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Study links mumps outbreaks to vaccine waning
A new study links recent mumps outbreaks to the waning of the mumps vaccine – which researchers believe wears off in an average of 27 years – and not to heterologous virus genotypes.
“These observations indicate the need for either innovative clinical trial designs to measure the benefit of extending vaccine dosing schedules or new vaccines to address the problem of waning vaccine-induced protection,” the study authors wrote. The findings appeared in Science Translational Medicine.
The numbers over the past 2 years are the highest numbers by far since 2000, with the exception of 2006. The CDC attributes the 2016 and 2017 numbers to factors such as “the known effectiveness of the vaccine, waning immunity following vaccination, and the intensity of exposure to the virus in close-contact settings [such as a college campus] coupled with behaviors that increase the risk of transmission.”
This year, as of Feb. 24, the CDC stated that it has received reports of 304 cases in 32 states and Washington.
For the new study, Joseph A. Lewnard, PhD, and Yonatan H. Grad, MD, PhD, of the Harvard School of Public Health, Boston, examined six studies and estimated that mumps vaccinations provide protection for an average of 27 years (95% confidence interval, 16-51 years). They also reported finding no evidence that the effectiveness of vaccines was affected by new heterologous virus genotypes.
Their analysis also determined that outbreaks in the late 1980s and early 1990s (among teens), and from 2006 to present (in young adults), “aligned with peaks in mumps susceptibility of these age groups predicted to be due to loss of vaccine-derived protection.”
The authors suggested that third doses of vaccine or an improved mumps vaccine could provide added protection. “Although congregated U.S. military populations resemble high-risk groups based on their age distribution and close-contact environments, no outbreaks have been reported in the military since a policy of administering an MMR dose to incoming recruits, regardless of vaccination history, was adopted in 1991,” the researchers wrote, referring to a 2008 study (Vaccine 2008, 26:494-501).
For now, however, “we expect population susceptibility to mumps to continue increasing as transient vaccine-derived immunity supersedes previous infection as the main determinant of mumps susceptibility in the U.S. population,” the authors wrote.
The study was funded by awards from the National Institute of General Medical Sciences and the Doris Duke Charitable Foundation. The study authors report grant funding (Pfizer) and consulting (Pfizer, GlaxoSmithKline) for work unrelated to the study.
SOURCE: Lenward JA et al. Sci Transl Med. 2018 Mar 21. doi: 10.1126/scitranslmed.aao5945.
A new study links recent mumps outbreaks to the waning of the mumps vaccine – which researchers believe wears off in an average of 27 years – and not to heterologous virus genotypes.
“These observations indicate the need for either innovative clinical trial designs to measure the benefit of extending vaccine dosing schedules or new vaccines to address the problem of waning vaccine-induced protection,” the study authors wrote. The findings appeared in Science Translational Medicine.
The numbers over the past 2 years are the highest numbers by far since 2000, with the exception of 2006. The CDC attributes the 2016 and 2017 numbers to factors such as “the known effectiveness of the vaccine, waning immunity following vaccination, and the intensity of exposure to the virus in close-contact settings [such as a college campus] coupled with behaviors that increase the risk of transmission.”
This year, as of Feb. 24, the CDC stated that it has received reports of 304 cases in 32 states and Washington.
For the new study, Joseph A. Lewnard, PhD, and Yonatan H. Grad, MD, PhD, of the Harvard School of Public Health, Boston, examined six studies and estimated that mumps vaccinations provide protection for an average of 27 years (95% confidence interval, 16-51 years). They also reported finding no evidence that the effectiveness of vaccines was affected by new heterologous virus genotypes.
Their analysis also determined that outbreaks in the late 1980s and early 1990s (among teens), and from 2006 to present (in young adults), “aligned with peaks in mumps susceptibility of these age groups predicted to be due to loss of vaccine-derived protection.”
The authors suggested that third doses of vaccine or an improved mumps vaccine could provide added protection. “Although congregated U.S. military populations resemble high-risk groups based on their age distribution and close-contact environments, no outbreaks have been reported in the military since a policy of administering an MMR dose to incoming recruits, regardless of vaccination history, was adopted in 1991,” the researchers wrote, referring to a 2008 study (Vaccine 2008, 26:494-501).
For now, however, “we expect population susceptibility to mumps to continue increasing as transient vaccine-derived immunity supersedes previous infection as the main determinant of mumps susceptibility in the U.S. population,” the authors wrote.
The study was funded by awards from the National Institute of General Medical Sciences and the Doris Duke Charitable Foundation. The study authors report grant funding (Pfizer) and consulting (Pfizer, GlaxoSmithKline) for work unrelated to the study.
SOURCE: Lenward JA et al. Sci Transl Med. 2018 Mar 21. doi: 10.1126/scitranslmed.aao5945.
A new study links recent mumps outbreaks to the waning of the mumps vaccine – which researchers believe wears off in an average of 27 years – and not to heterologous virus genotypes.
“These observations indicate the need for either innovative clinical trial designs to measure the benefit of extending vaccine dosing schedules or new vaccines to address the problem of waning vaccine-induced protection,” the study authors wrote. The findings appeared in Science Translational Medicine.
The numbers over the past 2 years are the highest numbers by far since 2000, with the exception of 2006. The CDC attributes the 2016 and 2017 numbers to factors such as “the known effectiveness of the vaccine, waning immunity following vaccination, and the intensity of exposure to the virus in close-contact settings [such as a college campus] coupled with behaviors that increase the risk of transmission.”
This year, as of Feb. 24, the CDC stated that it has received reports of 304 cases in 32 states and Washington.
For the new study, Joseph A. Lewnard, PhD, and Yonatan H. Grad, MD, PhD, of the Harvard School of Public Health, Boston, examined six studies and estimated that mumps vaccinations provide protection for an average of 27 years (95% confidence interval, 16-51 years). They also reported finding no evidence that the effectiveness of vaccines was affected by new heterologous virus genotypes.
Their analysis also determined that outbreaks in the late 1980s and early 1990s (among teens), and from 2006 to present (in young adults), “aligned with peaks in mumps susceptibility of these age groups predicted to be due to loss of vaccine-derived protection.”
The authors suggested that third doses of vaccine or an improved mumps vaccine could provide added protection. “Although congregated U.S. military populations resemble high-risk groups based on their age distribution and close-contact environments, no outbreaks have been reported in the military since a policy of administering an MMR dose to incoming recruits, regardless of vaccination history, was adopted in 1991,” the researchers wrote, referring to a 2008 study (Vaccine 2008, 26:494-501).
For now, however, “we expect population susceptibility to mumps to continue increasing as transient vaccine-derived immunity supersedes previous infection as the main determinant of mumps susceptibility in the U.S. population,” the authors wrote.
The study was funded by awards from the National Institute of General Medical Sciences and the Doris Duke Charitable Foundation. The study authors report grant funding (Pfizer) and consulting (Pfizer, GlaxoSmithKline) for work unrelated to the study.
SOURCE: Lenward JA et al. Sci Transl Med. 2018 Mar 21. doi: 10.1126/scitranslmed.aao5945.
FROM SCIENCE TRANSLATIONAL MEDICINE
Study links RA flares after joint replacement to disease activity, not medications
Patients with the most severe cases of rheumatoid arthritis are more likely to suffer flares after knee or hip replacement surgery, a new study finds, and it doesn’t seem to matter whether they stop taking biologics before their operation.
“We found that the majority of patients had active disease at the time of surgery, contrary to prior statements that RA patients have inactive disease at the time they go for hip or knee replacement. In fact, the majority – 65% of the patients – reported a flare of RA within 6 weeks of surgery,” lead author Susan M. Goodman, MD, of Cornell University and the Hospital for Special Surgery, New York, said in an interview. “Surprisingly, although more of the flaring patients were taking potent biologics that had been withheld preoperatively, the major risk factor for flares was their baseline disease activity.”
According to Dr. Goodman, the researchers launched the study to better understand how medical decisions prior to joint replacement surgery affect the progress of RA afterward.
In terms of continuing RA drug treatment, she said, “the decision really hinges on the risk of infection versus the risk of flare, and we didn’t know the usual course of events for these patients.”
In addition, she said, “many doctors incorrectly think that the majority of patients with RA have ‘burnt-out’ or inactive disease at the time of hip or knee replacement surgery.”
For the study, the researchers prospectively followed 120 patients who were to undergo joint replacement surgery. (The researchers initially approached 354 patients, of whom 169 declined to participate. Another 65 were dropped from the study for various reasons, including 42 who did not sufficiently fill out questionnaires and were deleted from the final analysis.)
The researchers tracked the patients before surgery and for 6 weeks after surgery. A majority of the patients were female (83%) and white (81%), with a mean age of 62 and a median RA symptom duration of 15 years. A total of 44% underwent hip replacement surgery while the rest underwent knee replacement surgery. Just over half of the patients were taking biologics, which were stopped prior to surgery, while glucocorticoids and methotrexate were usually continued.
Just under two-thirds of the patients flared within the first 6 weeks after surgery. The researchers didn’t find any connection between the flares and stopping biologics or using methotrexate. They did, however, link higher baseline RA activity to postsurgery flaring (odds ratio, 2.11; P = .015).
Dr. Goodman said that she and her colleagues continue to collect data to better understand flares and the link to disease severity. “The long-term implications of this are not yet known. We would like to know the effect on long-term functional outcome and complication rate.”
The National Institutes of Health, the Weill Cornell Clinical Translational Science Center, and the Block Family Foundation supported the study. Dr. Goodman disclosed receiving research funding from Novartis and Roche.
SOURCE: Goodman S et al. J Rheumatol. 2018 Mar 15. doi: 10.3899/jrheum.170366
Patients with the most severe cases of rheumatoid arthritis are more likely to suffer flares after knee or hip replacement surgery, a new study finds, and it doesn’t seem to matter whether they stop taking biologics before their operation.
“We found that the majority of patients had active disease at the time of surgery, contrary to prior statements that RA patients have inactive disease at the time they go for hip or knee replacement. In fact, the majority – 65% of the patients – reported a flare of RA within 6 weeks of surgery,” lead author Susan M. Goodman, MD, of Cornell University and the Hospital for Special Surgery, New York, said in an interview. “Surprisingly, although more of the flaring patients were taking potent biologics that had been withheld preoperatively, the major risk factor for flares was their baseline disease activity.”
According to Dr. Goodman, the researchers launched the study to better understand how medical decisions prior to joint replacement surgery affect the progress of RA afterward.
In terms of continuing RA drug treatment, she said, “the decision really hinges on the risk of infection versus the risk of flare, and we didn’t know the usual course of events for these patients.”
In addition, she said, “many doctors incorrectly think that the majority of patients with RA have ‘burnt-out’ or inactive disease at the time of hip or knee replacement surgery.”
For the study, the researchers prospectively followed 120 patients who were to undergo joint replacement surgery. (The researchers initially approached 354 patients, of whom 169 declined to participate. Another 65 were dropped from the study for various reasons, including 42 who did not sufficiently fill out questionnaires and were deleted from the final analysis.)
