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Three patients with acute lymphoblastic leukaemia are reported in whom Hodgkin's disease developed during chemotherapy-maintained remission. This association has been reported only once before. The pathogenesis of the Hodgkin's disease in these patients is discussed, including the possible role of anti-leukaemic therapy.

Fifty-six untreated patients with acute leukemia (38 acute myelogenous leukemia, 16 acute lymphoblastic leukemia, and 2 blast crisis of chronic granulocytic leukemia) were randomized on admission to one of three groups--one to receive oral anticandidal prophylaxis through the period of remission induction chemotherapy with nystatin, another to receive natamycin, and the third to receive no anticandidal prophylaxis. Neither of the first two groups show any advantage over the last and it is concluded that provided gut sterilization regimes are not employed, prophylactic oral anticandidal treatment is of no value in these patients and should be reserved until there is clinical evidence of infection.

Of 47 consecutive patients aged 15-60 years with acute non-myelogenous leukaemia (ANML) (40 acute lymphoblastic leukaemia (ALL); 5 acute Burkitt-like leukaemia (ABLL), 2 acute undifferentiated leukaemia (AUL) treated with a standard chemotherapy protocol (OPAL), 31 achieved complete remission (28/40(70%) of patients with ALL). CNS leukaemia occurred in 4/16 non-remitters, and in 6 patients who achieved complete remission (CR). CNS leukaemia occurred in all 5 patients with acute Burkitt-like leukaemia. 4/28 patients with ALL achieving CR had evidence of CSF involvement on cytocentrifuge examination shortly after CR. The apparent risk of early CNS disease suggests that prophylactic CNS therapy should be given early in the treatment of acute non-myelogenous leukaemia.

Fifty-one adults with acute lymphoblastic leukaemia were entered into a trial of intense initial chemotherapy and early "prophylaxis" of the central nervous system (CNS). Initial treatment with OPAL (Oncovin (vincristine), prednisolone, adriamycin (doxorubicin), and L-asparaginase (colaspase)) followed by craniospinal or cranial irradiation and intrathecal methotrexate produced remission in 36 patients (71%). Seventeen of these patients relapsed three to 18 months after the start of remission; the remainder had been in remission for 12 to 52 months by the end of the study. The predicted median duration of complete remission was 18.5 months. None of the four patients who initially had clinical evidence of CNS disease, three of whom also had leukaemic cells identical to those found in Burkitt's lymphoma, achieved remission. Those patients who initially had hepatomegaly or splenomegaly had a shorter remission than those without. The predicted median survival was 27 months in those who achieved complete remission, one month in those who did not, and 21 months overall. The addition of colaspase and doxorubicin to vincristine and prednisolone and the use of early CNS treatment clearly improved the remission rate among adults with acute lymphoblastic leukaemia, though the presence and length of remission was affected by the extent of disease at presentation. Burkitt-like leukaemia, which had a poor prognosis, is probably a separate disease and may benefit from a different therapeutic approach.