“We Are Not Done Changing”

Recently, the online version of JAMA published an original investigation titled, “Patient Mortality During Unannounced Accreditation Surveys at US Hospitals.” The purpose of this investigation was to determine the effect of heightened vigilance during unannounced accreditation surveys on safety and quality of inpatient care.

The authors found that there was a significant reduction in mortality in patients admitted during the week of surveys by The Joint Commission. The change was more significant in major teaching hospitals, where mortality fell from 6.41% to 5.93% during survey weeks, a 5.9% relative decrease. The positive effects of being monitored have been well documented in all kinds of arenas, such as hand washing and antibiotic stewardship. But mortality?

Also on The Hospital Leader…

• How Often Do You Ask This (Ineffective) Question? by Brad Flansbaum, DO, MPH, MHM• Building a Practice that People Want to Be a Part Of by Leslie Flores, MHA• A Need for Medicare Appeals Process Reform in Hospital Observation Care by Anne Sheehy, MD, MS, FHM

“We Are Not Done Changing”

Recently, the online version of JAMA published an original investigation titled, “Patient Mortality During Unannounced Accreditation Surveys at US Hospitals.” The purpose of this investigation was to determine the effect of heightened vigilance during unannounced accreditation surveys on safety and quality of inpatient care.

The authors found that there was a significant reduction in mortality in patients admitted during the week of surveys by The Joint Commission. The change was more significant in major teaching hospitals, where mortality fell from 6.41% to 5.93% during survey weeks, a 5.9% relative decrease. The positive effects of being monitored have been well documented in all kinds of arenas, such as hand washing and antibiotic stewardship. But mortality?

Also on The Hospital Leader…

• How Often Do You Ask This (Ineffective) Question? by Brad Flansbaum, DO, MPH, MHM• Building a Practice that People Want to Be a Part Of by Leslie Flores, MHA• A Need for Medicare Appeals Process Reform in Hospital Observation Care by Anne Sheehy, MD, MS, FHM

“We Are Not Done Changing”

Recently, the online version of JAMA published an original investigation titled, “Patient Mortality During Unannounced Accreditation Surveys at US Hospitals.” The purpose of this investigation was to determine the effect of heightened vigilance during unannounced accreditation surveys on safety and quality of inpatient care.

The authors found that there was a significant reduction in mortality in patients admitted during the week of surveys by The Joint Commission. The change was more significant in major teaching hospitals, where mortality fell from 6.41% to 5.93% during survey weeks, a 5.9% relative decrease. The positive effects of being monitored have been well documented in all kinds of arenas, such as hand washing and antibiotic stewardship. But mortality?

Also on The Hospital Leader…

• How Often Do You Ask This (Ineffective) Question? by Brad Flansbaum, DO, MPH, MHM• Building a Practice that People Want to Be a Part Of by Leslie Flores, MHA• A Need for Medicare Appeals Process Reform in Hospital Observation Care by Anne Sheehy, MD, MS, FHM

Aging equipment, valuable data, and an improperly trained workforce make health care IT extraordinarily vulnerable to external malfeasance, as demonstrated by the WannaCry virus episode that occurred this spring in the United Kingdom.

Computer hackers used a weakness in the operating system employed by the U.K. National Health Service, allowing the WannaCry virus to spread quickly across connected systems. The ransomware attack locked clinicians out of patient records and diagnostic machines that were connected, bringing patient care to a near standstill.

The attack lasted 3 days until Marcus Hutchins, a 22-year-old security researcher, stumbled onto a way to slow the spread of the virus enough to manage it, but not before nearly 60 million attacks had been conducted, Salim Neino, CEO of Kryptos Logic, testified June 15 at a joint hearing of two subcommittees of the House Science, Space & Technology Committee. Mr. Hutchins is employed by Kryptos Logic.

U.S. officials are keenly aware that a similar attack could happen here. In June, the federally sponsored Health Care Industry Cybersecurity Task Force issued a report on their year-long look at the state of the health care IT in this country. The task force was mandated by the Cybersecurity Act of 2015and formed in March 2016.

[email protected]

On Twitter @eaztweets

Aging equipment, valuable data, and an improperly trained workforce make health care IT extraordinarily vulnerable to external malfeasance, as demonstrated by the WannaCry virus episode that occurred this spring in the United Kingdom.

Computer hackers used a weakness in the operating system employed by the U.K. National Health Service, allowing the WannaCry virus to spread quickly across connected systems. The ransomware attack locked clinicians out of patient records and diagnostic machines that were connected, bringing patient care to a near standstill.

The attack lasted 3 days until Marcus Hutchins, a 22-year-old security researcher, stumbled onto a way to slow the spread of the virus enough to manage it, but not before nearly 60 million attacks had been conducted, Salim Neino, CEO of Kryptos Logic, testified June 15 at a joint hearing of two subcommittees of the House Science, Space & Technology Committee. Mr. Hutchins is employed by Kryptos Logic.

U.S. officials are keenly aware that a similar attack could happen here. In June, the federally sponsored Health Care Industry Cybersecurity Task Force issued a report on their year-long look at the state of the health care IT in this country. The task force was mandated by the Cybersecurity Act of 2015and formed in March 2016.

[email protected]

On Twitter @eaztweets

Aging equipment, valuable data, and an improperly trained workforce make health care IT extraordinarily vulnerable to external malfeasance, as demonstrated by the WannaCry virus episode that occurred this spring in the United Kingdom.

Computer hackers used a weakness in the operating system employed by the U.K. National Health Service, allowing the WannaCry virus to spread quickly across connected systems. The ransomware attack locked clinicians out of patient records and diagnostic machines that were connected, bringing patient care to a near standstill.

The attack lasted 3 days until Marcus Hutchins, a 22-year-old security researcher, stumbled onto a way to slow the spread of the virus enough to manage it, but not before nearly 60 million attacks had been conducted, Salim Neino, CEO of Kryptos Logic, testified June 15 at a joint hearing of two subcommittees of the House Science, Space & Technology Committee. Mr. Hutchins is employed by Kryptos Logic.

U.S. officials are keenly aware that a similar attack could happen here. In June, the federally sponsored Health Care Industry Cybersecurity Task Force issued a report on their year-long look at the state of the health care IT in this country. The task force was mandated by the Cybersecurity Act of 2015and formed in March 2016.

[email protected]

On Twitter @eaztweets

The House of Representatives has passed a bill that would cap damages in medical malpractice cases and impose a tighter time frame for legal challenges against physicians.

