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Autoimmune ITP transmitted by liver transplantation
933
Skull-duggery at a Royal College?
Autoimmune ITP transmitted by liver
Students of prehistoric man grow as old as the material they study, it seems; of the two, the fossils are by far the nicer. From the end of 1912 anthropologists and palaeontologists began to debate with acid vigour a handful of bones from a shallow gravel pit in Sussex. Years later those same men-older, no less tetchy, and little the wiser-were still at it. For a long time now we have known that their passion was directed at half the jaw of an orang-utang and bits of a not very old skull that in life had been nowhere near the Home Counties. Eoanthropus dawsoni was a hoax, and so were all the Piltdown finds. Frank Spencer has written an excellent, detailed account of the Piltdown story, setting it against a background of how 1 scientists, between roughly 1900 and 1950, saw the dawn of man. (The Piltdown Papers, that accompany this book, are not for the general reader, who would find the material dull and confusing.) Spencer does come up with a culprit, saving him for the end. The book is jointly published by the British Museum (Natural History), which is where the Uckfield solicitor, fossil enthusiast, and plagiarist Charles Dawson took his "fmd". It is in a very different museum-that of the Royal College of Surgeons of England-that Spencer gets his man, the anatomist Arthur Keith. Previous suspects, including Pierre Teilhard de Chardin and Arthur Conan Doyle, are argued away. As is W. J. Sollas, victim of near-deathbed revenge by the man he had kept waiting so long for his Oxford chair. Others went to their graves with a nod and a wink, including M. A. C. Hinton. In 1978 New Scientist ran a series of Piltdown articles in which Hinton was alleged to have tried to smoke out the hoaxer by planting an obvious fake, a hypothesis that Spencer does not spend time on. It is one of the frustrations of this book that the reader remains uncertain about how good the Piltdown fakes were; a joker and a fraudster would use different techniques and have different motives. Spencer’s accusation has, naturally, been ill-received by the Royal College and by the family, but it has not yet been countered. The prosecution case is no less, but no more, convincing than earlier ones. The hoaxer(s) must have had the means, the motive, and an ability to sustain behaviour consistent with the deed for many years. Keith died in 1955, two years after the fraud was exposed and forty-three after the formal presentation of Arthur Smith Woodward’s reconstruction at a meeting in London on Dec 18, 1912. Keith had the skills, but he cannot have salted the Piltdown site unaided. Dawson, a strong suspect in his own right, may have been the co-conspirator. Keith burned correspondence with Dawson and in an interview in 1953 he muddled dates, but there are plenty of chronological misrecollections in this tale. Spencer is unconvincing on motive. Why so studiously correct Smith Woodward’s model to one more supportive of his own view on the age of "dawn man" if he knew the thing to be a hoax? How would the Natural History Museum react? Keith’s fiercest opponent came from Manchester not South Kensington. In Keith’s own lifetime some anthropologists refused to accept that jaw and skull belonged to the same creature and the exposure of "Piltdown man" was greeted with relief-so, medium to long term Keith gained nothing. A key finding is an entry in Keith’s diary for 1912, in which he noted that he had written an account of "the meeting" two days before it happened. The meeting began at 8 o’clock on the Wednesday evening, and the British Medical Journal of that week does contain a remarkably detailed account entitled Discovery of a New Type of Fossil Man-more detail, Spencer claims, than could have been known beforehand by anyone who had not already visited the site. Spencer tells us nothing about press times at the BM] in those days; and he is asking us to accept that Keith and Smith Woodward were not on good enough terms for much site information to have been shared when Keith saw the specimens a few days before the meenng. The Piltdown forgery now has another suspect-but not at the level "beyond reasonable doubt" that this book seems to be
transplantation
or so
claiming.
Pltdol4m a Saennfic Forger. B, Frank Spencer London and Oxford. Natural Ht5torB Museum Publications Oxford Lmverstrv Press. 1990. Pp 272 yi7 95. 1 SBN’ 0-198585225 .
A
woman
with
primary biliary cirrhosis
became
severely
thrombocytopenic (platelet count 10 x l0"/l) 2 days after she received a liver transplant from a patient with a 26-year history of idiopathic thrombocytopenic purpura who died from an intracranial haemorrhage.1 A bone-marrow aspirate on day 5 showed normal megakaryocytes, so peripheral destruction of platelets was likely. She recovered only after an emergency retransplantation. The donor’s serum contained antibodies against glycoprotein complex IIb-IIIa (platelet surface constituents). These antibodies were identified in the recipient after transplantation and disappeared after treatment with intravenous gammaglobulin, plasma exchange, and retransplantation. Post-transfusion thrombocytopenia was thought to be an unlikely diagnosis because it occurs at least 5 days after a blood transfusion and because it is usually accompanied by the production of antibodies reactive with platelet-specific allo-antigens. The authors point out that the case indicates that livers from donors with autoimmune idiopathic thrombocytopenia and, by implication, any autoimmune condition should not be used for transplantation. They also say that the fact that the donor’s heart was given to a woman with idiopathic cardiomyopathy without complications developing is probably a reflection of the difference between the liver and the heart in lymphoid mass.