The researchers tracked the patients before surgery and for 6 weeks after surgery. A majority of the patients were female (83%) and white (81%), with a mean age of 62 and a median RA symptom duration of 15 years. A total of 44% underwent hip replacement surgery while the rest underwent knee replacement surgery. Just over half of the patients were taking biologics, which were stopped prior to surgery, while glucocorticoids and methotrexate were usually continued.
Just under two-thirds of the patients flared within the first 6 weeks after surgery. The researchers didn’t find any connection between the flares and stopping biologics or using methotrexate. They did, however, link higher baseline RA activity to postsurgery flaring (odds ratio, 2.11; P = .015).
Dr. Goodman said that she and her colleagues continue to collect data to better understand flares and the link to disease severity. “The long-term implications of this are not yet known. We would like to know the effect on long-term functional outcome and complication rate.”
The National Institutes of Health, the Weill Cornell Clinical Translational Science Center, and the Block Family Foundation supported the study. Dr. Goodman disclosed receiving research funding from Novartis and Roche.
SOURCE: Goodman S et al. J Rheumatol. 2018 Mar 15. doi: 10.3899/jrheum.170366
Patients with the most severe cases of rheumatoid arthritis are more likely to suffer flares after knee or hip replacement surgery, a new study finds, and it doesn’t seem to matter whether they stop taking biologics before their operation.
“We found that the majority of patients had active disease at the time of surgery, contrary to prior statements that RA patients have inactive disease at the time they go for hip or knee replacement. In fact, the majority – 65% of the patients – reported a flare of RA within 6 weeks of surgery,” lead author Susan M. Goodman, MD, of Cornell University and the Hospital for Special Surgery, New York, said in an interview. “Surprisingly, although more of the flaring patients were taking potent biologics that had been withheld preoperatively, the major risk factor for flares was their baseline disease activity.”
According to Dr. Goodman, the researchers launched the study to better understand how medical decisions prior to joint replacement surgery affect the progress of RA afterward.
In terms of continuing RA drug treatment, she said, “the decision really hinges on the risk of infection versus the risk of flare, and we didn’t know the usual course of events for these patients.”
In addition, she said, “many doctors incorrectly think that the majority of patients with RA have ‘burnt-out’ or inactive disease at the time of hip or knee replacement surgery.”
For the study, the researchers prospectively followed 120 patients who were to undergo joint replacement surgery. (The researchers initially approached 354 patients, of whom 169 declined to participate. Another 65 were dropped from the study for various reasons, including 42 who did not sufficiently fill out questionnaires and were deleted from the final analysis.)
The researchers tracked the patients before surgery and for 6 weeks after surgery. A majority of the patients were female (83%) and white (81%), with a mean age of 62 and a median RA symptom duration of 15 years. A total of 44% underwent hip replacement surgery while the rest underwent knee replacement surgery. Just over half of the patients were taking biologics, which were stopped prior to surgery, while glucocorticoids and methotrexate were usually continued.
Just under two-thirds of the patients flared within the first 6 weeks after surgery. The researchers didn’t find any connection between the flares and stopping biologics or using methotrexate. They did, however, link higher baseline RA activity to postsurgery flaring (odds ratio, 2.11; P = .015).
Dr. Goodman said that she and her colleagues continue to collect data to better understand flares and the link to disease severity. “The long-term implications of this are not yet known. We would like to know the effect on long-term functional outcome and complication rate.”
The National Institutes of Health, the Weill Cornell Clinical Translational Science Center, and the Block Family Foundation supported the study. Dr. Goodman disclosed receiving research funding from Novartis and Roche.
SOURCE: Goodman S et al. J Rheumatol. 2018 Mar 15. doi: 10.3899/jrheum.170366
FROM JOURNAL OF RHEUMATOLOGY
Key clinical point:
Major finding: Sixty-five percent of RA patients developed flares after joint replacement surgery, and it was more common in those with higher baseline RA activity (odds ratio, 2.11; P = .015).
Study details: Prospective study of 120 patients with RA who underwent hip replacement (44%) or knee replacement (56%).
Disclosures: The National Institutes of Health, the Weill Cornell Clinical Translational Science Center, and the Block Family Foundation supported the study. The lead author disclosed receiving research funding from Novartis and Roche.
Source: Goodman S et al. J Rheumatol. 2018 Mar 15. doi: 10.3899/jrheum.170366.
Alternative oxygen therapy reduces treatment failure in bronchiolitis
High-flow oxygen therapy outside the ICU boosts the likelihood that infants with bronchiolitis will avoid treatment failure and an escalation of treatment, a study finds.
“High flow can be safely used in general emergency wards and general pediatric ward settings in regional and metropolitan hospitals that have no immediate direct access to dedicated pediatric intensive care facilities,” study coauthor Andreas Schibler, MD, of University of Queensland in Australia, said in an interview. The findings were published March 22 in the New England Journal of Medicine.
“The typical treatment for bronchiolitis is supportive therapy, providing nutrition, fluids, and if needed respiratory support including provision of oxygen,” Dr. Schibler said.
The prognosis is generally goods thanks to improvements in intensive care, he said, which some infants need because the standard oxygen therapy provided in general pediatric wards is insufficient. The new study examines whether high-flow oxygen therapy through a cannula – which he said has become more common – reduces the risk of treatment failure in non-ICU therapy, compared with standard oxygen treatment.
Dr. Schibler and his colleagues tracked 1,472 patients under 12 months with bronchiolitis and a need for oxygen treatment who were randomly assigned to high-flow or standard oxygen therapy to maintain their oxygen saturation at 92%-98% or 94%-98%, depending on policy at the hospital. The subjects were patients at 17 hospitals in Australia and New Zealand.
A total of 739 infants received high-flow treatment that provided heated and humidified oxygen at a rate of 2 liters per kilogram of body weight per minute. The other 733 infants received standard oxygen therapy up to a maximum 2 liters per minute.
The treatment failed, requiring an escalation of care, in 87 of 739 patients (12%) in the high-flow group and 167 of 733 (23%) in the standard-therapy group. (risk difference = –11% points; 95% confidence interval, –15 to –7; P less than .001).
“The ease to use and simplicity of high flow made us recognize and think that this level of respiratory care can be provided outside intensive care,” Dr. Schibler said. “This was further supported by the observational fact that most of these infants with bronchiolitis showed a dramatically improved respiratory condition once on high flow.”
Dr. Schibler said there haven’t been any signs of adverse effects from high-flow oxygen therapy. As for the cost of the treatment, he said it is “likely offset by a reduced need for intensive care therapy or costs associated with transferring to a children’s hospital.”
What should physicians and hospitals take from the study findings? “If a hospital explores the option to use high flow in bronchiolitis, then start the therapy early in the disease process or once an oxygen requirement is recognized,” Dr. Schibler said. “Implementation of a solid and structured training program with a clear hospital guideline based on the evidence will ensure the staff who care for these patients will be empowered and comfortable to adjust the oxygen levels given by the high-flow equipment. The greater the confidence and comfort level for the nursing and respiratory technician staff the better for these infants, as they will sooner observe those infants who are not responding well and may require a higher level of care such as intensive care or they will recognize the infant who responds well.”
The National Health and Medical Research Council (Australia) and the Queensland Emergency Medical Research Fund provided funding, and sites received grant funding from various sources. Fisher & Paykel Healthcare, a respiratory care company based in Auckland, New Zealand, donated high-flow equipment and consumables and travel/accommodation support. Study authors reported various grants and other support.
SOURCE: Franklin D et al. N Engl J Med. 2018;378(12):1112-31.
High-flow oxygen therapy outside the ICU boosts the likelihood that infants with bronchiolitis will avoid treatment failure and an escalation of treatment, a study finds.
“High flow can be safely used in general emergency wards and general pediatric ward settings in regional and metropolitan hospitals that have no immediate direct access to dedicated pediatric intensive care facilities,” study coauthor Andreas Schibler, MD, of University of Queensland in Australia, said in an interview. The findings were published March 22 in the New England Journal of Medicine.
“The typical treatment for bronchiolitis is supportive therapy, providing nutrition, fluids, and if needed respiratory support including provision of oxygen,” Dr. Schibler said.
The prognosis is generally goods thanks to improvements in intensive care, he said, which some infants need because the standard oxygen therapy provided in general pediatric wards is insufficient. The new study examines whether high-flow oxygen therapy through a cannula – which he said has become more common – reduces the risk of treatment failure in non-ICU therapy, compared with standard oxygen treatment.
Dr. Schibler and his colleagues tracked 1,472 patients under 12 months with bronchiolitis and a need for oxygen treatment who were randomly assigned to high-flow or standard oxygen therapy to maintain their oxygen saturation at 92%-98% or 94%-98%, depending on policy at the hospital. The subjects were patients at 17 hospitals in Australia and New Zealand.
A total of 739 infants received high-flow treatment that provided heated and humidified oxygen at a rate of 2 liters per kilogram of body weight per minute. The other 733 infants received standard oxygen therapy up to a maximum 2 liters per minute.
The treatment failed, requiring an escalation of care, in 87 of 739 patients (12%) in the high-flow group and 167 of 733 (23%) in the standard-therapy group. (risk difference = –11% points; 95% confidence interval, –15 to –7; P less than .001).
“The ease to use and simplicity of high flow made us recognize and think that this level of respiratory care can be provided outside intensive care,” Dr. Schibler said. “This was further supported by the observational fact that most of these infants with bronchiolitis showed a dramatically improved respiratory condition once on high flow.”
Dr. Schibler said there haven’t been any signs of adverse effects from high-flow oxygen therapy. As for the cost of the treatment, he said it is “likely offset by a reduced need for intensive care therapy or costs associated with transferring to a children’s hospital.”
What should physicians and hospitals take from the study findings? “If a hospital explores the option to use high flow in bronchiolitis, then start the therapy early in the disease process or once an oxygen requirement is recognized,” Dr. Schibler said. “Implementation of a solid and structured training program with a clear hospital guideline based on the evidence will ensure the staff who care for these patients will be empowered and comfortable to adjust the oxygen levels given by the high-flow equipment. The greater the confidence and comfort level for the nursing and respiratory technician staff the better for these infants, as they will sooner observe those infants who are not responding well and may require a higher level of care such as intensive care or they will recognize the infant who responds well.”
The National Health and Medical Research Council (Australia) and the Queensland Emergency Medical Research Fund provided funding, and sites received grant funding from various sources. Fisher & Paykel Healthcare, a respiratory care company based in Auckland, New Zealand, donated high-flow equipment and consumables and travel/accommodation support. Study authors reported various grants and other support.
SOURCE: Franklin D et al. N Engl J Med. 2018;378(12):1112-31.
High-flow oxygen therapy outside the ICU boosts the likelihood that infants with bronchiolitis will avoid treatment failure and an escalation of treatment, a study finds.
“High flow can be safely used in general emergency wards and general pediatric ward settings in regional and metropolitan hospitals that have no immediate direct access to dedicated pediatric intensive care facilities,” study coauthor Andreas Schibler, MD, of University of Queensland in Australia, said in an interview. The findings were published March 22 in the New England Journal of Medicine.
