Jonathan Gardner

HARROGATE, ENGLAND — To better understand the genetic components of osteoporosis, a University of Edinburgh researcher is planning to study the relationship between the two in the isolated population of the Orkney Islands.

Dr. Stuart Ralston, professor of rheumatology and head of the school of molecular and clinical medicine at University of Edinburgh, said research has shown that bone mineral density (BMD) in osteoporosis patients is almost certainly regulated by genetic signals.

Genetic factors explain 60%–85% of the variance in BMD, including type I collagen affecting bone structure, vitamin D receptors affecting mineralization, estrogen receptors affecting hormone action, and interleukin-1 and interleukin −6 affecting inflammation. However, the effects of individual genes appear to be small and may be magnified only by the interactions of multiple genes.

Orkney—an archipelago of 70 or so islands about 10 miles off the northern tip of Scotland—is one of the more isolated regions of Europe, and it has good genealogical records, making it possible for researchers to get a clearer picture of the way genetics affects bone health, Dr. Ralston said.

Dr. Ralston said colleagues were already planning to test the Orkney Islands population for genetic factors related to cardiovascular disease, so he asked them to tack on the factors for osteoporosis as well.

“Linking studies conducted in general isolated populations are good,” Dr. Ralston said June 26 during a workshop at the annual conference of the National Osteoporosis Society.

“If you're going to study osteoporosis or any other complex disease, I would study an isolated population because you're more likely to find something,” Dr. Ralston said.

One study of the Icelandic population showed that a variation in the gene BMP2 in chromosome 20 was correlated to osteoporosis. That study found that variation was present in 5% of people with low BMD at spine or hip or a fracture, compared with 1% in the control population.

Dr Ralston said he confirmed that work with an isolated population in northeast Scotland, where 3% of fracture patients had that same variation, compared with 0.04% of the control population.

“It's still rare,” Dr. Ralston explained. “One of the advantages of studying an isolated population is that you're more likely to discover a gene. One of the disadvantages of this is, is it applicable for the rest of the world?”

The study will go beyond the BMP2 gene to include the entire human genome for correlations to osteoporosis. But even with research into the genetic components of osteoporosis, identifying a single marker that will help physicians identify likely hip fracture patients may be impossible, he said.

HARROGATE, ENGLAND — To better understand the genetic components of osteoporosis, a University of Edinburgh researcher is planning to study the relationship between the two in the isolated population of the Orkney Islands.

Dr. Stuart Ralston, professor of rheumatology and head of the school of molecular and clinical medicine at University of Edinburgh, said research has shown that bone mineral density (BMD) in osteoporosis patients is almost certainly regulated by genetic signals.

Genetic factors explain 60%–85% of the variance in BMD, including type I collagen affecting bone structure, vitamin D receptors affecting mineralization, estrogen receptors affecting hormone action, and interleukin-1 and interleukin −6 affecting inflammation. However, the effects of individual genes appear to be small and may be magnified only by the interactions of multiple genes.

Orkney—an archipelago of 70 or so islands about 10 miles off the northern tip of Scotland—is one of the more isolated regions of Europe, and it has good genealogical records, making it possible for researchers to get a clearer picture of the way genetics affects bone health, Dr. Ralston said.

Dr. Ralston said colleagues were already planning to test the Orkney Islands population for genetic factors related to cardiovascular disease, so he asked them to tack on the factors for osteoporosis as well.

“Linking studies conducted in general isolated populations are good,” Dr. Ralston said June 26 during a workshop at the annual conference of the National Osteoporosis Society.

“If you're going to study osteoporosis or any other complex disease, I would study an isolated population because you're more likely to find something,” Dr. Ralston said.

One study of the Icelandic population showed that a variation in the gene BMP2 in chromosome 20 was correlated to osteoporosis. That study found that variation was present in 5% of people with low BMD at spine or hip or a fracture, compared with 1% in the control population.

Dr Ralston said he confirmed that work with an isolated population in northeast Scotland, where 3% of fracture patients had that same variation, compared with 0.04% of the control population.

“It's still rare,” Dr. Ralston explained. “One of the advantages of studying an isolated population is that you're more likely to discover a gene. One of the disadvantages of this is, is it applicable for the rest of the world?”

The study will go beyond the BMP2 gene to include the entire human genome for correlations to osteoporosis. But even with research into the genetic components of osteoporosis, identifying a single marker that will help physicians identify likely hip fracture patients may be impossible, he said.

HARROGATE, ENGLAND — To better understand the genetic components of osteoporosis, a University of Edinburgh researcher is planning to study the relationship between the two in the isolated population of the Orkney Islands.

Dr. Stuart Ralston, professor of rheumatology and head of the school of molecular and clinical medicine at University of Edinburgh, said research has shown that bone mineral density (BMD) in osteoporosis patients is almost certainly regulated by genetic signals.

Genetic factors explain 60%–85% of the variance in BMD, including type I collagen affecting bone structure, vitamin D receptors affecting mineralization, estrogen receptors affecting hormone action, and interleukin-1 and interleukin −6 affecting inflammation. However, the effects of individual genes appear to be small and may be magnified only by the interactions of multiple genes.

Orkney—an archipelago of 70 or so islands about 10 miles off the northern tip of Scotland—is one of the more isolated regions of Europe, and it has good genealogical records, making it possible for researchers to get a clearer picture of the way genetics affects bone health, Dr. Ralston said.

Dr. Ralston said colleagues were already planning to test the Orkney Islands population for genetic factors related to cardiovascular disease, so he asked them to tack on the factors for osteoporosis as well.

“Linking studies conducted in general isolated populations are good,” Dr. Ralston said June 26 during a workshop at the annual conference of the National Osteoporosis Society.

“If you're going to study osteoporosis or any other complex disease, I would study an isolated population because you're more likely to find something,” Dr. Ralston said.

One study of the Icelandic population showed that a variation in the gene BMP2 in chromosome 20 was correlated to osteoporosis. That study found that variation was present in 5% of people with low BMD at spine or hip or a fracture, compared with 1% in the control population.

Dr Ralston said he confirmed that work with an isolated population in northeast Scotland, where 3% of fracture patients had that same variation, compared with 0.04% of the control population.

“It's still rare,” Dr. Ralston explained. “One of the advantages of studying an isolated population is that you're more likely to discover a gene. One of the disadvantages of this is, is it applicable for the rest of the world?”

The study will go beyond the BMP2 gene to include the entire human genome for correlations to osteoporosis. But even with research into the genetic components of osteoporosis, identifying a single marker that will help physicians identify likely hip fracture patients may be impossible, he said.

PARIS — To avert a worldwide pandemic sparked by a mutation of an infectious avian influenza, public health officials will need to begin containment efforts before it has spread to 50 humans and treat new cases within 2 days of infection, according to an expert who has developed a mathematical simulation of a potential pandemic.

If a form of the H5N1 virus that is more infectious to humans spreads outside an initial disease cluster, there is little public health authorities can do to keep it out of their countries, said Simon Cauchemez, Ph.D., of the division of epidemiology, public health, and primary care at Imperial College, London.

“For containment, the only option is to act very quickly at the source. Obviously, once the pandemic is international, you can't try to stop it. You can only decrease its magnitude. There's an option for containment at the source, but it will be very difficult to implement,” he said at the international conference on avian influenza in humans.

The simulation assumes any new pandemic strains would have the same transmission rates as earlier infections, including the 1918–1919 Spanish flu pandemic, he said.

Dr. Cauchemez's model assumes the outbreak originates in rural Southeast Asia, where in many cases, the H5N1 virus is endemic among birds. He noted that he designed the model to offer international public health authorities a way to contain the disease to a single geographic region, and if that fails, to help others control the size of the pandemic in their countries once it reaches them.

For now, the disease has been restricted largely to poultry and wild birds.

Most human infection results from close contact with birds. So far, 229 people have been infected, and 113 have died, according to data from the World Health Organization released July 4.

The World Health Organization has documented at least one case of human-to-human transmission. WHO officials do not believe that there was a mutation that made the virus any more transmissible between humans.