The House passed the Protecting Access to Care Act (H.R. 1215) on June 28 by a 218-210 vote. The bill, modeled after California’s Medical Injury Compensation Reform Act (MICRA), would limit noneconomic damages in medical malpractice cases to $250,000, restrict contingency fees charged by attorneys, and enforce a 3-year statute of limitations for liability lawsuits from the date of alleged injury. The legislation also includes a fair share rule in which defendants are liable only for the damages in direct proportion to their percentage of responsibility.

The American College of Physicians (ACP) praised the House for passing the bill, saying the time is ripe to develop and pass common-sense liability reforms.

“The American College of Physicians applauds the House of Representatives for its passage of a multifaceted approach to medical-liability reform,” Jack Ende, MD, ACP president, said in a statement. “ACP believes that any solution to improve the medical liability system in the U.S. should include a multifaceted approach, because no single program or law by itself is likely to achieve the goals of improving patient safety, ensuring fair compensation to patients, strengthening rather than undermining the patient-physician relationship, and reducing the economic costs associated with the current system.”

The American Association for Justice, a lobbying organization for plaintiffs’ attorneys, sent a letter to the House prior to the bill’s passage urging legislators to oppose the bill. More than 75 organizations signed the letter.

“Even if H.R. 1215 applied only to doctors and hospitals, recent studies clearly establish that its provisions would lead to more deaths and injuries, and increased health care costs due to a ‘broad relaxation of care,’ ” the letter stated. “... The latest statistics show that medical errors, most of which are preventable, are the third leading cause of death in America. This intolerable situation is perhaps all the more shocking because we already know about how to fix much of this problem. Congress should focus on improving patient safety and reducing deaths and injuries, not insulating negligent providers from accountability, harming patients, and saddling taxpayers with the cost.”

The legislation would apply to any patient who receives medical care provided via a federal program, such as Medicare or Medicaid, or via a subsidy or tax benefit, such as coverage purchased under the Affordable Care Act or a replacement. Medical care paid for via employer health plans also would fall under the legislation’s umbrella since insurance premiums receive federal tax exemptions. The bill would not preempt state medical malpractice laws that impose damage caps, whether higher or lower than $250,000, nor would the legislation affect the availability of economic damages, according to bill language.

As part of the H.R. 1215, courts could limit how much attorneys receive from a patient’s ultimate award. Specifically, courts would have the power to restrict payments from a plaintiff’s damage recovery to an attorney who claims a financial stake in the outcome by virtue of a contingent fee.

PIAA, a trade association representing medical liability insurers, said the House passage of the bill is a major victory for tort reform advocates. The bill is the first comprehensive medical liability reform legislation to be passed by either chamber of Congress in more than 5 years, according to PIAA.

[email protected]

On Twitter @legal_med

The House of Representatives has passed a bill that would cap damages in medical malpractice cases and impose a tighter time frame for legal challenges against physicians.

The House passed the Protecting Access to Care Act (H.R. 1215) on June 28 by a 218-210 vote. The bill, modeled after California’s Medical Injury Compensation Reform Act (MICRA), would limit noneconomic damages in medical malpractice cases to $250,000, restrict contingency fees charged by attorneys, and enforce a 3-year statute of limitations for liability lawsuits from the date of alleged injury. The legislation also includes a fair share rule in which defendants are liable only for the damages in direct proportion to their percentage of responsibility.

The American College of Physicians (ACP) praised the House for passing the bill, saying the time is ripe to develop and pass common-sense liability reforms.

“The American College of Physicians applauds the House of Representatives for its passage of a multifaceted approach to medical-liability reform,” Jack Ende, MD, ACP president, said in a statement. “ACP believes that any solution to improve the medical liability system in the U.S. should include a multifaceted approach, because no single program or law by itself is likely to achieve the goals of improving patient safety, ensuring fair compensation to patients, strengthening rather than undermining the patient-physician relationship, and reducing the economic costs associated with the current system.”

The American Association for Justice, a lobbying organization for plaintiffs’ attorneys, sent a letter to the House prior to the bill’s passage urging legislators to oppose the bill. More than 75 organizations signed the letter.

“Even if H.R. 1215 applied only to doctors and hospitals, recent studies clearly establish that its provisions would lead to more deaths and injuries, and increased health care costs due to a ‘broad relaxation of care,’ ” the letter stated. “... The latest statistics show that medical errors, most of which are preventable, are the third leading cause of death in America. This intolerable situation is perhaps all the more shocking because we already know about how to fix much of this problem. Congress should focus on improving patient safety and reducing deaths and injuries, not insulating negligent providers from accountability, harming patients, and saddling taxpayers with the cost.”

The legislation would apply to any patient who receives medical care provided via a federal program, such as Medicare or Medicaid, or via a subsidy or tax benefit, such as coverage purchased under the Affordable Care Act or a replacement. Medical care paid for via employer health plans also would fall under the legislation’s umbrella since insurance premiums receive federal tax exemptions. The bill would not preempt state medical malpractice laws that impose damage caps, whether higher or lower than $250,000, nor would the legislation affect the availability of economic damages, according to bill language.

As part of the H.R. 1215, courts could limit how much attorneys receive from a patient’s ultimate award. Specifically, courts would have the power to restrict payments from a plaintiff’s damage recovery to an attorney who claims a financial stake in the outcome by virtue of a contingent fee.

PIAA, a trade association representing medical liability insurers, said the House passage of the bill is a major victory for tort reform advocates. The bill is the first comprehensive medical liability reform legislation to be passed by either chamber of Congress in more than 5 years, according to PIAA.

[email protected]

On Twitter @legal_med

The House of Representatives has passed a bill that would cap damages in medical malpractice cases and impose a tighter time frame for legal challenges against physicians.

The House passed the Protecting Access to Care Act (H.R. 1215) on June 28 by a 218-210 vote. The bill, modeled after California’s Medical Injury Compensation Reform Act (MICRA), would limit noneconomic damages in medical malpractice cases to $250,000, restrict contingency fees charged by attorneys, and enforce a 3-year statute of limitations for liability lawsuits from the date of alleged injury. The legislation also includes a fair share rule in which defendants are liable only for the damages in direct proportion to their percentage of responsibility.

The American College of Physicians (ACP) praised the House for passing the bill, saying the time is ripe to develop and pass common-sense liability reforms.

“The American College of Physicians applauds the House of Representatives for its passage of a multifaceted approach to medical-liability reform,” Jack Ende, MD, ACP president, said in a statement. “ACP believes that any solution to improve the medical liability system in the U.S. should include a multifaceted approach, because no single program or law by itself is likely to achieve the goals of improving patient safety, ensuring fair compensation to patients, strengthening rather than undermining the patient-physician relationship, and reducing the economic costs associated with the current system.”