“The typical treatment for bronchiolitis is supportive therapy, providing nutrition, fluids, and if needed respiratory support including provision of oxygen,” Dr. Schibler said.
The prognosis is generally goods thanks to improvements in intensive care, he said, which some infants need because the standard oxygen therapy provided in general pediatric wards is insufficient. The new study examines whether high-flow oxygen therapy through a cannula – which he said has become more common – reduces the risk of treatment failure in non-ICU therapy, compared with standard oxygen treatment.
Dr. Schibler and his colleagues tracked 1,472 patients under 12 months with bronchiolitis and a need for oxygen treatment who were randomly assigned to high-flow or standard oxygen therapy to maintain their oxygen saturation at 92%-98% or 94%-98%, depending on policy at the hospital. The subjects were patients at 17 hospitals in Australia and New Zealand.
A total of 739 infants received high-flow treatment that provided heated and humidified oxygen at a rate of 2 liters per kilogram of body weight per minute. The other 733 infants received standard oxygen therapy up to a maximum 2 liters per minute.
The treatment failed, requiring an escalation of care, in 87 of 739 patients (12%) in the high-flow group and 167 of 733 (23%) in the standard-therapy group. (risk difference = –11% points; 95% confidence interval, –15 to –7; P less than .001).
“The ease to use and simplicity of high flow made us recognize and think that this level of respiratory care can be provided outside intensive care,” Dr. Schibler said. “This was further supported by the observational fact that most of these infants with bronchiolitis showed a dramatically improved respiratory condition once on high flow.”
Dr. Schibler said there haven’t been any signs of adverse effects from high-flow oxygen therapy. As for the cost of the treatment, he said it is “likely offset by a reduced need for intensive care therapy or costs associated with transferring to a children’s hospital.”
What should physicians and hospitals take from the study findings? “If a hospital explores the option to use high flow in bronchiolitis, then start the therapy early in the disease process or once an oxygen requirement is recognized,” Dr. Schibler said. “Implementation of a solid and structured training program with a clear hospital guideline based on the evidence will ensure the staff who care for these patients will be empowered and comfortable to adjust the oxygen levels given by the high-flow equipment. The greater the confidence and comfort level for the nursing and respiratory technician staff the better for these infants, as they will sooner observe those infants who are not responding well and may require a higher level of care such as intensive care or they will recognize the infant who responds well.”
The National Health and Medical Research Council (Australia) and the Queensland Emergency Medical Research Fund provided funding, and sites received grant funding from various sources. Fisher & Paykel Healthcare, a respiratory care company based in Auckland, New Zealand, donated high-flow equipment and consumables and travel/accommodation support. Study authors reported various grants and other support.
SOURCE: Franklin D et al. N Engl J Med. 2018;378(12):1112-31.
FROM THE NEW ENGLAND JOURNAL OF MEDICINE
Key clinical point: In non-ICUs, infants under 12 months with bronchiolitis are less likely to fail treatment if they are given high-flow oxygen therapy instead of standard oxygen therapy.
Major finding: Treatment failure occurred in 8 of 739 (12%) patients in the high-flow oxygen therapy group and 167 of 733 (23%) in the standard-therapy group.
Study details: Multicenter, randomized, controlled trial of 1,472 infants.
Disclosures: The National Health and Medical Research Council (Australia) and the Queensland Emergency Medical Research Fund provided funding, and sites received grant funding from various sources. Fisher & Paykel Healthcare, a respiratory care company based in Auckland, New Zealand, donated high-flow equipment/consumables and travel/accommodation support. Study authors reported various grants and other support.
Source: Franklin D et al. N Engl J Med 2018;378(12):1112-31.
Study finds AD accounts for hundreds of thousands of annual ED visits
SAN DIEGO – A new study finds that primary diagnoses of atopic dermatitis (AD) are made hundreds of thousands of times in United States emergency departments each year.
The numbers appear to be rising along with costs, researchers reported, and there are signs of disparities, with poorer people more likely to have an ED visit with a primary diagnosis of AD. The study was presented in a poster at the annual meeting of the American Academy of Dermatology.
He and his coauthor, Lauren Kwa, also with the department of dermatology at Northwestern, conducted the analysis to better understand the role of AD in emergency care. “Many AD patients experience severe, unpredictable flares and worsening chronic disease that warrant urgent treatment,” Dr. Silverberg said. “However, patients typically don’t have instant access to outpatient dermatological care and may be forced to turn to the urgent care setting.”
Indeed, he noted, “previous U.S. population–based studies showed that people with AD have higher odds of [ED] utilization than the rest of the population.”
He and Ms. Kwa examined 2006-2012 data from the Nationwide Emergency Department Sample, which includes information on about 20% of all emergency visits in the United States.
During that period, there were 1.86 million ED visits with a primary diagnosis of AD. The annual weighted prevalence of primary diagnoses of AD stayed fairly stable through the period, ranging from 2,589 to 2,769 per 1 million visits. However, the weighted prevalence of secondary AD diagnoses grew steadily from 1,227 per 1 million visits in 2006 to 1,533 per 1 million visits in 2012.
The researchers estimated that the total cost of annual costs of AD-related ED visits grew from $86.9 million in 2006 to $172.8 million in 2012 (P less than .05).
The study also linked primary diagnoses of AD to having Medicaid insurance or being uninsured, being poorer, or visiting hospitals in “micropolitan” areas (small urban communities such as Bozeman, Mont., and Durango, Colo.).
The study did not examine what medications were prescribed in the ED. However, Dr. Silverberg said, “my anecdotal experience has been that many AD patients are prescribed systemic steroids by nondermatologists in the [ED] setting. While these are rapidly effective, they typically have short-lived efficacy and result in rebound flares upon cessation. Patients are rarely counseled on appropriate skin care techniques or given long-term treatment approaches in the [ED] setting, which fails to achieve adequate long-term disease control.”
What’s next? “We are now studying how AD severity, disease course, and treatment impact [ED] utilization for AD,” Dr. Silverberg said.
No specific study funding was reported. He and Ms. Kwa report no relevant disclosures.
SOURCE: Silverberg, J et al. Poster 7021.
SAN DIEGO – A new study finds that primary diagnoses of atopic dermatitis (AD) are made hundreds of thousands of times in United States emergency departments each year.
The numbers appear to be rising along with costs, researchers reported, and there are signs of disparities, with poorer people more likely to have an ED visit with a primary diagnosis of AD. The study was presented in a poster at the annual meeting of the American Academy of Dermatology.
He and his coauthor, Lauren Kwa, also with the department of dermatology at Northwestern, conducted the analysis to better understand the role of AD in emergency care. “Many AD patients experience severe, unpredictable flares and worsening chronic disease that warrant urgent treatment,” Dr. Silverberg said. “However, patients typically don’t have instant access to outpatient dermatological care and may be forced to turn to the urgent care setting.”
Indeed, he noted, “previous U.S. population–based studies showed that people with AD have higher odds of [ED] utilization than the rest of the population.”
He and Ms. Kwa examined 2006-2012 data from the Nationwide Emergency Department Sample, which includes information on about 20% of all emergency visits in the United States.
During that period, there were 1.86 million ED visits with a primary diagnosis of AD. The annual weighted prevalence of primary diagnoses of AD stayed fairly stable through the period, ranging from 2,589 to 2,769 per 1 million visits. However, the weighted prevalence of secondary AD diagnoses grew steadily from 1,227 per 1 million visits in 2006 to 1,533 per 1 million visits in 2012.
The researchers estimated that the total cost of annual costs of AD-related ED visits grew from $86.9 million in 2006 to $172.8 million in 2012 (P less than .05).
The study also linked primary diagnoses of AD to having Medicaid insurance or being uninsured, being poorer, or visiting hospitals in “micropolitan” areas (small urban communities such as Bozeman, Mont., and Durango, Colo.).
The study did not examine what medications were prescribed in the ED. However, Dr. Silverberg said, “my anecdotal experience has been that many AD patients are prescribed systemic steroids by nondermatologists in the [ED] setting. While these are rapidly effective, they typically have short-lived efficacy and result in rebound flares upon cessation. Patients are rarely counseled on appropriate skin care techniques or given long-term treatment approaches in the [ED] setting, which fails to achieve adequate long-term disease control.”
What’s next? “We are now studying how AD severity, disease course, and treatment impact [ED] utilization for AD,” Dr. Silverberg said.
No specific study funding was reported. He and Ms. Kwa report no relevant disclosures.
SOURCE: Silverberg, J et al. Poster 7021.
SAN DIEGO – A new study finds that primary diagnoses of atopic dermatitis (AD) are made hundreds of thousands of times in United States emergency departments each year.
The numbers appear to be rising along with costs, researchers reported, and there are signs of disparities, with poorer people more likely to have an ED visit with a primary diagnosis of AD. The study was presented in a poster at the annual meeting of the American Academy of Dermatology.
He and his coauthor, Lauren Kwa, also with the department of dermatology at Northwestern, conducted the analysis to better understand the role of AD in emergency care. “Many AD patients experience severe, unpredictable flares and worsening chronic disease that warrant urgent treatment,” Dr. Silverberg said. “However, patients typically don’t have instant access to outpatient dermatological care and may be forced to turn to the urgent care setting.”
Indeed, he noted, “previous U.S. population–based studies showed that people with AD have higher odds of [ED] utilization than the rest of the population.”
He and Ms. Kwa examined 2006-2012 data from the Nationwide Emergency Department Sample, which includes information on about 20% of all emergency visits in the United States.
During that period, there were 1.86 million ED visits with a primary diagnosis of AD. The annual weighted prevalence of primary diagnoses of AD stayed fairly stable through the period, ranging from 2,589 to 2,769 per 1 million visits. However, the weighted prevalence of secondary AD diagnoses grew steadily from 1,227 per 1 million visits in 2006 to 1,533 per 1 million visits in 2012.
The researchers estimated that the total cost of annual costs of AD-related ED visits grew from $86.9 million in 2006 to $172.8 million in 2012 (P less than .05).
The study also linked primary diagnoses of AD to having Medicaid insurance or being uninsured, being poorer, or visiting hospitals in “micropolitan” areas (small urban communities such as Bozeman, Mont., and Durango, Colo.).
The study did not examine what medications were prescribed in the ED. However, Dr. Silverberg said, “my anecdotal experience has been that many AD patients are prescribed systemic steroids by nondermatologists in the [ED] setting. While these are rapidly effective, they typically have short-lived efficacy and result in rebound flares upon cessation. Patients are rarely counseled on appropriate skin care techniques or given long-term treatment approaches in the [ED] setting, which fails to achieve adequate long-term disease control.”
What’s next? “We are now studying how AD severity, disease course, and treatment impact [ED] utilization for AD,” Dr. Silverberg said.
No specific study funding was reported. He and Ms. Kwa report no relevant disclosures.
SOURCE: Silverberg, J et al. Poster 7021.
