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Interosseous tendon inflammation is common prior to RA
MAUI, HAWAII – Inflammation of the hand interosseous tendons found on MRI is a novel target in efforts to preempt the development and progression of rheumatoid arthritis, Paul Emery, MD, said at the 2019 Rheumatology Winter Clinical Symposium.
He and his coinvestigators have previously shown there is a high prevalence of interosseous tendon inflammation in the hands of patients with established RA, but now they’ve demonstrated that this phenomenon also occurs in anti–cyclic citrullinated peptide (CCP)–positive individuals at increased risk for RA, even before onset of clinical synovitis.
This finding is consistent with the notion that, even though RA is classically considered a disease of the synovial joints, the joint involvement is a relatively late phenomenon in the disease development process and extracapsular structures may be important early targets of RA-related inflammation. Indeed, the MRI finding of tenosynovitis of the wrist and finger flexor tendons is known to be the strongest predictor of progression to arthritis in patients with recent-onset arthralgia or other musculoskeletal symptoms but no clinical synovitis, according to Dr. Emery, professor of rheumatology and director of the University of Leeds (England) Musculoskeletal Biomedical Research Center.
Because the interosseous muscles of the hands play a critical role in hand function – pianists and other musicians not infrequently present to rheumatologists with overuse injuries of the muscles and their tendons – Dr. Emery and his coworkers decided to take a comprehensive look at interosseous tendon inflammation across the full spectrum of RA and pre-RA. They conducted a retrospective study of clinical and hand MRI data on 93 CCP-positive patients who presented with new-onset musculoskeletal symptoms but no clinical synovitis; 47 patients with early RA, all of whom were disease-modifying antirheumatic drug–naive; 28 patients with late RA as defined by at least 1 year of symptoms, anti-CCP and/or rheumatoid factor positivity, a Disease Activity Score in 28 joints (DAS28) of 3.2 or more, plus a history of exposure to one or more DMARDs at the time of their hand imaging; and 20 healthy controls.
The key finding is that the proportion of subjects with MRI evidence of interosseous tendon inflammation rose along the advancing RA continuum. It was present in 19% of the CCP-positive patients without clinical synovitis; 49% of the DMARD-naive early RA group; 57% of the late RA group; and in none of the healthy controls. Moreover, the number of inflamed interosseous tendons per patient also increased with RA progression.
A total of 12% of 507 nontender metacarpophalangeal joints showed MRI evidence of interosseous tendon inflammation, as did 28% of 141 tender ones (Ann Rheum Dis. 2019 Mar 23. doi: 10.1136/annrheumdis-2018-214331).
As part of the study, Dr. Emery and coinvestigators performed cadaveric dissections that demonstrated that the interosseous tendons don’t possess a tendon sheath and don’t directly communicate with the joint capsule.
A prospective study is warranted in order to confirm the observed association between interosseous tendon inflammation and clinical and subclinical synovitis and to establish the predictive value of hand MRI as a harbinger of RA, he noted.
Dr. Emery reported having no financial conflicts regarding his presentation.
MAUI, HAWAII – Inflammation of the hand interosseous tendons found on MRI is a novel target in efforts to preempt the development and progression of rheumatoid arthritis, Paul Emery, MD, said at the 2019 Rheumatology Winter Clinical Symposium.
He and his coinvestigators have previously shown there is a high prevalence of interosseous tendon inflammation in the hands of patients with established RA, but now they’ve demonstrated that this phenomenon also occurs in anti–cyclic citrullinated peptide (CCP)–positive individuals at increased risk for RA, even before onset of clinical synovitis.
This finding is consistent with the notion that, even though RA is classically considered a disease of the synovial joints, the joint involvement is a relatively late phenomenon in the disease development process and extracapsular structures may be important early targets of RA-related inflammation. Indeed, the MRI finding of tenosynovitis of the wrist and finger flexor tendons is known to be the strongest predictor of progression to arthritis in patients with recent-onset arthralgia or other musculoskeletal symptoms but no clinical synovitis, according to Dr. Emery, professor of rheumatology and director of the University of Leeds (England) Musculoskeletal Biomedical Research Center.
Because the interosseous muscles of the hands play a critical role in hand function – pianists and other musicians not infrequently present to rheumatologists with overuse injuries of the muscles and their tendons – Dr. Emery and his coworkers decided to take a comprehensive look at interosseous tendon inflammation across the full spectrum of RA and pre-RA. They conducted a retrospective study of clinical and hand MRI data on 93 CCP-positive patients who presented with new-onset musculoskeletal symptoms but no clinical synovitis; 47 patients with early RA, all of whom were disease-modifying antirheumatic drug–naive; 28 patients with late RA as defined by at least 1 year of symptoms, anti-CCP and/or rheumatoid factor positivity, a Disease Activity Score in 28 joints (DAS28) of 3.2 or more, plus a history of exposure to one or more DMARDs at the time of their hand imaging; and 20 healthy controls.
The key finding is that the proportion of subjects with MRI evidence of interosseous tendon inflammation rose along the advancing RA continuum. It was present in 19% of the CCP-positive patients without clinical synovitis; 49% of the DMARD-naive early RA group; 57% of the late RA group; and in none of the healthy controls. Moreover, the number of inflamed interosseous tendons per patient also increased with RA progression.
A total of 12% of 507 nontender metacarpophalangeal joints showed MRI evidence of interosseous tendon inflammation, as did 28% of 141 tender ones (Ann Rheum Dis. 2019 Mar 23. doi: 10.1136/annrheumdis-2018-214331).
As part of the study, Dr. Emery and coinvestigators performed cadaveric dissections that demonstrated that the interosseous tendons don’t possess a tendon sheath and don’t directly communicate with the joint capsule.
A prospective study is warranted in order to confirm the observed association between interosseous tendon inflammation and clinical and subclinical synovitis and to establish the predictive value of hand MRI as a harbinger of RA, he noted.
Dr. Emery reported having no financial conflicts regarding his presentation.
MAUI, HAWAII – Inflammation of the hand interosseous tendons found on MRI is a novel target in efforts to preempt the development and progression of rheumatoid arthritis, Paul Emery, MD, said at the 2019 Rheumatology Winter Clinical Symposium.
He and his coinvestigators have previously shown there is a high prevalence of interosseous tendon inflammation in the hands of patients with established RA, but now they’ve demonstrated that this phenomenon also occurs in anti–cyclic citrullinated peptide (CCP)–positive individuals at increased risk for RA, even before onset of clinical synovitis.
This finding is consistent with the notion that, even though RA is classically considered a disease of the synovial joints, the joint involvement is a relatively late phenomenon in the disease development process and extracapsular structures may be important early targets of RA-related inflammation. Indeed, the MRI finding of tenosynovitis of the wrist and finger flexor tendons is known to be the strongest predictor of progression to arthritis in patients with recent-onset arthralgia or other musculoskeletal symptoms but no clinical synovitis, according to Dr. Emery, professor of rheumatology and director of the University of Leeds (England) Musculoskeletal Biomedical Research Center.
Because the interosseous muscles of the hands play a critical role in hand function – pianists and other musicians not infrequently present to rheumatologists with overuse injuries of the muscles and their tendons – Dr. Emery and his coworkers decided to take a comprehensive look at interosseous tendon inflammation across the full spectrum of RA and pre-RA. They conducted a retrospective study of clinical and hand MRI data on 93 CCP-positive patients who presented with new-onset musculoskeletal symptoms but no clinical synovitis; 47 patients with early RA, all of whom were disease-modifying antirheumatic drug–naive; 28 patients with late RA as defined by at least 1 year of symptoms, anti-CCP and/or rheumatoid factor positivity, a Disease Activity Score in 28 joints (DAS28) of 3.2 or more, plus a history of exposure to one or more DMARDs at the time of their hand imaging; and 20 healthy controls.
The key finding is that the proportion of subjects with MRI evidence of interosseous tendon inflammation rose along the advancing RA continuum. It was present in 19% of the CCP-positive patients without clinical synovitis; 49% of the DMARD-naive early RA group; 57% of the late RA group; and in none of the healthy controls. Moreover, the number of inflamed interosseous tendons per patient also increased with RA progression.
A total of 12% of 507 nontender metacarpophalangeal joints showed MRI evidence of interosseous tendon inflammation, as did 28% of 141 tender ones (Ann Rheum Dis. 2019 Mar 23. doi: 10.1136/annrheumdis-2018-214331).
As part of the study, Dr. Emery and coinvestigators performed cadaveric dissections that demonstrated that the interosseous tendons don’t possess a tendon sheath and don’t directly communicate with the joint capsule.
A prospective study is warranted in order to confirm the observed association between interosseous tendon inflammation and clinical and subclinical synovitis and to establish the predictive value of hand MRI as a harbinger of RA, he noted.
Dr. Emery reported having no financial conflicts regarding his presentation.
REPORTING FROM RWCS 2019
Bringing hospitalist coverage to critical access hospitals
“As a hospitalist, I believe that my specialty improves care for inpatients,” said Ethan Kuperman, MD, MS, FHM, clinical associate professor of medicine at University of Iowa Health Care in Iowa City. “I want hospitalists involved with as many hospitals as possible because I believe we will lead to better patient outcomes.”
But, he adds, it’s not feasible to place dedicated hospitalists in every rural hospital in the United States – especially those running far below the average hospitalist census. “As a university, academic hospitalist, I wanted to make sure that the innovations and knowledge of the University of Iowa could penetrate into the greater community, and I wanted to strengthen the continuity of care between our partners in rural Iowa and our physical location in Iowa City,” he said.
Enter the virtual hospitalist: A telemedicine “virtual hospitalist” may expand capabilities at a fractional cost of an on-site provider.
Dr. Kuperman’s 6-month pilot program provided “virtual hospitalist” coverage to patients at a critical access hospital in rural Iowa.
“Our rural partners want to ensure that they are providing high-quality care within their communities and aren’t transferring patients without a good indication to larger centers,” he said. “For patients, this program means more of them can remain in their communities, surrounded by their families. I don’t think the virtual hospitalist program delivers equivalent care to the university hospital – I think we deliver better care because of that continuity with local providers and the ability of patients to remain in contact with their support structures.”
The study concludes that the virtual hospitalist model increased the percentage of ED patients who could safely receive their care locally, and a single virtual hospitalist may be able to cover multiple critical access hospitals simultaneously.
“We have the technology to deliver hospitalist expertise to rural hospitals through telehealth in a way that benefits patients, rural hospitals, and academic hospitals,” he said.
Reference
Kuperman E et al. The Virtual Hospitalist: A single-site implementation bringing hospitalist coverage to critical access hospitals. Journal of Hospital Medicine. Published online first 2018 Sep 26. doi: 10.12788/jhm.3061. Accessed 2018 Oct 2.
“As a hospitalist, I believe that my specialty improves care for inpatients,” said Ethan Kuperman, MD, MS, FHM, clinical associate professor of medicine at University of Iowa Health Care in Iowa City. “I want hospitalists involved with as many hospitals as possible because I believe we will lead to better patient outcomes.”
But, he adds, it’s not feasible to place dedicated hospitalists in every rural hospital in the United States – especially those running far below the average hospitalist census. “As a university, academic hospitalist, I wanted to make sure that the innovations and knowledge of the University of Iowa could penetrate into the greater community, and I wanted to strengthen the continuity of care between our partners in rural Iowa and our physical location in Iowa City,” he said.
Enter the virtual hospitalist: A telemedicine “virtual hospitalist” may expand capabilities at a fractional cost of an on-site provider.
Dr. Kuperman’s 6-month pilot program provided “virtual hospitalist” coverage to patients at a critical access hospital in rural Iowa.
“Our rural partners want to ensure that they are providing high-quality care within their communities and aren’t transferring patients without a good indication to larger centers,” he said. “For patients, this program means more of them can remain in their communities, surrounded by their families. I don’t think the virtual hospitalist program delivers equivalent care to the university hospital – I think we deliver better care because of that continuity with local providers and the ability of patients to remain in contact with their support structures.”
The study concludes that the virtual hospitalist model increased the percentage of ED patients who could safely receive their care locally, and a single virtual hospitalist may be able to cover multiple critical access hospitals simultaneously.
“We have the technology to deliver hospitalist expertise to rural hospitals through telehealth in a way that benefits patients, rural hospitals, and academic hospitals,” he said.
Reference
Kuperman E et al. The Virtual Hospitalist: A single-site implementation bringing hospitalist coverage to critical access hospitals. Journal of Hospital Medicine. Published online first 2018 Sep 26. doi: 10.12788/jhm.3061. Accessed 2018 Oct 2.
“As a hospitalist, I believe that my specialty improves care for inpatients,” said Ethan Kuperman, MD, MS, FHM, clinical associate professor of medicine at University of Iowa Health Care in Iowa City. “I want hospitalists involved with as many hospitals as possible because I believe we will lead to better patient outcomes.”
