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Intramuscular steroid injection reduced hip OA pain up to 12 weeks
Systemic treatment with an intramuscular glucocorticoid injection is effective, compared with placebo, in reducing pain in people with hip osteoarthritis for up to 12 weeks, a double-blinded, placebo-controlled, randomized trial suggests.
However, the study found benefit with intramuscular (IM) glucocorticoid injection at 2 weeks only when patients were at rest, and did not find any significant benefit with the injection in reducing pain while walking or in reducing Western Ontario and McMaster University Osteoarthritis Index (WOMAC) pain subscale scores. The report was published in Annals of the Rheumatic Diseases.
The multicenter, double-blinded, superiority trial randomized 106 patients with painful hip OA who were not responding to oral analgesics to either 40 mg triamcinolone acetate (n = 52) or placebo injection (n = 54) into the gluteus muscle. Overall, 73 patients (68%) were women, and the average age of the cohort was 64 years. Hip OA symptoms had occurred for at least 1 year in 70% of the patients.
The study’s three primary outcomes of hip pain severity 2 weeks after the injection on a 0-10 scale at rest and during walking and on the WOMAC pain subscale revealed inconsistent results with the treatment.
At the 2-week follow-up, patients who had received the IM glucocorticoid injection had a significant and clinically relevant difference in hip pain at rest (between-group difference = –1.3; 95% confidence interval, –2.3 to –0.3; P = .01). But at this time point there were no significant associations between glucocorticoid injection and hip pain during walking (difference = –0.9; 95% CI, –1.9 to 0.1; P = .07) and WOMAC pain subscale score (difference = –6.1; 95% CI, –13.4 to 1.2; P = .10), the researchers reported.
At 2-week follow-up, recipients of the glucocorticoid injection were significantly more likely to perceive improvement (relative risk = 1.7; 95% CI, 1.1 to 2.7; P = .02) or achieve OMERACT-OARSI level of response (RR = 2.0; 95% CI, 1.1 to 3.6; P = .03).
The authors described this finding as “surprising,” speculating that the 7-point Likert scale used to measure perceived improvement could have resulted in less power.
Nineteen patients in the glucocorticoid group reported 27 nonserious adverse events, compared with 13 patients in the placebo group who reported 18 adverse events.
The authors said the greatest effects of the glucocorticoid injection were seen at 4- to 12-week follow-up (the secondary outcomes of the study), instead of at the 2-week follow-up. For example, at 4-week follow-up, the glucocorticoid injection was associated with a significant hip pain reduction at rest (between-group difference = –1.2; 95% CI, –2.1 to –0.2; P = .01) and during walking (difference = –1.1; 95% CI, –2.0 to –0.2; P = .01). At 6 weeks, the corresponding figures for hip pain reduction were –1.4 at rest (95% CI, –2.4 to –0.5; P = .005) and –1.4 while walking (95% CI, –2.3 to –0.4; P = .004). The between-group differences were still significant at 12 weeks while at rest (difference = –1.2; 95% CI, –2.3 to –0.2; P = .02) and during walking (difference = –1.3; 95% CI, –2.2 to –0.3; P = .01).
Significant differences in favor of the glucocorticoid injection overall occurred on the WOMAC subscale scores for pain, function, and stiffness, as well as total Hip disability and Osteoarthritis Outcome Score for pain and total, intermittent, and constant pain measures on the Intermittent and Constant Osteoarthritis Pain scale. At 12 weeks, the between-group difference on the WOMAC total score was –9.4 (95% CI, –17.8 to –0.9; P = .03).
The researchers said it was surprising that hip pain reduction after IM glucocorticoid injection was still present at a similar degree at 12 weeks since previous studies had shown the effect usually peaked after 1-3 weeks.
“Our findings should be replicated in future research,” they said.
“An IM glucocorticoid injection showed effectiveness in patients with hip OA on one of the three primary outcomes at a 2 weeks post injection ... The effect is probably clinically relevant,” the authors concluded.
The investigators noted that in clinical practice patients are sometimes offered multiple injections per year, whereas in the current study patients received only one injection. There has also been concern that intra-articular glucocorticoid injections could cause toxicity to chondrocytes and potentially lead to OA progression, but the effect of a single IM injection is unknown.
Financial support for the study came from the Dutch Arthritis Foundation and the NutsOhra fund. Two of the authors reported receiving grants from several pharmaceutical companies, research consortia, and foundations.
SOURCE: Dorleijn D et al. Ann Rheum Dis. 2018 March 7. doi: 10.1136/annrheumdis-2017-212628
Systemic treatment with an intramuscular glucocorticoid injection is effective, compared with placebo, in reducing pain in people with hip osteoarthritis for up to 12 weeks, a double-blinded, placebo-controlled, randomized trial suggests.
However, the study found benefit with intramuscular (IM) glucocorticoid injection at 2 weeks only when patients were at rest, and did not find any significant benefit with the injection in reducing pain while walking or in reducing Western Ontario and McMaster University Osteoarthritis Index (WOMAC) pain subscale scores. The report was published in Annals of the Rheumatic Diseases.
The multicenter, double-blinded, superiority trial randomized 106 patients with painful hip OA who were not responding to oral analgesics to either 40 mg triamcinolone acetate (n = 52) or placebo injection (n = 54) into the gluteus muscle. Overall, 73 patients (68%) were women, and the average age of the cohort was 64 years. Hip OA symptoms had occurred for at least 1 year in 70% of the patients.
The study’s three primary outcomes of hip pain severity 2 weeks after the injection on a 0-10 scale at rest and during walking and on the WOMAC pain subscale revealed inconsistent results with the treatment.
At the 2-week follow-up, patients who had received the IM glucocorticoid injection had a significant and clinically relevant difference in hip pain at rest (between-group difference = –1.3; 95% confidence interval, –2.3 to –0.3; P = .01). But at this time point there were no significant associations between glucocorticoid injection and hip pain during walking (difference = –0.9; 95% CI, –1.9 to 0.1; P = .07) and WOMAC pain subscale score (difference = –6.1; 95% CI, –13.4 to 1.2; P = .10), the researchers reported.
At 2-week follow-up, recipients of the glucocorticoid injection were significantly more likely to perceive improvement (relative risk = 1.7; 95% CI, 1.1 to 2.7; P = .02) or achieve OMERACT-OARSI level of response (RR = 2.0; 95% CI, 1.1 to 3.6; P = .03).
The authors described this finding as “surprising,” speculating that the 7-point Likert scale used to measure perceived improvement could have resulted in less power.
Nineteen patients in the glucocorticoid group reported 27 nonserious adverse events, compared with 13 patients in the placebo group who reported 18 adverse events.
The authors said the greatest effects of the glucocorticoid injection were seen at 4- to 12-week follow-up (the secondary outcomes of the study), instead of at the 2-week follow-up. For example, at 4-week follow-up, the glucocorticoid injection was associated with a significant hip pain reduction at rest (between-group difference = –1.2; 95% CI, –2.1 to –0.2; P = .01) and during walking (difference = –1.1; 95% CI, –2.0 to –0.2; P = .01). At 6 weeks, the corresponding figures for hip pain reduction were –1.4 at rest (95% CI, –2.4 to –0.5; P = .005) and –1.4 while walking (95% CI, –2.3 to –0.4; P = .004). The between-group differences were still significant at 12 weeks while at rest (difference = –1.2; 95% CI, –2.3 to –0.2; P = .02) and during walking (difference = –1.3; 95% CI, –2.2 to –0.3; P = .01).
Significant differences in favor of the glucocorticoid injection overall occurred on the WOMAC subscale scores for pain, function, and stiffness, as well as total Hip disability and Osteoarthritis Outcome Score for pain and total, intermittent, and constant pain measures on the Intermittent and Constant Osteoarthritis Pain scale. At 12 weeks, the between-group difference on the WOMAC total score was –9.4 (95% CI, –17.8 to –0.9; P = .03).
The researchers said it was surprising that hip pain reduction after IM glucocorticoid injection was still present at a similar degree at 12 weeks since previous studies had shown the effect usually peaked after 1-3 weeks.
“Our findings should be replicated in future research,” they said.
“An IM glucocorticoid injection showed effectiveness in patients with hip OA on one of the three primary outcomes at a 2 weeks post injection ... The effect is probably clinically relevant,” the authors concluded.
The investigators noted that in clinical practice patients are sometimes offered multiple injections per year, whereas in the current study patients received only one injection. There has also been concern that intra-articular glucocorticoid injections could cause toxicity to chondrocytes and potentially lead to OA progression, but the effect of a single IM injection is unknown.
Financial support for the study came from the Dutch Arthritis Foundation and the NutsOhra fund. Two of the authors reported receiving grants from several pharmaceutical companies, research consortia, and foundations.
SOURCE: Dorleijn D et al. Ann Rheum Dis. 2018 March 7. doi: 10.1136/annrheumdis-2017-212628
Systemic treatment with an intramuscular glucocorticoid injection is effective, compared with placebo, in reducing pain in people with hip osteoarthritis for up to 12 weeks, a double-blinded, placebo-controlled, randomized trial suggests.
However, the study found benefit with intramuscular (IM) glucocorticoid injection at 2 weeks only when patients were at rest, and did not find any significant benefit with the injection in reducing pain while walking or in reducing Western Ontario and McMaster University Osteoarthritis Index (WOMAC) pain subscale scores. The report was published in Annals of the Rheumatic Diseases.
The multicenter, double-blinded, superiority trial randomized 106 patients with painful hip OA who were not responding to oral analgesics to either 40 mg triamcinolone acetate (n = 52) or placebo injection (n = 54) into the gluteus muscle. Overall, 73 patients (68%) were women, and the average age of the cohort was 64 years. Hip OA symptoms had occurred for at least 1 year in 70% of the patients.