But it is feared that the H5N1 virus eventually will mutate into a human-transmissible form. Because it is different from the seasonal form of flu and because health officials cannot predict the genetic makeup of a human-transmissible form of H5N1, vaccinating the population to prevent the spread of the disease is unlikely until the virus has already begun passing from human to human.

In the first affected country, the time from the first human-to-human case to the peak of the outbreak would be between 80 and 120 days, Dr. Cauchemez said.

Beyond treating the influenza cases in an initial outbreak cluster, if an outbreak is to be contained, public health officials need to consider actions such as prophylaxis of the flu patients' households, as well as the population in an area surrounding the flu patients. Other options that might be much more unpopular include closing schools to limit the spread of the virus and quarantining the entire region of an initial outbreak.

To contain an initial cluster of human-spread flu, officials must respond to an outbreak before it spreads to 50 people, new cases must be treated within the first 2 days, 3 million doses of antiviral medications must be available, and public health officials must act in multiple countries, Dr. Cauchemez said.

The simulation indicates that limiting the spread of disease once it enters a country will not be particularly effective, Dr. Cauchemez said. Once a country has an outbreak, the number of people infected with the flu is expected to increase by 10 times in a week or two, so “therefore if you succeeded in decreasing the number of cases 10-fold, you only buy 1 or 2 weeks,” he said.

The only way to prevent avian flu from entering a country is to keep out 99% of those people traveling from areas already affected by the pandemic, Dr. Cauchemez said. “So travel restrictions must be very, very effective—draconian—to have any significant impact,” he added.

Once avian flu enters a country, prophylaxis of a population near a disease cluster, closing schools and workplaces to limit the opportunity for the virus to spread, and prevaccinating children under age 16 would reduce the number of cases but not prevent the spread of the virus, Dr. Cauchemez said.

PARIS — To avert a worldwide pandemic sparked by a mutation of an infectious avian influenza, public health officials will need to begin containment efforts before it has spread to 50 humans and treat new cases within 2 days of infection, according to an expert who has developed a mathematical simulation of a potential pandemic.

If a form of the H5N1 virus that is more infectious to humans spreads outside an initial disease cluster, there is little public health authorities can do to keep it out of their countries, said Simon Cauchemez, Ph.D., of the division of epidemiology, public health, and primary care at Imperial College, London.

“For containment, the only option is to act very quickly at the source. Obviously, once the pandemic is international, you can't try to stop it. You can only decrease its magnitude. There's an option for containment at the source, but it will be very difficult to implement,” he said at the international conference on avian influenza in humans.

The simulation assumes any new pandemic strains would have the same transmission rates as earlier infections, including the 1918–1919 Spanish flu pandemic, he said.

Dr. Cauchemez's model assumes the outbreak originates in rural Southeast Asia, where in many cases, the H5N1 virus is endemic among birds. He noted that he designed the model to offer international public health authorities a way to contain the disease to a single geographic region, and if that fails, to help others control the size of the pandemic in their countries once it reaches them.

For now, the disease has been restricted largely to poultry and wild birds.

Most human infection results from close contact with birds. So far, 229 people have been infected, and 113 have died, according to data from the World Health Organization released July 4.

The World Health Organization has documented at least one case of human-to-human transmission. WHO officials do not believe that there was a mutation that made the virus any more transmissible between humans.

But it is feared that the H5N1 virus eventually will mutate into a human-transmissible form. Because it is different from the seasonal form of flu and because health officials cannot predict the genetic makeup of a human-transmissible form of H5N1, vaccinating the population to prevent the spread of the disease is unlikely until the virus has already begun passing from human to human.

In the first affected country, the time from the first human-to-human case to the peak of the outbreak would be between 80 and 120 days, Dr. Cauchemez said.

Beyond treating the influenza cases in an initial outbreak cluster, if an outbreak is to be contained, public health officials need to consider actions such as prophylaxis of the flu patients' households, as well as the population in an area surrounding the flu patients. Other options that might be much more unpopular include closing schools to limit the spread of the virus and quarantining the entire region of an initial outbreak.

To contain an initial cluster of human-spread flu, officials must respond to an outbreak before it spreads to 50 people, new cases must be treated within the first 2 days, 3 million doses of antiviral medications must be available, and public health officials must act in multiple countries, Dr. Cauchemez said.

The simulation indicates that limiting the spread of disease once it enters a country will not be particularly effective, Dr. Cauchemez said. Once a country has an outbreak, the number of people infected with the flu is expected to increase by 10 times in a week or two, so “therefore if you succeeded in decreasing the number of cases 10-fold, you only buy 1 or 2 weeks,” he said.

The only way to prevent avian flu from entering a country is to keep out 99% of those people traveling from areas already affected by the pandemic, Dr. Cauchemez said. “So travel restrictions must be very, very effective—draconian—to have any significant impact,” he added.

Once avian flu enters a country, prophylaxis of a population near a disease cluster, closing schools and workplaces to limit the opportunity for the virus to spread, and prevaccinating children under age 16 would reduce the number of cases but not prevent the spread of the virus, Dr. Cauchemez said.

PARIS — To avert a worldwide pandemic sparked by a mutation of an infectious avian influenza, public health officials will need to begin containment efforts before it has spread to 50 humans and treat new cases within 2 days of infection, according to an expert who has developed a mathematical simulation of a potential pandemic.

If a form of the H5N1 virus that is more infectious to humans spreads outside an initial disease cluster, there is little public health authorities can do to keep it out of their countries, said Simon Cauchemez, Ph.D., of the division of epidemiology, public health, and primary care at Imperial College, London.

“For containment, the only option is to act very quickly at the source. Obviously, once the pandemic is international, you can't try to stop it. You can only decrease its magnitude. There's an option for containment at the source, but it will be very difficult to implement,” he said at the international conference on avian influenza in humans.

The simulation assumes any new pandemic strains would have the same transmission rates as earlier infections, including the 1918–1919 Spanish flu pandemic, he said.

Dr. Cauchemez's model assumes the outbreak originates in rural Southeast Asia, where in many cases, the H5N1 virus is endemic among birds. He noted that he designed the model to offer international public health authorities a way to contain the disease to a single geographic region, and if that fails, to help others control the size of the pandemic in their countries once it reaches them.

For now, the disease has been restricted largely to poultry and wild birds.

Most human infection results from close contact with birds. So far, 229 people have been infected, and 113 have died, according to data from the World Health Organization released July 4.

The World Health Organization has documented at least one case of human-to-human transmission. WHO officials do not believe that there was a mutation that made the virus any more transmissible between humans.

But it is feared that the H5N1 virus eventually will mutate into a human-transmissible form. Because it is different from the seasonal form of flu and because health officials cannot predict the genetic makeup of a human-transmissible form of H5N1, vaccinating the population to prevent the spread of the disease is unlikely until the virus has already begun passing from human to human.

In the first affected country, the time from the first human-to-human case to the peak of the outbreak would be between 80 and 120 days, Dr. Cauchemez said.

Beyond treating the influenza cases in an initial outbreak cluster, if an outbreak is to be contained, public health officials need to consider actions such as prophylaxis of the flu patients' households, as well as the population in an area surrounding the flu patients. Other options that might be much more unpopular include closing schools to limit the spread of the virus and quarantining the entire region of an initial outbreak.

To contain an initial cluster of human-spread flu, officials must respond to an outbreak before it spreads to 50 people, new cases must be treated within the first 2 days, 3 million doses of antiviral medications must be available, and public health officials must act in multiple countries, Dr. Cauchemez said.

The simulation indicates that limiting the spread of disease once it enters a country will not be particularly effective, Dr. Cauchemez said. Once a country has an outbreak, the number of people infected with the flu is expected to increase by 10 times in a week or two, so “therefore if you succeeded in decreasing the number of cases 10-fold, you only buy 1 or 2 weeks,” he said.

The only way to prevent avian flu from entering a country is to keep out 99% of those people traveling from areas already affected by the pandemic, Dr. Cauchemez said. “So travel restrictions must be very, very effective—draconian—to have any significant impact,” he added.