But, he adds, it’s not feasible to place dedicated hospitalists in every rural hospital in the United States – especially those running far below the average hospitalist census. “As a university, academic hospitalist, I wanted to make sure that the innovations and knowledge of the University of Iowa could penetrate into the greater community, and I wanted to strengthen the continuity of care between our partners in rural Iowa and our physical location in Iowa City,” he said.
Enter the virtual hospitalist: A telemedicine “virtual hospitalist” may expand capabilities at a fractional cost of an on-site provider.
Dr. Kuperman’s 6-month pilot program provided “virtual hospitalist” coverage to patients at a critical access hospital in rural Iowa.
“Our rural partners want to ensure that they are providing high-quality care within their communities and aren’t transferring patients without a good indication to larger centers,” he said. “For patients, this program means more of them can remain in their communities, surrounded by their families. I don’t think the virtual hospitalist program delivers equivalent care to the university hospital – I think we deliver better care because of that continuity with local providers and the ability of patients to remain in contact with their support structures.”
The study concludes that the virtual hospitalist model increased the percentage of ED patients who could safely receive their care locally, and a single virtual hospitalist may be able to cover multiple critical access hospitals simultaneously.
“We have the technology to deliver hospitalist expertise to rural hospitals through telehealth in a way that benefits patients, rural hospitals, and academic hospitals,” he said.
Reference
Kuperman E et al. The Virtual Hospitalist: A single-site implementation bringing hospitalist coverage to critical access hospitals. Journal of Hospital Medicine. Published online first 2018 Sep 26. doi: 10.12788/jhm.3061. Accessed 2018 Oct 2.
Medicare-for-All gets first legislative hearing
Medicare-for-All – the health care proposal that could play a key role in the 2020 presidential elections – got its first airing on Capitol Hill April 30 as the House Rules Committee discussed H.R. 1384.
The Medicare for All Act of 2019, introduced Feb. 27 by Rep. Pramila Jayapal (D-Wash.) and Rep. Debbie Dingell (D-Mich.), would provide universal coverage at the time of birth in the United States or upon the establishment of residency. The bill would make it unlawful for a private health insurer to sell coverage that duplicates the benefits of the Medicare-for-All system, and would prohibit employers from providing health insurance coverage that is provided by the Medicare-for-All system. At press time, the bill currently had 108 cosponsors, all Democrats.
Given the challenges the bill will face getting through the Democrat-controlled House – and the likelihood that the Republican-controlled Senate won’t even touch it – one Rules Committee member questioned why the hearing was being held.
Rep. Debbie Lesko (D-Ariz.) acknowledged that there are problems with health care and called for bipartisanship, noting problems of this magnitude need both sides of the aisle working together, but said she does not think H.R. 1384 has any chance of passage.
“Most, if not all, Republicans in the House are probably going to vote against it if it gets up for a vote and certainly the Senate is not going to hear it,” Rep. Lesko said. “I don’t know why we are doing this.”
Witnesses called by the committee offered differing takes on whether Medicare-for-All is feasible in the United States.
“A Medicare-for-All system of the type envisioned in the Jayapal bill is a huge step from our current system, which relies largely on private insurers,” according to Dean Baker, PhD, senior economist at the Center for Economic and Policy Research. “The list of transition problems that would arise is too long to address here. However, I would argue that it is essential that any move to such a system be done piecemeal since a quick changeover would virtually guarantee confusion and quite possibly lead to some people going without care.”
Indeed, many ideas contained in a number of different Medicare-for-All proposals could be implemented “without a major reorganization of the health care system,” according to Sara Collins, PhD, vice president of health care coverage and access at The Commonwealth Fund. “For example, paying providers in commercial plans at prices closer to those in Medicare or allowing the secretary of Health and Human Services to negotiate prescription drug prices have potential to slow health care cost growth and would not require an immediate shift to a single-payer system.
“On the other hand,” she continued, “moving piecemeal also involves trade-offs including the possibility, based on the experience of the [Affordable Care Act], that additional steps may take some time to achieve.”
Grace-Marie Turner, president of the Galen Institute, noted that many people, regardless of whether their coverage is public or private or not at all, have frustrations with the current health care delivery system.
“But it is hard to see how consumers would be more empowered when dealing with a single government payer,” she said. “In a country that values diversity, will one program with one list of benefits and set of rules work for everyone?”
If physician payment under Medicare-for-All were closer to what Medicare currently pays, “physicians would see 30% cuts. These payment reductions would gradually grow over time,” Ms. Turner testified.
Despite discussion of pay cuts, doctors invited to testify spoke in favor of a single-payer system.
“All I want is to practice medicine in a world where I no longer have to watch a patient walk out of the ER without medical care that could save their life because they are worried about going bankrupt,” said Farzon Nahvi, MD, an emergency physician at New York University Medical Center who serves on the board of directors for the New York Metro chapter of Physicians for a National Health Program. “From my perspective on the ground, the solution has to involve approaching medical care in just the same way we approach educating our children, maintaining our roads, and supporting our troops. This means treating health care like any other public good and creating a universal health care system like Medicare-for-All so that when they’re at their most vulnerable, my patients never have to make any consideration except to simply do what they need to do in order to get better.”
Doris Browne, MD, immediate past president of the National Medical Association agreed, calling for the adoption of “a system of universal coverage that minimizes administrative medical costs. It does not matter what label is used. Such an undertaking must include preventive care, screening, early detection, and treatment. The coverage would allow patients the ability to chose their provider, primary care or specialist. Care should be the same no matter where you live, rural or urban, California or Mississippi, and not be restricted based on language, age, gender, or race/ethnicity.”
Rep. Jim McGovern (D-Mass.), chairman of the Rules Committee, wrapped up the hearing noting that, even with some dissenting viewpoints, “what we have shown today, I believe, is that Medicare-for-All is possible; that we can build on the principles of the Affordable Care Act to make even bolder reforms. Reforms that would give doctors like Dr. Browne and Dr. Nahvi the ability to treat patients and give them the best care every time without letting cost dictate medical decisions. ... If you walk away with nothing else today, know that we have the ability to do that. Medicare-for-All is possible. It is reasonable. It can move forward and I think it should.”
Medicare-for-All – the health care proposal that could play a key role in the 2020 presidential elections – got its first airing on Capitol Hill April 30 as the House Rules Committee discussed H.R. 1384.
The Medicare for All Act of 2019, introduced Feb. 27 by Rep. Pramila Jayapal (D-Wash.) and Rep. Debbie Dingell (D-Mich.), would provide universal coverage at the time of birth in the United States or upon the establishment of residency. The bill would make it unlawful for a private health insurer to sell coverage that duplicates the benefits of the Medicare-for-All system, and would prohibit employers from providing health insurance coverage that is provided by the Medicare-for-All system. At press time, the bill currently had 108 cosponsors, all Democrats.
Given the challenges the bill will face getting through the Democrat-controlled House – and the likelihood that the Republican-controlled Senate won’t even touch it – one Rules Committee member questioned why the hearing was being held.
Rep. Debbie Lesko (D-Ariz.) acknowledged that there are problems with health care and called for bipartisanship, noting problems of this magnitude need both sides of the aisle working together, but said she does not think H.R. 1384 has any chance of passage.
“Most, if not all, Republicans in the House are probably going to vote against it if it gets up for a vote and certainly the Senate is not going to hear it,” Rep. Lesko said. “I don’t know why we are doing this.”
Witnesses called by the committee offered differing takes on whether Medicare-for-All is feasible in the United States.
“A Medicare-for-All system of the type envisioned in the Jayapal bill is a huge step from our current system, which relies largely on private insurers,” according to Dean Baker, PhD, senior economist at the Center for Economic and Policy Research. “The list of transition problems that would arise is too long to address here. However, I would argue that it is essential that any move to such a system be done piecemeal since a quick changeover would virtually guarantee confusion and quite possibly lead to some people going without care.”
Indeed, many ideas contained in a number of different Medicare-for-All proposals could be implemented “without a major reorganization of the health care system,” according to Sara Collins, PhD, vice president of health care coverage and access at The Commonwealth Fund. “For example, paying providers in commercial plans at prices closer to those in Medicare or allowing the secretary of Health and Human Services to negotiate prescription drug prices have potential to slow health care cost growth and would not require an immediate shift to a single-payer system.
“On the other hand,” she continued, “moving piecemeal also involves trade-offs including the possibility, based on the experience of the [Affordable Care Act], that additional steps may take some time to achieve.”
Grace-Marie Turner, president of the Galen Institute, noted that many people, regardless of whether their coverage is public or private or not at all, have frustrations with the current health care delivery system.
“But it is hard to see how consumers would be more empowered when dealing with a single government payer,” she said. “In a country that values diversity, will one program with one list of benefits and set of rules work for everyone?”
If physician payment under Medicare-for-All were closer to what Medicare currently pays, “physicians would see 30% cuts. These payment reductions would gradually grow over time,” Ms. Turner testified.
Despite discussion of pay cuts, doctors invited to testify spoke in favor of a single-payer system.
“All I want is to practice medicine in a world where I no longer have to watch a patient walk out of the ER without medical care that could save their life because they are worried about going bankrupt,” said Farzon Nahvi, MD, an emergency physician at New York University Medical Center who serves on the board of directors for the New York Metro chapter of Physicians for a National Health Program. “From my perspective on the ground, the solution has to involve approaching medical care in just the same way we approach educating our children, maintaining our roads, and supporting our troops. This means treating health care like any other public good and creating a universal health care system like Medicare-for-All so that when they’re at their most vulnerable, my patients never have to make any consideration except to simply do what they need to do in order to get better.”
Doris Browne, MD, immediate past president of the National Medical Association agreed, calling for the adoption of “a system of universal coverage that minimizes administrative medical costs. It does not matter what label is used. Such an undertaking must include preventive care, screening, early detection, and treatment. The coverage would allow patients the ability to chose their provider, primary care or specialist. Care should be the same no matter where you live, rural or urban, California or Mississippi, and not be restricted based on language, age, gender, or race/ethnicity.”
Rep. Jim McGovern (D-Mass.), chairman of the Rules Committee, wrapped up the hearing noting that, even with some dissenting viewpoints, “what we have shown today, I believe, is that Medicare-for-All is possible; that we can build on the principles of the Affordable Care Act to make even bolder reforms. Reforms that would give doctors like Dr. Browne and Dr. Nahvi the ability to treat patients and give them the best care every time without letting cost dictate medical decisions. ... If you walk away with nothing else today, know that we have the ability to do that. Medicare-for-All is possible. It is reasonable. It can move forward and I think it should.”
Medicare-for-All – the health care proposal that could play a key role in the 2020 presidential elections – got its first airing on Capitol Hill April 30 as the House Rules Committee discussed H.R. 1384.
The Medicare for All Act of 2019, introduced Feb. 27 by Rep. Pramila Jayapal (D-Wash.) and Rep. Debbie Dingell (D-Mich.), would provide universal coverage at the time of birth in the United States or upon the establishment of residency. The bill would make it unlawful for a private health insurer to sell coverage that duplicates the benefits of the Medicare-for-All system, and would prohibit employers from providing health insurance coverage that is provided by the Medicare-for-All system. At press time, the bill currently had 108 cosponsors, all Democrats.
Given the challenges the bill will face getting through the Democrat-controlled House – and the likelihood that the Republican-controlled Senate won’t even touch it – one Rules Committee member questioned why the hearing was being held.
Rep. Debbie Lesko (D-Ariz.) acknowledged that there are problems with health care and called for bipartisanship, noting problems of this magnitude need both sides of the aisle working together, but said she does not think H.R. 1384 has any chance of passage.
“Most, if not all, Republicans in the House are probably going to vote against it if it gets up for a vote and certainly the Senate is not going to hear it,” Rep. Lesko said. “I don’t know why we are doing this.”
Witnesses called by the committee offered differing takes on whether Medicare-for-All is feasible in the United States.
“A Medicare-for-All system of the type envisioned in the Jayapal bill is a huge step from our current system, which relies largely on private insurers,” according to Dean Baker, PhD, senior economist at the Center for Economic and Policy Research. “The list of transition problems that would arise is too long to address here. However, I would argue that it is essential that any move to such a system be done piecemeal since a quick changeover would virtually guarantee confusion and quite possibly lead to some people going without care.”
Indeed, many ideas contained in a number of different Medicare-for-All proposals could be implemented “without a major reorganization of the health care system,” according to Sara Collins, PhD, vice president of health care coverage and access at The Commonwealth Fund. “For example, paying providers in commercial plans at prices closer to those in Medicare or allowing the secretary of Health and Human Services to negotiate prescription drug prices have potential to slow health care cost growth and would not require an immediate shift to a single-payer system.
“On the other hand,” she continued, “moving piecemeal also involves trade-offs including the possibility, based on the experience of the [Affordable Care Act], that additional steps may take some time to achieve.”
Grace-Marie Turner, president of the Galen Institute, noted that many people, regardless of whether their coverage is public or private or not at all, have frustrations with the current health care delivery system.