The study’s three primary outcomes of hip pain severity 2 weeks after the injection on a 0-10 scale at rest and during walking and on the WOMAC pain subscale revealed inconsistent results with the treatment.
At the 2-week follow-up, patients who had received the IM glucocorticoid injection had a significant and clinically relevant difference in hip pain at rest (between-group difference = –1.3; 95% confidence interval, –2.3 to –0.3; P = .01). But at this time point there were no significant associations between glucocorticoid injection and hip pain during walking (difference = –0.9; 95% CI, –1.9 to 0.1; P = .07) and WOMAC pain subscale score (difference = –6.1; 95% CI, –13.4 to 1.2; P = .10), the researchers reported.
At 2-week follow-up, recipients of the glucocorticoid injection were significantly more likely to perceive improvement (relative risk = 1.7; 95% CI, 1.1 to 2.7; P = .02) or achieve OMERACT-OARSI level of response (RR = 2.0; 95% CI, 1.1 to 3.6; P = .03).
The authors described this finding as “surprising,” speculating that the 7-point Likert scale used to measure perceived improvement could have resulted in less power.
Nineteen patients in the glucocorticoid group reported 27 nonserious adverse events, compared with 13 patients in the placebo group who reported 18 adverse events.
The authors said the greatest effects of the glucocorticoid injection were seen at 4- to 12-week follow-up (the secondary outcomes of the study), instead of at the 2-week follow-up. For example, at 4-week follow-up, the glucocorticoid injection was associated with a significant hip pain reduction at rest (between-group difference = –1.2; 95% CI, –2.1 to –0.2; P = .01) and during walking (difference = –1.1; 95% CI, –2.0 to –0.2; P = .01). At 6 weeks, the corresponding figures for hip pain reduction were –1.4 at rest (95% CI, –2.4 to –0.5; P = .005) and –1.4 while walking (95% CI, –2.3 to –0.4; P = .004). The between-group differences were still significant at 12 weeks while at rest (difference = –1.2; 95% CI, –2.3 to –0.2; P = .02) and during walking (difference = –1.3; 95% CI, –2.2 to –0.3; P = .01).
Significant differences in favor of the glucocorticoid injection overall occurred on the WOMAC subscale scores for pain, function, and stiffness, as well as total Hip disability and Osteoarthritis Outcome Score for pain and total, intermittent, and constant pain measures on the Intermittent and Constant Osteoarthritis Pain scale. At 12 weeks, the between-group difference on the WOMAC total score was –9.4 (95% CI, –17.8 to –0.9; P = .03).
The researchers said it was surprising that hip pain reduction after IM glucocorticoid injection was still present at a similar degree at 12 weeks since previous studies had shown the effect usually peaked after 1-3 weeks.
“Our findings should be replicated in future research,” they said.
“An IM glucocorticoid injection showed effectiveness in patients with hip OA on one of the three primary outcomes at a 2 weeks post injection ... The effect is probably clinically relevant,” the authors concluded.
The investigators noted that in clinical practice patients are sometimes offered multiple injections per year, whereas in the current study patients received only one injection. There has also been concern that intra-articular glucocorticoid injections could cause toxicity to chondrocytes and potentially lead to OA progression, but the effect of a single IM injection is unknown.
Financial support for the study came from the Dutch Arthritis Foundation and the NutsOhra fund. Two of the authors reported receiving grants from several pharmaceutical companies, research consortia, and foundations.
SOURCE: Dorleijn D et al. Ann Rheum Dis. 2018 March 7. doi: 10.1136/annrheumdis-2017-212628
FROM ANNALS OF THE RHEUMATIC DISEASES
Key clinical point:
Major finding: At 2 weeks, patients who had received the intramuscular glucocorticoid injection had a significant and clinically relevant difference in hip pain at rest (between-group difference = –1.3; 95% CI, –2.3 to –0.3; P = .01).
Study details: A 12-week, double blinded, placebo-controlled trial of 106 patients with hip OA randomized to 40 mg triamcinolone acetate or placebo injection.
Disclosures: Financial support for the study came from the Dutch Arthritis Foundation and the NutsOhra fund. Two of the authors reported receiving grants from several pharmaceutical companies, research consortia, and foundations.
Source: Dorleijn D et al. Ann Rheum Dis. 2018 Mar 7. doi: 10.1136/annrheumdis-2017-212628.
Swamp coolers not linked to dust mite sensitization in atopic children
ORLANDO – Swamp coolers – a low-cost alternative to air-conditioning in dry regions – weren’t found to increase sensitization to house dust mites or mold in atopic pediatric patients, researchers reported.
Neema Izadi, MD, and his associates say the findings, seen in a pediatric Colorado population in a study evaluating data over 10 years, could mean that not everyone at risk of dust mite and mold sensitization needs to avoid these cooling systems.
“Evaporative coolers have been shown to raise relative humidity by about 10%,” said Dr. Izadi, a pediatric allergy and immunology fellow at National Jewish Health, Denver, presenting at the joint congress of the American Academy of Asthma, Allergy and Immunology and the World Asthma Organization. “They work best in environments where the air is very warm and dry.”
House dust mites and mold thrive in higher humidity. Small studies performed in Colorado, Utah, and other locations have shown that the swamp coolers increase house dust mite allergen content, but there have been very few studies that have looked at actual sensitization. One smaller study in Nevada did find that the coolers increased sensitization to dust mites and mold.
In this study – thought to be the largest ever to look at this question – Dr. Izadi and his colleagues assessed data on patients aged 21 years and younger who were seen at National Jewish Health during 2008-2017 and who had at least one positive environmental skin-prick test. The average age was about 9 years. The cohort included 8,503 patients with sensitization to house dust mites and 9,286 with sensitization to mold. Researchers examined data on swamp coolers in their homes.
The researchers found that 29% of those with swamp coolers were dust-mite positive on skin testing, and 28% of those without one were positive. This was not a significant difference (P = .85). They found that 45% of those with the coolers were positive for sensitization to any mold, compared with 44% without one – also not a significant difference (P = .43).
They also found no difference according to age group, sex, or individually for atopic dermatitis, asthma, or allergic rhinitis.
He acknowledged that the study had no way to reliably account for patients who were transplants to Colorado, having moved there from somewhere else. The study also didn’t examine the age of homes, whether it had carpeting, or other factors.
He noted that the amount of time the coolers were run in the home was not examined and that “it might matter how much it is on.” This, he said, might account for differences in these results, compared with the Nevada study that did find a sensitization increase cause by the coolers.
“Evaporative coolers or swamp coolers are a great low-cost alternative in semiarid and arid environments – they can cut costs from 15%-35%,” Dr. Izadi said. “These data may indicate that it may be unnecessary to recommend that patients remove their swamp cooler, at least from a dust-mite and mold-sensitization standpoint.”
Dr. Izadi had no relevant financial disclosures.
SOURCE: Izadi N et al. AAAAI/WAO Joint Congress, Abstract 586
Susan Millard, MD, FCCP, comments: Swamp coolers are used in semi-arid and arid climates like Arizona, where I did my fellowship training but they didn't work well to keep apartments and homes cool enough if over about 100°F outside! The system is cheaper than air conditioning. So it is great to know that this type of cooling system does not cause more mold and dust mite allergies.
Susan Millard, MD, FCCP, comments: Swamp coolers are used in semi-arid and arid climates like Arizona, where I did my fellowship training but they didn't work well to keep apartments and homes cool enough if over about 100°F outside! The system is cheaper than air conditioning. So it is great to know that this type of cooling system does not cause more mold and dust mite allergies.
Susan Millard, MD, FCCP, comments: Swamp coolers are used in semi-arid and arid climates like Arizona, where I did my fellowship training but they didn't work well to keep apartments and homes cool enough if over about 100°F outside! The system is cheaper than air conditioning. So it is great to know that this type of cooling system does not cause more mold and dust mite allergies.
ORLANDO – Swamp coolers – a low-cost alternative to air-conditioning in dry regions – weren’t found to increase sensitization to house dust mites or mold in atopic pediatric patients, researchers reported.
Neema Izadi, MD, and his associates say the findings, seen in a pediatric Colorado population in a study evaluating data over 10 years, could mean that not everyone at risk of dust mite and mold sensitization needs to avoid these cooling systems.
“Evaporative coolers have been shown to raise relative humidity by about 10%,” said Dr. Izadi, a pediatric allergy and immunology fellow at National Jewish Health, Denver, presenting at the joint congress of the American Academy of Asthma, Allergy and Immunology and the World Asthma Organization. “They work best in environments where the air is very warm and dry.”
House dust mites and mold thrive in higher humidity. Small studies performed in Colorado, Utah, and other locations have shown that the swamp coolers increase house dust mite allergen content, but there have been very few studies that have looked at actual sensitization. One smaller study in Nevada did find that the coolers increased sensitization to dust mites and mold.
In this study – thought to be the largest ever to look at this question – Dr. Izadi and his colleagues assessed data on patients aged 21 years and younger who were seen at National Jewish Health during 2008-2017 and who had at least one positive environmental skin-prick test. The average age was about 9 years. The cohort included 8,503 patients with sensitization to house dust mites and 9,286 with sensitization to mold. Researchers examined data on swamp coolers in their homes.
The researchers found that 29% of those with swamp coolers were dust-mite positive on skin testing, and 28% of those without one were positive. This was not a significant difference (P = .85). They found that 45% of those with the coolers were positive for sensitization to any mold, compared with 44% without one – also not a significant difference (P = .43).
They also found no difference according to age group, sex, or individually for atopic dermatitis, asthma, or allergic rhinitis.
He acknowledged that the study had no way to reliably account for patients who were transplants to Colorado, having moved there from somewhere else. The study also didn’t examine the age of homes, whether it had carpeting, or other factors.
He noted that the amount of time the coolers were run in the home was not examined and that “it might matter how much it is on.” This, he said, might account for differences in these results, compared with the Nevada study that did find a sensitization increase cause by the coolers.
