User login
How Far Does a Cough Travel?
A single cough can propel as many as 3,000 droplets into the air at a velocity of 6 to 28 m/s. The droplets travel in what classic fluid mechanics calls a “2-stage jet”: the starting jet (when the cough starts) and interrupted jet (when the cough stops). After the original cough ends, a “leading vortex” carries particles forward, but as the momentum slows, particles fall out of the jet according to researchers from the University of Hong Kong and Shenzhen Institute of Research and Innovation, both in China, who studied cough trajectories and the implications for disease transmission in buildings.
Once the penetration velocity drops below 0.01 m/s, environmental factors, such as ventilation and human body temperature, begin to influence the flow. Beyond 1 to 2 m, the exhaled air stream dissolves into the room airflow, and the pathogen-containing droplets or droplet nuclei are dispersed according to the global airflow in the room.
When a cough doesn’t last long, the researchers say, the velocity of fine particles decays significantly after the jet is interrupted. However, even short coughs have consequences: Pathogen-containing droplets as large as ≥ 5 µm in diameter can be directly deposited on the nasal or oral mucosa of a nearby “new host.”
But coughs differ in many ways, including how far and wide they send the droplets. The researchers conducted experiments to help determine spread by discharging dyed or particle-filled water into a water tank. They examined 3 different temporal exit velocity profiles: pulsation, sinusoidal, and real-cough.
The “most striking phenomenon,” the researchers say, is that the particle clouds of all 3 sizes of particles (small [8-14 µm], medium [57-68 µm], large [96-114 µm]) penetrated almost the same distance at different time steps. In other words, large particles can travel as far as fine particles.
The cough flow’s maximum penetration distance was 53.4 to 69.7 opening diameter. That is, for a mouth opening to a diameter of 2 cm, the large particles could penetrate 1 to 1.4 m in a “real cough case,” they note. Cough duration was important in determining the spread range of particles. Their maximum travel distance was “much enhanced” in a long starting jet, especially for small particles.
Source:
Wei J, Li Y. PLoS One. 2017;12(1): e0169235.
doi: 10.1371/journal.pone.0169235.
A single cough can propel as many as 3,000 droplets into the air at a velocity of 6 to 28 m/s. The droplets travel in what classic fluid mechanics calls a “2-stage jet”: the starting jet (when the cough starts) and interrupted jet (when the cough stops). After the original cough ends, a “leading vortex” carries particles forward, but as the momentum slows, particles fall out of the jet according to researchers from the University of Hong Kong and Shenzhen Institute of Research and Innovation, both in China, who studied cough trajectories and the implications for disease transmission in buildings.
Once the penetration velocity drops below 0.01 m/s, environmental factors, such as ventilation and human body temperature, begin to influence the flow. Beyond 1 to 2 m, the exhaled air stream dissolves into the room airflow, and the pathogen-containing droplets or droplet nuclei are dispersed according to the global airflow in the room.
When a cough doesn’t last long, the researchers say, the velocity of fine particles decays significantly after the jet is interrupted. However, even short coughs have consequences: Pathogen-containing droplets as large as ≥ 5 µm in diameter can be directly deposited on the nasal or oral mucosa of a nearby “new host.”
But coughs differ in many ways, including how far and wide they send the droplets. The researchers conducted experiments to help determine spread by discharging dyed or particle-filled water into a water tank. They examined 3 different temporal exit velocity profiles: pulsation, sinusoidal, and real-cough.
The “most striking phenomenon,” the researchers say, is that the particle clouds of all 3 sizes of particles (small [8-14 µm], medium [57-68 µm], large [96-114 µm]) penetrated almost the same distance at different time steps. In other words, large particles can travel as far as fine particles.
The cough flow’s maximum penetration distance was 53.4 to 69.7 opening diameter. That is, for a mouth opening to a diameter of 2 cm, the large particles could penetrate 1 to 1.4 m in a “real cough case,” they note. Cough duration was important in determining the spread range of particles. Their maximum travel distance was “much enhanced” in a long starting jet, especially for small particles.
Source:
Wei J, Li Y. PLoS One. 2017;12(1): e0169235.
doi: 10.1371/journal.pone.0169235.
A single cough can propel as many as 3,000 droplets into the air at a velocity of 6 to 28 m/s. The droplets travel in what classic fluid mechanics calls a “2-stage jet”: the starting jet (when the cough starts) and interrupted jet (when the cough stops). After the original cough ends, a “leading vortex” carries particles forward, but as the momentum slows, particles fall out of the jet according to researchers from the University of Hong Kong and Shenzhen Institute of Research and Innovation, both in China, who studied cough trajectories and the implications for disease transmission in buildings.
Once the penetration velocity drops below 0.01 m/s, environmental factors, such as ventilation and human body temperature, begin to influence the flow. Beyond 1 to 2 m, the exhaled air stream dissolves into the room airflow, and the pathogen-containing droplets or droplet nuclei are dispersed according to the global airflow in the room.
When a cough doesn’t last long, the researchers say, the velocity of fine particles decays significantly after the jet is interrupted. However, even short coughs have consequences: Pathogen-containing droplets as large as ≥ 5 µm in diameter can be directly deposited on the nasal or oral mucosa of a nearby “new host.”
But coughs differ in many ways, including how far and wide they send the droplets. The researchers conducted experiments to help determine spread by discharging dyed or particle-filled water into a water tank. They examined 3 different temporal exit velocity profiles: pulsation, sinusoidal, and real-cough.
The “most striking phenomenon,” the researchers say, is that the particle clouds of all 3 sizes of particles (small [8-14 µm], medium [57-68 µm], large [96-114 µm]) penetrated almost the same distance at different time steps. In other words, large particles can travel as far as fine particles.
The cough flow’s maximum penetration distance was 53.4 to 69.7 opening diameter. That is, for a mouth opening to a diameter of 2 cm, the large particles could penetrate 1 to 1.4 m in a “real cough case,” they note. Cough duration was important in determining the spread range of particles. Their maximum travel distance was “much enhanced” in a long starting jet, especially for small particles.
Source:
Wei J, Li Y. PLoS One. 2017;12(1): e0169235.
doi: 10.1371/journal.pone.0169235.
Racial disparity in cervical cancer deaths higher than previously reported
Corrected mortality rates for cervical cancer indicate a greater disparity between races, according to a report in Cancer.
Because previous estimates did not adjust for women who’d had a hysterectomy or who were otherwise not at risk for cervical cancer, investigators performed a “corrected” analysis using data from the Behavioral Risk Factor Surveillance System and from the National Center for Health Statistics and the National Cancer Institute’s Surveillance, Epidemiology, and End Results program, for the years 2002 through 2012.
The corrected mortality rate in black women is 10.1 per 100,000 women (95% confidence interval, 9.6-10.6) and 4.7 per 100,000 in white women (95% CI, 4.6-4.8), an overall difference of 44%. The previous, uncorrected mortality rate for black women was 5.7 per 100,000 (95% CI, 5.5-6.0) and 3.2 per 100,000 (95% CI, 3.1-3.2) for white women, reported Anne F. Rositch, PhD, of Johns Hopkins Bloomberg School of Public Health, Baltimore, and her colleagues.
The corrected findings do not indicate a rise in the overall cervical cancer death rate, but do show that the disparity between the races is higher, despite declines in such deaths among black women over the years: The corrected analysis over the decade showed that the rate of decrease in cervical cancer mortality rates was 0.8% in white women and 3.6% in black women (P less than .05), Dr. Rositch and her associates reported (Cancer 2017 Jan 23 doi: 10.1002/cncr.30507). Both corrected and uncorrected rates were significantly higher in older black women, especially those 85 years and older at 18.6 per 100,000 (95% CI, 15.4-21.7) before correction, and 37.2 per 100,000 (95% CI, 31.0-43.5) after correction.
“Future research should focus on overcoming the underlying factors that contribute to this mortality gap (differential follow-up for abnormal Papanicolaou test results and barriers to care after diagnosis) and on determining why black women and older women receive different and inadequate treatment for the same disease,” wrote Dr. Rositch and her colleagues.
The elimination of mortality differences across the two races in women aged 20-29 years and those 35-39 years was “encouraging ... because these age cohorts correspond to the patients who are most likely to have been vaccinated against the human papillomavirus (HPV) virus,” Heather J. Dalton, MD, and John Farley, MD, of Creighton University School of Medicine at St. Joseph’s Hospital and Medical Center, Phoenix, Ariz., wrote in an accompanying editorial (Cancer 2017 Jan. 23 doi: 10.1002/cncr.30501).
High-risk HPV infections and lack of adequate screening are the “only factors definitely associated with the incidence of cervical cancer,” they noted.
[email protected]
On Twitter @whitneymcknight
Corrected mortality rates for cervical cancer indicate a greater disparity between races, according to a report in Cancer.
Because previous estimates did not adjust for women who’d had a hysterectomy or who were otherwise not at risk for cervical cancer, investigators performed a “corrected” analysis using data from the Behavioral Risk Factor Surveillance System and from the National Center for Health Statistics and the National Cancer Institute’s Surveillance, Epidemiology, and End Results program, for the years 2002 through 2012.
The corrected mortality rate in black women is 10.1 per 100,000 women (95% confidence interval, 9.6-10.6) and 4.7 per 100,000 in white women (95% CI, 4.6-4.8), an overall difference of 44%. The previous, uncorrected mortality rate for black women was 5.7 per 100,000 (95% CI, 5.5-6.0) and 3.2 per 100,000 (95% CI, 3.1-3.2) for white women, reported Anne F. Rositch, PhD, of Johns Hopkins Bloomberg School of Public Health, Baltimore, and her colleagues.
The corrected findings do not indicate a rise in the overall cervical cancer death rate, but do show that the disparity between the races is higher, despite declines in such deaths among black women over the years: The corrected analysis over the decade showed that the rate of decrease in cervical cancer mortality rates was 0.8% in white women and 3.6% in black women (P less than .05), Dr. Rositch and her associates reported (Cancer 2017 Jan 23 doi: 10.1002/cncr.30507). Both corrected and uncorrected rates were significantly higher in older black women, especially those 85 years and older at 18.6 per 100,000 (95% CI, 15.4-21.7) before correction, and 37.2 per 100,000 (95% CI, 31.0-43.5) after correction.
“Future research should focus on overcoming the underlying factors that contribute to this mortality gap (differential follow-up for abnormal Papanicolaou test results and barriers to care after diagnosis) and on determining why black women and older women receive different and inadequate treatment for the same disease,” wrote Dr. Rositch and her colleagues.
The elimination of mortality differences across the two races in women aged 20-29 years and those 35-39 years was “encouraging ... because these age cohorts correspond to the patients who are most likely to have been vaccinated against the human papillomavirus (HPV) virus,” Heather J. Dalton, MD, and John Farley, MD, of Creighton University School of Medicine at St. Joseph’s Hospital and Medical Center, Phoenix, Ariz., wrote in an accompanying editorial (Cancer 2017 Jan. 23 doi: 10.1002/cncr.30501).
High-risk HPV infections and lack of adequate screening are the “only factors definitely associated with the incidence of cervical cancer,” they noted.
[email protected]
On Twitter @whitneymcknight
Corrected mortality rates for cervical cancer indicate a greater disparity between races, according to a report in Cancer.
Because previous estimates did not adjust for women who’d had a hysterectomy or who were otherwise not at risk for cervical cancer, investigators performed a “corrected” analysis using data from the Behavioral Risk Factor Surveillance System and from the National Center for Health Statistics and the National Cancer Institute’s Surveillance, Epidemiology, and End Results program, for the years 2002 through 2012.
