BSE-CJD pages
A High Court judge last week held the Department of Health and the Medical Research Council to blame for the deaths of young adults from Creutzfeldt-Jakob disease (CJD) who had been treated with human growth hormone.
In the first compensation claim over a pharmaceutical product to succeed in the British courts, Mr Justice Morland ruled that the two bodies were negligent in not passing on concerns raised by scientists that would probably have led to the treatment's suspension from July 1977. The decision means that only the families of patients who started the treatment after 1 July 1977 will be entitled to compensation.
The judge held, in effect, that had the Department of Health and the MRC fulfilled their duty of care, patients such as Patrick Baldwin, who was treated between October 1977 and 1980, would never have undergone the treatment and contracted CJD. He died in 1992 aged 30, leaving two daughters now aged 9 and 10, who are in line for substantial compensation, which has still to be assessed. The test case was brought by eight of the 16 families of recipients of human growth hormone who have died from CJD since 1985, and by three others who are dying from the disease. In addition, 87 claimants in whom CJD has not been diagnosed but who are claiming compensation for psychological trauma, hope to have their case heard next year.
Patrick Baldwin in late 1992. His family is in
line for compensation following his death from CJD
PHOTO: EMPICS/GRAHAM CHADWICK
The MRC ran the growth hormone programme as a clinical
trial from 1959 until 1 July 1977, when the programme was taken over by the Department of Health. Nearly 2,000 children were treated with the hormone - extracted from the pituitaries of cadavers - between 1959 and 1985, until reports of the first deaths from CJD in the United States, after which synthetic hormone was used. The MRC retained responsibility for collecting and processing pituitaries until 1980.
In October 1976 a veterinary scientist, Dr Alan Dickinson of the Agricultural Research Council, who was working on scrapie, telephoned the MRC to alert officials to the risk of transmission of CJD through human growth hormone. In a letter in February 1977 he made four suggestions to improve the safety of the hormone. Two were never acted on, a third was only partly implemented, and the fourth - excluding the use of pituitaries from cases with dementia - was not put into force until 1980. Two virologists, Professor Cedric Mims of Guy's Hospital and Professor Peter Wildy of Cambridge University, were consulted by the MRC, but not until December 1977. Professor Wildy replied: "Any clinician who uses growth hormone must be made aware of the gruesome possibilities and their imponderable probabilities." But while the scientific steering committee overseeing the manufacture of the hormone were told, the clinicians' committee was "deliberately kept in the dark," the judge said. Charles Brook, professor of paediatric endocrinology at University College London Hospitals and Great Ormond Street Children's Hospital and a member of the clinicians' committee, gave evidence that he had never seen the letters from Dr Dickinson and the two virologists before the trial and he was "appalled" by them.
CLARE DYER,
legal correspondent, BMJ
Accepted facts about the agent responsible for bovine spongiform encephalopathy (BSE) are rare; two of those on which there is good agreement took a knock from scientists at a meeting organised by the North West Public Health Alliance in Liverpool last week. Suspicion is increasing that the agent may not have originated from scrapie and that cows may transmit it to their calves.
Until now, BSE has been explained by the contamination of animal feed by the carcases of sheep affected by scrapie. Its appearance in the mid-1980s was attributed to changes in the rendering process, which had previously destroyed the scrapie agent. But Kevin Taylor, deputy chief veterinary officer at the Ministry of Agriculture, Fisheries and Food said the problem with this theory is that none of the 20 strains in scrapie resembles BSE.
Few researchers doubt that feeding rendered down bovine carcases to cows was an extremely efficient way of spreading disease, but the disease in question may have originated in cows rather than sheep. Strain tying on the cases found in humans of the new variant of Creutzfeldt-Jakob disease (CJD) would be available later this year and should shed more light on the situation, said Martin Zeidler, research registrar at the National CJD Surveillance Unit.
In view of this risk, the government has sought to exclude from cattle feed any material that might convey BSE. If contaminated animal feed is solely responsible for cases of BSE then this strategy should lead to its eradication. Yet two thirds of cattle with recent notifications of BSE have been born after the ruminant feed ban, said Mr Taylor. Poor compliance by farmers is one explanation, but two other possibilities exist.
The first is vertical transmission, whereby cows pass the disease on to their calves. The second is environmental contamination, a theory supported by Iceland's experience. Some Icelandic farms replaced their sheep population with new stock, yet within a few years the new stock was affected with scrapie. Unless poor compliance with the feed ban was solely to blame then BSE could remain endemic within British herds, said Professor Morgan.
TONY DELAMOTHE,
BMJ