The American Association for Justice, a lobbying organization for plaintiffs’ attorneys, sent a letter to the House prior to the bill’s passage urging legislators to oppose the bill. More than 75 organizations signed the letter.

“Even if H.R. 1215 applied only to doctors and hospitals, recent studies clearly establish that its provisions would lead to more deaths and injuries, and increased health care costs due to a ‘broad relaxation of care,’ ” the letter stated. “... The latest statistics show that medical errors, most of which are preventable, are the third leading cause of death in America. This intolerable situation is perhaps all the more shocking because we already know about how to fix much of this problem. Congress should focus on improving patient safety and reducing deaths and injuries, not insulating negligent providers from accountability, harming patients, and saddling taxpayers with the cost.”

The legislation would apply to any patient who receives medical care provided via a federal program, such as Medicare or Medicaid, or via a subsidy or tax benefit, such as coverage purchased under the Affordable Care Act or a replacement. Medical care paid for via employer health plans also would fall under the legislation’s umbrella since insurance premiums receive federal tax exemptions. The bill would not preempt state medical malpractice laws that impose damage caps, whether higher or lower than $250,000, nor would the legislation affect the availability of economic damages, according to bill language.

As part of the H.R. 1215, courts could limit how much attorneys receive from a patient’s ultimate award. Specifically, courts would have the power to restrict payments from a plaintiff’s damage recovery to an attorney who claims a financial stake in the outcome by virtue of a contingent fee.

PIAA, a trade association representing medical liability insurers, said the House passage of the bill is a major victory for tort reform advocates. The bill is the first comprehensive medical liability reform legislation to be passed by either chamber of Congress in more than 5 years, according to PIAA.

[email protected]

On Twitter @legal_med

NEW YORK – Minimally invasive mitral valve surgery provides outcomes that match those of conventional sternotomy without increasing use of resources, and lower costs after surgery offset potentially higher operation costs, according to a single-center, propensity-matched analysis of almost 500 patients presented at the meeting sponsored by the American Association for Thoracic Surgery.

“Minimally invasive mitral surgery has excellent outcomes with fewer transfusions and less time ventilated in this representative cohort,” said Robert Hawkins, MD, of the University of Virginia, Charlottesville, in reporting the results.

“While operative times were longer, surgical costs remained statistically similar, and minimally invasive mitral surgery was associated with similar total costs in more complex mitral cases.”

NEW YORK – Minimally invasive mitral valve surgery provides outcomes that match those of conventional sternotomy without increasing use of resources, and lower costs after surgery offset potentially higher operation costs, according to a single-center, propensity-matched analysis of almost 500 patients presented at the meeting sponsored by the American Association for Thoracic Surgery.

“Minimally invasive mitral surgery has excellent outcomes with fewer transfusions and less time ventilated in this representative cohort,” said Robert Hawkins, MD, of the University of Virginia, Charlottesville, in reporting the results.

“While operative times were longer, surgical costs remained statistically similar, and minimally invasive mitral surgery was associated with similar total costs in more complex mitral cases.”

NEW YORK – Minimally invasive mitral valve surgery provides outcomes that match those of conventional sternotomy without increasing use of resources, and lower costs after surgery offset potentially higher operation costs, according to a single-center, propensity-matched analysis of almost 500 patients presented at the meeting sponsored by the American Association for Thoracic Surgery.

“Minimally invasive mitral surgery has excellent outcomes with fewer transfusions and less time ventilated in this representative cohort,” said Robert Hawkins, MD, of the University of Virginia, Charlottesville, in reporting the results.

“While operative times were longer, surgical costs remained statistically similar, and minimally invasive mitral surgery was associated with similar total costs in more complex mitral cases.”

Diffuse large B-cell lymphoma

LUGANO, SWITZERLAND—The chimeric antigen receptor (CAR) T-cell therapy JCAR017 can produce “potent and durable” responses in patients with relapsed/refractory, aggressive diffuse large B-cell lymphoma (DLBCL), according to an investigator from the TRANSCEND NHL 001 trial.

In this phase 1 trial, JCAR017, given after lymphodepleting chemotherapy, produced an overall response rate (ORR) of 76% and a complete response (CR) rate of 52%.

At 3 months of follow-up, the ORR was 51%, and the CR rate was 39%.

Responses were seen even in poor-risk subgroups, noted study investigator Jeremy Abramson, MD, of Massachusetts General Hospital Cancer Center in Boston.

“TRANSCEND NHL 001 is the first multicenter study of a CD19-directed CAR T-cell product with a fixed CD4 and CD8 composition to deliver potent and durable responses in high-risk subsets in DLBCL,” Dr Abramson said.

He presented data from the trial at the 2017 International Conference on Malignant Lymphoma (ICML) as abstract 128. The research was sponsored by Juno Therapeutics, the company developing JCAR017.

Patients

Dr Abramson presented data on 55 patients with relapsed/refractory non-Hodgkin lymphoma. Forty patients had DLBCL not otherwise specified, 14 had transformed DLBCL, and 1 had grade 3B follicular lymphoma. Fifteen patients had double- or triple-hit lymphoma.

The patients’ median age was 61 (range, 29-82), and 69% were male. Eighty-seven percent of patients (n=48) had an ECOG status of 0 to 1. Two patients had central nervous system involvement.

The patients had received a median of 3 prior lines of therapy (range, 1-11). Seventy-six percent of patients (n=42) were chemo-refractory, 7% (n=4) had received an allogeneic transplant, and 44% (n=24) had received an autologous transplant.

Treatment

Patients received 1 of 2 doses of JCAR017 after fludarabine/cyclophosphamide lymphodepletion.

Thirty patients received a single dose of JCAR017 at 5 x 10⁷ CAR cells (dose-level 1, single [DL1S]).

Six patients received 2 doses of 5 x 10⁷ CAR cells (dose-level 1, double [DL1D]).

Nineteen patients received a single dose of 1 x 10⁸ CAR cells (dose-level 2, single [DL2S]).

Safety

More than 90% of patients experienced a treatment-emergent adverse event (AE), and 60% had a treatment-related AE.

Treatment-emergent AEs occurring in more than 20% of patients included cytokine release syndrome (CRS), fatigue, nausea, constipation, decreased appetite, diarrhea, hypotension, neutropenia, anemia, and thrombocytopenia.

One patient had a grade 5 AE of diffuse alveolar damage that was thought to be related to fludarabine, cyclophosphamide, and JCAR017.

Another patient had a grade 5 AE of multiorgan failure that was considered unrelated to study treatment and due to disease progression.

