A prespecified analysis of a large global trial of patients with symptomatic heart failure with mildly reduced and preserved ejection fraction “seals the deal” on the efficacy of sodium-glucose cotransporter 2 (SGLT2) inhibitors to manage and improve their symptoms.

The prespecified analysis of the DELIVER (Dapagliflozin Evaluation to Improve the Lives of Patients with Preserved Ejection Fraction Heart Failure) trial included 5,795 patients with mildly reduced and preserved ejection fraction who completed the Kansas City Cardiomyopathy Questionnaire (KCCQ) after taking the SGLT2 inhibitor dapagliflozin or placebo. The results were published online in the Journal of the American College of Cardiology.

“We’ve known from studies prior to DELIVER that SGLT2 inhibitors have been shown to improve health status, patient symptoms and quality of life among those that are living with heart failure and mildly reduced [HFmrEF] and preserved [HFpEF] ejection fraction,” lead author Mikhail N. Kosiborod, MD, vice president for research at Saint Luke’s Health System, and codirector of the St. Luke’s Michael and Marly Haverty Cardiometabolic Center of Excellence at St. Luke’s Mid America Heart Institute, Kansas City, Mo., said in an interview. “But the picture was incomplete for a number of different reasons, partly because the previous studies were either relatively modest in size, geographically limited, or suggested potential attenuation of these benefits in patients with completely normal ejection fraction.”

Specifically, the study authors noted the EMPEROR-Preserved trial of the SGLT2 inhibitor empagliflozin showed improvement in health status vs. placebo across the range of EF except in those with normal EF of 65% or greater. The PRESERVED-HF trial of dapagliflozin demonstrated a more robust response than EMPEROR-Preserved or DELIVER, but PRESERVED-HF patients were recruited only in the United States and had more debilitating HF symptoms at baseline.

“Because of the results of the DELIVER trial and because of how large, extensive, and inclusive the trial was, it really seals the deal on the value of SGLT2 inhibitors in patients with heart failure,” said Dr. Kosiborod, who is also a professor of medicine at the University of Missouri–Kansas City.

The DELIVER analysis found that the effects of dapagliflozin on reducing cardiovascular death and worsening HF were greatest in patients who had the most debilitating symptoms at baseline, measured as KCCQ total symptom score (TSS) as 63 or less, the lowest of three tertiles used in the analysis. At baseline, these patients had the highest rates of CV death or worsening HF than those in the other two tertiles: KCCQ-TSS of 63-84, and greater than 84.

Compared with placebo, treated patients in the lowest KCCQ-TSS quartile had a 30% reduction in risk for the primary composite outcome, which consisted of time to first CV death or HF event (hazard ratio, 0.70; 95% confidence interval, 0.58-0.84; P < .001). In the second tertile, the relative risk reduction was 19% (HR, 0.81; 95% CI, 0.65-1.01; P < .006), and the highest quartile showed no significant difference between treatment and placebo (HR, 1.07; 95% CI, 0.83-1.37; P < .62).

“The most important take home message is that the SGLT2 inhibitor dapagliflozin significantly improved patient symptoms as measured by the Kansas City Cardiomyopathy Questionnaire symptom score,” Dr. Kosiborod said. “It improved those symptoms within 1 month and those benefits were sustained out to 8 months.”

DELIVER patients also showed improvement in all other key KCCQ domains across the board, he added. “In addition, dapagliflozin also improved the proportion of patients who had small, moderate, and large improvements in a responder analysis. So really, by every measure that we had, dapagliflozin had a significant beneficial effect.”

The DELIVER results taken collectively with the EMPEROR-Preserved and PRESERVED-HF trials cinch the deal for SGLT2 inhibitors, Dr. Kosiborod said. “They deliver on the triple goal of care in patients with heart failure. They reduce the risk of cardiovascular death and worsening heart failure and they improve patient symptoms, function and quality of life – and they accomplish that across the entire continuum of heart failure regardless of ejection fraction, regardless of whether patients are hospitalized or in an ambulatory setting, regardless of age or background therapies or other comorbidities.”

He added: “It’s a pretty historic development because we haven’t had that before.”

AstraZeneca funded the DELIVER trial. Dr. Kosiborod disclosed financial relationships with Alnylam, Amgen, Applied Therapeutics, Bayer, Boehringer Ingelheim, Cytokinetics, Dexcom, Eli Lilly, Esperion Therapeutics, Janssen, Lexicon, Merck (Diabetes and Cardiovascular), Novo Nordisk, Sanofi, Pharmacosmos and Vifor Pharma.
 

A prespecified analysis of a large global trial of patients with symptomatic heart failure with mildly reduced and preserved ejection fraction “seals the deal” on the efficacy of sodium-glucose cotransporter 2 (SGLT2) inhibitors to manage and improve their symptoms.

The prespecified analysis of the DELIVER (Dapagliflozin Evaluation to Improve the Lives of Patients with Preserved Ejection Fraction Heart Failure) trial included 5,795 patients with mildly reduced and preserved ejection fraction who completed the Kansas City Cardiomyopathy Questionnaire (KCCQ) after taking the SGLT2 inhibitor dapagliflozin or placebo. The results were published online in the Journal of the American College of Cardiology.

“We’ve known from studies prior to DELIVER that SGLT2 inhibitors have been shown to improve health status, patient symptoms and quality of life among those that are living with heart failure and mildly reduced [HFmrEF] and preserved [HFpEF] ejection fraction,” lead author Mikhail N. Kosiborod, MD, vice president for research at Saint Luke’s Health System, and codirector of the St. Luke’s Michael and Marly Haverty Cardiometabolic Center of Excellence at St. Luke’s Mid America Heart Institute, Kansas City, Mo., said in an interview. “But the picture was incomplete for a number of different reasons, partly because the previous studies were either relatively modest in size, geographically limited, or suggested potential attenuation of these benefits in patients with completely normal ejection fraction.”

Specifically, the study authors noted the EMPEROR-Preserved trial of the SGLT2 inhibitor empagliflozin showed improvement in health status vs. placebo across the range of EF except in those with normal EF of 65% or greater. The PRESERVED-HF trial of dapagliflozin demonstrated a more robust response than EMPEROR-Preserved or DELIVER, but PRESERVED-HF patients were recruited only in the United States and had more debilitating HF symptoms at baseline.

“Because of the results of the DELIVER trial and because of how large, extensive, and inclusive the trial was, it really seals the deal on the value of SGLT2 inhibitors in patients with heart failure,” said Dr. Kosiborod, who is also a professor of medicine at the University of Missouri–Kansas City.

The DELIVER analysis found that the effects of dapagliflozin on reducing cardiovascular death and worsening HF were greatest in patients who had the most debilitating symptoms at baseline, measured as KCCQ total symptom score (TSS) as 63 or less, the lowest of three tertiles used in the analysis. At baseline, these patients had the highest rates of CV death or worsening HF than those in the other two tertiles: KCCQ-TSS of 63-84, and greater than 84.

Compared with placebo, treated patients in the lowest KCCQ-TSS quartile had a 30% reduction in risk for the primary composite outcome, which consisted of time to first CV death or HF event (hazard ratio, 0.70; 95% confidence interval, 0.58-0.84; P < .001). In the second tertile, the relative risk reduction was 19% (HR, 0.81; 95% CI, 0.65-1.01; P < .006), and the highest quartile showed no significant difference between treatment and placebo (HR, 1.07; 95% CI, 0.83-1.37; P < .62).

“The most important take home message is that the SGLT2 inhibitor dapagliflozin significantly improved patient symptoms as measured by the Kansas City Cardiomyopathy Questionnaire symptom score,” Dr. Kosiborod said. “It improved those symptoms within 1 month and those benefits were sustained out to 8 months.”

DELIVER patients also showed improvement in all other key KCCQ domains across the board, he added. “In addition, dapagliflozin also improved the proportion of patients who had small, moderate, and large improvements in a responder analysis. So really, by every measure that we had, dapagliflozin had a significant beneficial effect.”

The DELIVER results taken collectively with the EMPEROR-Preserved and PRESERVED-HF trials cinch the deal for SGLT2 inhibitors, Dr. Kosiborod said. “They deliver on the triple goal of care in patients with heart failure. They reduce the risk of cardiovascular death and worsening heart failure and they improve patient symptoms, function and quality of life – and they accomplish that across the entire continuum of heart failure regardless of ejection fraction, regardless of whether patients are hospitalized or in an ambulatory setting, regardless of age or background therapies or other comorbidities.”

He added: “It’s a pretty historic development because we haven’t had that before.”

AstraZeneca funded the DELIVER trial. Dr. Kosiborod disclosed financial relationships with Alnylam, Amgen, Applied Therapeutics, Bayer, Boehringer Ingelheim, Cytokinetics, Dexcom, Eli Lilly, Esperion Therapeutics, Janssen, Lexicon, Merck (Diabetes and Cardiovascular), Novo Nordisk, Sanofi, Pharmacosmos and Vifor Pharma.
 

A prespecified analysis of a large global trial of patients with symptomatic heart failure with mildly reduced and preserved ejection fraction “seals the deal” on the efficacy of sodium-glucose cotransporter 2 (SGLT2) inhibitors to manage and improve their symptoms.

The prespecified analysis of the DELIVER (Dapagliflozin Evaluation to Improve the Lives of Patients with Preserved Ejection Fraction Heart Failure) trial included 5,795 patients with mildly reduced and preserved ejection fraction who completed the Kansas City Cardiomyopathy Questionnaire (KCCQ) after taking the SGLT2 inhibitor dapagliflozin or placebo. The results were published online in the Journal of the American College of Cardiology.

“We’ve known from studies prior to DELIVER that SGLT2 inhibitors have been shown to improve health status, patient symptoms and quality of life among those that are living with heart failure and mildly reduced [HFmrEF] and preserved [HFpEF] ejection fraction,” lead author Mikhail N. Kosiborod, MD, vice president for research at Saint Luke’s Health System, and codirector of the St. Luke’s Michael and Marly Haverty Cardiometabolic Center of Excellence at St. Luke’s Mid America Heart Institute, Kansas City, Mo., said in an interview. “But the picture was incomplete for a number of different reasons, partly because the previous studies were either relatively modest in size, geographically limited, or suggested potential attenuation of these benefits in patients with completely normal ejection fraction.”

Specifically, the study authors noted the EMPEROR-Preserved trial of the SGLT2 inhibitor empagliflozin showed improvement in health status vs. placebo across the range of EF except in those with normal EF of 65% or greater. The PRESERVED-HF trial of dapagliflozin demonstrated a more robust response than EMPEROR-Preserved or DELIVER, but PRESERVED-HF patients were recruited only in the United States and had more debilitating HF symptoms at baseline.

“Because of the results of the DELIVER trial and because of how large, extensive, and inclusive the trial was, it really seals the deal on the value of SGLT2 inhibitors in patients with heart failure,” said Dr. Kosiborod, who is also a professor of medicine at the University of Missouri–Kansas City.

The DELIVER analysis found that the effects of dapagliflozin on reducing cardiovascular death and worsening HF were greatest in patients who had the most debilitating symptoms at baseline, measured as KCCQ total symptom score (TSS) as 63 or less, the lowest of three tertiles used in the analysis. At baseline, these patients had the highest rates of CV death or worsening HF than those in the other two tertiles: KCCQ-TSS of 63-84, and greater than 84.

Compared with placebo, treated patients in the lowest KCCQ-TSS quartile had a 30% reduction in risk for the primary composite outcome, which consisted of time to first CV death or HF event (hazard ratio, 0.70; 95% confidence interval, 0.58-0.84; P < .001). In the second tertile, the relative risk reduction was 19% (HR, 0.81; 95% CI, 0.65-1.01; P < .006), and the highest quartile showed no significant difference between treatment and placebo (HR, 1.07; 95% CI, 0.83-1.37; P < .62).

“The most important take home message is that the SGLT2 inhibitor dapagliflozin significantly improved patient symptoms as measured by the Kansas City Cardiomyopathy Questionnaire symptom score,” Dr. Kosiborod said. “It improved those symptoms within 1 month and those benefits were sustained out to 8 months.”

DELIVER patients also showed improvement in all other key KCCQ domains across the board, he added. “In addition, dapagliflozin also improved the proportion of patients who had small, moderate, and large improvements in a responder analysis. So really, by every measure that we had, dapagliflozin had a significant beneficial effect.”

The DELIVER results taken collectively with the EMPEROR-Preserved and PRESERVED-HF trials cinch the deal for SGLT2 inhibitors, Dr. Kosiborod said. “They deliver on the triple goal of care in patients with heart failure. They reduce the risk of cardiovascular death and worsening heart failure and they improve patient symptoms, function and quality of life – and they accomplish that across the entire continuum of heart failure regardless of ejection fraction, regardless of whether patients are hospitalized or in an ambulatory setting, regardless of age or background therapies or other comorbidities.”

He added: “It’s a pretty historic development because we haven’t had that before.”

AstraZeneca funded the DELIVER trial. Dr. Kosiborod disclosed financial relationships with Alnylam, Amgen, Applied Therapeutics, Bayer, Boehringer Ingelheim, Cytokinetics, Dexcom, Eli Lilly, Esperion Therapeutics, Janssen, Lexicon, Merck (Diabetes and Cardiovascular), Novo Nordisk, Sanofi, Pharmacosmos and Vifor Pharma.
 

