High Proportion of Hodgkin-Like Large B-Cell Proliferations Associated with Background Peripheral T-Cell Lymphoma — A Diagnostic Pitfall
LHC Tan, AKW Lee, LL Chiu, ESC Koay. Singapore General Hospital, Singapore, Singapore; National University Hospital, Singapore, Singapore; National University of Singapore, Singapore, Singapore
Background: The latest WHO lymphoma classification recognizes an entity dubbed “B-cell lymphoma, unclassifiable with features intermediate between diffuse large B-cell lymphoma (DLBCL) and classical Hodgkin lymphoma (CHL)”. In our Singaporean practice, we have encountered other forms of large B-cell (LBC) proliferation that do not fit these entities, arising in background peripheral T-cell lymphoma (PTCL).
Design: 45 of such cases were reviewed immunohistologically and by PCR for clonality of T-cell receptor (TCR) and immunoglobulin heavy chain (IGH) gene rearrangements. All established variants of HL and LBCL, including T-cell/histiocyte-rich and lymphomatoid granulomatosis, were excluded according to WHO criteria.
Results: The mean patient age was 59 (range 27-88) years, with a male:female ratio of 1.8; 77.8% were Chinese. 82.2% had nodal presentation, none mediastinal. 46.7% were initially wrongly diagnosed; 9 (20%) were labelled “non-neoplastic”, (7 “atypical lymphoid hyperplasia”, 1 “dermatopathic lymphadenopathy” and 1 “plasma cell-variant Castleman's disease”). 42 cases (93.3%) had background immunomorphological features interpretable as PTCL, with monoclonal TCR gene rearrangements in 23/35 (65.7%). 20 cases (47.6% of PTCL) were angioimmunoblastic (AITL), 3 of which showed synchronous TCR and IGH clonality, the latter transient in 1 case (also the one of 4 with hyperplastic GC). A case each of AITL recurred as either DLBCL or CHL, neither with initially demonstrable IGH clonality. 3 cases amounted to composite unspecified PTCL-CHL, 2 of which, together with an additional 3 cases, were originally misinterpreted as some form of HL, including a case called CHL involving marrow with a discordant nodal diagnosis of LBCL. 2 other marrow cases showed either spontaneous disappearance of LBC or phenotypic change from CD20+/CD30- to CD20-/CD30+, supporting a primary diagnosis of PTCL despite lack of demonstrable TCR clonality. Another AITL with TCR monoclonality but IGH polyclonality disclosed transient plasmacellular lambda light chain restriction in marrow, mimicking marginal zone lymphoma with extreme plasmacytic differentiation.
Conclusions: Whenever LBC proliferations atypical of DLBCL or HL are encountered, it would be prudent to exclude background PTCL by immunomolecular scrutiny.
Wednesday, March 24, 2010 9:30 AM
Poster Session V # 206, Wednesday Morning