LEUKAEMIA IN YOUNG CHILDREN

960 * TABLE II-COHORT DATA*

be excessive in the brains of schizophrenic patients.6.7 Were any such excess to be found, this could still, on our formulation of events, have a primary basis in neurodevelopmental deviance. The atrophy of normal ageing, which is subject to large individual differences, may interact with the consequences of developmental anomaly in schizophrenia to determine not just cerebral morphology but also the clinical picture and the response to treatment.8

developmental abnormality) might

Department of Clinical Pharmacology, Royal College of Surgeons in Ireland,

I

Dublin 2, Ireland

JOHN L. WADDINGTON

Cluain Mhuire Family Centre, Blackrock, Co Dublin

EADBHARD O’CALLAGHAN CONALL LARKIN

O’Callaghan E, Larkin C, Redmond O, Stack J, Ennis JT, Waddington JL. "Early onset schizophrenia" after teenage head injury: a case report with magnetic resonance imaging. Br J Psychiatry 1988; 153: 394-96. 2. Nagata K, Basugi N, Fukushima T, et al. A quantitative study of physiological cerebral atrophy with ageing: a statistical analysis of the normal range. Neuroradiology 1987; 1

29: 327-32. 3. Stafford JL, Albert MS, Naeser MA, Sandor T, Garvey AJ. Age-related differences in

computed tomographic scan measurements. Arch Neurol 1988; 45: 409-15. DGC, Johnstone EC, Crow TJ, Frith CD, Jagoe JR, Kreel L. Lateral ventricular size in schizophrenia. relationship to the disease process and its clinical manifestations Psychol Med 1985; 15: 27-41. 5. Rossi A, Stratta P, Casacchia M, D’Albenzio L, Schiazza G, De Donatis M. Age and duration of illness as predictors of ventncular brain ratio (VBR) size in chronic schizophrenic patients. Acta Psychiatr Scand 1987; 76: 256-60. 6. Roberts GW, Colter N, Lofthouse R, Bogerts B, Zech M, Crow TJ. Gliosis in schizophrenia: a survey. Biol Psychiatry 1986; 21: 1043-50. 7. Casanova MF, Stevens JR, Bigelow LB. Gliosis in schizophrenia. Biol Psychiatry

4. Owens

1987; 22: 1172-75. 8.

Waddington JL The ageing brain, neuroleptic drugs and the enigma of schizophrenia. Ir J Med Sci 1988; 157: 135-41.

LEUKAEMIA IN YOUNG CHILDREN

SiR,—The unusual pattern of leukaemia in young children in Scotland, reported by Dr Gibson and colleagues (Sept 10, p 630) prompted us to examine the Leukaemia Research Fund data collection survey’s registrations for cases in other parts of the UK. We looked at all new registrations from Jan 1,1984, to July 31,1988. In view of possible concern about cases subsequent to the Chernobyl radioactivity accident, we grouped the children, by address at diagnosis, into those who might have received relatively more radioactive fallout (Cumbria, South Wales, and Yorkshire health regions) and less fallout (Trent and the South-West England health regions) according to the distribution described by Clark and Smith.l The survey does not cover the whole of the UK, and only those parts for which data collection began on Jan 1, 1984, with continuation to the present and covering entire counties are used here. The data are presented by annual age-specific rates for any leukaemia in children diagnosed before their fifth birthday and by birth cohort for children born in 1983-87. The annual rates (table I) show stability of case occurrence by area. This stability makes the Scottish observation more striking. The rates for Cumbria are higher but numbers are small and the increase is confined to children born before 1986. Birth cohort data (table II) more accurately reflect temporal trends, through factors influencing events during gestation and shortly after birth. The 1988 numbers have been estimated on the basis of the first seven months of registration and the patterns in previous years. In table II there is no evidence for higher rates related to the Chernobyl accident (ie, the 1986 or 1987 cohorts). TABLE I-CHILDHOOD LEUKAEMIA IN SELECTED PARTS OF ENGLAND AND WALES I

I

1984-88* J

*Expressed as number of cases (and rate per 100 000 person-years) for ages 0-4 combined pooled sexes, by year of diagnosis. tIncomplete ascertamment; no rates given.

with

I

I

I

born 1983-87 and diagnosed up to July, 1988. No adjustment for migration or death. Number of cases (rate per 100 000 live births). tadjusted numbers and rates YOB =year of birth. *Cohorts of

cases

However, if there is an effect it will become more apparent over the next 2 years. The unusually high predicted figure for young cases in the 1987 birth cohort (n = 10) is based on 5 cases found earlier this year (none from Cumbria or Wales). These cohorts will need a lapse of time for further cases to occur before any interpretation can be placed upon them, and it would be dangerous to predict a trend on the basis of these preliminary data. There is, on this basis, a clear place for routine birth cohort analysis of childhood incidence data. The Leukaemia Research Fund Centre in Leeds is planning such an exercise. Funded by the Leukaemia Research Fund. We thank haematologists and paediatric oncologists in different parts of England and Wales for their collaboration and Mr Jon Dunnington, Mr Jim Miller, and Miss Lorraine Harvey. Leukaemia Research Fund Centre for Clinical Epidemiology, 17 Springfield Mount, Leeds LS2 9NG

1. Clark MJ, Smith FB. Wet and dry deposition of

RAY A. CARTWRIGHT PATRICIA A. MCKINNEY FREDA E. ALEXANDER JAMES RICKETTS Chernobyl releases. Nature 1988; 332:

245-49.

TREATMENT OF ESSENTIAL THROMBOCYTHAEMIA BY ALPHA 2a INTERFERON

SIR,-Dr Giles and colleagues (July 9, p 70) report experience with alpha interferon (IFN-0c) in essential thrombocythaemia. Twelve patients were treated with IFN-a2b (’Intron’; KirbyWarrick) and six with IFN-02a (’Roferon’, Roche). The dose was 3 x 106 units daily, rising to 5 x 106units at day 30 if the platelet count remained above 600 x 109f1. All patients had a better than 50% decrease in platelet count by day 28 and counts remained below 600 x 109/1 for 2-5 months since induction therapy, with a decrease in dose of IFN-a. Results were similar in four patients previously treated with chemotherapy. No difference was seen between IFN-a2a and IFN-cz2b’ Our experience differs considerably. We treated twelve patients with essential thrombocythaemia with roferon. In the first six patients (two had been previously treated with chemotherapy), the daily dose was 9 x 106 units for 2 months, followed by 6 x 106 units every 2 days for 4 months. Platelet count decreased by 50% in all patients between day 7 and 21, and were below 400 x 109/1 between days 7 and 50 (table). Side-effects (asthenia, lethargy, myalgia, alopecia, and weight loss) were seen at varying intensities in all patients and led to withdrawal of two patients. Except for one patient who remained in remission (platelet count below 600 x 109/1) after a year, the three other patients became resistant to therapy between days 90 and 150. Side-effects prevented dose increases. Six other patients (two had been previously treated with chemotherapy) received 4.5 x 106 units daily for 2 months and then every 2 days for 4 months (or even 3 x 106 units daily every 2 days). Decreases of 50% in platelet count were seen later than in the first group, occurring between days 15 and 120, and counts below 600 x 109/1 were observed in four patients between days 15 and 45. Levels below 400 x 109 were not observed. Side-effects were less intense than in the first group but led to withdrawal of two patients at 3 and 4 months. Platelet count remained below 600 x 109/1 in only