“Evaporative coolers or swamp coolers are a great low-cost alternative in semiarid and arid environments – they can cut costs from 15%-35%,” Dr. Izadi said. “These data may indicate that it may be unnecessary to recommend that patients remove their swamp cooler, at least from a dust-mite and mold-sensitization standpoint.”
Dr. Izadi had no relevant financial disclosures.
SOURCE: Izadi N et al. AAAAI/WAO Joint Congress, Abstract 586
ORLANDO – Swamp coolers – a low-cost alternative to air-conditioning in dry regions – weren’t found to increase sensitization to house dust mites or mold in atopic pediatric patients, researchers reported.
Neema Izadi, MD, and his associates say the findings, seen in a pediatric Colorado population in a study evaluating data over 10 years, could mean that not everyone at risk of dust mite and mold sensitization needs to avoid these cooling systems.
“Evaporative coolers have been shown to raise relative humidity by about 10%,” said Dr. Izadi, a pediatric allergy and immunology fellow at National Jewish Health, Denver, presenting at the joint congress of the American Academy of Asthma, Allergy and Immunology and the World Asthma Organization. “They work best in environments where the air is very warm and dry.”
House dust mites and mold thrive in higher humidity. Small studies performed in Colorado, Utah, and other locations have shown that the swamp coolers increase house dust mite allergen content, but there have been very few studies that have looked at actual sensitization. One smaller study in Nevada did find that the coolers increased sensitization to dust mites and mold.
In this study – thought to be the largest ever to look at this question – Dr. Izadi and his colleagues assessed data on patients aged 21 years and younger who were seen at National Jewish Health during 2008-2017 and who had at least one positive environmental skin-prick test. The average age was about 9 years. The cohort included 8,503 patients with sensitization to house dust mites and 9,286 with sensitization to mold. Researchers examined data on swamp coolers in their homes.
The researchers found that 29% of those with swamp coolers were dust-mite positive on skin testing, and 28% of those without one were positive. This was not a significant difference (P = .85). They found that 45% of those with the coolers were positive for sensitization to any mold, compared with 44% without one – also not a significant difference (P = .43).
They also found no difference according to age group, sex, or individually for atopic dermatitis, asthma, or allergic rhinitis.
He acknowledged that the study had no way to reliably account for patients who were transplants to Colorado, having moved there from somewhere else. The study also didn’t examine the age of homes, whether it had carpeting, or other factors.
He noted that the amount of time the coolers were run in the home was not examined and that “it might matter how much it is on.” This, he said, might account for differences in these results, compared with the Nevada study that did find a sensitization increase cause by the coolers.
“Evaporative coolers or swamp coolers are a great low-cost alternative in semiarid and arid environments – they can cut costs from 15%-35%,” Dr. Izadi said. “These data may indicate that it may be unnecessary to recommend that patients remove their swamp cooler, at least from a dust-mite and mold-sensitization standpoint.”
Dr. Izadi had no relevant financial disclosures.
SOURCE: Izadi N et al. AAAAI/WAO Joint Congress, Abstract 586
REPORTING FROM AAAAI/WAO JOINT CONGRESS
Key clinical point:
Major finding: Researchers found that 29% of those with swamp coolers were dust-mite positive on skin testing, and 28% of those without one were as well. This was not a significant difference (P = .85).
Study details: A retrospective review of more than 17,000 cases of atopic children aged 21 years and younger who were seen at National Jewish Health and had a positive environmental skin prick test.
Disclosures: Dr. Izadi had no relevant financial disclosures.
Source: Izadi N et al. AAAAI/WAO Joint Congress, Abstract 586
MDedge Daily News: Have ‘The Talk’ about medical marijuana
, uniformity comes to inflammatory bowel disease severity, diabetes drives the nation’s drug bills, and there’s pushback against new blood sugar targets.
Listen to the MDedge Daily News podcast for all the details on today’s top news.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
, uniformity comes to inflammatory bowel disease severity, diabetes drives the nation’s drug bills, and there’s pushback against new blood sugar targets.
Listen to the MDedge Daily News podcast for all the details on today’s top news.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
, uniformity comes to inflammatory bowel disease severity, diabetes drives the nation’s drug bills, and there’s pushback against new blood sugar targets.
Listen to the MDedge Daily News podcast for all the details on today’s top news.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Does Your Work Trigger Asthma?
As many as 1 in 5 asthma-related deaths in the US is due to occupational exposure—and many could be prevented, according to CDC researchers.
The researchers analyzed reports from 1999-2016 of asthma-related mortality and occupations of the people involved. Of 3,396 deaths (3,396 in 2015 alone), between 11% and 21% were due to occupational exposures. Health care workers and construction workers were at highest risk.
By industry, the highest number of deaths were among men working in construction (13%) and women in health care (14%). By occupation, the most deaths were among men construction trades workers (11%) and women office and administrative support workers (9%).
The researchers note that ongoing exposure to cleaners, disinfectants, and antibiotics, all can trigger asthma. But they also point out that steps can be successfully taken to limit the type of exposure that exacerbates asthma symptoms, such as replacing powdered latex gloves with powder-free natural rubber latex or nonlatex gloves.
In an interview with MD Magazine, principle investigator Jacek Mazurek, MD, PhD, said there’s also an opportunity for health care providers to intervene more effectively. “Inadequate screening of workers for occupational exposures by health providers and lack of recognition of associations between workplace exposures and asthma symptoms remain the main reasons for underrecognition and underdiagnosis of work-related asthma.”
The Occupational Safety and Health Administration offers guidance for diagnosing work-related asthma at https://www.osha.gov/SLTC/occupationalasthma/.
As many as 1 in 5 asthma-related deaths in the US is due to occupational exposure—and many could be prevented, according to CDC researchers.
The researchers analyzed reports from 1999-2016 of asthma-related mortality and occupations of the people involved. Of 3,396 deaths (3,396 in 2015 alone), between 11% and 21% were due to occupational exposures. Health care workers and construction workers were at highest risk.
By industry, the highest number of deaths were among men working in construction (13%) and women in health care (14%). By occupation, the most deaths were among men construction trades workers (11%) and women office and administrative support workers (9%).
The researchers note that ongoing exposure to cleaners, disinfectants, and antibiotics, all can trigger asthma. But they also point out that steps can be successfully taken to limit the type of exposure that exacerbates asthma symptoms, such as replacing powdered latex gloves with powder-free natural rubber latex or nonlatex gloves.
In an interview with MD Magazine, principle investigator Jacek Mazurek, MD, PhD, said there’s also an opportunity for health care providers to intervene more effectively. “Inadequate screening of workers for occupational exposures by health providers and lack of recognition of associations between workplace exposures and asthma symptoms remain the main reasons for underrecognition and underdiagnosis of work-related asthma.”
The Occupational Safety and Health Administration offers guidance for diagnosing work-related asthma at https://www.osha.gov/SLTC/occupationalasthma/.
As many as 1 in 5 asthma-related deaths in the US is due to occupational exposure—and many could be prevented, according to CDC researchers.
The researchers analyzed reports from 1999-2016 of asthma-related mortality and occupations of the people involved. Of 3,396 deaths (3,396 in 2015 alone), between 11% and 21% were due to occupational exposures. Health care workers and construction workers were at highest risk.
By industry, the highest number of deaths were among men working in construction (13%) and women in health care (14%). By occupation, the most deaths were among men construction trades workers (11%) and women office and administrative support workers (9%).
The researchers note that ongoing exposure to cleaners, disinfectants, and antibiotics, all can trigger asthma. But they also point out that steps can be successfully taken to limit the type of exposure that exacerbates asthma symptoms, such as replacing powdered latex gloves with powder-free natural rubber latex or nonlatex gloves.
In an interview with MD Magazine, principle investigator Jacek Mazurek, MD, PhD, said there’s also an opportunity for health care providers to intervene more effectively. “Inadequate screening of workers for occupational exposures by health providers and lack of recognition of associations between workplace exposures and asthma symptoms remain the main reasons for underrecognition and underdiagnosis of work-related asthma.”
The Occupational Safety and Health Administration offers guidance for diagnosing work-related asthma at https://www.osha.gov/SLTC/occupationalasthma/.
Reversal agent exhibits efficacy in patients with major bleeding
ORLANDO—Interim trial results suggest andexanet alfa can reverse the activity of factor Xa inhibitors in patients with acute major bleeding.
Andexanet alfa reduced median anti-factor Xa inhibitor activity by 91% in patients taking apixaban, 88% in those taking rivaroxaban, and 75% in patients taking enoxaparin.
Eleven percent of patients experienced thrombotic events, and 12% of patients died.
Stuart J. Connolly, MD, of McMaster University in Hamilton, Ontario, Canada, presented these results at the American College of Cardiology’s 67th Annual Scientific Session & Expo (ACC.18, abstract 409-14).
The trial, known as ANNEXA-4, was sponsored by Portola Pharmaceuticals, Inc.
“These data are particularly compelling when you consider the high-risk profile of the ANNEXA-4 population, which includes a substantial number of elderly patients presenting with intracranial hemorrhage and anticoagulated for venous thromboembolism, and the lack of any FDA- or EMA-approved reversal agent for these patients,” Dr Connolly said.
“The interim efficacy and safety data continue to support the promising role of AndexXa [the brand name for andexanet alfa] as an antidote to reverse anticoagulation in factor Xa-associated bleeding.”
Andexanet alfa is a recombinant modified factor Xa molecule designed to bind to and disable factor Xa inhibitors, thereby allowing factor Xa produced by the body to play its normal role in the formation of blood clots.
In earlier trials of healthy volunteers, andexanet alfa reversed the anticoagulant effect of factor Xa inhibitors without any significant safety problems.
ANNEXA-4 is an ongoing trial of andexanet alfa in patients experiencing major bleeding while taking factor Xa inhibitors.
