlos D Hunter; Courtney S Schaffert; Lynell W Klassen
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7.  Fast food diet mouse: novel small animal model of NASH with ballooning, progressive fibrosis, and high physiological fidelity to the human condition.

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8.  Inter-observer variability in histopathological assessment of liver biopsies taken in a pediatric open label therapeutic program for chronic HBV infection treatment.

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Journal:  World J Gastroenterol       Date:  2006-03-21       Impact factor: 5.742

9.  Evaluation of the aspartate aminotransferase/platelet ratio index and enhanced liver fibrosis tests to detect significant fibrosis due to chronic hepatitis C.

Authors:  John R Petersen; Heather L Stevenson; Krishna S Kasturi; Ashutosh Naniwadekar; Julie Parkes; Richard Cross; William M Rosenberg; Shu-Yuan Xiao; Ned Snyder
Journal:  J Clin Gastroenterol       Date:  2014-04       Impact factor: 3.062

10.  The murine coronavirus nucleocapsid gene is a determinant of virulence.

Authors:  Timothy J Cowley; Simon Y Long; Susan R Weiss
Journal:  J Virol       Date:  2009-12-09       Impact factor: 5.103

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