Once avian flu enters a country, prophylaxis of a population near a disease cluster, closing schools and workplaces to limit the opportunity for the virus to spread, and prevaccinating children under age 16 would reduce the number of cases but not prevent the spread of the virus, Dr. Cauchemez said.

PARIS — The number of avian influenza outbreaks in animals, particularly wild animals, has hit a seasonal lull, and world animal health experts believe it may reflect the end of the spring bird migration season.

The World Health Organization reports that the number of human deaths resulting from infection with the H5N1 avian flu this year already has exceeded the total for 2005, and the total number of human infections has nearly matched the 95 of last year. Yet experts from Paris-based OIE, the World Organization for Animal Health, said they've received fewer notifications of outbreaks in animals in recent months.

“Fewer outbreaks are reported and, especially in Europe where we found most of the outbreaks, we assume that the animals that may be affected, that carry the virus, already moved to other places,” Dr. Christianne Bruschke, project manager with OIE, said at an international conference on avian influenza in humans.

“In poultry we get fewer reports, but we know there are places like Indonesia where we know the virus is endemic, so it's very difficult to report every individual outbreak,” she noted in an interview.

In addition, many of the countries where avian flu is endemic do not have the necessary scientific resources to chase every report of avian flu.

The role of wild birds in the spread of avian flu worldwide is unclear. Dr. Bruschke said less than 1% of wild birds in Asia and Africa have been found to be infected.

A scientific conference of OIE and the United Nations Food and Agriculture Organization in late spring concluded that the poultry trade, legal and illegal, is the chief means of the spread of the disease. But wild birds have been responsible for carrying the disease to regions far removed from poultry outbreaks and may serve as a permanent “reservoir” of the disease, it was concluded at that conference.

In her presentation, Dr. Bruschke said that OIE is in the final stages of setting up a “global early warning system” to help prevent further spread of the disease in animals. The international approach will focus on combating disease outbreaks in poultry. Among the necessary tools will be compensation for poultry farmers whose flocks are infected, giving them an incentive to report an outbreak.

“It's still an animal disease and should be controlled at the animal source,” she said. “The risk of pandemic can be minimized if we act quickly to reduce the virus load in poultry.”

PARIS — The number of avian influenza outbreaks in animals, particularly wild animals, has hit a seasonal lull, and world animal health experts believe it may reflect the end of the spring bird migration season.

The World Health Organization reports that the number of human deaths resulting from infection with the H5N1 avian flu this year already has exceeded the total for 2005, and the total number of human infections has nearly matched the 95 of last year. Yet experts from Paris-based OIE, the World Organization for Animal Health, said they've received fewer notifications of outbreaks in animals in recent months.

“Fewer outbreaks are reported and, especially in Europe where we found most of the outbreaks, we assume that the animals that may be affected, that carry the virus, already moved to other places,” Dr. Christianne Bruschke, project manager with OIE, said at an international conference on avian influenza in humans.

“In poultry we get fewer reports, but we know there are places like Indonesia where we know the virus is endemic, so it's very difficult to report every individual outbreak,” she noted in an interview.

In addition, many of the countries where avian flu is endemic do not have the necessary scientific resources to chase every report of avian flu.

The role of wild birds in the spread of avian flu worldwide is unclear. Dr. Bruschke said less than 1% of wild birds in Asia and Africa have been found to be infected.

A scientific conference of OIE and the United Nations Food and Agriculture Organization in late spring concluded that the poultry trade, legal and illegal, is the chief means of the spread of the disease. But wild birds have been responsible for carrying the disease to regions far removed from poultry outbreaks and may serve as a permanent “reservoir” of the disease, it was concluded at that conference.

In her presentation, Dr. Bruschke said that OIE is in the final stages of setting up a “global early warning system” to help prevent further spread of the disease in animals. The international approach will focus on combating disease outbreaks in poultry. Among the necessary tools will be compensation for poultry farmers whose flocks are infected, giving them an incentive to report an outbreak.

“It's still an animal disease and should be controlled at the animal source,” she said. “The risk of pandemic can be minimized if we act quickly to reduce the virus load in poultry.”

PARIS — The number of avian influenza outbreaks in animals, particularly wild animals, has hit a seasonal lull, and world animal health experts believe it may reflect the end of the spring bird migration season.

The World Health Organization reports that the number of human deaths resulting from infection with the H5N1 avian flu this year already has exceeded the total for 2005, and the total number of human infections has nearly matched the 95 of last year. Yet experts from Paris-based OIE, the World Organization for Animal Health, said they've received fewer notifications of outbreaks in animals in recent months.

“Fewer outbreaks are reported and, especially in Europe where we found most of the outbreaks, we assume that the animals that may be affected, that carry the virus, already moved to other places,” Dr. Christianne Bruschke, project manager with OIE, said at an international conference on avian influenza in humans.

“In poultry we get fewer reports, but we know there are places like Indonesia where we know the virus is endemic, so it's very difficult to report every individual outbreak,” she noted in an interview.

In addition, many of the countries where avian flu is endemic do not have the necessary scientific resources to chase every report of avian flu.

The role of wild birds in the spread of avian flu worldwide is unclear. Dr. Bruschke said less than 1% of wild birds in Asia and Africa have been found to be infected.

A scientific conference of OIE and the United Nations Food and Agriculture Organization in late spring concluded that the poultry trade, legal and illegal, is the chief means of the spread of the disease. But wild birds have been responsible for carrying the disease to regions far removed from poultry outbreaks and may serve as a permanent “reservoir” of the disease, it was concluded at that conference.

In her presentation, Dr. Bruschke said that OIE is in the final stages of setting up a “global early warning system” to help prevent further spread of the disease in animals. The international approach will focus on combating disease outbreaks in poultry. Among the necessary tools will be compensation for poultry farmers whose flocks are infected, giving them an incentive to report an outbreak.

“It's still an animal disease and should be controlled at the animal source,” she said. “The risk of pandemic can be minimized if we act quickly to reduce the virus load in poultry.”

Variant Creutzfeldt-Jakob disease could have an incubation time of 30 years or longer and could affect a wider population than currently forecast, according to new research on patients with a similar human prion disease.

Researchers examined 11 recent cases of kuru, a prion protein disease that became an epidemic in the mid-1900s among several groups of Papua New Guinea natives, resulting from their ritual cannibalism, reported John Collinge, Ph.D., a professor of neurology at University College London, and his colleagues (Lancet 2006;367:2068–74).

Cannibalism practices were banned by the Australian authorities in the mid-1950s, and researchers are confident they have been nonexistent since 1960. However, because kuru disease still affects Papua New Guinea natives, researchers have been able to determine long incubation times.

Dr. Collinge and his colleagues monitored 11 cases of kuru disease in Papua New Guinea beginning in 1996, with disease onset between November 1994 and October 2001. The average age of patient onset was 46 years or older.

The oldest patient at disease onset was a 63-year-old man in 1996. The minimum incubation time for the patient was 36 years. However, because young boys traditionally stopped participating in the cannibalism ritual around the age of 7 years, the likely incubation period was 56 years, the researchers reported.

The mean incubation period for kuru is currently estimated to be about 12 years.

Of the 11 patients, 8 were heterozygous for valine and methionine at codon 129 of the human prion protein gene. That distribution of heterozygous genotypes within the kuru patients did not, however, differ markedly from the surrounding population.

Although kuru disease's lethality arose from intraspecies recycling of infectious prions, the results of the latest research suggest that prion diseases, such as variant Creutzfeldt-Jakob disease (vCJD), may have longer incubation times than current models now pose.

Genetic transmission barriers may limit the number of people who acquire vCJD by consuming meat infected with bovine spongiform encephalopathy (BSE). Those who have already suffered from the disease may have been genetically predisposed to have shorter incubation times. Meanwhile, the research on kuru patients demonstrates that prion diseases can also have very long incubation times, “approaching (and perhaps exceeding) the typical human life span,” according to the researchers.

“Therefore, a human BSE epidemic may be multiphasic, and recent estimates of the size of the vCJD epidemic based on uniform genetic susceptibility could be substantial underestimations,” they wrote.

