Pathologic and clinical features of 77 Hodgkin's lymphoma patients treated in a lymphoma protocol (LNH87): a GELA study.
Between 1987 and 1993, 77 of 2855 lymphomas included in the LNH87 protocol of the GELA as non-Hodgkin lymphoma (NHL) and reviewed by a panel of pathologists had a diagnosis changed to Hodgkin lymphoma (HL). Some of these lymphomas had been initially interpreted as anaplastic large-cell lymphoma Hodgkin-like (ALCL-HL subtype). The purpose of this study was to analyze the histologic pitfalls initially encountered, to define more clearly the diagnostic criteria of lymphomas placed in the gray zone around HL, and to follow the survival of these 77 patients affected with HL and initially treated with NHL regimens. The 77 cases of HL were reviewed by three hematopathologists and immunostained with a large panel of antibodies, including CD30, CD15, CD3, CD20, CD45, CD43, LMP-1, EMA, BNH-9, TiA1, and ALK1. Each case was classified according to the Lukes-Rye system and the British National Lymphoma Investigation (BNLI) grading. The initial clinical presentation of patients was analyzed, and the overall and event-free survival rates of the 77 patients were estimated. Among the 77 HLs, 46 were misinterpreted as NHL by primary individual pathologists (12 as ALCL, 8 as ALCL-HL, 12 as peripheral T-cell lymphoma (PTCL), 6 as B-cell lymphoma, and 8 as unclassifiable NHL). The other 31 cases had been first considered by the panel as consistent with ALCL-HL (n = 18) or with PTCL (n = 13) and were changed later in view of an immunophenotype concordant with HL. Fifty-five percent of the patients completed the full NHL treatment. The 5-year event-free and overall survival rates were 54% and 77%, respectively. The current results indicate that lymphomas initially called ALCL-HL should not be regarded as a variant of ALCL, but as HL. The clinical consequences of misdiagnoses seem to be a lower event-free survival rate compared with that of classical HL, probably because of more relapses of initially inappropriately treated HL.
Cazals-Hatem
D
D
Service d'Anatomie Pathologique, Hôpital Beaujon, AP-HP, Clichy, France. dominique.cazals-haten@bjn.ap-hop-paris.fr
André
M
M
Mounier
N
N
Copin
M C
MC
Divine
M
M
Berger
F
F
Bosly
A
A
Kerneis
Y
Y
Brière
J
J
Quesnel
B
B
Diebold
J
J
Gaulard
P
P
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000378:metabolism; D001761:Bleomycin / Q000627:therapeutic use*; D003520:Cyclophosphamide / Q000627:therapeutic use*; D003937:Diagnosis, Differential; D004317:Doxorubicin / Q000627:therapeutic use*; D005260:Female; D006689:Hodgkin Disease / Q000188:drug therapy / Q000378:metabolism / Q000401:mortality / Q000473:pathology*; D006801:Humans; D007124:Immunoenzyme Techniques; D016130:Immunophenotyping; D017728:Lymphoma, Large-Cell, Anaplastic / Q000175:diagnosis; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000378:metabolism; D011241:Prednisone / Q000627:therapeutic use*; D015996:Survival Rate; D016896:Treatment Outcome; D014751:Vindesine / Q000627:therapeutic use*
D014408:Biomarkers, Tumor; D009363:Neoplasm Proteins; D001761:Bleomycin; D004317:Doxorubicin; D003520:Cyclophosphamide; D014751:Vindesine; D011241:Prednisone