The corrected mortality rate in black women is 10.1 per 100,000 women (95% confidence interval, 9.6-10.6) and 4.7 per 100,000 in white women (95% CI, 4.6-4.8), an overall difference of 44%. The previous, uncorrected mortality rate for black women was 5.7 per 100,000 (95% CI, 5.5-6.0) and 3.2 per 100,000 (95% CI, 3.1-3.2) for white women, reported Anne F. Rositch, PhD, of Johns Hopkins Bloomberg School of Public Health, Baltimore, and her colleagues.
The corrected findings do not indicate a rise in the overall cervical cancer death rate, but do show that the disparity between the races is higher, despite declines in such deaths among black women over the years: The corrected analysis over the decade showed that the rate of decrease in cervical cancer mortality rates was 0.8% in white women and 3.6% in black women (P less than .05), Dr. Rositch and her associates reported (Cancer 2017 Jan 23 doi: 10.1002/cncr.30507). Both corrected and uncorrected rates were significantly higher in older black women, especially those 85 years and older at 18.6 per 100,000 (95% CI, 15.4-21.7) before correction, and 37.2 per 100,000 (95% CI, 31.0-43.5) after correction.
“Future research should focus on overcoming the underlying factors that contribute to this mortality gap (differential follow-up for abnormal Papanicolaou test results and barriers to care after diagnosis) and on determining why black women and older women receive different and inadequate treatment for the same disease,” wrote Dr. Rositch and her colleagues.
The elimination of mortality differences across the two races in women aged 20-29 years and those 35-39 years was “encouraging ... because these age cohorts correspond to the patients who are most likely to have been vaccinated against the human papillomavirus (HPV) virus,” Heather J. Dalton, MD, and John Farley, MD, of Creighton University School of Medicine at St. Joseph’s Hospital and Medical Center, Phoenix, Ariz., wrote in an accompanying editorial (Cancer 2017 Jan. 23 doi: 10.1002/cncr.30501).
High-risk HPV infections and lack of adequate screening are the “only factors definitely associated with the incidence of cervical cancer,” they noted.
[email protected]
On Twitter @whitneymcknight
FROM CANCER
Key clinical point:
Major finding: Black women die from cervical cancer at a rate of 10.1 per 100,000 women; the rate for white women is 4.7 per 100,000, a 44% disparity.
Data source: National population database study from 2002 to 2012, adjusted for women not at risk for cervical cancer.
Disclosures: Dr. Patti E. Gravitt reported support from Hologic for research not related to this study.
Does Cannabidiol Affect Seizure Severity?
HOUSTON—Pharmaceutical-grade cannabidiol (CBD) may reduce seizure severity in adults and children with medically refractory epilepsy, according to an open-label trial described at the 70th Annual Meeting of the American Epilepsy Society. A controlled trial to confirm the drug’s effect may be warranted.
Jennifer L. DeWolfe, DO, Associate Professor of Neurology at the University of Alabama at Birmingham, and colleagues conducted a state-sponsored compassionate-use study of CBD in patients with refractory epilepsy. Patients received Epidiolex (a CBD formulation developed by GW Pharmaceuticals) in addition to their antiepileptic drugs. Eligible participants were adults and children with epilepsy confirmed by video EEG. Participants were required to have failed four antiepileptic drugs and had to have had four countable seizures per month. Exclusion criteria included psychogenic nonepileptic seizures confirmed by video EEG and prior CBD use.
Measuring Seizure Severity Over Time
The investigators measured participants’ seizure frequency and used the Chalfont Seizure Severity Scale to measure seizure severity. The scale solicits information about various factors, such as whether the patient lost awareness, dropped an object, fell, or was injured. The total possible score on the scale is 178, and the score increases with seizure severity. Changes of 10 or more points were considered significant. The researchers particularly focused on participants’ most frequent seizure type, which the Chalfont Seizure Severity Scale names the Type 1 seizure.
Dr. DeWolfe and colleagues measured patients’ total seizure severity scores and severity scores for Type 1 seizures at baseline, three months, and six months. To compare the scores, the researchers calculated time-weighted average values. They also examined percent change in seizures; seizure severity in adults, children, and all patients; and severity in responders and nonresponders. Responders were defined as patients who had a reduction in seizure frequency of more than 50%. The analysis included 81 participants, approximately half of whom were children. At the time of the analysis, 57 patients had undergone evaluation at three months, and 47 patients had undergone evaluation at six months. At baseline, the majority of patients had at least two types of seizures.
Seizure Severity Was Reduced
The total change in Chalfont Seizure Severity Scale score at three months was significant for adults, children, and all patients. The change remained significant at six months. The difference in the percent change in seizure severity between responders and nonresponders was significant at three months, but not at six months.
The change in severity of Type 1 seizures was significant for adults, children, and all patients at three months and at six months. The difference between responders and nonresponders in change in severity of Type 1 seizures was significant at three months, but not at six months.
At three months, the majority of adults, the majority of all patients, the majority of responders, and the majority of nonresponders had a reduction in seizure severity of at least 10 points. Approximately one-third of children had a reduction in seizure severity of at least 10 points at three months. At six months, the majority of adults, children, all patients, responders, and nonresponders had a decrease in seizure severity of at least 10 points. Patients’ average seizure severity tended to increase at six months, compared with the three-month point, but was still significantly lower than at baseline.
“One of the things I find most exciting is [that] … even if you were considered a nonresponder, you still had improvement in seizure severity,” said Dr. DeWolfe. She and her colleagues plan to examine the data by seizure type (eg, absence or tonic-clonic), to identify which factors measured by the Chalfont Seizure Severity Scale contributed most to the reductions in seizure severity, and to examine whether the effect of CBD on levels of antiepileptic drugs contributed to the change in seizure severity. The findings of this open-label trial suggest that CBD may improve seizure severity in people with medically refractory epilepsy. Randomized placebo-controlled studies are needed to further evaluate the effects of CBD on seizure severity.
—Erik Greb
Suggested Reading
Devinsky O, Marsh E, Friedman D, et al. Cannabidiol in patients with treatment-resistant epilepsy: an open-label interventional trial. Lancet Neurol. 2016;15(3):270-278.
Porter BE, Jacobson C. Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy. Epilepsy Behav. 2013;29(3):574-577.
HOUSTON—Pharmaceutical-grade cannabidiol (CBD) may reduce seizure severity in adults and children with medically refractory epilepsy, according to an open-label trial described at the 70th Annual Meeting of the American Epilepsy Society. A controlled trial to confirm the drug’s effect may be warranted.
Jennifer L. DeWolfe, DO, Associate Professor of Neurology at the University of Alabama at Birmingham, and colleagues conducted a state-sponsored compassionate-use study of CBD in patients with refractory epilepsy. Patients received Epidiolex (a CBD formulation developed by GW Pharmaceuticals) in addition to their antiepileptic drugs. Eligible participants were adults and children with epilepsy confirmed by video EEG. Participants were required to have failed four antiepileptic drugs and had to have had four countable seizures per month. Exclusion criteria included psychogenic nonepileptic seizures confirmed by video EEG and prior CBD use.
Measuring Seizure Severity Over Time
The investigators measured participants’ seizure frequency and used the Chalfont Seizure Severity Scale to measure seizure severity. The scale solicits information about various factors, such as whether the patient lost awareness, dropped an object, fell, or was injured. The total possible score on the scale is 178, and the score increases with seizure severity. Changes of 10 or more points were considered significant. The researchers particularly focused on participants’ most frequent seizure type, which the Chalfont Seizure Severity Scale names the Type 1 seizure.
Dr. DeWolfe and colleagues measured patients’ total seizure severity scores and severity scores for Type 1 seizures at baseline, three months, and six months. To compare the scores, the researchers calculated time-weighted average values. They also examined percent change in seizures; seizure severity in adults, children, and all patients; and severity in responders and nonresponders. Responders were defined as patients who had a reduction in seizure frequency of more than 50%. The analysis included 81 participants, approximately half of whom were children. At the time of the analysis, 57 patients had undergone evaluation at three months, and 47 patients had undergone evaluation at six months. At baseline, the majority of patients had at least two types of seizures.
Seizure Severity Was Reduced
The total change in Chalfont Seizure Severity Scale score at three months was significant for adults, children, and all patients. The change remained significant at six months. The difference in the percent change in seizure severity between responders and nonresponders was significant at three months, but not at six months.
The change in severity of Type 1 seizures was significant for adults, children, and all patients at three months and at six months. The difference between responders and nonresponders in change in severity of Type 1 seizures was significant at three months, but not at six months.
At three months, the majority of adults, the majority of all patients, the majority of responders, and the majority of nonresponders had a reduction in seizure severity of at least 10 points. Approximately one-third of children had a reduction in seizure severity of at least 10 points at three months. At six months, the majority of adults, children, all patients, responders, and nonresponders had a decrease in seizure severity of at least 10 points. Patients’ average seizure severity tended to increase at six months, compared with the three-month point, but was still significantly lower than at baseline.
“One of the things I find most exciting is [that] … even if you were considered a nonresponder, you still had improvement in seizure severity,” said Dr. DeWolfe. She and her colleagues plan to examine the data by seizure type (eg, absence or tonic-clonic), to identify which factors measured by the Chalfont Seizure Severity Scale contributed most to the reductions in seizure severity, and to examine whether the effect of CBD on levels of antiepileptic drugs contributed to the change in seizure severity. The findings of this open-label trial suggest that CBD may improve seizure severity in people with medically refractory epilepsy. Randomized placebo-controlled studies are needed to further evaluate the effects of CBD on seizure severity.
—Erik Greb
Suggested Reading
Devinsky O, Marsh E, Friedman D, et al. Cannabidiol in patients with treatment-resistant epilepsy: an open-label interventional trial. Lancet Neurol. 2016;15(3):270-278.
Porter BE, Jacobson C. Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy. Epilepsy Behav. 2013;29(3):574-577.
HOUSTON—Pharmaceutical-grade cannabidiol (CBD) may reduce seizure severity in adults and children with medically refractory epilepsy, according to an open-label trial described at the 70th Annual Meeting of the American Epilepsy Society. A controlled trial to confirm the drug’s effect may be warranted.
Jennifer L. DeWolfe, DO, Associate Professor of Neurology at the University of Alabama at Birmingham, and colleagues conducted a state-sponsored compassionate-use study of CBD in patients with refractory epilepsy. Patients received Epidiolex (a CBD formulation developed by GW Pharmaceuticals) in addition to their antiepileptic drugs. Eligible participants were adults and children with epilepsy confirmed by video EEG. Participants were required to have failed four antiepileptic drugs and had to have had four countable seizures per month. Exclusion criteria included psychogenic nonepileptic seizures confirmed by video EEG and prior CBD use.
Measuring Seizure Severity Over Time
The investigators measured participants’ seizure frequency and used the Chalfont Seizure Severity Scale to measure seizure severity. The scale solicits information about various factors, such as whether the patient lost awareness, dropped an object, fell, or was injured. The total possible score on the scale is 178, and the score increases with seizure severity. Changes of 10 or more points were considered significant. The researchers particularly focused on participants’ most frequent seizure type, which the Chalfont Seizure Severity Scale names the Type 1 seizure.
Dr. DeWolfe and colleagues measured patients’ total seizure severity scores and severity scores for Type 1 seizures at baseline, three months, and six months. To compare the scores, the researchers calculated time-weighted average values. They also examined percent change in seizures; seizure severity in adults, children, and all patients; and severity in responders and nonresponders. Responders were defined as patients who had a reduction in seizure frequency of more than 50%. The analysis included 81 participants, approximately half of whom were children. At the time of the analysis, 57 patients had undergone evaluation at three months, and 47 patients had undergone evaluation at six months. At baseline, the majority of patients had at least two types of seizures.
Seizure Severity Was Reduced
The total change in Chalfont Seizure Severity Scale score at three months was significant for adults, children, and all patients. The change remained significant at six months. The difference in the percent change in seizure severity between responders and nonresponders was significant at three months, but not at six months.