“Genes implicated in species-barrier effects, which would further increase both the mean and range of human BSE incubation periods, are also probably relevant. In this context, a human epidemic will be difficult to accurately model until such modifier loci are identified and their gene frequencies in the population can be measured.”

Variant Creutzfeldt-Jakob disease could have an incubation time of 30 years or longer and could affect a wider population than currently forecast, according to new research on patients with a similar human prion disease.

Researchers examined 11 recent cases of kuru, a prion protein disease that became an epidemic in the mid-1900s among several groups of Papua New Guinea natives, resulting from their ritual cannibalism, reported John Collinge, Ph.D., a professor of neurology at University College London, and his colleagues (Lancet 2006;367:2068–74).

Cannibalism practices were banned by the Australian authorities in the mid-1950s, and researchers are confident they have been nonexistent since 1960. However, because kuru disease still affects Papua New Guinea natives, researchers have been able to determine long incubation times.

Dr. Collinge and his colleagues monitored 11 cases of kuru disease in Papua New Guinea beginning in 1996, with disease onset between November 1994 and October 2001. The average age of patient onset was 46 years or older.

The oldest patient at disease onset was a 63-year-old man in 1996. The minimum incubation time for the patient was 36 years. However, because young boys traditionally stopped participating in the cannibalism ritual around the age of 7 years, the likely incubation period was 56 years, the researchers reported.

The mean incubation period for kuru is currently estimated to be about 12 years.

Of the 11 patients, 8 were heterozygous for valine and methionine at codon 129 of the human prion protein gene. That distribution of heterozygous genotypes within the kuru patients did not, however, differ markedly from the surrounding population.

Although kuru disease's lethality arose from intraspecies recycling of infectious prions, the results of the latest research suggest that prion diseases, such as variant Creutzfeldt-Jakob disease (vCJD), may have longer incubation times than current models now pose.

Genetic transmission barriers may limit the number of people who acquire vCJD by consuming meat infected with bovine spongiform encephalopathy (BSE). Those who have already suffered from the disease may have been genetically predisposed to have shorter incubation times. Meanwhile, the research on kuru patients demonstrates that prion diseases can also have very long incubation times, “approaching (and perhaps exceeding) the typical human life span,” according to the researchers.

“Therefore, a human BSE epidemic may be multiphasic, and recent estimates of the size of the vCJD epidemic based on uniform genetic susceptibility could be substantial underestimations,” they wrote.

“Genes implicated in species-barrier effects, which would further increase both the mean and range of human BSE incubation periods, are also probably relevant. In this context, a human epidemic will be difficult to accurately model until such modifier loci are identified and their gene frequencies in the population can be measured.”

Variant Creutzfeldt-Jakob disease could have an incubation time of 30 years or longer and could affect a wider population than currently forecast, according to new research on patients with a similar human prion disease.

Researchers examined 11 recent cases of kuru, a prion protein disease that became an epidemic in the mid-1900s among several groups of Papua New Guinea natives, resulting from their ritual cannibalism, reported John Collinge, Ph.D., a professor of neurology at University College London, and his colleagues (Lancet 2006;367:2068–74).

Cannibalism practices were banned by the Australian authorities in the mid-1950s, and researchers are confident they have been nonexistent since 1960. However, because kuru disease still affects Papua New Guinea natives, researchers have been able to determine long incubation times.

Dr. Collinge and his colleagues monitored 11 cases of kuru disease in Papua New Guinea beginning in 1996, with disease onset between November 1994 and October 2001. The average age of patient onset was 46 years or older.

The oldest patient at disease onset was a 63-year-old man in 1996. The minimum incubation time for the patient was 36 years. However, because young boys traditionally stopped participating in the cannibalism ritual around the age of 7 years, the likely incubation period was 56 years, the researchers reported.

The mean incubation period for kuru is currently estimated to be about 12 years.

Of the 11 patients, 8 were heterozygous for valine and methionine at codon 129 of the human prion protein gene. That distribution of heterozygous genotypes within the kuru patients did not, however, differ markedly from the surrounding population.

Although kuru disease's lethality arose from intraspecies recycling of infectious prions, the results of the latest research suggest that prion diseases, such as variant Creutzfeldt-Jakob disease (vCJD), may have longer incubation times than current models now pose.

Genetic transmission barriers may limit the number of people who acquire vCJD by consuming meat infected with bovine spongiform encephalopathy (BSE). Those who have already suffered from the disease may have been genetically predisposed to have shorter incubation times. Meanwhile, the research on kuru patients demonstrates that prion diseases can also have very long incubation times, “approaching (and perhaps exceeding) the typical human life span,” according to the researchers.

“Therefore, a human BSE epidemic may be multiphasic, and recent estimates of the size of the vCJD epidemic based on uniform genetic susceptibility could be substantial underestimations,” they wrote.

“Genes implicated in species-barrier effects, which would further increase both the mean and range of human BSE incubation periods, are also probably relevant. In this context, a human epidemic will be difficult to accurately model until such modifier loci are identified and their gene frequencies in the population can be measured.”

An anti-infective drug now used to treat illnesses from waterborne parasites also can shorten the course of rotavirus in children, results of a small study have shown.

In a trial of 38 children treated at Cairo (Egypt) University Children's Hospital, treatment with nitazoxanide more than halved the time spent in a hospital for treatment of diarrhea resulting from a rotavirus infection (Lancet 2006;doi:10.1016/S0140-6736(06)68852-1).

Nitazoxanide (Alinia) is approved for treatment of Cryptosporidium parvum and Giardia lamblia in the United States. Its manufacturer, Romark Laboratories, also has filed an investigational new drug application with the Food and Drug Administration to test its effectiveness as a treatment for chronic hepatitis C.

Romark was a sponsor of this study, and its lead investigator, Jean-Francois Rossignol, is a professor at the Romark Institute for Medical Research, Tampa, Fla., as well as a shareholder in the company.

Rotavirus kills about 500,000 children a year, mostly in underdeveloped countries where poor nutrition makes children more vulnerable.

A vaccine had been developed for the virus, but that Wyeth vaccine—RotaShield—was pulled from the market in 1999 because of a higher rate of intussusception linked to the vaccine.

The FDA approved a new live vaccine, RotaTeq (Merck & Co.), for the United States in February.

The study randomized 50 children younger than 12 years suffering from diarrhea into groups treated with a 3-day course of nitazoxanide in an oral suspension or a placebo to test the length of time until disease resolution.

All received routine care, including fluid replacement therapy and nutritional management of diarrhea. Twelve children were excluded because rotavirus was not found to be the cause of their diarrhea, the researchers said.

The median time from first dose to disease resolution was 31 hours among the children treated with nitazoxanide, compared with 75 hours for the children in the placebo group, Dr. Rossignol and associates reported.

The two groups were not significantly different in their demographic makeup, symptoms, nutritional status, or the length of time they had experienced diarrhea or hospitalization as a result of the diarrhea. Most of the study patients were malnourished with reduced immunity. In both groups, early responders tended to be better-nourished, had been sick longer, and had been in the hospital longer when receiving the first dose, the investigators wrote.

Dr. Rossignol and associates added that despite laboratory results indicating otherwise, they cannot rule out the possibility that hidden pathogens might have affected the results of the study, although coinfections with rotavirus are rare.

The investigators also noted that they did not take stool samples during the study to assess the relationship between the clinical response and the rotavirus excretion.

An anti-infective drug now used to treat illnesses from waterborne parasites also can shorten the course of rotavirus in children, results of a small study have shown.

In a trial of 38 children treated at Cairo (Egypt) University Children's Hospital, treatment with nitazoxanide more than halved the time spent in a hospital for treatment of diarrhea resulting from a rotavirus infection (Lancet 2006;doi:10.1016/S0140-6736(06)68852-1).

Nitazoxanide (Alinia) is approved for treatment of Cryptosporidium parvum and Giardia lamblia in the United States. Its manufacturer, Romark Laboratories, also has filed an investigational new drug application with the Food and Drug Administration to test its effectiveness as a treatment for chronic hepatitis C.