Dr Connolly presented safety outcomes for 227 trial subjects and adjudicated efficacy outcomes for 132 subjects. All subjects presented with acute major bleeding within 18 hours of taking a factor Xa inhibitor, including apixaban, rivaroxaban, enoxaparin, and edoxaban.
The patients received andexanet alfa given as a bolus dose over 20 to 30 minutes, followed by a 2-hour (120 minute) infusion. The dosage was determined based on the specific factor Xa inhibitor the patients were taking and how long it had been since their last dose.
The patients were evaluated for 30 days after andexanet alfa administration.
Efficacy
The median age of the efficacy population (n=137) was 77, and 51% (n=70) were male. Indications for anticoagulation included atrial fibrillation (Afib, 76%, n=104), venous thromboembolism (VTE, 28%, n=38), and both Afib and VTE (4%, n=6).
Patients were receiving apixaban (n=68), rivaroxaban (n=54), or enoxaparin (n=10). None of these patients had received edoxaban.
Types of bleeding included intracranial hemorrhage (ICH, 57%, n=78), gastrointestinal (GI) bleeding (31%, n=43), and “other” bleeding (12%, n=16).
The researchers assessed andexanet alfa’s efficacy in terms of 2 co-primary endpoints—reduction in anti-factor Xa inhibitor activity and achievement of clinical hemostasis by 12 hours after administration. Hemostatic efficacy was assessed by an independent endpoint adjudication committee as “excellent,” “good,” or “poor/none.”
After the bolus dose of andexanet alfa, the median anti-factor Xa inhibitor activity was reduced by 91% for patients taking apixaban, 88% for those taking rivaroxaban, and 75% for those taking enoxaparin.
For patients taking rivaroxaban, the median anti-factor Xa inhibitor activity was reduced by 88% at the end of the bolus dose, 87% at the end of the infusion, 42% at 4 hours, 49% at 8 hours, and 60% at 12 hours.
For patients taking apixaban, the median anti-factor Xa inhibitor activity was reduced by 91% at the end of the bolus dose, 91% at the end of the infusion, 36% at 4 hours, 30% at 8 hours, and 35% at 12 hours.
Overall, 83% of patients had “excellent” or “good” clinical hemostasis, and 17% had “poor/none.”
Hemostasis was deemed excellent or good in 83% of patients on rivaroxaban, 82% of those on apixaban, and 80% of those on enoxaparin. It was excellent/good in 86% of patients with GI bleeding, 81% of patients with ICH, and 80% of patients with bleeding at other sites.
Safety
The median age of the safety population (n=227) was 77, and 52% (n=117) were male. Indications for anticoagulation included Afib (78%, n=178), VTE (23%, n=52), and both Afib and VTE (4%, n=8).
Patients were receiving apixaban (n=117), rivaroxaban (n=90), enoxaparin (n=17), and edoxaban (n=3). Types of bleeding included ICH (61%, n=139), GI (27%, n=62), and “other” (12%, n=26).
During the 30-day follow-up period, the rate of thrombotic events was 11% (n=24) for the entire population and 12% (n=17) among patients with ICH.
The mortality rate for all patients was 12% (n=27). Eleven deaths were due to cardiovascular causes.
According to Dr Connolly, these rates of adverse events are in line with what would be expected given the underlying medical condition of the patients in the trial and the fact that many (43%) had not resumed anticoagulant treatment in the 30-day follow-up period.
Two patients experienced an infusion reaction.
None of the patients developed antibodies to factor Xa or factor X, and there were no neutralizing antibodies to andexanet alfa.
ORLANDO—Interim trial results suggest andexanet alfa can reverse the activity of factor Xa inhibitors in patients with acute major bleeding.
Andexanet alfa reduced median anti-factor Xa inhibitor activity by 91% in patients taking apixaban, 88% in those taking rivaroxaban, and 75% in patients taking enoxaparin.
Eleven percent of patients experienced thrombotic events, and 12% of patients died.
Stuart J. Connolly, MD, of McMaster University in Hamilton, Ontario, Canada, presented these results at the American College of Cardiology’s 67th Annual Scientific Session & Expo (ACC.18, abstract 409-14).
The trial, known as ANNEXA-4, was sponsored by Portola Pharmaceuticals, Inc.
“These data are particularly compelling when you consider the high-risk profile of the ANNEXA-4 population, which includes a substantial number of elderly patients presenting with intracranial hemorrhage and anticoagulated for venous thromboembolism, and the lack of any FDA- or EMA-approved reversal agent for these patients,” Dr Connolly said.
“The interim efficacy and safety data continue to support the promising role of AndexXa [the brand name for andexanet alfa] as an antidote to reverse anticoagulation in factor Xa-associated bleeding.”
Andexanet alfa is a recombinant modified factor Xa molecule designed to bind to and disable factor Xa inhibitors, thereby allowing factor Xa produced by the body to play its normal role in the formation of blood clots.
In earlier trials of healthy volunteers, andexanet alfa reversed the anticoagulant effect of factor Xa inhibitors without any significant safety problems.
ANNEXA-4 is an ongoing trial of andexanet alfa in patients experiencing major bleeding while taking factor Xa inhibitors.
Dr Connolly presented safety outcomes for 227 trial subjects and adjudicated efficacy outcomes for 132 subjects. All subjects presented with acute major bleeding within 18 hours of taking a factor Xa inhibitor, including apixaban, rivaroxaban, enoxaparin, and edoxaban.
The patients received andexanet alfa given as a bolus dose over 20 to 30 minutes, followed by a 2-hour (120 minute) infusion. The dosage was determined based on the specific factor Xa inhibitor the patients were taking and how long it had been since their last dose.
The patients were evaluated for 30 days after andexanet alfa administration.
Efficacy
The median age of the efficacy population (n=137) was 77, and 51% (n=70) were male. Indications for anticoagulation included atrial fibrillation (Afib, 76%, n=104), venous thromboembolism (VTE, 28%, n=38), and both Afib and VTE (4%, n=6).
Patients were receiving apixaban (n=68), rivaroxaban (n=54), or enoxaparin (n=10). None of these patients had received edoxaban.
Types of bleeding included intracranial hemorrhage (ICH, 57%, n=78), gastrointestinal (GI) bleeding (31%, n=43), and “other” bleeding (12%, n=16).
The researchers assessed andexanet alfa’s efficacy in terms of 2 co-primary endpoints—reduction in anti-factor Xa inhibitor activity and achievement of clinical hemostasis by 12 hours after administration. Hemostatic efficacy was assessed by an independent endpoint adjudication committee as “excellent,” “good,” or “poor/none.”
After the bolus dose of andexanet alfa, the median anti-factor Xa inhibitor activity was reduced by 91% for patients taking apixaban, 88% for those taking rivaroxaban, and 75% for those taking enoxaparin.
For patients taking rivaroxaban, the median anti-factor Xa inhibitor activity was reduced by 88% at the end of the bolus dose, 87% at the end of the infusion, 42% at 4 hours, 49% at 8 hours, and 60% at 12 hours.
For patients taking apixaban, the median anti-factor Xa inhibitor activity was reduced by 91% at the end of the bolus dose, 91% at the end of the infusion, 36% at 4 hours, 30% at 8 hours, and 35% at 12 hours.
Overall, 83% of patients had “excellent” or “good” clinical hemostasis, and 17% had “poor/none.”
Hemostasis was deemed excellent or good in 83% of patients on rivaroxaban, 82% of those on apixaban, and 80% of those on enoxaparin. It was excellent/good in 86% of patients with GI bleeding, 81% of patients with ICH, and 80% of patients with bleeding at other sites.
Safety
The median age of the safety population (n=227) was 77, and 52% (n=117) were male. Indications for anticoagulation included Afib (78%, n=178), VTE (23%, n=52), and both Afib and VTE (4%, n=8).
Patients were receiving apixaban (n=117), rivaroxaban (n=90), enoxaparin (n=17), and edoxaban (n=3). Types of bleeding included ICH (61%, n=139), GI (27%, n=62), and “other” (12%, n=26).
During the 30-day follow-up period, the rate of thrombotic events was 11% (n=24) for the entire population and 12% (n=17) among patients with ICH.
The mortality rate for all patients was 12% (n=27). Eleven deaths were due to cardiovascular causes.
According to Dr Connolly, these rates of adverse events are in line with what would be expected given the underlying medical condition of the patients in the trial and the fact that many (43%) had not resumed anticoagulant treatment in the 30-day follow-up period.
Two patients experienced an infusion reaction.
None of the patients developed antibodies to factor Xa or factor X, and there were no neutralizing antibodies to andexanet alfa.
ORLANDO—Interim trial results suggest andexanet alfa can reverse the activity of factor Xa inhibitors in patients with acute major bleeding.
Andexanet alfa reduced median anti-factor Xa inhibitor activity by 91% in patients taking apixaban, 88% in those taking rivaroxaban, and 75% in patients taking enoxaparin.
Eleven percent of patients experienced thrombotic events, and 12% of patients died.
Stuart J. Connolly, MD, of McMaster University in Hamilton, Ontario, Canada, presented these results at the American College of Cardiology’s 67th Annual Scientific Session & Expo (ACC.18, abstract 409-14).
The trial, known as ANNEXA-4, was sponsored by Portola Pharmaceuticals, Inc.
“These data are particularly compelling when you consider the high-risk profile of the ANNEXA-4 population, which includes a substantial number of elderly patients presenting with intracranial hemorrhage and anticoagulated for venous thromboembolism, and the lack of any FDA- or EMA-approved reversal agent for these patients,” Dr Connolly said.
“The interim efficacy and safety data continue to support the promising role of AndexXa [the brand name for andexanet alfa] as an antidote to reverse anticoagulation in factor Xa-associated bleeding.”
Andexanet alfa is a recombinant modified factor Xa molecule designed to bind to and disable factor Xa inhibitors, thereby allowing factor Xa produced by the body to play its normal role in the formation of blood clots.