PJ, McCarthy LJ, Filo RS. Transmission of idiopathic (autoimmune) thrombocytopenic purpura by liver transplantation. N Engl J Med 1990; 323: 807-11.
1. Friend
The cost of
clozapine
neuroleptic drug, is potentially very of schizophrenia, but in practice its severely limited by an associated risk of agranulocytosis. It is used, often successfully, when other treatments have failed, but its effects on the white-cell count have to be monitored closely. In the UK, where the provision of a patient monitoring system was made a mandatory part of the product licence, the drug’s manufacturer, Sandoz, insists that all prescribers and dispensers of clozapine and all patients taking the drug are registered with the company. Patients’ blood samples (taken weekly for the first 18 weeks of treatment and fortnightly thereafter) are sent for analysis to a central laboratory and the results are sent both to Sandoz and to the prescribing psychiatrist. A year’s treatment in the UK, including the analyses, costs about 1500. National Health Service patients, however, pay only the standard prescription charge, or nothing at all if exempt. Things are very different in the United States, where the cost of clozapine (more than three times as much as in the UK, making it one of the most expensive therapeutic drugs available there) and the refusal of some state Medicaid programmes to pick up the tab put the treatment way beyond the reach of most patients. Clozapine was released for clinical use in the USA in February, 1990 (at roughly the same time as in the UK), but so far only about 5500 US patients are taking it. Carl Salzman, a psychiatrist at Harvard Medical School, ascribes the high price of clozapine in the United States to "bundling", an unusual form of monopoly in which the availability of the drug is linked to a mandatory distribution and monitoring system.1 Collecting blood samples and distributing the drug, which in the UK are carried out by the NHS, are in the USA subcontracted to a commercial agency (which, according to Salzman, charges a phlebotomy fee even to hospitals whose own staff take the blood samples.) Furthermore, in the United States supplies of clozapine are not held by pharmacies but are released by the distributors week by week for individual patients who have had a satisfactory blood result. Salzman argues that the work of Sandoz’s expensive Clozapine Patient Monitoring System (CPMS), set up to comply with the Food and Drug Administration’s safety requirements, might be done just as effectively and more cheaply in existing facilities in universities and major hospitals. Sandoz, however, would be unlikely to consider relinquishing control of monitoring (for-fear, Clozapine (’Clozaril’),
useful in the usefulness is
a new
treatment
Skull-duggery at a Royal College?
Autoimmune ITP transmitted by liver
Students of prehistoric man grow as old as the material they study, it seems; of the two, the fossils are by far the nicer. From the end of 1912 anthropologists and palaeontologists began to debate with acid vigour a handful of bones from a shallow gravel pit in Sussex. Years later those same men-older, no less tetchy, and little the wiser-were still at it. For a long time now we have known that their passion was directed at half the jaw of an orang-utang and bits of a not very old skull that in life had been nowhere near the Home Counties. Eoanthropus dawsoni was a hoax, and so were all the Piltdown finds. Frank Spencer has written an excellent, detailed account of the Piltdown story, setting it against a background of how 1 scientists, between roughly 1900 and 1950, saw the dawn of man. (The Piltdown Papers, that accompany this book, are not for the general reader, who would find the material dull and confusing.) Spencer does come up with a culprit, saving him for the end. The book is jointly published by the British Museum (Natural History), which is where the Uckfield solicitor, fossil enthusiast, and plagiarist Charles Dawson took his "fmd". It is in a very different museum-that of the Royal College of Surgeons of England-that Spencer gets his man, the anatomist Arthur Keith. Previous suspects, including Pierre Teilhard de Chardin and Arthur Conan Doyle, are argued away. As is W. J. Sollas, victim of near-deathbed revenge by the man he had kept waiting so long for his Oxford chair. Others went to their graves with a nod and a wink, including M. A. C. Hinton. In 1978 New Scientist ran a series of Piltdown articles in which Hinton was alleged to have tried to smoke out the hoaxer by planting an obvious fake, a hypothesis that Spencer does not spend time on. It is one of the frustrations of this book that the reader remains uncertain about how good the Piltdown fakes were; a joker and a fraudster would use different techniques and have different motives. Spencer’s accusation has, naturally, been ill-received by the Royal College and by the family, but it has not yet been countered. The prosecution case is no less, but no more, convincing than earlier ones. The hoaxer(s) must have had the means, the motive, and an ability to sustain behaviour consistent with the deed for many years. Keith died in 1955, two years after the fraud was exposed and forty-three after the formal presentation of Arthur Smith Woodward’s reconstruction at a meeting in London on Dec 18, 1912. Keith had the skills, but he cannot have salted the Piltdown site unaided. Dawson, a strong suspect in his own right, may have been the co-conspirator. Keith burned correspondence with Dawson and in an interview in 1953 he muddled dates, but there are plenty of chronological misrecollections in this tale. Spencer is unconvincing on motive. Why so studiously correct Smith Woodward’s model to one more supportive of his own view on the age of "dawn man" if he knew the thing to be a hoax? How would the Natural History Museum react? Keith’s fiercest opponent came from Manchester not South Kensington. In Keith’s own lifetime some anthropologists refused to accept that jaw and skull belonged to the same creature and the exposure of "Piltdown man" was greeted with relief-so, medium to long term Keith gained nothing. A key finding is an entry in Keith’s diary for 1912, in which he noted that he had written an account of "the meeting" two days before it happened. The meeting began at 8 o’clock on the Wednesday evening, and the British Medical Journal of that week does contain a remarkably detailed account entitled Discovery of a New Type of Fossil Man-more detail, Spencer claims, than could have been known beforehand by anyone who had not already visited the site. Spencer tells us nothing about press times at the BM] in those days; and he is asking us to accept that Keith and Smith Woodward were not on good enough terms for much site information to have been shared when Keith saw the specimens a few days before the meenng. The Piltdown forgery now has another suspect-but not at the level "beyond reasonable doubt" that this book seems to be
transplantation
or so
claiming.