LAS VEGAS – Improving diversity in dermatology starts with education, Susan C. Taylor, MD, said in a presentation at Medscape Live’s annual Las Vegas Dermatology Seminar, where she led a panel discussion on opportunities to improve diversity in the specialty.

The growing ethnic minority population in the United States “underscores the need for medical education to ensure dermatologists are prepared to provide quality care for patients of diverse racial and ethnic backgrounds,” said Dr. Taylor, the Bernett L. Johnson Jr., MD, Professor, and vice chair for diversity, equity, and inclusion in the department of dermatology at the University of Pennsylvania.

Improving education includes diversifying resource material, she said. A recent study in the Journal of the American Academy of Dermatology showed the representation of skin tones on Google searches for skin conditions was mostly light skin (91.7%), although non-Hispanic Whites account for less than two-thirds (approximately 60%) of the U.S. population, she said. Many people with darker skin tones “are not finding people who look like themselves” when they search skin conditions online, she noted.

The lack of diversity in images occurs not only on Google, “but in our textbooks, which are the foundational resources for our students,” said Nada M. Elbuluk, MD, founder and director of the Skin of Color and Pigmentary Disorders Program at the University of Southern California, Los Angeles. She also established the Dermatology Diversity and Inclusion Program at USC.

Although more than 13% of Americans are Black, only 3% of dermatologists in the United States are Black, Dr. Callender noted. Similarly, 4.2% of dermatologists in the United States are Hispanic or Latino, but these groups make up more than 18% of the general U.S. population, according to a recent study, she said.

Cheryl M. Burgess, MD, founder and medical director of the Center for Dermatology and Dermatologic Surgery in Washington, presented a roadmap of strategies for improving diversity in dermatology, starting with increasing STEM education at the high school and college levels among all populations and increasing the pipeline of underrepresented students to medical schools.

Then, faculty should work to increase interest in dermatology among underrepresented medical students and increase the numbers of underrepresented medical students in dermatology residency programs, said Dr. Burgess, assistant clinical professor of dermatology at Georgetown University and George Washington University, Washington.

“The more diversity we have in our specialty, the more we learn from each other,” and increased diversity can promote new research questions, said Andrew F. Alexis, MD, vice chair for diversity and inclusion in the department of dermatology and professor of clinical dermatology at Weill Cornell Medicine, New York.

Increasing the diversity of populations in clinical trials is another important strategy to improve diversity in dermatology, he emphasized.

Mentoring is an excellent way to help underrepresented students develop and pursue a career in dermatology, the panelists agreed. Time is precious for everyone, so don’t hesitate to use Zoom and other technology to help connect with mentees, Dr. Burgess advised.

Dr. Taylor added that mentoring doesn’t have to be a huge time commitment, it can be as simple as volunteering once a year at a school career forum. “It is so gratifying to have these young people looking up to you,” she said.

The panelists disclosed relationships with multiple companies, but none were relevant to this panel discussion. MedscapeLive and this news organization are owned by the same parent company.

LAS VEGAS – Improving diversity in dermatology starts with education, Susan C. Taylor, MD, said in a presentation at Medscape Live’s annual Las Vegas Dermatology Seminar, where she led a panel discussion on opportunities to improve diversity in the specialty.

The growing ethnic minority population in the United States “underscores the need for medical education to ensure dermatologists are prepared to provide quality care for patients of diverse racial and ethnic backgrounds,” said Dr. Taylor, the Bernett L. Johnson Jr., MD, Professor, and vice chair for diversity, equity, and inclusion in the department of dermatology at the University of Pennsylvania.

Improving education includes diversifying resource material, she said. A recent study in the Journal of the American Academy of Dermatology showed the representation of skin tones on Google searches for skin conditions was mostly light skin (91.7%), although non-Hispanic Whites account for less than two-thirds (approximately 60%) of the U.S. population, she said. Many people with darker skin tones “are not finding people who look like themselves” when they search skin conditions online, she noted.

The lack of diversity in images occurs not only on Google, “but in our textbooks, which are the foundational resources for our students,” said Nada M. Elbuluk, MD, founder and director of the Skin of Color and Pigmentary Disorders Program at the University of Southern California, Los Angeles. She also established the Dermatology Diversity and Inclusion Program at USC.

Although more than 13% of Americans are Black, only 3% of dermatologists in the United States are Black, Dr. Callender noted. Similarly, 4.2% of dermatologists in the United States are Hispanic or Latino, but these groups make up more than 18% of the general U.S. population, according to a recent study, she said.

Cheryl M. Burgess, MD, founder and medical director of the Center for Dermatology and Dermatologic Surgery in Washington, presented a roadmap of strategies for improving diversity in dermatology, starting with increasing STEM education at the high school and college levels among all populations and increasing the pipeline of underrepresented students to medical schools.

Then, faculty should work to increase interest in dermatology among underrepresented medical students and increase the numbers of underrepresented medical students in dermatology residency programs, said Dr. Burgess, assistant clinical professor of dermatology at Georgetown University and George Washington University, Washington.

“The more diversity we have in our specialty, the more we learn from each other,” and increased diversity can promote new research questions, said Andrew F. Alexis, MD, vice chair for diversity and inclusion in the department of dermatology and professor of clinical dermatology at Weill Cornell Medicine, New York.

Increasing the diversity of populations in clinical trials is another important strategy to improve diversity in dermatology, he emphasized.

Mentoring is an excellent way to help underrepresented students develop and pursue a career in dermatology, the panelists agreed. Time is precious for everyone, so don’t hesitate to use Zoom and other technology to help connect with mentees, Dr. Burgess advised.

Dr. Taylor added that mentoring doesn’t have to be a huge time commitment, it can be as simple as volunteering once a year at a school career forum. “It is so gratifying to have these young people looking up to you,” she said.

The panelists disclosed relationships with multiple companies, but none were relevant to this panel discussion. MedscapeLive and this news organization are owned by the same parent company.

LAS VEGAS – Improving diversity in dermatology starts with education, Susan C. Taylor, MD, said in a presentation at Medscape Live’s annual Las Vegas Dermatology Seminar, where she led a panel discussion on opportunities to improve diversity in the specialty.

The growing ethnic minority population in the United States “underscores the need for medical education to ensure dermatologists are prepared to provide quality care for patients of diverse racial and ethnic backgrounds,” said Dr. Taylor, the Bernett L. Johnson Jr., MD, Professor, and vice chair for diversity, equity, and inclusion in the department of dermatology at the University of Pennsylvania.

Improving education includes diversifying resource material, she said. A recent study in the Journal of the American Academy of Dermatology showed the representation of skin tones on Google searches for skin conditions was mostly light skin (91.7%), although non-Hispanic Whites account for less than two-thirds (approximately 60%) of the U.S. population, she said. Many people with darker skin tones “are not finding people who look like themselves” when they search skin conditions online, she noted.

The lack of diversity in images occurs not only on Google, “but in our textbooks, which are the foundational resources for our students,” said Nada M. Elbuluk, MD, founder and director of the Skin of Color and Pigmentary Disorders Program at the University of Southern California, Los Angeles. She also established the Dermatology Diversity and Inclusion Program at USC.

Although more than 13% of Americans are Black, only 3% of dermatologists in the United States are Black, Dr. Callender noted. Similarly, 4.2% of dermatologists in the United States are Hispanic or Latino, but these groups make up more than 18% of the general U.S. population, according to a recent study, she said.

Cheryl M. Burgess, MD, founder and medical director of the Center for Dermatology and Dermatologic Surgery in Washington, presented a roadmap of strategies for improving diversity in dermatology, starting with increasing STEM education at the high school and college levels among all populations and increasing the pipeline of underrepresented students to medical schools.

Then, faculty should work to increase interest in dermatology among underrepresented medical students and increase the numbers of underrepresented medical students in dermatology residency programs, said Dr. Burgess, assistant clinical professor of dermatology at Georgetown University and George Washington University, Washington.

“The more diversity we have in our specialty, the more we learn from each other,” and increased diversity can promote new research questions, said Andrew F. Alexis, MD, vice chair for diversity and inclusion in the department of dermatology and professor of clinical dermatology at Weill Cornell Medicine, New York.

Increasing the diversity of populations in clinical trials is another important strategy to improve diversity in dermatology, he emphasized.

Mentoring is an excellent way to help underrepresented students develop and pursue a career in dermatology, the panelists agreed. Time is precious for everyone, so don’t hesitate to use Zoom and other technology to help connect with mentees, Dr. Burgess advised.

Dr. Taylor added that mentoring doesn’t have to be a huge time commitment, it can be as simple as volunteering once a year at a school career forum. “It is so gratifying to have these young people looking up to you,” she said.

The panelists disclosed relationships with multiple companies, but none were relevant to this panel discussion. MedscapeLive and this news organization are owned by the same parent company.

At least once a week, dermatologist Kelly Stankiewicz, MD, meets with patients who believe that fillers can help them achieve any lip shape. Some reach for their smartphones to show her images and say: “I want my lips to look just like this.”

Those images may help Dr. Stankiewicz understand patient preferences in terms of lip size and proportion, but she points out that shape is unique to each person. “I tell them: ‘All we can do is enhance that lip shape with filler. We can’t give you somebody else’s lip shape with an injection of filler.’ ”

During a virtual course on laser and aesthetic skin therapy, she and Omar A. Ibrahimi, MD, PhD, dispelled this and other false dogmas that they hear from some clinicians who practice aesthetic medicine and the patients who see them.

Wait 1 year before treating traumatic and surgical scars with vascular and fractional CO2 lasers. “I don’t think this is controversial anymore, because there is a boatload of data, which has shown that early treatment can prevent hypertrophic scarring and promote scar maturation,” said Dr. Stankiewicz, who practices dermatology in Park City, Utah. “Histology has also shown more organized dermal collagen from early treatment. Of course, there will be situations where you may want to hold off, like doing an ablative fractional [laser treatment] over the scar of a joint replacement ... where you may risk infection.” In her clinic, she routinely treats scars on the same day as suture removal, “as long as the healing looks appropriate.”

Dr. Ibrahimi, a dermatologist and medical director of the Connecticut Skin Institute, Stamford, also jumps on treating scars early. For a patient with postacne erythema, for example, he will use a pulsed-dye laser, which he believes will prevent scars from becoming atrophic.

Used equipment is a better investment than new equipment. While purchasing used laser and light devices can save money, especially when starting out, be wary of potential pitfalls, including the fact that many devices have disposable tips. “If your laser isn’t certified or you’re not the authorized owner of the device, you won’t be able to buy the disposables,” Dr. Stankiewicz noted. “So, before you buy a used device, ensure that you can buy them.”

Also, consider the cost of service if the device breaks down, she advised. Some lasers are complicated to service and others have codes set by the manufacturer so that only contracted engineers can work on them. “Otherwise, third-party engineers and service providers have to figure out how to crack the code to get into the machine,” she said. “If you’re in the situation where you have to ask the manufacturer to service your device, you have to pay a lot of money to recertify your device. Then you’ve lost all the savings you thought you made by buying a used machine.” She prefers to negotiate a good deal on a new device. “Often, a very good deal on a new device can rival the offer of a used one.”

Dr. Ibrahimi recalled buying a used fractional laser that came with a 30-day guarantee, but it stopped working around day 45. “I didn’t have much recourse there,” he said during the meeting, which was sponsored by Harvard Medical School, Massachusetts General Hospital, and the Wellman Center for Photomedicine. “You can’t go back to the company [for repair] unless you pay a recertification fee.”

Avoid exercise after Botox treatment. Although inverted yoga poses and lying down should be avoided for several hours after receiving Botox, there are no other limits to other forms of exercise post treatment, Dr. Stankiewicz said. If she suspects that a patient will develop bruising on one or more injection sites, she treats the areas with a laser. “Doing this on the same day as Botox treatment doesn’t always stop or treat bruising, many times it does.”

Another myth she hears is that it is not safe to fly in an airplane after Botox treatment. “That recommendation comes from the fact that the atmospheric pressure is lower in an airplane, so we worry about the risk of Botox spread,” Dr. Stankiewicz said. “But I practice at 7,000 feet above sea level, which is the same atmospheric pressure as that in an airplane,” she added, noting Botox is administered throughout the day in her practice and she does not see increased complications or worry about spread.

Clinician self-treatment is okay. In the opinion of Dr. Stankiewicz, aesthetic clinicians who treat themselves “have a fool for a patient.” She added: “Although no one is going to blame you and may not even know if you give yourself a little Botox touch-up at home, glorifying self-treatment on social media must stop. It’s dangerous and it can be ineffective.”

Self-treatment can also impair judgment and the objectivity of cosmetic therapies. “Also, when you’re pointing a laser at your own face and posting it on social media, it gives viewers the impression that this is not a serious medical treatment when it really is,” she emphasized. In addition, “when you treat yourself, you lose the ability to see the proper clinical endpoint. You also lose the ability to see the angle and the appropriate position for injection to avoid intervascular occlusion.”

Neither Dr. Stankiewicz nor Dr. Ibrahimi reported having relevant financial disclosures.

At least once a week, dermatologist Kelly Stankiewicz, MD, meets with patients who believe that fillers can help them achieve any lip shape. Some reach for their smartphones to show her images and say: “I want my lips to look just like this.”