REPORTING FROM AAD 18
Key clinical point: ED visits for atopic dermatitis are common, and their numbers are growing.
Major finding: An estimated 1.86 million ED visits in the United States from 2006 to 2012 were linked to a primary diagnosis of AD.
Study details: Analysis of data from the Nationwide Emergency Department Sample for 2006-2016.
Disclosures: No study funding was reported. The authors had no relevant disclosures.
Source: Silverberg J et al. Poster 7021.
VIDEO: The return of Kaposi’s sarcoma
SAN DIEGO – Dermatologists, who served as crucial sentinels during the early years of the AIDS epidemic, should be alert for dermatologic signs and symptoms of HIV infection, according to Toby Maurer, MD, professor of clinical dermatology at the University of California, San Francisco.
“We’re now seeing a lot of HIV-infected patients presenting once again with skin symptoms,” including new-onset psoriasis, poorly controlled seborrheic dermatitis, and even Kaposi’s sarcoma, she said in a video interview at the annual meeting of the American Academy of Dermatology.
The upswing in cases of Kaposi’s sarcoma “comes as a shock to many dermatologists; they thought Kaposi’s sarcoma was a thing of the past,” added Dr. Maurer, who presented on HIV-associated skin conditions at the meeting.
“My whole plea is to remember that HIV has not gone away, that it keeps showing up, and that the skin symptoms absolutely show up,” she said. “It’s not on the radar as much as it should be.”
In her presentation, Dr. Maurer, who is also chief of dermatology at San Francisco General Hospital, said HIV and HIV medications have a variety of impacts on skin. For example, psoriasis gets worse when patients are off medication and better when they’re on it, she said, while molluscum contagiosum and herpes simplex can actually worsen when patients start HIV drugs. And, she said, a late start of AIDS drugs can worsen eczema.
In the interview, she discussed the impact of starting antiretrovirals late into the infection, when CD4 counts are low, on skin conditions, as well as possible reasons behind the increase in Kaposi’s sarcoma, and interactions between systemic dermatologic medications and some antiretrovirals.
Dr. Maurer reports no relevant disclosures.
SAN DIEGO – Dermatologists, who served as crucial sentinels during the early years of the AIDS epidemic, should be alert for dermatologic signs and symptoms of HIV infection, according to Toby Maurer, MD, professor of clinical dermatology at the University of California, San Francisco.
“We’re now seeing a lot of HIV-infected patients presenting once again with skin symptoms,” including new-onset psoriasis, poorly controlled seborrheic dermatitis, and even Kaposi’s sarcoma, she said in a video interview at the annual meeting of the American Academy of Dermatology.
The upswing in cases of Kaposi’s sarcoma “comes as a shock to many dermatologists; they thought Kaposi’s sarcoma was a thing of the past,” added Dr. Maurer, who presented on HIV-associated skin conditions at the meeting.
“My whole plea is to remember that HIV has not gone away, that it keeps showing up, and that the skin symptoms absolutely show up,” she said. “It’s not on the radar as much as it should be.”
In her presentation, Dr. Maurer, who is also chief of dermatology at San Francisco General Hospital, said HIV and HIV medications have a variety of impacts on skin. For example, psoriasis gets worse when patients are off medication and better when they’re on it, she said, while molluscum contagiosum and herpes simplex can actually worsen when patients start HIV drugs. And, she said, a late start of AIDS drugs can worsen eczema.
In the interview, she discussed the impact of starting antiretrovirals late into the infection, when CD4 counts are low, on skin conditions, as well as possible reasons behind the increase in Kaposi’s sarcoma, and interactions between systemic dermatologic medications and some antiretrovirals.
Dr. Maurer reports no relevant disclosures.
SAN DIEGO – Dermatologists, who served as crucial sentinels during the early years of the AIDS epidemic, should be alert for dermatologic signs and symptoms of HIV infection, according to Toby Maurer, MD, professor of clinical dermatology at the University of California, San Francisco.
“We’re now seeing a lot of HIV-infected patients presenting once again with skin symptoms,” including new-onset psoriasis, poorly controlled seborrheic dermatitis, and even Kaposi’s sarcoma, she said in a video interview at the annual meeting of the American Academy of Dermatology.
The upswing in cases of Kaposi’s sarcoma “comes as a shock to many dermatologists; they thought Kaposi’s sarcoma was a thing of the past,” added Dr. Maurer, who presented on HIV-associated skin conditions at the meeting.
“My whole plea is to remember that HIV has not gone away, that it keeps showing up, and that the skin symptoms absolutely show up,” she said. “It’s not on the radar as much as it should be.”
In her presentation, Dr. Maurer, who is also chief of dermatology at San Francisco General Hospital, said HIV and HIV medications have a variety of impacts on skin. For example, psoriasis gets worse when patients are off medication and better when they’re on it, she said, while molluscum contagiosum and herpes simplex can actually worsen when patients start HIV drugs. And, she said, a late start of AIDS drugs can worsen eczema.
In the interview, she discussed the impact of starting antiretrovirals late into the infection, when CD4 counts are low, on skin conditions, as well as possible reasons behind the increase in Kaposi’s sarcoma, and interactions between systemic dermatologic medications and some antiretrovirals.
Dr. Maurer reports no relevant disclosures.
REPORTING FROM AAD 18
Free testosterone linked to frailty in older men
A new study provides more evidence of a link between lower free testosterone levels and higher levels of frailty in older men, but a researcher says proof of a causal connection remains elusive.
“Our study demonstrates clear associations between testosterone and frailty progression, and, although causality and directionality of the hormone/frailty relationships require clarification, the results presented here make a strong case for large interventional trials of testosterone therapy in frail men to determine whether such treatment would be beneficial,” lead author Agnieszka Swiecicka, MD, of the andrology research unit in the division of diabetes, endocrinology, and gastroenterology at the University of Manchester (England), said in an interview.
As Dr. Swiecicka noted, “in men, testosterone levels decline with age, and it has been suggested that this phenomenon might play a role in the development of frailty.”
However, evidence is limited, and studies have offered conflicting results Dr. Swiecicka said.
For the new study, the researchers prospectively tracked 3,369 community-dwelling men aged 40-79 years from eight European centers. Hundreds were excluded for various reasons or lost to follow-up, and 2,278 men were ultimately included.
The average age was 58 years, and the average body mass index was 28 kg/m2.
Hormone measurements were performed, and frailty was tracked via frailty status (FS, n = 2,278) and frailty phenotype (FP, n = 1,980).
After adjusting their statistics to account for various factors, the researchers were able to link only free testosterone – and not testosterone or dihydrotestosterone – to changes in frailty index (FI). They linked each standard deviation improvement in free testosterone level at baseline to a –2.8% change in FI over 4 years (95% confidence interval, –4.9 to –0.3, P = .030).
“Higher free testosterone levels were associated with a lower risk of worsening frailty status. The direction of this association was consistent regardless of the frailty construct used (FI and FP),” Dr. Swiecicka said. “Higher androgen remained significantly associated with improving frailty status, as assessed by FI, despite age adjustment, suggesting that these relationships cannot be explained by age-related differences in androgen levels.”
Overall, “sex hormones are associated with the development/worsening of frailty in middle-aged and older men, but these relationships vary between different constructs of frailty assessment,” Dr. Swiecicka said. “In light of the findings, a therapeutic role for testosterone in the context of physical frailty prevention or alleviation remains an attractive possibility that should be further explored.”
The study was published in the Journal of Clinical Endocrinology and Metabolism.
In an interview, Steve Borst, PhD, of the University of Florida, questioned the study’s approach because it looks only at baseline hormone levels. “What would be much more interesting to study would be changes in hormone levels vs. changes in frailty,” he said.
Dr. Borst added that researchers already know that “the relationship between testosterone and frailty is both large in magnitude and causal in nature.”
He pointed to his group’s research that linked testosterone injections to an increase in muscle strength, and he said others have linked testosterone administration to an increase in bone density. “While these measures are not exactly the same as frailty index,” he said, “it is well established that lower body muscle strength keeps older people in an independent living state and that the changes in bone mineral density are enough to account for protection against fracture.”
John Morley, MBBCh, of Saint Louis University, said in an interview that testosterone has a role in combating frailty. “But it’s not like it’s going to turn people into super people,” he said.
He added that “we shouldn’t say ‘Let’s do testosterone before we do exercise.’ It’s better to do resistance exercise than it is to take testosterone. But most older males are loath to do any physical work to make themselves better. That’s just human nature.”
The study was funded by various European research-based organizations. The study authors reported multiple disclosures. Dr. Morley reports no disclosures.
SOURCE: Swiecicka A et al. J Clin Endocrinol Metab. 2018 Feb;103(2):701-9.
A new study provides more evidence of a link between lower free testosterone levels and higher levels of frailty in older men, but a researcher says proof of a causal connection remains elusive.
“Our study demonstrates clear associations between testosterone and frailty progression, and, although causality and directionality of the hormone/frailty relationships require clarification, the results presented here make a strong case for large interventional trials of testosterone therapy in frail men to determine whether such treatment would be beneficial,” lead author Agnieszka Swiecicka, MD, of the andrology research unit in the division of diabetes, endocrinology, and gastroenterology at the University of Manchester (England), said in an interview.
As Dr. Swiecicka noted, “in men, testosterone levels decline with age, and it has been suggested that this phenomenon might play a role in the development of frailty.”
However, evidence is limited, and studies have offered conflicting results Dr. Swiecicka said.
For the new study, the researchers prospectively tracked 3,369 community-dwelling men aged 40-79 years from eight European centers. Hundreds were excluded for various reasons or lost to follow-up, and 2,278 men were ultimately included.
The average age was 58 years, and the average body mass index was 28 kg/m2.
Hormone measurements were performed, and frailty was tracked via frailty status (FS, n = 2,278) and frailty phenotype (FP, n = 1,980).
After adjusting their statistics to account for various factors, the researchers were able to link only free testosterone – and not testosterone or dihydrotestosterone – to changes in frailty index (FI). They linked each standard deviation improvement in free testosterone level at baseline to a –2.8% change in FI over 4 years (95% confidence interval, –4.9 to –0.3, P = .030).
“Higher free testosterone levels were associated with a lower risk of worsening frailty status. The direction of this association was consistent regardless of the frailty construct used (FI and FP),” Dr. Swiecicka said. “Higher androgen remained significantly associated with improving frailty status, as assessed by FI, despite age adjustment, suggesting that these relationships cannot be explained by age-related differences in androgen levels.”
Overall, “sex hormones are associated with the development/worsening of frailty in middle-aged and older men, but these relationships vary between different constructs of frailty assessment,” Dr. Swiecicka said. “In light of the findings, a therapeutic role for testosterone in the context of physical frailty prevention or alleviation remains an attractive possibility that should be further explored.”
The study was published in the Journal of Clinical Endocrinology and Metabolism.
In an interview, Steve Borst, PhD, of the University of Florida, questioned the study’s approach because it looks only at baseline hormone levels. “What would be much more interesting to study would be changes in hormone levels vs. changes in frailty,” he said.
