357 tarianism. The student trained in scientific thought would be and would ask for hard data. Pharmaceutical industries would suffer financially because their claims would be rejected as profit biased. There are a few inherent snags and contradictions in teaching science in medical schools. First, somebody must teach it to teachers. Secondly, those who grasp complex problems of epistemology will become humble because they find that the definite answers they were looking for did not exist. Their newly acquired awareness of ignorance will be of no use in their role of doctor from whom patients will expect to have knowledge. Sir George Pickering’ summarised this beautifully: "From the time of Galen to our own ... medicine always presented a facade of systematic knowledge, or alleged knowledge, Infor, like religion, medicine could not tolerate ignorance tellectual nihilism is the very stuff of which scientists are made, but it is scarcely convenient for a practising physician." Thirdly, doctors are split by the dichotomy of wishing to be taken seriously as scientists and, at the same time, to retain their elitist power and pomp.23 While the scientist freely shares his knowledge and ignorance in discussion, the doctor keeps his patient in darkness by necessity or habit. While science can play with general hypotheses at leisure, the doctor must give an instant ad-hoc judgement or treatment for an individual patient. Another problem, clearly exposed by Professor Campbell, is essentialism in medical thought. Contemporary medicine continues to be based on an aristotelian classification of diseases. In the grey area of non-health, new nosological territories are being charted and named after their discoverers, as if they have existed since the creation. Beyond this area lies the Blessed Land of Normal, often referred to in the mythology of medicine but never mapped. The Classical Case is viewed as materialisation of the Idea or Essence of Disease, as if all diseases were disorders of kind and not of degree. One of the first critics of Professor Campbell, Dr West (Jan. 31, p. 242), says: "A clear description of a rash is just as much a part of science as a definition of a kilopascal ..." In fact, neither has anything to do with nature and processes of science with which Professor Campbell is concerned. The first is just a description (i.e., an observational statement) and the other is an arbitrary definition. It was Aristotle who believed that science consists of definitions and by defining everything we would know everything; but that was more than 2000 years
encouraged to question "experience"
...
"early" group were admitted within 9 h, and, though the sumthey were treated in this period, the details
mary states that given in the text
effects of
variance with this claim. At best, the cysteamine only be assessed in the six "early" and the results seem to confirm our earlier finding of are at
can
patients, almost complete protection against paracetamol hepatotoxicity.’ The Newcastle workers, however, seem reluctant to accept this, despite the fact that in these patients the maximum levels of aspartate aminotransferase (A.S.T.) and ferritin were significantly lower with less histological evidence of liver damage. In most of the comparisons made by Douglas et al. the data from the six "early" and the twelve "late" patients were pooled even though most of the late group were admitted and treated far too late for cysteamine to be effective. Their conclusions are not valid. The "paracetamol index" described by Douglas et al. is inappropriate and further confuses the issue. There is enormous individual variation in the plasma-paracetamol half-life after overdosage,6 and it is possible for the plasma concentration to be well above and well below the line in fig. 1 of their paper at different times in the same patient. The value obtained for the paracetamol index may thus depend more on the time that the patient is admitted after ingestion than on the severity of intoxication. Furthermore, it can be calculated that even if the plasma concentrations decline in parallel with the line in their fig. 1 the "paracetamol index" at any given time will itself decrease exponentially with a half-time of 3 h. We have treated nineteen severely poisoned patients with cysteamine given within 10 h (mean 6-8 h) of ingestion of paracetamol. All but one had a plasma-paracetamol well above the line in fig. 1 in the article by Douglas et al. None had significant hepatic or renal damage, and there were no deaths. In
PROTECTIVE EFFECT OF CYSTEAMINE GIVEN WITHIN
10 h OF
INGESTION
IN PATIENTS WITH SEVERE PARACETAMOL POISONING
ago. Mater Misericordiæ Dublin, Ireland.
Hospital,
PETR SKRABANEK
CYSTEAMINE FOR PARACETAMOL POISONING
S 1000 units/I), and three died in hepatic failure (see table). Furthermore, many of our treated patients were at risk because of alcoholism or previous consumption of drugs causing induction of hepatic microsomal enzymes 7 -an important aspect not considered by Douglas et al. Seven other patients who could not be given cysteamine for 11.5-26-5 h after overdosage all developed severe hepatic necrosis (mean A.S.T. > 4470 units/1). Our results with cysteamine given within 10 h to patients with severe paracetamol poisoning reinforce our previously expressed reservationsconcerning the ethics of controlled trials of cysteamine in this situation. We hope that the confusing report by Douglas et al. will not cause cysteamine to be withheld from patients at risk of severe liver damage or death after paracetamol overdosage. Regional Poisoning Treatment Centre, and University Department of Therapeutics, Royal Infirmary, Edinburgh EH3 9YW.
L. F. PRESCOTT
J. PARK A. T. PROUDFOOT
6. Prescott, L. F., Wright, N., Roscoe, P., Brown, S. S. ibid. 1971, i, 519. 7. Wright, N., Prescott, L. F. Scott. med. J. 1973, 18, 56. 8. Prescott, L. F., Matthew, H. Lancet, 1974, i, 998.