COPENHAGEN – Older veterans who had sleep disturbances were at a 30% greater risk of developing dementia, according to a retrospective analysis of 200,000 medical records presented at the Alzheimer’s Association International Conference 2014.

And having posttraumatic stress disorder (PTSD) in addition to sleep disturbances put veterans at an 80% greater risk.

"As veterans are turning 65 and older, it’s important for us to understand who in that population is at an increased risk of developing dementia, so when we have that therapy or lifestyle intervention, we can intervene at that point," said Heather M. Snyder, Ph.D., director of medical and scientific operations at the Alzheimer’s Association. Dr. Snyder was not involved in the study.

For the study, researchers studied the records of veterans 55 years and older for 8 years. They found that almost 11% of the veterans with sleep disturbance developed dementia, compared with 9% of those without sleep disturbance, almost a 30% risk increase. The results were similar for veterans who had sleep apnea and nonapnea insomnia.

Meanwhile, researchers found no significant interaction between sleep disturbance and traumatic brain injury or PTSD, with regard to increased risk of dementia. However, veterans who had both PTSD and sleep disturbance had an 80% increased risk of developing dementia.

In a video interview, Dr. Kristine Yaffe, professor of psychiatry and neurology at the University of California, San Francisco, explains the study’s findings, shares practice pearls, and discusses the implications for younger veterans.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – Older veterans who had sleep disturbances were at a 30% greater risk of developing dementia, according to a retrospective analysis of 200,000 medical records presented at the Alzheimer’s Association International Conference 2014.

And having posttraumatic stress disorder (PTSD) in addition to sleep disturbances put veterans at an 80% greater risk.

"As veterans are turning 65 and older, it’s important for us to understand who in that population is at an increased risk of developing dementia, so when we have that therapy or lifestyle intervention, we can intervene at that point," said Heather M. Snyder, Ph.D., director of medical and scientific operations at the Alzheimer’s Association. Dr. Snyder was not involved in the study.

For the study, researchers studied the records of veterans 55 years and older for 8 years. They found that almost 11% of the veterans with sleep disturbance developed dementia, compared with 9% of those without sleep disturbance, almost a 30% risk increase. The results were similar for veterans who had sleep apnea and nonapnea insomnia.

Meanwhile, researchers found no significant interaction between sleep disturbance and traumatic brain injury or PTSD, with regard to increased risk of dementia. However, veterans who had both PTSD and sleep disturbance had an 80% increased risk of developing dementia.

In a video interview, Dr. Kristine Yaffe, professor of psychiatry and neurology at the University of California, San Francisco, explains the study’s findings, shares practice pearls, and discusses the implications for younger veterans.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – Older veterans who had sleep disturbances were at a 30% greater risk of developing dementia, according to a retrospective analysis of 200,000 medical records presented at the Alzheimer’s Association International Conference 2014.

And having posttraumatic stress disorder (PTSD) in addition to sleep disturbances put veterans at an 80% greater risk.

"As veterans are turning 65 and older, it’s important for us to understand who in that population is at an increased risk of developing dementia, so when we have that therapy or lifestyle intervention, we can intervene at that point," said Heather M. Snyder, Ph.D., director of medical and scientific operations at the Alzheimer’s Association. Dr. Snyder was not involved in the study.

For the study, researchers studied the records of veterans 55 years and older for 8 years. They found that almost 11% of the veterans with sleep disturbance developed dementia, compared with 9% of those without sleep disturbance, almost a 30% risk increase. The results were similar for veterans who had sleep apnea and nonapnea insomnia.

Meanwhile, researchers found no significant interaction between sleep disturbance and traumatic brain injury or PTSD, with regard to increased risk of dementia. However, veterans who had both PTSD and sleep disturbance had an 80% increased risk of developing dementia.

In a video interview, Dr. Kristine Yaffe, professor of psychiatry and neurology at the University of California, San Francisco, explains the study’s findings, shares practice pearls, and discusses the implications for younger veterans.

[email protected]

On Twitter @naseemmiller

Researcher in the lab

Credit: Darren Baker

In recreating the structure of prothrombin, researchers have improved their understanding of how the clotting factor functions.

By deleting a disordered linker region, they were able to visualize the complete structure of prothrombin.

This deleted version was activated to thrombin much faster than the intact version of prothrombin.

And results suggested that cofactor Va enhances the activation of prothrombin by altering the architecture of the linker.

Enrico Di Cera, MD, of Saint Louis University in Missouri, and his colleagues reported these findings in PNAS.

Last year, Dr Di Cera’s team published the first structure of prothrombin. This structure lacked a domain responsible for interaction with membranes, and certain other sections were not detected by X-ray analysis.

Though the researchers were able to crystallize the protein, there were disordered regions in the structure they could not see.

Within prothrombin, there are 2 kringle domains connected by a linker region that intrigued the researchers because of its intrinsic disorder.

“We deleted this linker, and crystals grew in a few days instead of months, revealing, for the first time, the full architecture of prothrombin,” Dr Di Cera said.

The crystal structure revealed a contorted conformation where the domains are not vertically stacked, kringle-1 comes close to the protease domain, and the Gla-domain contacts kringle-2.

The researchers also found the deleted version of prothrombin is activated to thrombin much faster than intact prothrombin.

Specifically, deletion of the linker reduced the enhancement of thrombin generation by cofactor Va from the more than 3000-fold observed with wild-type prothrombin to 60-fold. So it appears that deletion of the linker mimics the effect of cofactor Va on prothrombin activation.

“It took us almost 2 years to discover that the disordered linker was the key,” Dr Di Cera said. “Finally, prothrombin revealed its secrets, and, with that, the molecular mechanism of a key reaction of blood clotting finally becomes amenable to rational drug design for therapeutic intervention.”

Researcher in the lab

Credit: Darren Baker

In recreating the structure of prothrombin, researchers have improved their understanding of how the clotting factor functions.

By deleting a disordered linker region, they were able to visualize the complete structure of prothrombin.

This deleted version was activated to thrombin much faster than the intact version of prothrombin.

And results suggested that cofactor Va enhances the activation of prothrombin by altering the architecture of the linker.

Enrico Di Cera, MD, of Saint Louis University in Missouri, and his colleagues reported these findings in PNAS.

Last year, Dr Di Cera’s team published the first structure of prothrombin. This structure lacked a domain responsible for interaction with membranes, and certain other sections were not detected by X-ray analysis.

Though the researchers were able to crystallize the protein, there were disordered regions in the structure they could not see.

Within prothrombin, there are 2 kringle domains connected by a linker region that intrigued the researchers because of its intrinsic disorder.