Romark was a sponsor of this study, and its lead investigator, Jean-Francois Rossignol, is a professor at the Romark Institute for Medical Research, Tampa, Fla., as well as a shareholder in the company.

Rotavirus kills about 500,000 children a year, mostly in underdeveloped countries where poor nutrition makes children more vulnerable.

A vaccine had been developed for the virus, but that Wyeth vaccine—RotaShield—was pulled from the market in 1999 because of a higher rate of intussusception linked to the vaccine.

The FDA approved a new live vaccine, RotaTeq (Merck & Co.), for the United States in February.

The study randomized 50 children younger than 12 years suffering from diarrhea into groups treated with a 3-day course of nitazoxanide in an oral suspension or a placebo to test the length of time until disease resolution.

All received routine care, including fluid replacement therapy and nutritional management of diarrhea. Twelve children were excluded because rotavirus was not found to be the cause of their diarrhea, the researchers said.

The median time from first dose to disease resolution was 31 hours among the children treated with nitazoxanide, compared with 75 hours for the children in the placebo group, Dr. Rossignol and associates reported.

The two groups were not significantly different in their demographic makeup, symptoms, nutritional status, or the length of time they had experienced diarrhea or hospitalization as a result of the diarrhea. Most of the study patients were malnourished with reduced immunity. In both groups, early responders tended to be better-nourished, had been sick longer, and had been in the hospital longer when receiving the first dose, the investigators wrote.

Dr. Rossignol and associates added that despite laboratory results indicating otherwise, they cannot rule out the possibility that hidden pathogens might have affected the results of the study, although coinfections with rotavirus are rare.

The investigators also noted that they did not take stool samples during the study to assess the relationship between the clinical response and the rotavirus excretion.

An anti-infective drug now used to treat illnesses from waterborne parasites also can shorten the course of rotavirus in children, results of a small study have shown.

In a trial of 38 children treated at Cairo (Egypt) University Children's Hospital, treatment with nitazoxanide more than halved the time spent in a hospital for treatment of diarrhea resulting from a rotavirus infection (Lancet 2006;doi:10.1016/S0140-6736(06)68852-1).

Nitazoxanide (Alinia) is approved for treatment of Cryptosporidium parvum and Giardia lamblia in the United States. Its manufacturer, Romark Laboratories, also has filed an investigational new drug application with the Food and Drug Administration to test its effectiveness as a treatment for chronic hepatitis C.

Romark was a sponsor of this study, and its lead investigator, Jean-Francois Rossignol, is a professor at the Romark Institute for Medical Research, Tampa, Fla., as well as a shareholder in the company.

Rotavirus kills about 500,000 children a year, mostly in underdeveloped countries where poor nutrition makes children more vulnerable.

A vaccine had been developed for the virus, but that Wyeth vaccine—RotaShield—was pulled from the market in 1999 because of a higher rate of intussusception linked to the vaccine.

The FDA approved a new live vaccine, RotaTeq (Merck & Co.), for the United States in February.

The study randomized 50 children younger than 12 years suffering from diarrhea into groups treated with a 3-day course of nitazoxanide in an oral suspension or a placebo to test the length of time until disease resolution.

All received routine care, including fluid replacement therapy and nutritional management of diarrhea. Twelve children were excluded because rotavirus was not found to be the cause of their diarrhea, the researchers said.

The median time from first dose to disease resolution was 31 hours among the children treated with nitazoxanide, compared with 75 hours for the children in the placebo group, Dr. Rossignol and associates reported.

The two groups were not significantly different in their demographic makeup, symptoms, nutritional status, or the length of time they had experienced diarrhea or hospitalization as a result of the diarrhea. Most of the study patients were malnourished with reduced immunity. In both groups, early responders tended to be better-nourished, had been sick longer, and had been in the hospital longer when receiving the first dose, the investigators wrote.

Dr. Rossignol and associates added that despite laboratory results indicating otherwise, they cannot rule out the possibility that hidden pathogens might have affected the results of the study, although coinfections with rotavirus are rare.

The investigators also noted that they did not take stool samples during the study to assess the relationship between the clinical response and the rotavirus excretion.

African Americans are two to three times more likely to die from systemic lupus erythematosus than are whites, a disparity that is higher than the risk of mortality from all causes, according to an analysis of U.S. death and hospitalization statistics.

Dr. Eswar Krishnan of the University of Pittsburgh and Helen B. Hubert, Ph.D., of Stanford (Calif.) University wrote that the greater lupus mortality risk suggests that biologic rather than socioeconomic factors may be responsible.

The study examined death statistics from the National Center for Health Statistics at the Centers for Disease Control and Prevention from 1979 to 1998. Investigators also analyzed data from the Nationwide Inpatient Sample, a database run by the Agency for Healthcare Research and Quality taken from the discharge summaries of a 20% stratified sample of hospitals in the United States from 1993 to 2002 (Ann. Rheum. Dis. 2006;[Epub ahead of print, doi:10.1136/ard.2005.040907]).

For African American women, the lupus mortality risk was 3.91 times that of white women, compared with 1.24 for death from all causes. For African American men, the lupus mortality risk was 2.4 times that of white men, compared with 1.36 for deaths from all causes.

The mean age at which women were hospitalized for lupus was 43 years for African Americans and 53 years for whites. For men, the mean age at hospitalization for lupus was 43 years for African Americans and 58 years for whites. For lupus patients who died, the mean age among African Americans was 49 years; for whites, the mean age was 64 years.

The lupus death rate increased for both African American and white women from 1979 to 1998. The death rate for African American men held steady while decreasing for white men, which resulted in an increase in the relative death risk ratio for African American men.

Insurance status did not influence relative mortality risk, suggesting that the ethnic differences may be biologic, the researchers said. Such a suggestion is supported by research indicating that African Americans are diagnosed with lupus 6 years younger than are whites on average and were more likely to show such symptoms as discoid lupus.

“Our findings have important clinical and public health implications,” the investigators wrote, adding that African Americans are less likely to receive preventative health services than are whites. Therefore, many of the excess deaths among African Americans with lupus may be the result of preventable cardiovascular, infectious, and renal complications. Aggressive intervention with increased exercise, control of hypertension and hyperlipidemia, smoking cessation, and management of other risk factors may eliminate the excess mortality seen in African Americans with lupus, according to the investigators.

African Americans are two to three times more likely to die from systemic lupus erythematosus than are whites, a disparity that is higher than the risk of mortality from all causes, according to an analysis of U.S. death and hospitalization statistics.

Dr. Eswar Krishnan of the University of Pittsburgh and Helen B. Hubert, Ph.D., of Stanford (Calif.) University wrote that the greater lupus mortality risk suggests that biologic rather than socioeconomic factors may be responsible.

The study examined death statistics from the National Center for Health Statistics at the Centers for Disease Control and Prevention from 1979 to 1998. Investigators also analyzed data from the Nationwide Inpatient Sample, a database run by the Agency for Healthcare Research and Quality taken from the discharge summaries of a 20% stratified sample of hospitals in the United States from 1993 to 2002 (Ann. Rheum. Dis. 2006;[Epub ahead of print, doi:10.1136/ard.2005.040907]).

For African American women, the lupus mortality risk was 3.91 times that of white women, compared with 1.24 for death from all causes. For African American men, the lupus mortality risk was 2.4 times that of white men, compared with 1.36 for deaths from all causes.

The mean age at which women were hospitalized for lupus was 43 years for African Americans and 53 years for whites. For men, the mean age at hospitalization for lupus was 43 years for African Americans and 58 years for whites. For lupus patients who died, the mean age among African Americans was 49 years; for whites, the mean age was 64 years.

The lupus death rate increased for both African American and white women from 1979 to 1998. The death rate for African American men held steady while decreasing for white men, which resulted in an increase in the relative death risk ratio for African American men.

Insurance status did not influence relative mortality risk, suggesting that the ethnic differences may be biologic, the researchers said. Such a suggestion is supported by research indicating that African Americans are diagnosed with lupus 6 years younger than are whites on average and were more likely to show such symptoms as discoid lupus.

