Opiate-receptor expression sets pain sensitivity ariations in the gene for the opiate receptor could explain why one person’s pinprick is another’s painful jab, say researchers at the US National Institute of Drug Abuse and Johns Hopkins University School of Medicine (Baltimore, MD, USA). “Many people assume the way we respond to pain is voluntary. ‘Just put up with it’ has been a common recommendation for years”, says lead author George Uhl. Now it seems that pain sensitivity and response to pain medications, could in part be genetically determined. Uhl and his colleagues altered the gene for the opiate receptor in several mice strains to reflect the genetic variations seen in people. Mice expressing fewer receptors were more sensitive to pain at baseline, say the researchers, and needed more morphine to quell the pain. In mice with half the usual number of receptors, response to morphine was halved, indicating a dose response (Proc Natl Acad Sci USA 1999; 96: 7752–55). Human studies also suggest a link between variations in the gene for the
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opiate receptor and pain sensitivity, says Uhl, and positron emission tomography scans indicate that receptor numbers vary widely in people. The new results, he adds, suggest that receptor measurement could be used before surgery to predict patient response to opioid analgesia, and to improve management of chronic pain. Such tests “could help patients who get labelled as complainers or fakers, but who may really have a deficiency in their inherent ability to respond to analgesics”, comments Douglas Merrill, spokesperson for the American Society of Anesthesiologists. But he warns that although the findings are “fascinating”, it is far too early to draw firm conclusions. Uhl is more optimistic and predicts that the receptor could be included in a pharmacogenomic screen within a year or two. But such assessments will “have to be treated with respect because the differences we’re seeing in pain sensitivity could also affect addictability to opiate drugs”.
n July 20, Frank Dobson, the UK Secretary of State for Health, announced that a new meningitis C vaccine will be launched in the UK this autumn, a year ahead of schedule. The vaccine will be provided on the National Health Service, he said, but because supplies of the vaccine are limited, “it will have to be targeted at the babies, children, and young people at most risk”. Last year, about 1500 people were infected by group C meningococci in the UK, and of these 150—mainly children and young people—died. The new immunisation programme should start in October in time to prevent the seasonal rise in cases. In the first instance, the vaccine will be available to: ● babies getting their diphtheria, tetanus, whooping cough, polio, and Haemophilus influenzae b vaccination at 2, 3, and 4 months;
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Ehrlichiosis agent A new agent for ehrlichiosis has been isolated from four patients in the USA. Ehrlichia DNA found in these patients had the same nucleotide sequence as that of Ehrlichia ewingii, an agent previously reported as a cause of ehrlichiosis in dogs (N Engl J Med 1999; 341: 148–55). Surgery audit On July 21, the Society of Cardiothoracic Surgeons of Great Britain and Ireland published an audit of adult cardiac surgery in the UK. It details a relatively constant 2–3% operative mortality rate for coronary artery bypass surgery during the past 20 years.
US FDA again stops urokinase sales
children having their first measles, mumps, and rubella vaccination at about 13 months; ● young people aged 15–17 years. Children aged between 4 months and 1 year will be recalled for immunisation with the vaccine. Dobson said that stocks of the vaccine, which has been tested for safety and efficacy in 4500 UK children and young adults and more than 21 000 similar individuals elsewhere, were not sufficient to permit vaccination of young people going to college for the first time. This high-risk group, he said, would be offered the existing vaccine, which is effective for about 3 years. The government’s move was welcomed by the British Medical Association who said the immunisation programme would “fill a gap in protection”.
or the second time in 6 months, the US FDA has told Abbott Laboratories to cease shipments of its clotbusting drug urokinase (Abbokinase). On July 16, the FDA said that it is again concerned that Abbott cannot confirm that the product, derived from neonatal kidney cells, is free of infection. The agency first halted urokinase shipments in December, 1998, citing similar concerns. A month later, it allowed sales to resume, but warned physicians that urokinase posed a risk of transmitting infectious diseases. In February, Public Citizen’s Health Research Group alleged that the kidney cells were being harvested from aborted fetuses and dead newborn babies at hospitals in Cali, Columbia, without proper consent from or screening of the mothers. The FDA now says that over the past few months, Abbott has reported that six batches of urokinase that were in process, but not ready for sale, were contaminated with reovirus. Another batch was contaminated with mycoplasma. “These recent findings of contamination and Abbott’s inability to locate the source of the problem have raised further concerns at FDA about Abbott’s entire manufacturing process for Abbokinase”, said the FDA. No more sales will be allowed until Abbott documents the source of the contamination, and assures that the cells have been obtained legally, and that the final product is infection-free.
Jane Bradbury
Alicia Ault
Marilynn Larkin
New meningitis C vaccine to be used in UK
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News in brief
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THE LANCET • Vol 354 • July 24, 1999