“We deleted this linker, and crystals grew in a few days instead of months, revealing, for the first time, the full architecture of prothrombin,” Dr Di Cera said.

The crystal structure revealed a contorted conformation where the domains are not vertically stacked, kringle-1 comes close to the protease domain, and the Gla-domain contacts kringle-2.

The researchers also found the deleted version of prothrombin is activated to thrombin much faster than intact prothrombin.

Specifically, deletion of the linker reduced the enhancement of thrombin generation by cofactor Va from the more than 3000-fold observed with wild-type prothrombin to 60-fold. So it appears that deletion of the linker mimics the effect of cofactor Va on prothrombin activation.

“It took us almost 2 years to discover that the disordered linker was the key,” Dr Di Cera said. “Finally, prothrombin revealed its secrets, and, with that, the molecular mechanism of a key reaction of blood clotting finally becomes amenable to rational drug design for therapeutic intervention.”

Researcher in the lab

Credit: Darren Baker

In recreating the structure of prothrombin, researchers have improved their understanding of how the clotting factor functions.

By deleting a disordered linker region, they were able to visualize the complete structure of prothrombin.

This deleted version was activated to thrombin much faster than the intact version of prothrombin.

And results suggested that cofactor Va enhances the activation of prothrombin by altering the architecture of the linker.

Enrico Di Cera, MD, of Saint Louis University in Missouri, and his colleagues reported these findings in PNAS.

Last year, Dr Di Cera’s team published the first structure of prothrombin. This structure lacked a domain responsible for interaction with membranes, and certain other sections were not detected by X-ray analysis.

Though the researchers were able to crystallize the protein, there were disordered regions in the structure they could not see.

Within prothrombin, there are 2 kringle domains connected by a linker region that intrigued the researchers because of its intrinsic disorder.

“We deleted this linker, and crystals grew in a few days instead of months, revealing, for the first time, the full architecture of prothrombin,” Dr Di Cera said.

The crystal structure revealed a contorted conformation where the domains are not vertically stacked, kringle-1 comes close to the protease domain, and the Gla-domain contacts kringle-2.

The researchers also found the deleted version of prothrombin is activated to thrombin much faster than intact prothrombin.

Specifically, deletion of the linker reduced the enhancement of thrombin generation by cofactor Va from the more than 3000-fold observed with wild-type prothrombin to 60-fold. So it appears that deletion of the linker mimics the effect of cofactor Va on prothrombin activation.

“It took us almost 2 years to discover that the disordered linker was the key,” Dr Di Cera said. “Finally, prothrombin revealed its secrets, and, with that, the molecular mechanism of a key reaction of blood clotting finally becomes amenable to rational drug design for therapeutic intervention.”

Prescriptions

Credit: CDC

A new assay can be used to determine if a product actually contains the antimalarial drug artesunate, according to a paper published in the journal Talanta.

The testing system looks about as simple, and is almost as cheap, as a sheet of paper.

But it’s actually a colorimetric assay consumers could use to tell whether or not they are getting the medication they paid for—artesunate.

The assay also verifies that an adequate level of the drug is present.

“There are laboratory methods to analyze medications such as this, but they often are not available or widely used in the developing world, where malaria kills thousands of people every year,” said study author Vincent Remcho, PhD, of Oregon State University in Corvallis.

“What we need are inexpensive, accurate assays that can detect adulterated pharmaceuticals in the field, simple enough that anyone can use them. Our technology should provide that.”

The technology is an application of microfluidics in which a film is impressed onto paper that can then detect the presence and level of artesunate in a product.

A single pill can be crushed and dissolved in water. When a drop of the solution is placed on the paper, it turns yellow if the drug is present. The intensity of the color indicates the level of the drug, which can be compared to a simple color chart.

The system can also include another step. The researchers created an iPhone app that could be used to measure the color and tell with an even higher degree of accuracy both the presence and level of artesunate.

“This is conceptually similar to what we do with integrated circuit chips in computers, but we’re pushing fluids around instead of electrons, to reveal chemical information that’s useful to us,” Dr Remcho said. “Chemical communication is how Mother Nature does it, and the long-term applications of this approach really are mind-blowing.”

Aside from ensuring patients receive the appropriate treatment, the assay could help government officials combat the larger problem of drug counterfeiting. Researchers have found that, in some places in the developing world, more than 80% of outlets are selling counterfeit pharmaceuticals.

Dr Remcho and his colleagues also believe their technique could be expanded for a wide range of other medical conditions, pharmaceutical and diagnostic tests, pathogen detection, environmental analysis, and other uses.

Prescriptions

Credit: CDC

A new assay can be used to determine if a product actually contains the antimalarial drug artesunate, according to a paper published in the journal Talanta.

The testing system looks about as simple, and is almost as cheap, as a sheet of paper.

But it’s actually a colorimetric assay consumers could use to tell whether or not they are getting the medication they paid for—artesunate.

The assay also verifies that an adequate level of the drug is present.

“There are laboratory methods to analyze medications such as this, but they often are not available or widely used in the developing world, where malaria kills thousands of people every year,” said study author Vincent Remcho, PhD, of Oregon State University in Corvallis.

“What we need are inexpensive, accurate assays that can detect adulterated pharmaceuticals in the field, simple enough that anyone can use them. Our technology should provide that.”

The technology is an application of microfluidics in which a film is impressed onto paper that can then detect the presence and level of artesunate in a product.

A single pill can be crushed and dissolved in water. When a drop of the solution is placed on the paper, it turns yellow if the drug is present. The intensity of the color indicates the level of the drug, which can be compared to a simple color chart.

The system can also include another step. The researchers created an iPhone app that could be used to measure the color and tell with an even higher degree of accuracy both the presence and level of artesunate.

“This is conceptually similar to what we do with integrated circuit chips in computers, but we’re pushing fluids around instead of electrons, to reveal chemical information that’s useful to us,” Dr Remcho said. “Chemical communication is how Mother Nature does it, and the long-term applications of this approach really are mind-blowing.”

Aside from ensuring patients receive the appropriate treatment, the assay could help government officials combat the larger problem of drug counterfeiting. Researchers have found that, in some places in the developing world, more than 80% of outlets are selling counterfeit pharmaceuticals.

Dr Remcho and his colleagues also believe their technique could be expanded for a wide range of other medical conditions, pharmaceutical and diagnostic tests, pathogen detection, environmental analysis, and other uses.

Prescriptions

Credit: CDC

A new assay can be used to determine if a product actually contains the antimalarial drug artesunate, according to a paper published in the journal Talanta.