Those images may help Dr. Stankiewicz understand patient preferences in terms of lip size and proportion, but she points out that shape is unique to each person. “I tell them: ‘All we can do is enhance that lip shape with filler. We can’t give you somebody else’s lip shape with an injection of filler.’ ”

During a virtual course on laser and aesthetic skin therapy, she and Omar A. Ibrahimi, MD, PhD, dispelled this and other false dogmas that they hear from some clinicians who practice aesthetic medicine and the patients who see them.

Wait 1 year before treating traumatic and surgical scars with vascular and fractional CO2 lasers. “I don’t think this is controversial anymore, because there is a boatload of data, which has shown that early treatment can prevent hypertrophic scarring and promote scar maturation,” said Dr. Stankiewicz, who practices dermatology in Park City, Utah. “Histology has also shown more organized dermal collagen from early treatment. Of course, there will be situations where you may want to hold off, like doing an ablative fractional [laser treatment] over the scar of a joint replacement ... where you may risk infection.” In her clinic, she routinely treats scars on the same day as suture removal, “as long as the healing looks appropriate.”

Dr. Ibrahimi, a dermatologist and medical director of the Connecticut Skin Institute, Stamford, also jumps on treating scars early. For a patient with postacne erythema, for example, he will use a pulsed-dye laser, which he believes will prevent scars from becoming atrophic.

Used equipment is a better investment than new equipment. While purchasing used laser and light devices can save money, especially when starting out, be wary of potential pitfalls, including the fact that many devices have disposable tips. “If your laser isn’t certified or you’re not the authorized owner of the device, you won’t be able to buy the disposables,” Dr. Stankiewicz noted. “So, before you buy a used device, ensure that you can buy them.”

Also, consider the cost of service if the device breaks down, she advised. Some lasers are complicated to service and others have codes set by the manufacturer so that only contracted engineers can work on them. “Otherwise, third-party engineers and service providers have to figure out how to crack the code to get into the machine,” she said. “If you’re in the situation where you have to ask the manufacturer to service your device, you have to pay a lot of money to recertify your device. Then you’ve lost all the savings you thought you made by buying a used machine.” She prefers to negotiate a good deal on a new device. “Often, a very good deal on a new device can rival the offer of a used one.”

Dr. Ibrahimi recalled buying a used fractional laser that came with a 30-day guarantee, but it stopped working around day 45. “I didn’t have much recourse there,” he said during the meeting, which was sponsored by Harvard Medical School, Massachusetts General Hospital, and the Wellman Center for Photomedicine. “You can’t go back to the company [for repair] unless you pay a recertification fee.”

Avoid exercise after Botox treatment. Although inverted yoga poses and lying down should be avoided for several hours after receiving Botox, there are no other limits to other forms of exercise post treatment, Dr. Stankiewicz said. If she suspects that a patient will develop bruising on one or more injection sites, she treats the areas with a laser. “Doing this on the same day as Botox treatment doesn’t always stop or treat bruising, many times it does.”

Another myth she hears is that it is not safe to fly in an airplane after Botox treatment. “That recommendation comes from the fact that the atmospheric pressure is lower in an airplane, so we worry about the risk of Botox spread,” Dr. Stankiewicz said. “But I practice at 7,000 feet above sea level, which is the same atmospheric pressure as that in an airplane,” she added, noting Botox is administered throughout the day in her practice and she does not see increased complications or worry about spread.

Clinician self-treatment is okay. In the opinion of Dr. Stankiewicz, aesthetic clinicians who treat themselves “have a fool for a patient.” She added: “Although no one is going to blame you and may not even know if you give yourself a little Botox touch-up at home, glorifying self-treatment on social media must stop. It’s dangerous and it can be ineffective.”

Self-treatment can also impair judgment and the objectivity of cosmetic therapies. “Also, when you’re pointing a laser at your own face and posting it on social media, it gives viewers the impression that this is not a serious medical treatment when it really is,” she emphasized. In addition, “when you treat yourself, you lose the ability to see the proper clinical endpoint. You also lose the ability to see the angle and the appropriate position for injection to avoid intervascular occlusion.”

Neither Dr. Stankiewicz nor Dr. Ibrahimi reported having relevant financial disclosures.

At least once a week, dermatologist Kelly Stankiewicz, MD, meets with patients who believe that fillers can help them achieve any lip shape. Some reach for their smartphones to show her images and say: “I want my lips to look just like this.”

Those images may help Dr. Stankiewicz understand patient preferences in terms of lip size and proportion, but she points out that shape is unique to each person. “I tell them: ‘All we can do is enhance that lip shape with filler. We can’t give you somebody else’s lip shape with an injection of filler.’ ”

During a virtual course on laser and aesthetic skin therapy, she and Omar A. Ibrahimi, MD, PhD, dispelled this and other false dogmas that they hear from some clinicians who practice aesthetic medicine and the patients who see them.

Wait 1 year before treating traumatic and surgical scars with vascular and fractional CO2 lasers. “I don’t think this is controversial anymore, because there is a boatload of data, which has shown that early treatment can prevent hypertrophic scarring and promote scar maturation,” said Dr. Stankiewicz, who practices dermatology in Park City, Utah. “Histology has also shown more organized dermal collagen from early treatment. Of course, there will be situations where you may want to hold off, like doing an ablative fractional [laser treatment] over the scar of a joint replacement ... where you may risk infection.” In her clinic, she routinely treats scars on the same day as suture removal, “as long as the healing looks appropriate.”

Dr. Ibrahimi, a dermatologist and medical director of the Connecticut Skin Institute, Stamford, also jumps on treating scars early. For a patient with postacne erythema, for example, he will use a pulsed-dye laser, which he believes will prevent scars from becoming atrophic.

Used equipment is a better investment than new equipment. While purchasing used laser and light devices can save money, especially when starting out, be wary of potential pitfalls, including the fact that many devices have disposable tips. “If your laser isn’t certified or you’re not the authorized owner of the device, you won’t be able to buy the disposables,” Dr. Stankiewicz noted. “So, before you buy a used device, ensure that you can buy them.”

Also, consider the cost of service if the device breaks down, she advised. Some lasers are complicated to service and others have codes set by the manufacturer so that only contracted engineers can work on them. “Otherwise, third-party engineers and service providers have to figure out how to crack the code to get into the machine,” she said. “If you’re in the situation where you have to ask the manufacturer to service your device, you have to pay a lot of money to recertify your device. Then you’ve lost all the savings you thought you made by buying a used machine.” She prefers to negotiate a good deal on a new device. “Often, a very good deal on a new device can rival the offer of a used one.”

Dr. Ibrahimi recalled buying a used fractional laser that came with a 30-day guarantee, but it stopped working around day 45. “I didn’t have much recourse there,” he said during the meeting, which was sponsored by Harvard Medical School, Massachusetts General Hospital, and the Wellman Center for Photomedicine. “You can’t go back to the company [for repair] unless you pay a recertification fee.”

Avoid exercise after Botox treatment. Although inverted yoga poses and lying down should be avoided for several hours after receiving Botox, there are no other limits to other forms of exercise post treatment, Dr. Stankiewicz said. If she suspects that a patient will develop bruising on one or more injection sites, she treats the areas with a laser. “Doing this on the same day as Botox treatment doesn’t always stop or treat bruising, many times it does.”

Another myth she hears is that it is not safe to fly in an airplane after Botox treatment. “That recommendation comes from the fact that the atmospheric pressure is lower in an airplane, so we worry about the risk of Botox spread,” Dr. Stankiewicz said. “But I practice at 7,000 feet above sea level, which is the same atmospheric pressure as that in an airplane,” she added, noting Botox is administered throughout the day in her practice and she does not see increased complications or worry about spread.

Clinician self-treatment is okay. In the opinion of Dr. Stankiewicz, aesthetic clinicians who treat themselves “have a fool for a patient.” She added: “Although no one is going to blame you and may not even know if you give yourself a little Botox touch-up at home, glorifying self-treatment on social media must stop. It’s dangerous and it can be ineffective.”

Self-treatment can also impair judgment and the objectivity of cosmetic therapies. “Also, when you’re pointing a laser at your own face and posting it on social media, it gives viewers the impression that this is not a serious medical treatment when it really is,” she emphasized. In addition, “when you treat yourself, you lose the ability to see the proper clinical endpoint. You also lose the ability to see the angle and the appropriate position for injection to avoid intervascular occlusion.”

Neither Dr. Stankiewicz nor Dr. Ibrahimi reported having relevant financial disclosures.

Metabolic syndrome is associated with a significantly increased risk for gout in young men, but the risk can be mitigated by improvement in individual components of the syndrome, based on data from a pair of population-based studies totaling more than 4 million individuals.

Gout remains the most common type of inflammatory arthritis in men, and the rate has been rising among younger adults, Yeonghee Eun, MD, PhD, of Sungkyunkwan University, Seoul, South Korea, and colleagues wrote. An increasing body of evidence suggests a link between gout and metabolic syndrome (MetS), but large studies have been lacking, especially in younger adults.

In a study published in Frontiers in Medicine, the researchers reviewed data from 3,569,104 men aged 20-39 years who underwent a health checkup between 2009 and 2012 in South Korea, based on the Korean National Health Insurance Service. The primary outcome of incident gout was identified using claims data. The mean age of the participants was 31.5 years.

Over a mean follow-up of 7.4 years, the incidence of gout was 3.36 per 1,000 person-years. The risk of developing gout was more than twice as high among individuals who met MetS criteria than in those who did not (adjusted hazard ratio, 2.44).

MetS was defined as the presence of at least two of the following components: hypertriglyceridemia, abdominal obesity, reduced HDL cholesterol, elevated blood pressure, and elevated fasting glucose.

Overall, individuals with all five MetS components had a fivefold increase in gout risk, compared with people who did not have MetS (aHR, 5.24). In an analysis of each component of MetS, hypertriglyceridemia and abdominal obesity showed the strongest association with gout (aHRs of 2.08 and 2.33, respectively).

The impact of MetS on risk of incident gout was greater in younger participants, which suggests that the management of MetS in young people should be emphasized, the researchers said.

In a further analysis of body mass index subgroups, MetS had the greatest impact on gout risk for individuals who were underweight (aHR, 3.82). “In particular, in the underweight group, the risk of gout increased 10-fold when abdominal obesity was present,” the researchers said.

The study was limited by several factors including potential selection bias and potential overestimation of gout incidence because of the use of diagnostic codes, the researchers noted. Other limitations included lack of control for nutritional or dietary risk factors and the inability to include cases that occurred after the study period.

However, findings were strengthened by the large number of participants with MetS who were underweight or normal weight, the researchers wrote. More research on the mechanism of action is needed, but the data suggest that MetS is a key risk factor in the development of gout in young men.

In a second study, published in Arthritis & Rheumatology, Dr. Eun and colleagues examined associations between MetS changes and incident gout in young men. Although previous studies have shown that changes in MetS status can alter the risk of cardiovascular events, atrial fibrillation, end-stage renal disease, and all-cause mortality, the impact of these changes on gout has not been well studied, they said. The researchers used the same study cohort, the National Health Insurance Service database in South Korea. They reviewed data from 1,293,166 individuals aged 20-39 years. Of these, 18,473 were diagnosed with gout for an incidence rate 3.36/1,000 person-years. The researchers compared gout incidence for men who met criteria for MetS at three health checkups and those without MetS.

Overall, patients with MetS at all three checkups had a nearly fourfold higher risk of gout than those who never had MetS, with an adjusted hazard ratio of 3.82, the researchers wrote. The development of MetS over the study period more than doubled the risk of gout, but recovery from MetS reduced incident gout risk by approximately 50% (aHR, 0.52).

In findings similar to the Frontiers in Medicine study, the greatest associations with gout were noted for changes in elevated triglycerides and changes in abdominal obesity; aHRs for development and recovery for elevated triglycerides were 1.74 and 0.56, respectively, and for abdominal obesity, 1.94 and 0.69, respectively.

More research is needed to explore the mechanism by which both abdominal obesity and elevated triglycerides drive the development of gout, the researchers wrote in their discussion.

Also similar to the Frontiers study, the associations among changes in MetS and incident gout were greater for the youngest participants (in their 20s) and in the underweight or normal weight BMI groups.

Limitations of the second study included possible selection bias because of the study population of workplace employees who participated in regular health checks and the lack of data on women or on men aged 40 years and older, the researchers noted. Other limitations included possible misclassification of MetS because of varying health checkup results and drug claims, and lack of data on serum urate, which prevented assessment of hyperuricemia as a cause of gout.

However, the results were strengthened by the large sample size and suggest that MetS is a modifiable risk factor for gout, the researchers concluded.

Neither of the studies received outside funding. The researchers had no financial conflicts to disclose.

Metabolic syndrome is associated with a significantly increased risk for gout in young men, but the risk can be mitigated by improvement in individual components of the syndrome, based on data from a pair of population-based studies totaling more than 4 million individuals.

Gout remains the most common type of inflammatory arthritis in men, and the rate has been rising among younger adults, Yeonghee Eun, MD, PhD, of Sungkyunkwan University, Seoul, South Korea, and colleagues wrote. An increasing body of evidence suggests a link between gout and metabolic syndrome (MetS), but large studies have been lacking, especially in younger adults.