The rate of grade 1/2 CRS was 33% (n=18), and the rate of grade 3/4 CRS was 2% (n=1). The rate of grade 1/2 neurotoxicity was 6% (n=3), and the rate of grade 3/4 neurotoxicity was 16% (n=9).

There were no deaths from CRS or neurotoxicity. The median time to onset of CRS was 5 days (range, 1-23), and the median time to onset of neurotoxicity was 11 days (range, 5-23).

“JCAR017 toxicities have, thus far, been relatively low and highly manageable at all dose levels tested, with a favorable safety profile that may enable outpatient administration,” Dr Abramson said.

Response

Fifty-four patients were evaluable for response. The ORR was 76%, and the CR rate was 52%. At 3 months of follow-up, the ORR was 51%, and the CR rate was 39%.

Dr Abramson noted that there was a dose-response relationship.

Overall, in the DL1S cohort, the ORR was 80%, and the CR rate was 53%. In the DL2S cohort, the ORR was 72%, and the CR rate was 50%. In the DL1D cohort, the ORR was 67%, and the CR rate was 50%.

At 3 months, in the DL1S cohort, the ORR was 46%, and the CR rate was 33%. In the DL2S cohort, the ORR was 64%, and the CR rate was 46%. In the DL1D cohort, the ORR and CR rate were both 50%.

Dr Abramson also noted that JCAR017 could produce a high response rate in poor-risk subgroups.

At 3 months, the ORR was 91% in patients who relapsed less than 12 months after transplant, 82% in patients with double- or triple-hit lymphoma, 48% in patients who had never achieved a CR, 47% in chemo-refractory patients, 31% in patients with primary refractory lymphoma, and 24% in patients with stable disease or progression after last chemotherapy.

Diffuse large B-cell lymphoma

LUGANO, SWITZERLAND—The chimeric antigen receptor (CAR) T-cell therapy JCAR017 can produce “potent and durable” responses in patients with relapsed/refractory, aggressive diffuse large B-cell lymphoma (DLBCL), according to an investigator from the TRANSCEND NHL 001 trial.

In this phase 1 trial, JCAR017, given after lymphodepleting chemotherapy, produced an overall response rate (ORR) of 76% and a complete response (CR) rate of 52%.

At 3 months of follow-up, the ORR was 51%, and the CR rate was 39%.

Responses were seen even in poor-risk subgroups, noted study investigator Jeremy Abramson, MD, of Massachusetts General Hospital Cancer Center in Boston.

“TRANSCEND NHL 001 is the first multicenter study of a CD19-directed CAR T-cell product with a fixed CD4 and CD8 composition to deliver potent and durable responses in high-risk subsets in DLBCL,” Dr Abramson said.

He presented data from the trial at the 2017 International Conference on Malignant Lymphoma (ICML) as abstract 128. The research was sponsored by Juno Therapeutics, the company developing JCAR017.

Patients

Dr Abramson presented data on 55 patients with relapsed/refractory non-Hodgkin lymphoma. Forty patients had DLBCL not otherwise specified, 14 had transformed DLBCL, and 1 had grade 3B follicular lymphoma. Fifteen patients had double- or triple-hit lymphoma.

The patients’ median age was 61 (range, 29-82), and 69% were male. Eighty-seven percent of patients (n=48) had an ECOG status of 0 to 1. Two patients had central nervous system involvement.

The patients had received a median of 3 prior lines of therapy (range, 1-11). Seventy-six percent of patients (n=42) were chemo-refractory, 7% (n=4) had received an allogeneic transplant, and 44% (n=24) had received an autologous transplant.

Treatment

Patients received 1 of 2 doses of JCAR017 after fludarabine/cyclophosphamide lymphodepletion.

Thirty patients received a single dose of JCAR017 at 5 x 10⁷ CAR cells (dose-level 1, single [DL1S]).

Six patients received 2 doses of 5 x 10⁷ CAR cells (dose-level 1, double [DL1D]).

Nineteen patients received a single dose of 1 x 10⁸ CAR cells (dose-level 2, single [DL2S]).

Safety

More than 90% of patients experienced a treatment-emergent adverse event (AE), and 60% had a treatment-related AE.

Treatment-emergent AEs occurring in more than 20% of patients included cytokine release syndrome (CRS), fatigue, nausea, constipation, decreased appetite, diarrhea, hypotension, neutropenia, anemia, and thrombocytopenia.

One patient had a grade 5 AE of diffuse alveolar damage that was thought to be related to fludarabine, cyclophosphamide, and JCAR017.

Another patient had a grade 5 AE of multiorgan failure that was considered unrelated to study treatment and due to disease progression.

The rate of grade 1/2 CRS was 33% (n=18), and the rate of grade 3/4 CRS was 2% (n=1). The rate of grade 1/2 neurotoxicity was 6% (n=3), and the rate of grade 3/4 neurotoxicity was 16% (n=9).

There were no deaths from CRS or neurotoxicity. The median time to onset of CRS was 5 days (range, 1-23), and the median time to onset of neurotoxicity was 11 days (range, 5-23).

“JCAR017 toxicities have, thus far, been relatively low and highly manageable at all dose levels tested, with a favorable safety profile that may enable outpatient administration,” Dr Abramson said.

Response

Fifty-four patients were evaluable for response. The ORR was 76%, and the CR rate was 52%. At 3 months of follow-up, the ORR was 51%, and the CR rate was 39%.

Dr Abramson noted that there was a dose-response relationship.

Overall, in the DL1S cohort, the ORR was 80%, and the CR rate was 53%. In the DL2S cohort, the ORR was 72%, and the CR rate was 50%. In the DL1D cohort, the ORR was 67%, and the CR rate was 50%.

At 3 months, in the DL1S cohort, the ORR was 46%, and the CR rate was 33%. In the DL2S cohort, the ORR was 64%, and the CR rate was 46%. In the DL1D cohort, the ORR and CR rate were both 50%.

Dr Abramson also noted that JCAR017 could produce a high response rate in poor-risk subgroups.

At 3 months, the ORR was 91% in patients who relapsed less than 12 months after transplant, 82% in patients with double- or triple-hit lymphoma, 48% in patients who had never achieved a CR, 47% in chemo-refractory patients, 31% in patients with primary refractory lymphoma, and 24% in patients with stable disease or progression after last chemotherapy.

Diffuse large B-cell lymphoma

LUGANO, SWITZERLAND—The chimeric antigen receptor (CAR) T-cell therapy JCAR017 can produce “potent and durable” responses in patients with relapsed/refractory, aggressive diffuse large B-cell lymphoma (DLBCL), according to an investigator from the TRANSCEND NHL 001 trial.