Dr. Borst added that researchers already know that “the relationship between testosterone and frailty is both large in magnitude and causal in nature.”
He pointed to his group’s research that linked testosterone injections to an increase in muscle strength, and he said others have linked testosterone administration to an increase in bone density. “While these measures are not exactly the same as frailty index,” he said, “it is well established that lower body muscle strength keeps older people in an independent living state and that the changes in bone mineral density are enough to account for protection against fracture.”
John Morley, MBBCh, of Saint Louis University, said in an interview that testosterone has a role in combating frailty. “But it’s not like it’s going to turn people into super people,” he said.
He added that “we shouldn’t say ‘Let’s do testosterone before we do exercise.’ It’s better to do resistance exercise than it is to take testosterone. But most older males are loath to do any physical work to make themselves better. That’s just human nature.”
The study was funded by various European research-based organizations. The study authors reported multiple disclosures. Dr. Morley reports no disclosures.
SOURCE: Swiecicka A et al. J Clin Endocrinol Metab. 2018 Feb;103(2):701-9.
A new study provides more evidence of a link between lower free testosterone levels and higher levels of frailty in older men, but a researcher says proof of a causal connection remains elusive.
“Our study demonstrates clear associations between testosterone and frailty progression, and, although causality and directionality of the hormone/frailty relationships require clarification, the results presented here make a strong case for large interventional trials of testosterone therapy in frail men to determine whether such treatment would be beneficial,” lead author Agnieszka Swiecicka, MD, of the andrology research unit in the division of diabetes, endocrinology, and gastroenterology at the University of Manchester (England), said in an interview.
As Dr. Swiecicka noted, “in men, testosterone levels decline with age, and it has been suggested that this phenomenon might play a role in the development of frailty.”
However, evidence is limited, and studies have offered conflicting results Dr. Swiecicka said.
For the new study, the researchers prospectively tracked 3,369 community-dwelling men aged 40-79 years from eight European centers. Hundreds were excluded for various reasons or lost to follow-up, and 2,278 men were ultimately included.
The average age was 58 years, and the average body mass index was 28 kg/m2.
Hormone measurements were performed, and frailty was tracked via frailty status (FS, n = 2,278) and frailty phenotype (FP, n = 1,980).
After adjusting their statistics to account for various factors, the researchers were able to link only free testosterone – and not testosterone or dihydrotestosterone – to changes in frailty index (FI). They linked each standard deviation improvement in free testosterone level at baseline to a –2.8% change in FI over 4 years (95% confidence interval, –4.9 to –0.3, P = .030).
“Higher free testosterone levels were associated with a lower risk of worsening frailty status. The direction of this association was consistent regardless of the frailty construct used (FI and FP),” Dr. Swiecicka said. “Higher androgen remained significantly associated with improving frailty status, as assessed by FI, despite age adjustment, suggesting that these relationships cannot be explained by age-related differences in androgen levels.”
Overall, “sex hormones are associated with the development/worsening of frailty in middle-aged and older men, but these relationships vary between different constructs of frailty assessment,” Dr. Swiecicka said. “In light of the findings, a therapeutic role for testosterone in the context of physical frailty prevention or alleviation remains an attractive possibility that should be further explored.”
The study was published in the Journal of Clinical Endocrinology and Metabolism.
In an interview, Steve Borst, PhD, of the University of Florida, questioned the study’s approach because it looks only at baseline hormone levels. “What would be much more interesting to study would be changes in hormone levels vs. changes in frailty,” he said.
Dr. Borst added that researchers already know that “the relationship between testosterone and frailty is both large in magnitude and causal in nature.”
He pointed to his group’s research that linked testosterone injections to an increase in muscle strength, and he said others have linked testosterone administration to an increase in bone density. “While these measures are not exactly the same as frailty index,” he said, “it is well established that lower body muscle strength keeps older people in an independent living state and that the changes in bone mineral density are enough to account for protection against fracture.”
John Morley, MBBCh, of Saint Louis University, said in an interview that testosterone has a role in combating frailty. “But it’s not like it’s going to turn people into super people,” he said.
He added that “we shouldn’t say ‘Let’s do testosterone before we do exercise.’ It’s better to do resistance exercise than it is to take testosterone. But most older males are loath to do any physical work to make themselves better. That’s just human nature.”
The study was funded by various European research-based organizations. The study authors reported multiple disclosures. Dr. Morley reports no disclosures.
SOURCE: Swiecicka A et al. J Clin Endocrinol Metab. 2018 Feb;103(2):701-9.
FROM THE JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
Key clinical point: Free testosterone levels are linked to frailty in older men.
Major finding: For each standard deviation improvement in free testosterone level at baseline, frailty index was 2.8% lower at 4 years. (95% CI, –4.9% to –0.3%, P = .030)
Study details: Prospective cohort study of 3,369 men aged 40-79 years at eight European centers.
Disclosures: The study was funded by various European research-based organizations. The investigators reported multiple disclosures.
Source: Swiecicka A et al. J Clin Endocrinol Metab. 2018 Feb;103(2):701-9.
Study: Natpara slightly boosts health-related QoL in hypoparathyroidism
A new industry-funded analysis suggests that recombinant human parathyroid hormone, an extraordinarily expensive treatment for hypoparathyroidism, produces slight improvement in some health-related quality of life (HRQoL) domains.
While researchers didn’t find any statistically significant between-group differences vs. a placebo, the study lead author said the positive findings about within-group differences reflect her experiences with some patients. “They’re telling me they feel much better, and they don’t have emergency room visits,” endocrinologist Tamara J. Vokes, MD, of the University of Chicago, said in an interview.
And, she said, as reflected in the findings, she’s seen that those with the lowest HRQoL levels at baseline especially show signs of improvement.
The treatment, known as rhPTH(1-84) or Natpara, was approved by the Food and Drug Administration as a treatment for hypoparathyroidism in 2015. The FDA stated that the drug “is only for people who do not respond well to treatment with calcium and active forms of vitamin D alone, because it may increase the possible risk of bone cancer, known as osteosarcoma.”
Pharmacies list the drug as costing $9,500-$9,900 per month with a coupon or discount. According to the new study, research has shown that quality of life is often impaired in patients who have tried the traditional hypoparathyroidism treatments of calcium supplements and vitamin D. Dr. Vokes and her colleagues aimed to expand upon previous studies of HRQoL that did not reach conclusions or failed to include controls.
They examined findings of a previous multinational, randomized, placebo-controlled study of 122 adults with hypoparathyroidism. Average age was 48 years, and roughly 80% of the patients were women.
After their serum calcium levels were adjusted through medication, the patients were randomly assigned to placebo (n = 39) or rhPTH(1-84) (n = 83, starting dose of 50 mg/d that could be raised to 100 mg/d).
The study, which appears in the Journal of Clinical Endocrinology and Metabolism, analyzes the changes in HRQoL from baseline to 24 weeks per the 36-Item Short-Form Health Survey (SF-36).
The researchers found no significant between-group differences. However, those who took the drug did see statistically significant improvements in 4 of 10 domains: physical component summary score (P = .004), body pain (P = .05), general health (P = .05), and vitality (P less than .001). The changes were small, with the vitality score improving the most, from a mean SF-36 score of 49.5 to 53.
In some cases, she said, she’s seen QoL improve in patients whom she normally wouldn’t consider candidates for the medication. “I would have not have recommended PTH for them, but they insisted on taking it, and they report feeling better.”
This may be a placebo effect, she said. Even so, “if someone doesn’t feel well, it’s worth it at least to try to use PTH and see whether they improve.”
She added that lack of well-being is a preexisting condition for some hypoparathyroidism patients. “I’ve seen quite a number of them who have what we call premorbid personality disorder. They didn’t feel well and weren’t happy, and when you get hypoparathyroidism, you’re more unwell and unhappy.”
With medication, however, “you’re a bit less unhappy but you’re still miserable,” she said.
Carol Greenlee, MD, an endocrinologist in Grand Junction, Colo., said in an interview that she saw a patient in a clinical study who had experienced a marked improvement in QoL. However, she said, “it will be the cost of the PTH that is the burden.”
For her part, Dr. Vokes cautioned that it’s important to take special care with patients taking Natpara. “You can’t just give this injection and say, ‘Goodbye, you will be better.’ It requires following certain protocol, frequent monitoring of the blood levels. Be sure the patient has access to the lab, and insurance that covers the test.”
Dr. Greenlee reported no relevant disclosures. The study was funded by Shire Human Genetic Therapies, and the initial clinical trial was funded by NPS Pharmaceuticals, a wholly owned indirect subsidiary. Dr. Vokes reported consulting for Shire and serving as an investigator for the initial clinical trial. Other study authors reported serving as clinical investigators and/or consulting for Shire, and three authors are employees of Shire.
SOURCE: Vokes, TJ et al. J Clin Endocrinol Metab. 2018 Feb 1;103(2):722-31
A new industry-funded analysis suggests that recombinant human parathyroid hormone, an extraordinarily expensive treatment for hypoparathyroidism, produces slight improvement in some health-related quality of life (HRQoL) domains.
While researchers didn’t find any statistically significant between-group differences vs. a placebo, the study lead author said the positive findings about within-group differences reflect her experiences with some patients. “They’re telling me they feel much better, and they don’t have emergency room visits,” endocrinologist Tamara J. Vokes, MD, of the University of Chicago, said in an interview.
And, she said, as reflected in the findings, she’s seen that those with the lowest HRQoL levels at baseline especially show signs of improvement.
The treatment, known as rhPTH(1-84) or Natpara, was approved by the Food and Drug Administration as a treatment for hypoparathyroidism in 2015. The FDA stated that the drug “is only for people who do not respond well to treatment with calcium and active forms of vitamin D alone, because it may increase the possible risk of bone cancer, known as osteosarcoma.”
Pharmacies list the drug as costing $9,500-$9,900 per month with a coupon or discount. According to the new study, research has shown that quality of life is often impaired in patients who have tried the traditional hypoparathyroidism treatments of calcium supplements and vitamin D. Dr. Vokes and her colleagues aimed to expand upon previous studies of HRQoL that did not reach conclusions or failed to include controls.
They examined findings of a previous multinational, randomized, placebo-controlled study of 122 adults with hypoparathyroidism. Average age was 48 years, and roughly 80% of the patients were women.
After their serum calcium levels were adjusted through medication, the patients were randomly assigned to placebo (n = 39) or rhPTH(1-84) (n = 83, starting dose of 50 mg/d that could be raised to 100 mg/d).
The study, which appears in the Journal of Clinical Endocrinology and Metabolism, analyzes the changes in HRQoL from baseline to 24 weeks per the 36-Item Short-Form Health Survey (SF-36).
The researchers found no significant between-group differences. However, those who took the drug did see statistically significant improvements in 4 of 10 domains: physical component summary score (P = .004), body pain (P = .05), general health (P = .05), and vitality (P less than .001). The changes were small, with the vitality score improving the most, from a mean SF-36 score of 49.5 to 53.