In a study published in Frontiers in Medicine, the researchers reviewed data from 3,569,104 men aged 20-39 years who underwent a health checkup between 2009 and 2012 in South Korea, based on the Korean National Health Insurance Service. The primary outcome of incident gout was identified using claims data. The mean age of the participants was 31.5 years.

Over a mean follow-up of 7.4 years, the incidence of gout was 3.36 per 1,000 person-years. The risk of developing gout was more than twice as high among individuals who met MetS criteria than in those who did not (adjusted hazard ratio, 2.44).

MetS was defined as the presence of at least two of the following components: hypertriglyceridemia, abdominal obesity, reduced HDL cholesterol, elevated blood pressure, and elevated fasting glucose.

Overall, individuals with all five MetS components had a fivefold increase in gout risk, compared with people who did not have MetS (aHR, 5.24). In an analysis of each component of MetS, hypertriglyceridemia and abdominal obesity showed the strongest association with gout (aHRs of 2.08 and 2.33, respectively).

The impact of MetS on risk of incident gout was greater in younger participants, which suggests that the management of MetS in young people should be emphasized, the researchers said.

In a further analysis of body mass index subgroups, MetS had the greatest impact on gout risk for individuals who were underweight (aHR, 3.82). “In particular, in the underweight group, the risk of gout increased 10-fold when abdominal obesity was present,” the researchers said.

The study was limited by several factors including potential selection bias and potential overestimation of gout incidence because of the use of diagnostic codes, the researchers noted. Other limitations included lack of control for nutritional or dietary risk factors and the inability to include cases that occurred after the study period.

However, findings were strengthened by the large number of participants with MetS who were underweight or normal weight, the researchers wrote. More research on the mechanism of action is needed, but the data suggest that MetS is a key risk factor in the development of gout in young men.

In a second study, published in Arthritis & Rheumatology, Dr. Eun and colleagues examined associations between MetS changes and incident gout in young men. Although previous studies have shown that changes in MetS status can alter the risk of cardiovascular events, atrial fibrillation, end-stage renal disease, and all-cause mortality, the impact of these changes on gout has not been well studied, they said. The researchers used the same study cohort, the National Health Insurance Service database in South Korea. They reviewed data from 1,293,166 individuals aged 20-39 years. Of these, 18,473 were diagnosed with gout for an incidence rate 3.36/1,000 person-years. The researchers compared gout incidence for men who met criteria for MetS at three health checkups and those without MetS.

Overall, patients with MetS at all three checkups had a nearly fourfold higher risk of gout than those who never had MetS, with an adjusted hazard ratio of 3.82, the researchers wrote. The development of MetS over the study period more than doubled the risk of gout, but recovery from MetS reduced incident gout risk by approximately 50% (aHR, 0.52).

In findings similar to the Frontiers in Medicine study, the greatest associations with gout were noted for changes in elevated triglycerides and changes in abdominal obesity; aHRs for development and recovery for elevated triglycerides were 1.74 and 0.56, respectively, and for abdominal obesity, 1.94 and 0.69, respectively.

More research is needed to explore the mechanism by which both abdominal obesity and elevated triglycerides drive the development of gout, the researchers wrote in their discussion.

Also similar to the Frontiers study, the associations among changes in MetS and incident gout were greater for the youngest participants (in their 20s) and in the underweight or normal weight BMI groups.

Limitations of the second study included possible selection bias because of the study population of workplace employees who participated in regular health checks and the lack of data on women or on men aged 40 years and older, the researchers noted. Other limitations included possible misclassification of MetS because of varying health checkup results and drug claims, and lack of data on serum urate, which prevented assessment of hyperuricemia as a cause of gout.

However, the results were strengthened by the large sample size and suggest that MetS is a modifiable risk factor for gout, the researchers concluded.

Neither of the studies received outside funding. The researchers had no financial conflicts to disclose.

Metabolic syndrome is associated with a significantly increased risk for gout in young men, but the risk can be mitigated by improvement in individual components of the syndrome, based on data from a pair of population-based studies totaling more than 4 million individuals.

Gout remains the most common type of inflammatory arthritis in men, and the rate has been rising among younger adults, Yeonghee Eun, MD, PhD, of Sungkyunkwan University, Seoul, South Korea, and colleagues wrote. An increasing body of evidence suggests a link between gout and metabolic syndrome (MetS), but large studies have been lacking, especially in younger adults.

In a study published in Frontiers in Medicine, the researchers reviewed data from 3,569,104 men aged 20-39 years who underwent a health checkup between 2009 and 2012 in South Korea, based on the Korean National Health Insurance Service. The primary outcome of incident gout was identified using claims data. The mean age of the participants was 31.5 years.

Over a mean follow-up of 7.4 years, the incidence of gout was 3.36 per 1,000 person-years. The risk of developing gout was more than twice as high among individuals who met MetS criteria than in those who did not (adjusted hazard ratio, 2.44).

MetS was defined as the presence of at least two of the following components: hypertriglyceridemia, abdominal obesity, reduced HDL cholesterol, elevated blood pressure, and elevated fasting glucose.

Overall, individuals with all five MetS components had a fivefold increase in gout risk, compared with people who did not have MetS (aHR, 5.24). In an analysis of each component of MetS, hypertriglyceridemia and abdominal obesity showed the strongest association with gout (aHRs of 2.08 and 2.33, respectively).

The impact of MetS on risk of incident gout was greater in younger participants, which suggests that the management of MetS in young people should be emphasized, the researchers said.

In a further analysis of body mass index subgroups, MetS had the greatest impact on gout risk for individuals who were underweight (aHR, 3.82). “In particular, in the underweight group, the risk of gout increased 10-fold when abdominal obesity was present,” the researchers said.

The study was limited by several factors including potential selection bias and potential overestimation of gout incidence because of the use of diagnostic codes, the researchers noted. Other limitations included lack of control for nutritional or dietary risk factors and the inability to include cases that occurred after the study period.

However, findings were strengthened by the large number of participants with MetS who were underweight or normal weight, the researchers wrote. More research on the mechanism of action is needed, but the data suggest that MetS is a key risk factor in the development of gout in young men.

In a second study, published in Arthritis & Rheumatology, Dr. Eun and colleagues examined associations between MetS changes and incident gout in young men. Although previous studies have shown that changes in MetS status can alter the risk of cardiovascular events, atrial fibrillation, end-stage renal disease, and all-cause mortality, the impact of these changes on gout has not been well studied, they said. The researchers used the same study cohort, the National Health Insurance Service database in South Korea. They reviewed data from 1,293,166 individuals aged 20-39 years. Of these, 18,473 were diagnosed with gout for an incidence rate 3.36/1,000 person-years. The researchers compared gout incidence for men who met criteria for MetS at three health checkups and those without MetS.

Overall, patients with MetS at all three checkups had a nearly fourfold higher risk of gout than those who never had MetS, with an adjusted hazard ratio of 3.82, the researchers wrote. The development of MetS over the study period more than doubled the risk of gout, but recovery from MetS reduced incident gout risk by approximately 50% (aHR, 0.52).

In findings similar to the Frontiers in Medicine study, the greatest associations with gout were noted for changes in elevated triglycerides and changes in abdominal obesity; aHRs for development and recovery for elevated triglycerides were 1.74 and 0.56, respectively, and for abdominal obesity, 1.94 and 0.69, respectively.

More research is needed to explore the mechanism by which both abdominal obesity and elevated triglycerides drive the development of gout, the researchers wrote in their discussion.

Also similar to the Frontiers study, the associations among changes in MetS and incident gout were greater for the youngest participants (in their 20s) and in the underweight or normal weight BMI groups.

Limitations of the second study included possible selection bias because of the study population of workplace employees who participated in regular health checks and the lack of data on women or on men aged 40 years and older, the researchers noted. Other limitations included possible misclassification of MetS because of varying health checkup results and drug claims, and lack of data on serum urate, which prevented assessment of hyperuricemia as a cause of gout.

However, the results were strengthened by the large sample size and suggest that MetS is a modifiable risk factor for gout, the researchers concluded.

Neither of the studies received outside funding. The researchers had no financial conflicts to disclose.

A panel of advisers to the Food and Drug Administration has recommended against approval of omecamtiv mecarbil (Cytokinetics) for the treatment of heart failure with reduced ejection fraction (HFrEF).

Omecamtiv mecarbil is a first-in-class, selective cardiac myosin activator designed to improve cardiac performance.

Wikimedia Commons/FitzColinGerald/Creative Commons License

The FDA Cardiovascular and Renal Drugs Advisory Committee on Dec. 13 voted 8 to 3 (with no abstentions) that the benefits of omecamtiv mecarbil do not outweigh the risks for HFrEF.

Those who voted in favor of the drug cited the clinical benefit (albeit small) and good safety profile of the drug as well as the unmet need for new treatments.

C. Noel Bairey Merz, MD, Cedars-Sinai Medical Center, Los Angeles, said she voted yes “on the basis of need,” and her personal experience, as well as the data presented, that “up to half of severe heart failure patients are intolerant of guidelines directed medical therapy.”

Christopher M. O’Connor, MD, with Inova Heart and Vascular Institute, Falls Church, Va., who also voted in favor of approval for the drug, cited the “important unmet need,” and said he believes “a path was constructed in which one could go forward safely and with enhanced efficacy.

“It may be a narrow path, but I think it’s a path that would afford a lot of benefit to this high-risk patient population,” said Dr. O’Connor.

Those who voted against approval generally felt the benefit was not large enough and that more data are needed, given this is a first-in-class agent.

Julia B. Lewis, MD, Vanderbilt Medical Center, Nashville, Tenn., who voted no, said she was concerned that, despite the large size of the trial, “a more positive effect could not have been found.” She was also concerned that there was no benefit on quality of life or any other secondary outcomes. 

David J. Moliterno, MD, University of Kentucky Medical Center, Lexington, who also voted no, felt the benefits were “more singular and that being a modest reduction primarily limited to fewer outpatient visits.” Dr. Moliterno, like many of the committee members who voted no, called for more study.

The committee’s decision was based on results from the phase 3 GALACTIC-HF trial, which enrolled 8,256 patients with HFrEF who were at risk of hospitalization and death, despite standard-of-care therapy.

As previously reported by this news organization, omecamtiv mecarbil produced a positive result for the study’s primary endpoint, with a 2.1% absolute reduction in the combined rate of cardiovascular (CV) death, first HF hospitalization, or first urgent visit for HF, compared with placebo during a median follow-up of about 22 months.

This represented an 8% relative risk reduction and broke down as a 0.6% absolute drop in CV death, compared with placebo, a 0.7% cut in HF hospitalization, and a 0.8% drop in urgent outpatient HF visits.

The results were presented at the American Heart Association 2020 scientific sessions and simultaneously published in the New England Journal of Medicine.

In a statement, Robert I. Blum, president and CEO of Cytokinetics, said, “We are disappointed there was not a greater consensus amongst committee members relating to the benefit-risk of omecamtiv mecarbil, and we maintain our conviction in the strength of evidence supporting its potential benefit for patients suffering from HFrEF.”

He added that the company plans to engage constructively with the FDA as it completes its review of the application for omecamtiv mecarbil. 

The drug has a Prescription Drug User Fee Act target date of Feb. 28, 2023.

A version of this article first appeared on Medscape.com.

A panel of advisers to the Food and Drug Administration has recommended against approval of omecamtiv mecarbil (Cytokinetics) for the treatment of heart failure with reduced ejection fraction (HFrEF).

Omecamtiv mecarbil is a first-in-class, selective cardiac myosin activator designed to improve cardiac performance.

Wikimedia Commons/FitzColinGerald/Creative Commons License

The FDA Cardiovascular and Renal Drugs Advisory Committee on Dec. 13 voted 8 to 3 (with no abstentions) that the benefits of omecamtiv mecarbil do not outweigh the risks for HFrEF.

Those who voted in favor of the drug cited the clinical benefit (albeit small) and good safety profile of the drug as well as the unmet need for new treatments.

C. Noel Bairey Merz, MD, Cedars-Sinai Medical Center, Los Angeles, said she voted yes “on the basis of need,” and her personal experience, as well as the data presented, that “up to half of severe heart failure patients are intolerant of guidelines directed medical therapy.”

Christopher M. O’Connor, MD, with Inova Heart and Vascular Institute, Falls Church, Va., who also voted in favor of approval for the drug, cited the “important unmet need,” and said he believes “a path was constructed in which one could go forward safely and with enhanced efficacy.

“It may be a narrow path, but I think it’s a path that would afford a lot of benefit to this high-risk patient population,” said Dr. O’Connor.

Those who voted against approval generally felt the benefit was not large enough and that more data are needed, given this is a first-in-class agent.

Julia B. Lewis, MD, Vanderbilt Medical Center, Nashville, Tenn., who voted no, said she was concerned that, despite the large size of the trial, “a more positive effect could not have been found.” She was also concerned that there was no benefit on quality of life or any other secondary outcomes. 

David J. Moliterno, MD, University of Kentucky Medical Center, Lexington, who also voted no, felt the benefits were “more singular and that being a modest reduction primarily limited to fewer outpatient visits.” Dr. Moliterno, like many of the committee members who voted no, called for more study.

The committee’s decision was based on results from the phase 3 GALACTIC-HF trial, which enrolled 8,256 patients with HFrEF who were at risk of hospitalization and death, despite standard-of-care therapy.