The change in severity of Type 1 seizures was significant for adults, children, and all patients at three months and at six months. The difference between responders and nonresponders in change in severity of Type 1 seizures was significant at three months, but not at six months.
At three months, the majority of adults, the majority of all patients, the majority of responders, and the majority of nonresponders had a reduction in seizure severity of at least 10 points. Approximately one-third of children had a reduction in seizure severity of at least 10 points at three months. At six months, the majority of adults, children, all patients, responders, and nonresponders had a decrease in seizure severity of at least 10 points. Patients’ average seizure severity tended to increase at six months, compared with the three-month point, but was still significantly lower than at baseline.
“One of the things I find most exciting is [that] … even if you were considered a nonresponder, you still had improvement in seizure severity,” said Dr. DeWolfe. She and her colleagues plan to examine the data by seizure type (eg, absence or tonic-clonic), to identify which factors measured by the Chalfont Seizure Severity Scale contributed most to the reductions in seizure severity, and to examine whether the effect of CBD on levels of antiepileptic drugs contributed to the change in seizure severity. The findings of this open-label trial suggest that CBD may improve seizure severity in people with medically refractory epilepsy. Randomized placebo-controlled studies are needed to further evaluate the effects of CBD on seizure severity.
—Erik Greb
Suggested Reading
Devinsky O, Marsh E, Friedman D, et al. Cannabidiol in patients with treatment-resistant epilepsy: an open-label interventional trial. Lancet Neurol. 2016;15(3):270-278.
Porter BE, Jacobson C. Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy. Epilepsy Behav. 2013;29(3):574-577.
CMS makes economics of primary care ACOs more appealing
As you may have read, accountable care organizations have met uneven success over the last several years. But, when they are broken down into categories, physician-sponsored ACOs have done better, particularly those with a strong primary care core.
This is true for several reasons.
In this transition period from a fee-for-service payment system that rewards volume and expensive inpatient care to a pay-for-value system, some ACOs set up by health systems or specialists envisioned the savings coming through lower utilization of their services. They had an inherent impediment to fully committing to keeping people well and avoiding acute care. In contrast, primary care providers are free to be all in with population health value-based programs.
However, because the fee-for-service system has historically left primary care physicians at the bottom of the compensation food chain, we have a “can’t get there from here” dilemma. It is a cruel irony that the group best suited to stretch America’s health care dollar and benefit both professionally and financially usually does not have the capital to create and operate an ACO for the roughly 18 months before shared savings are distributed.
The Centers for Medicare & Medicaid Services has tried to mitigate this by offering financial support for small, non–health system ACOs, particularly those in rural areas. Some of those enrolled ACOs are primary care driven and have been among the most successful in the MSSP.
Nonetheless, the upfront costs, paired with the long delay for the sole economic return on the investment – shared savings – have combined to be deal killers for many promising would-be primary care ACOs.
New upfront payments are game changers
A successful ACO will be assigned one or more patient populations and be given a minimum of 50% of the savings for the overall costs for those populations, if the quality of their health is maintained or improved.
To excise avoidable waste, the ACO looks at gaps in care for those populations – frequent emergency department use for nonemergencies, avoidably high levels of diabetes and obesity, too-high readmission rates, unnecessarily high postacute care costs, etc. They then use evidence-based best team care practices – from patient self care and prevention, to multispecialty coordination and PCMH care management.
Why? Because these proved to give the highest impact on quality and reducing costs. To achieve significant shared savings, the costs are usually measured for a calendar year, then it takes about 6 months for the claims to be reported and paid. Thus, the shared savings check to the ACO will arrive about 18 months after all this is started.
The CMS has also figured out that primary care physician care coordination and management drive quality and savings. The agency knows that incentivizing this type of care, the very type calculated to create ACO success, will net significant savings to the Medicare program.
For example, the pilot project for preventing diabetes will be expanded, because Medicare hopes to save several thousand dollars a year per beneficiary in health care costs.
In a blog entry the day the expanded population health management codes were announced, the CMS acting administrator wrote that, “Over time, if the clinicians qualified to provide these services were to fully provide these services to all eligible beneficiaries, the increase would be as much as $4 billion or more in additional support for care coordination and patient-centered care.”
CMS revenue streams to support ACO success-driving activities include:
• Value-based screening and counseling codes to decrease downstream costs.
• Upward adjustment of evaluation and management reimbursement for assessment of care and care plan development for mobility-impaired patients.
• Annual wellness visits.
• Prolonged E&M services that accrue outside of a patient visit.
• Collaboration with mental health specialists.
• Comprehensive assessment and care planning for patients with cognitive impairment.
• Expansion of the diabetes prevention pilot program; diabetes prevention and diabetes education are two separate services.
• Transitional care management for high-risk patients post discharge.
• Structured obesity management.
The 2017 Medicare fee schedule smoothed some of the bumps in administering and being paid for chronic care management (CCM) services, and it added codes with increased reimbursement aligned with increased complexity of comorbidities/illness.
Perhaps the biggest new payment boost for primary care to engage in ACO high-value activities is actually the Merit-Based Incentive Payment System (MIPS) under MACRA, the Medicare Access and CHIP Reauthorization Act of 2015.
Under MACRA, all Medicare compensation for physicians will be determined by relative delivery of quality and efficient care. Experts are recommending that primary care physicians participate in non–risk-taking ACOs to optimize MIPS value scoring, while also reducing administrative burdens of compliance. Use an ACO’s analytics to support collaborative care and provide the reports required under MIPS.
Let’s be smart about it
According to Gordon Wilhoit, MD, a practicing physician and chief medical officer of an all–primary-care-physician ACO in South Carolina, “This is a no brainer. Start first with your MSSP ACO high-value game plan, then align the complementary care coordination codes, CCM, MIPS, and other revenue stream and reporting activities with it. Now, primary care physicians can finance their ACO and MIPS care coordination efforts with a stream of ongoing payments from these care management codes.
“One of my colleagues saw a 27% increase in revenues in 6 months just from providing and billing for this type of care,” Dr. Wilhoit explained. “And, not counting shared savings or MIPS incentive payments, our office’s reimbursement from these care management codes now exceeds our fee-for-service income, which has not decreased.”
Even with these payments, the CMS will reduce overall net expenditures. Your impact on health care will be more powerful as a manager of the team addressing patients’ overall health than reacting to patient sickness one at a time. The patients you impact the most may be ones you don’t actually see. Your empowerment to practice medicine the right way will continue to grow.
Now, finally, you may start getting compensation that takes away the last big hurdle to creating the infrastructure you need to succeed.
Mr. Bobbitt is a head of the health law group at the Smith Anderson law firm in Raleigh, N.C. He is president of, and Dr. Wilhoit is a consultant with, Value Health Partners, LLC, a health care strategic consulting company. He has years of experience assisting physicians form integrated delivery systems. He has spoken and written nationally to primary care physicians on the strategies and practicalities of forming or joining ACOs. This article is meant to be educational and does not constitute legal advice. For additional information, readers may contact the author at either [email protected] or 919-906-4054.
As you may have read, accountable care organizations have met uneven success over the last several years. But, when they are broken down into categories, physician-sponsored ACOs have done better, particularly those with a strong primary care core.
This is true for several reasons.
In this transition period from a fee-for-service payment system that rewards volume and expensive inpatient care to a pay-for-value system, some ACOs set up by health systems or specialists envisioned the savings coming through lower utilization of their services. They had an inherent impediment to fully committing to keeping people well and avoiding acute care. In contrast, primary care providers are free to be all in with population health value-based programs.
However, because the fee-for-service system has historically left primary care physicians at the bottom of the compensation food chain, we have a “can’t get there from here” dilemma. It is a cruel irony that the group best suited to stretch America’s health care dollar and benefit both professionally and financially usually does not have the capital to create and operate an ACO for the roughly 18 months before shared savings are distributed.
The Centers for Medicare & Medicaid Services has tried to mitigate this by offering financial support for small, non–health system ACOs, particularly those in rural areas. Some of those enrolled ACOs are primary care driven and have been among the most successful in the MSSP.
Nonetheless, the upfront costs, paired with the long delay for the sole economic return on the investment – shared savings – have combined to be deal killers for many promising would-be primary care ACOs.
New upfront payments are game changers
A successful ACO will be assigned one or more patient populations and be given a minimum of 50% of the savings for the overall costs for those populations, if the quality of their health is maintained or improved.
To excise avoidable waste, the ACO looks at gaps in care for those populations – frequent emergency department use for nonemergencies, avoidably high levels of diabetes and obesity, too-high readmission rates, unnecessarily high postacute care costs, etc. They then use evidence-based best team care practices – from patient self care and prevention, to multispecialty coordination and PCMH care management.
Why? Because these proved to give the highest impact on quality and reducing costs. To achieve significant shared savings, the costs are usually measured for a calendar year, then it takes about 6 months for the claims to be reported and paid. Thus, the shared savings check to the ACO will arrive about 18 months after all this is started.
The CMS has also figured out that primary care physician care coordination and management drive quality and savings. The agency knows that incentivizing this type of care, the very type calculated to create ACO success, will net significant savings to the Medicare program.
For example, the pilot project for preventing diabetes will be expanded, because Medicare hopes to save several thousand dollars a year per beneficiary in health care costs.
In a blog entry the day the expanded population health management codes were announced, the CMS acting administrator wrote that, “Over time, if the clinicians qualified to provide these services were to fully provide these services to all eligible beneficiaries, the increase would be as much as $4 billion or more in additional support for care coordination and patient-centered care.”
CMS revenue streams to support ACO success-driving activities include:
• Value-based screening and counseling codes to decrease downstream costs.
• Upward adjustment of evaluation and management reimbursement for assessment of care and care plan development for mobility-impaired patients.
• Annual wellness visits.
• Prolonged E&M services that accrue outside of a patient visit.
• Collaboration with mental health specialists.
• Comprehensive assessment and care planning for patients with cognitive impairment.
• Expansion of the diabetes prevention pilot program; diabetes prevention and diabetes education are two separate services.
• Transitional care management for high-risk patients post discharge.
• Structured obesity management.
The 2017 Medicare fee schedule smoothed some of the bumps in administering and being paid for chronic care management (CCM) services, and it added codes with increased reimbursement aligned with increased complexity of comorbidities/illness.
Perhaps the biggest new payment boost for primary care to engage in ACO high-value activities is actually the Merit-Based Incentive Payment System (MIPS) under MACRA, the Medicare Access and CHIP Reauthorization Act of 2015.
Under MACRA, all Medicare compensation for physicians will be determined by relative delivery of quality and efficient care. Experts are recommending that primary care physicians participate in non–risk-taking ACOs to optimize MIPS value scoring, while also reducing administrative burdens of compliance. Use an ACO’s analytics to support collaborative care and provide the reports required under MIPS.
Let’s be smart about it
According to Gordon Wilhoit, MD, a practicing physician and chief medical officer of an all–primary-care-physician ACO in South Carolina, “This is a no brainer. Start first with your MSSP ACO high-value game plan, then align the complementary care coordination codes, CCM, MIPS, and other revenue stream and reporting activities with it. Now, primary care physicians can finance their ACO and MIPS care coordination efforts with a stream of ongoing payments from these care management codes.
“One of my colleagues saw a 27% increase in revenues in 6 months just from providing and billing for this type of care,” Dr. Wilhoit explained. “And, not counting shared savings or MIPS incentive payments, our office’s reimbursement from these care management codes now exceeds our fee-for-service income, which has not decreased.”
Even with these payments, the CMS will reduce overall net expenditures. Your impact on health care will be more powerful as a manager of the team addressing patients’ overall health than reacting to patient sickness one at a time. The patients you impact the most may be ones you don’t actually see. Your empowerment to practice medicine the right way will continue to grow.