In some cases, she said, she’s seen QoL improve in patients whom she normally wouldn’t consider candidates for the medication. “I would have not have recommended PTH for them, but they insisted on taking it, and they report feeling better.”
This may be a placebo effect, she said. Even so, “if someone doesn’t feel well, it’s worth it at least to try to use PTH and see whether they improve.”
She added that lack of well-being is a preexisting condition for some hypoparathyroidism patients. “I’ve seen quite a number of them who have what we call premorbid personality disorder. They didn’t feel well and weren’t happy, and when you get hypoparathyroidism, you’re more unwell and unhappy.”
With medication, however, “you’re a bit less unhappy but you’re still miserable,” she said.
Carol Greenlee, MD, an endocrinologist in Grand Junction, Colo., said in an interview that she saw a patient in a clinical study who had experienced a marked improvement in QoL. However, she said, “it will be the cost of the PTH that is the burden.”
For her part, Dr. Vokes cautioned that it’s important to take special care with patients taking Natpara. “You can’t just give this injection and say, ‘Goodbye, you will be better.’ It requires following certain protocol, frequent monitoring of the blood levels. Be sure the patient has access to the lab, and insurance that covers the test.”
Dr. Greenlee reported no relevant disclosures. The study was funded by Shire Human Genetic Therapies, and the initial clinical trial was funded by NPS Pharmaceuticals, a wholly owned indirect subsidiary. Dr. Vokes reported consulting for Shire and serving as an investigator for the initial clinical trial. Other study authors reported serving as clinical investigators and/or consulting for Shire, and three authors are employees of Shire.
SOURCE: Vokes, TJ et al. J Clin Endocrinol Metab. 2018 Feb 1;103(2):722-31
A new industry-funded analysis suggests that recombinant human parathyroid hormone, an extraordinarily expensive treatment for hypoparathyroidism, produces slight improvement in some health-related quality of life (HRQoL) domains.
While researchers didn’t find any statistically significant between-group differences vs. a placebo, the study lead author said the positive findings about within-group differences reflect her experiences with some patients. “They’re telling me they feel much better, and they don’t have emergency room visits,” endocrinologist Tamara J. Vokes, MD, of the University of Chicago, said in an interview.
And, she said, as reflected in the findings, she’s seen that those with the lowest HRQoL levels at baseline especially show signs of improvement.
The treatment, known as rhPTH(1-84) or Natpara, was approved by the Food and Drug Administration as a treatment for hypoparathyroidism in 2015. The FDA stated that the drug “is only for people who do not respond well to treatment with calcium and active forms of vitamin D alone, because it may increase the possible risk of bone cancer, known as osteosarcoma.”
Pharmacies list the drug as costing $9,500-$9,900 per month with a coupon or discount. According to the new study, research has shown that quality of life is often impaired in patients who have tried the traditional hypoparathyroidism treatments of calcium supplements and vitamin D. Dr. Vokes and her colleagues aimed to expand upon previous studies of HRQoL that did not reach conclusions or failed to include controls.
They examined findings of a previous multinational, randomized, placebo-controlled study of 122 adults with hypoparathyroidism. Average age was 48 years, and roughly 80% of the patients were women.
After their serum calcium levels were adjusted through medication, the patients were randomly assigned to placebo (n = 39) or rhPTH(1-84) (n = 83, starting dose of 50 mg/d that could be raised to 100 mg/d).
The study, which appears in the Journal of Clinical Endocrinology and Metabolism, analyzes the changes in HRQoL from baseline to 24 weeks per the 36-Item Short-Form Health Survey (SF-36).
The researchers found no significant between-group differences. However, those who took the drug did see statistically significant improvements in 4 of 10 domains: physical component summary score (P = .004), body pain (P = .05), general health (P = .05), and vitality (P less than .001). The changes were small, with the vitality score improving the most, from a mean SF-36 score of 49.5 to 53.
In some cases, she said, she’s seen QoL improve in patients whom she normally wouldn’t consider candidates for the medication. “I would have not have recommended PTH for them, but they insisted on taking it, and they report feeling better.”
This may be a placebo effect, she said. Even so, “if someone doesn’t feel well, it’s worth it at least to try to use PTH and see whether they improve.”
She added that lack of well-being is a preexisting condition for some hypoparathyroidism patients. “I’ve seen quite a number of them who have what we call premorbid personality disorder. They didn’t feel well and weren’t happy, and when you get hypoparathyroidism, you’re more unwell and unhappy.”
With medication, however, “you’re a bit less unhappy but you’re still miserable,” she said.
Carol Greenlee, MD, an endocrinologist in Grand Junction, Colo., said in an interview that she saw a patient in a clinical study who had experienced a marked improvement in QoL. However, she said, “it will be the cost of the PTH that is the burden.”
For her part, Dr. Vokes cautioned that it’s important to take special care with patients taking Natpara. “You can’t just give this injection and say, ‘Goodbye, you will be better.’ It requires following certain protocol, frequent monitoring of the blood levels. Be sure the patient has access to the lab, and insurance that covers the test.”
Dr. Greenlee reported no relevant disclosures. The study was funded by Shire Human Genetic Therapies, and the initial clinical trial was funded by NPS Pharmaceuticals, a wholly owned indirect subsidiary. Dr. Vokes reported consulting for Shire and serving as an investigator for the initial clinical trial. Other study authors reported serving as clinical investigators and/or consulting for Shire, and three authors are employees of Shire.
SOURCE: Vokes, TJ et al. J Clin Endocrinol Metab. 2018 Feb 1;103(2):722-31
FROM THE JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
Key clinical point: Health-related quality of life (HRQoL) may improve slightly in patients on recombinant human parathyroid hormone for hypoparathyroidism.
Major finding: In 4 of 10 SF-36 domains, HRQoL improved in within-group analysis. There was no statistically significant improvement vs. placebo.
Study details: A 24-week analysis of previous drug vs. placebo clinical trial of 122 adults with hypoparathyroidism.
Disclosures: Shire Human Genetic Therapies funded the study, and the initial clinical trial was funded by NPS Pharmaceuticals, a wholly owned indirect subsidiary. The researchers reported various relationships to Shire, including employment.
Source: Vokes TJ et al. J Clin Endocrinol Metab. 2018 Feb 1;103(2):722-31.
VIDEO: With new therapies available, it’s the ‘decade of eczema,’ researcher says
SAN DIEGO – A long dry spell in the development of new atopic dermatitis (AD) medications came to an end in 2016 with the approval of a topical treatment, and last year brought the first biologic for AD to the market. With more targets and potential treatments being studied, “it’s the decade of eczema,” according to a leading researcher.
And I think we’ll have many more approvals in the next few years,” said Emma Guttman, MD, PhD, said in a video interview at the annual meeting of the American Academy of Dermatology, where she was presenting a talk on the translational revolution in atopic dermatitis.
In the interview, she also discussed research showing that children with AD don’t have the same distribution of lesions as adults, and a study of young children, which found that during an early stage of the disease, when compared with adults, they showed much higher increases in Th17 similar to that seen in psoriasis. It will be interesting to see if “some drugs that work for psoriasis may work in children,” said Dr. Guttman, professor of dermatology and director of the laboratory of inflammatory skin diseases at the Icahn School of Medicine at Mount Sinai, New York.
Dr. Guttman disclosed research support, consulting, or lecture fees from Regeneron, Sanofi, Pfizer, and other companies developing AD treatments.
SAN DIEGO – A long dry spell in the development of new atopic dermatitis (AD) medications came to an end in 2016 with the approval of a topical treatment, and last year brought the first biologic for AD to the market. With more targets and potential treatments being studied, “it’s the decade of eczema,” according to a leading researcher.
And I think we’ll have many more approvals in the next few years,” said Emma Guttman, MD, PhD, said in a video interview at the annual meeting of the American Academy of Dermatology, where she was presenting a talk on the translational revolution in atopic dermatitis.
In the interview, she also discussed research showing that children with AD don’t have the same distribution of lesions as adults, and a study of young children, which found that during an early stage of the disease, when compared with adults, they showed much higher increases in Th17 similar to that seen in psoriasis. It will be interesting to see if “some drugs that work for psoriasis may work in children,” said Dr. Guttman, professor of dermatology and director of the laboratory of inflammatory skin diseases at the Icahn School of Medicine at Mount Sinai, New York.
Dr. Guttman disclosed research support, consulting, or lecture fees from Regeneron, Sanofi, Pfizer, and other companies developing AD treatments.
SAN DIEGO – A long dry spell in the development of new atopic dermatitis (AD) medications came to an end in 2016 with the approval of a topical treatment, and last year brought the first biologic for AD to the market. With more targets and potential treatments being studied, “it’s the decade of eczema,” according to a leading researcher.
And I think we’ll have many more approvals in the next few years,” said Emma Guttman, MD, PhD, said in a video interview at the annual meeting of the American Academy of Dermatology, where she was presenting a talk on the translational revolution in atopic dermatitis.
In the interview, she also discussed research showing that children with AD don’t have the same distribution of lesions as adults, and a study of young children, which found that during an early stage of the disease, when compared with adults, they showed much higher increases in Th17 similar to that seen in psoriasis. It will be interesting to see if “some drugs that work for psoriasis may work in children,” said Dr. Guttman, professor of dermatology and director of the laboratory of inflammatory skin diseases at the Icahn School of Medicine at Mount Sinai, New York.
Dr. Guttman disclosed research support, consulting, or lecture fees from Regeneron, Sanofi, Pfizer, and other companies developing AD treatments.
REPORTING FROM AAD 18
Extended-interval dosing of natalizumab linked to lower risk of PML
SAN DIEGO – A large industry-funded study of the multiple sclerosis drug natalizumab suggests that physicians can dramatically lower the likelihood of progressive multifocal leukoencephalopathy in patients at higher risk of the condition by increasing the interval between doses.
Previous research has suggested that natalizumab (Tysabri) doesn’t lose efficacy when given less frequently.
Dr. Zhovtis Ryerson presented the study findings at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.
As a 2014 report explains, natalizumab is a “highly effective disease-modifying therapy for the treatment of relapsing forms of multiple sclerosis,” but the risk of progressive multifocal leukoencephalopathy (PML) “has largely contributed to it being relegated to a second-line position” (Ther Adv Chronic Dis. 2014 Mar;5[2]:62-8).
Patients previously exposed to John Cunningham (JC) virus are at higher risk of PML, a rare viral brain disease that can be severely disabling or deadly. A 2017 report estimated the combined cumulative PML probability at 2.7% (with previous immunosuppressant use) and 1.7% (no previous immunosuppressant use) over 6 years in patients with signs of exposure to the JC virus (Lancet Neurol. 2017 Nov;16[11]:925-33). According to Dr. Zhovtis Ryerson, natalizumab manufacturer Biogen reported in December 2017 that it has confirmed 756 cases of PML in natalizumab-treated patients, all except for 3 in MS patients.
Doctors are wary in the at-risk patient population. “In general,” she said, “clinicians treating patients who are JC virus positive, and therefore have a risk for PML, may not utilize the drug or may take the patient off it after 2 years, which is when the risk goes up.”