The testing system looks about as simple, and is almost as cheap, as a sheet of paper.

But it’s actually a colorimetric assay consumers could use to tell whether or not they are getting the medication they paid for—artesunate.

The assay also verifies that an adequate level of the drug is present.

“There are laboratory methods to analyze medications such as this, but they often are not available or widely used in the developing world, where malaria kills thousands of people every year,” said study author Vincent Remcho, PhD, of Oregon State University in Corvallis.

“What we need are inexpensive, accurate assays that can detect adulterated pharmaceuticals in the field, simple enough that anyone can use them. Our technology should provide that.”

The technology is an application of microfluidics in which a film is impressed onto paper that can then detect the presence and level of artesunate in a product.

A single pill can be crushed and dissolved in water. When a drop of the solution is placed on the paper, it turns yellow if the drug is present. The intensity of the color indicates the level of the drug, which can be compared to a simple color chart.

The system can also include another step. The researchers created an iPhone app that could be used to measure the color and tell with an even higher degree of accuracy both the presence and level of artesunate.

“This is conceptually similar to what we do with integrated circuit chips in computers, but we’re pushing fluids around instead of electrons, to reveal chemical information that’s useful to us,” Dr Remcho said. “Chemical communication is how Mother Nature does it, and the long-term applications of this approach really are mind-blowing.”

Aside from ensuring patients receive the appropriate treatment, the assay could help government officials combat the larger problem of drug counterfeiting. Researchers have found that, in some places in the developing world, more than 80% of outlets are selling counterfeit pharmaceuticals.

Dr Remcho and his colleagues also believe their technique could be expanded for a wide range of other medical conditions, pharmaceutical and diagnostic tests, pathogen detection, environmental analysis, and other uses.

Drug release in a cancer cell

Credit: PNAS

A new model suggests we should be targeting cancers’ weaknesses instead of their strengths.

An article in BioEssays proposes that cancers form when recently evolved genes are damaged, and cancer cells have to revert to using older, inappropriate genetic pathways.

So we should create treatments that take advantage of capabilities humans have developed more recently—such as the adaptive immune system—instead of trying to target older capabilities—such as the innate immune system and cell proliferation.

“The rapid proliferation of cancer cells is an ancient, default capability that became regulated during the evolution of multicellularity about a billion years ago,” said study author Charley Lineweaver, PhD, of The Australian National University in Canberra.

“Our model suggests that cancer progression is the accumulation of damage to the more recently acquired genes. Without the regulation of these recent genes, cell physiology reverts to earlier programs, such as unregulated cell proliferation.”

To develop their model, Dr Lineweaver and his colleagues turned to knowledge uncovered by genome sequencing in a range of our distant relatives, including fish, coral, and sponges.

This knowledge has allowed scientists to establish the order in which genes evolved and is the basis of the new therapeutic implications of the model, Dr Lineweaver said.

He noted that the standard model of cancer development suggests that selection produces the acquired capabilities of cancer—such as sustained proliferative signaling and evading apoptosis—and they evolve during the lifetime of the patient.

But Dr Lineweaver’s model suggests the capabilities of cancer are acquired atavisms. They are activated during early embryogenesis and wound healing and reactivated inappropriately during carcinogenesis.

The most recent capabilities—mammalian and vertebrate capabilities—are the least entrenched in cancer. So they should be targeted with therapy.

The older capabilities—last eukaryotic common ancestor (LECA) capabilities, stem eukaryote capabilities, and the earliest evolved capabilities—are maintained in cancer and are therefore difficult to target.

For example, some human ATP binding cassette (ABC) transporters are ancient, and some are quite recent. Dr Lineweaver and his colleagues found that older ABC proteins were more likely to be active in cancer.

So the researchers believe we should create treatments that can be expelled by the newer ABC transporters. That way, normal cells will expel the treatment, but cancer cells will not.

Another potential treatment avenue, according to Dr Lineweaver, is targeting the adaptive immune system.

“The adaptive immune system that humans have has evolved relatively recently, and it seems cancer cells do not have the ability to talk to and be protected by it,” he noted.

“The new therapeutic strategies we are proposing target these weaknesses. These strategies are very different from current therapies, which attack cancer’s strength—its ability to proliferate rapidly.”

Drug release in a cancer cell

Credit: PNAS

A new model suggests we should be targeting cancers’ weaknesses instead of their strengths.

An article in BioEssays proposes that cancers form when recently evolved genes are damaged, and cancer cells have to revert to using older, inappropriate genetic pathways.

So we should create treatments that take advantage of capabilities humans have developed more recently—such as the adaptive immune system—instead of trying to target older capabilities—such as the innate immune system and cell proliferation.

“The rapid proliferation of cancer cells is an ancient, default capability that became regulated during the evolution of multicellularity about a billion years ago,” said study author Charley Lineweaver, PhD, of The Australian National University in Canberra.

“Our model suggests that cancer progression is the accumulation of damage to the more recently acquired genes. Without the regulation of these recent genes, cell physiology reverts to earlier programs, such as unregulated cell proliferation.”

To develop their model, Dr Lineweaver and his colleagues turned to knowledge uncovered by genome sequencing in a range of our distant relatives, including fish, coral, and sponges.

This knowledge has allowed scientists to establish the order in which genes evolved and is the basis of the new therapeutic implications of the model, Dr Lineweaver said.

He noted that the standard model of cancer development suggests that selection produces the acquired capabilities of cancer—such as sustained proliferative signaling and evading apoptosis—and they evolve during the lifetime of the patient.

But Dr Lineweaver’s model suggests the capabilities of cancer are acquired atavisms. They are activated during early embryogenesis and wound healing and reactivated inappropriately during carcinogenesis.

The most recent capabilities—mammalian and vertebrate capabilities—are the least entrenched in cancer. So they should be targeted with therapy.

The older capabilities—last eukaryotic common ancestor (LECA) capabilities, stem eukaryote capabilities, and the earliest evolved capabilities—are maintained in cancer and are therefore difficult to target.

For example, some human ATP binding cassette (ABC) transporters are ancient, and some are quite recent. Dr Lineweaver and his colleagues found that older ABC proteins were more likely to be active in cancer.

So the researchers believe we should create treatments that can be expelled by the newer ABC transporters. That way, normal cells will expel the treatment, but cancer cells will not.

Another potential treatment avenue, according to Dr Lineweaver, is targeting the adaptive immune system.

“The adaptive immune system that humans have has evolved relatively recently, and it seems cancer cells do not have the ability to talk to and be protected by it,” he noted.