As previously reported by this news organization, omecamtiv mecarbil produced a positive result for the study’s primary endpoint, with a 2.1% absolute reduction in the combined rate of cardiovascular (CV) death, first HF hospitalization, or first urgent visit for HF, compared with placebo during a median follow-up of about 22 months.

This represented an 8% relative risk reduction and broke down as a 0.6% absolute drop in CV death, compared with placebo, a 0.7% cut in HF hospitalization, and a 0.8% drop in urgent outpatient HF visits.

The results were presented at the American Heart Association 2020 scientific sessions and simultaneously published in the New England Journal of Medicine.

In a statement, Robert I. Blum, president and CEO of Cytokinetics, said, “We are disappointed there was not a greater consensus amongst committee members relating to the benefit-risk of omecamtiv mecarbil, and we maintain our conviction in the strength of evidence supporting its potential benefit for patients suffering from HFrEF.”

He added that the company plans to engage constructively with the FDA as it completes its review of the application for omecamtiv mecarbil. 

The drug has a Prescription Drug User Fee Act target date of Feb. 28, 2023.

A version of this article first appeared on Medscape.com.

A panel of advisers to the Food and Drug Administration has recommended against approval of omecamtiv mecarbil (Cytokinetics) for the treatment of heart failure with reduced ejection fraction (HFrEF).

Omecamtiv mecarbil is a first-in-class, selective cardiac myosin activator designed to improve cardiac performance.

Wikimedia Commons/FitzColinGerald/Creative Commons License

The FDA Cardiovascular and Renal Drugs Advisory Committee on Dec. 13 voted 8 to 3 (with no abstentions) that the benefits of omecamtiv mecarbil do not outweigh the risks for HFrEF.

Those who voted in favor of the drug cited the clinical benefit (albeit small) and good safety profile of the drug as well as the unmet need for new treatments.

C. Noel Bairey Merz, MD, Cedars-Sinai Medical Center, Los Angeles, said she voted yes “on the basis of need,” and her personal experience, as well as the data presented, that “up to half of severe heart failure patients are intolerant of guidelines directed medical therapy.”

Christopher M. O’Connor, MD, with Inova Heart and Vascular Institute, Falls Church, Va., who also voted in favor of approval for the drug, cited the “important unmet need,” and said he believes “a path was constructed in which one could go forward safely and with enhanced efficacy.

“It may be a narrow path, but I think it’s a path that would afford a lot of benefit to this high-risk patient population,” said Dr. O’Connor.

Those who voted against approval generally felt the benefit was not large enough and that more data are needed, given this is a first-in-class agent.

Julia B. Lewis, MD, Vanderbilt Medical Center, Nashville, Tenn., who voted no, said she was concerned that, despite the large size of the trial, “a more positive effect could not have been found.” She was also concerned that there was no benefit on quality of life or any other secondary outcomes. 

David J. Moliterno, MD, University of Kentucky Medical Center, Lexington, who also voted no, felt the benefits were “more singular and that being a modest reduction primarily limited to fewer outpatient visits.” Dr. Moliterno, like many of the committee members who voted no, called for more study.

The committee’s decision was based on results from the phase 3 GALACTIC-HF trial, which enrolled 8,256 patients with HFrEF who were at risk of hospitalization and death, despite standard-of-care therapy.

As previously reported by this news organization, omecamtiv mecarbil produced a positive result for the study’s primary endpoint, with a 2.1% absolute reduction in the combined rate of cardiovascular (CV) death, first HF hospitalization, or first urgent visit for HF, compared with placebo during a median follow-up of about 22 months.

This represented an 8% relative risk reduction and broke down as a 0.6% absolute drop in CV death, compared with placebo, a 0.7% cut in HF hospitalization, and a 0.8% drop in urgent outpatient HF visits.

The results were presented at the American Heart Association 2020 scientific sessions and simultaneously published in the New England Journal of Medicine.

In a statement, Robert I. Blum, president and CEO of Cytokinetics, said, “We are disappointed there was not a greater consensus amongst committee members relating to the benefit-risk of omecamtiv mecarbil, and we maintain our conviction in the strength of evidence supporting its potential benefit for patients suffering from HFrEF.”

He added that the company plans to engage constructively with the FDA as it completes its review of the application for omecamtiv mecarbil. 

The drug has a Prescription Drug User Fee Act target date of Feb. 28, 2023.

A version of this article first appeared on Medscape.com.

Maybe the cow was late for its appointment

It’s been a long day running the front desk at your doctor’s office. People calling in prescriptions, a million appointments, you’ve been running yourself ragged keeping things together. Finally, it’s almost closing time. The last patient of the day has just checked out and you turn back to the waiting room, expecting to see it blessedly empty.

Instead, a 650-pound cow is staring at you.

“I’m sorry, sir or madam, we’re about to close.”

Moo.
 

tilo/Thinkstock

We can see that decision in your eyes

The cliché that eyes are the windows to the soul doesn’t tell the whole story about how telling eyes really are. It’s all about how they move. In a recent study, researchers determined that a type of eye movement known as a saccade reveals your choice before you even decide.

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Saccades involve the eyes jumping from one fixation point to another, senior author Alaa Ahmed of the University of Colorado, Boulder, explained in a statement from the university. Saccade vigor was the key in how aligned the type of decisions were made by the 22 study participants.

In the study, subjects walked on a treadmill at varied inclines for a period of time. Then they sat in front of a monitor and a high-speed camera that tracked their eye movements as the monitor presented them with a series of exercise options. The participants had only 4 seconds to choose between them.

After they made their choices, participants went back on the treadmill to perform the exercises they had chosen. The researchers found that participants’ eyes jumped between the options slowly then faster to the option they eventually picked. The more impulsive decision-makers also tended to move their eyes even more rapidly before slowing down after a decision was made, making it pretty conclusive that the eyes were revealing their choices.

The way your eyes shift gives you away without saying a thing. Might be wise, then, to wear sunglasses to your next poker tournament.
 

Let them eat soap

Okay, we admit it: LOTME spends a lot of time in the bathroom. Today, though, we’re interested in the sinks. Specifically, the P-traps under the sinks. You know, the curvy bit that keeps sewer gas from wafting back into the room?

PxHere

Well, researchers from the University of Reading (England) recently found some fungi while examining a bunch of sinks on the university’s Whiteknights campus. “It isn’t a big surprise to find fungi in a warm, wet environment. But sinks and P-traps have thus far been overlooked as potential reservoirs of these microorganisms,” they said in a written statement.

Samples collected from 289 P-traps contained “a very similar community of yeasts and molds, showing that sinks in use in public environments share a role as reservoirs of fungal organisms,” they noted.

The fungi living in the traps survived conditions with high temperatures, low pH, and little in the way of nutrients. So what were they eating? Some varieties, they said, “use detergents, found in soap, as a source of carbon-rich food.” We’ll repeat that last part: They used the soap as food.

WARNING: Rant Ahead.

There are a lot of cleaning products for sale that say they will make your home safe by killing 99.9% of germs and bacteria. Not fungi, exactly, but we’re still talking microorganisms. Molds, bacteria, and viruses are all stuff that can infect humans and make them sick.

So you kill 99.9% of them. Great, but that leaves 0.1% that you just made angry. And what do they do next? They learn to eat soap. Then University of Reading investigators find out that all the extra hand washing going on during the COVID-19 pandemic was “clogging up sinks with nasty disease-causing bacteria.”

These are microorganisms we’re talking about people. They’ve been at this for a billion years! Rats can’t beat them, cockroaches won’t stop them – Earth’s ultimate survivors are powerless against the invisible horde.

We’re doomed.

Maybe the cow was late for its appointment

It’s been a long day running the front desk at your doctor’s office. People calling in prescriptions, a million appointments, you’ve been running yourself ragged keeping things together. Finally, it’s almost closing time. The last patient of the day has just checked out and you turn back to the waiting room, expecting to see it blessedly empty.

Instead, a 650-pound cow is staring at you.

“I’m sorry, sir or madam, we’re about to close.”

Moo.
 

tilo/Thinkstock

We can see that decision in your eyes

The cliché that eyes are the windows to the soul doesn’t tell the whole story about how telling eyes really are. It’s all about how they move. In a recent study, researchers determined that a type of eye movement known as a saccade reveals your choice before you even decide.

pxfuel

Saccades involve the eyes jumping from one fixation point to another, senior author Alaa Ahmed of the University of Colorado, Boulder, explained in a statement from the university. Saccade vigor was the key in how aligned the type of decisions were made by the 22 study participants.

In the study, subjects walked on a treadmill at varied inclines for a period of time. Then they sat in front of a monitor and a high-speed camera that tracked their eye movements as the monitor presented them with a series of exercise options. The participants had only 4 seconds to choose between them.

After they made their choices, participants went back on the treadmill to perform the exercises they had chosen. The researchers found that participants’ eyes jumped between the options slowly then faster to the option they eventually picked. The more impulsive decision-makers also tended to move their eyes even more rapidly before slowing down after a decision was made, making it pretty conclusive that the eyes were revealing their choices.

The way your eyes shift gives you away without saying a thing. Might be wise, then, to wear sunglasses to your next poker tournament.
 

Let them eat soap

Okay, we admit it: LOTME spends a lot of time in the bathroom. Today, though, we’re interested in the sinks. Specifically, the P-traps under the sinks. You know, the curvy bit that keeps sewer gas from wafting back into the room?

PxHere

Well, researchers from the University of Reading (England) recently found some fungi while examining a bunch of sinks on the university’s Whiteknights campus. “It isn’t a big surprise to find fungi in a warm, wet environment. But sinks and P-traps have thus far been overlooked as potential reservoirs of these microorganisms,” they said in a written statement.

Samples collected from 289 P-traps contained “a very similar community of yeasts and molds, showing that sinks in use in public environments share a role as reservoirs of fungal organisms,” they noted.

The fungi living in the traps survived conditions with high temperatures, low pH, and little in the way of nutrients. So what were they eating? Some varieties, they said, “use detergents, found in soap, as a source of carbon-rich food.” We’ll repeat that last part: They used the soap as food.

WARNING: Rant Ahead.

There are a lot of cleaning products for sale that say they will make your home safe by killing 99.9% of germs and bacteria. Not fungi, exactly, but we’re still talking microorganisms. Molds, bacteria, and viruses are all stuff that can infect humans and make them sick.

So you kill 99.9% of them. Great, but that leaves 0.1% that you just made angry. And what do they do next? They learn to eat soap. Then University of Reading investigators find out that all the extra hand washing going on during the COVID-19 pandemic was “clogging up sinks with nasty disease-causing bacteria.”

These are microorganisms we’re talking about people. They’ve been at this for a billion years! Rats can’t beat them, cockroaches won’t stop them – Earth’s ultimate survivors are powerless against the invisible horde.

We’re doomed.

Maybe the cow was late for its appointment

It’s been a long day running the front desk at your doctor’s office. People calling in prescriptions, a million appointments, you’ve been running yourself ragged keeping things together. Finally, it’s almost closing time. The last patient of the day has just checked out and you turn back to the waiting room, expecting to see it blessedly empty.

Instead, a 650-pound cow is staring at you.

“I’m sorry, sir or madam, we’re about to close.”

Moo.
 

tilo/Thinkstock

We can see that decision in your eyes

The cliché that eyes are the windows to the soul doesn’t tell the whole story about how telling eyes really are. It’s all about how they move. In a recent study, researchers determined that a type of eye movement known as a saccade reveals your choice before you even decide.

pxfuel

Saccades involve the eyes jumping from one fixation point to another, senior author Alaa Ahmed of the University of Colorado, Boulder, explained in a statement from the university. Saccade vigor was the key in how aligned the type of decisions were made by the 22 study participants.

In the study, subjects walked on a treadmill at varied inclines for a period of time. Then they sat in front of a monitor and a high-speed camera that tracked their eye movements as the monitor presented them with a series of exercise options. The participants had only 4 seconds to choose between them.

After they made their choices, participants went back on the treadmill to perform the exercises they had chosen. The researchers found that participants’ eyes jumped between the options slowly then faster to the option they eventually picked. The more impulsive decision-makers also tended to move their eyes even more rapidly before slowing down after a decision was made, making it pretty conclusive that the eyes were revealing their choices.

The way your eyes shift gives you away without saying a thing. Might be wise, then, to wear sunglasses to your next poker tournament.
 

Let them eat soap

Okay, we admit it: LOTME spends a lot of time in the bathroom. Today, though, we’re interested in the sinks. Specifically, the P-traps under the sinks. You know, the curvy bit that keeps sewer gas from wafting back into the room?

PxHere

Well, researchers from the University of Reading (England) recently found some fungi while examining a bunch of sinks on the university’s Whiteknights campus. “It isn’t a big surprise to find fungi in a warm, wet environment. But sinks and P-traps have thus far been overlooked as potential reservoirs of these microorganisms,” they said in a written statement.

Samples collected from 289 P-traps contained “a very similar community of yeasts and molds, showing that sinks in use in public environments share a role as reservoirs of fungal organisms,” they noted.

The fungi living in the traps survived conditions with high temperatures, low pH, and little in the way of nutrients. So what were they eating? Some varieties, they said, “use detergents, found in soap, as a source of carbon-rich food.” We’ll repeat that last part: They used the soap as food.

WARNING: Rant Ahead.