“But it is hard to see how consumers would be more empowered when dealing with a single government payer,” she said. “In a country that values diversity, will one program with one list of benefits and set of rules work for everyone?”
If physician payment under Medicare-for-All were closer to what Medicare currently pays, “physicians would see 30% cuts. These payment reductions would gradually grow over time,” Ms. Turner testified.
Despite discussion of pay cuts, doctors invited to testify spoke in favor of a single-payer system.
“All I want is to practice medicine in a world where I no longer have to watch a patient walk out of the ER without medical care that could save their life because they are worried about going bankrupt,” said Farzon Nahvi, MD, an emergency physician at New York University Medical Center who serves on the board of directors for the New York Metro chapter of Physicians for a National Health Program. “From my perspective on the ground, the solution has to involve approaching medical care in just the same way we approach educating our children, maintaining our roads, and supporting our troops. This means treating health care like any other public good and creating a universal health care system like Medicare-for-All so that when they’re at their most vulnerable, my patients never have to make any consideration except to simply do what they need to do in order to get better.”
Doris Browne, MD, immediate past president of the National Medical Association agreed, calling for the adoption of “a system of universal coverage that minimizes administrative medical costs. It does not matter what label is used. Such an undertaking must include preventive care, screening, early detection, and treatment. The coverage would allow patients the ability to chose their provider, primary care or specialist. Care should be the same no matter where you live, rural or urban, California or Mississippi, and not be restricted based on language, age, gender, or race/ethnicity.”
Rep. Jim McGovern (D-Mass.), chairman of the Rules Committee, wrapped up the hearing noting that, even with some dissenting viewpoints, “what we have shown today, I believe, is that Medicare-for-All is possible; that we can build on the principles of the Affordable Care Act to make even bolder reforms. Reforms that would give doctors like Dr. Browne and Dr. Nahvi the ability to treat patients and give them the best care every time without letting cost dictate medical decisions. ... If you walk away with nothing else today, know that we have the ability to do that. Medicare-for-All is possible. It is reasonable. It can move forward and I think it should.”
REPORTING FROM THE HOUSE RULES COMMITTEE
Out-of-pocket costs for neurologic medications rise sharply
The out-of-pocket cost of multiple sclerosis (MS) treatments increased the most, with a 20-fold increase during that time. The average out-of-pocket cost for MS therapy was $15/month in 2004, compared with $309/month in 2016. Patients also had to pay more for brand name medications for peripheral neuropathy, dementia, and Parkinson’s disease, researchers said.
“Out-of-pocket costs vary widely both across and within conditions,” said study author Brian C. Callaghan, MD, an assistant professor of neurology at the University of Michigan in Ann Arbor, and research colleagues. “To minimize patient financial burden, neurologists require access to precise cost information when making treatment decisions.”
Prior studies have found that high drug costs “can create burdens such as medical debt, skipping food or other essentials, or even not taking drugs as often as necessary,” Dr. Callaghan said in a news release.
To assess how out-of-pocket costs affect patients with neurologic conditions, the investigators analyzed data from a large, privately insured health care claims database. They determined medication costs for patients with MS, peripheral neuropathy, epilepsy, dementia, and Parkinson’s disease who were seen by outpatient neurologists. They also compared costs for high-deductible and traditional plans and explored cumulative out-of-pocket costs during the first 2 years after diagnosis.
The analysis examined the five most commonly prescribed drugs by neurologists for each condition based on Medicare data. In addition, the researchers included in their analysis all approved MS medications, lacosamide as a brand name epilepsy drug, and venlafaxine, a peripheral neuropathy medication that transitioned from brand to generic.
In all, the study population included 105,355 patients with MS, 314,530 with peripheral neuropathy, 281,073 with epilepsy, 120,720 with dementia, and 90,801 with Parkinson’s disease.
In 2016, patients in high-deductible health plans had an average monthly out-of-pocket expense that was approximately twice that of patients not in those plans – $661 versus $246 among patients with MS, and $40 versus $18 among patients with epilepsy.
In the 2 years after diagnosis in 2012 or 2013, cumulative out-of-pocket costs for patients with MS were a mean of $2,238, but costs varied widely. Cumulative costs were no more than $90 for patients in the bottom 5% of expenses, whereas they exceeded $9,800 for patients in the top 5% of expenses. Among patients with epilepsy, cumulative out-of-pocket costs were $230 in the 2 years after diagnosis.
“In 2004, out-of-pocket costs were of such low magnitude that physicians could typically ignore these costs for most patients and not adversely affect the financial status of patients or their adherence to medications. However, by 2016, out-of-pockets costs have risen to the point where neurologists should consider out-of-pocket costs for most medications and for most patients,” Dr. Callaghan and colleagues wrote.
Ralph L. Sacco, MD, president of the American Academy of Neurology (AAN), said in a news release that the AAN has created a Neurology Drug Pricing Task Force and is advocating for better drug-pricing policies. “This study provides important information to help us better understand how these problems can directly affect our patients,” Dr. Sacco said.
“Everyone deserves affordable access to the medications that will be most beneficial, but if the drugs are too expensive, people may simply not take them, possibly leading to medical complications and higher costs later,” Dr. Sacco said.
The study was supported by the AAN. Several authors are supported by National Institutes of Health grants. Dr. Callaghan receives research support from Impeto Medical and performs consulting work.
SOURCE: Callaghan BC et al. Neurology. 2019 May 1. doi: 10.1212/WNL.0000000000007564.
The out-of-pocket cost of multiple sclerosis (MS) treatments increased the most, with a 20-fold increase during that time. The average out-of-pocket cost for MS therapy was $15/month in 2004, compared with $309/month in 2016. Patients also had to pay more for brand name medications for peripheral neuropathy, dementia, and Parkinson’s disease, researchers said.
“Out-of-pocket costs vary widely both across and within conditions,” said study author Brian C. Callaghan, MD, an assistant professor of neurology at the University of Michigan in Ann Arbor, and research colleagues. “To minimize patient financial burden, neurologists require access to precise cost information when making treatment decisions.”
Prior studies have found that high drug costs “can create burdens such as medical debt, skipping food or other essentials, or even not taking drugs as often as necessary,” Dr. Callaghan said in a news release.
To assess how out-of-pocket costs affect patients with neurologic conditions, the investigators analyzed data from a large, privately insured health care claims database. They determined medication costs for patients with MS, peripheral neuropathy, epilepsy, dementia, and Parkinson’s disease who were seen by outpatient neurologists. They also compared costs for high-deductible and traditional plans and explored cumulative out-of-pocket costs during the first 2 years after diagnosis.
The analysis examined the five most commonly prescribed drugs by neurologists for each condition based on Medicare data. In addition, the researchers included in their analysis all approved MS medications, lacosamide as a brand name epilepsy drug, and venlafaxine, a peripheral neuropathy medication that transitioned from brand to generic.
In all, the study population included 105,355 patients with MS, 314,530 with peripheral neuropathy, 281,073 with epilepsy, 120,720 with dementia, and 90,801 with Parkinson’s disease.
In 2016, patients in high-deductible health plans had an average monthly out-of-pocket expense that was approximately twice that of patients not in those plans – $661 versus $246 among patients with MS, and $40 versus $18 among patients with epilepsy.
In the 2 years after diagnosis in 2012 or 2013, cumulative out-of-pocket costs for patients with MS were a mean of $2,238, but costs varied widely. Cumulative costs were no more than $90 for patients in the bottom 5% of expenses, whereas they exceeded $9,800 for patients in the top 5% of expenses. Among patients with epilepsy, cumulative out-of-pocket costs were $230 in the 2 years after diagnosis.
“In 2004, out-of-pocket costs were of such low magnitude that physicians could typically ignore these costs for most patients and not adversely affect the financial status of patients or their adherence to medications. However, by 2016, out-of-pockets costs have risen to the point where neurologists should consider out-of-pocket costs for most medications and for most patients,” Dr. Callaghan and colleagues wrote.
Ralph L. Sacco, MD, president of the American Academy of Neurology (AAN), said in a news release that the AAN has created a Neurology Drug Pricing Task Force and is advocating for better drug-pricing policies. “This study provides important information to help us better understand how these problems can directly affect our patients,” Dr. Sacco said.
“Everyone deserves affordable access to the medications that will be most beneficial, but if the drugs are too expensive, people may simply not take them, possibly leading to medical complications and higher costs later,” Dr. Sacco said.
The study was supported by the AAN. Several authors are supported by National Institutes of Health grants. Dr. Callaghan receives research support from Impeto Medical and performs consulting work.
SOURCE: Callaghan BC et al. Neurology. 2019 May 1. doi: 10.1212/WNL.0000000000007564.
The out-of-pocket cost of multiple sclerosis (MS) treatments increased the most, with a 20-fold increase during that time. The average out-of-pocket cost for MS therapy was $15/month in 2004, compared with $309/month in 2016. Patients also had to pay more for brand name medications for peripheral neuropathy, dementia, and Parkinson’s disease, researchers said.
“Out-of-pocket costs vary widely both across and within conditions,” said study author Brian C. Callaghan, MD, an assistant professor of neurology at the University of Michigan in Ann Arbor, and research colleagues. “To minimize patient financial burden, neurologists require access to precise cost information when making treatment decisions.”
Prior studies have found that high drug costs “can create burdens such as medical debt, skipping food or other essentials, or even not taking drugs as often as necessary,” Dr. Callaghan said in a news release.
To assess how out-of-pocket costs affect patients with neurologic conditions, the investigators analyzed data from a large, privately insured health care claims database. They determined medication costs for patients with MS, peripheral neuropathy, epilepsy, dementia, and Parkinson’s disease who were seen by outpatient neurologists. They also compared costs for high-deductible and traditional plans and explored cumulative out-of-pocket costs during the first 2 years after diagnosis.
The analysis examined the five most commonly prescribed drugs by neurologists for each condition based on Medicare data. In addition, the researchers included in their analysis all approved MS medications, lacosamide as a brand name epilepsy drug, and venlafaxine, a peripheral neuropathy medication that transitioned from brand to generic.
In all, the study population included 105,355 patients with MS, 314,530 with peripheral neuropathy, 281,073 with epilepsy, 120,720 with dementia, and 90,801 with Parkinson’s disease.
In 2016, patients in high-deductible health plans had an average monthly out-of-pocket expense that was approximately twice that of patients not in those plans – $661 versus $246 among patients with MS, and $40 versus $18 among patients with epilepsy.
In the 2 years after diagnosis in 2012 or 2013, cumulative out-of-pocket costs for patients with MS were a mean of $2,238, but costs varied widely. Cumulative costs were no more than $90 for patients in the bottom 5% of expenses, whereas they exceeded $9,800 for patients in the top 5% of expenses. Among patients with epilepsy, cumulative out-of-pocket costs were $230 in the 2 years after diagnosis.
“In 2004, out-of-pocket costs were of such low magnitude that physicians could typically ignore these costs for most patients and not adversely affect the financial status of patients or their adherence to medications. However, by 2016, out-of-pockets costs have risen to the point where neurologists should consider out-of-pocket costs for most medications and for most patients,” Dr. Callaghan and colleagues wrote.
Ralph L. Sacco, MD, president of the American Academy of Neurology (AAN), said in a news release that the AAN has created a Neurology Drug Pricing Task Force and is advocating for better drug-pricing policies. “This study provides important information to help us better understand how these problems can directly affect our patients,” Dr. Sacco said.
“Everyone deserves affordable access to the medications that will be most beneficial, but if the drugs are too expensive, people may simply not take them, possibly leading to medical complications and higher costs later,” Dr. Sacco said.
The study was supported by the AAN. Several authors are supported by National Institutes of Health grants. Dr. Callaghan receives research support from Impeto Medical and performs consulting work.
SOURCE: Callaghan BC et al. Neurology. 2019 May 1. doi: 10.1212/WNL.0000000000007564.
FROM NEUROLOGY
Empty words, Captain Bacteria, and the perils of vampire facials
And now, 37 words from our sponsor
If you’re looking for gluten-free news of the health and medical sciences that’s low in sugar, we here at LOTME Farms promise to use no artificial colors or flavors to tell you about a study of the health claims on cereal boxes.
Researchers identified 37 such claims that appeared on the boxes of 460 different breakfast cereals and grouped them into four categories: adding positives (high fiber, probiotics), not adding negatives (GMO free, no high-fructose corn syrup), removing negatives (low cholesterol, no trans fat), and not removing positives (made with whole grains, fresh).
What they found is that words matter: None of the 37 claims explicitly said that the product inside would make people healthier or help them lose weight, but that was how respondents interpreted them. There is, of course, a reason none of the products claimed to improve health. “The correlation between the type of ‘healthy’ claim made and the actual nutritional quality of the breakfast cereal was almost zero,” investigator Pierre Chandon said.
This is, perhaps, not such a surprise. But we here at the pure, all-natural LOTME deal with facts, which are low in calories and contain no artificial growth hormones, and we would never insult (NEW LOTME LIGHT! NO ARTIFICIAL SWEETENERS!) our wholesome, low-fat readers by resorting (TRY FRESH LOTME ORGANIC!) to hyperbole or doublespeak. Not a chance (MMM … HOMEMADE LOTME).