“The new therapeutic strategies we are proposing target these weaknesses. These strategies are very different from current therapies, which attack cancer’s strength—its ability to proliferate rapidly.”

Drug release in a cancer cell

Credit: PNAS

A new model suggests we should be targeting cancers’ weaknesses instead of their strengths.

An article in BioEssays proposes that cancers form when recently evolved genes are damaged, and cancer cells have to revert to using older, inappropriate genetic pathways.

So we should create treatments that take advantage of capabilities humans have developed more recently—such as the adaptive immune system—instead of trying to target older capabilities—such as the innate immune system and cell proliferation.

“The rapid proliferation of cancer cells is an ancient, default capability that became regulated during the evolution of multicellularity about a billion years ago,” said study author Charley Lineweaver, PhD, of The Australian National University in Canberra.

“Our model suggests that cancer progression is the accumulation of damage to the more recently acquired genes. Without the regulation of these recent genes, cell physiology reverts to earlier programs, such as unregulated cell proliferation.”

To develop their model, Dr Lineweaver and his colleagues turned to knowledge uncovered by genome sequencing in a range of our distant relatives, including fish, coral, and sponges.

This knowledge has allowed scientists to establish the order in which genes evolved and is the basis of the new therapeutic implications of the model, Dr Lineweaver said.

He noted that the standard model of cancer development suggests that selection produces the acquired capabilities of cancer—such as sustained proliferative signaling and evading apoptosis—and they evolve during the lifetime of the patient.

But Dr Lineweaver’s model suggests the capabilities of cancer are acquired atavisms. They are activated during early embryogenesis and wound healing and reactivated inappropriately during carcinogenesis.

The most recent capabilities—mammalian and vertebrate capabilities—are the least entrenched in cancer. So they should be targeted with therapy.

The older capabilities—last eukaryotic common ancestor (LECA) capabilities, stem eukaryote capabilities, and the earliest evolved capabilities—are maintained in cancer and are therefore difficult to target.

For example, some human ATP binding cassette (ABC) transporters are ancient, and some are quite recent. Dr Lineweaver and his colleagues found that older ABC proteins were more likely to be active in cancer.

So the researchers believe we should create treatments that can be expelled by the newer ABC transporters. That way, normal cells will expel the treatment, but cancer cells will not.

Another potential treatment avenue, according to Dr Lineweaver, is targeting the adaptive immune system.

“The adaptive immune system that humans have has evolved relatively recently, and it seems cancer cells do not have the ability to talk to and be protected by it,” he noted.

“The new therapeutic strategies we are proposing target these weaknesses. These strategies are very different from current therapies, which attack cancer’s strength—its ability to proliferate rapidly.”

Nurses administering

chemo to a cancer patient

Credit: Rhoda Baer

The nursing workforce in the US has grown substantially in recent years, and this is only partly due to an increase in nursing graduates, according to a new study.

The research revealed that registered nurses (RNs) are putting off retirement for longer than they have in the past.

From 1991 to 2012, 24% of RNs who were working at age 50 remained working as late as age 69. From 1969 to 1990, however, only 9% of nurses were still working at age 69.

These findings appear in Health Affairs.

“We estimate this trend accounts for about a quarter of an unexpected surge in the supply of registered nurses that the nation has experienced in recent years,” said study author David Auerbach, PhD, of RAND Corporation in Boston. “This may provide advantages to parts of the US healthcare system.”

The researchers noted that the RN workforce has surpassed forecasts from a decade ago, growing to 2.7 million in 2012 instead of peaking at 2.2 million as predicted. While much of the difference is the result of a surge in new nursing graduates, the size of the workforce is particularly sensitive to changes in retirement age.

Dr Auerbach and his colleagues uncovered the trend of delaying retirement by analyzing data from the Current Population Survey and the American Community Survey.

The team included all respondents aged 23 to 69 who reported being employed as an RN during the week of the relevant survey from 1969 to 2012. There were 70,724 RNs who responded to the Current Population Survey and 307,187 who responded to the American Community Survey.

The researchers found that, from 1969 to 1990, for a given number of RNs working at age 50, 47% were still working at age 62. From 1991 to 2012, 74% of RNs were working at age 62.

The trend of RNs delaying retirement, which largely predates the recent recession, extended nursing careers by 2.5 years after age 50 and increased the 2012 RN workforce by 136,000 people, according to the researchers.

The team said the reasons older RNs are working longer is unclear, but it is likely part of an overall trend that has seen more Americans—particularly women—stay in the workforce longer because of lengthening life expectancy and the satisfaction they derive from employment.

Nurses administering

chemo to a cancer patient

Credit: Rhoda Baer

The nursing workforce in the US has grown substantially in recent years, and this is only partly due to an increase in nursing graduates, according to a new study.

The research revealed that registered nurses (RNs) are putting off retirement for longer than they have in the past.

From 1991 to 2012, 24% of RNs who were working at age 50 remained working as late as age 69. From 1969 to 1990, however, only 9% of nurses were still working at age 69.

These findings appear in Health Affairs.

“We estimate this trend accounts for about a quarter of an unexpected surge in the supply of registered nurses that the nation has experienced in recent years,” said study author David Auerbach, PhD, of RAND Corporation in Boston. “This may provide advantages to parts of the US healthcare system.”

The researchers noted that the RN workforce has surpassed forecasts from a decade ago, growing to 2.7 million in 2012 instead of peaking at 2.2 million as predicted. While much of the difference is the result of a surge in new nursing graduates, the size of the workforce is particularly sensitive to changes in retirement age.

Dr Auerbach and his colleagues uncovered the trend of delaying retirement by analyzing data from the Current Population Survey and the American Community Survey.

The team included all respondents aged 23 to 69 who reported being employed as an RN during the week of the relevant survey from 1969 to 2012. There were 70,724 RNs who responded to the Current Population Survey and 307,187 who responded to the American Community Survey.

The researchers found that, from 1969 to 1990, for a given number of RNs working at age 50, 47% were still working at age 62. From 1991 to 2012, 74% of RNs were working at age 62.

The trend of RNs delaying retirement, which largely predates the recent recession, extended nursing careers by 2.5 years after age 50 and increased the 2012 RN workforce by 136,000 people, according to the researchers.

The team said the reasons older RNs are working longer is unclear, but it is likely part of an overall trend that has seen more Americans—particularly women—stay in the workforce longer because of lengthening life expectancy and the satisfaction they derive from employment.