There are a lot of cleaning products for sale that say they will make your home safe by killing 99.9% of germs and bacteria. Not fungi, exactly, but we’re still talking microorganisms. Molds, bacteria, and viruses are all stuff that can infect humans and make them sick.

So you kill 99.9% of them. Great, but that leaves 0.1% that you just made angry. And what do they do next? They learn to eat soap. Then University of Reading investigators find out that all the extra hand washing going on during the COVID-19 pandemic was “clogging up sinks with nasty disease-causing bacteria.”

These are microorganisms we’re talking about people. They’ve been at this for a billion years! Rats can’t beat them, cockroaches won’t stop them – Earth’s ultimate survivors are powerless against the invisible horde.

We’re doomed.

Exposure to inhaled agents in the workplace could be putting people at risk of developing rheumatoid arthritis, according to research published in Annals of the Rheumatic Diseases.

In an analysis of data from the long-running Swedish Epidemiological Investigation of RA (EIRA) population-based cohort study, there was a 21% increased risk of RA and a 25% increased risk of anti–citrullinated protein antibody (ACPA)–positive RA associated with exposure to any occupationally inhaled agent.

LOOK PHOTO / Fotolia.com

“We have investigated a number of occupational airborne exposures and found that exposure for those agents infer a high risk for RA,” Lars Klareskog, MD, PhD, senior professor of rheumatology at the Karolinska Institute and Karolinska University Hospital (Solna) in Stockholm, said in an interview.

Dr. Klareskog, who is one of the lead authors of the published work, added that the risk is particularly high in individuals who had a genetic susceptibility and in those who smoked.

“The importance of this is that it further demonstrates that exposures to the lung may trigger immune reactions associated with the major subset of rheumatoid arthritis,” Dr. Klareskog said. “Second, it shows that those exposed to these agents should be very keen to not smoke.” “These findings further implicate the respiratory tract mucosa in ACPA-positive RA pathogenesis,” agreed Vanessa L. Kronzer, MD, of the Mayo Clinic in Rochester, Minn., and Jeffrey A. Sparks, MD, MMSc, of Brigham and Women’s Hospital and Harvard Medical School, both in Boston.

They also “impress the need for public policy initiatives related to occupational inhalants to prevent RA,” they suggested in an editorial.

Multiple occupational inhalable exposures assessed

In the analysis, the researchers assessed exposure to 32 inhalable agents in people with (n = 4,033) and without RA (n = 6,485). The list of agents considered included detergents, diesel engine exhaust, fine particulate matter, solvents, and agricultural chemicals.

A total of 17 agents showed a positive association with an increased risk of ACPA-positive RA. Dr. Kronzer and Dr. Sparks noted that breathing in insecticides and fungicides at work was associated with the highest odds ratios for having ACPA-positive RA (both 2.38).

“Importantly, both the number and duration of exposures exhibited a dose-response effect on RA risk,” the editorialists said.

They also picked out that there was “a gene-environment interaction for RA risk for certain inhalants,” including diesel engine exhaust, asbestos, carbon monoxide, and quartz dust.

Smoking amplified the risk for ACPA-positive RA associated with certain agents, such as detergents, and adding in genetic susceptibility for a third exposure increased the risk still further.

A key message is that there are many agents that can affect the airways and increase the risk of RA rather than there being a specific one, Dr. Klareskog said.

“On one hand, it’s a message of public health,” he said. Many public health authorities are aware of the potential risks of inhaled agents on the lung, “but this just adds another dimension that it’s bad also for rheumatoid arthritis.” Thus, greater efforts to help protect people from being exposed at work may be needed.

From the individual’s perspective, “if you have RA or other immune diseases in your family, then you may know that you’re at increased risk,” Dr. Klareskog said. The message here is perhaps to “be aware, [protect yourself], and stop smoking.”

The EIRA study was supported by funding from the Swedish Research Foundation for Health, Working Life, and Welfare, the Swedish Research Council, the AFA foundation, Region Stockholm, King Gustaf V’s 80-year foundation, and the Swedish Rheumatic Foundation. Dr. Klareskog and coauthors had no competing interests to disclose. Dr. Kronzer and Dr. Sparks had no disclosures of relevance to their comments.

Exposure to inhaled agents in the workplace could be putting people at risk of developing rheumatoid arthritis, according to research published in Annals of the Rheumatic Diseases.

In an analysis of data from the long-running Swedish Epidemiological Investigation of RA (EIRA) population-based cohort study, there was a 21% increased risk of RA and a 25% increased risk of anti–citrullinated protein antibody (ACPA)–positive RA associated with exposure to any occupationally inhaled agent.

LOOK PHOTO / Fotolia.com

“We have investigated a number of occupational airborne exposures and found that exposure for those agents infer a high risk for RA,” Lars Klareskog, MD, PhD, senior professor of rheumatology at the Karolinska Institute and Karolinska University Hospital (Solna) in Stockholm, said in an interview.

Dr. Klareskog, who is one of the lead authors of the published work, added that the risk is particularly high in individuals who had a genetic susceptibility and in those who smoked.

“The importance of this is that it further demonstrates that exposures to the lung may trigger immune reactions associated with the major subset of rheumatoid arthritis,” Dr. Klareskog said. “Second, it shows that those exposed to these agents should be very keen to not smoke.” “These findings further implicate the respiratory tract mucosa in ACPA-positive RA pathogenesis,” agreed Vanessa L. Kronzer, MD, of the Mayo Clinic in Rochester, Minn., and Jeffrey A. Sparks, MD, MMSc, of Brigham and Women’s Hospital and Harvard Medical School, both in Boston.

They also “impress the need for public policy initiatives related to occupational inhalants to prevent RA,” they suggested in an editorial.

Multiple occupational inhalable exposures assessed

In the analysis, the researchers assessed exposure to 32 inhalable agents in people with (n = 4,033) and without RA (n = 6,485). The list of agents considered included detergents, diesel engine exhaust, fine particulate matter, solvents, and agricultural chemicals.

A total of 17 agents showed a positive association with an increased risk of ACPA-positive RA. Dr. Kronzer and Dr. Sparks noted that breathing in insecticides and fungicides at work was associated with the highest odds ratios for having ACPA-positive RA (both 2.38).

“Importantly, both the number and duration of exposures exhibited a dose-response effect on RA risk,” the editorialists said.

They also picked out that there was “a gene-environment interaction for RA risk for certain inhalants,” including diesel engine exhaust, asbestos, carbon monoxide, and quartz dust.

Smoking amplified the risk for ACPA-positive RA associated with certain agents, such as detergents, and adding in genetic susceptibility for a third exposure increased the risk still further.

A key message is that there are many agents that can affect the airways and increase the risk of RA rather than there being a specific one, Dr. Klareskog said.

“On one hand, it’s a message of public health,” he said. Many public health authorities are aware of the potential risks of inhaled agents on the lung, “but this just adds another dimension that it’s bad also for rheumatoid arthritis.” Thus, greater efforts to help protect people from being exposed at work may be needed.

From the individual’s perspective, “if you have RA or other immune diseases in your family, then you may know that you’re at increased risk,” Dr. Klareskog said. The message here is perhaps to “be aware, [protect yourself], and stop smoking.”

The EIRA study was supported by funding from the Swedish Research Foundation for Health, Working Life, and Welfare, the Swedish Research Council, the AFA foundation, Region Stockholm, King Gustaf V’s 80-year foundation, and the Swedish Rheumatic Foundation. Dr. Klareskog and coauthors had no competing interests to disclose. Dr. Kronzer and Dr. Sparks had no disclosures of relevance to their comments.

Exposure to inhaled agents in the workplace could be putting people at risk of developing rheumatoid arthritis, according to research published in Annals of the Rheumatic Diseases.

In an analysis of data from the long-running Swedish Epidemiological Investigation of RA (EIRA) population-based cohort study, there was a 21% increased risk of RA and a 25% increased risk of anti–citrullinated protein antibody (ACPA)–positive RA associated with exposure to any occupationally inhaled agent.

LOOK PHOTO / Fotolia.com

“We have investigated a number of occupational airborne exposures and found that exposure for those agents infer a high risk for RA,” Lars Klareskog, MD, PhD, senior professor of rheumatology at the Karolinska Institute and Karolinska University Hospital (Solna) in Stockholm, said in an interview.

Dr. Klareskog, who is one of the lead authors of the published work, added that the risk is particularly high in individuals who had a genetic susceptibility and in those who smoked.

“The importance of this is that it further demonstrates that exposures to the lung may trigger immune reactions associated with the major subset of rheumatoid arthritis,” Dr. Klareskog said. “Second, it shows that those exposed to these agents should be very keen to not smoke.” “These findings further implicate the respiratory tract mucosa in ACPA-positive RA pathogenesis,” agreed Vanessa L. Kronzer, MD, of the Mayo Clinic in Rochester, Minn., and Jeffrey A. Sparks, MD, MMSc, of Brigham and Women’s Hospital and Harvard Medical School, both in Boston.

They also “impress the need for public policy initiatives related to occupational inhalants to prevent RA,” they suggested in an editorial.

Multiple occupational inhalable exposures assessed

In the analysis, the researchers assessed exposure to 32 inhalable agents in people with (n = 4,033) and without RA (n = 6,485). The list of agents considered included detergents, diesel engine exhaust, fine particulate matter, solvents, and agricultural chemicals.

A total of 17 agents showed a positive association with an increased risk of ACPA-positive RA. Dr. Kronzer and Dr. Sparks noted that breathing in insecticides and fungicides at work was associated with the highest odds ratios for having ACPA-positive RA (both 2.38).

“Importantly, both the number and duration of exposures exhibited a dose-response effect on RA risk,” the editorialists said.

They also picked out that there was “a gene-environment interaction for RA risk for certain inhalants,” including diesel engine exhaust, asbestos, carbon monoxide, and quartz dust.

Smoking amplified the risk for ACPA-positive RA associated with certain agents, such as detergents, and adding in genetic susceptibility for a third exposure increased the risk still further.

A key message is that there are many agents that can affect the airways and increase the risk of RA rather than there being a specific one, Dr. Klareskog said.

“On one hand, it’s a message of public health,” he said. Many public health authorities are aware of the potential risks of inhaled agents on the lung, “but this just adds another dimension that it’s bad also for rheumatoid arthritis.” Thus, greater efforts to help protect people from being exposed at work may be needed.

From the individual’s perspective, “if you have RA or other immune diseases in your family, then you may know that you’re at increased risk,” Dr. Klareskog said. The message here is perhaps to “be aware, [protect yourself], and stop smoking.”

The EIRA study was supported by funding from the Swedish Research Foundation for Health, Working Life, and Welfare, the Swedish Research Council, the AFA foundation, Region Stockholm, King Gustaf V’s 80-year foundation, and the Swedish Rheumatic Foundation. Dr. Klareskog and coauthors had no competing interests to disclose. Dr. Kronzer and Dr. Sparks had no disclosures of relevance to their comments.

Sir Augustus d’Este (1794-1848) described the circumstances preceding his development of neurological symptoms as follows:¹ “I travelled from Ramsgate to the Highlands of Scotland for the purpose of passing some days with a Relation for whom I had the affection of a Son. On my arrival I found him dead. Shortly after the funeral I was obliged to have my letters read to me, and their answers written for me, as my eyes were so attacked that when fixed upon minute objects indistinctness of vision was the consequence: Soon after I went to Ireland, and without any thing having been done to my eyes, they completely recovered their strength and distinctness of vision…" He then described a clinical course of relapsing-remitting neurologic symptoms merging into a progressive stage of unrelenting illness, most fitting with what we know today as multiple sclerosis (MS).¹ Why did Sir Augustus d'Este connect the event of the unexpected death to the onset of a lifelong neurologic disease?

Jean-Martin Charcot first described MS in a way close to what we know it as today. Charcot considered stress a factor in MS. He linked grief, vexation, and adverse changes in social circumstances to the onset of MS at that time.² I, as a practicing MS specialist, am surprised neither by Sir Augustus d'Este's diary nor by Charcot's earlier assessments of MS triggers.³ As I write this narrative, I think of the many times I heard from people diagnosed with MS. "It happened to me because of stress" is a statement not estranged from my daily clinical practice

MS as a multifactorial disease

It is tempting to make a case for emotional stress as a cause of MS, but one must remember that MS is a very complex disease with unclear etiologies. MS, a treatable but not yet curable disease, is the interplay between the genetics of the host and numerous environmental factors that exploit a susceptible immune system leading to unrelenting immune dysregulation.⁴ Recent studies have brought some pieces of this intricate puzzle together. The role of Epstein-Barr virus (EBV) in the pathogenesis of MS is being dissected.⁵ The possible synergy between vitamin D deficiency, EBV, and certain genetic variations is being studied.⁶ The roles of smoking, environmental toxins, obesity, diet, Western lifestyle, and the gut microbiome are some of the top areas of clinical, translational, and basic research.^7-11 But what about emotional stress? Where does it fit, if anywhere, in the current research paradigm?

Emotional stress and MS—Causality or not?