Now, finally, you may start getting compensation that takes away the last big hurdle to creating the infrastructure you need to succeed.
Mr. Bobbitt is a head of the health law group at the Smith Anderson law firm in Raleigh, N.C. He is president of, and Dr. Wilhoit is a consultant with, Value Health Partners, LLC, a health care strategic consulting company. He has years of experience assisting physicians form integrated delivery systems. He has spoken and written nationally to primary care physicians on the strategies and practicalities of forming or joining ACOs. This article is meant to be educational and does not constitute legal advice. For additional information, readers may contact the author at either [email protected] or 919-906-4054.
As you may have read, accountable care organizations have met uneven success over the last several years. But, when they are broken down into categories, physician-sponsored ACOs have done better, particularly those with a strong primary care core.
This is true for several reasons.
In this transition period from a fee-for-service payment system that rewards volume and expensive inpatient care to a pay-for-value system, some ACOs set up by health systems or specialists envisioned the savings coming through lower utilization of their services. They had an inherent impediment to fully committing to keeping people well and avoiding acute care. In contrast, primary care providers are free to be all in with population health value-based programs.
However, because the fee-for-service system has historically left primary care physicians at the bottom of the compensation food chain, we have a “can’t get there from here” dilemma. It is a cruel irony that the group best suited to stretch America’s health care dollar and benefit both professionally and financially usually does not have the capital to create and operate an ACO for the roughly 18 months before shared savings are distributed.
The Centers for Medicare & Medicaid Services has tried to mitigate this by offering financial support for small, non–health system ACOs, particularly those in rural areas. Some of those enrolled ACOs are primary care driven and have been among the most successful in the MSSP.
Nonetheless, the upfront costs, paired with the long delay for the sole economic return on the investment – shared savings – have combined to be deal killers for many promising would-be primary care ACOs.
New upfront payments are game changers
A successful ACO will be assigned one or more patient populations and be given a minimum of 50% of the savings for the overall costs for those populations, if the quality of their health is maintained or improved.
To excise avoidable waste, the ACO looks at gaps in care for those populations – frequent emergency department use for nonemergencies, avoidably high levels of diabetes and obesity, too-high readmission rates, unnecessarily high postacute care costs, etc. They then use evidence-based best team care practices – from patient self care and prevention, to multispecialty coordination and PCMH care management.
Why? Because these proved to give the highest impact on quality and reducing costs. To achieve significant shared savings, the costs are usually measured for a calendar year, then it takes about 6 months for the claims to be reported and paid. Thus, the shared savings check to the ACO will arrive about 18 months after all this is started.
The CMS has also figured out that primary care physician care coordination and management drive quality and savings. The agency knows that incentivizing this type of care, the very type calculated to create ACO success, will net significant savings to the Medicare program.
For example, the pilot project for preventing diabetes will be expanded, because Medicare hopes to save several thousand dollars a year per beneficiary in health care costs.
In a blog entry the day the expanded population health management codes were announced, the CMS acting administrator wrote that, “Over time, if the clinicians qualified to provide these services were to fully provide these services to all eligible beneficiaries, the increase would be as much as $4 billion or more in additional support for care coordination and patient-centered care.”
CMS revenue streams to support ACO success-driving activities include:
• Value-based screening and counseling codes to decrease downstream costs.
• Upward adjustment of evaluation and management reimbursement for assessment of care and care plan development for mobility-impaired patients.
• Annual wellness visits.
• Prolonged E&M services that accrue outside of a patient visit.
• Collaboration with mental health specialists.
• Comprehensive assessment and care planning for patients with cognitive impairment.
• Expansion of the diabetes prevention pilot program; diabetes prevention and diabetes education are two separate services.
• Transitional care management for high-risk patients post discharge.
• Structured obesity management.
The 2017 Medicare fee schedule smoothed some of the bumps in administering and being paid for chronic care management (CCM) services, and it added codes with increased reimbursement aligned with increased complexity of comorbidities/illness.
Perhaps the biggest new payment boost for primary care to engage in ACO high-value activities is actually the Merit-Based Incentive Payment System (MIPS) under MACRA, the Medicare Access and CHIP Reauthorization Act of 2015.
Under MACRA, all Medicare compensation for physicians will be determined by relative delivery of quality and efficient care. Experts are recommending that primary care physicians participate in non–risk-taking ACOs to optimize MIPS value scoring, while also reducing administrative burdens of compliance. Use an ACO’s analytics to support collaborative care and provide the reports required under MIPS.
Let’s be smart about it
According to Gordon Wilhoit, MD, a practicing physician and chief medical officer of an all–primary-care-physician ACO in South Carolina, “This is a no brainer. Start first with your MSSP ACO high-value game plan, then align the complementary care coordination codes, CCM, MIPS, and other revenue stream and reporting activities with it. Now, primary care physicians can finance their ACO and MIPS care coordination efforts with a stream of ongoing payments from these care management codes.
“One of my colleagues saw a 27% increase in revenues in 6 months just from providing and billing for this type of care,” Dr. Wilhoit explained. “And, not counting shared savings or MIPS incentive payments, our office’s reimbursement from these care management codes now exceeds our fee-for-service income, which has not decreased.”
Even with these payments, the CMS will reduce overall net expenditures. Your impact on health care will be more powerful as a manager of the team addressing patients’ overall health than reacting to patient sickness one at a time. The patients you impact the most may be ones you don’t actually see. Your empowerment to practice medicine the right way will continue to grow.
Now, finally, you may start getting compensation that takes away the last big hurdle to creating the infrastructure you need to succeed.
Mr. Bobbitt is a head of the health law group at the Smith Anderson law firm in Raleigh, N.C. He is president of, and Dr. Wilhoit is a consultant with, Value Health Partners, LLC, a health care strategic consulting company. He has years of experience assisting physicians form integrated delivery systems. He has spoken and written nationally to primary care physicians on the strategies and practicalities of forming or joining ACOs. This article is meant to be educational and does not constitute legal advice. For additional information, readers may contact the author at either [email protected] or 919-906-4054.
Psychiatric Comorbidities Are Common in Newly Diagnosed Pediatric Epilepsy
HOUSTON—Nearly one in three children diagnosed with new-onset epilepsy presents with psychiatric diagnoses at the onset, according to research presented at the 70th Annual Meeting of the American Epilepsy Society.
This finding “tells us that when kids are coming in, even if they are only having psychiatric symptoms at their onset of epilepsy, they should be referred for some treatment to help them possibly mitigate the development of these psychiatric diagnoses in the first year,” said Julia Doss, PsyD, Pediatric Psychologist at the Minnesota Epilepsy Group in Saint Paul.
About three years ago, the Minnesota Epilepsy Group, a private practice group that consults with the United Hospital and Children’s Hospitals and Clinics of Minnesota, launched a New Onset Pediatric Epilepsy (NOPE) clinic. At this clinic, referred patients undergo a psychologic evaluation, neuropsychologic testing, and medical evaluation in the same day. Psychologic assessment measures include the Clinical Interview with parent and patient, the Strengths and Difficulties Questionnaire (SDQ), and the Revised Children’s Anxiety and Depression Scale (RCADS).
Researchers evaluated 96 patients in the clinic who had presented for their first NOPE clinic visit within eight weeks of their epilepsy diagnosis. More than half were male, and patients ranged in age from 3 to 18. Dr. Doss and her colleagues separated the children into the following three groups: ages 3 to 6 (group 1), ages 7 to 11 (group 2), and ages 12 to 18 (group 3). Based on the Clinical Interview, none of the patients in group 1 screened positive for depression or anxiety, but 16% met criteria for some other behavioral disorder. However, among patients in group 2, the percentages who met criteria for depression, anxiety, and other behavioral disorders were 13%, 25%, and 13%, respectively. The corresponding percentages for patients in group 3 were 29%, 38%, and 10%.
Of the 96 patients evaluated, 64 parents completed all of the questions on the SDQ. The researchers observed significant correlations between parent response and diagnoses assigned on the Clinical Interview for behavior diagnoses and anxiety diagnoses) but not for depression diagnoses.
“Despite the correlations on both behavior and anxiety responses and clinical diagnoses assigned, parents still only reported significant concerns in about half of the children that were given diagnoses,” said Dr. Doss.
The comparison of RCADS scores between parent and child demonstrated moderate to strong correlation on the following scales: separation anxiety, generalized anxiety, obsessive/compulsive, and depression.
Small sample size was a key limitation in this study, said Dr. Doss. “Early evaluation or at least screening is necessary in all of our kids who present with an epilepsy diagnosis, because more than 30% develop psychiatric disorders within the first year of their diagnosis,” said Dr. Doss. “That’s one in three, so if we can start to better evaluate that early and get them funneled into treatment early, we might be able to prevent some of these problems from becoming lifelong issues.”
—Doug Brunk
Suggested Reading
Asato MR, Doss JL, Piloplys S. Clinic-friendly screening for cognitive and mental health problems in school-aged youth with epilepsy. Epilepsy Behav. 2015;48:97-102.
Piloplys S, Doss J, Siddarth P, et al. Risk factors for comorbid psychopathology in youth with psychogenic nonepileptic seizures. Seizure. 2016;38:32-37.
HOUSTON—Nearly one in three children diagnosed with new-onset epilepsy presents with psychiatric diagnoses at the onset, according to research presented at the 70th Annual Meeting of the American Epilepsy Society.
This finding “tells us that when kids are coming in, even if they are only having psychiatric symptoms at their onset of epilepsy, they should be referred for some treatment to help them possibly mitigate the development of these psychiatric diagnoses in the first year,” said Julia Doss, PsyD, Pediatric Psychologist at the Minnesota Epilepsy Group in Saint Paul.
About three years ago, the Minnesota Epilepsy Group, a private practice group that consults with the United Hospital and Children’s Hospitals and Clinics of Minnesota, launched a New Onset Pediatric Epilepsy (NOPE) clinic. At this clinic, referred patients undergo a psychologic evaluation, neuropsychologic testing, and medical evaluation in the same day. Psychologic assessment measures include the Clinical Interview with parent and patient, the Strengths and Difficulties Questionnaire (SDQ), and the Revised Children’s Anxiety and Depression Scale (RCADS).
Researchers evaluated 96 patients in the clinic who had presented for their first NOPE clinic visit within eight weeks of their epilepsy diagnosis. More than half were male, and patients ranged in age from 3 to 18. Dr. Doss and her colleagues separated the children into the following three groups: ages 3 to 6 (group 1), ages 7 to 11 (group 2), and ages 12 to 18 (group 3). Based on the Clinical Interview, none of the patients in group 1 screened positive for depression or anxiety, but 16% met criteria for some other behavioral disorder. However, among patients in group 2, the percentages who met criteria for depression, anxiety, and other behavioral disorders were 13%, 25%, and 13%, respectively. The corresponding percentages for patients in group 3 were 29%, 38%, and 10%.
Of the 96 patients evaluated, 64 parents completed all of the questions on the SDQ. The researchers observed significant correlations between parent response and diagnoses assigned on the Clinical Interview for behavior diagnoses and anxiety diagnoses) but not for depression diagnoses.
“Despite the correlations on both behavior and anxiety responses and clinical diagnoses assigned, parents still only reported significant concerns in about half of the children that were given diagnoses,” said Dr. Doss.
The comparison of RCADS scores between parent and child demonstrated moderate to strong correlation on the following scales: separation anxiety, generalized anxiety, obsessive/compulsive, and depression.
Small sample size was a key limitation in this study, said Dr. Doss. “Early evaluation or at least screening is necessary in all of our kids who present with an epilepsy diagnosis, because more than 30% develop psychiatric disorders within the first year of their diagnosis,” said Dr. Doss. “That’s one in three, so if we can start to better evaluate that early and get them funneled into treatment early, we might be able to prevent some of these problems from becoming lifelong issues.”