In this phase 1 trial, JCAR017, given after lymphodepleting chemotherapy, produced an overall response rate (ORR) of 76% and a complete response (CR) rate of 52%.

At 3 months of follow-up, the ORR was 51%, and the CR rate was 39%.

Responses were seen even in poor-risk subgroups, noted study investigator Jeremy Abramson, MD, of Massachusetts General Hospital Cancer Center in Boston.

“TRANSCEND NHL 001 is the first multicenter study of a CD19-directed CAR T-cell product with a fixed CD4 and CD8 composition to deliver potent and durable responses in high-risk subsets in DLBCL,” Dr Abramson said.

He presented data from the trial at the 2017 International Conference on Malignant Lymphoma (ICML) as abstract 128. The research was sponsored by Juno Therapeutics, the company developing JCAR017.

Patients

Dr Abramson presented data on 55 patients with relapsed/refractory non-Hodgkin lymphoma. Forty patients had DLBCL not otherwise specified, 14 had transformed DLBCL, and 1 had grade 3B follicular lymphoma. Fifteen patients had double- or triple-hit lymphoma.

The patients’ median age was 61 (range, 29-82), and 69% were male. Eighty-seven percent of patients (n=48) had an ECOG status of 0 to 1. Two patients had central nervous system involvement.

The patients had received a median of 3 prior lines of therapy (range, 1-11). Seventy-six percent of patients (n=42) were chemo-refractory, 7% (n=4) had received an allogeneic transplant, and 44% (n=24) had received an autologous transplant.

Treatment

Patients received 1 of 2 doses of JCAR017 after fludarabine/cyclophosphamide lymphodepletion.

Thirty patients received a single dose of JCAR017 at 5 x 10⁷ CAR cells (dose-level 1, single [DL1S]).

Six patients received 2 doses of 5 x 10⁷ CAR cells (dose-level 1, double [DL1D]).

Nineteen patients received a single dose of 1 x 10⁸ CAR cells (dose-level 2, single [DL2S]).

Safety

More than 90% of patients experienced a treatment-emergent adverse event (AE), and 60% had a treatment-related AE.

Treatment-emergent AEs occurring in more than 20% of patients included cytokine release syndrome (CRS), fatigue, nausea, constipation, decreased appetite, diarrhea, hypotension, neutropenia, anemia, and thrombocytopenia.

One patient had a grade 5 AE of diffuse alveolar damage that was thought to be related to fludarabine, cyclophosphamide, and JCAR017.

Another patient had a grade 5 AE of multiorgan failure that was considered unrelated to study treatment and due to disease progression.

The rate of grade 1/2 CRS was 33% (n=18), and the rate of grade 3/4 CRS was 2% (n=1). The rate of grade 1/2 neurotoxicity was 6% (n=3), and the rate of grade 3/4 neurotoxicity was 16% (n=9).

There were no deaths from CRS or neurotoxicity. The median time to onset of CRS was 5 days (range, 1-23), and the median time to onset of neurotoxicity was 11 days (range, 5-23).

“JCAR017 toxicities have, thus far, been relatively low and highly manageable at all dose levels tested, with a favorable safety profile that may enable outpatient administration,” Dr Abramson said.

Response

Fifty-four patients were evaluable for response. The ORR was 76%, and the CR rate was 52%. At 3 months of follow-up, the ORR was 51%, and the CR rate was 39%.

Dr Abramson noted that there was a dose-response relationship.

Overall, in the DL1S cohort, the ORR was 80%, and the CR rate was 53%. In the DL2S cohort, the ORR was 72%, and the CR rate was 50%. In the DL1D cohort, the ORR was 67%, and the CR rate was 50%.

At 3 months, in the DL1S cohort, the ORR was 46%, and the CR rate was 33%. In the DL2S cohort, the ORR was 64%, and the CR rate was 46%. In the DL1D cohort, the ORR and CR rate were both 50%.

Dr Abramson also noted that JCAR017 could produce a high response rate in poor-risk subgroups.

At 3 months, the ORR was 91% in patients who relapsed less than 12 months after transplant, 82% in patients with double- or triple-hit lymphoma, 48% in patients who had never achieved a CR, 47% in chemo-refractory patients, 31% in patients with primary refractory lymphoma, and 24% in patients with stable disease or progression after last chemotherapy.

Image by Betty Pace

The European Medicines Agency (EMA) has granted GBT440 access to the agency’s PRIority MEdicines (PRIME) program.

GBT440 is being developed by Global Blood Therapeutics, Inc. as a potentially disease-modifying therapy for sickle cell disease (SCD).

GBT440 works by increasing hemoglobin’s affinity for oxygen. Since oxygenated sickle hemoglobin does not polymerize, it is believed that GBT440 blocks polymerization and the resultant sickling of red blood cells.

If GBT440 can restore normal hemoglobin function and improve oxygen delivery, the therapy may be capable of modifying the progression of SCD.

About PRIME

The goal of the EMA’s PRIME program is to accelerate the development of therapies that may offer a major advantage over existing treatments or benefit patients with no treatment options.

Through PRIME, the EMA offers early and enhanced support to developers in order to optimize development plans and speed regulatory evaluations to potentially bring therapies to patients more quickly.

To be accepted for PRIME, a therapy must demonstrate the potential to benefit patients with unmet medical need through early clinical or nonclinical data.

Phase 1/2 trial

The GBT440 acceptance in the PRIME program was supported by data from an ongoing phase 1/2 trial (GBT440-001) in which researchers are evaluating the safety, tolerability, pharmacokinetics, and pharmacodynamics of GBT440 in healthy subjects and adults with SCD.

Data from this trial were presented at the 2016 ASH Annual Meeting.

At that time, there were 41 SCD patients who had been receiving GBT440 for up to 6 months.

All of these patients experienced a “profound and durable” reduction in hemolysis, as assessed by hemoglobin, reticulocytes, and/or bilirubin, according to Global Blood Therapeutics.

Patients treated with GBT440 for at least 90 days demonstrated a “clinically significant” increase in hemoglobin (greater than 1 g/dL increase) when compared with placebo-treated patients (46% vs 0%; P=0.006).

Patients treated with GBT440 also had a sustained reduction in irreversibly sickled cells when compared with placebo-treated patients (-76.6% vs +9.7%; P<0.001).

The most common treatment-related adverse events were grade 1/2 headache and gastrointestinal disorders. These events occurred in similar rates in the placebo and GBT440 arms. There were no drug-related serious or severe adverse events.

No sickle cell crises events occurred while participants were on GBT440. Exercise testing data showed normal tissue oxygen delivery (no change in oxygen consumption compared to placebo).