In the scientific method, several criteria must be proven for an element to be suspected in the etiology of a disease.¹² First, the suspect element must be present before the disease starts—i.e., a temporal association. Second, there must be a plausible biological explanation of how the suspect element acts in the disease's causation. Third, other variables that could confound the picture must be controlled for or dismissed. It is clear that no single factor is the cause of MS. By now, MS is agreed upon as a disease caused by multiple factors, some of which remain to be unraveled.⁹ The term "cause" has been utilized more recently by many authors when referring to EBV in relation to MS development, reasoning that in one study, in a small number of individuals with MS, EBV infection preceded the MS clinical diagnosis.¹³ Thus, the temporal association was provided. But does MS start at the onset of clinical symptoms?

For Sir Augustus d'Este, the disease may have started years before he visited the Highlands of Scotland, but only at that visit did MS become clinically apparent. So, the emotional trauma may have acted as a "trigger" for an MS flare-up rather than being a "cause" of MS. This might be a more plausible explanation of the association between emotional trauma and MS development. However, MS pathogenesis is complex, and one could argue that the disease starts many years before the first clinical symptoms that lead to diagnosis.

The MS prodrome has been demonstrated by several studies that suggest that MS may start many years before the clinical diagnosis.¹⁴ Radiologically isolated syndrome (RIS) further argues that MS may be clinically dormant for years, and clinical symptoms may not appear until later in the disease process.¹⁵ One may think that immune attacks on the optic nerves, spinal cord, or areas of the brainstem might be readily symptomatic compared to attacks on other structures of the central nervous system (e.g., periventricular or juxtacortical brain areas) that may be clinically silent. So, while for Sir Augustus d'Este it seemed that the disease started at the time of his visit to the Highlands of Scotland, it is equally plausible that it started years before the first clinical attack. Nevertheless, how could emotional stress play a role in the pathophysiology of MS?

Stress and the Immune System

At times of chronic stress, one may become more susceptible to infections. Reactivation of certain viruses can lead to oral ulcers, increased common cold symptoms, or other illnesses. For example, stress can reactivate herpes simplex type 1 and interestingly, EBV.^16,17 In MS, the immune system is dysregulated and has an autoimmune component. The effect of acute emotional stress differs from that of chronic stress.¹⁸ Several studies have examined the immune responses to both forms of stress.^19-21

Interestingly, acute stress activates cell-mediated immunity, increases immune cell trafficking to areas of injury, and, importantly, increases blood-brain barrier (BBB) permeability by activating resident mast cells in the brain and other areas, including the optic nerves.^22,23 Mast cell activation leads to BBB disruption, which is a key early step in the pathogenesis of MS. Thus, it is plausible that the proinflammatory changes associated with acute stress could be implicated in the pathogenesis of MS. This contrasts with chronic stress, which attenuates various immune responses, including suppressing cell-mediated immunity, but also dysregulate the immune system.

One could establish a biological plausibility for stress playing a role in the proinflammatory responses in MS. Whether it is causal or not, scientists can further explore the potential biologic explanations. While studying the association between acute stress and MS development or disease activity is difficult, several groups have examined the potential association. Many studies, however, have limitations due to the difficult nature of studying such an association, especially in quantifying or defining acute stress in general.

A limited number of studies on MS and stress: What do we know? And what are the challenges?

Rare studies have reported a potential association between MS development and stressful life events, while others reported no association.^24-26 Also, some studies observed an increase in MS relapses or the development of new magnetic resonance imaging (MRI) lesions following stressful life events or wartime, while others failed to show such an association.^26-30 There are few studies directly addressing the potential association between acute emotional stress and MS. The results of published studies are variable, and limitations are numerous. Limitations include the difficulty in measuring acute emotional stress, difficulty in its prediction, and ethical challenges of experimental design and recruiting participants. So, studies have focused on observational aspects, retrospective reviews, and surveys of memories prone to various biases. Rarely was the design of these clinical studies prospective. A few prospective studies reported an association between stressful life events and increased MS relapses and increased number of brain lesions.^27,31,32 Rare clinical trials have attempted to test stress reduction strategies and reported on the modest improvement of patient-reported outcomes and, in one study, a modest improvement in new MRI lesions.^33-35

Overall, several lines of evidence support a potential association between acute emotional stress and MS. Yet, the association is challenging to study, and future research might focus on stress-mitigation strategies and improving coping mechanisms in persons living with MS. It is important to note that it will be very difficult to design prospective studies to examine the potential association between acute emotional trauma and the development of de novo MS. Such studies will require a large number of participants (e.g., hundreds of thousands), long durations of follow-up (e.g., decades), and ways to classify repeated stressful events. An alternative approach is to ask persons newly diagnosed with MS at the time of initial diagnosis about any temporal association between their first symptom and stressful life events. However, this approach would provide some information on any association between the two, but not on causality of the disease itself.

Conclusion

The potential association between acute emotional stress and MS dates to the times of early descriptions of MS. Yet, research has been very limited and challenging. To date, the potential association remains elusive. Lines of evidence, while with limitations, have provided possible biologic explanations for the relationship between MS symptom onset and acute emotional stress. Although avoiding acute emotional stress is nearly impossible, incorporating global stress-coping strategies in early childhood education and secondary education might theoretically have potential beneficial effects on the subsequent risk of MS development or symptom flare-up, depending on a variety of factors.

But for now, when patients and colleagues ask me, “Can acute emotional stress be a ‘trigger’ for MS symptomology?,” my answer will remain, “Potentially, until proven otherwise.”

Sir Augustus d’Este (1794-1848) described the circumstances preceding his development of neurological symptoms as follows:¹ “I travelled from Ramsgate to the Highlands of Scotland for the purpose of passing some days with a Relation for whom I had the affection of a Son. On my arrival I found him dead. Shortly after the funeral I was obliged to have my letters read to me, and their answers written for me, as my eyes were so attacked that when fixed upon minute objects indistinctness of vision was the consequence: Soon after I went to Ireland, and without any thing having been done to my eyes, they completely recovered their strength and distinctness of vision…" He then described a clinical course of relapsing-remitting neurologic symptoms merging into a progressive stage of unrelenting illness, most fitting with what we know today as multiple sclerosis (MS).¹ Why did Sir Augustus d'Este connect the event of the unexpected death to the onset of a lifelong neurologic disease?

Jean-Martin Charcot first described MS in a way close to what we know it as today. Charcot considered stress a factor in MS. He linked grief, vexation, and adverse changes in social circumstances to the onset of MS at that time.² I, as a practicing MS specialist, am surprised neither by Sir Augustus d'Este's diary nor by Charcot's earlier assessments of MS triggers.³ As I write this narrative, I think of the many times I heard from people diagnosed with MS. "It happened to me because of stress" is a statement not estranged from my daily clinical practice

MS as a multifactorial disease

It is tempting to make a case for emotional stress as a cause of MS, but one must remember that MS is a very complex disease with unclear etiologies. MS, a treatable but not yet curable disease, is the interplay between the genetics of the host and numerous environmental factors that exploit a susceptible immune system leading to unrelenting immune dysregulation.⁴ Recent studies have brought some pieces of this intricate puzzle together. The role of Epstein-Barr virus (EBV) in the pathogenesis of MS is being dissected.⁵ The possible synergy between vitamin D deficiency, EBV, and certain genetic variations is being studied.⁶ The roles of smoking, environmental toxins, obesity, diet, Western lifestyle, and the gut microbiome are some of the top areas of clinical, translational, and basic research.^7-11 But what about emotional stress? Where does it fit, if anywhere, in the current research paradigm?

Emotional stress and MS—Causality or not?

In the scientific method, several criteria must be proven for an element to be suspected in the etiology of a disease.¹² First, the suspect element must be present before the disease starts—i.e., a temporal association. Second, there must be a plausible biological explanation of how the suspect element acts in the disease's causation. Third, other variables that could confound the picture must be controlled for or dismissed. It is clear that no single factor is the cause of MS. By now, MS is agreed upon as a disease caused by multiple factors, some of which remain to be unraveled.⁹ The term "cause" has been utilized more recently by many authors when referring to EBV in relation to MS development, reasoning that in one study, in a small number of individuals with MS, EBV infection preceded the MS clinical diagnosis.¹³ Thus, the temporal association was provided. But does MS start at the onset of clinical symptoms?

For Sir Augustus d'Este, the disease may have started years before he visited the Highlands of Scotland, but only at that visit did MS become clinically apparent. So, the emotional trauma may have acted as a "trigger" for an MS flare-up rather than being a "cause" of MS. This might be a more plausible explanation of the association between emotional trauma and MS development. However, MS pathogenesis is complex, and one could argue that the disease starts many years before the first clinical symptoms that lead to diagnosis.

The MS prodrome has been demonstrated by several studies that suggest that MS may start many years before the clinical diagnosis.¹⁴ Radiologically isolated syndrome (RIS) further argues that MS may be clinically dormant for years, and clinical symptoms may not appear until later in the disease process.¹⁵ One may think that immune attacks on the optic nerves, spinal cord, or areas of the brainstem might be readily symptomatic compared to attacks on other structures of the central nervous system (e.g., periventricular or juxtacortical brain areas) that may be clinically silent. So, while for Sir Augustus d'Este it seemed that the disease started at the time of his visit to the Highlands of Scotland, it is equally plausible that it started years before the first clinical attack. Nevertheless, how could emotional stress play a role in the pathophysiology of MS?

Stress and the Immune System

At times of chronic stress, one may become more susceptible to infections. Reactivation of certain viruses can lead to oral ulcers, increased common cold symptoms, or other illnesses. For example, stress can reactivate herpes simplex type 1 and interestingly, EBV.^16,17 In MS, the immune system is dysregulated and has an autoimmune component. The effect of acute emotional stress differs from that of chronic stress.¹⁸ Several studies have examined the immune responses to both forms of stress.^19-21

Interestingly, acute stress activates cell-mediated immunity, increases immune cell trafficking to areas of injury, and, importantly, increases blood-brain barrier (BBB) permeability by activating resident mast cells in the brain and other areas, including the optic nerves.^22,23 Mast cell activation leads to BBB disruption, which is a key early step in the pathogenesis of MS. Thus, it is plausible that the proinflammatory changes associated with acute stress could be implicated in the pathogenesis of MS. This contrasts with chronic stress, which attenuates various immune responses, including suppressing cell-mediated immunity, but also dysregulate the immune system.

One could establish a biological plausibility for stress playing a role in the proinflammatory responses in MS. Whether it is causal or not, scientists can further explore the potential biologic explanations. While studying the association between acute stress and MS development or disease activity is difficult, several groups have examined the potential association. Many studies, however, have limitations due to the difficult nature of studying such an association, especially in quantifying or defining acute stress in general.

A limited number of studies on MS and stress: What do we know? And what are the challenges?

Rare studies have reported a potential association between MS development and stressful life events, while others reported no association.^24-26 Also, some studies observed an increase in MS relapses or the development of new magnetic resonance imaging (MRI) lesions following stressful life events or wartime, while others failed to show such an association.^26-30 There are few studies directly addressing the potential association between acute emotional stress and MS. The results of published studies are variable, and limitations are numerous. Limitations include the difficulty in measuring acute emotional stress, difficulty in its prediction, and ethical challenges of experimental design and recruiting participants. So, studies have focused on observational aspects, retrospective reviews, and surveys of memories prone to various biases. Rarely was the design of these clinical studies prospective. A few prospective studies reported an association between stressful life events and increased MS relapses and increased number of brain lesions.^27,31,32 Rare clinical trials have attempted to test stress reduction strategies and reported on the modest improvement of patient-reported outcomes and, in one study, a modest improvement in new MRI lesions.^33-35

Overall, several lines of evidence support a potential association between acute emotional stress and MS. Yet, the association is challenging to study, and future research might focus on stress-mitigation strategies and improving coping mechanisms in persons living with MS. It is important to note that it will be very difficult to design prospective studies to examine the potential association between acute emotional trauma and the development of de novo MS. Such studies will require a large number of participants (e.g., hundreds of thousands), long durations of follow-up (e.g., decades), and ways to classify repeated stressful events. An alternative approach is to ask persons newly diagnosed with MS at the time of initial diagnosis about any temporal association between their first symptom and stressful life events. However, this approach would provide some information on any association between the two, but not on causality of the disease itself.

Conclusion

The potential association between acute emotional stress and MS dates to the times of early descriptions of MS. Yet, research has been very limited and challenging. To date, the potential association remains elusive. Lines of evidence, while with limitations, have provided possible biologic explanations for the relationship between MS symptom onset and acute emotional stress. Although avoiding acute emotional stress is nearly impossible, incorporating global stress-coping strategies in early childhood education and secondary education might theoretically have potential beneficial effects on the subsequent risk of MS development or symptom flare-up, depending on a variety of factors.

But for now, when patients and colleagues ask me, “Can acute emotional stress be a ‘trigger’ for MS symptomology?,” my answer will remain, “Potentially, until proven otherwise.”

Sir Augustus d’Este (1794-1848) described the circumstances preceding his development of neurological symptoms as follows:¹ “I travelled from Ramsgate to the Highlands of Scotland for the purpose of passing some days with a Relation for whom I had the affection of a Son. On my arrival I found him dead. Shortly after the funeral I was obliged to have my letters read to me, and their answers written for me, as my eyes were so attacked that when fixed upon minute objects indistinctness of vision was the consequence: Soon after I went to Ireland, and without any thing having been done to my eyes, they completely recovered their strength and distinctness of vision…" He then described a clinical course of relapsing-remitting neurologic symptoms merging into a progressive stage of unrelenting illness, most fitting with what we know today as multiple sclerosis (MS).¹ Why did Sir Augustus d'Este connect the event of the unexpected death to the onset of a lifelong neurologic disease?