—Doug Brunk
Suggested Reading
Asato MR, Doss JL, Piloplys S. Clinic-friendly screening for cognitive and mental health problems in school-aged youth with epilepsy. Epilepsy Behav. 2015;48:97-102.
Piloplys S, Doss J, Siddarth P, et al. Risk factors for comorbid psychopathology in youth with psychogenic nonepileptic seizures. Seizure. 2016;38:32-37.
HOUSTON—Nearly one in three children diagnosed with new-onset epilepsy presents with psychiatric diagnoses at the onset, according to research presented at the 70th Annual Meeting of the American Epilepsy Society.
This finding “tells us that when kids are coming in, even if they are only having psychiatric symptoms at their onset of epilepsy, they should be referred for some treatment to help them possibly mitigate the development of these psychiatric diagnoses in the first year,” said Julia Doss, PsyD, Pediatric Psychologist at the Minnesota Epilepsy Group in Saint Paul.
About three years ago, the Minnesota Epilepsy Group, a private practice group that consults with the United Hospital and Children’s Hospitals and Clinics of Minnesota, launched a New Onset Pediatric Epilepsy (NOPE) clinic. At this clinic, referred patients undergo a psychologic evaluation, neuropsychologic testing, and medical evaluation in the same day. Psychologic assessment measures include the Clinical Interview with parent and patient, the Strengths and Difficulties Questionnaire (SDQ), and the Revised Children’s Anxiety and Depression Scale (RCADS).
Researchers evaluated 96 patients in the clinic who had presented for their first NOPE clinic visit within eight weeks of their epilepsy diagnosis. More than half were male, and patients ranged in age from 3 to 18. Dr. Doss and her colleagues separated the children into the following three groups: ages 3 to 6 (group 1), ages 7 to 11 (group 2), and ages 12 to 18 (group 3). Based on the Clinical Interview, none of the patients in group 1 screened positive for depression or anxiety, but 16% met criteria for some other behavioral disorder. However, among patients in group 2, the percentages who met criteria for depression, anxiety, and other behavioral disorders were 13%, 25%, and 13%, respectively. The corresponding percentages for patients in group 3 were 29%, 38%, and 10%.
Of the 96 patients evaluated, 64 parents completed all of the questions on the SDQ. The researchers observed significant correlations between parent response and diagnoses assigned on the Clinical Interview for behavior diagnoses and anxiety diagnoses) but not for depression diagnoses.
“Despite the correlations on both behavior and anxiety responses and clinical diagnoses assigned, parents still only reported significant concerns in about half of the children that were given diagnoses,” said Dr. Doss.
The comparison of RCADS scores between parent and child demonstrated moderate to strong correlation on the following scales: separation anxiety, generalized anxiety, obsessive/compulsive, and depression.
Small sample size was a key limitation in this study, said Dr. Doss. “Early evaluation or at least screening is necessary in all of our kids who present with an epilepsy diagnosis, because more than 30% develop psychiatric disorders within the first year of their diagnosis,” said Dr. Doss. “That’s one in three, so if we can start to better evaluate that early and get them funneled into treatment early, we might be able to prevent some of these problems from becoming lifelong issues.”
—Doug Brunk
Suggested Reading
Asato MR, Doss JL, Piloplys S. Clinic-friendly screening for cognitive and mental health problems in school-aged youth with epilepsy. Epilepsy Behav. 2015;48:97-102.
Piloplys S, Doss J, Siddarth P, et al. Risk factors for comorbid psychopathology in youth with psychogenic nonepileptic seizures. Seizure. 2016;38:32-37.
Dementia Prevalence Is Increased in Patients With Heart Failure
NEW ORLEANS—Elderly patients with heart failure have a significantly increased prevalence of dementia and mild cognitive impairment (MCI), compared with people of similar age without heart failure, according to an analysis of data collected from more than 6,000 US residents enrolled in a long-term observational study.
Patients diagnosed with either heart failure with reduced ejection fraction or heart failure with preserved ejection fraction had an 89% increased prevalence of dementia and a 41% increased prevalence of MCI, compared with people from the same cohort who did not develop heart failure. Investigators adjusted their analysis for several demographic and clinical variables, said Lucy S. Witt, MD, a researcher at the University of North Carolina in Chapel Hill, at the American Heart Association Scientific Sessions 2016. She speculated that the link between heart failure and dementia and MCI might result from impaired cerebral perfusion in patients with heart failure or from effects from heart failure medications.
“Our findings suggest that clinicians should have a higher suspicion for cognitive impairment in patients with heart failure, regardless of other, more classic risk factors,” she said. “This knowledge could prompt physicians to perform testing [for dementia and MCI], initiate conversations regarding the goals of care or advance care planning, and discuss appropriate living situations” for their patients with heart failure.
The analysis used data collected for the Atherosclerosis Risk in Communities (ARIC) study, which began in 1987 and enrolled a randomly selected representative cohort of approximately 16,000 women and men between ages 45 and 64 who resided in any of four US communities. Dr. Witt specifically focused on the data collected from 6,431 of the participants who returned for a fifth follow-up examination between 2011 and 2013, including 5,490 people without heart failure, whose average age was 76, and 941 participants with heart failure, whose average age was 78.
The adjusted rate of dementia prevalence at the fifth follow-up visit was 5.6% among those without heart failure and 7.0% in those with heart failure. The examinations also found MCI in an adjusted 21.5% of those without heart failure and in 26.2% of those with heart failure, said Dr. Witt. Adjustments were for factors such as age, sex, location, education, hypertension, diabetes, depression, alcohol and tobacco use, cerebrovascular disease, and marital status.
The relative risk for dementia among patients with heart failure was roughly similar, regardless of whether ARIC participants had a reduced or preserved left ventricular ejection fraction, she said.
ARIC is funded by the National Heart, Lung, and Blood Institute. Dr. Witt had no disclosures.
—Mitchel L. Zoler
Suggested Reading
Adelborg K, Horváth-Puhó E, Ording A, et al. Heart failure and risk of dementia: a Danish nationwide population-based cohort study. Eur J Heart Fail. 2016 Sep 9 [Epub ahead of print].
Ampadu J, Morley JE. Heart failure and cognitive dysfunction. Int J Cardiol. 2015;178:12-23.
Rusanen M, Kivipelto M, Levälahti E, et al. Heart diseases and long-term risk of dementia and Alzheimer’s disease: a population-based CAIDE study. J Alzheimers Dis. 2014;42(1):183-191.
NEW ORLEANS—Elderly patients with heart failure have a significantly increased prevalence of dementia and mild cognitive impairment (MCI), compared with people of similar age without heart failure, according to an analysis of data collected from more than 6,000 US residents enrolled in a long-term observational study.
Patients diagnosed with either heart failure with reduced ejection fraction or heart failure with preserved ejection fraction had an 89% increased prevalence of dementia and a 41% increased prevalence of MCI, compared with people from the same cohort who did not develop heart failure. Investigators adjusted their analysis for several demographic and clinical variables, said Lucy S. Witt, MD, a researcher at the University of North Carolina in Chapel Hill, at the American Heart Association Scientific Sessions 2016. She speculated that the link between heart failure and dementia and MCI might result from impaired cerebral perfusion in patients with heart failure or from effects from heart failure medications.
“Our findings suggest that clinicians should have a higher suspicion for cognitive impairment in patients with heart failure, regardless of other, more classic risk factors,” she said. “This knowledge could prompt physicians to perform testing [for dementia and MCI], initiate conversations regarding the goals of care or advance care planning, and discuss appropriate living situations” for their patients with heart failure.
The analysis used data collected for the Atherosclerosis Risk in Communities (ARIC) study, which began in 1987 and enrolled a randomly selected representative cohort of approximately 16,000 women and men between ages 45 and 64 who resided in any of four US communities. Dr. Witt specifically focused on the data collected from 6,431 of the participants who returned for a fifth follow-up examination between 2011 and 2013, including 5,490 people without heart failure, whose average age was 76, and 941 participants with heart failure, whose average age was 78.
The adjusted rate of dementia prevalence at the fifth follow-up visit was 5.6% among those without heart failure and 7.0% in those with heart failure. The examinations also found MCI in an adjusted 21.5% of those without heart failure and in 26.2% of those with heart failure, said Dr. Witt. Adjustments were for factors such as age, sex, location, education, hypertension, diabetes, depression, alcohol and tobacco use, cerebrovascular disease, and marital status.
The relative risk for dementia among patients with heart failure was roughly similar, regardless of whether ARIC participants had a reduced or preserved left ventricular ejection fraction, she said.
ARIC is funded by the National Heart, Lung, and Blood Institute. Dr. Witt had no disclosures.
—Mitchel L. Zoler
Suggested Reading
Adelborg K, Horváth-Puhó E, Ording A, et al. Heart failure and risk of dementia: a Danish nationwide population-based cohort study. Eur J Heart Fail. 2016 Sep 9 [Epub ahead of print].
Ampadu J, Morley JE. Heart failure and cognitive dysfunction. Int J Cardiol. 2015;178:12-23.
Rusanen M, Kivipelto M, Levälahti E, et al. Heart diseases and long-term risk of dementia and Alzheimer’s disease: a population-based CAIDE study. J Alzheimers Dis. 2014;42(1):183-191.
NEW ORLEANS—Elderly patients with heart failure have a significantly increased prevalence of dementia and mild cognitive impairment (MCI), compared with people of similar age without heart failure, according to an analysis of data collected from more than 6,000 US residents enrolled in a long-term observational study.
Patients diagnosed with either heart failure with reduced ejection fraction or heart failure with preserved ejection fraction had an 89% increased prevalence of dementia and a 41% increased prevalence of MCI, compared with people from the same cohort who did not develop heart failure. Investigators adjusted their analysis for several demographic and clinical variables, said Lucy S. Witt, MD, a researcher at the University of North Carolina in Chapel Hill, at the American Heart Association Scientific Sessions 2016. She speculated that the link between heart failure and dementia and MCI might result from impaired cerebral perfusion in patients with heart failure or from effects from heart failure medications.
“Our findings suggest that clinicians should have a higher suspicion for cognitive impairment in patients with heart failure, regardless of other, more classic risk factors,” she said. “This knowledge could prompt physicians to perform testing [for dementia and MCI], initiate conversations regarding the goals of care or advance care planning, and discuss appropriate living situations” for their patients with heart failure.
The analysis used data collected for the Atherosclerosis Risk in Communities (ARIC) study, which began in 1987 and enrolled a randomly selected representative cohort of approximately 16,000 women and men between ages 45 and 64 who resided in any of four US communities. Dr. Witt specifically focused on the data collected from 6,431 of the participants who returned for a fifth follow-up examination between 2011 and 2013, including 5,490 people without heart failure, whose average age was 76, and 941 participants with heart failure, whose average age was 78.
The adjusted rate of dementia prevalence at the fifth follow-up visit was 5.6% among those without heart failure and 7.0% in those with heart failure. The examinations also found MCI in an adjusted 21.5% of those without heart failure and in 26.2% of those with heart failure, said Dr. Witt. Adjustments were for factors such as age, sex, location, education, hypertension, diabetes, depression, alcohol and tobacco use, cerebrovascular disease, and marital status.
The relative risk for dementia among patients with heart failure was roughly similar, regardless of whether ARIC participants had a reduced or preserved left ventricular ejection fraction, she said.
ARIC is funded by the National Heart, Lung, and Blood Institute. Dr. Witt had no disclosures.
—Mitchel L. Zoler
Suggested Reading
Adelborg K, Horváth-Puhó E, Ording A, et al. Heart failure and risk of dementia: a Danish nationwide population-based cohort study. Eur J Heart Fail. 2016 Sep 9 [Epub ahead of print].