Nurses administering

chemo to a cancer patient

Credit: Rhoda Baer

The nursing workforce in the US has grown substantially in recent years, and this is only partly due to an increase in nursing graduates, according to a new study.

The research revealed that registered nurses (RNs) are putting off retirement for longer than they have in the past.

From 1991 to 2012, 24% of RNs who were working at age 50 remained working as late as age 69. From 1969 to 1990, however, only 9% of nurses were still working at age 69.

These findings appear in Health Affairs.

“We estimate this trend accounts for about a quarter of an unexpected surge in the supply of registered nurses that the nation has experienced in recent years,” said study author David Auerbach, PhD, of RAND Corporation in Boston. “This may provide advantages to parts of the US healthcare system.”

The researchers noted that the RN workforce has surpassed forecasts from a decade ago, growing to 2.7 million in 2012 instead of peaking at 2.2 million as predicted. While much of the difference is the result of a surge in new nursing graduates, the size of the workforce is particularly sensitive to changes in retirement age.

Dr Auerbach and his colleagues uncovered the trend of delaying retirement by analyzing data from the Current Population Survey and the American Community Survey.

The team included all respondents aged 23 to 69 who reported being employed as an RN during the week of the relevant survey from 1969 to 2012. There were 70,724 RNs who responded to the Current Population Survey and 307,187 who responded to the American Community Survey.

The researchers found that, from 1969 to 1990, for a given number of RNs working at age 50, 47% were still working at age 62. From 1991 to 2012, 74% of RNs were working at age 62.

The trend of RNs delaying retirement, which largely predates the recent recession, extended nursing careers by 2.5 years after age 50 and increased the 2012 RN workforce by 136,000 people, according to the researchers.

The team said the reasons older RNs are working longer is unclear, but it is likely part of an overall trend that has seen more Americans—particularly women—stay in the workforce longer because of lengthening life expectancy and the satisfaction they derive from employment.

The Society of Hospital Medicine (SHM) is supporting a Congressional push to tweak which admissions factors are taken into consideration in the federal Hospital Readmissions Reduction Program.

Hospitalist and SHM President Burke Kealey, MD, SFHM, says that the Establishing Beneficiary Equity in the Hospital Readmission Program Act (H.R. 4188) would help "level the playing field."

Sponsored by U.S. Representative James Renacci (R-Ohio), the proposal seeks to "exclude from the program admissions related to transplants, end-stage renal disease, burns, trauma, psychosis, or substance abuse." It also would require the U.S. Department of Health & Human Services (HHS) "in applying requirements for the excess readmission ratio to provide for a risk adjustment" that would take into account the percentage of inpatients eligible for both Medicare and Medicaid to avoid unfairly penalizing hospitals that treat the most vulnerable populations.

"We feel that some hospitals may be being unfairly handled in this program," Dr. Kealey says. "Those are the hospitals that are having to deal with more complex populations or lower-SES [socioeconomic status] populations. Those are the hospitalists that actually need the most resources to help prevent readmissions, and they end up losing in this whole equation."

In a letter to Rep. Renacci outlining SHM's support for the bill, Dr. Kealey notes that the current readmissions reduction program "needs fine-tuning to better account for preventable readmission."

Dr. Kealey also says he believes attempts by HHS to address readmissions are well-intentioned. However, as the program is implemented, he wants the government to be flexible in dealing with hospitals, particularly those dealing with complex populations or large groups of low-SES patients.

"We feel [these are] valuable programs, and in general, they help move the country in the right direction," Dr. Kealey says. "But they certainly need to be open and available to be modified and changed to fit conditions better."

SHM's program to reduce hospital readmissions, Project BOOST, is accepting applications to its 2014 cohort through August 30. TH

Visit our website for more information on hospital readmissions penalties.

The Society of Hospital Medicine (SHM) is supporting a Congressional push to tweak which admissions factors are taken into consideration in the federal Hospital Readmissions Reduction Program.

Hospitalist and SHM President Burke Kealey, MD, SFHM, says that the Establishing Beneficiary Equity in the Hospital Readmission Program Act (H.R. 4188) would help "level the playing field."

Sponsored by U.S. Representative James Renacci (R-Ohio), the proposal seeks to "exclude from the program admissions related to transplants, end-stage renal disease, burns, trauma, psychosis, or substance abuse." It also would require the U.S. Department of Health & Human Services (HHS) "in applying requirements for the excess readmission ratio to provide for a risk adjustment" that would take into account the percentage of inpatients eligible for both Medicare and Medicaid to avoid unfairly penalizing hospitals that treat the most vulnerable populations.

"We feel that some hospitals may be being unfairly handled in this program," Dr. Kealey says. "Those are the hospitals that are having to deal with more complex populations or lower-SES [socioeconomic status] populations. Those are the hospitalists that actually need the most resources to help prevent readmissions, and they end up losing in this whole equation."

In a letter to Rep. Renacci outlining SHM's support for the bill, Dr. Kealey notes that the current readmissions reduction program "needs fine-tuning to better account for preventable readmission."

Dr. Kealey also says he believes attempts by HHS to address readmissions are well-intentioned. However, as the program is implemented, he wants the government to be flexible in dealing with hospitals, particularly those dealing with complex populations or large groups of low-SES patients.

"We feel [these are] valuable programs, and in general, they help move the country in the right direction," Dr. Kealey says. "But they certainly need to be open and available to be modified and changed to fit conditions better."

SHM's program to reduce hospital readmissions, Project BOOST, is accepting applications to its 2014 cohort through August 30. TH

Visit our website for more information on hospital readmissions penalties.

The Society of Hospital Medicine (SHM) is supporting a Congressional push to tweak which admissions factors are taken into consideration in the federal Hospital Readmissions Reduction Program.

Hospitalist and SHM President Burke Kealey, MD, SFHM, says that the Establishing Beneficiary Equity in the Hospital Readmission Program Act (H.R. 4188) would help "level the playing field."

Sponsored by U.S. Representative James Renacci (R-Ohio), the proposal seeks to "exclude from the program admissions related to transplants, end-stage renal disease, burns, trauma, psychosis, or substance abuse." It also would require the U.S. Department of Health & Human Services (HHS) "in applying requirements for the excess readmission ratio to provide for a risk adjustment" that would take into account the percentage of inpatients eligible for both Medicare and Medicaid to avoid unfairly penalizing hospitals that treat the most vulnerable populations.

"We feel that some hospitals may be being unfairly handled in this program," Dr. Kealey says. "Those are the hospitals that are having to deal with more complex populations or lower-SES [socioeconomic status] populations. Those are the hospitalists that actually need the most resources to help prevent readmissions, and they end up losing in this whole equation."