Image by Betty Pace

The European Medicines Agency (EMA) has granted GBT440 access to the agency’s PRIority MEdicines (PRIME) program.

GBT440 is being developed by Global Blood Therapeutics, Inc. as a potentially disease-modifying therapy for sickle cell disease (SCD).

GBT440 works by increasing hemoglobin’s affinity for oxygen. Since oxygenated sickle hemoglobin does not polymerize, it is believed that GBT440 blocks polymerization and the resultant sickling of red blood cells.

If GBT440 can restore normal hemoglobin function and improve oxygen delivery, the therapy may be capable of modifying the progression of SCD.

About PRIME

The goal of the EMA’s PRIME program is to accelerate the development of therapies that may offer a major advantage over existing treatments or benefit patients with no treatment options.

Through PRIME, the EMA offers early and enhanced support to developers in order to optimize development plans and speed regulatory evaluations to potentially bring therapies to patients more quickly.

To be accepted for PRIME, a therapy must demonstrate the potential to benefit patients with unmet medical need through early clinical or nonclinical data.

Phase 1/2 trial

The GBT440 acceptance in the PRIME program was supported by data from an ongoing phase 1/2 trial (GBT440-001) in which researchers are evaluating the safety, tolerability, pharmacokinetics, and pharmacodynamics of GBT440 in healthy subjects and adults with SCD.

Data from this trial were presented at the 2016 ASH Annual Meeting.

At that time, there were 41 SCD patients who had been receiving GBT440 for up to 6 months.

All of these patients experienced a “profound and durable” reduction in hemolysis, as assessed by hemoglobin, reticulocytes, and/or bilirubin, according to Global Blood Therapeutics.

Patients treated with GBT440 for at least 90 days demonstrated a “clinically significant” increase in hemoglobin (greater than 1 g/dL increase) when compared with placebo-treated patients (46% vs 0%; P=0.006).

Patients treated with GBT440 also had a sustained reduction in irreversibly sickled cells when compared with placebo-treated patients (-76.6% vs +9.7%; P<0.001).

The most common treatment-related adverse events were grade 1/2 headache and gastrointestinal disorders. These events occurred in similar rates in the placebo and GBT440 arms. There were no drug-related serious or severe adverse events.

No sickle cell crises events occurred while participants were on GBT440. Exercise testing data showed normal tissue oxygen delivery (no change in oxygen consumption compared to placebo).

Image by Betty Pace

The European Medicines Agency (EMA) has granted GBT440 access to the agency’s PRIority MEdicines (PRIME) program.

GBT440 is being developed by Global Blood Therapeutics, Inc. as a potentially disease-modifying therapy for sickle cell disease (SCD).

GBT440 works by increasing hemoglobin’s affinity for oxygen. Since oxygenated sickle hemoglobin does not polymerize, it is believed that GBT440 blocks polymerization and the resultant sickling of red blood cells.

If GBT440 can restore normal hemoglobin function and improve oxygen delivery, the therapy may be capable of modifying the progression of SCD.

About PRIME

The goal of the EMA’s PRIME program is to accelerate the development of therapies that may offer a major advantage over existing treatments or benefit patients with no treatment options.

Through PRIME, the EMA offers early and enhanced support to developers in order to optimize development plans and speed regulatory evaluations to potentially bring therapies to patients more quickly.

To be accepted for PRIME, a therapy must demonstrate the potential to benefit patients with unmet medical need through early clinical or nonclinical data.

Phase 1/2 trial

The GBT440 acceptance in the PRIME program was supported by data from an ongoing phase 1/2 trial (GBT440-001) in which researchers are evaluating the safety, tolerability, pharmacokinetics, and pharmacodynamics of GBT440 in healthy subjects and adults with SCD.

Data from this trial were presented at the 2016 ASH Annual Meeting.

At that time, there were 41 SCD patients who had been receiving GBT440 for up to 6 months.

All of these patients experienced a “profound and durable” reduction in hemolysis, as assessed by hemoglobin, reticulocytes, and/or bilirubin, according to Global Blood Therapeutics.

Patients treated with GBT440 for at least 90 days demonstrated a “clinically significant” increase in hemoglobin (greater than 1 g/dL increase) when compared with placebo-treated patients (46% vs 0%; P=0.006).

Patients treated with GBT440 also had a sustained reduction in irreversibly sickled cells when compared with placebo-treated patients (-76.6% vs +9.7%; P<0.001).

The most common treatment-related adverse events were grade 1/2 headache and gastrointestinal disorders. These events occurred in similar rates in the placebo and GBT440 arms. There were no drug-related serious or severe adverse events.

No sickle cell crises events occurred while participants were on GBT440. Exercise testing data showed normal tissue oxygen delivery (no change in oxygen consumption compared to placebo).

Antihemophilic factor

The European Commission has granted orphan medicinal product designation to CB 2679d/ISU304, a clinical stage drug candidate for hemophilia B.

CB 2679d/ISU304 is a next-generation coagulation factor IX variant that may allow for subcutaneous prophylactic treatment of individuals with hemophilia B.

The product is being developed by Catalyst Biosciences, Inc. and ISU Abxis.

Earlier this month, ISU Abxis completed dosing in the first of up to 5 patient cohorts in a phase 1/2 trial of CB 2679d/ISU304 in individuals with severe hemophilia B.

Catalyst Biosciences and ISU Abxis plan to have data from this trial by the end of this year.

About orphan designation

Orphan designation provides regulatory and financial incentives for companies to develop and market therapies that treat life-threatening or chronically debilitating conditions affecting no more than 5 in 10,000 people in the European Union, and where no satisfactory treatment is available.

Orphan designation provides a 10-year period of marketing exclusivity if the drug receives regulatory approval.

The designation also provides incentives for companies seeking protocol assistance from the European Medicines Agency during the product development phase and direct access to the centralized authorization procedure.

Antihemophilic factor

The European Commission has granted orphan medicinal product designation to CB 2679d/ISU304, a clinical stage drug candidate for hemophilia B.

CB 2679d/ISU304 is a next-generation coagulation factor IX variant that may allow for subcutaneous prophylactic treatment of individuals with hemophilia B.

The product is being developed by Catalyst Biosciences, Inc. and ISU Abxis.

Earlier this month, ISU Abxis completed dosing in the first of up to 5 patient cohorts in a phase 1/2 trial of CB 2679d/ISU304 in individuals with severe hemophilia B.

Catalyst Biosciences and ISU Abxis plan to have data from this trial by the end of this year.