Some physicians have experimented with longer intervals between treatments of 300 mg given intravenously, administering it every 5-8 weeks instead of every 4 weeks, with an eye on not extending the interval for too long “because MS disease activity returns after 12 weeks of withholding therapy,” Dr. Zhovtis Ryerson said.
In 2016, Dr. Zhovtis Ryerson and colleagues reported in a retrospective analysis that natalizumab dosing intervals of up to 8 weeks, 5 days didn’t affect the drug’s efficacy (J Neurol Neurosurg Psychiatry. 2016 Aug;87[8]:885-9).
For the primary analyses in the new study – whether dosing history in the last 18 months of natalizumab treatment affects PML – researchers tracked 1,988 patients who took the drug via an extended interval schedule and 13,132 who took it via a standard interval. The patients were tracked in the mandated TOUCH Prescribing Program; all participants showed signs of exposure to the JC virus.
The two groups were similar at about 68% female, an average age at first infusion of about 43, and a median number of about 48 natalizumab infusions.
For patients without previous immunosuppressant use who had received 49-60 doses, the researchers estimated the incidence of PML per 1,000 patients as 1.23 in the extended-interval group and 3.96 in the standard-interval group. The numbers were slightly higher for those who received 61-72 doses. At 48 or fewer doses, there were no PML cases in patients on extended-interval dosing.
“The data showed highly significant risk reductions of up to 94%,” Dr. Zhovtis Ryerson said.
Moving forward, “in collaboration with Biogen, we have more sensitivity analysis to be done to assure that our conclusions on this are correct,” she said. “Furthermore, more evidence of efficacy of extended-interval dosing natalizumab is needed, and we hope to move forward with a prospective, randomized, controlled trial to give clinicians the highest level of evidence we can.”
The study was funded by Biogen. Dr. Zhovtis Ryerson reported personal compensation from Teva, speaker/advisory board activities for Biogen, and research support from Biogen. Seven other authors reported being Biogen employees. Other authors reported no disclosures or various disclosures, including connections to Biogen.
SOURCE: Zhovtis R et al. ACTRIMS Forum 2018 Abstract LB250.
SAN DIEGO – A large industry-funded study of the multiple sclerosis drug natalizumab suggests that physicians can dramatically lower the likelihood of progressive multifocal leukoencephalopathy in patients at higher risk of the condition by increasing the interval between doses.
Previous research has suggested that natalizumab (Tysabri) doesn’t lose efficacy when given less frequently.
Dr. Zhovtis Ryerson presented the study findings at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.
As a 2014 report explains, natalizumab is a “highly effective disease-modifying therapy for the treatment of relapsing forms of multiple sclerosis,” but the risk of progressive multifocal leukoencephalopathy (PML) “has largely contributed to it being relegated to a second-line position” (Ther Adv Chronic Dis. 2014 Mar;5[2]:62-8).
Patients previously exposed to John Cunningham (JC) virus are at higher risk of PML, a rare viral brain disease that can be severely disabling or deadly. A 2017 report estimated the combined cumulative PML probability at 2.7% (with previous immunosuppressant use) and 1.7% (no previous immunosuppressant use) over 6 years in patients with signs of exposure to the JC virus (Lancet Neurol. 2017 Nov;16[11]:925-33). According to Dr. Zhovtis Ryerson, natalizumab manufacturer Biogen reported in December 2017 that it has confirmed 756 cases of PML in natalizumab-treated patients, all except for 3 in MS patients.
Doctors are wary in the at-risk patient population. “In general,” she said, “clinicians treating patients who are JC virus positive, and therefore have a risk for PML, may not utilize the drug or may take the patient off it after 2 years, which is when the risk goes up.”
Some physicians have experimented with longer intervals between treatments of 300 mg given intravenously, administering it every 5-8 weeks instead of every 4 weeks, with an eye on not extending the interval for too long “because MS disease activity returns after 12 weeks of withholding therapy,” Dr. Zhovtis Ryerson said.
In 2016, Dr. Zhovtis Ryerson and colleagues reported in a retrospective analysis that natalizumab dosing intervals of up to 8 weeks, 5 days didn’t affect the drug’s efficacy (J Neurol Neurosurg Psychiatry. 2016 Aug;87[8]:885-9).
For the primary analyses in the new study – whether dosing history in the last 18 months of natalizumab treatment affects PML – researchers tracked 1,988 patients who took the drug via an extended interval schedule and 13,132 who took it via a standard interval. The patients were tracked in the mandated TOUCH Prescribing Program; all participants showed signs of exposure to the JC virus.
The two groups were similar at about 68% female, an average age at first infusion of about 43, and a median number of about 48 natalizumab infusions.
For patients without previous immunosuppressant use who had received 49-60 doses, the researchers estimated the incidence of PML per 1,000 patients as 1.23 in the extended-interval group and 3.96 in the standard-interval group. The numbers were slightly higher for those who received 61-72 doses. At 48 or fewer doses, there were no PML cases in patients on extended-interval dosing.
“The data showed highly significant risk reductions of up to 94%,” Dr. Zhovtis Ryerson said.
Moving forward, “in collaboration with Biogen, we have more sensitivity analysis to be done to assure that our conclusions on this are correct,” she said. “Furthermore, more evidence of efficacy of extended-interval dosing natalizumab is needed, and we hope to move forward with a prospective, randomized, controlled trial to give clinicians the highest level of evidence we can.”
The study was funded by Biogen. Dr. Zhovtis Ryerson reported personal compensation from Teva, speaker/advisory board activities for Biogen, and research support from Biogen. Seven other authors reported being Biogen employees. Other authors reported no disclosures or various disclosures, including connections to Biogen.
SOURCE: Zhovtis R et al. ACTRIMS Forum 2018 Abstract LB250.
SAN DIEGO – A large industry-funded study of the multiple sclerosis drug natalizumab suggests that physicians can dramatically lower the likelihood of progressive multifocal leukoencephalopathy in patients at higher risk of the condition by increasing the interval between doses.
Previous research has suggested that natalizumab (Tysabri) doesn’t lose efficacy when given less frequently.
Dr. Zhovtis Ryerson presented the study findings at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.
As a 2014 report explains, natalizumab is a “highly effective disease-modifying therapy for the treatment of relapsing forms of multiple sclerosis,” but the risk of progressive multifocal leukoencephalopathy (PML) “has largely contributed to it being relegated to a second-line position” (Ther Adv Chronic Dis. 2014 Mar;5[2]:62-8).
Patients previously exposed to John Cunningham (JC) virus are at higher risk of PML, a rare viral brain disease that can be severely disabling or deadly. A 2017 report estimated the combined cumulative PML probability at 2.7% (with previous immunosuppressant use) and 1.7% (no previous immunosuppressant use) over 6 years in patients with signs of exposure to the JC virus (Lancet Neurol. 2017 Nov;16[11]:925-33). According to Dr. Zhovtis Ryerson, natalizumab manufacturer Biogen reported in December 2017 that it has confirmed 756 cases of PML in natalizumab-treated patients, all except for 3 in MS patients.
Doctors are wary in the at-risk patient population. “In general,” she said, “clinicians treating patients who are JC virus positive, and therefore have a risk for PML, may not utilize the drug or may take the patient off it after 2 years, which is when the risk goes up.”
Some physicians have experimented with longer intervals between treatments of 300 mg given intravenously, administering it every 5-8 weeks instead of every 4 weeks, with an eye on not extending the interval for too long “because MS disease activity returns after 12 weeks of withholding therapy,” Dr. Zhovtis Ryerson said.
In 2016, Dr. Zhovtis Ryerson and colleagues reported in a retrospective analysis that natalizumab dosing intervals of up to 8 weeks, 5 days didn’t affect the drug’s efficacy (J Neurol Neurosurg Psychiatry. 2016 Aug;87[8]:885-9).
For the primary analyses in the new study – whether dosing history in the last 18 months of natalizumab treatment affects PML – researchers tracked 1,988 patients who took the drug via an extended interval schedule and 13,132 who took it via a standard interval. The patients were tracked in the mandated TOUCH Prescribing Program; all participants showed signs of exposure to the JC virus.
The two groups were similar at about 68% female, an average age at first infusion of about 43, and a median number of about 48 natalizumab infusions.
For patients without previous immunosuppressant use who had received 49-60 doses, the researchers estimated the incidence of PML per 1,000 patients as 1.23 in the extended-interval group and 3.96 in the standard-interval group. The numbers were slightly higher for those who received 61-72 doses. At 48 or fewer doses, there were no PML cases in patients on extended-interval dosing.
“The data showed highly significant risk reductions of up to 94%,” Dr. Zhovtis Ryerson said.
Moving forward, “in collaboration with Biogen, we have more sensitivity analysis to be done to assure that our conclusions on this are correct,” she said. “Furthermore, more evidence of efficacy of extended-interval dosing natalizumab is needed, and we hope to move forward with a prospective, randomized, controlled trial to give clinicians the highest level of evidence we can.”
The study was funded by Biogen. Dr. Zhovtis Ryerson reported personal compensation from Teva, speaker/advisory board activities for Biogen, and research support from Biogen. Seven other authors reported being Biogen employees. Other authors reported no disclosures or various disclosures, including connections to Biogen.
SOURCE: Zhovtis R et al. ACTRIMS Forum 2018 Abstract LB250.
REPORTING FROM ACTRIMS FORUM 2018
Key clinical point: , compared with standard-interval dosing in patients who showed signs of exposure to the JC virus.
Major finding: Estimated incidence of PML per 1,000 patients was 1.23 in an extended-interval group and 3.96 in a standard-interval group among those who had received 49-60 natalizumab doses.
Study details: 18-month analysis of multiple sclerosis patients on natalizumab who showed signs of exposure to the JC virus: 1,988 on extended-interval dosing and 13,132 on standard-interval dosing.
Disclosures: The study was funded by Biogen, and multiple study authors report being employees of Biogen or having other relationships to the company.
Source: Zhovtis R et al. ACTRIMS Forum 2018, Abstract LB250.
Is MS caused by one-two punch of pinworm and Epstein-Barr virus?
SAN DIEGO – What causes multiple sclerosis (MS)? A team of Scottish researchers offers a new theory that it’s triggered in part by a one-two punch of infection with pinworm – a common condition in the United States, especially among children – and the Epstein-Barr virus (EBV).
The theory identifies pinworm as the prime suspect to be the “missing link” that explains why EBV and MS are so tightly connected, said Patrick Kearns, MBChB, a graduate student at Harvard T.H. Chan School of Public Health in Boston.
Dr. Kearns is the lead author of two reports about the possible role of pinworm that were presented at ACTRIMS Forum 2018, which is held by the Americas Committee for Treatment and Research in Multiple Sclerosis. He spoke in an interview.
Dr. Kearns and his colleagues focused on a well-known cluster of MS cases that began to appear in the Faroe Islands – a Danish possession in the North Atlantic – during World War II. The cases began to appear after British troops occupied the islands.