In a letter to Rep. Renacci outlining SHM's support for the bill, Dr. Kealey notes that the current readmissions reduction program "needs fine-tuning to better account for preventable readmission."

Dr. Kealey also says he believes attempts by HHS to address readmissions are well-intentioned. However, as the program is implemented, he wants the government to be flexible in dealing with hospitals, particularly those dealing with complex populations or large groups of low-SES patients.

"We feel [these are] valuable programs, and in general, they help move the country in the right direction," Dr. Kealey says. "But they certainly need to be open and available to be modified and changed to fit conditions better."

SHM's program to reduce hospital readmissions, Project BOOST, is accepting applications to its 2014 cohort through August 30. TH

Visit our website for more information on hospital readmissions penalties.

A new report that shows efforts to prevent central-line-associated bloodstream infections (CLABSIs) saved the government at least $640 million over nearly 20 years is an example of how effective prevention campaigns can be, a veteran hospitalist says.

"The major idea of this report was to show us that complications like bloodstream infections are preventable," says Ketino Kobaidze MD, PhD, FHM, assistant professor of medicine and associate site director of the division of hospital medicine at the Emory University School of Medicine in Atlanta. "When you prevent these things, you can locate other things. That's what the major message is to any kind of healthcare provider."

Published in the June issue of Health Affairs, the report examines the results of CDC programs from 1990 to 2008 to prevent CLABSIs in critical care units and how prevention helped the Centers for Medicaid & Medicare Services (CMS) reduce the amount of reimbursement paid to hospitals for treating such infections.

The authors reported that from 1990 to 2008, between 40,556 and 75,067 CLABSIs were avoided in Medicare and Medicaid patients treated in critical care units. This resulted in:

• Net savings ranging from $640 million to $1.8 billion;

• Net savings per case ranging from $15,780 to $24,391; and

• Per dollar rate of return on CDC investments between $3.88 and $23.85.

"Now, you're basically expected for it to not happen at all," says Dr. Kobaidze, referring to a rule implemented by CMS in 2008 that ended reimbursements to hospitals for treating CLABSIs that weren't present upon admission.

With that rule, CMS included 10 categories of hospital-acquired conditions (HACs) for the payment provision rule, including stage III and IV pressure ulcers and falls that occur while the patient is in the hospital. The rule was updated in 2013 to include HACs related to surgical site infection with cardiac implantable electronic devices and iatrogenic pneumothorax with venous catheterization. TH 

Visit our website for more information on bloodstream infection prevention.

A new report that shows efforts to prevent central-line-associated bloodstream infections (CLABSIs) saved the government at least $640 million over nearly 20 years is an example of how effective prevention campaigns can be, a veteran hospitalist says.

"The major idea of this report was to show us that complications like bloodstream infections are preventable," says Ketino Kobaidze MD, PhD, FHM, assistant professor of medicine and associate site director of the division of hospital medicine at the Emory University School of Medicine in Atlanta. "When you prevent these things, you can locate other things. That's what the major message is to any kind of healthcare provider."

Published in the June issue of Health Affairs, the report examines the results of CDC programs from 1990 to 2008 to prevent CLABSIs in critical care units and how prevention helped the Centers for Medicaid & Medicare Services (CMS) reduce the amount of reimbursement paid to hospitals for treating such infections.

The authors reported that from 1990 to 2008, between 40,556 and 75,067 CLABSIs were avoided in Medicare and Medicaid patients treated in critical care units. This resulted in:

• Net savings ranging from $640 million to $1.8 billion;

• Net savings per case ranging from $15,780 to $24,391; and

• Per dollar rate of return on CDC investments between $3.88 and $23.85.

"Now, you're basically expected for it to not happen at all," says Dr. Kobaidze, referring to a rule implemented by CMS in 2008 that ended reimbursements to hospitals for treating CLABSIs that weren't present upon admission.

With that rule, CMS included 10 categories of hospital-acquired conditions (HACs) for the payment provision rule, including stage III and IV pressure ulcers and falls that occur while the patient is in the hospital. The rule was updated in 2013 to include HACs related to surgical site infection with cardiac implantable electronic devices and iatrogenic pneumothorax with venous catheterization. TH 

Visit our website for more information on bloodstream infection prevention.

A new report that shows efforts to prevent central-line-associated bloodstream infections (CLABSIs) saved the government at least $640 million over nearly 20 years is an example of how effective prevention campaigns can be, a veteran hospitalist says.

"The major idea of this report was to show us that complications like bloodstream infections are preventable," says Ketino Kobaidze MD, PhD, FHM, assistant professor of medicine and associate site director of the division of hospital medicine at the Emory University School of Medicine in Atlanta. "When you prevent these things, you can locate other things. That's what the major message is to any kind of healthcare provider."

Published in the June issue of Health Affairs, the report examines the results of CDC programs from 1990 to 2008 to prevent CLABSIs in critical care units and how prevention helped the Centers for Medicaid & Medicare Services (CMS) reduce the amount of reimbursement paid to hospitals for treating such infections.

The authors reported that from 1990 to 2008, between 40,556 and 75,067 CLABSIs were avoided in Medicare and Medicaid patients treated in critical care units. This resulted in:

• Net savings ranging from $640 million to $1.8 billion;

• Net savings per case ranging from $15,780 to $24,391; and

• Per dollar rate of return on CDC investments between $3.88 and $23.85.

"Now, you're basically expected for it to not happen at all," says Dr. Kobaidze, referring to a rule implemented by CMS in 2008 that ended reimbursements to hospitals for treating CLABSIs that weren't present upon admission.

With that rule, CMS included 10 categories of hospital-acquired conditions (HACs) for the payment provision rule, including stage III and IV pressure ulcers and falls that occur while the patient is in the hospital. The rule was updated in 2013 to include HACs related to surgical site infection with cardiac implantable electronic devices and iatrogenic pneumothorax with venous catheterization. TH 

Visit our website for more information on bloodstream infection prevention.

Summer months can be dreadful for patients with atopic dermatitis. The chlorine, heat, and humidity can lead to flares. Furthermore, noncompliance with skin care regimens because of changing summer routines, travel, and the use of hotel products can exacerbate even the calmest skin disease.

Share these tips with your patients to help them keep their atopic skin under control in the summer heat, and stop flares before they start.

• Rinse the skin well after swimming. Chlorine and saltwater can dry out the skin. Showers after swimming in chlorinated pools can help retain the skin’s natural oils.