In earlier trials of healthy volunteers, andexanet alfa reversed the anticoagulant effect of factor Xa inhibitors without any significant safety problems.
ANNEXA-4 is an ongoing trial of andexanet alfa in patients experiencing major bleeding while taking factor Xa inhibitors.
Dr Connolly presented safety outcomes for 227 trial subjects and adjudicated efficacy outcomes for 132 subjects. All subjects presented with acute major bleeding within 18 hours of taking a factor Xa inhibitor, including apixaban, rivaroxaban, enoxaparin, and edoxaban.
The patients received andexanet alfa given as a bolus dose over 20 to 30 minutes, followed by a 2-hour (120 minute) infusion. The dosage was determined based on the specific factor Xa inhibitor the patients were taking and how long it had been since their last dose.
The patients were evaluated for 30 days after andexanet alfa administration.
Efficacy
The median age of the efficacy population (n=137) was 77, and 51% (n=70) were male. Indications for anticoagulation included atrial fibrillation (Afib, 76%, n=104), venous thromboembolism (VTE, 28%, n=38), and both Afib and VTE (4%, n=6).
Patients were receiving apixaban (n=68), rivaroxaban (n=54), or enoxaparin (n=10). None of these patients had received edoxaban.
Types of bleeding included intracranial hemorrhage (ICH, 57%, n=78), gastrointestinal (GI) bleeding (31%, n=43), and “other” bleeding (12%, n=16).
The researchers assessed andexanet alfa’s efficacy in terms of 2 co-primary endpoints—reduction in anti-factor Xa inhibitor activity and achievement of clinical hemostasis by 12 hours after administration. Hemostatic efficacy was assessed by an independent endpoint adjudication committee as “excellent,” “good,” or “poor/none.”
After the bolus dose of andexanet alfa, the median anti-factor Xa inhibitor activity was reduced by 91% for patients taking apixaban, 88% for those taking rivaroxaban, and 75% for those taking enoxaparin.
For patients taking rivaroxaban, the median anti-factor Xa inhibitor activity was reduced by 88% at the end of the bolus dose, 87% at the end of the infusion, 42% at 4 hours, 49% at 8 hours, and 60% at 12 hours.
For patients taking apixaban, the median anti-factor Xa inhibitor activity was reduced by 91% at the end of the bolus dose, 91% at the end of the infusion, 36% at 4 hours, 30% at 8 hours, and 35% at 12 hours.
Overall, 83% of patients had “excellent” or “good” clinical hemostasis, and 17% had “poor/none.”
Hemostasis was deemed excellent or good in 83% of patients on rivaroxaban, 82% of those on apixaban, and 80% of those on enoxaparin. It was excellent/good in 86% of patients with GI bleeding, 81% of patients with ICH, and 80% of patients with bleeding at other sites.
Safety
The median age of the safety population (n=227) was 77, and 52% (n=117) were male. Indications for anticoagulation included Afib (78%, n=178), VTE (23%, n=52), and both Afib and VTE (4%, n=8).
Patients were receiving apixaban (n=117), rivaroxaban (n=90), enoxaparin (n=17), and edoxaban (n=3). Types of bleeding included ICH (61%, n=139), GI (27%, n=62), and “other” (12%, n=26).
During the 30-day follow-up period, the rate of thrombotic events was 11% (n=24) for the entire population and 12% (n=17) among patients with ICH.
The mortality rate for all patients was 12% (n=27). Eleven deaths were due to cardiovascular causes.
According to Dr Connolly, these rates of adverse events are in line with what would be expected given the underlying medical condition of the patients in the trial and the fact that many (43%) had not resumed anticoagulant treatment in the 30-day follow-up period.
Two patients experienced an infusion reaction.
None of the patients developed antibodies to factor Xa or factor X, and there were no neutralizing antibodies to andexanet alfa.
Heme implicated in adverse transfusion outcomes
Free heme plays a key role in the adverse effects associated with massive transfusion of stored red blood cells (RBCs), according to researchers.
Experiments in a mouse model of trauma hemorrhage revealed a greater risk of mortality from bacterial pneumonia in mice that received transfusions of blood stored for 14 days, rather than fresh blood.
This greater risk was dependent upon free heme, which is released from RBCs during storage and upon transfusion.
In a study of human trauma patients, researchers found the amount of heme was proportional to the amount of blood transfused.
Brant M. Wagener, MD, PhD, of University of Alabama at Birmingham, and his colleagues detailed these findings in PLOS Medicine.
In the mouse model of trauma hemorrhage, the researchers resuscitated mice using either fresh blood (stored for 0 days) or blood stored for 2 weeks. (A 2-week storage of mouse blood approximates storage of human RBCs for 42 days.)
Two days after transfusion, the mice were challenged by instilling the lungs with the bacteria Pseudomonas aeruginosa.
Mice that received the stored blood had a significant increase in bacterial lung injury, as shown by higher mortality, and increased fluid accumulation and bacterial numbers in the lungs.
The researchers identified the connection between free heme and infection susceptibility/severity in 2 ways.
First, Pseudomonas aeruginosa-induced mortality was completely prevented by the addition of hemopexin, a scavenging protein that removes free heme from the blood.
Second, adding an inhibitor of toll-like receptor 4 (TLR4), or genetically removing TLR4 from mice, also prevented bacteria-induced mortality. Free heme—which is known to induce inflammatory injury to major organs in diseases like sickle cell or sepsis—acts, in part, by activating TLR4.
The researchers also found that transfusion with stored blood induced release of the inflammation mediator high mobility group box 1 (HMGB1). But an anti-HMGB1 antibody protected mice from bacteria-induced mortality.
The anti-HMGB1 antibody also restored macrophage-dependent phagocytosis of Pseudomonas aeruginosa in vitro.
Tissue culture experiments had revealed that free heme inhibits macrophages from ingesting Pseudomonas aeruginosa, and the addition of free heme increases permeability in endothelial cells.
Finally, in a 16-month study, the researchers found that human trauma-hemorrhage patients who received large amounts of transfused blood were also receiving amounts of free heme sufficient to overwhelm the normal amounts of hemopexin found in a person’s blood.
The researchers said this work underscores the need to confirm whether the storage age of transfused RBCs correlates with increasing levels of free heme after transfusion. The team would also like to establish whether patients with low ratios of hemopexin to free heme have a greater risk for adverse outcomes after massive transfusions.
Free heme plays a key role in the adverse effects associated with massive transfusion of stored red blood cells (RBCs), according to researchers.
Experiments in a mouse model of trauma hemorrhage revealed a greater risk of mortality from bacterial pneumonia in mice that received transfusions of blood stored for 14 days, rather than fresh blood.
This greater risk was dependent upon free heme, which is released from RBCs during storage and upon transfusion.
In a study of human trauma patients, researchers found the amount of heme was proportional to the amount of blood transfused.
Brant M. Wagener, MD, PhD, of University of Alabama at Birmingham, and his colleagues detailed these findings in PLOS Medicine.
In the mouse model of trauma hemorrhage, the researchers resuscitated mice using either fresh blood (stored for 0 days) or blood stored for 2 weeks. (A 2-week storage of mouse blood approximates storage of human RBCs for 42 days.)
Two days after transfusion, the mice were challenged by instilling the lungs with the bacteria Pseudomonas aeruginosa.
Mice that received the stored blood had a significant increase in bacterial lung injury, as shown by higher mortality, and increased fluid accumulation and bacterial numbers in the lungs.
The researchers identified the connection between free heme and infection susceptibility/severity in 2 ways.
First, Pseudomonas aeruginosa-induced mortality was completely prevented by the addition of hemopexin, a scavenging protein that removes free heme from the blood.
Second, adding an inhibitor of toll-like receptor 4 (TLR4), or genetically removing TLR4 from mice, also prevented bacteria-induced mortality. Free heme—which is known to induce inflammatory injury to major organs in diseases like sickle cell or sepsis—acts, in part, by activating TLR4.
The researchers also found that transfusion with stored blood induced release of the inflammation mediator high mobility group box 1 (HMGB1). But an anti-HMGB1 antibody protected mice from bacteria-induced mortality.
The anti-HMGB1 antibody also restored macrophage-dependent phagocytosis of Pseudomonas aeruginosa in vitro.
Tissue culture experiments had revealed that free heme inhibits macrophages from ingesting Pseudomonas aeruginosa, and the addition of free heme increases permeability in endothelial cells.
Finally, in a 16-month study, the researchers found that human trauma-hemorrhage patients who received large amounts of transfused blood were also receiving amounts of free heme sufficient to overwhelm the normal amounts of hemopexin found in a person’s blood.
The researchers said this work underscores the need to confirm whether the storage age of transfused RBCs correlates with increasing levels of free heme after transfusion. The team would also like to establish whether patients with low ratios of hemopexin to free heme have a greater risk for adverse outcomes after massive transfusions.
Free heme plays a key role in the adverse effects associated with massive transfusion of stored red blood cells (RBCs), according to researchers.
Experiments in a mouse model of trauma hemorrhage revealed a greater risk of mortality from bacterial pneumonia in mice that received transfusions of blood stored for 14 days, rather than fresh blood.
This greater risk was dependent upon free heme, which is released from RBCs during storage and upon transfusion.
In a study of human trauma patients, researchers found the amount of heme was proportional to the amount of blood transfused.
Brant M. Wagener, MD, PhD, of University of Alabama at Birmingham, and his colleagues detailed these findings in PLOS Medicine.
In the mouse model of trauma hemorrhage, the researchers resuscitated mice using either fresh blood (stored for 0 days) or blood stored for 2 weeks. (A 2-week storage of mouse blood approximates storage of human RBCs for 42 days.)
Two days after transfusion, the mice were challenged by instilling the lungs with the bacteria Pseudomonas aeruginosa.