Now, who’s up for a bowl of Froot Loops?
Captain Bacteria: Civil War
In the never-ending struggle of bacteria versus the world, Clostridium difficile has become a particularly stubborn foe. It is far more likely to be resistant to antibiotics, and the antibiotics that can do the job are either incredibly expensive or destroy the patient’s entire microbiota. However, we may have a new ally in the fight against C. diff: other bacteria.
Specifically, we’re talking about fecal transplants. According to an article published in the Journal of the American Osteopathic Association, the wide variety of bacteria that get transferred into the body along with the poop can block C. diff’s ability to germinate and produce the toxins that affect the human body. The treatment is especially beneficial for patients with C. diff whose microbiotas have been compromised by some other treatment, like chemotherapy, antibiotics, or proton pump inhibitors.
We here at LOTME would like to take a moment to salute the brave bacteria in our guts, fighting the good fight against those who would do us harm, and to the fecal transplants that let our own bacteria join the battle. Poop, you never let us down!
Dracula side effects
The Kim Kardashian effect is having dire ramifications. Back in 2013, the social media influencer posted a photo of herself getting a “vampire facial” – a dermatologic procedure in which a person’s own blood is injected into their face as a way to freshen and rejuvenate their skin. At least they aren’t drinking it.
Vampire facials have skyrocketed in popularity since, despite the ick factor. Unfortunately, it seems to be as dangerous as an encounter with a real vampire: Recently, two people in New Mexico were diagnosed with HIV after getting vampire facials.
The New Mexico Department of Health noted that both cases have been traced to the same spa, which was shut down in 2018 after at least three government agencies noted its lack of attention to hygiene and cleanliness. Warning to all: Just because a Kardashian does it doesn’t mean you should, too.
Shave that beard, Fido
The adage “a dog’s mouth is cleaner than a person’s” is getting an upgrade and this time it’s backed by science. A clinic in Zurich looked at the pathogenic microorganisms that reside in men’s beards and dogs’ fur and guess what – the beards were dirtier.
Despite beards’ manly cache among Millennials and hipsters, the results many have some reaching for the razor. The clinicians took a look at the bacterial load of colony-forming units of human-pathogenic microorganisms, and compared samples of beards and dog’s necks (since dogs don’t have beards, but how cute would that be?). They found high microbial counts in all beard samples, but only 23 of 30 dogs’ hair samples. Half of the human subjects carried so much bacteria that they were in danger of illness, the researchers noted.
Does this mean men are dirty? Or are dogs clean? The clinicians didn’t survey the men on their habits so it could be likely that they spend lots of time rolling around in the grass or drinking water from the toilet. More research is definitely needed here.
And now, 37 words from our sponsor
If you’re looking for gluten-free news of the health and medical sciences that’s low in sugar, we here at LOTME Farms promise to use no artificial colors or flavors to tell you about a study of the health claims on cereal boxes.
Researchers identified 37 such claims that appeared on the boxes of 460 different breakfast cereals and grouped them into four categories: adding positives (high fiber, probiotics), not adding negatives (GMO free, no high-fructose corn syrup), removing negatives (low cholesterol, no trans fat), and not removing positives (made with whole grains, fresh).
What they found is that words matter: None of the 37 claims explicitly said that the product inside would make people healthier or help them lose weight, but that was how respondents interpreted them. There is, of course, a reason none of the products claimed to improve health. “The correlation between the type of ‘healthy’ claim made and the actual nutritional quality of the breakfast cereal was almost zero,” investigator Pierre Chandon said.
This is, perhaps, not such a surprise. But we here at the pure, all-natural LOTME deal with facts, which are low in calories and contain no artificial growth hormones, and we would never insult (NEW LOTME LIGHT! NO ARTIFICIAL SWEETENERS!) our wholesome, low-fat readers by resorting (TRY FRESH LOTME ORGANIC!) to hyperbole or doublespeak. Not a chance (MMM … HOMEMADE LOTME).
Now, who’s up for a bowl of Froot Loops?
Captain Bacteria: Civil War
In the never-ending struggle of bacteria versus the world, Clostridium difficile has become a particularly stubborn foe. It is far more likely to be resistant to antibiotics, and the antibiotics that can do the job are either incredibly expensive or destroy the patient’s entire microbiota. However, we may have a new ally in the fight against C. diff: other bacteria.
Specifically, we’re talking about fecal transplants. According to an article published in the Journal of the American Osteopathic Association, the wide variety of bacteria that get transferred into the body along with the poop can block C. diff’s ability to germinate and produce the toxins that affect the human body. The treatment is especially beneficial for patients with C. diff whose microbiotas have been compromised by some other treatment, like chemotherapy, antibiotics, or proton pump inhibitors.
We here at LOTME would like to take a moment to salute the brave bacteria in our guts, fighting the good fight against those who would do us harm, and to the fecal transplants that let our own bacteria join the battle. Poop, you never let us down!
Dracula side effects
The Kim Kardashian effect is having dire ramifications. Back in 2013, the social media influencer posted a photo of herself getting a “vampire facial” – a dermatologic procedure in which a person’s own blood is injected into their face as a way to freshen and rejuvenate their skin. At least they aren’t drinking it.
Vampire facials have skyrocketed in popularity since, despite the ick factor. Unfortunately, it seems to be as dangerous as an encounter with a real vampire: Recently, two people in New Mexico were diagnosed with HIV after getting vampire facials.
The New Mexico Department of Health noted that both cases have been traced to the same spa, which was shut down in 2018 after at least three government agencies noted its lack of attention to hygiene and cleanliness. Warning to all: Just because a Kardashian does it doesn’t mean you should, too.
Shave that beard, Fido
The adage “a dog’s mouth is cleaner than a person’s” is getting an upgrade and this time it’s backed by science. A clinic in Zurich looked at the pathogenic microorganisms that reside in men’s beards and dogs’ fur and guess what – the beards were dirtier.
Despite beards’ manly cache among Millennials and hipsters, the results many have some reaching for the razor. The clinicians took a look at the bacterial load of colony-forming units of human-pathogenic microorganisms, and compared samples of beards and dog’s necks (since dogs don’t have beards, but how cute would that be?). They found high microbial counts in all beard samples, but only 23 of 30 dogs’ hair samples. Half of the human subjects carried so much bacteria that they were in danger of illness, the researchers noted.
Does this mean men are dirty? Or are dogs clean? The clinicians didn’t survey the men on their habits so it could be likely that they spend lots of time rolling around in the grass or drinking water from the toilet. More research is definitely needed here.
And now, 37 words from our sponsor
If you’re looking for gluten-free news of the health and medical sciences that’s low in sugar, we here at LOTME Farms promise to use no artificial colors or flavors to tell you about a study of the health claims on cereal boxes.
Researchers identified 37 such claims that appeared on the boxes of 460 different breakfast cereals and grouped them into four categories: adding positives (high fiber, probiotics), not adding negatives (GMO free, no high-fructose corn syrup), removing negatives (low cholesterol, no trans fat), and not removing positives (made with whole grains, fresh).
What they found is that words matter: None of the 37 claims explicitly said that the product inside would make people healthier or help them lose weight, but that was how respondents interpreted them. There is, of course, a reason none of the products claimed to improve health. “The correlation between the type of ‘healthy’ claim made and the actual nutritional quality of the breakfast cereal was almost zero,” investigator Pierre Chandon said.
This is, perhaps, not such a surprise. But we here at the pure, all-natural LOTME deal with facts, which are low in calories and contain no artificial growth hormones, and we would never insult (NEW LOTME LIGHT! NO ARTIFICIAL SWEETENERS!) our wholesome, low-fat readers by resorting (TRY FRESH LOTME ORGANIC!) to hyperbole or doublespeak. Not a chance (MMM … HOMEMADE LOTME).
Now, who’s up for a bowl of Froot Loops?
Captain Bacteria: Civil War
In the never-ending struggle of bacteria versus the world, Clostridium difficile has become a particularly stubborn foe. It is far more likely to be resistant to antibiotics, and the antibiotics that can do the job are either incredibly expensive or destroy the patient’s entire microbiota. However, we may have a new ally in the fight against C. diff: other bacteria.
Specifically, we’re talking about fecal transplants. According to an article published in the Journal of the American Osteopathic Association, the wide variety of bacteria that get transferred into the body along with the poop can block C. diff’s ability to germinate and produce the toxins that affect the human body. The treatment is especially beneficial for patients with C. diff whose microbiotas have been compromised by some other treatment, like chemotherapy, antibiotics, or proton pump inhibitors.
We here at LOTME would like to take a moment to salute the brave bacteria in our guts, fighting the good fight against those who would do us harm, and to the fecal transplants that let our own bacteria join the battle. Poop, you never let us down!
Dracula side effects
The Kim Kardashian effect is having dire ramifications. Back in 2013, the social media influencer posted a photo of herself getting a “vampire facial” – a dermatologic procedure in which a person’s own blood is injected into their face as a way to freshen and rejuvenate their skin. At least they aren’t drinking it.
Vampire facials have skyrocketed in popularity since, despite the ick factor. Unfortunately, it seems to be as dangerous as an encounter with a real vampire: Recently, two people in New Mexico were diagnosed with HIV after getting vampire facials.
The New Mexico Department of Health noted that both cases have been traced to the same spa, which was shut down in 2018 after at least three government agencies noted its lack of attention to hygiene and cleanliness. Warning to all: Just because a Kardashian does it doesn’t mean you should, too.
Shave that beard, Fido
The adage “a dog’s mouth is cleaner than a person’s” is getting an upgrade and this time it’s backed by science. A clinic in Zurich looked at the pathogenic microorganisms that reside in men’s beards and dogs’ fur and guess what – the beards were dirtier.
Despite beards’ manly cache among Millennials and hipsters, the results many have some reaching for the razor. The clinicians took a look at the bacterial load of colony-forming units of human-pathogenic microorganisms, and compared samples of beards and dog’s necks (since dogs don’t have beards, but how cute would that be?). They found high microbial counts in all beard samples, but only 23 of 30 dogs’ hair samples. Half of the human subjects carried so much bacteria that they were in danger of illness, the researchers noted.
Does this mean men are dirty? Or are dogs clean? The clinicians didn’t survey the men on their habits so it could be likely that they spend lots of time rolling around in the grass or drinking water from the toilet. More research is definitely needed here.
Are guidelines relevant?
The recent publication of the changes and current levels of evidence for the guidelines from the American College of Cardiology, American Heart Association, and the European Society of Cardiology once again indicates that the level of high-quality scientific data supporting the decision making process is limited.
Of the thousands of recommendations among the guidelines provided, level A data – which is supported by at least two randomized, controlled trials (RCT), arguably the gold standard for the proof of benefit of a treatment program – was available in only 8.5% of ACC/AHA recommendations and in 14.2% of ESC recommendations. The recent review covering guidelines published from 2008 to 2018 has changed very little since the previous review carried out on data collected between 1999 and 2014 (JAMA. 2019 Mar 19;321[11]:1069-80). Admittedly, by the nature of their design, RCTs represent a very special subset of any disease process but they are the best we can do. The remainder of the guidelines is supported by nonrandomized data and consensus opinion of “experts.” The absence of randomized data in the rest of the guidelines creates an area of uncertainty between clinical practice and outcomes.
Guidelines have been with us for almost 30 years and have provided a near “cookbook recipe” for the treatment of almost the totality of cardiovascular care, both in the United States and Europe. There is little evidence that guideline dissemination results in a beneficial effect on cardiovascular care, instead reflecting the contemporary published research and informed opinion of our generation.
Despite the limitation of hard data based on RCTs, cardiovascular mortality has leveled off in the last few years. Although there are a number of areas that could be investigated with more focused and practical RCTs, there has been little enthusiasm by either the National Heart, Lung, and Blood Institute or the pharmaceutical or device industries to investigate existing cardiovascular drugs and/or devices to better elucidate nuanced therapy for subsets of heart disease that remain in the uncertain data areas. In fact, the current report shows that there has been little change in guidelines in the last 10 years. Most effort has been focused on new drug development and application.
Much of the advance in cardiovascular care and decrease in mortality is a result of the development of new drugs for the treatment of hypertension, management of hypercholesterolemia, and MI, together with coronary angiography and its interventional permutations of the previous 50 years. Those advances are now part of our knowledge base, our therapeutic DNA, and in the absence of some new scientific breakthrough, there is little to expect from future guideline development. Medical students and house officers are being taught as fact what we found as exciting new therapy just a few short years ago. Guidelines are now part of textbook knowledge and until new clinical outcome are reported, guidelines will probably serve a useful reference material but will not lead to much change in clinical care.
Even so, treating the patient in the clinic and in the hospital still requires the doctor to practice the “art” of medicine and to synthesize therapy based on the paucity of scientific data and quasi knowledge acquired over a generation.
