Buenas Tarreas

1184

BRITISH MEDICAL JOURNAL

VOLUME 294

9 mY 1987

year at school, as well as to their parents. A few genetic clinics are necessary to provide this service; ophthalmological support is essential for an accurate diagnosis, itself a prerequisite for meaningful genetic counselling. The "new genetics," with prenatal diagnosis by chorion biopsy of genetically determined disorders, hasdramatically changed the prospects of secondary prevention. Among the conditions that may now be diagnosed early in pregnancy are X linked retinitis pigmentosa,9 choroideraemia,'0 and retinoblastoma."I This list should increase over the next few years, with additional- autosomal recessive, autosomal dominant, and X linked conditions. Hence secondary prevention of genetically determined diseases willbecome increasingly important. This is yet another reason why genetic counselling should be made available to all visually handicapped children and their families. BARRiE JAY
Professor of Clinical Ophthalmology, University of London, Moorfields Eye Hospital, London EC1V 2PD
I Sorsby A. The causes of blindness inEngland and Waks. London: HMSO, 1950. 2 Sorsby A. The incidence and causes of blindnessin Englad and Waks 1948-1962. London: HMSO, 1966. 3 Sorsby A. The incidence and causes of blindness in England and Waks 1963-68. London: HMSO, 1972. 4 Department of Health and Social Security. Blindness and partial sighs in England 1969-1976. London: HMSO, 1979. (DHSS reports on public health and medical subjects No 129.) 5 Fraser GR, Friedmann AI. The causes of blindness in childhood. Baltimore:Johns Hopkins Press,

1967..
6 Schappert-Kimmniiser J. Causes of severe visual impairment in children and their prevention. Doc 7 Phillips CI, Levy AM, Newton M, Stokoe NL. Blindness in schoolchildren: importance of heredity, congenital cataract and prematurity. Brtis Ophthalmol (in press). 8 Carter CO. Prevention ofblindness from retinitis pigmentosa-discussion. Trans Ophthalmol Soc
9Bhattacharya SS, Wright AF, Clayton JF, et al. Close genetic linkage between X-linked retinitis pigmentosa and a restriction fragment length polymorphism identified by recombinant DNA

Ophihalmol 1975;39:213-341.
UK 1978;98:311-2.

probe L1.28. Nature 1984j309:253-5. 10 Nussbaum RL, Lewis RA, Lesko JG, Ferrell R. Choroideremia is linked to the restriction fragment length polymorphism DXYSI atXql3-21. AmJ Hum Genet 1985;37:565-75. 11 Sparkes RS, Murphree AL, Lingua RW, et al. Gene for hereditary retinoblastoma assigned to human chromosome 13 by linkage to esterase D. Science 1983;219:971-3.

Laboratory control of oral anticoagulants
A several fold variation in the mean warfarin dose in different geographical locations has been reported in a recent international survey.' The main cause ofthe variation was the tissue thromboplastin in the test for the prothrombin time. North American centres, which used rabbit brain thromboplastin almost exclusively, gave more warfarin than centres elsewhere, which used human brain reagents. This problem was resolved in Britain with the introduction in 1969 of the national--system for anticoagulant control by the British Society for Haematology. Asingle reagent, British comparative thromboplastin, was adopted as the national reference preparation and was linked to a national system of reporting the British ratio. British comparative thromboplastin was a designated batch of the routine reagent, Manchester comparative thromboplastin, which until recently was employed by over 95% of British hospitals. This human brain tissue extract had tobe withdrawn in early 1986 because of the possible risk of contamination by human immunodeficiency virus tissue from the central nervous system. Other thromboplastin reagents are now again being used to estimate the prothrombin time in British hospitals. Does this matter or has the problem been solved by

the prothrombin time standardisation system based on international normalised ratios-...