Frequency of clonal intraepithelial T lymphocyte proliferations in XXXX , @entity66 , and refractory @entity1593 .

@entity1 @entity404 @entity1593 @entity66 @entity5 @entity1066 @entity784 @entity11112 @entity194 @entity405
BACKGROUND: Clonal T cell receptor (TCR) gene rearrangements and loss of T cell antigens such as @entity405 and @entity11112 in intraepithelial lymphocytes (IELs) may indicate the development of an @entity784 ( @entity784 ) in @entity1 with refractory @entity1593 . AIMS: To define the diagnostic value of these markers in duodenal biopsies from @entity1 with @entity194 as a result of various underlying disorders. @entity1 AND METHODS: Duodenal biopsies from eight @entity1 with @entity66 and five @entity1 with @entity194 caused by defined disorders were compared with three @entity1 with refractory @entity1593 evolving into overt @entity784 , two @entity1 with @entity1066 , and with eight @entity1 with overt @entity784 , for expression of CD3, @entity404 , @entity405 , and @entity11112 in IELs using immunohistochemistry and for clonal TCR-gamma gene rearrangements using polymerase chain reaction. In addition, biopsies from six consecutive @entity1 with refractory @entity1593 of uncertain cause were examined. RESULTS: Clonal TCR-gamma gene rearrangements were found in all resected @entity5 of @entity1 with @entity784 , in 3/8 duodenal biopsies of @entity1 with @entity784 , in 2/2 @entity1 with @entity1066 , in 2/3 @entity1 with refractory @entity1593 evolving into overt @entity784 , and in 1/6 @entity1 with refractory @entity1593 . No rearrangements were found in biopsies from @entity1 with refractory @entity1593 caused by defined disorders or those with @entity66 . Clonality in duodenal biopsies was associated with an abnormal phenotype of IELs in all cases and in all but one case in @entity1 with evidence of underlying @entity66 . Specificity for detection of an @entity784 using immunohistology was 77% for @entity405 and for @entity11112 staining, and 100% for detection of a clonal TCR-gamma gene rearrangement. Sensitivity was 62% for staining with @entity405 and clonality investigation, while sensitivity reached 100% for @entity11112 staining in all investigated @entity1 with @entity784 . CONCLUSIONS: Clonal proliferations of phenotypically abnormal IELs in refractory @entity1593 represent an early manifestation of @entity784 , for which the term " @entity1593 -like @entity784 " is proposed. This constellation is also found in duodenal biopsies from @entity1 with an overt @entity784 and is not related to other @entity1593 , resulting in a high specificity for detection of an @entity784 or refractory @entity1593 evolving into @entity784 . Overt @entity784 may develop directly from @entity66 without a precursor lesion (refractory @entity1593 with clonal IELs) being demonstrable in duodenal biopsies or via a " @entity1593 -like @entity784 ". This latter entity is a complication of @entity66 .