Ampadu J, Morley JE. Heart failure and cognitive dysfunction. Int J Cardiol. 2015;178:12-23.
Rusanen M, Kivipelto M, Levälahti E, et al. Heart diseases and long-term risk of dementia and Alzheimer’s disease: a population-based CAIDE study. J Alzheimers Dis. 2014;42(1):183-191.
Study Identifies Predictors of Poor Outcome in Status Epilepticus
HOUSTON—Predictors of poor outcomes in patients with status epilepticus admitted to the neurointensive care unit include complex partial status epilepticus (CPSE), refractory status epilepticus, or the development of nonconvulsive status epilepticus (NCSE), according to research presented at the 70th Annual Meeting of the American Epilepsy Society.
“Not a lot of data exist as to what predicts the poor outcomes and what’s known about the outcome in patients with status epilepticus,” said Advait Mahulikar, MD, a neurology resident at Wayne State University in Detroit.
Dr. Mahulikar and colleagues retrospectively reviewed data from 100 patients with status epilepticus who were admitted to the neurointensive care unit at Detroit Medical Center from November 2013 to January 2016. Variables of interest included patient demographics, initial presentation, refractoriness to treatment, presence or absence of underlying etiology, past history of epilepsy, and use of benzodiazepines on admission. NCSE was another variable of interest, either from initial presentation or developed during the course of convulsive status epilepticus. A good outcome was defined as a Glasgow Outcome Scale (GOS) score of 4 or 5
The mean age of the 100 patients was 58; 53% were male, 84% were African American, and 70% had a history of epilepsy. The median hospital length of stay was seven days and the median neurointensive care unit length of stay was three days. Good outcomes occurred in 69 patients.
Neither age nor gender predicted poor outcome, and there was no difference in outcome between structural and nonstructural causes of status epilepticus. However, prior history of epilepsy was a strong negative predictor of poor outcome. Fourteen out of 70 patients (20%) with a prior history of epilepsy had a poor outcome. “The theory is that [these patients] were already on treatment for epilepsy in the past and that affected their outcome in a positive way,” said Dr. Mahulikar.
When outcome was analyzed based on status semiology on initial presentation, poor outcome was observed in 16 of the 37 patients (43%) with CPSE, nine of 48 patients (19%) with generalized convulsive status epilepticus, all patients with myoclonic status epilepticus (n = 2), and three of nine (33%) who had NCSE. The type of status epilepticus was unknown for four patients, one of whom had an unknown outcome. NCSE at any time during the hospital course was seen in 31 patients; 14 (45%) had a poor outcome.
The mean number of ventilator days was higher in patients with NCSE than in those without NCSE (9.2 vs 1.6 days) and also higher in those with new-onset seizures than in those without (7.8 vs. 2.9 days). Analysis of methods of treatment revealed that only seven of 31 (22.5%) patients who received adequate benzodiazepine dosing had poor outcomes.
“The take-home message is to diagnose NCSE as early as possible,” said Dr. Mahulikar. Neurologists may attribute some cases incorrectly to metabolic or autoimmune causes on their initial presentation. “Treat aggressively at the beginning,” Dr. Mahulikar advised.
—Doug Brunk
Suggested Reading
Power KN, Gramstad A, Gilhus NE, Englesen BA. Prognostic factors of status epilepticus in adults. Epileptic Disord. 2016;18(3):297-304.
Sutter R, De Marchis GM, Semmlack S, et al. Anesthetics and outcome in status epilepticus: A matched two-center cohort study. CNS Drugs. 2017;31(1):655-674.
HOUSTON—Predictors of poor outcomes in patients with status epilepticus admitted to the neurointensive care unit include complex partial status epilepticus (CPSE), refractory status epilepticus, or the development of nonconvulsive status epilepticus (NCSE), according to research presented at the 70th Annual Meeting of the American Epilepsy Society.
“Not a lot of data exist as to what predicts the poor outcomes and what’s known about the outcome in patients with status epilepticus,” said Advait Mahulikar, MD, a neurology resident at Wayne State University in Detroit.
Dr. Mahulikar and colleagues retrospectively reviewed data from 100 patients with status epilepticus who were admitted to the neurointensive care unit at Detroit Medical Center from November 2013 to January 2016. Variables of interest included patient demographics, initial presentation, refractoriness to treatment, presence or absence of underlying etiology, past history of epilepsy, and use of benzodiazepines on admission. NCSE was another variable of interest, either from initial presentation or developed during the course of convulsive status epilepticus. A good outcome was defined as a Glasgow Outcome Scale (GOS) score of 4 or 5
The mean age of the 100 patients was 58; 53% were male, 84% were African American, and 70% had a history of epilepsy. The median hospital length of stay was seven days and the median neurointensive care unit length of stay was three days. Good outcomes occurred in 69 patients.
Neither age nor gender predicted poor outcome, and there was no difference in outcome between structural and nonstructural causes of status epilepticus. However, prior history of epilepsy was a strong negative predictor of poor outcome. Fourteen out of 70 patients (20%) with a prior history of epilepsy had a poor outcome. “The theory is that [these patients] were already on treatment for epilepsy in the past and that affected their outcome in a positive way,” said Dr. Mahulikar.
When outcome was analyzed based on status semiology on initial presentation, poor outcome was observed in 16 of the 37 patients (43%) with CPSE, nine of 48 patients (19%) with generalized convulsive status epilepticus, all patients with myoclonic status epilepticus (n = 2), and three of nine (33%) who had NCSE. The type of status epilepticus was unknown for four patients, one of whom had an unknown outcome. NCSE at any time during the hospital course was seen in 31 patients; 14 (45%) had a poor outcome.
The mean number of ventilator days was higher in patients with NCSE than in those without NCSE (9.2 vs 1.6 days) and also higher in those with new-onset seizures than in those without (7.8 vs. 2.9 days). Analysis of methods of treatment revealed that only seven of 31 (22.5%) patients who received adequate benzodiazepine dosing had poor outcomes.
“The take-home message is to diagnose NCSE as early as possible,” said Dr. Mahulikar. Neurologists may attribute some cases incorrectly to metabolic or autoimmune causes on their initial presentation. “Treat aggressively at the beginning,” Dr. Mahulikar advised.
—Doug Brunk
Suggested Reading
Power KN, Gramstad A, Gilhus NE, Englesen BA. Prognostic factors of status epilepticus in adults. Epileptic Disord. 2016;18(3):297-304.
Sutter R, De Marchis GM, Semmlack S, et al. Anesthetics and outcome in status epilepticus: A matched two-center cohort study. CNS Drugs. 2017;31(1):655-674.
HOUSTON—Predictors of poor outcomes in patients with status epilepticus admitted to the neurointensive care unit include complex partial status epilepticus (CPSE), refractory status epilepticus, or the development of nonconvulsive status epilepticus (NCSE), according to research presented at the 70th Annual Meeting of the American Epilepsy Society.
“Not a lot of data exist as to what predicts the poor outcomes and what’s known about the outcome in patients with status epilepticus,” said Advait Mahulikar, MD, a neurology resident at Wayne State University in Detroit.
Dr. Mahulikar and colleagues retrospectively reviewed data from 100 patients with status epilepticus who were admitted to the neurointensive care unit at Detroit Medical Center from November 2013 to January 2016. Variables of interest included patient demographics, initial presentation, refractoriness to treatment, presence or absence of underlying etiology, past history of epilepsy, and use of benzodiazepines on admission. NCSE was another variable of interest, either from initial presentation or developed during the course of convulsive status epilepticus. A good outcome was defined as a Glasgow Outcome Scale (GOS) score of 4 or 5
The mean age of the 100 patients was 58; 53% were male, 84% were African American, and 70% had a history of epilepsy. The median hospital length of stay was seven days and the median neurointensive care unit length of stay was three days. Good outcomes occurred in 69 patients.
Neither age nor gender predicted poor outcome, and there was no difference in outcome between structural and nonstructural causes of status epilepticus. However, prior history of epilepsy was a strong negative predictor of poor outcome. Fourteen out of 70 patients (20%) with a prior history of epilepsy had a poor outcome. “The theory is that [these patients] were already on treatment for epilepsy in the past and that affected their outcome in a positive way,” said Dr. Mahulikar.
When outcome was analyzed based on status semiology on initial presentation, poor outcome was observed in 16 of the 37 patients (43%) with CPSE, nine of 48 patients (19%) with generalized convulsive status epilepticus, all patients with myoclonic status epilepticus (n = 2), and three of nine (33%) who had NCSE. The type of status epilepticus was unknown for four patients, one of whom had an unknown outcome. NCSE at any time during the hospital course was seen in 31 patients; 14 (45%) had a poor outcome.
The mean number of ventilator days was higher in patients with NCSE than in those without NCSE (9.2 vs 1.6 days) and also higher in those with new-onset seizures than in those without (7.8 vs. 2.9 days). Analysis of methods of treatment revealed that only seven of 31 (22.5%) patients who received adequate benzodiazepine dosing had poor outcomes.
“The take-home message is to diagnose NCSE as early as possible,” said Dr. Mahulikar. Neurologists may attribute some cases incorrectly to metabolic or autoimmune causes on their initial presentation. “Treat aggressively at the beginning,” Dr. Mahulikar advised.
—Doug Brunk
Suggested Reading
Power KN, Gramstad A, Gilhus NE, Englesen BA. Prognostic factors of status epilepticus in adults. Epileptic Disord. 2016;18(3):297-304.
Sutter R, De Marchis GM, Semmlack S, et al. Anesthetics and outcome in status epilepticus: A matched two-center cohort study. CNS Drugs. 2017;31(1):655-674.
Trump administration reinstates global gag rule on abortion
President Trump has reinstated and expanded the Mexico City policy prohibiting foreign nongovernmental organizations from offering counseling or referrals for abortion services if they receive funding from the U.S. government.
Mr. Trump’s executive order on Jan. 23 was not unexpected given his conservative platform on reproductive health care; however, he has taken the policy – also known as the global gag rule – further than his predecessors.
Originally instituted under President Reagan, the Mexico City Policy required overseas organizations to certify that they would not “perform or actively promote abortion as a method of family planning” using non–U.S. funds in order to receive family planning aid from the U.S. government. The policy has been rescinded and enforced periodically since 1984, based on the ideologic slant of successive U.S. administrations.
The Trump iteration of the Mexico City Policy “extends the requirements of the reinstated memorandum to global health assistance furnished by all departments and agencies,” according to the White House.
Planned Parenthood Global condemned the expanded policy, which now affects international organizations working on any U.S.–funded global health initiative, including HIV/AIDS prevention and treatment, maternal and child health, and Zika virus programs. These groups will be stripped of all U.S. aid if they also provide abortion counseling, referrals, or services for abortion, even with their own funds.
“This is an unprecedented move, and the most extreme executive action we’ve seen of its kind,” Latanya Mapp Frett, executive director, said in a statement. “The global gag rule, as it existed under previous anti–women’s health presidents, was deeply harmful. But this action will be catastrophic for all communities, especially those relying on U.S. funding to address HIV/AIDS and maternal health care, and the fight against Zika.”
The expansion of the Mexico City Policy “certainly does presage negative things for abortion and contraception” under the new administration, said Sarah W. Prager, MD, of the department of obstetrics and gynecology at the University of Washington, Seattle. “Another example is the [Jan. 24] passage in the House of Representatives of H.R. 7, which would make permanent the Hyde Amendment and deny our most disadvantaged women access to abortion.”
The American Association of Pro-Life Obstetricians and Gynecologists took a different stance. “The Mexico City Policy was instituted to prevent the U.S. from forcing taxpayers to fund abortion overseas,” said Donna J. Harrison, MD, executive director. “This policy has been intermittently in place since 1984 and represents no departure from previous policies implemented by pro-life presidents.”