The appreciation that much is unknown gives the doctor the humility required to be sensitive to patient needs and their symptoms and the aspiration for new, science-based data. This is still part of the excitement of being a doctor.
Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.
The recent publication of the changes and current levels of evidence for the guidelines from the American College of Cardiology, American Heart Association, and the European Society of Cardiology once again indicates that the level of high-quality scientific data supporting the decision making process is limited.
Of the thousands of recommendations among the guidelines provided, level A data – which is supported by at least two randomized, controlled trials (RCT), arguably the gold standard for the proof of benefit of a treatment program – was available in only 8.5% of ACC/AHA recommendations and in 14.2% of ESC recommendations. The recent review covering guidelines published from 2008 to 2018 has changed very little since the previous review carried out on data collected between 1999 and 2014 (JAMA. 2019 Mar 19;321[11]:1069-80). Admittedly, by the nature of their design, RCTs represent a very special subset of any disease process but they are the best we can do. The remainder of the guidelines is supported by nonrandomized data and consensus opinion of “experts.” The absence of randomized data in the rest of the guidelines creates an area of uncertainty between clinical practice and outcomes.
Guidelines have been with us for almost 30 years and have provided a near “cookbook recipe” for the treatment of almost the totality of cardiovascular care, both in the United States and Europe. There is little evidence that guideline dissemination results in a beneficial effect on cardiovascular care, instead reflecting the contemporary published research and informed opinion of our generation.
Despite the limitation of hard data based on RCTs, cardiovascular mortality has leveled off in the last few years. Although there are a number of areas that could be investigated with more focused and practical RCTs, there has been little enthusiasm by either the National Heart, Lung, and Blood Institute or the pharmaceutical or device industries to investigate existing cardiovascular drugs and/or devices to better elucidate nuanced therapy for subsets of heart disease that remain in the uncertain data areas. In fact, the current report shows that there has been little change in guidelines in the last 10 years. Most effort has been focused on new drug development and application.
Much of the advance in cardiovascular care and decrease in mortality is a result of the development of new drugs for the treatment of hypertension, management of hypercholesterolemia, and MI, together with coronary angiography and its interventional permutations of the previous 50 years. Those advances are now part of our knowledge base, our therapeutic DNA, and in the absence of some new scientific breakthrough, there is little to expect from future guideline development. Medical students and house officers are being taught as fact what we found as exciting new therapy just a few short years ago. Guidelines are now part of textbook knowledge and until new clinical outcome are reported, guidelines will probably serve a useful reference material but will not lead to much change in clinical care.
Even so, treating the patient in the clinic and in the hospital still requires the doctor to practice the “art” of medicine and to synthesize therapy based on the paucity of scientific data and quasi knowledge acquired over a generation.
The appreciation that much is unknown gives the doctor the humility required to be sensitive to patient needs and their symptoms and the aspiration for new, science-based data. This is still part of the excitement of being a doctor.
Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.
The recent publication of the changes and current levels of evidence for the guidelines from the American College of Cardiology, American Heart Association, and the European Society of Cardiology once again indicates that the level of high-quality scientific data supporting the decision making process is limited.
Of the thousands of recommendations among the guidelines provided, level A data – which is supported by at least two randomized, controlled trials (RCT), arguably the gold standard for the proof of benefit of a treatment program – was available in only 8.5% of ACC/AHA recommendations and in 14.2% of ESC recommendations. The recent review covering guidelines published from 2008 to 2018 has changed very little since the previous review carried out on data collected between 1999 and 2014 (JAMA. 2019 Mar 19;321[11]:1069-80). Admittedly, by the nature of their design, RCTs represent a very special subset of any disease process but they are the best we can do. The remainder of the guidelines is supported by nonrandomized data and consensus opinion of “experts.” The absence of randomized data in the rest of the guidelines creates an area of uncertainty between clinical practice and outcomes.
Guidelines have been with us for almost 30 years and have provided a near “cookbook recipe” for the treatment of almost the totality of cardiovascular care, both in the United States and Europe. There is little evidence that guideline dissemination results in a beneficial effect on cardiovascular care, instead reflecting the contemporary published research and informed opinion of our generation.
Despite the limitation of hard data based on RCTs, cardiovascular mortality has leveled off in the last few years. Although there are a number of areas that could be investigated with more focused and practical RCTs, there has been little enthusiasm by either the National Heart, Lung, and Blood Institute or the pharmaceutical or device industries to investigate existing cardiovascular drugs and/or devices to better elucidate nuanced therapy for subsets of heart disease that remain in the uncertain data areas. In fact, the current report shows that there has been little change in guidelines in the last 10 years. Most effort has been focused on new drug development and application.
Much of the advance in cardiovascular care and decrease in mortality is a result of the development of new drugs for the treatment of hypertension, management of hypercholesterolemia, and MI, together with coronary angiography and its interventional permutations of the previous 50 years. Those advances are now part of our knowledge base, our therapeutic DNA, and in the absence of some new scientific breakthrough, there is little to expect from future guideline development. Medical students and house officers are being taught as fact what we found as exciting new therapy just a few short years ago. Guidelines are now part of textbook knowledge and until new clinical outcome are reported, guidelines will probably serve a useful reference material but will not lead to much change in clinical care.
Even so, treating the patient in the clinic and in the hospital still requires the doctor to practice the “art” of medicine and to synthesize therapy based on the paucity of scientific data and quasi knowledge acquired over a generation.
The appreciation that much is unknown gives the doctor the humility required to be sensitive to patient needs and their symptoms and the aspiration for new, science-based data. This is still part of the excitement of being a doctor.
Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.
Increase in pediatric thyroid cancers: overdiagnosis or something more?
Thyroid cancer rates are on the rise in U.S. pediatric patients, a large epidemiologic study shows, and researchers say the trend can’t be explained away purely as overdiagnosis.
However, the extent of a real increase in clinically significant cancers and what might be causing that increase remains unclear, according to authors of the study and two related editorials appearing in the journal Cancer.
Cases of pediatric differentiated thyroid cancer (DTC) cases increased by 4.43% per year in the study, which was based on data from 39 U.S. cancer registries. Increases were seen in both smaller early-stage and larger late-stage tumors, leading study authors to assert that the trend was “unlikely to be explained solely by increased medical surveillance or improved detection.”
“Environmental and individual factors may also have affected rising trends,” said Meredith S. Shiels, PhD, of the National Cancer Institute and coauthors in a report on the study.
A true increase in pediatric thyroid cancer incidence is a possibility, authors of a related editorial said; however, they also expressed concern that inferences drawn from this U.S. cancer epidemiology data may be “artifactual.”
“We believe that first it is most important to closely examine the reasons for the increase that could be attributable to overdiagnosis, given this appears to be a likely explanation,” said authors of one editorial, including Amy Y. Chen, MD, MPH, of Emory University, Atlanta, and Louise Davies, MD, MS, of the Dartmouth Institute for Health Policy and Clinical Practice in Lebanon, N.H.
Overdiagnosis does occur, but the “real component” of the rise in thyroid cancer incidence cannot be ignored, according to a second editorial by David Goldenberg, MD, of Penn State University, Hershey.
“Although many authors are quick to explain the rise in thyroid cancer as an artifact of the overdiagnosis of clinically insignificant thyroid cancers, multiple groups all over the world have shown that this is not sufficient to explain the rise in thyroid cancer,” Dr. Goldenberg said in his editorial.
New data in pediatric patients
Pediatric DTCs are rare, representing just 2%-4% of pediatric malignancies, and they’re particularly rare in relation to adult cases, comprising about 2.3% of thyroid cancer diagnoses overall, according to Dr. Shiels and coauthors of the current study.
“The rarity of pediatric DTC, the lack of information on histologic features, or both have prevented prior studies from analyzing trends by tumor size or cancer stage at diagnosis,” they said.
To address this knowledge gap, Dr. Shiels and colleagues analyzed a total of 7,296 primary DTCs in children aged 0-19 years in data obtained from the North American Association of Central Cancer Registries. Ninety-one percent of these pediatric patients had papillary thyroid cancer, 83% were female, and 76% were between the ages of 15 to 19 years.
The rate of pediatric DTCs increased from 4.77 per million in 1998 to 8.82 per million in 2013, representing an increase of 4.43% per year, they found.
Both localized and more aggressive tumors increased in incidence over that time period, they also found. The annual increase was 4.06% for local stage at diagnosis, 5.68% for regional, and 8.55% for distant disease.
Similarly, increases were seen in small and large tumors alike. The annual percentage increase was 9.46% for tumors smaller than 1 cm, and 4.69% for tumors greater than 2 cm, according to the report.
Looking at age, investigators found that the increases in incidence were significant only for 10- to 19-year-olds, while significant increases were consistently observed for both sexes and for all races and ethnicities.
Overdiagnosis vs. environmental factors and lifestyle changes
If further investigations point to detection of subclinical disease as the cause of the increases in pediatric DTC incidence then initiatives may be needed to curtail use of CT scans, ultrasound, and needle biopsies, as has been done in adults, Dr. Chen and Dr. Davies said in their editorial.
“When the American Thyroid Association modified their guidelines for needle biopsy of nodules to discourage sampling of small lesions, a corresponding decrease in incidence rates was observed, suggesting that, indeed, overdiagnosis was the culprit,” they said.
Although it’s not clear what environmental factors or lifestyle changes are driving an increase, obesity has been consistently linked to increases in thyroid cancer, Dr. Goldenberg said. Conversely, smoking has been linked to reduced thyroid cancer risk, which means reduced prevalence of smoking in the community could potentially contribute to increased thyroid cancer incidence.
“It is our role as physicians to protect our patients from complacency and undertreatment,” he concluded in his editorial. “Explaining away thyroid cancers as being subclinical or clinically insignificant is reminiscent of days past when we told our patients: ‘Don’t worry, it’s good cancer.’ ”
The research by Dr. Shiels and colleagues was supported by the Intramural Research Program of the National Cancer Institute. Dr. Shiels and coauthors made no conflict of interest disclosures related to their report.
SOURCE: Shiels MO et al. Cancer. 2019 Apr 23. doi: 10.1002/cncr.32125.
Thyroid cancer rates are on the rise in U.S. pediatric patients, a large epidemiologic study shows, and researchers say the trend can’t be explained away purely as overdiagnosis.
However, the extent of a real increase in clinically significant cancers and what might be causing that increase remains unclear, according to authors of the study and two related editorials appearing in the journal Cancer.
Cases of pediatric differentiated thyroid cancer (DTC) cases increased by 4.43% per year in the study, which was based on data from 39 U.S. cancer registries. Increases were seen in both smaller early-stage and larger late-stage tumors, leading study authors to assert that the trend was “unlikely to be explained solely by increased medical surveillance or improved detection.”
“Environmental and individual factors may also have affected rising trends,” said Meredith S. Shiels, PhD, of the National Cancer Institute and coauthors in a report on the study.
A true increase in pediatric thyroid cancer incidence is a possibility, authors of a related editorial said; however, they also expressed concern that inferences drawn from this U.S. cancer epidemiology data may be “artifactual.”
“We believe that first it is most important to closely examine the reasons for the increase that could be attributable to overdiagnosis, given this appears to be a likely explanation,” said authors of one editorial, including Amy Y. Chen, MD, MPH, of Emory University, Atlanta, and Louise Davies, MD, MS, of the Dartmouth Institute for Health Policy and Clinical Practice in Lebanon, N.H.
Overdiagnosis does occur, but the “real component” of the rise in thyroid cancer incidence cannot be ignored, according to a second editorial by David Goldenberg, MD, of Penn State University, Hershey.
“Although many authors are quick to explain the rise in thyroid cancer as an artifact of the overdiagnosis of clinically insignificant thyroid cancers, multiple groups all over the world have shown that this is not sufficient to explain the rise in thyroid cancer,” Dr. Goldenberg said in his editorial.
New data in pediatric patients
Pediatric DTCs are rare, representing just 2%-4% of pediatric malignancies, and they’re particularly rare in relation to adult cases, comprising about 2.3% of thyroid cancer diagnoses overall, according to Dr. Shiels and coauthors of the current study.
“The rarity of pediatric DTC, the lack of information on histologic features, or both have prevented prior studies from analyzing trends by tumor size or cancer stage at diagnosis,” they said.
To address this knowledge gap, Dr. Shiels and colleagues analyzed a total of 7,296 primary DTCs in children aged 0-19 years in data obtained from the North American Association of Central Cancer Registries. Ninety-one percent of these pediatric patients had papillary thyroid cancer, 83% were female, and 76% were between the ages of 15 to 19 years.
The rate of pediatric DTCs increased from 4.77 per million in 1998 to 8.82 per million in 2013, representing an increase of 4.43% per year, they found.
Both localized and more aggressive tumors increased in incidence over that time period, they also found. The annual increase was 4.06% for local stage at diagnosis, 5.68% for regional, and 8.55% for distant disease.
Similarly, increases were seen in small and large tumors alike. The annual percentage increase was 9.46% for tumors smaller than 1 cm, and 4.69% for tumors greater than 2 cm, according to the report.