Mice that received the stored blood had a significant increase in bacterial lung injury, as shown by higher mortality, and increased fluid accumulation and bacterial numbers in the lungs.
The researchers identified the connection between free heme and infection susceptibility/severity in 2 ways.
First, Pseudomonas aeruginosa-induced mortality was completely prevented by the addition of hemopexin, a scavenging protein that removes free heme from the blood.
Second, adding an inhibitor of toll-like receptor 4 (TLR4), or genetically removing TLR4 from mice, also prevented bacteria-induced mortality. Free heme—which is known to induce inflammatory injury to major organs in diseases like sickle cell or sepsis—acts, in part, by activating TLR4.
The researchers also found that transfusion with stored blood induced release of the inflammation mediator high mobility group box 1 (HMGB1). But an anti-HMGB1 antibody protected mice from bacteria-induced mortality.
The anti-HMGB1 antibody also restored macrophage-dependent phagocytosis of Pseudomonas aeruginosa in vitro.
Tissue culture experiments had revealed that free heme inhibits macrophages from ingesting Pseudomonas aeruginosa, and the addition of free heme increases permeability in endothelial cells.
Finally, in a 16-month study, the researchers found that human trauma-hemorrhage patients who received large amounts of transfused blood were also receiving amounts of free heme sufficient to overwhelm the normal amounts of hemopexin found in a person’s blood.
The researchers said this work underscores the need to confirm whether the storage age of transfused RBCs correlates with increasing levels of free heme after transfusion. The team would also like to establish whether patients with low ratios of hemopexin to free heme have a greater risk for adverse outcomes after massive transfusions.
Lymphoma, breast cancer survivors have greater risk of CHF
ORLANDO—Results of a retrospective study showed that survivors of lymphoma or breast cancer had a significantly greater risk of congestive heart failure (CHF) than patients who did not have cancer.
This increased risk was observed as early as a year after cancer diagnosis but was still present 20 years after diagnosis.
Overall, 1 in 10 cancer patients had CHF at the 20-year mark.
“The majority of patients do not develop heart failure, but our research helps us recognize the factors associated with it and the importance of appropriate heart care following cancer treatment,” said Carolyn Larsen, MD, of the Mayo Clinic in Rochester, Minnesota.
“Our research suggests that periodic cardiac imaging to monitor for heart damage may be needed for some cancer patients, even if they have no signs of heart damage initially after chemotherapy. Additionally, it emphasizes that working to live a heart-healthy lifestyle is important for cancer patients and survivors to reduce the overall risk of heart disease.”
Dr Larsen and her colleagues presented this research as a poster (abstract 1105-066) at the American College of Cardiology’s 67th Annual Scientific Session & Expo (ACC.18).
Patients
Using data from the Rochester Epidemiology Project, the researchers retrospectively tracked CHF cases in 900 cancer patients and 1550 non-cancer patients. Patients were treated in Olmsted County in Minnesota from 1985 to 2010.
For both patient groups, the median age at baseline was about 53, a little more than 90% of each group was white, and nearly 80% of each group was female.
Six to 7% of patients had diabetes, and about 30% of each group had hypertension. Thirty-eight percent of each group had hyperlipidemia, and 31% were obese.
Five percent of cancer patients and 2% of controls had coronary artery disease (P<0.001). This was the only significant difference in baseline characteristics.
Cancer patients had been diagnosed with non-Hodgkin lymphoma (28%), Hodgkin lymphoma (9%), or breast cancer (64%). Forty-seven percent had received radiation, including right chest (21%), left chest (23%), and mediastinal (4%).
Eighty-four percent of patients had received anthracycline therapy. The median doxorubicin isotoxic dose was 240 mg/m2.
At baseline, 12% of cancer patients were on beta-blockers, 8% were on angiotensin converting enzyme inhibitors, 4% were on angiotensin receptor blockers, and 11% were on statins.
Results
Cancer patients were more than 3 times as likely as controls to develop CHF. The hazard ratio (HR) was 3.6 (P<0.01) in an analysis adjusted for age, gender, diabetes, hypertension, coronary artery disease, dyslipidemia, and obesity at baseline.
The increased CHF risk among cancer patients was evident after the first year from cancer diagnosis and persisted at 20 years of follow-up.
“The risk of heart failure doesn’t go away after a couple of years,” Dr Larsen said. “It’s a long-term issue that patients need to discuss with their doctors and use as motivation to stay heart healthy.”
The incidence of CHF—in cancer patients and controls, respectively—was as follows:
- 1 year—1.5% vs 0.1%
- 5 years—3.1% vs 0.9%
- 10 years—5.0% vs 2%
- 20 years—10.1% vs 5.8%.
A multivariable analysis in the cancer patients revealed a few independent risk factors for CHF, including:
- Doxorubicin isotoxic dose ≥ 300 mg/m2 (HR=2.34, P=0.003)
- Age at diagnosis (HR=3.06 for age ≥ 80 vs 60-69, P=0.01)
- Coronary artery disease at diagnosis (HR=2.27, P=0.04)
- Diabetes mellitus at diagnosis (HR=2.39, P<0.01).
Dr Larsen said additional research is needed to determine why diabetes carries a greater risk than other traditional risk factors, such as high blood pressure, in this group.
Mitigating risk
These findings raise important questions about what the appropriate surveillance should be for heart problems post-cancer treatment, Dr Larsen said. She believes more frequent cardiac imaging may be warranted in some patients to detect signs of CHF earlier.
“It’s an area that needs to be better defined,” Dr Larsen said. “An echocardiogram is usually done 6 to 12 months after cancer treatment with an anthracycline, but how often should it be done after that? We need to be more vigilant in making sure we try to prevent or control heart issues post-cancer care, especially in light of the growing appreciation of the connection between some cancer treatments and heart disease.”
Dr Larsen also noted that patients themselves can play a role in decreasing their risk of CHF, even if they are starting at a disadvantage.
A heart-healthy lifestyle—maintaining a normal body weight, regular exercise, and controlling other risk factors such as high blood pressure, diabetes, and high cholesterol—can help lower the risk of heart disease and CHF.
“If patients know they have received a drug treatment that might increase their risk of heart failure, it’s even more important to take care of the aspects of their life that they can control to reduce their risk as much as possible and to work with their medical care team to detect issues as early as possible,” Dr Larsen said.
ORLANDO—Results of a retrospective study showed that survivors of lymphoma or breast cancer had a significantly greater risk of congestive heart failure (CHF) than patients who did not have cancer.
This increased risk was observed as early as a year after cancer diagnosis but was still present 20 years after diagnosis.
Overall, 1 in 10 cancer patients had CHF at the 20-year mark.
“The majority of patients do not develop heart failure, but our research helps us recognize the factors associated with it and the importance of appropriate heart care following cancer treatment,” said Carolyn Larsen, MD, of the Mayo Clinic in Rochester, Minnesota.
“Our research suggests that periodic cardiac imaging to monitor for heart damage may be needed for some cancer patients, even if they have no signs of heart damage initially after chemotherapy. Additionally, it emphasizes that working to live a heart-healthy lifestyle is important for cancer patients and survivors to reduce the overall risk of heart disease.”
Dr Larsen and her colleagues presented this research as a poster (abstract 1105-066) at the American College of Cardiology’s 67th Annual Scientific Session & Expo (ACC.18).
Patients
Using data from the Rochester Epidemiology Project, the researchers retrospectively tracked CHF cases in 900 cancer patients and 1550 non-cancer patients. Patients were treated in Olmsted County in Minnesota from 1985 to 2010.
For both patient groups, the median age at baseline was about 53, a little more than 90% of each group was white, and nearly 80% of each group was female.
Six to 7% of patients had diabetes, and about 30% of each group had hypertension. Thirty-eight percent of each group had hyperlipidemia, and 31% were obese.
Five percent of cancer patients and 2% of controls had coronary artery disease (P<0.001). This was the only significant difference in baseline characteristics.
Cancer patients had been diagnosed with non-Hodgkin lymphoma (28%), Hodgkin lymphoma (9%), or breast cancer (64%). Forty-seven percent had received radiation, including right chest (21%), left chest (23%), and mediastinal (4%).
Eighty-four percent of patients had received anthracycline therapy. The median doxorubicin isotoxic dose was 240 mg/m2.
At baseline, 12% of cancer patients were on beta-blockers, 8% were on angiotensin converting enzyme inhibitors, 4% were on angiotensin receptor blockers, and 11% were on statins.
Results
Cancer patients were more than 3 times as likely as controls to develop CHF. The hazard ratio (HR) was 3.6 (P<0.01) in an analysis adjusted for age, gender, diabetes, hypertension, coronary artery disease, dyslipidemia, and obesity at baseline.
The increased CHF risk among cancer patients was evident after the first year from cancer diagnosis and persisted at 20 years of follow-up.
“The risk of heart failure doesn’t go away after a couple of years,” Dr Larsen said. “It’s a long-term issue that patients need to discuss with their doctors and use as motivation to stay heart healthy.”
The incidence of CHF—in cancer patients and controls, respectively—was as follows:
- 1 year—1.5% vs 0.1%
- 5 years—3.1% vs 0.9%
- 10 years—5.0% vs 2%
- 20 years—10.1% vs 5.8%.
A multivariable analysis in the cancer patients revealed a few independent risk factors for CHF, including:
- Doxorubicin isotoxic dose ≥ 300 mg/m2 (HR=2.34, P=0.003)
- Age at diagnosis (HR=3.06 for age ≥ 80 vs 60-69, P=0.01)
- Coronary artery disease at diagnosis (HR=2.27, P=0.04)
- Diabetes mellitus at diagnosis (HR=2.39, P<0.01).
Dr Larsen said additional research is needed to determine why diabetes carries a greater risk than other traditional risk factors, such as high blood pressure, in this group.