AAPLOG supports reinstating this policy because elective abortion “is not a part of essential women’s health care, and, in fact, is an elective procedure,” Dr. Harrison said.
President Trump has reinstated and expanded the Mexico City policy prohibiting foreign nongovernmental organizations from offering counseling or referrals for abortion services if they receive funding from the U.S. government.
Mr. Trump’s executive order on Jan. 23 was not unexpected given his conservative platform on reproductive health care; however, he has taken the policy – also known as the global gag rule – further than his predecessors.
Originally instituted under President Reagan, the Mexico City Policy required overseas organizations to certify that they would not “perform or actively promote abortion as a method of family planning” using non–U.S. funds in order to receive family planning aid from the U.S. government. The policy has been rescinded and enforced periodically since 1984, based on the ideologic slant of successive U.S. administrations.
The Trump iteration of the Mexico City Policy “extends the requirements of the reinstated memorandum to global health assistance furnished by all departments and agencies,” according to the White House.
Planned Parenthood Global condemned the expanded policy, which now affects international organizations working on any U.S.–funded global health initiative, including HIV/AIDS prevention and treatment, maternal and child health, and Zika virus programs. These groups will be stripped of all U.S. aid if they also provide abortion counseling, referrals, or services for abortion, even with their own funds.
“This is an unprecedented move, and the most extreme executive action we’ve seen of its kind,” Latanya Mapp Frett, executive director, said in a statement. “The global gag rule, as it existed under previous anti–women’s health presidents, was deeply harmful. But this action will be catastrophic for all communities, especially those relying on U.S. funding to address HIV/AIDS and maternal health care, and the fight against Zika.”
The expansion of the Mexico City Policy “certainly does presage negative things for abortion and contraception” under the new administration, said Sarah W. Prager, MD, of the department of obstetrics and gynecology at the University of Washington, Seattle. “Another example is the [Jan. 24] passage in the House of Representatives of H.R. 7, which would make permanent the Hyde Amendment and deny our most disadvantaged women access to abortion.”
The American Association of Pro-Life Obstetricians and Gynecologists took a different stance. “The Mexico City Policy was instituted to prevent the U.S. from forcing taxpayers to fund abortion overseas,” said Donna J. Harrison, MD, executive director. “This policy has been intermittently in place since 1984 and represents no departure from previous policies implemented by pro-life presidents.”
AAPLOG supports reinstating this policy because elective abortion “is not a part of essential women’s health care, and, in fact, is an elective procedure,” Dr. Harrison said.
President Trump has reinstated and expanded the Mexico City policy prohibiting foreign nongovernmental organizations from offering counseling or referrals for abortion services if they receive funding from the U.S. government.
Mr. Trump’s executive order on Jan. 23 was not unexpected given his conservative platform on reproductive health care; however, he has taken the policy – also known as the global gag rule – further than his predecessors.
Originally instituted under President Reagan, the Mexico City Policy required overseas organizations to certify that they would not “perform or actively promote abortion as a method of family planning” using non–U.S. funds in order to receive family planning aid from the U.S. government. The policy has been rescinded and enforced periodically since 1984, based on the ideologic slant of successive U.S. administrations.
The Trump iteration of the Mexico City Policy “extends the requirements of the reinstated memorandum to global health assistance furnished by all departments and agencies,” according to the White House.
Planned Parenthood Global condemned the expanded policy, which now affects international organizations working on any U.S.–funded global health initiative, including HIV/AIDS prevention and treatment, maternal and child health, and Zika virus programs. These groups will be stripped of all U.S. aid if they also provide abortion counseling, referrals, or services for abortion, even with their own funds.
“This is an unprecedented move, and the most extreme executive action we’ve seen of its kind,” Latanya Mapp Frett, executive director, said in a statement. “The global gag rule, as it existed under previous anti–women’s health presidents, was deeply harmful. But this action will be catastrophic for all communities, especially those relying on U.S. funding to address HIV/AIDS and maternal health care, and the fight against Zika.”
The expansion of the Mexico City Policy “certainly does presage negative things for abortion and contraception” under the new administration, said Sarah W. Prager, MD, of the department of obstetrics and gynecology at the University of Washington, Seattle. “Another example is the [Jan. 24] passage in the House of Representatives of H.R. 7, which would make permanent the Hyde Amendment and deny our most disadvantaged women access to abortion.”
The American Association of Pro-Life Obstetricians and Gynecologists took a different stance. “The Mexico City Policy was instituted to prevent the U.S. from forcing taxpayers to fund abortion overseas,” said Donna J. Harrison, MD, executive director. “This policy has been intermittently in place since 1984 and represents no departure from previous policies implemented by pro-life presidents.”
AAPLOG supports reinstating this policy because elective abortion “is not a part of essential women’s health care, and, in fact, is an elective procedure,” Dr. Harrison said.
Incidence of IBD is elevated in hidradenitis suppurativa patients
Individuals with hidradenitis suppurativa (HS) may be at significantly greater risk of inflammatory bowel conditions such as Crohn’s disease and ulcerative colitis, according to a Danish populationwide cohort study.
“In HS patients presenting with gastrointestinal complaints, timely referral for gastroenterological evaluation of IBD [inflammatory bowel disease] may be appropriate,” Alexander Egeberg, MD, of the University of Copenhagen and his coauthors wrote.
Similarly, the incidence of ulcerative colitis was about 1.8-fold higher among individuals with HS, compared with controls (1.3% vs. 0.7%; OR, 1.75; P less than .002), and the incidence of “unspecified” inflammatory bowel disease was 3.4-fold higher (0.7% vs. 0.1%; OR, 3.40; P less than .007), according to a paper published online in the Journal of Investigative Dermatology.
Dr. Egeberg and his coauthors reported that HS and inflammatory bowel disease similarities suggest a shared pathogenesis, including the worsening effect of smoking on both conditions; the appearance of scarring and sinus tract formation; the apparent involvement of T-helper 17 cells, interleukin-23, and tumor necrosis factor; and the coinvolvement of genes such as SULT1B1 and SULT1E1 (J Invest Dermatol. 2017 Jan 13. doi: 10.1016/j.jid.2016.11.040).
“Finally, an increased prevalence of spondylarthropathy has been reported in patients with IBD as well as in those with HS, raising the hypothesis that genetic, epigenetic, and/or environmental factors cooperate to lead to dysregulated inflammatory pathways across these immune-mediated diseases,” the authors wrote.
While previous study evidence linking HS and IBD has been inconsistent, the authors said their findings suggested an increased incidence of IBD in individuals with HS – ranging from 0.13 to 0.97 per 1,000 HS patients per year.
They acknowledged that the study population was predominantly of Northern European descent, and the results might not be generalizable to patients of other ethnicities. They also noted that patients with HS identified by hospital diagnoses may therefore have had greater comorbidity than patients sampled from a population setting.
The study was funded by Eli Lilly, and one author is an employee of Eli Lilly. Five other authors declared research funding, grants, consultancies, honoraria, consultancy, and board positions for various pharmaceutical companies, including Eli Lilly.
Individuals with hidradenitis suppurativa (HS) may be at significantly greater risk of inflammatory bowel conditions such as Crohn’s disease and ulcerative colitis, according to a Danish populationwide cohort study.
“In HS patients presenting with gastrointestinal complaints, timely referral for gastroenterological evaluation of IBD [inflammatory bowel disease] may be appropriate,” Alexander Egeberg, MD, of the University of Copenhagen and his coauthors wrote.
Similarly, the incidence of ulcerative colitis was about 1.8-fold higher among individuals with HS, compared with controls (1.3% vs. 0.7%; OR, 1.75; P less than .002), and the incidence of “unspecified” inflammatory bowel disease was 3.4-fold higher (0.7% vs. 0.1%; OR, 3.40; P less than .007), according to a paper published online in the Journal of Investigative Dermatology.
Dr. Egeberg and his coauthors reported that HS and inflammatory bowel disease similarities suggest a shared pathogenesis, including the worsening effect of smoking on both conditions; the appearance of scarring and sinus tract formation; the apparent involvement of T-helper 17 cells, interleukin-23, and tumor necrosis factor; and the coinvolvement of genes such as SULT1B1 and SULT1E1 (J Invest Dermatol. 2017 Jan 13. doi: 10.1016/j.jid.2016.11.040).
“Finally, an increased prevalence of spondylarthropathy has been reported in patients with IBD as well as in those with HS, raising the hypothesis that genetic, epigenetic, and/or environmental factors cooperate to lead to dysregulated inflammatory pathways across these immune-mediated diseases,” the authors wrote.
While previous study evidence linking HS and IBD has been inconsistent, the authors said their findings suggested an increased incidence of IBD in individuals with HS – ranging from 0.13 to 0.97 per 1,000 HS patients per year.
They acknowledged that the study population was predominantly of Northern European descent, and the results might not be generalizable to patients of other ethnicities. They also noted that patients with HS identified by hospital diagnoses may therefore have had greater comorbidity than patients sampled from a population setting.
The study was funded by Eli Lilly, and one author is an employee of Eli Lilly. Five other authors declared research funding, grants, consultancies, honoraria, consultancy, and board positions for various pharmaceutical companies, including Eli Lilly.
Individuals with hidradenitis suppurativa (HS) may be at significantly greater risk of inflammatory bowel conditions such as Crohn’s disease and ulcerative colitis, according to a Danish populationwide cohort study.
“In HS patients presenting with gastrointestinal complaints, timely referral for gastroenterological evaluation of IBD [inflammatory bowel disease] may be appropriate,” Alexander Egeberg, MD, of the University of Copenhagen and his coauthors wrote.
Similarly, the incidence of ulcerative colitis was about 1.8-fold higher among individuals with HS, compared with controls (1.3% vs. 0.7%; OR, 1.75; P less than .002), and the incidence of “unspecified” inflammatory bowel disease was 3.4-fold higher (0.7% vs. 0.1%; OR, 3.40; P less than .007), according to a paper published online in the Journal of Investigative Dermatology.
Dr. Egeberg and his coauthors reported that HS and inflammatory bowel disease similarities suggest a shared pathogenesis, including the worsening effect of smoking on both conditions; the appearance of scarring and sinus tract formation; the apparent involvement of T-helper 17 cells, interleukin-23, and tumor necrosis factor; and the coinvolvement of genes such as SULT1B1 and SULT1E1 (J Invest Dermatol. 2017 Jan 13. doi: 10.1016/j.jid.2016.11.040).
“Finally, an increased prevalence of spondylarthropathy has been reported in patients with IBD as well as in those with HS, raising the hypothesis that genetic, epigenetic, and/or environmental factors cooperate to lead to dysregulated inflammatory pathways across these immune-mediated diseases,” the authors wrote.
While previous study evidence linking HS and IBD has been inconsistent, the authors said their findings suggested an increased incidence of IBD in individuals with HS – ranging from 0.13 to 0.97 per 1,000 HS patients per year.
They acknowledged that the study population was predominantly of Northern European descent, and the results might not be generalizable to patients of other ethnicities. They also noted that patients with HS identified by hospital diagnoses may therefore have had greater comorbidity than patients sampled from a population setting.
The study was funded by Eli Lilly, and one author is an employee of Eli Lilly. Five other authors declared research funding, grants, consultancies, honoraria, consultancy, and board positions for various pharmaceutical companies, including Eli Lilly.
FROM THE JOURNAL OF INVESTIGATIVE DERMATOLOGY
Key clinical point: Individuals with hidradenitis suppurativa may be at significantly greater risk of inflammatory bowel conditions such as Crohn’s disease and ulcerative colitis.
Major finding: The baseline prevalence of Crohn’s disease is twofold higher, and ulcerative colitis is about 1.8-fold higher, in individuals with hidradenitis suppurativa, compared with the general population.