Looking at age, investigators found that the increases in incidence were significant only for 10- to 19-year-olds, while significant increases were consistently observed for both sexes and for all races and ethnicities.
Overdiagnosis vs. environmental factors and lifestyle changes
If further investigations point to detection of subclinical disease as the cause of the increases in pediatric DTC incidence then initiatives may be needed to curtail use of CT scans, ultrasound, and needle biopsies, as has been done in adults, Dr. Chen and Dr. Davies said in their editorial.
“When the American Thyroid Association modified their guidelines for needle biopsy of nodules to discourage sampling of small lesions, a corresponding decrease in incidence rates was observed, suggesting that, indeed, overdiagnosis was the culprit,” they said.
Although it’s not clear what environmental factors or lifestyle changes are driving an increase, obesity has been consistently linked to increases in thyroid cancer, Dr. Goldenberg said. Conversely, smoking has been linked to reduced thyroid cancer risk, which means reduced prevalence of smoking in the community could potentially contribute to increased thyroid cancer incidence.
“It is our role as physicians to protect our patients from complacency and undertreatment,” he concluded in his editorial. “Explaining away thyroid cancers as being subclinical or clinically insignificant is reminiscent of days past when we told our patients: ‘Don’t worry, it’s good cancer.’ ”
The research by Dr. Shiels and colleagues was supported by the Intramural Research Program of the National Cancer Institute. Dr. Shiels and coauthors made no conflict of interest disclosures related to their report.
SOURCE: Shiels MO et al. Cancer. 2019 Apr 23. doi: 10.1002/cncr.32125.
Thyroid cancer rates are on the rise in U.S. pediatric patients, a large epidemiologic study shows, and researchers say the trend can’t be explained away purely as overdiagnosis.
However, the extent of a real increase in clinically significant cancers and what might be causing that increase remains unclear, according to authors of the study and two related editorials appearing in the journal Cancer.
Cases of pediatric differentiated thyroid cancer (DTC) cases increased by 4.43% per year in the study, which was based on data from 39 U.S. cancer registries. Increases were seen in both smaller early-stage and larger late-stage tumors, leading study authors to assert that the trend was “unlikely to be explained solely by increased medical surveillance or improved detection.”
“Environmental and individual factors may also have affected rising trends,” said Meredith S. Shiels, PhD, of the National Cancer Institute and coauthors in a report on the study.
A true increase in pediatric thyroid cancer incidence is a possibility, authors of a related editorial said; however, they also expressed concern that inferences drawn from this U.S. cancer epidemiology data may be “artifactual.”
“We believe that first it is most important to closely examine the reasons for the increase that could be attributable to overdiagnosis, given this appears to be a likely explanation,” said authors of one editorial, including Amy Y. Chen, MD, MPH, of Emory University, Atlanta, and Louise Davies, MD, MS, of the Dartmouth Institute for Health Policy and Clinical Practice in Lebanon, N.H.
Overdiagnosis does occur, but the “real component” of the rise in thyroid cancer incidence cannot be ignored, according to a second editorial by David Goldenberg, MD, of Penn State University, Hershey.
“Although many authors are quick to explain the rise in thyroid cancer as an artifact of the overdiagnosis of clinically insignificant thyroid cancers, multiple groups all over the world have shown that this is not sufficient to explain the rise in thyroid cancer,” Dr. Goldenberg said in his editorial.
New data in pediatric patients
Pediatric DTCs are rare, representing just 2%-4% of pediatric malignancies, and they’re particularly rare in relation to adult cases, comprising about 2.3% of thyroid cancer diagnoses overall, according to Dr. Shiels and coauthors of the current study.
“The rarity of pediatric DTC, the lack of information on histologic features, or both have prevented prior studies from analyzing trends by tumor size or cancer stage at diagnosis,” they said.
To address this knowledge gap, Dr. Shiels and colleagues analyzed a total of 7,296 primary DTCs in children aged 0-19 years in data obtained from the North American Association of Central Cancer Registries. Ninety-one percent of these pediatric patients had papillary thyroid cancer, 83% were female, and 76% were between the ages of 15 to 19 years.
The rate of pediatric DTCs increased from 4.77 per million in 1998 to 8.82 per million in 2013, representing an increase of 4.43% per year, they found.
Both localized and more aggressive tumors increased in incidence over that time period, they also found. The annual increase was 4.06% for local stage at diagnosis, 5.68% for regional, and 8.55% for distant disease.
Similarly, increases were seen in small and large tumors alike. The annual percentage increase was 9.46% for tumors smaller than 1 cm, and 4.69% for tumors greater than 2 cm, according to the report.
Looking at age, investigators found that the increases in incidence were significant only for 10- to 19-year-olds, while significant increases were consistently observed for both sexes and for all races and ethnicities.
Overdiagnosis vs. environmental factors and lifestyle changes
If further investigations point to detection of subclinical disease as the cause of the increases in pediatric DTC incidence then initiatives may be needed to curtail use of CT scans, ultrasound, and needle biopsies, as has been done in adults, Dr. Chen and Dr. Davies said in their editorial.
“When the American Thyroid Association modified their guidelines for needle biopsy of nodules to discourage sampling of small lesions, a corresponding decrease in incidence rates was observed, suggesting that, indeed, overdiagnosis was the culprit,” they said.
Although it’s not clear what environmental factors or lifestyle changes are driving an increase, obesity has been consistently linked to increases in thyroid cancer, Dr. Goldenberg said. Conversely, smoking has been linked to reduced thyroid cancer risk, which means reduced prevalence of smoking in the community could potentially contribute to increased thyroid cancer incidence.
“It is our role as physicians to protect our patients from complacency and undertreatment,” he concluded in his editorial. “Explaining away thyroid cancers as being subclinical or clinically insignificant is reminiscent of days past when we told our patients: ‘Don’t worry, it’s good cancer.’ ”
The research by Dr. Shiels and colleagues was supported by the Intramural Research Program of the National Cancer Institute. Dr. Shiels and coauthors made no conflict of interest disclosures related to their report.
SOURCE: Shiels MO et al. Cancer. 2019 Apr 23. doi: 10.1002/cncr.32125.
FROM CANCER
Type 2 diabetes bumps up short-term risk for bone fracture
LOS ANGELES – results from a large community-based study have shown.
“Osteoporotic fractures are a significant public health burden, causing high morbidity, mortality, and associated health care costs,” Elizabeth J. Samelson, PhD, said in an interview in advance of the annual scientific and clinical congress of the American Association of Clinical Endocrinologists. “Risk of fractures are higher in patients with type 2 diabetes. Further, outcomes are worse in type 2 diabetes patients, with greater frequency of complications following a fracture.”
Given the projected increase in type 2 diabetes in the U.S. population, Dr. Samelson, an associate scientist at the Marcus Institute for Aging Research at Hebrew SeniorLife and Harvard Medical School, Boston, and colleagues set out to evaluate the short- and long-term risks of bone fractures associated with the disease. They drew from 2,105 women and 1,130 men who participated in the Framingham Original and Offspring Cohorts and whose baseline osteoporosis visit was around 1990. Type 2 diabetes was defined as having a fasting plasma glucose of greater than 125 mg/dL or being on treatment for the disease. Incident fractures excluded finger, toe, skull, face, and pathologic fractures, and the researchers used repeated measures analyses to estimate hazard ratios for the association between type 2 diabetes, type 2 diabetes medication use, and type 2 diabetes duration and incident fracture, adjusted for age, sex, height, and weight.
The mean age of the study participants was 67 years, and the mean follow-up was 9 years. The prevalence of type 2 diabetes in women and men was 7% and 13%, respectively, and 63% and 51% of those were on medication for the disease. The mean duration of diabetes was 8 years.
Dr. Samelson and colleagues found that the cumulative incidence of fracture was 37% in women with type 2 diabetes and 30% in those without the disease. Meanwhile, the cumulative incidence of fracture was 11% in men with type 2 diabetes and 16% in those without the disease. The researchers also found that type 2 diabetes was associated with 1-year fracture risk in women (hazard ratio, 2.23), but not in men.
In the entire study population, longer duration of type 2 diabetes increased the 2-year fracture risk (HR, 1.28), as did the use of any type 2 diabetes medication (HR, 1.70). The researchers observed no statistically significant differences between type 2 diabetes and long-term incidence of fracture.
“Previous studies have contributed to understanding the higher incidence of fractures and worse outcomes in type 2 diabetes, [but] the current study demonstrated that patients [with type 2 diabetes] have 50% to 100% higher short-term [1- to 2-year] risk of fracture independent of clinical risk factors, whereas long-term [10-year] risk of fracture was similar in [patients with] type 2 diabetes and those who do not have [the disease],” Dr. Samelson said. “The current study has some inherent limitations of observational studies, including a lack of definitive determination of causality and that the results are not generalizable to patients with similar demographics. The study, however, is robust in the availability of detailed clinical information, which allows for control of multiple confounding variables.”
Dr. Samelson reported having no financial disclosures. Coauthors Setareh Williams, PhD, and Rich Weiss, MD, are employees and shareholders of Radius Health Inc.
LOS ANGELES – results from a large community-based study have shown.
“Osteoporotic fractures are a significant public health burden, causing high morbidity, mortality, and associated health care costs,” Elizabeth J. Samelson, PhD, said in an interview in advance of the annual scientific and clinical congress of the American Association of Clinical Endocrinologists. “Risk of fractures are higher in patients with type 2 diabetes. Further, outcomes are worse in type 2 diabetes patients, with greater frequency of complications following a fracture.”
Given the projected increase in type 2 diabetes in the U.S. population, Dr. Samelson, an associate scientist at the Marcus Institute for Aging Research at Hebrew SeniorLife and Harvard Medical School, Boston, and colleagues set out to evaluate the short- and long-term risks of bone fractures associated with the disease. They drew from 2,105 women and 1,130 men who participated in the Framingham Original and Offspring Cohorts and whose baseline osteoporosis visit was around 1990. Type 2 diabetes was defined as having a fasting plasma glucose of greater than 125 mg/dL or being on treatment for the disease. Incident fractures excluded finger, toe, skull, face, and pathologic fractures, and the researchers used repeated measures analyses to estimate hazard ratios for the association between type 2 diabetes, type 2 diabetes medication use, and type 2 diabetes duration and incident fracture, adjusted for age, sex, height, and weight.
The mean age of the study participants was 67 years, and the mean follow-up was 9 years. The prevalence of type 2 diabetes in women and men was 7% and 13%, respectively, and 63% and 51% of those were on medication for the disease. The mean duration of diabetes was 8 years.
Dr. Samelson and colleagues found that the cumulative incidence of fracture was 37% in women with type 2 diabetes and 30% in those without the disease. Meanwhile, the cumulative incidence of fracture was 11% in men with type 2 diabetes and 16% in those without the disease. The researchers also found that type 2 diabetes was associated with 1-year fracture risk in women (hazard ratio, 2.23), but not in men.
In the entire study population, longer duration of type 2 diabetes increased the 2-year fracture risk (HR, 1.28), as did the use of any type 2 diabetes medication (HR, 1.70). The researchers observed no statistically significant differences between type 2 diabetes and long-term incidence of fracture.
“Previous studies have contributed to understanding the higher incidence of fractures and worse outcomes in type 2 diabetes, [but] the current study demonstrated that patients [with type 2 diabetes] have 50% to 100% higher short-term [1- to 2-year] risk of fracture independent of clinical risk factors, whereas long-term [10-year] risk of fracture was similar in [patients with] type 2 diabetes and those who do not have [the disease],” Dr. Samelson said. “The current study has some inherent limitations of observational studies, including a lack of definitive determination of causality and that the results are not generalizable to patients with similar demographics. The study, however, is robust in the availability of detailed clinical information, which allows for control of multiple confounding variables.”
Dr. Samelson reported having no financial disclosures. Coauthors Setareh Williams, PhD, and Rich Weiss, MD, are employees and shareholders of Radius Health Inc.
LOS ANGELES – results from a large community-based study have shown.
“Osteoporotic fractures are a significant public health burden, causing high morbidity, mortality, and associated health care costs,” Elizabeth J. Samelson, PhD, said in an interview in advance of the annual scientific and clinical congress of the American Association of Clinical Endocrinologists. “Risk of fractures are higher in patients with type 2 diabetes. Further, outcomes are worse in type 2 diabetes patients, with greater frequency of complications following a fracture.”
Given the projected increase in type 2 diabetes in the U.S. population, Dr. Samelson, an associate scientist at the Marcus Institute for Aging Research at Hebrew SeniorLife and Harvard Medical School, Boston, and colleagues set out to evaluate the short- and long-term risks of bone fractures associated with the disease. They drew from 2,105 women and 1,130 men who participated in the Framingham Original and Offspring Cohorts and whose baseline osteoporosis visit was around 1990. Type 2 diabetes was defined as having a fasting plasma glucose of greater than 125 mg/dL or being on treatment for the disease. Incident fractures excluded finger, toe, skull, face, and pathologic fractures, and the researchers used repeated measures analyses to estimate hazard ratios for the association between type 2 diabetes, type 2 diabetes medication use, and type 2 diabetes duration and incident fracture, adjusted for age, sex, height, and weight.