Mitigating risk
These findings raise important questions about what the appropriate surveillance should be for heart problems post-cancer treatment, Dr Larsen said. She believes more frequent cardiac imaging may be warranted in some patients to detect signs of CHF earlier.
“It’s an area that needs to be better defined,” Dr Larsen said. “An echocardiogram is usually done 6 to 12 months after cancer treatment with an anthracycline, but how often should it be done after that? We need to be more vigilant in making sure we try to prevent or control heart issues post-cancer care, especially in light of the growing appreciation of the connection between some cancer treatments and heart disease.”
Dr Larsen also noted that patients themselves can play a role in decreasing their risk of CHF, even if they are starting at a disadvantage.
A heart-healthy lifestyle—maintaining a normal body weight, regular exercise, and controlling other risk factors such as high blood pressure, diabetes, and high cholesterol—can help lower the risk of heart disease and CHF.
“If patients know they have received a drug treatment that might increase their risk of heart failure, it’s even more important to take care of the aspects of their life that they can control to reduce their risk as much as possible and to work with their medical care team to detect issues as early as possible,” Dr Larsen said.
ORLANDO—Results of a retrospective study showed that survivors of lymphoma or breast cancer had a significantly greater risk of congestive heart failure (CHF) than patients who did not have cancer.
This increased risk was observed as early as a year after cancer diagnosis but was still present 20 years after diagnosis.
Overall, 1 in 10 cancer patients had CHF at the 20-year mark.
“The majority of patients do not develop heart failure, but our research helps us recognize the factors associated with it and the importance of appropriate heart care following cancer treatment,” said Carolyn Larsen, MD, of the Mayo Clinic in Rochester, Minnesota.
“Our research suggests that periodic cardiac imaging to monitor for heart damage may be needed for some cancer patients, even if they have no signs of heart damage initially after chemotherapy. Additionally, it emphasizes that working to live a heart-healthy lifestyle is important for cancer patients and survivors to reduce the overall risk of heart disease.”
Dr Larsen and her colleagues presented this research as a poster (abstract 1105-066) at the American College of Cardiology’s 67th Annual Scientific Session & Expo (ACC.18).
Patients
Using data from the Rochester Epidemiology Project, the researchers retrospectively tracked CHF cases in 900 cancer patients and 1550 non-cancer patients. Patients were treated in Olmsted County in Minnesota from 1985 to 2010.
For both patient groups, the median age at baseline was about 53, a little more than 90% of each group was white, and nearly 80% of each group was female.
Six to 7% of patients had diabetes, and about 30% of each group had hypertension. Thirty-eight percent of each group had hyperlipidemia, and 31% were obese.
Five percent of cancer patients and 2% of controls had coronary artery disease (P<0.001). This was the only significant difference in baseline characteristics.
Cancer patients had been diagnosed with non-Hodgkin lymphoma (28%), Hodgkin lymphoma (9%), or breast cancer (64%). Forty-seven percent had received radiation, including right chest (21%), left chest (23%), and mediastinal (4%).
Eighty-four percent of patients had received anthracycline therapy. The median doxorubicin isotoxic dose was 240 mg/m2.
At baseline, 12% of cancer patients were on beta-blockers, 8% were on angiotensin converting enzyme inhibitors, 4% were on angiotensin receptor blockers, and 11% were on statins.
Results
Cancer patients were more than 3 times as likely as controls to develop CHF. The hazard ratio (HR) was 3.6 (P<0.01) in an analysis adjusted for age, gender, diabetes, hypertension, coronary artery disease, dyslipidemia, and obesity at baseline.
The increased CHF risk among cancer patients was evident after the first year from cancer diagnosis and persisted at 20 years of follow-up.
“The risk of heart failure doesn’t go away after a couple of years,” Dr Larsen said. “It’s a long-term issue that patients need to discuss with their doctors and use as motivation to stay heart healthy.”
The incidence of CHF—in cancer patients and controls, respectively—was as follows:
- 1 year—1.5% vs 0.1%
- 5 years—3.1% vs 0.9%
- 10 years—5.0% vs 2%
- 20 years—10.1% vs 5.8%.
A multivariable analysis in the cancer patients revealed a few independent risk factors for CHF, including:
- Doxorubicin isotoxic dose ≥ 300 mg/m2 (HR=2.34, P=0.003)
- Age at diagnosis (HR=3.06 for age ≥ 80 vs 60-69, P=0.01)
- Coronary artery disease at diagnosis (HR=2.27, P=0.04)
- Diabetes mellitus at diagnosis (HR=2.39, P<0.01).
Dr Larsen said additional research is needed to determine why diabetes carries a greater risk than other traditional risk factors, such as high blood pressure, in this group.
Mitigating risk
These findings raise important questions about what the appropriate surveillance should be for heart problems post-cancer treatment, Dr Larsen said. She believes more frequent cardiac imaging may be warranted in some patients to detect signs of CHF earlier.
“It’s an area that needs to be better defined,” Dr Larsen said. “An echocardiogram is usually done 6 to 12 months after cancer treatment with an anthracycline, but how often should it be done after that? We need to be more vigilant in making sure we try to prevent or control heart issues post-cancer care, especially in light of the growing appreciation of the connection between some cancer treatments and heart disease.”
Dr Larsen also noted that patients themselves can play a role in decreasing their risk of CHF, even if they are starting at a disadvantage.
A heart-healthy lifestyle—maintaining a normal body weight, regular exercise, and controlling other risk factors such as high blood pressure, diabetes, and high cholesterol—can help lower the risk of heart disease and CHF.
“If patients know they have received a drug treatment that might increase their risk of heart failure, it’s even more important to take care of the aspects of their life that they can control to reduce their risk as much as possible and to work with their medical care team to detect issues as early as possible,” Dr Larsen said.
His Old Pain Is Back
ANSWER
The radiograph demonstrates a fracture within the femoral neck. These types of fractures, which are slightly angulated and located at the base of the neck, are typically referred to as basicervical femur fractures.
Prompt orthopedic surgery consultation was obtained, and the patient underwent an open reduction and internal fixation of his fracture.
ANSWER
The radiograph demonstrates a fracture within the femoral neck. These types of fractures, which are slightly angulated and located at the base of the neck, are typically referred to as basicervical femur fractures.
Prompt orthopedic surgery consultation was obtained, and the patient underwent an open reduction and internal fixation of his fracture.
ANSWER
The radiograph demonstrates a fracture within the femoral neck. These types of fractures, which are slightly angulated and located at the base of the neck, are typically referred to as basicervical femur fractures.
Prompt orthopedic surgery consultation was obtained, and the patient underwent an open reduction and internal fixation of his fracture.
You are called in for a neurosurgical consult of a 60-year-old man who underwent a lumbar decompression approximately 18 months ago. For the past several weeks, he has been experiencing worsening back pain that radiates down his left leg; at times, he has to use his cane and walker. The patient denies any acute injury or trauma preceding the pain; however, last night he slipped and fell in his bedroom, which made it much worse.
Medical history is significant for hypertension and hyperlipidemia. The patient responded well to his previous back surgery. The emergency department clinician is concerned that his symptoms may be caused by a new lumbar stenosis at an adjacent level.
On exam, you note a mildly obese male who appears uncomfortable but is in no obvious distress. His vital signs are stable. He has some tenderness within his left hip. Distally, his strength is good, and there is no evidence of neurovascular compromise. Internal and external rotation causes some discomfort.
A portable pelvic radiograph is obtained (shown). What is your impression?
PASI responses with biologics similar among white, nonwhite individuals, study finds
MIAMI – Skin clearance rates among people with moderate to severe plaque psoriasis treated with brodalumab were superior to clearance rates among those treated with ustekinumab in a study that also provided comparisons between white and nonwhite patients.
In the study, presented in a poster at the 2018 Orlando Dermatology Aesthetic and Clinical Conference, there were no significant difference in overall efficacy, safety, or health-related quality of life outcomes between white and nonwhite patients treated with either biologic.
Additional analyses specific to patients with skin of color can be beneficial, Amy McMichael, MD, one of the investigators, said in an interview. “Patients with skin of color experience differences in psoriasis-related symptoms,” noted Dr. McMichael, chair of dermatology at Wake Forest Baptist Medical Center in Winston-Salem, N.C. “Greater degrees of skin involvement have been shown in African-American patients, as have differences in erythema, scaling, dyspigmentation, and plaque thickness.”
She and her colleagues evaluated 1,849 participants in phase 3 brodalumab clinical trials, which included ustekinumab-treated patients as a comparison group. Approximately 10% of the AMAGINE-2 and AMAGINE-3 study populations were skin of color participants. The results reported at the meeting were from their ad hoc study of 12-week induction findings from the 52-week clinical trials.
At week 12, 70% of white and 63% of nonwhite participants treated with ustekinumab achieved a Psoriasis Area and Severity Index (PASI) 75. At the same time, 86% of white and 88% of nonwhite patients treated with brodalumab achieved the same outcome. Similarly, PASI 90 and PASI 100 scores did not differ significantly between the 1,667 white and 182 skin of color participants.
The two biologics act on different aspects of the molecular pathway involved in psoriasis. Brodalumab (Siliq) specifically blocks the interleukin-17 receptor, whereas other biologics used to treat psoriasis, including ustekinumab (Stelara), an IL-12 and -23 antagonist, target upstream molecules in the inflammatory pathway. Dr. McMichael said, “The superior skin clearance rates seen in patients treated with brodalumab may be due to its target being a receptor as opposed to a ligand.”
Treatment-emergent adverse event rates were similar between the white and nonwhite patients. Treatment-emergent adverse events were reported in 58% and 57% of the white brodalumab and ustekinumab groups, respectively, and in 53% and 47% of the nonwhite brodalumab and ustekinumab groups, respectively. Serious adverse events occurred in 1.2% and 1.1% of the white brodalumab and ustekinumab cohorts, respectively, and in 1.7% and 0% of the nonwhite participants, respectively.