Data source: A population-based cohort study in 7,732 patients with a hospital diagnosis of hidradenitis suppurativa, and 4,354,137 controls.
Disclosures: The study was funded by Eli Lilly, and one author is an employee of Eli Lilly. Five other authors declared research funding, grants, consultancies, honoraria, consultancy, and board positions for various pharmaceutical companies, including Eli Lilly.
Evidence supports efficacy of topical skin products for photoaging reversal
MIAMI – Topical skin care products are evolving along with evidence in the literature supporting their efficacy; these products include serums, lotions, and cleansers with DNA repair enzymes or epidermal growth factor as active ingredients, according to Ron Moy, MD.
Importantly, some of these formulations not only show efficacy to reverse the signs of photodamage to skin and to promote rejuvenation, but may have a role in skin cancer prevention as well, said Dr. Moy, a dermatologist and facial plastic surgeon in private practice in Beverly Hills, Calif.
More investigators are assessing the mechanisms and potential advantages of DNA repair, Dr. Moy said at the Orlando Dermatology Aesthetic and Clinical Conference. In 2015, the Nobel Prize in Chemistry was awarded to scientists who discovered key mechanisms underlying DNA repair. “Since then, DNA repair has gotten a lot more attention,” he said.
Evidence suggests a person’s DNA repair capability can modulate colon cancer risk. Also, smokers with a low level of DNA repair enzymes carry a higher risk for lung cancer, and DNA repair genes can predict ovarian cancer and lung cancer survival, Dr. Moy said.
“It is still not entirely understood how everything ties together,” he said. “But the work on DNA repair is convincing, more convincing than work on antioxidants or retinoids.” Although antioxidants look favorable in experimental and animal studies, for example, “generally the published work on antioxidants does not give you good clinical results,” he said.
DNA repair enzymes have a beneficial effect on the proto-oncogene hyperexpression in human skin and ultraviolet light telomere shortening, according to an experimental pilot study in the Journal of Drugs in Dermatology (2013 Sep;12[9]:1017-21).
Also, a DNA repair enzyme derived from bacteria, T4 endonuclease V, showed promise in an older study of 30 patients with xeroderma pigmentosum (Lancet. 2001 Mar 24;357[9260]:926-9). Those affected carry a higher risk overall for any skin cancer, compared with the general population. The DNA repair enzyme group had fewer new actinic keratoses and fewer new basal cell carcinoma, squamous cell carcinomas, and melanoma lesions at 1 year, compared with a vehicle-only group at 1 year.
Another class of DNA repair molecules, photolyases, is newer than T4 endonuclease V and “might work even better,” Dr. Moy said.
“There is evidence that DNA enzymes are very effective and helpful in preventing skin cancer,” he pointed out. One mechanism is the ability of exogenous DNA repair enzymes to bolster intrinsic DNA in the fight against carcinogenesis, according to a review article Dr. Moy and his colleagues published in the Journal of Drugs in Dermatology (2015 Mar;14[3]:297-303).
The role of human epidermal growth factor for improving skin appearance and tightening is another area of active research and promise.
“It basically thickens and tightens skin,” Dr. Moy explained. “It works better on thinner skin, including the eyelids and neck.” Ultrasound objectively demonstrates gains in skin thickness. Studies also show improvement in acne scars following application of epidermal growth factor.
In addition, epidermal growth factor can enhance the appearance of solar purpura. In fact, this is the dermatologic condition with the most convincing evidence supporting its use so far, Dr. Moy said. Clinical studies have shown that epidermal growth factor along with other active ingredients also can improve acne scars and eye bags.
During the question and answer session at the ODAC conference, moderator Susan Weinkle, MD, a dermatologist and Mohs surgeon in private practice in Bradenton, Fla., asked Dr. Moy which epidermal growth factor product he recommends.
“There are a lot of different growth factors. Epidermal growth factors are not all the same,” said Dr. Moy, who is the founder of DNA EGF Renewal, a company that manufactures skin care products containing epidermal growth factor and DNA repair enzymes.
When pressed for the name of his growth factor product by Dr. Weinkle and an uproar from the audience, Dr. Moy chose to stay noncommercial, pointing attendees to his website instead: www.dnaegfrenewal.com.
Dr. Moy is founder of DNA EGF Renewal in Beverly Hills, Calif.
MIAMI – Topical skin care products are evolving along with evidence in the literature supporting their efficacy; these products include serums, lotions, and cleansers with DNA repair enzymes or epidermal growth factor as active ingredients, according to Ron Moy, MD.
Importantly, some of these formulations not only show efficacy to reverse the signs of photodamage to skin and to promote rejuvenation, but may have a role in skin cancer prevention as well, said Dr. Moy, a dermatologist and facial plastic surgeon in private practice in Beverly Hills, Calif.
More investigators are assessing the mechanisms and potential advantages of DNA repair, Dr. Moy said at the Orlando Dermatology Aesthetic and Clinical Conference. In 2015, the Nobel Prize in Chemistry was awarded to scientists who discovered key mechanisms underlying DNA repair. “Since then, DNA repair has gotten a lot more attention,” he said.
Evidence suggests a person’s DNA repair capability can modulate colon cancer risk. Also, smokers with a low level of DNA repair enzymes carry a higher risk for lung cancer, and DNA repair genes can predict ovarian cancer and lung cancer survival, Dr. Moy said.
“It is still not entirely understood how everything ties together,” he said. “But the work on DNA repair is convincing, more convincing than work on antioxidants or retinoids.” Although antioxidants look favorable in experimental and animal studies, for example, “generally the published work on antioxidants does not give you good clinical results,” he said.
DNA repair enzymes have a beneficial effect on the proto-oncogene hyperexpression in human skin and ultraviolet light telomere shortening, according to an experimental pilot study in the Journal of Drugs in Dermatology (2013 Sep;12[9]:1017-21).
Also, a DNA repair enzyme derived from bacteria, T4 endonuclease V, showed promise in an older study of 30 patients with xeroderma pigmentosum (Lancet. 2001 Mar 24;357[9260]:926-9). Those affected carry a higher risk overall for any skin cancer, compared with the general population. The DNA repair enzyme group had fewer new actinic keratoses and fewer new basal cell carcinoma, squamous cell carcinomas, and melanoma lesions at 1 year, compared with a vehicle-only group at 1 year.
Another class of DNA repair molecules, photolyases, is newer than T4 endonuclease V and “might work even better,” Dr. Moy said.
“There is evidence that DNA enzymes are very effective and helpful in preventing skin cancer,” he pointed out. One mechanism is the ability of exogenous DNA repair enzymes to bolster intrinsic DNA in the fight against carcinogenesis, according to a review article Dr. Moy and his colleagues published in the Journal of Drugs in Dermatology (2015 Mar;14[3]:297-303).
The role of human epidermal growth factor for improving skin appearance and tightening is another area of active research and promise.
“It basically thickens and tightens skin,” Dr. Moy explained. “It works better on thinner skin, including the eyelids and neck.” Ultrasound objectively demonstrates gains in skin thickness. Studies also show improvement in acne scars following application of epidermal growth factor.
In addition, epidermal growth factor can enhance the appearance of solar purpura. In fact, this is the dermatologic condition with the most convincing evidence supporting its use so far, Dr. Moy said. Clinical studies have shown that epidermal growth factor along with other active ingredients also can improve acne scars and eye bags.
During the question and answer session at the ODAC conference, moderator Susan Weinkle, MD, a dermatologist and Mohs surgeon in private practice in Bradenton, Fla., asked Dr. Moy which epidermal growth factor product he recommends.
“There are a lot of different growth factors. Epidermal growth factors are not all the same,” said Dr. Moy, who is the founder of DNA EGF Renewal, a company that manufactures skin care products containing epidermal growth factor and DNA repair enzymes.
When pressed for the name of his growth factor product by Dr. Weinkle and an uproar from the audience, Dr. Moy chose to stay noncommercial, pointing attendees to his website instead: www.dnaegfrenewal.com.
Dr. Moy is founder of DNA EGF Renewal in Beverly Hills, Calif.
MIAMI – Topical skin care products are evolving along with evidence in the literature supporting their efficacy; these products include serums, lotions, and cleansers with DNA repair enzymes or epidermal growth factor as active ingredients, according to Ron Moy, MD.
Importantly, some of these formulations not only show efficacy to reverse the signs of photodamage to skin and to promote rejuvenation, but may have a role in skin cancer prevention as well, said Dr. Moy, a dermatologist and facial plastic surgeon in private practice in Beverly Hills, Calif.
More investigators are assessing the mechanisms and potential advantages of DNA repair, Dr. Moy said at the Orlando Dermatology Aesthetic and Clinical Conference. In 2015, the Nobel Prize in Chemistry was awarded to scientists who discovered key mechanisms underlying DNA repair. “Since then, DNA repair has gotten a lot more attention,” he said.
Evidence suggests a person’s DNA repair capability can modulate colon cancer risk. Also, smokers with a low level of DNA repair enzymes carry a higher risk for lung cancer, and DNA repair genes can predict ovarian cancer and lung cancer survival, Dr. Moy said.
“It is still not entirely understood how everything ties together,” he said. “But the work on DNA repair is convincing, more convincing than work on antioxidants or retinoids.” Although antioxidants look favorable in experimental and animal studies, for example, “generally the published work on antioxidants does not give you good clinical results,” he said.
DNA repair enzymes have a beneficial effect on the proto-oncogene hyperexpression in human skin and ultraviolet light telomere shortening, according to an experimental pilot study in the Journal of Drugs in Dermatology (2013 Sep;12[9]:1017-21).
Also, a DNA repair enzyme derived from bacteria, T4 endonuclease V, showed promise in an older study of 30 patients with xeroderma pigmentosum (Lancet. 2001 Mar 24;357[9260]:926-9). Those affected carry a higher risk overall for any skin cancer, compared with the general population. The DNA repair enzyme group had fewer new actinic keratoses and fewer new basal cell carcinoma, squamous cell carcinomas, and melanoma lesions at 1 year, compared with a vehicle-only group at 1 year.
Another class of DNA repair molecules, photolyases, is newer than T4 endonuclease V and “might work even better,” Dr. Moy said.
“There is evidence that DNA enzymes are very effective and helpful in preventing skin cancer,” he pointed out. One mechanism is the ability of exogenous DNA repair enzymes to bolster intrinsic DNA in the fight against carcinogenesis, according to a review article Dr. Moy and his colleagues published in the Journal of Drugs in Dermatology (2015 Mar;14[3]:297-303).
The role of human epidermal growth factor for improving skin appearance and tightening is another area of active research and promise.
“It basically thickens and tightens skin,” Dr. Moy explained. “It works better on thinner skin, including the eyelids and neck.” Ultrasound objectively demonstrates gains in skin thickness. Studies also show improvement in acne scars following application of epidermal growth factor.
In addition, epidermal growth factor can enhance the appearance of solar purpura. In fact, this is the dermatologic condition with the most convincing evidence supporting its use so far, Dr. Moy said. Clinical studies have shown that epidermal growth factor along with other active ingredients also can improve acne scars and eye bags.
During the question and answer session at the ODAC conference, moderator Susan Weinkle, MD, a dermatologist and Mohs surgeon in private practice in Bradenton, Fla., asked Dr. Moy which epidermal growth factor product he recommends.
“There are a lot of different growth factors. Epidermal growth factors are not all the same,” said Dr. Moy, who is the founder of DNA EGF Renewal, a company that manufactures skin care products containing epidermal growth factor and DNA repair enzymes.
When pressed for the name of his growth factor product by Dr. Weinkle and an uproar from the audience, Dr. Moy chose to stay noncommercial, pointing attendees to his website instead: www.dnaegfrenewal.com.
Dr. Moy is founder of DNA EGF Renewal in Beverly Hills, Calif.
EXPERT ANALYSIS FROM ODAC 2017