“Many of the occupation soldiers were from the Scottish Highlands, where the MS prevalence is quite high: 90 cases per 100,000, comparable to the northern U.S.,” according to a National MS Society summary about MS clusters.
In a theory that spawned controversy, the late neurologist John Kurtzke, MD, speculated that the British soldiers brought a transmissible agent to the islands, which triggered MS cases.
Could the agent be EBV alone? The authors of the new studies don’t think so, although they note that EBV is “robustly linked” to MS. Indeed, a 2012 meta-analysis reported that the virus “appears to be present in 100% of MS patients,” based on studies considered to be the strongest (Mult Scler. 2013 Feb;19[2]:162-6).
The authors of the new reports note that, while EBV infection “appears necessary,” it is “clearly not sufficient” to cause the disease on its own.
“Certainly almost everyone gets EBV eventually,” Dr. Kearns said. “So mere presence of the virus is certainly not sufficient for causing the disease. But it seems still to be necessary, and timing of infection might be everything.”
So what’s the missing piece of the puzzle?
Dr. Kearns began to think it might be the lowly pinworm after helping a colleague by analyzing data from appendicitis samples in children. He noted that uninflamed samples often had pinworms in them, but the inflamed samples often didn’t, which suggested that “the rate of pinworms in normal appendices must be very high in the healthy pediatric population at any given time.”
More data confirmed this to be true, and medical literature told Dr. Kearns that pinworms were common in high latitudes – places where people often are especially prone to MS.
“Most remarkably, they are known to have very little migration and stay spatially stable in populations over long periods of time,” Dr. Kearns said, “and typically everyone in an affected population will encounter them because their eggs are transmitted in household dust.”
And, he said, “they are known to be common in soldiers who live in military accommodation.”
According to the Centers for Disease Control and Prevention, pinworm prevalence can be as high as 50% in at-risk groups – children, caregivers of infected children, and people who live in institutions. Pinworms, which are spread through ingestion, are often asymptomatic but may cause anal itching and trigger bacterial infections.
The researchers suggest that pinworm infection comes first, followed by EBV infection. This makes sense because “late EBV infection in the form of infectious mononucleosis is known to be a risk factor for MS,” Dr. Kearns said.
The one-two punch of pinworm and then EBV is a plausible theory “because EBV lives in memory B cells, which are known to be important in MS and could be specific for the previous exposure to pinworm,” Dr. Kearns said. “However, this is very speculative and some researchers will argue this is very unlikely to be the case. But I think there is a chance it could explain some of the epidemiology, so I’m keen to try and test the theory if I can.”
What’s next? Dr. Kearns wants to explore data from Scotland in search of areas of high and low MS incidence that could offer insight into environmental triggers.
He added that the development of a serological blood test to prove a history of pinworm infection would be “the most effective way to prove or disprove this theory.”
“I have approached an investigator who has a track record of doing this for other infections and have been encouraged that he thinks that it would be achievable,” he said. “But this will definitely take time and funding.”
No specific funding was reported. The study authors reported no relevant disclosures.
SOURCE: Kearns P et al. ACTRIMS Forum 2018, Abstracts LB257 and LB264.
SAN DIEGO – What causes multiple sclerosis (MS)? A team of Scottish researchers offers a new theory that it’s triggered in part by a one-two punch of infection with pinworm – a common condition in the United States, especially among children – and the Epstein-Barr virus (EBV).
The theory identifies pinworm as the prime suspect to be the “missing link” that explains why EBV and MS are so tightly connected, said Patrick Kearns, MBChB, a graduate student at Harvard T.H. Chan School of Public Health in Boston.
Dr. Kearns is the lead author of two reports about the possible role of pinworm that were presented at ACTRIMS Forum 2018, which is held by the Americas Committee for Treatment and Research in Multiple Sclerosis. He spoke in an interview.
Dr. Kearns and his colleagues focused on a well-known cluster of MS cases that began to appear in the Faroe Islands – a Danish possession in the North Atlantic – during World War II. The cases began to appear after British troops occupied the islands.
“Many of the occupation soldiers were from the Scottish Highlands, where the MS prevalence is quite high: 90 cases per 100,000, comparable to the northern U.S.,” according to a National MS Society summary about MS clusters.
In a theory that spawned controversy, the late neurologist John Kurtzke, MD, speculated that the British soldiers brought a transmissible agent to the islands, which triggered MS cases.
Could the agent be EBV alone? The authors of the new studies don’t think so, although they note that EBV is “robustly linked” to MS. Indeed, a 2012 meta-analysis reported that the virus “appears to be present in 100% of MS patients,” based on studies considered to be the strongest (Mult Scler. 2013 Feb;19[2]:162-6).
The authors of the new reports note that, while EBV infection “appears necessary,” it is “clearly not sufficient” to cause the disease on its own.
“Certainly almost everyone gets EBV eventually,” Dr. Kearns said. “So mere presence of the virus is certainly not sufficient for causing the disease. But it seems still to be necessary, and timing of infection might be everything.”
So what’s the missing piece of the puzzle?
Dr. Kearns began to think it might be the lowly pinworm after helping a colleague by analyzing data from appendicitis samples in children. He noted that uninflamed samples often had pinworms in them, but the inflamed samples often didn’t, which suggested that “the rate of pinworms in normal appendices must be very high in the healthy pediatric population at any given time.”
More data confirmed this to be true, and medical literature told Dr. Kearns that pinworms were common in high latitudes – places where people often are especially prone to MS.
“Most remarkably, they are known to have very little migration and stay spatially stable in populations over long periods of time,” Dr. Kearns said, “and typically everyone in an affected population will encounter them because their eggs are transmitted in household dust.”
And, he said, “they are known to be common in soldiers who live in military accommodation.”
According to the Centers for Disease Control and Prevention, pinworm prevalence can be as high as 50% in at-risk groups – children, caregivers of infected children, and people who live in institutions. Pinworms, which are spread through ingestion, are often asymptomatic but may cause anal itching and trigger bacterial infections.
The researchers suggest that pinworm infection comes first, followed by EBV infection. This makes sense because “late EBV infection in the form of infectious mononucleosis is known to be a risk factor for MS,” Dr. Kearns said.
The one-two punch of pinworm and then EBV is a plausible theory “because EBV lives in memory B cells, which are known to be important in MS and could be specific for the previous exposure to pinworm,” Dr. Kearns said. “However, this is very speculative and some researchers will argue this is very unlikely to be the case. But I think there is a chance it could explain some of the epidemiology, so I’m keen to try and test the theory if I can.”
What’s next? Dr. Kearns wants to explore data from Scotland in search of areas of high and low MS incidence that could offer insight into environmental triggers.
He added that the development of a serological blood test to prove a history of pinworm infection would be “the most effective way to prove or disprove this theory.”
“I have approached an investigator who has a track record of doing this for other infections and have been encouraged that he thinks that it would be achievable,” he said. “But this will definitely take time and funding.”
No specific funding was reported. The study authors reported no relevant disclosures.
SOURCE: Kearns P et al. ACTRIMS Forum 2018, Abstracts LB257 and LB264.
SAN DIEGO – What causes multiple sclerosis (MS)? A team of Scottish researchers offers a new theory that it’s triggered in part by a one-two punch of infection with pinworm – a common condition in the United States, especially among children – and the Epstein-Barr virus (EBV).
The theory identifies pinworm as the prime suspect to be the “missing link” that explains why EBV and MS are so tightly connected, said Patrick Kearns, MBChB, a graduate student at Harvard T.H. Chan School of Public Health in Boston.
Dr. Kearns is the lead author of two reports about the possible role of pinworm that were presented at ACTRIMS Forum 2018, which is held by the Americas Committee for Treatment and Research in Multiple Sclerosis. He spoke in an interview.
Dr. Kearns and his colleagues focused on a well-known cluster of MS cases that began to appear in the Faroe Islands – a Danish possession in the North Atlantic – during World War II. The cases began to appear after British troops occupied the islands.
“Many of the occupation soldiers were from the Scottish Highlands, where the MS prevalence is quite high: 90 cases per 100,000, comparable to the northern U.S.,” according to a National MS Society summary about MS clusters.
In a theory that spawned controversy, the late neurologist John Kurtzke, MD, speculated that the British soldiers brought a transmissible agent to the islands, which triggered MS cases.
Could the agent be EBV alone? The authors of the new studies don’t think so, although they note that EBV is “robustly linked” to MS. Indeed, a 2012 meta-analysis reported that the virus “appears to be present in 100% of MS patients,” based on studies considered to be the strongest (Mult Scler. 2013 Feb;19[2]:162-6).
The authors of the new reports note that, while EBV infection “appears necessary,” it is “clearly not sufficient” to cause the disease on its own.
“Certainly almost everyone gets EBV eventually,” Dr. Kearns said. “So mere presence of the virus is certainly not sufficient for causing the disease. But it seems still to be necessary, and timing of infection might be everything.”
So what’s the missing piece of the puzzle?
Dr. Kearns began to think it might be the lowly pinworm after helping a colleague by analyzing data from appendicitis samples in children. He noted that uninflamed samples often had pinworms in them, but the inflamed samples often didn’t, which suggested that “the rate of pinworms in normal appendices must be very high in the healthy pediatric population at any given time.”
More data confirmed this to be true, and medical literature told Dr. Kearns that pinworms were common in high latitudes – places where people often are especially prone to MS.
“Most remarkably, they are known to have very little migration and stay spatially stable in populations over long periods of time,” Dr. Kearns said, “and typically everyone in an affected population will encounter them because their eggs are transmitted in household dust.”
And, he said, “they are known to be common in soldiers who live in military accommodation.”
According to the Centers for Disease Control and Prevention, pinworm prevalence can be as high as 50% in at-risk groups – children, caregivers of infected children, and people who live in institutions. Pinworms, which are spread through ingestion, are often asymptomatic but may cause anal itching and trigger bacterial infections.
The researchers suggest that pinworm infection comes first, followed by EBV infection. This makes sense because “late EBV infection in the form of infectious mononucleosis is known to be a risk factor for MS,” Dr. Kearns said.
The one-two punch of pinworm and then EBV is a plausible theory “because EBV lives in memory B cells, which are known to be important in MS and could be specific for the previous exposure to pinworm,” Dr. Kearns said. “However, this is very speculative and some researchers will argue this is very unlikely to be the case. But I think there is a chance it could explain some of the epidemiology, so I’m keen to try and test the theory if I can.”
What’s next? Dr. Kearns wants to explore data from Scotland in search of areas of high and low MS incidence that could offer insight into environmental triggers.
He added that the development of a serological blood test to prove a history of pinworm infection would be “the most effective way to prove or disprove this theory.”
“I have approached an investigator who has a track record of doing this for other infections and have been encouraged that he thinks that it would be achievable,” he said. “But this will definitely take time and funding.”
No specific funding was reported. The study authors reported no relevant disclosures.
SOURCE: Kearns P et al. ACTRIMS Forum 2018, Abstracts LB257 and LB264.
REPORTING FROM ACTRIMS FORUM 2018