“Our findings have important clinical and public health implications,” the investigators wrote, adding that African Americans are less likely to receive preventative health services than are whites. Therefore, many of the excess deaths among African Americans with lupus may be the result of preventable cardiovascular, infectious, and renal complications. Aggressive intervention with increased exercise, control of hypertension and hyperlipidemia, smoking cessation, and management of other risk factors may eliminate the excess mortality seen in African Americans with lupus, according to the investigators.

African Americans are two to three times more likely to die from systemic lupus erythematosus than are whites, a disparity that is higher than the risk of mortality from all causes, according to an analysis of U.S. death and hospitalization statistics.

Dr. Eswar Krishnan of the University of Pittsburgh and Helen B. Hubert, Ph.D., of Stanford (Calif.) University wrote that the greater lupus mortality risk suggests that biologic rather than socioeconomic factors may be responsible.

The study examined death statistics from the National Center for Health Statistics at the Centers for Disease Control and Prevention from 1979 to 1998. Investigators also analyzed data from the Nationwide Inpatient Sample, a database run by the Agency for Healthcare Research and Quality taken from the discharge summaries of a 20% stratified sample of hospitals in the United States from 1993 to 2002 (Ann. Rheum. Dis. 2006;[Epub ahead of print, doi:10.1136/ard.2005.040907]).

For African American women, the lupus mortality risk was 3.91 times that of white women, compared with 1.24 for death from all causes. For African American men, the lupus mortality risk was 2.4 times that of white men, compared with 1.36 for deaths from all causes.

The mean age at which women were hospitalized for lupus was 43 years for African Americans and 53 years for whites. For men, the mean age at hospitalization for lupus was 43 years for African Americans and 58 years for whites. For lupus patients who died, the mean age among African Americans was 49 years; for whites, the mean age was 64 years.

The lupus death rate increased for both African American and white women from 1979 to 1998. The death rate for African American men held steady while decreasing for white men, which resulted in an increase in the relative death risk ratio for African American men.

Insurance status did not influence relative mortality risk, suggesting that the ethnic differences may be biologic, the researchers said. Such a suggestion is supported by research indicating that African Americans are diagnosed with lupus 6 years younger than are whites on average and were more likely to show such symptoms as discoid lupus.

“Our findings have important clinical and public health implications,” the investigators wrote, adding that African Americans are less likely to receive preventative health services than are whites. Therefore, many of the excess deaths among African Americans with lupus may be the result of preventable cardiovascular, infectious, and renal complications. Aggressive intervention with increased exercise, control of hypertension and hyperlipidemia, smoking cessation, and management of other risk factors may eliminate the excess mortality seen in African Americans with lupus, according to the investigators.

GLASGOW, SCOTLAND — Swiss researchers have identified a hormonal precursor that may make it easier for physicians to identify patients suffering from sepsis, according to a study presented at the 8th European Congress of Endocrinology.

The substance is copeptin, a precursor to vasopressin, which is produced when the body undergoes stress, such as septic shock. Vasopressin is unstable and has a short half-life, making it difficult to use in identifying patients who are suffering from sepsis. Copeptin, on the other hand, is more stable and is derived from the same precursor molecule.

A team of researchers from the departments of endocrinology and internal medicine at University Hospital, Basel, Switzerland, led by Dr. Mirjam Christ-Crain, evaluated 101 consecutive critically ill patients over a 9-month period and compared their relative serum copeptin levels with relative copeptin levels in 50 healthy control subjects. Copeptin levels were measured at admission, day 2, and hospital discharge or death.

Copeptin levels were identified in the blood using a test that will soon be available commercially from the German medical equipment manufacturer Brahms AG.

Of the 101 critically ill patients, 53 had sepsis, severe sepsis, or septic shock; 48 had systemic inflammatory response syndrome (SIRS).

At admission, patients with SIRS had a median copeptin level of 27.6 pmol/L of blood, those with sepsis 50 pmol/L, those with severe sepsis 73.6 pmol/L, and those with septic shock 171.5 pmol/L. In comparison, healthy controls had a median copeptin level of 5 pmol/L, Dr. Christ-Crain said.

Patients with sepsis, severe sepsis, or septic shock who died had median copeptin blood levels of 171.5 pmol/L, compared with 86.8 pmol/L among those who survived.

Septicemia is the 10th-leading cause of death in the United States, claiming 33,464 lives in 2004, according to the Centers for Disease Control and Prevention.

“Copeptin is a novel tool to assess the prognosis of sepsis,” Dr. Christ-Crain observed. “It might help to guide the resource allocation of hospital care to those patients especially in need for intensive surveillance.”

ELSEVIER GLOBAL MEDICAL NEWS

GLASGOW, SCOTLAND — Swiss researchers have identified a hormonal precursor that may make it easier for physicians to identify patients suffering from sepsis, according to a study presented at the 8th European Congress of Endocrinology.

The substance is copeptin, a precursor to vasopressin, which is produced when the body undergoes stress, such as septic shock. Vasopressin is unstable and has a short half-life, making it difficult to use in identifying patients who are suffering from sepsis. Copeptin, on the other hand, is more stable and is derived from the same precursor molecule.

A team of researchers from the departments of endocrinology and internal medicine at University Hospital, Basel, Switzerland, led by Dr. Mirjam Christ-Crain, evaluated 101 consecutive critically ill patients over a 9-month period and compared their relative serum copeptin levels with relative copeptin levels in 50 healthy control subjects. Copeptin levels were measured at admission, day 2, and hospital discharge or death.

Copeptin levels were identified in the blood using a test that will soon be available commercially from the German medical equipment manufacturer Brahms AG.

Of the 101 critically ill patients, 53 had sepsis, severe sepsis, or septic shock; 48 had systemic inflammatory response syndrome (SIRS).

At admission, patients with SIRS had a median copeptin level of 27.6 pmol/L of blood, those with sepsis 50 pmol/L, those with severe sepsis 73.6 pmol/L, and those with septic shock 171.5 pmol/L. In comparison, healthy controls had a median copeptin level of 5 pmol/L, Dr. Christ-Crain said.

Patients with sepsis, severe sepsis, or septic shock who died had median copeptin blood levels of 171.5 pmol/L, compared with 86.8 pmol/L among those who survived.

Septicemia is the 10th-leading cause of death in the United States, claiming 33,464 lives in 2004, according to the Centers for Disease Control and Prevention.

“Copeptin is a novel tool to assess the prognosis of sepsis,” Dr. Christ-Crain observed. “It might help to guide the resource allocation of hospital care to those patients especially in need for intensive surveillance.”

ELSEVIER GLOBAL MEDICAL NEWS

GLASGOW, SCOTLAND — Swiss researchers have identified a hormonal precursor that may make it easier for physicians to identify patients suffering from sepsis, according to a study presented at the 8th European Congress of Endocrinology.

The substance is copeptin, a precursor to vasopressin, which is produced when the body undergoes stress, such as septic shock. Vasopressin is unstable and has a short half-life, making it difficult to use in identifying patients who are suffering from sepsis. Copeptin, on the other hand, is more stable and is derived from the same precursor molecule.

A team of researchers from the departments of endocrinology and internal medicine at University Hospital, Basel, Switzerland, led by Dr. Mirjam Christ-Crain, evaluated 101 consecutive critically ill patients over a 9-month period and compared their relative serum copeptin levels with relative copeptin levels in 50 healthy control subjects. Copeptin levels were measured at admission, day 2, and hospital discharge or death.

Copeptin levels were identified in the blood using a test that will soon be available commercially from the German medical equipment manufacturer Brahms AG.

Of the 101 critically ill patients, 53 had sepsis, severe sepsis, or septic shock; 48 had systemic inflammatory response syndrome (SIRS).

At admission, patients with SIRS had a median copeptin level of 27.6 pmol/L of blood, those with sepsis 50 pmol/L, those with severe sepsis 73.6 pmol/L, and those with septic shock 171.5 pmol/L. In comparison, healthy controls had a median copeptin level of 5 pmol/L, Dr. Christ-Crain said.