Jean-Martin Charcot first described MS in a way close to what we know it as today. Charcot considered stress a factor in MS. He linked grief, vexation, and adverse changes in social circumstances to the onset of MS at that time.² I, as a practicing MS specialist, am surprised neither by Sir Augustus d'Este's diary nor by Charcot's earlier assessments of MS triggers.³ As I write this narrative, I think of the many times I heard from people diagnosed with MS. "It happened to me because of stress" is a statement not estranged from my daily clinical practice

MS as a multifactorial disease

It is tempting to make a case for emotional stress as a cause of MS, but one must remember that MS is a very complex disease with unclear etiologies. MS, a treatable but not yet curable disease, is the interplay between the genetics of the host and numerous environmental factors that exploit a susceptible immune system leading to unrelenting immune dysregulation.⁴ Recent studies have brought some pieces of this intricate puzzle together. The role of Epstein-Barr virus (EBV) in the pathogenesis of MS is being dissected.⁵ The possible synergy between vitamin D deficiency, EBV, and certain genetic variations is being studied.⁶ The roles of smoking, environmental toxins, obesity, diet, Western lifestyle, and the gut microbiome are some of the top areas of clinical, translational, and basic research.^7-11 But what about emotional stress? Where does it fit, if anywhere, in the current research paradigm?

Emotional stress and MS—Causality or not?

In the scientific method, several criteria must be proven for an element to be suspected in the etiology of a disease.¹² First, the suspect element must be present before the disease starts—i.e., a temporal association. Second, there must be a plausible biological explanation of how the suspect element acts in the disease's causation. Third, other variables that could confound the picture must be controlled for or dismissed. It is clear that no single factor is the cause of MS. By now, MS is agreed upon as a disease caused by multiple factors, some of which remain to be unraveled.⁹ The term "cause" has been utilized more recently by many authors when referring to EBV in relation to MS development, reasoning that in one study, in a small number of individuals with MS, EBV infection preceded the MS clinical diagnosis.¹³ Thus, the temporal association was provided. But does MS start at the onset of clinical symptoms?

For Sir Augustus d'Este, the disease may have started years before he visited the Highlands of Scotland, but only at that visit did MS become clinically apparent. So, the emotional trauma may have acted as a "trigger" for an MS flare-up rather than being a "cause" of MS. This might be a more plausible explanation of the association between emotional trauma and MS development. However, MS pathogenesis is complex, and one could argue that the disease starts many years before the first clinical symptoms that lead to diagnosis.

The MS prodrome has been demonstrated by several studies that suggest that MS may start many years before the clinical diagnosis.¹⁴ Radiologically isolated syndrome (RIS) further argues that MS may be clinically dormant for years, and clinical symptoms may not appear until later in the disease process.¹⁵ One may think that immune attacks on the optic nerves, spinal cord, or areas of the brainstem might be readily symptomatic compared to attacks on other structures of the central nervous system (e.g., periventricular or juxtacortical brain areas) that may be clinically silent. So, while for Sir Augustus d'Este it seemed that the disease started at the time of his visit to the Highlands of Scotland, it is equally plausible that it started years before the first clinical attack. Nevertheless, how could emotional stress play a role in the pathophysiology of MS?

Stress and the Immune System

At times of chronic stress, one may become more susceptible to infections. Reactivation of certain viruses can lead to oral ulcers, increased common cold symptoms, or other illnesses. For example, stress can reactivate herpes simplex type 1 and interestingly, EBV.^16,17 In MS, the immune system is dysregulated and has an autoimmune component. The effect of acute emotional stress differs from that of chronic stress.¹⁸ Several studies have examined the immune responses to both forms of stress.^19-21

Interestingly, acute stress activates cell-mediated immunity, increases immune cell trafficking to areas of injury, and, importantly, increases blood-brain barrier (BBB) permeability by activating resident mast cells in the brain and other areas, including the optic nerves.^22,23 Mast cell activation leads to BBB disruption, which is a key early step in the pathogenesis of MS. Thus, it is plausible that the proinflammatory changes associated with acute stress could be implicated in the pathogenesis of MS. This contrasts with chronic stress, which attenuates various immune responses, including suppressing cell-mediated immunity, but also dysregulate the immune system.

One could establish a biological plausibility for stress playing a role in the proinflammatory responses in MS. Whether it is causal or not, scientists can further explore the potential biologic explanations. While studying the association between acute stress and MS development or disease activity is difficult, several groups have examined the potential association. Many studies, however, have limitations due to the difficult nature of studying such an association, especially in quantifying or defining acute stress in general.

A limited number of studies on MS and stress: What do we know? And what are the challenges?

Rare studies have reported a potential association between MS development and stressful life events, while others reported no association.^24-26 Also, some studies observed an increase in MS relapses or the development of new magnetic resonance imaging (MRI) lesions following stressful life events or wartime, while others failed to show such an association.^26-30 There are few studies directly addressing the potential association between acute emotional stress and MS. The results of published studies are variable, and limitations are numerous. Limitations include the difficulty in measuring acute emotional stress, difficulty in its prediction, and ethical challenges of experimental design and recruiting participants. So, studies have focused on observational aspects, retrospective reviews, and surveys of memories prone to various biases. Rarely was the design of these clinical studies prospective. A few prospective studies reported an association between stressful life events and increased MS relapses and increased number of brain lesions.^27,31,32 Rare clinical trials have attempted to test stress reduction strategies and reported on the modest improvement of patient-reported outcomes and, in one study, a modest improvement in new MRI lesions.^33-35

Overall, several lines of evidence support a potential association between acute emotional stress and MS. Yet, the association is challenging to study, and future research might focus on stress-mitigation strategies and improving coping mechanisms in persons living with MS. It is important to note that it will be very difficult to design prospective studies to examine the potential association between acute emotional trauma and the development of de novo MS. Such studies will require a large number of participants (e.g., hundreds of thousands), long durations of follow-up (e.g., decades), and ways to classify repeated stressful events. An alternative approach is to ask persons newly diagnosed with MS at the time of initial diagnosis about any temporal association between their first symptom and stressful life events. However, this approach would provide some information on any association between the two, but not on causality of the disease itself.

Conclusion

The potential association between acute emotional stress and MS dates to the times of early descriptions of MS. Yet, research has been very limited and challenging. To date, the potential association remains elusive. Lines of evidence, while with limitations, have provided possible biologic explanations for the relationship between MS symptom onset and acute emotional stress. Although avoiding acute emotional stress is nearly impossible, incorporating global stress-coping strategies in early childhood education and secondary education might theoretically have potential beneficial effects on the subsequent risk of MS development or symptom flare-up, depending on a variety of factors.

But for now, when patients and colleagues ask me, “Can acute emotional stress be a ‘trigger’ for MS symptomology?,” my answer will remain, “Potentially, until proven otherwise.”

Key clinical point: Although a few biomarkers can assist in distinguishing psoriatic arthritis (PsA) from psoriasis or osteoarthritis, a precise diagnostic biomarker that can distinguish PsA from osteoarthritis and most other chronic inflammatory diseases has not yet been identified.

Major finding: Serum cartilage oligometrix metalloproteinase levels were significantly increased in patients with PsA compared with control individuals without chronic inflammatory diseases (standardized mean difference [SMD] 2.305; P = .003) and patients with osteoarthritis (SMD 0.783; P = .046). Serum matrix metalloproteinase-3 levels were significantly higher in patients with PsA vs psoriasis (SMD 0.419; P = .006) but could not distinguish patients with PsA from control individuals.

Study details: Findings are from a meta-analysis of 124 studies including patients with PsA.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Wirth T et al. Biomarkers in psoriatic arthritis: A meta-analysis and systematic review. Front Immunol. 2022;13:1054539 (Nov 30). Doi: 10.3389/fimmu.2022.1054539

Key clinical point: Although a few biomarkers can assist in distinguishing psoriatic arthritis (PsA) from psoriasis or osteoarthritis, a precise diagnostic biomarker that can distinguish PsA from osteoarthritis and most other chronic inflammatory diseases has not yet been identified.

Major finding: Serum cartilage oligometrix metalloproteinase levels were significantly increased in patients with PsA compared with control individuals without chronic inflammatory diseases (standardized mean difference [SMD] 2.305; P = .003) and patients with osteoarthritis (SMD 0.783; P = .046). Serum matrix metalloproteinase-3 levels were significantly higher in patients with PsA vs psoriasis (SMD 0.419; P = .006) but could not distinguish patients with PsA from control individuals.

Study details: Findings are from a meta-analysis of 124 studies including patients with PsA.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Wirth T et al. Biomarkers in psoriatic arthritis: A meta-analysis and systematic review. Front Immunol. 2022;13:1054539 (Nov 30). Doi: 10.3389/fimmu.2022.1054539

Key clinical point: Although a few biomarkers can assist in distinguishing psoriatic arthritis (PsA) from psoriasis or osteoarthritis, a precise diagnostic biomarker that can distinguish PsA from osteoarthritis and most other chronic inflammatory diseases has not yet been identified.

Major finding: Serum cartilage oligometrix metalloproteinase levels were significantly increased in patients with PsA compared with control individuals without chronic inflammatory diseases (standardized mean difference [SMD] 2.305; P = .003) and patients with osteoarthritis (SMD 0.783; P = .046). Serum matrix metalloproteinase-3 levels were significantly higher in patients with PsA vs psoriasis (SMD 0.419; P = .006) but could not distinguish patients with PsA from control individuals.

Study details: Findings are from a meta-analysis of 124 studies including patients with PsA.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Wirth T et al. Biomarkers in psoriatic arthritis: A meta-analysis and systematic review. Front Immunol. 2022;13:1054539 (Nov 30). Doi: 10.3389/fimmu.2022.1054539

Key clinical point: Axial psoriatic arthritis (PsA) can be categorized as a distinct subtype of PsA because it exhibits clinical and radiological symptoms that are different from those of ankylosing spondylitis (AS) with psoriasis.

Major finding: Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27-negative axial PsA had lesser inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001) along with a higher prevalence of nail disease (P = .009) and were more likely to present with psoriasis before spondyloarthritis onset (P = .020). However, patients with HLA-B27-positive axial PsA vs AS and psoriasis reported lesser structural damage as revealed by Bath Ankylosing Spondylitis Radiology Index scores (P < .001).

Study details: This cross-sectional study included 109 patients with axial PsA and 127 patients with AS and current presentation or a history of skin psoriasis from the REGISPONSER registry.

Disclosures: The REGISPONSER registry is funded by the Spanish Society for Rheumatology. The authors declared no conflicts of interest.

Source: Michelena X et al. Characterising the axial phenotype of psoriatic arthritis: a study comparing axial psoriatic arthritis and ankylosing spondylitis with psoriasis from the REGISPONSER registry. RMD Open. 2022;8:e002513 (Dec 5). Doi: 10.1136/rmdopen-2022-002513

Key clinical point: Axial psoriatic arthritis (PsA) can be categorized as a distinct subtype of PsA because it exhibits clinical and radiological symptoms that are different from those of ankylosing spondylitis (AS) with psoriasis.

Major finding: Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27-negative axial PsA had lesser inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001) along with a higher prevalence of nail disease (P = .009) and were more likely to present with psoriasis before spondyloarthritis onset (P = .020). However, patients with HLA-B27-positive axial PsA vs AS and psoriasis reported lesser structural damage as revealed by Bath Ankylosing Spondylitis Radiology Index scores (P < .001).

Study details: This cross-sectional study included 109 patients with axial PsA and 127 patients with AS and current presentation or a history of skin psoriasis from the REGISPONSER registry.

Disclosures: The REGISPONSER registry is funded by the Spanish Society for Rheumatology. The authors declared no conflicts of interest.

Source: Michelena X et al. Characterising the axial phenotype of psoriatic arthritis: a study comparing axial psoriatic arthritis and ankylosing spondylitis with psoriasis from the REGISPONSER registry. RMD Open. 2022;8:e002513 (Dec 5). Doi: 10.1136/rmdopen-2022-002513

Key clinical point: Axial psoriatic arthritis (PsA) can be categorized as a distinct subtype of PsA because it exhibits clinical and radiological symptoms that are different from those of ankylosing spondylitis (AS) with psoriasis.

Major finding: Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27-negative axial PsA had lesser inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001) along with a higher prevalence of nail disease (P = .009) and were more likely to present with psoriasis before spondyloarthritis onset (P = .020). However, patients with HLA-B27-positive axial PsA vs AS and psoriasis reported lesser structural damage as revealed by Bath Ankylosing Spondylitis Radiology Index scores (P < .001).

Study details: This cross-sectional study included 109 patients with axial PsA and 127 patients with AS and current presentation or a history of skin psoriasis from the REGISPONSER registry.

Disclosures: The REGISPONSER registry is funded by the Spanish Society for Rheumatology. The authors declared no conflicts of interest.

Source: Michelena X et al. Characterising the axial phenotype of psoriatic arthritis: a study comparing axial psoriatic arthritis and ankylosing spondylitis with psoriasis from the REGISPONSER registry. RMD Open. 2022;8:e002513 (Dec 5). Doi: 10.1136/rmdopen-2022-002513