The mean age of the study participants was 67 years, and the mean follow-up was 9 years. The prevalence of type 2 diabetes in women and men was 7% and 13%, respectively, and 63% and 51% of those were on medication for the disease. The mean duration of diabetes was 8 years.
Dr. Samelson and colleagues found that the cumulative incidence of fracture was 37% in women with type 2 diabetes and 30% in those without the disease. Meanwhile, the cumulative incidence of fracture was 11% in men with type 2 diabetes and 16% in those without the disease. The researchers also found that type 2 diabetes was associated with 1-year fracture risk in women (hazard ratio, 2.23), but not in men.
In the entire study population, longer duration of type 2 diabetes increased the 2-year fracture risk (HR, 1.28), as did the use of any type 2 diabetes medication (HR, 1.70). The researchers observed no statistically significant differences between type 2 diabetes and long-term incidence of fracture.
“Previous studies have contributed to understanding the higher incidence of fractures and worse outcomes in type 2 diabetes, [but] the current study demonstrated that patients [with type 2 diabetes] have 50% to 100% higher short-term [1- to 2-year] risk of fracture independent of clinical risk factors, whereas long-term [10-year] risk of fracture was similar in [patients with] type 2 diabetes and those who do not have [the disease],” Dr. Samelson said. “The current study has some inherent limitations of observational studies, including a lack of definitive determination of causality and that the results are not generalizable to patients with similar demographics. The study, however, is robust in the availability of detailed clinical information, which allows for control of multiple confounding variables.”
Dr. Samelson reported having no financial disclosures. Coauthors Setareh Williams, PhD, and Rich Weiss, MD, are employees and shareholders of Radius Health Inc.
REPORTING FROM AACE 2019
Induction trough levels predicted ustekinumab response in Crohn’s disease
For patients with Crohn’s disease, therapeutic drug monitoring helped identify early primary nonresponders to induction with ustekinumab, according to researchers. The report is in Clinical Gastroenterology and Hepatology.
At week 8, median trough levels of ustekinumab were 6.0 mcg per mL (interquartile range, 3.1-8.0) among patients who achieved a primary response to induction at week 16, versus 1.3 mcg/mL (IQR, 0.9-5.6 ) among primary nonresponders (P = .03). An 8-week ustekinumab trough level cutoff of 2.0 mcg/mL distinguished week 16 responders from nonresponders with an area under the receiver operating curve (AUROC) of 0.75, wrote Ninon Soufflet of University Claude Bernard Lyon 1 in France, and associates. The researchers recommended “dedicated studies” to assess whether escalating the dose of ustekinumab can benefit patients with lower trough levels at week 8.
Few studies have explored biomarkers for response to ustekinumab induction therapy. Hence, the researchers assessed the relative utility of ustekinumab trough levels, C-reactive protein (CRP) levels, and fecal calprotectin levels for predicting early primary nonresponse. All 51 study participants had active luminal Crohn’s disease and received body weight–based intravenous infusions of ustekinumab at baseline, followed by subcutaneous injections of 90 mg. Primary nonresponders did not achieve steroid-free clinical and biochemical remission at week 16, defined as a Harvey-Bradshaw Index (HBI) of 4 points or less, a CRP level under 5 mg/L, and a fecal calprotectin level under 250 mcg/g. Week 16 was chosen to account for any delayed responders, the researchers noted.
A total of 32 patients (63%) achieved remission to ustekinumab induction therapy by week 16. An 8-week trough level of 2.0 mcg/mL was found to be optimal and distinguished primary nonresponders from responders with a sensitivity of 87%, a specificity of 66%, a positive predictive value of 82%, and a negative predictive value of 75%. In prior studies, optimal thresholds exceeded 3.3 mcg/mL for achieving remission and 4.5 mcg/mL at week 26 for achieving endoscopic response, the researchers noted. They said that this discrepancy might reflect different time points for evaluation, assays for measuring ustekinumab, patient populations, and a lack of endoscopic data in their study. “The relatively small sample size and the short period of follow-up evaluation [were] substantial limitations” they acknowledged.
In this study, levels of CRP did not change significantly between weeks 0 and 16 among either responders or nonresponders. In contrast, fecal calprotectin levels dropped rapidly and significantly over time only in responders. Median fecal calprotectin levels were 1,612 mcg/g of stools at week 0 versus 374 mcg/g at week 4 and 339 mcg/g at week 8. The finding “confirms the value of this biomarker, as previously shown in inflammatory bowel disease with anti–tumor necrosis factor,” the researchers wrote.
The investigators did not acknowledge external funding sources. Dr. Soufflet reported having no conflicts of interest. The senior author and three coinvestigators disclosed ties to MSD, AbbVie, Tillots, and several other pharmaceutical companies.
SOURCE: Soufflet N et al. Clin Gastroenterol Hepatol. 2019 Mar 6. doi: 10.1016/j.cgh.2019.02.042. https://www.cghjournal.org/article/S1542-3565(19)30248-4/abstract
For patients with Crohn’s disease, therapeutic drug monitoring helped identify early primary nonresponders to induction with ustekinumab, according to researchers. The report is in Clinical Gastroenterology and Hepatology.
At week 8, median trough levels of ustekinumab were 6.0 mcg per mL (interquartile range, 3.1-8.0) among patients who achieved a primary response to induction at week 16, versus 1.3 mcg/mL (IQR, 0.9-5.6 ) among primary nonresponders (P = .03). An 8-week ustekinumab trough level cutoff of 2.0 mcg/mL distinguished week 16 responders from nonresponders with an area under the receiver operating curve (AUROC) of 0.75, wrote Ninon Soufflet of University Claude Bernard Lyon 1 in France, and associates. The researchers recommended “dedicated studies” to assess whether escalating the dose of ustekinumab can benefit patients with lower trough levels at week 8.
Few studies have explored biomarkers for response to ustekinumab induction therapy. Hence, the researchers assessed the relative utility of ustekinumab trough levels, C-reactive protein (CRP) levels, and fecal calprotectin levels for predicting early primary nonresponse. All 51 study participants had active luminal Crohn’s disease and received body weight–based intravenous infusions of ustekinumab at baseline, followed by subcutaneous injections of 90 mg. Primary nonresponders did not achieve steroid-free clinical and biochemical remission at week 16, defined as a Harvey-Bradshaw Index (HBI) of 4 points or less, a CRP level under 5 mg/L, and a fecal calprotectin level under 250 mcg/g. Week 16 was chosen to account for any delayed responders, the researchers noted.
A total of 32 patients (63%) achieved remission to ustekinumab induction therapy by week 16. An 8-week trough level of 2.0 mcg/mL was found to be optimal and distinguished primary nonresponders from responders with a sensitivity of 87%, a specificity of 66%, a positive predictive value of 82%, and a negative predictive value of 75%. In prior studies, optimal thresholds exceeded 3.3 mcg/mL for achieving remission and 4.5 mcg/mL at week 26 for achieving endoscopic response, the researchers noted. They said that this discrepancy might reflect different time points for evaluation, assays for measuring ustekinumab, patient populations, and a lack of endoscopic data in their study. “The relatively small sample size and the short period of follow-up evaluation [were] substantial limitations” they acknowledged.
In this study, levels of CRP did not change significantly between weeks 0 and 16 among either responders or nonresponders. In contrast, fecal calprotectin levels dropped rapidly and significantly over time only in responders. Median fecal calprotectin levels were 1,612 mcg/g of stools at week 0 versus 374 mcg/g at week 4 and 339 mcg/g at week 8. The finding “confirms the value of this biomarker, as previously shown in inflammatory bowel disease with anti–tumor necrosis factor,” the researchers wrote.
The investigators did not acknowledge external funding sources. Dr. Soufflet reported having no conflicts of interest. The senior author and three coinvestigators disclosed ties to MSD, AbbVie, Tillots, and several other pharmaceutical companies.
SOURCE: Soufflet N et al. Clin Gastroenterol Hepatol. 2019 Mar 6. doi: 10.1016/j.cgh.2019.02.042. https://www.cghjournal.org/article/S1542-3565(19)30248-4/abstract
For patients with Crohn’s disease, therapeutic drug monitoring helped identify early primary nonresponders to induction with ustekinumab, according to researchers. The report is in Clinical Gastroenterology and Hepatology.
At week 8, median trough levels of ustekinumab were 6.0 mcg per mL (interquartile range, 3.1-8.0) among patients who achieved a primary response to induction at week 16, versus 1.3 mcg/mL (IQR, 0.9-5.6 ) among primary nonresponders (P = .03). An 8-week ustekinumab trough level cutoff of 2.0 mcg/mL distinguished week 16 responders from nonresponders with an area under the receiver operating curve (AUROC) of 0.75, wrote Ninon Soufflet of University Claude Bernard Lyon 1 in France, and associates. The researchers recommended “dedicated studies” to assess whether escalating the dose of ustekinumab can benefit patients with lower trough levels at week 8.
Few studies have explored biomarkers for response to ustekinumab induction therapy. Hence, the researchers assessed the relative utility of ustekinumab trough levels, C-reactive protein (CRP) levels, and fecal calprotectin levels for predicting early primary nonresponse. All 51 study participants had active luminal Crohn’s disease and received body weight–based intravenous infusions of ustekinumab at baseline, followed by subcutaneous injections of 90 mg. Primary nonresponders did not achieve steroid-free clinical and biochemical remission at week 16, defined as a Harvey-Bradshaw Index (HBI) of 4 points or less, a CRP level under 5 mg/L, and a fecal calprotectin level under 250 mcg/g. Week 16 was chosen to account for any delayed responders, the researchers noted.
A total of 32 patients (63%) achieved remission to ustekinumab induction therapy by week 16. An 8-week trough level of 2.0 mcg/mL was found to be optimal and distinguished primary nonresponders from responders with a sensitivity of 87%, a specificity of 66%, a positive predictive value of 82%, and a negative predictive value of 75%. In prior studies, optimal thresholds exceeded 3.3 mcg/mL for achieving remission and 4.5 mcg/mL at week 26 for achieving endoscopic response, the researchers noted. They said that this discrepancy might reflect different time points for evaluation, assays for measuring ustekinumab, patient populations, and a lack of endoscopic data in their study. “The relatively small sample size and the short period of follow-up evaluation [were] substantial limitations” they acknowledged.
In this study, levels of CRP did not change significantly between weeks 0 and 16 among either responders or nonresponders. In contrast, fecal calprotectin levels dropped rapidly and significantly over time only in responders. Median fecal calprotectin levels were 1,612 mcg/g of stools at week 0 versus 374 mcg/g at week 4 and 339 mcg/g at week 8. The finding “confirms the value of this biomarker, as previously shown in inflammatory bowel disease with anti–tumor necrosis factor,” the researchers wrote.
The investigators did not acknowledge external funding sources. Dr. Soufflet reported having no conflicts of interest. The senior author and three coinvestigators disclosed ties to MSD, AbbVie, Tillots, and several other pharmaceutical companies.
SOURCE: Soufflet N et al. Clin Gastroenterol Hepatol. 2019 Mar 6. doi: 10.1016/j.cgh.2019.02.042. https://www.cghjournal.org/article/S1542-3565(19)30248-4/abstract
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Ribavirin boosts HCV genotype 3 eradication in compensated cirrhotic patients
VIENNA – In patients with compensated cirrhosis infected with genotype 3 hepatitis C virus, adding ribavirin to a usual antiviral regimen of sofosbuvir and velpatasvir significantly boosted the rate of sustained virologic response in a review of more than 14,000 English residents entered in a national registry starting in 2017.
With ribavirin added to a sofosbuvir plus velpatasvir regimen for 12 weeks of treatment, the three-drug combination produced a 98% rate of sustained virologic response after 12 weeks (SVR12) in 196 treated patients, Kate Drysdale, MBBCh, said at the meeting sponsored by the European Association for the Study of the Liver. In contrast, 218 compensated cirrhosis patients who received a 12-week regimen of sofosbuvir plus velpatasvir (Epclusa) but without ribavirin had an SVR12 rate of just under 92%, a statistically significant difference, compared with the rate among patients who also received ribavirin, said Dr. Drysdale, a gastroenterologist at Bart’s Health and Queen Mary University of London. The SVR12 rate among 167 compensated cirrhotic patients treated for 12 weeks with the combination of glecaprevir plus pibrentasvir (Mavyret) was 96%, and not statistically different from the patients who received three drugs including ribavirin. The sofosbuvir, velpatasvir, ribavirin combination also outperformed the combination of sofosbuvir plus daclatasvir (Daklinza) and ribavirin, which produced an SVR12 of 92% in 868 patients. The SVR12 rate is the percentage of patients with undetectable hepatitis C virus (HCV) 12 or more weeks after the end of treatment.