• Avoid hot tubs. Cracks and fissures in atopic skin can become infected in hot tubs with Staphylococcus and Pseudomonas. Advise your atopic patients to avoid hot tubs, even if they claim the tubs have been cleaned.

• Bring your own products. Many soaps and shower gels available in hotels and resorts are extremely drying, and may contain ingredients that could irritate atopic skin.

• Don’t switch from thick creams to thin lotions just because it is summer. Remind your patients that a thin lotion does not provide the same occlusive and humectant properties as thicker creams, although they are not as easy to apply, and can feel thick and sticky on the skin with humidity.

• In case of an active eczema flare, topical steroids should be used and sun exposure should be avoided. Topical steroids are the most effective treatment when used correctly. However, any occurrence of hypopigmentation as a result of their use becomes more evident if the skin tans around the area of treatment.

• Wear physical sunscreen. This seems obvious, but most chemical blockers – even the formulations made for babies – can burn on cracked, inflamed skin. Instead, stress to your patients that they use a physical blocker made of pure titanium dioxide or zinc oxide on inflamed skin.

• Oral steroids and sun do not mix. Oral steroids can be potent photosensitizers. If they are needed, UV exposure should be avoided.

Dr. Talakoub and Dr. Wesley are co-contributors to a monthly Aesthetic Dermatology column in Skin & Allergy News. Dr. Talakoub is in private practice at McLean (Va.) Dermatology Center. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub.

Summer months can be dreadful for patients with atopic dermatitis. The chlorine, heat, and humidity can lead to flares. Furthermore, noncompliance with skin care regimens because of changing summer routines, travel, and the use of hotel products can exacerbate even the calmest skin disease.

Share these tips with your patients to help them keep their atopic skin under control in the summer heat, and stop flares before they start.

• Rinse the skin well after swimming. Chlorine and saltwater can dry out the skin. Showers after swimming in chlorinated pools can help retain the skin’s natural oils.

• Avoid hot tubs. Cracks and fissures in atopic skin can become infected in hot tubs with Staphylococcus and Pseudomonas. Advise your atopic patients to avoid hot tubs, even if they claim the tubs have been cleaned.

• Bring your own products. Many soaps and shower gels available in hotels and resorts are extremely drying, and may contain ingredients that could irritate atopic skin.

• Don’t switch from thick creams to thin lotions just because it is summer. Remind your patients that a thin lotion does not provide the same occlusive and humectant properties as thicker creams, although they are not as easy to apply, and can feel thick and sticky on the skin with humidity.

• In case of an active eczema flare, topical steroids should be used and sun exposure should be avoided. Topical steroids are the most effective treatment when used correctly. However, any occurrence of hypopigmentation as a result of their use becomes more evident if the skin tans around the area of treatment.

• Wear physical sunscreen. This seems obvious, but most chemical blockers – even the formulations made for babies – can burn on cracked, inflamed skin. Instead, stress to your patients that they use a physical blocker made of pure titanium dioxide or zinc oxide on inflamed skin.

• Oral steroids and sun do not mix. Oral steroids can be potent photosensitizers. If they are needed, UV exposure should be avoided.

Dr. Talakoub and Dr. Wesley are co-contributors to a monthly Aesthetic Dermatology column in Skin & Allergy News. Dr. Talakoub is in private practice at McLean (Va.) Dermatology Center. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub.

Summer months can be dreadful for patients with atopic dermatitis. The chlorine, heat, and humidity can lead to flares. Furthermore, noncompliance with skin care regimens because of changing summer routines, travel, and the use of hotel products can exacerbate even the calmest skin disease.

Share these tips with your patients to help them keep their atopic skin under control in the summer heat, and stop flares before they start.

• Rinse the skin well after swimming. Chlorine and saltwater can dry out the skin. Showers after swimming in chlorinated pools can help retain the skin’s natural oils.

• Avoid hot tubs. Cracks and fissures in atopic skin can become infected in hot tubs with Staphylococcus and Pseudomonas. Advise your atopic patients to avoid hot tubs, even if they claim the tubs have been cleaned.

• Bring your own products. Many soaps and shower gels available in hotels and resorts are extremely drying, and may contain ingredients that could irritate atopic skin.

• Don’t switch from thick creams to thin lotions just because it is summer. Remind your patients that a thin lotion does not provide the same occlusive and humectant properties as thicker creams, although they are not as easy to apply, and can feel thick and sticky on the skin with humidity.

• In case of an active eczema flare, topical steroids should be used and sun exposure should be avoided. Topical steroids are the most effective treatment when used correctly. However, any occurrence of hypopigmentation as a result of their use becomes more evident if the skin tans around the area of treatment.

• Wear physical sunscreen. This seems obvious, but most chemical blockers – even the formulations made for babies – can burn on cracked, inflamed skin. Instead, stress to your patients that they use a physical blocker made of pure titanium dioxide or zinc oxide on inflamed skin.

• Oral steroids and sun do not mix. Oral steroids can be potent photosensitizers. If they are needed, UV exposure should be avoided.

Dr. Talakoub and Dr. Wesley are co-contributors to a monthly Aesthetic Dermatology column in Skin & Allergy News. Dr. Talakoub is in private practice at McLean (Va.) Dermatology Center. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub.

Standardized research methods are needed to advance efforts toward reducing the costs and high burden of chronic low back pain, according to a multidisciplinary NIH Task Force report published online ahead of print May 30 in Spine.

The article introduces a set of proposed research standards to help in comparing the results of chronic low back pain studies. The Task Force co-chairs were Drs. Richard A. Deyo of Oregon Health and Science University, and Samuel F. Dworkin of the University of Washington in Seattle.

“Researchers use varied inclusion criteria, definitions, baseline assessments, and outcome measures, which impede comparisons and consensus,” the Task Force wrote.

To address this issue, the Task Force followed a structured approach to developing a set of standards for chronic low back pain research. Overriding issues included defining the problem of chronic low back pain, identifying the minimum dataset that should be collected in chronic low back pain research, assessing its impact on patients’ lives, and defining the best outcomes to evaluate treatment effectiveness.

The Task Force recommends that chronic low back pain be defined as back pain that lasts at least 3 months and causing pain on at least half of days over the past 6 months. Their recommended definition does not include ratings of pain severity.

In terms of impact, the Task Force recommends focusing on how back pain affects patients’ lives. They recommend a 9-item chronic low back pain “Impact Score” that incorporates ratings of pain intensity, interference with normal activities, and functional ability.

A key point for the Task Force was to define a minimum set of data to be gathered in any study of chronic low back pain. The recommended dataset included legal or workers compensation issues, previous treatments, and important contributing factors (eg, smoking, obesity, substance abuse, and widespread pain).