About orphan designation

Orphan designation provides regulatory and financial incentives for companies to develop and market therapies that treat life-threatening or chronically debilitating conditions affecting no more than 5 in 10,000 people in the European Union, and where no satisfactory treatment is available.

Orphan designation provides a 10-year period of marketing exclusivity if the drug receives regulatory approval.

The designation also provides incentives for companies seeking protocol assistance from the European Medicines Agency during the product development phase and direct access to the centralized authorization procedure.

Antihemophilic factor

The European Commission has granted orphan medicinal product designation to CB 2679d/ISU304, a clinical stage drug candidate for hemophilia B.

CB 2679d/ISU304 is a next-generation coagulation factor IX variant that may allow for subcutaneous prophylactic treatment of individuals with hemophilia B.

The product is being developed by Catalyst Biosciences, Inc. and ISU Abxis.

Earlier this month, ISU Abxis completed dosing in the first of up to 5 patient cohorts in a phase 1/2 trial of CB 2679d/ISU304 in individuals with severe hemophilia B.

Catalyst Biosciences and ISU Abxis plan to have data from this trial by the end of this year.

About orphan designation

Orphan designation provides regulatory and financial incentives for companies to develop and market therapies that treat life-threatening or chronically debilitating conditions affecting no more than 5 in 10,000 people in the European Union, and where no satisfactory treatment is available.

Orphan designation provides a 10-year period of marketing exclusivity if the drug receives regulatory approval.

The designation also provides incentives for companies seeking protocol assistance from the European Medicines Agency during the product development phase and direct access to the centralized authorization procedure.

Patients with sickle cell disease have abnormalities of plasma lipoproteins that likely contribute to the disease’s characteristic vasculopathy and would not be addressed by simple red blood cell transfusion, suggesting that it may be time to rethink treatment strategy, according to a new study.

Previous research has shown that sickle cell disease (SCD) is associated with perturbations of cholesterol metabolism, according to the investigators, who were led by Eric Soupene, PhD, of the Children’s Hospital Oakland (Calif.) Research Institute. In particular, altered interactions of HDL particles appear to play a role.

For the study, the investigators analyzed 31 plasma samples obtained from patients with SCD during routine clinic visits and, in a subset, during vaso-occlusive crises, and 12 plasma samples obtained from healthy individuals serving as controls.

Main results showed that the patients with SCD had reduced levels of HDL₃ particles (which play roles in macrophage handling of cholesterol and endothelial protection) and altered functionality of HDL₂ particles, possibly as a compensatory mechanism (Exp Biol Med [Maywood]. 2017 Jan 1:1535370217706966. doi: 10.1177/1535370217706966). These changes were more pronounced during vaso-occlusive episodes.

In addition, endothelial cells exposed to lipoproteins from patients exhibited enhanced formation of inflammatory mediators, and this response could be blocked by treatment with hemopexin, a naturally occurring protein that scavenges heme.

“These findings indicate a significant imbalance of lipoprotein function,” the investigators write. “Our study adds to the growing evidence that the dysfunctional red blood cell ... in SCD affects the plasma environment, which contributes significantly in the vasculopathy that defines the disease.”

“The use of [red blood cell] concentrates in transfusion therapy of SCD patients underestimates the importance of the dysfunctional plasma compartment, and transfusion of whole blood or plasma may be warranted,” they propose. Furthermore, “[hemopexin] may provide an additional option to reduce inflammatory pathways by lowering the burden of cell-free heme.”

Study details

In the study, the investigators carried out a series of laboratory experiments comparing the quantity and function of lipoproteins between patients with SCD and healthy individuals. Patients receiving transfusion recently or on a long-term basis were not eligible, but patients receiving hydroxyurea were.

Results of gel electrophoresis showed that, compared with healthy individuals, patients with SCD not having a vaso-occlusive episode had a mean ratio of HDL₂ to HDL₃ that was 1.4 times higher (P less than .006), according to the published data. Moreover, the ratio for patients rose further on the 1st day of a vaso-occlusive episode (P = .005), so that the difference became even more pronounced.

Incubation of red blood cells with plasma from healthy individuals did not alter the HDL₂ to HDL₃ ratio, whereas incubation with plasma from patients with SCD increased this ratio.

When a fluorescent assay was used to assess oxidation, HDL₂ from patients with SCD had altered function, whereby it had greater antioxidant capacity than HDL₂ from healthy individuals. In fact, its antioxidant capacity was now very similar to that of HDL₃.

Endothelial cells showed a greater increase in expression of long pentraxin 3, an acute phase protein produced in response to inflammatory stimuli, when exposed to HDL₂ from patients with SCD as compared with HDL₂ from healthy individuals (P less than .05). Hemopexin, the heme scavenger, nearly abolished this increase for SCD patients (P = .003) but had little effect for healthy individuals.

“This links hemolysis to lipoprotein-mediated inflammation in SCD, and hemopexin treatment could be considered,” the investigators maintain.

Dr. Soupene disclosed that he had no relevant conflicts of interest.

Patients with sickle cell disease have abnormalities of plasma lipoproteins that likely contribute to the disease’s characteristic vasculopathy and would not be addressed by simple red blood cell transfusion, suggesting that it may be time to rethink treatment strategy, according to a new study.

Previous research has shown that sickle cell disease (SCD) is associated with perturbations of cholesterol metabolism, according to the investigators, who were led by Eric Soupene, PhD, of the Children’s Hospital Oakland (Calif.) Research Institute. In particular, altered interactions of HDL particles appear to play a role.

For the study, the investigators analyzed 31 plasma samples obtained from patients with SCD during routine clinic visits and, in a subset, during vaso-occlusive crises, and 12 plasma samples obtained from healthy individuals serving as controls.

Main results showed that the patients with SCD had reduced levels of HDL₃ particles (which play roles in macrophage handling of cholesterol and endothelial protection) and altered functionality of HDL₂ particles, possibly as a compensatory mechanism (Exp Biol Med [Maywood]. 2017 Jan 1:1535370217706966. doi: 10.1177/1535370217706966). These changes were more pronounced during vaso-occlusive episodes.

In addition, endothelial cells exposed to lipoproteins from patients exhibited enhanced formation of inflammatory mediators, and this response could be blocked by treatment with hemopexin, a naturally occurring protein that scavenges heme.

“These findings indicate a significant imbalance of lipoprotein function,” the investigators write. “Our study adds to the growing evidence that the dysfunctional red blood cell ... in SCD affects the plasma environment, which contributes significantly in the vasculopathy that defines the disease.”

