Effective treatment for rhinopulmonary mucormycosis in a boy with leukaemia 557 Effective treatment for rhinopulmonary mucormycosis in a boy with leukaemia

suMMARY Lymphoblastic leukaemia in a 3-year-old child was complicated by rhinopulmonary mucor-mycosis. This was successfully treated by surgical resection of the nasal mass, pulmonary lobectomy, combined with amphotericin. Effective treatment of childhood lymphoblastic leukaemia has been associated with an increased Myer et al., 1972). Successful management of rhinopulmonary mucormycosis in childhood malig-nancy has not been reported. Case history In July 1971, a 3i-year-old white boy with a leucocyte count of 7 * 7 x 109/1 was diagnosed as having acute lymphoblastic leukaemia (ALL). Chemotherapy was begun with daily prednisolone (40 mg/m2) and weekly vincristine (1 * 5 mg/M2). Once in remission at 4 weeks, central nervous system prophylaxis was given (2000 rads to the craniospinal axis over 13 days with weekly injections x 2 of intrathecal metho-trexate 0 5 mg/kg). Maintenance was with daily 6-mercaptopurine (50 mg/M2), weekly oral metho-trexate (20 mg/M2), and cyclophosphamide (200 mg/m2), with vincristine and prednisolone pulses every 3 months. In May 1974 the child developed a right hemi-paresis and a left 3rd and right 6th and 7thcranial nerve palsies. Fundoscopy was normal and there was no meningismus. Investigations identified a 2-3 cm mass to the left of the midline at midbrain level, deviating the 3rd ventricle to the right. Lumbar thecal pressure was normal with CSF glucose 65 mg/ 100 ml (3-6 mmol/l) and protein 38 mg/100 ml (0 * 38 g/l), with no cells. Abnormal vascularitywasconfirmed on carotidarteriography. Biopsywas deferred because of the lesion site but a trial of irradiation to a total dose of 4000 rads (2500 rads to whole brain and 1500 rads to midbrain) over 18 days produced slight improvement in limb power only. This was considered to suggest a new tumour, not a leukaemic or encephalopathic lesion. Computerised axial tomography_(CAT) showed an increase in tumour size. Leukaemic therapy was stopped and oral 1-(2-chloroethyl)-3 cyclohexyl-1 nitroso-urea (CCNU) began (100 mg/m2) orally every 6 weeks. Between the first two dosages the tumour enlarged by a further 20% with neovascularity, but the child remained clinically well at school. Neither bone marrow nor CSF showed evidence of leukaemic relapse until April 1976 (22 months after stopping antileukaemic treatment) when he developed a left-sided broncho-pneumonia coincident with haematological relapse. Leukaemic therapy was restarted and CCNU stopped. Remission was again achieved after one month. CAT scan showed calcification without further enlargement of the midbrain lesion. One month later (2 years after the development of hemi-paresis) he …