Patients with sepsis, severe sepsis, or septic shock who died had median copeptin blood levels of 171.5 pmol/L, compared with 86.8 pmol/L among those who survived.

Septicemia is the 10th-leading cause of death in the United States, claiming 33,464 lives in 2004, according to the Centers for Disease Control and Prevention.

“Copeptin is a novel tool to assess the prognosis of sepsis,” Dr. Christ-Crain observed. “It might help to guide the resource allocation of hospital care to those patients especially in need for intensive surveillance.”

ELSEVIER GLOBAL MEDICAL NEWS

GLASGOW, SCOTLAND — Swiss researchers have identified a hormonal precursor that may make it easier for physicians to identify patients suffering from sepsis, according to a study presented at the 8th European Congress of Endocrinology.

The substance is copeptin, a precursor to vasopressin, which is produced when the body undergoes stress such as septic shock. Vasopressin is unstable and has a short half-life, making it difficult to use to identify patients suffering from sepsis. Copeptin, on the other hand, is more stable and is derived from the same precursor molecule.

A team of researchers from the departments of endocrinology and internal medicine at University Hospital, Basel, Switzerland, led by Dr. Mirjam Christ-Crain, evaluated 101 consecutive critically ill patients over a 9-month period and compared their relative serum copeptin levels with those of 50 healthy controls. Copeptin levels were measured at admission, day 2, and hospital discharge or death.

Copeptin levels were identified in the blood using a test that will soon be available commercially from the German medical equipment manufacturer Brahms.

Of the 101 critically ill patients, 53 had sepsis, severe sepsis, or septic shock; 48 had systemic inflammatory response syndrome (SIRS).

At admission, patients with SIRS had a median copeptin level of 27.6 pmol/L of blood, those with sepsis 50 pmol/L, those with severe sepsis 73.6 pmol/L, and those with septic shock 171.5 pmol/L. In comparison, healthy controls had a median copeptin level of 5 pmol/L, Dr. Christ-Crain said.

Patients with sepsis, severe sepsis, or septic shock who died had median copeptin blood levels of 171.5 pmol/L, compared with 86.8 pmol/L among those who survived.

Septicemia is the 10th leading cause of death in the United States, claiming 33,464 lives in 2004, according to the Centers for Disease Control and Prevention.

“Copeptin is a novel tool to assess the prognosis of sepsis,” Dr. Christ-Crain said. “It might help to guide the resource allocation of hospital care to those patients especially in need for intensive surveillance.”

ELSEVIER GLOBAL MEDICAL NEWS

GLASGOW, SCOTLAND — Swiss researchers have identified a hormonal precursor that may make it easier for physicians to identify patients suffering from sepsis, according to a study presented at the 8th European Congress of Endocrinology.

The substance is copeptin, a precursor to vasopressin, which is produced when the body undergoes stress such as septic shock. Vasopressin is unstable and has a short half-life, making it difficult to use to identify patients suffering from sepsis. Copeptin, on the other hand, is more stable and is derived from the same precursor molecule.

A team of researchers from the departments of endocrinology and internal medicine at University Hospital, Basel, Switzerland, led by Dr. Mirjam Christ-Crain, evaluated 101 consecutive critically ill patients over a 9-month period and compared their relative serum copeptin levels with those of 50 healthy controls. Copeptin levels were measured at admission, day 2, and hospital discharge or death.

Copeptin levels were identified in the blood using a test that will soon be available commercially from the German medical equipment manufacturer Brahms.

Of the 101 critically ill patients, 53 had sepsis, severe sepsis, or septic shock; 48 had systemic inflammatory response syndrome (SIRS).

At admission, patients with SIRS had a median copeptin level of 27.6 pmol/L of blood, those with sepsis 50 pmol/L, those with severe sepsis 73.6 pmol/L, and those with septic shock 171.5 pmol/L. In comparison, healthy controls had a median copeptin level of 5 pmol/L, Dr. Christ-Crain said.

Patients with sepsis, severe sepsis, or septic shock who died had median copeptin blood levels of 171.5 pmol/L, compared with 86.8 pmol/L among those who survived.

Septicemia is the 10th leading cause of death in the United States, claiming 33,464 lives in 2004, according to the Centers for Disease Control and Prevention.

“Copeptin is a novel tool to assess the prognosis of sepsis,” Dr. Christ-Crain said. “It might help to guide the resource allocation of hospital care to those patients especially in need for intensive surveillance.”

ELSEVIER GLOBAL MEDICAL NEWS

GLASGOW, SCOTLAND — Swiss researchers have identified a hormonal precursor that may make it easier for physicians to identify patients suffering from sepsis, according to a study presented at the 8th European Congress of Endocrinology.

The substance is copeptin, a precursor to vasopressin, which is produced when the body undergoes stress such as septic shock. Vasopressin is unstable and has a short half-life, making it difficult to use to identify patients suffering from sepsis. Copeptin, on the other hand, is more stable and is derived from the same precursor molecule.

A team of researchers from the departments of endocrinology and internal medicine at University Hospital, Basel, Switzerland, led by Dr. Mirjam Christ-Crain, evaluated 101 consecutive critically ill patients over a 9-month period and compared their relative serum copeptin levels with those of 50 healthy controls. Copeptin levels were measured at admission, day 2, and hospital discharge or death.

Copeptin levels were identified in the blood using a test that will soon be available commercially from the German medical equipment manufacturer Brahms.

Of the 101 critically ill patients, 53 had sepsis, severe sepsis, or septic shock; 48 had systemic inflammatory response syndrome (SIRS).

At admission, patients with SIRS had a median copeptin level of 27.6 pmol/L of blood, those with sepsis 50 pmol/L, those with severe sepsis 73.6 pmol/L, and those with septic shock 171.5 pmol/L. In comparison, healthy controls had a median copeptin level of 5 pmol/L, Dr. Christ-Crain said.

Patients with sepsis, severe sepsis, or septic shock who died had median copeptin blood levels of 171.5 pmol/L, compared with 86.8 pmol/L among those who survived.

Septicemia is the 10th leading cause of death in the United States, claiming 33,464 lives in 2004, according to the Centers for Disease Control and Prevention.

“Copeptin is a novel tool to assess the prognosis of sepsis,” Dr. Christ-Crain said. “It might help to guide the resource allocation of hospital care to those patients especially in need for intensive surveillance.”

ELSEVIER GLOBAL MEDICAL NEWS

Drug regulators in the United States and Europe have announced "intensified" information sharing and dialogue aimed at increasing cooperation in drug approval and surveillance activities in the world's two largest pharmaceutical markets.

At a March review meeting in Brussels, representatives from the Food and Drug Administration, the European Medicines Agency, and the European Commission judged as a success the implementation of a confidentiality agreement that has enabled greater transatlantic information sharing and dialogue on pharmaceutical regulations protecting 753 million people in 26 countries.

The three agencies hope to particularly strengthen joint activities on vaccines in preparation for potential pandemic flu outbreaks, as well as cancer, children's, and orphan drugs, and pharmacogenomics. Future activities will address counterfeit medicines.

The original agreement, signed in September 2003, paved the way for quarterly exchanges on information on new drug applications, regulatory guidance, and inspections of manufacturing plants, which began in 2004. The agreement also authorized ad hoc exchanges of information on drug safety and public health, including advance notice of significant regulatory actions such as pulling drugs from the market.

Such an exchange prevents other agencies from issuing contradictory advice when one agency takes significant regulatory action.

The ad hoc exchanges also have enabled "parallel" scientific guidance for drug applicants seeking the advice of the three agencies on how to proceed with research at such milestones as the conclusion of clinical trials. The first such parallel scientific meeting occurred in September 2003, and as part of the initial confidentiality arrangement a 1-year pilot project was initiated in 2005.

The focus of those parallel meetings is breakthrough drugs, those for rare conditions, medication for children, or other new medicines considered important.

The three agencies agreed to extend the pilot project, although the document released by the agencies did not give a time period. A spokesman for the European Commission said the meetings do not guarantee joint scientific advice from the three agencies but give applicants better guidance on how to proceed if they are seeking international drug approvals.