For outcomes, the Task Force concluded there was no set definition of what degree of improvement should be considered “clinically important.” Likewise, there was no consensus on the use of combined outcome measures, time frame for improvement, or adverse effects.

Finally, testing and developing new combined outcome measures was identified as an important aspect of future research, more specifically, other included approaches to predicting treatment results and studies to evaluate and improve the minimum dataset.

Overall, the recommendations stress the importance of getting a fuller picture of the patient’s medical history, even more so than the physical examination. On the other hand, the Task Force specified no standard laboratory or imaging tests, citing the lack of association with patient functioning or symptoms. Evaluations of depression, sleep disturbance, physical functioning, and catastrophic thinking were rated as important for all groups of patients with chronic low back pain.

The Task Force hopes that their recommended standards reflect the “complex, intertwined factors” affecting the development and clinical course of chronic low back pain. The NIH Pain Consortium has approved the recommendations and advises that investigators should incorporate them into NIH grant proposals. “As adopted by the NIH, these recommendations have the potential to standardize methods for identifying chronic low back pain research cases, describe research subjects, and compare published reports.” The Task Force added that recommendations should be subject to periodic validation and refinement in years ahead.

Standardized research methods are needed to advance efforts toward reducing the costs and high burden of chronic low back pain, according to a multidisciplinary NIH Task Force report published online ahead of print May 30 in Spine.

The article introduces a set of proposed research standards to help in comparing the results of chronic low back pain studies. The Task Force co-chairs were Drs. Richard A. Deyo of Oregon Health and Science University, and Samuel F. Dworkin of the University of Washington in Seattle.

“Researchers use varied inclusion criteria, definitions, baseline assessments, and outcome measures, which impede comparisons and consensus,” the Task Force wrote.

To address this issue, the Task Force followed a structured approach to developing a set of standards for chronic low back pain research. Overriding issues included defining the problem of chronic low back pain, identifying the minimum dataset that should be collected in chronic low back pain research, assessing its impact on patients’ lives, and defining the best outcomes to evaluate treatment effectiveness.

The Task Force recommends that chronic low back pain be defined as back pain that lasts at least 3 months and causing pain on at least half of days over the past 6 months. Their recommended definition does not include ratings of pain severity.

In terms of impact, the Task Force recommends focusing on how back pain affects patients’ lives. They recommend a 9-item chronic low back pain “Impact Score” that incorporates ratings of pain intensity, interference with normal activities, and functional ability.

A key point for the Task Force was to define a minimum set of data to be gathered in any study of chronic low back pain. The recommended dataset included legal or workers compensation issues, previous treatments, and important contributing factors (eg, smoking, obesity, substance abuse, and widespread pain).

For outcomes, the Task Force concluded there was no set definition of what degree of improvement should be considered “clinically important.” Likewise, there was no consensus on the use of combined outcome measures, time frame for improvement, or adverse effects.

Finally, testing and developing new combined outcome measures was identified as an important aspect of future research, more specifically, other included approaches to predicting treatment results and studies to evaluate and improve the minimum dataset.

Overall, the recommendations stress the importance of getting a fuller picture of the patient’s medical history, even more so than the physical examination. On the other hand, the Task Force specified no standard laboratory or imaging tests, citing the lack of association with patient functioning or symptoms. Evaluations of depression, sleep disturbance, physical functioning, and catastrophic thinking were rated as important for all groups of patients with chronic low back pain.

The Task Force hopes that their recommended standards reflect the “complex, intertwined factors” affecting the development and clinical course of chronic low back pain. The NIH Pain Consortium has approved the recommendations and advises that investigators should incorporate them into NIH grant proposals. “As adopted by the NIH, these recommendations have the potential to standardize methods for identifying chronic low back pain research cases, describe research subjects, and compare published reports.” The Task Force added that recommendations should be subject to periodic validation and refinement in years ahead.

Standardized research methods are needed to advance efforts toward reducing the costs and high burden of chronic low back pain, according to a multidisciplinary NIH Task Force report published online ahead of print May 30 in Spine.

The article introduces a set of proposed research standards to help in comparing the results of chronic low back pain studies. The Task Force co-chairs were Drs. Richard A. Deyo of Oregon Health and Science University, and Samuel F. Dworkin of the University of Washington in Seattle.

“Researchers use varied inclusion criteria, definitions, baseline assessments, and outcome measures, which impede comparisons and consensus,” the Task Force wrote.

To address this issue, the Task Force followed a structured approach to developing a set of standards for chronic low back pain research. Overriding issues included defining the problem of chronic low back pain, identifying the minimum dataset that should be collected in chronic low back pain research, assessing its impact on patients’ lives, and defining the best outcomes to evaluate treatment effectiveness.

The Task Force recommends that chronic low back pain be defined as back pain that lasts at least 3 months and causing pain on at least half of days over the past 6 months. Their recommended definition does not include ratings of pain severity.

In terms of impact, the Task Force recommends focusing on how back pain affects patients’ lives. They recommend a 9-item chronic low back pain “Impact Score” that incorporates ratings of pain intensity, interference with normal activities, and functional ability.

A key point for the Task Force was to define a minimum set of data to be gathered in any study of chronic low back pain. The recommended dataset included legal or workers compensation issues, previous treatments, and important contributing factors (eg, smoking, obesity, substance abuse, and widespread pain).

For outcomes, the Task Force concluded there was no set definition of what degree of improvement should be considered “clinically important.” Likewise, there was no consensus on the use of combined outcome measures, time frame for improvement, or adverse effects.

Finally, testing and developing new combined outcome measures was identified as an important aspect of future research, more specifically, other included approaches to predicting treatment results and studies to evaluate and improve the minimum dataset.

Overall, the recommendations stress the importance of getting a fuller picture of the patient’s medical history, even more so than the physical examination. On the other hand, the Task Force specified no standard laboratory or imaging tests, citing the lack of association with patient functioning or symptoms. Evaluations of depression, sleep disturbance, physical functioning, and catastrophic thinking were rated as important for all groups of patients with chronic low back pain.

The Task Force hopes that their recommended standards reflect the “complex, intertwined factors” affecting the development and clinical course of chronic low back pain. The NIH Pain Consortium has approved the recommendations and advises that investigators should incorporate them into NIH grant proposals. “As adopted by the NIH, these recommendations have the potential to standardize methods for identifying chronic low back pain research cases, describe research subjects, and compare published reports.” The Task Force added that recommendations should be subject to periodic validation and refinement in years ahead.