1329 within normal limits may avoid ectopic and even prevent secondary hyperparathyroidism while allowing other bone diseases to progress. The continued use of oral phosphate binders risks phosphate depletion, causing bone disease,9 or symptoms related to In our low intracellular nucleotide concentration. 10 inverse correlation between plasmasignificant patients, phosphate and osteoid area suggests that the mineralisation defect is common when plasma-phosphate is within or below the normal range defined in individuals without renal failure (fig. 2). and
only
phosphorus
Royal South Hants Hospital, Southampton S09 4PE.
M. C. BISHOP.
EFFECTS OF HEPARIN DERIVED FROM DIFFERENT TISSUES ON PLASMA-PHOSPHOLIPIDS AND PLATELET AGGREGATION
SiR,-Mr Gillett and Dr Besterman (Nov. 24, p. 1204) report that no differences exist between the effects of two commercial heparin preparations from different animal tissue sources on plasma-lysolecithin formation or on collagen-induced platelet aggregation in man. These results are very interesting, but need to be compared with eight different degrees of response in aggregation of washed platelets in the presence of calcium ions and at a final concentration of 70 international units of heparin, with eight different commercial preparations of heparin, reported by Eika.11 Department of Pathology Frenchay Hospital,
R. D. EASTHAM.
Bristol BS16 1LE.
HISTOCOMPATIBILITY ANTIGENS, DISEASE, AND MORAL DILEMMAS
SIR,-Professor Burch and Dr Rowell (Nov. 24, p. 1208) have stated the moral dilemma which could arise if medical science makes further progress in identifying genetic predictors of disease. In terms of their belief that unpredictable stochastic processes 12 serve to initiate diseases in those at genetic risk, Burch and Rowell are right to suggest that predictive knowledge would not yield preventive power and that such knowledge could thus do more harm than good. However, they fail to emphasise that only a minority of individuals with an at-risk " genotype (such as HL-A27) actually develop the " predicted " disease (such as ankylosing spondylitis).13 Furthermore, there is evidence that predictable (and preventable) environmental causes can initiate disease in those at genetic risk; for example, it appears that paralytic poliomyelitis resulted from the interaction of the virus with susceptible HL-A genotypes.14Rather than baulking at the initial bitter taste of these new " fruits of the tree of knowledge ", we should digest and absorb them; knowledge of genetic factors predisposing to disease may help to identify environmental causes and allow us to choose a better environment for certain genotypes. Research should therefore be encouraged, not restricted. The worry raised in the mind of someone who finds that he is predisposed to a disease for which no prophylaxis is known can be minimised by the normal medical procedure of revealing about the prognosis, "
9. Bloom, W. L., Flinchum, D. J. Am. med. Ass. 1960, 174, 1327. 10. Lichtman, M. A., Miller, D. R., Freeman, R. B. New Engl. J. Med. 1969, 280, 240. 11. Eiks, C. Scand. J. Hœmat. 1972, 9, 480. 12. Burch, P. R. J., Rowell, R. G. Q. Rev. Biol. 1965, 40, 252. 13. Brewerton, D. A., Caffrey, M., Hart, F. D., James, D. C. O., Nicholls, A., Sturrock, R. D. Lancet, 1973, i, 904. 14. Morris, P. J., Pietsch, M. C. ibid. Oct. 13, 1973, p. 847.
as
and the
calcification
much as is appropriate for the individual patient particular disease.
Department of the Regius Professor of Medicine, Radcliffe Infirmary, Oxford OX2 6HE.
J. D. MATHEWS.
ULTRASONIC CEPHALOMETRY SIR,-It seems from the tone of Mr Campbell’s letter (Nov. 17, p. 1145) in response to the editorial (Oct. 20, p. 892) that our paper1 has been taken as a personal criticism of his work. If this is so, then we take this opportunity to apologise, for such was not our intent; indeed, we pointed out that we analysed the data from his paper2 because it was the only published work we could find giving sufficient detail against which a meaningful comparison could be made. There are interesting points raised by his letter upon which we should like to comment. (1) As Campbell suggests, our abilities in the use of ultrasonic techniques may be limited. We would point out, however, that in Newcastle two years’ experience with the assistance of a medical physics department with a special interest in ultrasonic techniques was gained before the trial was undertaken; in Aberdeen there had been many more years’ experience in this field. We can therefore claim that the results we obtained are perhaps reasonably representative of those which will be attained in a teaching maternity unit. Campbell’s suggestion implies that the usefulness of fetal cephalometry is further limited by the supply of those who can do it better. (2) While not detailing the " crucial signs " for the correct alignment of the ultrasonic beam, we stated that we followed the methods previously described by Campbell himself. It now appears that " about ten measurements in the transcoronal plane " are necessary to ensure that the correct diameter has been obtained. Mr Campbell3 stated previously that about 50 patients can be scanned per day; assuming a working day of 7 hours non-stop this means an average of just over 8 minutes per patient. Our experience is that ten independent transcoronal readings per patient could require 15-20 minutes. (3) We appreciated that our paper was somewhat technical and in an attempt to make it palatable we may have telescoped our arguments excessively. We defined what we believe to be three major, and independent, sources of error in the ultrasonic determination of the rate of growth of the fetal head. Perhaps we should expand briefly on the third source of error, the physical limitations which Campbell dismisses as " either non-entities or of negligible significance ". We have said that the ultrasonic B.P.D. measurement is essentially a measurement of the time between two echoes as displayed on the A-scan. The relationship between this and the physical length of the B.P.D. depends on many factors including:
(a) The speed
with which the ultrasonic pulse is propagated each of the tissues within the fetal head and the thickness of each tissue; (b) the shapes of the echo pulses reflected from the two sides of the head (these will be influenced by the geometry of the tissue layers adjacent to the skull, their acoustic properties, and the ultrasonic frequency); (c) the shape of the ultrasonic beam within the vicinity of the fetal head (this depends on the distance and acoustic characteristic across
Davison, J. M., Lind, T., Farr, V., Whittingham, T. A. J. Obstet. Gynœc. Br. Commonw. 1973, 80, 769. 2. Campbell, S. ibid. 1970, 77, 1057. 3. Campbell, S. Proceedings of the 2nd Study Group of the Royal College of Obstetricians and Gynæcologists, 1971 (edited by S. Clayton and R. Beard). 1.