Dr. Drysdale cautioned that the data have not yet been put through a multivariate analysis, but the results so far provide “a strong indication that ribavirin may not be as insignificant” as many have recently presumed. “Ribavirin has been set aside because it was thought not to add to the SVR12, but if patients get only one go at treatment, we must be sure their first treatment is the best one,” Dr. Drysdale said in an interview. If ribavirin can be shown to make a significant contribution to treatment efficacy “then we should think more widely about using it when patients tolerate it.”
The analysis included too few patients with either current decompensated cirrhosis or a history of decompensated cirrhosis to make any statistically meaningful comparisons of the treatment subgroups among these patients. And among patients with genotype 3 HCV infection and without cirrhosis, none of the treatments used in practice showed any statistically significant differences in the SVR12 rates they produced. Among patients without cirrhosis the most commonly used regimens by far were an 8-week course of glecaprevir plus pibrentasvir in 731 patients or a 12-week course of sofosbuvir plus velpatasvir in 1,184 patients. Both regimens had SVR12 rates in noncirrhotic patients of 97%, regardless of whether patients had no, mild, or moderate liver fibrosis.
The study used data collected in an English national registry of HCV-infected patients treated with direct-acting antiviral drugs starting in 2017. Dr. Drysdale and her associates narrowed down the total database of more than 37,000 English adults who received some HCV therapy during the period to 14,603 who received a complete, valid regimen and had follow-up SVR12 information available. The overall SVR12 rate among all these patients was 95.59%, and among the patients infected by genotype 3 virus the SVR12 rate was 95.03%. Dr. Drysdale’s analysis focused primarily on the roughly one-third of patients in the study group infected with genotype 3 HCV, the genotype that historically has presented unique treatment challenges (Drugs. 2017 Feb;77[2]:131-44).
Another finding Dr. Drysdale reported was that as liver disease severity worsened from no fibrosis to mild or moderate fibrosis, and then to compensated cirrhosis or decompensation, the SVR12 rate steadily diminished. Among genotype 3 patients, the SVR12 rate fell from about 97% among patients without any fibrosis to about 87% among those with decompensated cirrhosis. Although this observation had been made before, this finding in such a large number of treated patients adds significant new evidence to support this pattern. It also adds further support to the idea of screening for HCV infection among higher-risk, asymptomatic people to optimize their prospects for virus eradication with treatment.
“If patients get much better treatment outcomes before they become cirrhotic then we should try to find these HCV-infected people before they develop symptoms,” Dr. Drysdale said.
Dr. Drysdale reported no disclosures.
SOURCE: Drysdale K et al. J Hepatol. 2019 April;70(1):e131.
The results from Dr. Drysdale’s analysis confirm what had previously been proposed by other investigators that, in a subgroup of patients with cirrhosis and infected with hepatitis C virus (HCV) genotype 3, adding ribavirin to a regimen of direct-acting antiviral drugs can increase efficacy. But the new study included no data to address the prevalence of HCV genetic variants with resistance mutations that necessitate adding ribavirin. We have known that, in patients with cirrhosis and infected with resistant genotype 3 HCV, adding ribavirin is necessary. In many locations resistance testing is not possible; in those circumstances, adding ribavirin to the treatment should be routinely done.
Thomas Berg, MD, is professor and head of hepatology at University Hospital in Leipzig, Germany. He has received personal fees and research support from several companies. He made these comments in an interview.
The results from Dr. Drysdale’s analysis confirm what had previously been proposed by other investigators that, in a subgroup of patients with cirrhosis and infected with hepatitis C virus (HCV) genotype 3, adding ribavirin to a regimen of direct-acting antiviral drugs can increase efficacy. But the new study included no data to address the prevalence of HCV genetic variants with resistance mutations that necessitate adding ribavirin. We have known that, in patients with cirrhosis and infected with resistant genotype 3 HCV, adding ribavirin is necessary. In many locations resistance testing is not possible; in those circumstances, adding ribavirin to the treatment should be routinely done.
Thomas Berg, MD, is professor and head of hepatology at University Hospital in Leipzig, Germany. He has received personal fees and research support from several companies. He made these comments in an interview.
The results from Dr. Drysdale’s analysis confirm what had previously been proposed by other investigators that, in a subgroup of patients with cirrhosis and infected with hepatitis C virus (HCV) genotype 3, adding ribavirin to a regimen of direct-acting antiviral drugs can increase efficacy. But the new study included no data to address the prevalence of HCV genetic variants with resistance mutations that necessitate adding ribavirin. We have known that, in patients with cirrhosis and infected with resistant genotype 3 HCV, adding ribavirin is necessary. In many locations resistance testing is not possible; in those circumstances, adding ribavirin to the treatment should be routinely done.
Thomas Berg, MD, is professor and head of hepatology at University Hospital in Leipzig, Germany. He has received personal fees and research support from several companies. He made these comments in an interview.
VIENNA – In patients with compensated cirrhosis infected with genotype 3 hepatitis C virus, adding ribavirin to a usual antiviral regimen of sofosbuvir and velpatasvir significantly boosted the rate of sustained virologic response in a review of more than 14,000 English residents entered in a national registry starting in 2017.
With ribavirin added to a sofosbuvir plus velpatasvir regimen for 12 weeks of treatment, the three-drug combination produced a 98% rate of sustained virologic response after 12 weeks (SVR12) in 196 treated patients, Kate Drysdale, MBBCh, said at the meeting sponsored by the European Association for the Study of the Liver. In contrast, 218 compensated cirrhosis patients who received a 12-week regimen of sofosbuvir plus velpatasvir (Epclusa) but without ribavirin had an SVR12 rate of just under 92%, a statistically significant difference, compared with the rate among patients who also received ribavirin, said Dr. Drysdale, a gastroenterologist at Bart’s Health and Queen Mary University of London. The SVR12 rate among 167 compensated cirrhotic patients treated for 12 weeks with the combination of glecaprevir plus pibrentasvir (Mavyret) was 96%, and not statistically different from the patients who received three drugs including ribavirin. The sofosbuvir, velpatasvir, ribavirin combination also outperformed the combination of sofosbuvir plus daclatasvir (Daklinza) and ribavirin, which produced an SVR12 of 92% in 868 patients. The SVR12 rate is the percentage of patients with undetectable hepatitis C virus (HCV) 12 or more weeks after the end of treatment.
Dr. Drysdale cautioned that the data have not yet been put through a multivariate analysis, but the results so far provide “a strong indication that ribavirin may not be as insignificant” as many have recently presumed. “Ribavirin has been set aside because it was thought not to add to the SVR12, but if patients get only one go at treatment, we must be sure their first treatment is the best one,” Dr. Drysdale said in an interview. If ribavirin can be shown to make a significant contribution to treatment efficacy “then we should think more widely about using it when patients tolerate it.”
The analysis included too few patients with either current decompensated cirrhosis or a history of decompensated cirrhosis to make any statistically meaningful comparisons of the treatment subgroups among these patients. And among patients with genotype 3 HCV infection and without cirrhosis, none of the treatments used in practice showed any statistically significant differences in the SVR12 rates they produced. Among patients without cirrhosis the most commonly used regimens by far were an 8-week course of glecaprevir plus pibrentasvir in 731 patients or a 12-week course of sofosbuvir plus velpatasvir in 1,184 patients. Both regimens had SVR12 rates in noncirrhotic patients of 97%, regardless of whether patients had no, mild, or moderate liver fibrosis.
The study used data collected in an English national registry of HCV-infected patients treated with direct-acting antiviral drugs starting in 2017. Dr. Drysdale and her associates narrowed down the total database of more than 37,000 English adults who received some HCV therapy during the period to 14,603 who received a complete, valid regimen and had follow-up SVR12 information available. The overall SVR12 rate among all these patients was 95.59%, and among the patients infected by genotype 3 virus the SVR12 rate was 95.03%. Dr. Drysdale’s analysis focused primarily on the roughly one-third of patients in the study group infected with genotype 3 HCV, the genotype that historically has presented unique treatment challenges (Drugs. 2017 Feb;77[2]:131-44).
Another finding Dr. Drysdale reported was that as liver disease severity worsened from no fibrosis to mild or moderate fibrosis, and then to compensated cirrhosis or decompensation, the SVR12 rate steadily diminished. Among genotype 3 patients, the SVR12 rate fell from about 97% among patients without any fibrosis to about 87% among those with decompensated cirrhosis. Although this observation had been made before, this finding in such a large number of treated patients adds significant new evidence to support this pattern. It also adds further support to the idea of screening for HCV infection among higher-risk, asymptomatic people to optimize their prospects for virus eradication with treatment.
“If patients get much better treatment outcomes before they become cirrhotic then we should try to find these HCV-infected people before they develop symptoms,” Dr. Drysdale said.
Dr. Drysdale reported no disclosures.
SOURCE: Drysdale K et al. J Hepatol. 2019 April;70(1):e131.
VIENNA – In patients with compensated cirrhosis infected with genotype 3 hepatitis C virus, adding ribavirin to a usual antiviral regimen of sofosbuvir and velpatasvir significantly boosted the rate of sustained virologic response in a review of more than 14,000 English residents entered in a national registry starting in 2017.
With ribavirin added to a sofosbuvir plus velpatasvir regimen for 12 weeks of treatment, the three-drug combination produced a 98% rate of sustained virologic response after 12 weeks (SVR12) in 196 treated patients, Kate Drysdale, MBBCh, said at the meeting sponsored by the European Association for the Study of the Liver. In contrast, 218 compensated cirrhosis patients who received a 12-week regimen of sofosbuvir plus velpatasvir (Epclusa) but without ribavirin had an SVR12 rate of just under 92%, a statistically significant difference, compared with the rate among patients who also received ribavirin, said Dr. Drysdale, a gastroenterologist at Bart’s Health and Queen Mary University of London. The SVR12 rate among 167 compensated cirrhotic patients treated for 12 weeks with the combination of glecaprevir plus pibrentasvir (Mavyret) was 96%, and not statistically different from the patients who received three drugs including ribavirin. The sofosbuvir, velpatasvir, ribavirin combination also outperformed the combination of sofosbuvir plus daclatasvir (Daklinza) and ribavirin, which produced an SVR12 of 92% in 868 patients. The SVR12 rate is the percentage of patients with undetectable hepatitis C virus (HCV) 12 or more weeks after the end of treatment.
Dr. Drysdale cautioned that the data have not yet been put through a multivariate analysis, but the results so far provide “a strong indication that ribavirin may not be as insignificant” as many have recently presumed. “Ribavirin has been set aside because it was thought not to add to the SVR12, but if patients get only one go at treatment, we must be sure their first treatment is the best one,” Dr. Drysdale said in an interview. If ribavirin can be shown to make a significant contribution to treatment efficacy “then we should think more widely about using it when patients tolerate it.”
The analysis included too few patients with either current decompensated cirrhosis or a history of decompensated cirrhosis to make any statistically meaningful comparisons of the treatment subgroups among these patients. And among patients with genotype 3 HCV infection and without cirrhosis, none of the treatments used in practice showed any statistically significant differences in the SVR12 rates they produced. Among patients without cirrhosis the most commonly used regimens by far were an 8-week course of glecaprevir plus pibrentasvir in 731 patients or a 12-week course of sofosbuvir plus velpatasvir in 1,184 patients. Both regimens had SVR12 rates in noncirrhotic patients of 97%, regardless of whether patients had no, mild, or moderate liver fibrosis.
The study used data collected in an English national registry of HCV-infected patients treated with direct-acting antiviral drugs starting in 2017. Dr. Drysdale and her associates narrowed down the total database of more than 37,000 English adults who received some HCV therapy during the period to 14,603 who received a complete, valid regimen and had follow-up SVR12 information available. The overall SVR12 rate among all these patients was 95.59%, and among the patients infected by genotype 3 virus the SVR12 rate was 95.03%. Dr. Drysdale’s analysis focused primarily on the roughly one-third of patients in the study group infected with genotype 3 HCV, the genotype that historically has presented unique treatment challenges (Drugs. 2017 Feb;77[2]:131-44).
Another finding Dr. Drysdale reported was that as liver disease severity worsened from no fibrosis to mild or moderate fibrosis, and then to compensated cirrhosis or decompensation, the SVR12 rate steadily diminished. Among genotype 3 patients, the SVR12 rate fell from about 97% among patients without any fibrosis to about 87% among those with decompensated cirrhosis. Although this observation had been made before, this finding in such a large number of treated patients adds significant new evidence to support this pattern. It also adds further support to the idea of screening for HCV infection among higher-risk, asymptomatic people to optimize their prospects for virus eradication with treatment.
“If patients get much better treatment outcomes before they become cirrhotic then we should try to find these HCV-infected people before they develop symptoms,” Dr. Drysdale said.
Dr. Drysdale reported no disclosures.
SOURCE: Drysdale K et al. J Hepatol. 2019 April;70(1):e131.
REPORTING FROM ILC 2019