Pltdol4m a Saennfic Forger. B, Frank Spencer London and Oxford. Natural Ht5torB Museum Publications Oxford Lmverstrv Press. 1990. Pp 272 yi7 95. 1 SBN’ 0-198585225 .
A
woman
with
primary biliary cirrhosis
became
severely
thrombocytopenic (platelet count 10 x l0"/l) 2 days after she received a liver transplant from a patient with a 26-year history of idiopathic thrombocytopenic purpura who died from an intracranial haemorrhage.1 A bone-marrow aspirate on day 5 showed normal megakaryocytes, so peripheral destruction of platelets was likely. She recovered only after an emergency retransplantation. The donor’s serum contained antibodies against glycoprotein complex IIb-IIIa (platelet surface constituents). These antibodies were identified in the recipient after transplantation and disappeared after treatment with intravenous gammaglobulin, plasma exchange, and retransplantation. Post-transfusion thrombocytopenia was thought to be an unlikely diagnosis because it occurs at least 5 days after a blood transfusion and because it is usually accompanied by the production of antibodies reactive with platelet-specific allo-antigens. The authors point out that the case indicates that livers from donors with autoimmune idiopathic thrombocytopenia and, by implication, any autoimmune condition should not be used for transplantation. They also say that the fact that the donor’s heart was given to a woman with idiopathic cardiomyopathy without complications developing is probably a reflection of the difference between the liver and the heart in lymphoid mass.
PJ, McCarthy LJ, Filo RS. Transmission of idiopathic (autoimmune) thrombocytopenic purpura by liver transplantation. N Engl J Med 1990; 323: 807-11.
1. Friend
The cost of
clozapine
neuroleptic drug, is potentially very of schizophrenia, but in practice its severely limited by an associated risk of agranulocytosis. It is used, often successfully, when other treatments have failed, but its effects on the white-cell count have to be monitored closely. In the UK, where the provision of a patient monitoring system was made a mandatory part of the product licence, the drug’s manufacturer, Sandoz, insists that all prescribers and dispensers of clozapine and all patients taking the drug are registered with the company. Patients’ blood samples (taken weekly for the first 18 weeks of treatment and fortnightly thereafter) are sent for analysis to a central laboratory and the results are sent both to Sandoz and to the prescribing psychiatrist. A year’s treatment in the UK, including the analyses, costs about 1500. National Health Service patients, however, pay only the standard prescription charge, or nothing at all if exempt. Things are very different in the United States, where the cost of clozapine (more than three times as much as in the UK, making it one of the most expensive therapeutic drugs available there) and the refusal of some state Medicaid programmes to pick up the tab put the treatment way beyond the reach of most patients. Clozapine was released for clinical use in the USA in February, 1990 (at roughly the same time as in the UK), but so far only about 5500 US patients are taking it. Carl Salzman, a psychiatrist at Harvard Medical School, ascribes the high price of clozapine in the United States to "bundling", an unusual form of monopoly in which the availability of the drug is linked to a mandatory distribution and monitoring system.1 Collecting blood samples and distributing the drug, which in the UK are carried out by the NHS, are in the USA subcontracted to a commercial agency (which, according to Salzman, charges a phlebotomy fee even to hospitals whose own staff take the blood samples.) Furthermore, in the United States supplies of clozapine are not held by pharmacies but are released by the distributors week by week for individual patients who have had a satisfactory blood result. Salzman argues that the work of Sandoz’s expensive Clozapine Patient Monitoring System (CPMS), set up to comply with the Food and Drug Administration’s safety requirements, might be done just as effectively and more cheaply in existing facilities in universities and major hospitals. Sandoz, however, would be unlikely to consider relinquishing control of monitoring (for-fear, Clozapine (’Clozaril’),
useful in the usefulness is
a new
treatment