“The use of [red blood cell] concentrates in transfusion therapy of SCD patients underestimates the importance of the dysfunctional plasma compartment, and transfusion of whole blood or plasma may be warranted,” they propose. Furthermore, “[hemopexin] may provide an additional option to reduce inflammatory pathways by lowering the burden of cell-free heme.”

Study details

In the study, the investigators carried out a series of laboratory experiments comparing the quantity and function of lipoproteins between patients with SCD and healthy individuals. Patients receiving transfusion recently or on a long-term basis were not eligible, but patients receiving hydroxyurea were.

Results of gel electrophoresis showed that, compared with healthy individuals, patients with SCD not having a vaso-occlusive episode had a mean ratio of HDL₂ to HDL₃ that was 1.4 times higher (P less than .006), according to the published data. Moreover, the ratio for patients rose further on the 1st day of a vaso-occlusive episode (P = .005), so that the difference became even more pronounced.

Incubation of red blood cells with plasma from healthy individuals did not alter the HDL₂ to HDL₃ ratio, whereas incubation with plasma from patients with SCD increased this ratio.

When a fluorescent assay was used to assess oxidation, HDL₂ from patients with SCD had altered function, whereby it had greater antioxidant capacity than HDL₂ from healthy individuals. In fact, its antioxidant capacity was now very similar to that of HDL₃.

Endothelial cells showed a greater increase in expression of long pentraxin 3, an acute phase protein produced in response to inflammatory stimuli, when exposed to HDL₂ from patients with SCD as compared with HDL₂ from healthy individuals (P less than .05). Hemopexin, the heme scavenger, nearly abolished this increase for SCD patients (P = .003) but had little effect for healthy individuals.

“This links hemolysis to lipoprotein-mediated inflammation in SCD, and hemopexin treatment could be considered,” the investigators maintain.

Dr. Soupene disclosed that he had no relevant conflicts of interest.

Patients with sickle cell disease have abnormalities of plasma lipoproteins that likely contribute to the disease’s characteristic vasculopathy and would not be addressed by simple red blood cell transfusion, suggesting that it may be time to rethink treatment strategy, according to a new study.

Previous research has shown that sickle cell disease (SCD) is associated with perturbations of cholesterol metabolism, according to the investigators, who were led by Eric Soupene, PhD, of the Children’s Hospital Oakland (Calif.) Research Institute. In particular, altered interactions of HDL particles appear to play a role.

For the study, the investigators analyzed 31 plasma samples obtained from patients with SCD during routine clinic visits and, in a subset, during vaso-occlusive crises, and 12 plasma samples obtained from healthy individuals serving as controls.

Main results showed that the patients with SCD had reduced levels of HDL₃ particles (which play roles in macrophage handling of cholesterol and endothelial protection) and altered functionality of HDL₂ particles, possibly as a compensatory mechanism (Exp Biol Med [Maywood]. 2017 Jan 1:1535370217706966. doi: 10.1177/1535370217706966). These changes were more pronounced during vaso-occlusive episodes.

In addition, endothelial cells exposed to lipoproteins from patients exhibited enhanced formation of inflammatory mediators, and this response could be blocked by treatment with hemopexin, a naturally occurring protein that scavenges heme.

“These findings indicate a significant imbalance of lipoprotein function,” the investigators write. “Our study adds to the growing evidence that the dysfunctional red blood cell ... in SCD affects the plasma environment, which contributes significantly in the vasculopathy that defines the disease.”

“The use of [red blood cell] concentrates in transfusion therapy of SCD patients underestimates the importance of the dysfunctional plasma compartment, and transfusion of whole blood or plasma may be warranted,” they propose. Furthermore, “[hemopexin] may provide an additional option to reduce inflammatory pathways by lowering the burden of cell-free heme.”

Study details

In the study, the investigators carried out a series of laboratory experiments comparing the quantity and function of lipoproteins between patients with SCD and healthy individuals. Patients receiving transfusion recently or on a long-term basis were not eligible, but patients receiving hydroxyurea were.

Results of gel electrophoresis showed that, compared with healthy individuals, patients with SCD not having a vaso-occlusive episode had a mean ratio of HDL₂ to HDL₃ that was 1.4 times higher (P less than .006), according to the published data. Moreover, the ratio for patients rose further on the 1st day of a vaso-occlusive episode (P = .005), so that the difference became even more pronounced.

Incubation of red blood cells with plasma from healthy individuals did not alter the HDL₂ to HDL₃ ratio, whereas incubation with plasma from patients with SCD increased this ratio.

When a fluorescent assay was used to assess oxidation, HDL₂ from patients with SCD had altered function, whereby it had greater antioxidant capacity than HDL₂ from healthy individuals. In fact, its antioxidant capacity was now very similar to that of HDL₃.

Endothelial cells showed a greater increase in expression of long pentraxin 3, an acute phase protein produced in response to inflammatory stimuli, when exposed to HDL₂ from patients with SCD as compared with HDL₂ from healthy individuals (P less than .05). Hemopexin, the heme scavenger, nearly abolished this increase for SCD patients (P = .003) but had little effect for healthy individuals.

“This links hemolysis to lipoprotein-mediated inflammation in SCD, and hemopexin treatment could be considered,” the investigators maintain.

Dr. Soupene disclosed that he had no relevant conflicts of interest.

LAS VEGAS – Metabolic syndrome is not causally related to hand osteoarthritis, according to data from the Framingham Offspring Study.

The new Framingham analysis, which features rigorous longitudinal follow-up, puts a serious dent in the popular hypothesis that metabolic syndrome is a risk factor for osteoarthritis through the proposed mechanism of systemic inflammation, Ida K. Haugen, MD, said at the World Congress on Osteoarthritis.

Bruce Jancin/Frontline Medical News

[email protected]

LAS VEGAS – Metabolic syndrome is not causally related to hand osteoarthritis, according to data from the Framingham Offspring Study.

The new Framingham analysis, which features rigorous longitudinal follow-up, puts a serious dent in the popular hypothesis that metabolic syndrome is a risk factor for osteoarthritis through the proposed mechanism of systemic inflammation, Ida K. Haugen, MD, said at the World Congress on Osteoarthritis.

Bruce Jancin/Frontline Medical News

[email protected]

LAS VEGAS – Metabolic syndrome is not causally related to hand osteoarthritis, according to data from the Framingham Offspring Study.

The new Framingham analysis, which features rigorous longitudinal follow-up, puts a serious dent in the popular hypothesis that metabolic syndrome is a risk factor for osteoarthritis through the proposed mechanism of systemic inflammation, Ida K. Haugen, MD, said at the World Congress on Osteoarthritis.

Bruce Jancin/Frontline Medical News

[email protected]