2ND MALIGNANT-TUMORS IN CHILDHOOD HODGKINS-DISEASE

This study was undertaken to determine the treatment-specific incidenc e of second malignant tumours (SMT) in childhood Hodgkin's disease. Th e institutional databases at The Hospital for Sick Children, the Princ ess Margaret Hospital, and the Toronto-Bayview Regional Cancer Centre were reviewed for the years 1958-1993. Three hundred and forty-three c onsecutive newly diagnosed children were evaluated. The overall 30 yea r cumulative SMT incidence was 31%. The 20 year SMT incidence was grea ter for patients who relapsed (n = 129), 27%, compared with patients w ho remained relapse free (n = 214), 13%. For patients with stage 1-3B disease who remained relapse free, the 10 year SMT rate was 7% for pat ients who were surgically staged and treated with extended field radia tion treatment (EF RT) (35 G), compared with 3% in clinically staged p atients treated with MOPP (six cycles) and EF RT (25-30 G). To date th ere is no significant difference in the oncogenicity of these treatmen t protocols. However, EF RT alone was less effective in disease contro l. For stages 1-3B, 62% of patients relapsed after EF RT alone compare d with 18% after bimodal treatment. Therefore treatment intensificatio n due to relapse was more frequent in the former group. The overall 10 year SMT incidence for patients treated with these protocols was 11% and 3%, respectively. The 20 year SMT incidence following EF RT alone was 24%. We conclude that SMTs were a common late complication in chil dhood Hodgkin's disease and are a limiting factor in the achievement o f cure. The incidence of SMTs was increased in children who required r etreatment and was minimal in children who remained in a first complet e remission. Therefore the initial treatment strategy in childhood Hod gkin's disease must be to minimize the risk of relapse, in order to av oid the morbidity and mortality associated with both relapse and SMT i nduction, and to achieve this objective with a primary treatment proto col of low oncogenicity. (C) 1996 Wiley-Liss, Inc.