Drug regulators in the United States and Europe have announced "intensified" information sharing and dialogue aimed at increasing cooperation in drug approval and surveillance activities in the world's two largest pharmaceutical markets.

At a March review meeting in Brussels, representatives from the Food and Drug Administration, the European Medicines Agency, and the European Commission judged as a success the implementation of a confidentiality agreement that has enabled greater transatlantic information sharing and dialogue on pharmaceutical regulations protecting 753 million people in 26 countries.

The three agencies hope to particularly strengthen joint activities on vaccines in preparation for potential pandemic flu outbreaks, as well as cancer, children's, and orphan drugs, and pharmacogenomics. Future activities will address counterfeit medicines.

The original agreement, signed in September 2003, paved the way for quarterly exchanges on information on new drug applications, regulatory guidance, and inspections of manufacturing plants, which began in 2004. The agreement also authorized ad hoc exchanges of information on drug safety and public health, including advance notice of significant regulatory actions such as pulling drugs from the market.

Such an exchange prevents other agencies from issuing contradictory advice when one agency takes significant regulatory action.

The ad hoc exchanges also have enabled "parallel" scientific guidance for drug applicants seeking the advice of the three agencies on how to proceed with research at such milestones as the conclusion of clinical trials. The first such parallel scientific meeting occurred in September 2003, and as part of the initial confidentiality arrangement a 1-year pilot project was initiated in 2005.

The focus of those parallel meetings is breakthrough drugs, those for rare conditions, medication for children, or other new medicines considered important.

The three agencies agreed to extend the pilot project, although the document released by the agencies did not give a time period. A spokesman for the European Commission said the meetings do not guarantee joint scientific advice from the three agencies but give applicants better guidance on how to proceed if they are seeking international drug approvals.

Drug regulators in the United States and Europe have announced "intensified" information sharing and dialogue aimed at increasing cooperation in drug approval and surveillance activities in the world's two largest pharmaceutical markets.

At a March review meeting in Brussels, representatives from the Food and Drug Administration, the European Medicines Agency, and the European Commission judged as a success the implementation of a confidentiality agreement that has enabled greater transatlantic information sharing and dialogue on pharmaceutical regulations protecting 753 million people in 26 countries.

The three agencies hope to particularly strengthen joint activities on vaccines in preparation for potential pandemic flu outbreaks, as well as cancer, children's, and orphan drugs, and pharmacogenomics. Future activities will address counterfeit medicines.

The original agreement, signed in September 2003, paved the way for quarterly exchanges on information on new drug applications, regulatory guidance, and inspections of manufacturing plants, which began in 2004. The agreement also authorized ad hoc exchanges of information on drug safety and public health, including advance notice of significant regulatory actions such as pulling drugs from the market.

Such an exchange prevents other agencies from issuing contradictory advice when one agency takes significant regulatory action.

The ad hoc exchanges also have enabled "parallel" scientific guidance for drug applicants seeking the advice of the three agencies on how to proceed with research at such milestones as the conclusion of clinical trials. The first such parallel scientific meeting occurred in September 2003, and as part of the initial confidentiality arrangement a 1-year pilot project was initiated in 2005.

The focus of those parallel meetings is breakthrough drugs, those for rare conditions, medication for children, or other new medicines considered important.

The three agencies agreed to extend the pilot project, although the document released by the agencies did not give a time period. A spokesman for the European Commission said the meetings do not guarantee joint scientific advice from the three agencies but give applicants better guidance on how to proceed if they are seeking international drug approvals.

U.S. and European drug regulators have announced “intensified” information sharing and dialogue aimed at increasing cooperation in drug approval and surveillance activities in the world's two largest pharmaceutical markets.

At a March meeting in Brussels, Food and Drug Administration, European Medicines Agency, and European Commission representatives judged as a success the implementation of a confidentiality agreement that has enabled greater transatlantic information sharing and dialogue on pharmaceutical regulations protecting 753 million people in 26 countries. The three agencies hope to particularly strengthen joint activities on vaccines in preparation for potential pandemic flu outbreaks, as well as cancer, children's, and orphan drugs, and pharmacogenomics. Future activities will address counterfeit medicines.

The original agreement, signed in September 2003, paved the way for quarterly exchanges on information on new drug applications, regulatory guidance, and inspections of manufacturing plants, which began in 2004. The pact also authorized ad hoc exchanges of information on drug safety and public health, including advance notice of significant regulatory actions such as pulling drugs from the market.

Such an exchange prevents other agencies from issuing contradictory advice when one agency takes significant regulatory action. The ad hoc exchanges also have enabled “parallel” scientific guidance for drug applicants seeking the advice of the three agencies on how to proceed with research at such milestones as the conclusion of clinical trials. The first such parallel scientific meeting occurred in September 2003, and as part of the initial confidentiality arrangement a 1-year pilot project was initiated in 2005.

The focus of those parallel meetings is breakthrough drugs, those for rare conditions, medication for children, or other new medicines considered important.

The three agencies agreed to extend the pilot project; the document released by the agencies did not say for how long.

U.S. and European drug regulators have announced “intensified” information sharing and dialogue aimed at increasing cooperation in drug approval and surveillance activities in the world's two largest pharmaceutical markets.

At a March meeting in Brussels, Food and Drug Administration, European Medicines Agency, and European Commission representatives judged as a success the implementation of a confidentiality agreement that has enabled greater transatlantic information sharing and dialogue on pharmaceutical regulations protecting 753 million people in 26 countries. The three agencies hope to particularly strengthen joint activities on vaccines in preparation for potential pandemic flu outbreaks, as well as cancer, children's, and orphan drugs, and pharmacogenomics. Future activities will address counterfeit medicines.

The original agreement, signed in September 2003, paved the way for quarterly exchanges on information on new drug applications, regulatory guidance, and inspections of manufacturing plants, which began in 2004. The pact also authorized ad hoc exchanges of information on drug safety and public health, including advance notice of significant regulatory actions such as pulling drugs from the market.

Such an exchange prevents other agencies from issuing contradictory advice when one agency takes significant regulatory action. The ad hoc exchanges also have enabled “parallel” scientific guidance for drug applicants seeking the advice of the three agencies on how to proceed with research at such milestones as the conclusion of clinical trials. The first such parallel scientific meeting occurred in September 2003, and as part of the initial confidentiality arrangement a 1-year pilot project was initiated in 2005.

The focus of those parallel meetings is breakthrough drugs, those for rare conditions, medication for children, or other new medicines considered important.

The three agencies agreed to extend the pilot project; the document released by the agencies did not say for how long.

U.S. and European drug regulators have announced “intensified” information sharing and dialogue aimed at increasing cooperation in drug approval and surveillance activities in the world's two largest pharmaceutical markets.

At a March meeting in Brussels, Food and Drug Administration, European Medicines Agency, and European Commission representatives judged as a success the implementation of a confidentiality agreement that has enabled greater transatlantic information sharing and dialogue on pharmaceutical regulations protecting 753 million people in 26 countries. The three agencies hope to particularly strengthen joint activities on vaccines in preparation for potential pandemic flu outbreaks, as well as cancer, children's, and orphan drugs, and pharmacogenomics. Future activities will address counterfeit medicines.

The original agreement, signed in September 2003, paved the way for quarterly exchanges on information on new drug applications, regulatory guidance, and inspections of manufacturing plants, which began in 2004. The pact also authorized ad hoc exchanges of information on drug safety and public health, including advance notice of significant regulatory actions such as pulling drugs from the market.

Such an exchange prevents other agencies from issuing contradictory advice when one agency takes significant regulatory action. The ad hoc exchanges also have enabled “parallel” scientific guidance for drug applicants seeking the advice of the three agencies on how to proceed with research at such milestones as the conclusion of clinical trials. The first such parallel scientific meeting occurred in September 2003, and as part of the initial confidentiality arrangement a 1-year pilot project was initiated in 2005.

The focus of those parallel meetings is breakthrough drugs, those for rare conditions, medication for children, or other new medicines considered important.

The three agencies agreed to extend the pilot project; the document released by the agencies did not say for how long.