The investigators also assessed health-related quality of life and again found outcomes were similar between white and nonwhite participants. For example, among those treated with brodalumab, 80% of white and 78% of nonwhite patients achieved a score improvement of 5 or greater on the Dermatology Life Quality Index. Of those randomized to ustekinumab, 76% of white patients and 73% of nonwhite patients achieved the same outcome.
“We plan to perform a further analysis evaluating the Dr. McMichael said. Additionally, a population-based study to investigate treatment patterns in patients with psoriasis across racial and socioeconomic groups could also shed light on how patients with skin of color manage their psoriasis, she added.
Dr. McMichael’s disclosures include having been an investigator for Allergan, Incyte, and Samumed and a consultant to Aclaris, Galderma, IntraDerm, Johnson & Johnson, Merz, Pfizer, and Procter & Gamble.
SOURCE: McMichael A et al. ODAC 2018.
MIAMI – Skin clearance rates among people with moderate to severe plaque psoriasis treated with brodalumab were superior to clearance rates among those treated with ustekinumab in a study that also provided comparisons between white and nonwhite patients.
In the study, presented in a poster at the 2018 Orlando Dermatology Aesthetic and Clinical Conference, there were no significant difference in overall efficacy, safety, or health-related quality of life outcomes between white and nonwhite patients treated with either biologic.
Additional analyses specific to patients with skin of color can be beneficial, Amy McMichael, MD, one of the investigators, said in an interview. “Patients with skin of color experience differences in psoriasis-related symptoms,” noted Dr. McMichael, chair of dermatology at Wake Forest Baptist Medical Center in Winston-Salem, N.C. “Greater degrees of skin involvement have been shown in African-American patients, as have differences in erythema, scaling, dyspigmentation, and plaque thickness.”
She and her colleagues evaluated 1,849 participants in phase 3 brodalumab clinical trials, which included ustekinumab-treated patients as a comparison group. Approximately 10% of the AMAGINE-2 and AMAGINE-3 study populations were skin of color participants. The results reported at the meeting were from their ad hoc study of 12-week induction findings from the 52-week clinical trials.
At week 12, 70% of white and 63% of nonwhite participants treated with ustekinumab achieved a Psoriasis Area and Severity Index (PASI) 75. At the same time, 86% of white and 88% of nonwhite patients treated with brodalumab achieved the same outcome. Similarly, PASI 90 and PASI 100 scores did not differ significantly between the 1,667 white and 182 skin of color participants.
The two biologics act on different aspects of the molecular pathway involved in psoriasis. Brodalumab (Siliq) specifically blocks the interleukin-17 receptor, whereas other biologics used to treat psoriasis, including ustekinumab (Stelara), an IL-12 and -23 antagonist, target upstream molecules in the inflammatory pathway. Dr. McMichael said, “The superior skin clearance rates seen in patients treated with brodalumab may be due to its target being a receptor as opposed to a ligand.”
Treatment-emergent adverse event rates were similar between the white and nonwhite patients. Treatment-emergent adverse events were reported in 58% and 57% of the white brodalumab and ustekinumab groups, respectively, and in 53% and 47% of the nonwhite brodalumab and ustekinumab groups, respectively. Serious adverse events occurred in 1.2% and 1.1% of the white brodalumab and ustekinumab cohorts, respectively, and in 1.7% and 0% of the nonwhite participants, respectively.
The investigators also assessed health-related quality of life and again found outcomes were similar between white and nonwhite participants. For example, among those treated with brodalumab, 80% of white and 78% of nonwhite patients achieved a score improvement of 5 or greater on the Dermatology Life Quality Index. Of those randomized to ustekinumab, 76% of white patients and 73% of nonwhite patients achieved the same outcome.
“We plan to perform a further analysis evaluating the Dr. McMichael said. Additionally, a population-based study to investigate treatment patterns in patients with psoriasis across racial and socioeconomic groups could also shed light on how patients with skin of color manage their psoriasis, she added.
Dr. McMichael’s disclosures include having been an investigator for Allergan, Incyte, and Samumed and a consultant to Aclaris, Galderma, IntraDerm, Johnson & Johnson, Merz, Pfizer, and Procter & Gamble.
SOURCE: McMichael A et al. ODAC 2018.
MIAMI – Skin clearance rates among people with moderate to severe plaque psoriasis treated with brodalumab were superior to clearance rates among those treated with ustekinumab in a study that also provided comparisons between white and nonwhite patients.
In the study, presented in a poster at the 2018 Orlando Dermatology Aesthetic and Clinical Conference, there were no significant difference in overall efficacy, safety, or health-related quality of life outcomes between white and nonwhite patients treated with either biologic.
Additional analyses specific to patients with skin of color can be beneficial, Amy McMichael, MD, one of the investigators, said in an interview. “Patients with skin of color experience differences in psoriasis-related symptoms,” noted Dr. McMichael, chair of dermatology at Wake Forest Baptist Medical Center in Winston-Salem, N.C. “Greater degrees of skin involvement have been shown in African-American patients, as have differences in erythema, scaling, dyspigmentation, and plaque thickness.”
She and her colleagues evaluated 1,849 participants in phase 3 brodalumab clinical trials, which included ustekinumab-treated patients as a comparison group. Approximately 10% of the AMAGINE-2 and AMAGINE-3 study populations were skin of color participants. The results reported at the meeting were from their ad hoc study of 12-week induction findings from the 52-week clinical trials.
At week 12, 70% of white and 63% of nonwhite participants treated with ustekinumab achieved a Psoriasis Area and Severity Index (PASI) 75. At the same time, 86% of white and 88% of nonwhite patients treated with brodalumab achieved the same outcome. Similarly, PASI 90 and PASI 100 scores did not differ significantly between the 1,667 white and 182 skin of color participants.
The two biologics act on different aspects of the molecular pathway involved in psoriasis. Brodalumab (Siliq) specifically blocks the interleukin-17 receptor, whereas other biologics used to treat psoriasis, including ustekinumab (Stelara), an IL-12 and -23 antagonist, target upstream molecules in the inflammatory pathway. Dr. McMichael said, “The superior skin clearance rates seen in patients treated with brodalumab may be due to its target being a receptor as opposed to a ligand.”
Treatment-emergent adverse event rates were similar between the white and nonwhite patients. Treatment-emergent adverse events were reported in 58% and 57% of the white brodalumab and ustekinumab groups, respectively, and in 53% and 47% of the nonwhite brodalumab and ustekinumab groups, respectively. Serious adverse events occurred in 1.2% and 1.1% of the white brodalumab and ustekinumab cohorts, respectively, and in 1.7% and 0% of the nonwhite participants, respectively.
The investigators also assessed health-related quality of life and again found outcomes were similar between white and nonwhite participants. For example, among those treated with brodalumab, 80% of white and 78% of nonwhite patients achieved a score improvement of 5 or greater on the Dermatology Life Quality Index. Of those randomized to ustekinumab, 76% of white patients and 73% of nonwhite patients achieved the same outcome.
“We plan to perform a further analysis evaluating the Dr. McMichael said. Additionally, a population-based study to investigate treatment patterns in patients with psoriasis across racial and socioeconomic groups could also shed light on how patients with skin of color manage their psoriasis, she added.
Dr. McMichael’s disclosures include having been an investigator for Allergan, Incyte, and Samumed and a consultant to Aclaris, Galderma, IntraDerm, Johnson & Johnson, Merz, Pfizer, and Procter & Gamble.
SOURCE: McMichael A et al. ODAC 2018.
REPORTING FROM ODAC 2018
Key clinical point: Responses to brodalumab and ustekinumab were comparable in nonwhite and white patients with psoriasis.
Major finding: At week 12, 70% of white and 63% of nonwhite participants treated with ustekinumab achieved PASI 75, a nonsignificant difference.
Study details: An ad hoc comparison of week 12 phase 3 study data in 1,849 patients including 182 patients with skin of color.
Disclosures: Dr. McMichael’s disclosures include having been an investigator for Allergan, Incyte, and Samumed; and a consultant to Aclaris, Galderma, IntraDerm, Johnson & Johnson, Merz, Pfizer, and Procter & Gamble.
Source: McMichael A et al. ODAC 2018.
Is there a resilience deficit?
Even if you have never experienced a symptom of burnout, you probably have at least one colleague who has. In the last decade, collateral damage from physician burnout has earned it a place on the agenda of the American Academy of Pediatrics and most other physician organizations.
When one steps back and takes a longer view, burnout is simply a poor fit between physicians and their roles. An increasing number of physicians are finding themselves in jobs in which – for a variety of reasons – they feel uncomfortable. Eventually, the discomfort resulting from that poor fit becomes so unbearable the only solution is to change jobs or retire.
However, an article in Pediatrics entitled “Seeking professional resilience” addresses burnout from the perspective that physician vulnerability is a major contributor to the problem (Pediatrics. 2018, Feb 1. doi: 10.1542/peds.2017-2388). The author, Abby R. Rosenberg, MD, suggests that one solution to burnout is helping physicians learn how “to maintain physical and emotional well-being in the face of adversity,” that is, “resilience.”
It turns out that the recent buzz surrounding “resilience” has drawn a throng of theorists. I guess if we can have chaos theory, we can have resilience theories. Dr. Rosenberg sorts these theories into three categories based on whether they consider resilience an intrinsic trait, a process of adaptation, or an outcome. She offers an alternative description in which resilience is conceived as “a process of harnessing the resources we need to sustain well-being.” Dr. Rosenberg’s suggestions of how this harnessing process can be achieved are certainly worth reading, but I fear that most physicians threatened with burnout won’t have the time or the composure to follow her recommendations. Fifty years of watching physicians both thrive and flame out has convinced me that in most cases, resilience is an intrinsic trait gifted to the recipient at birth.
I am sure there are older physicians who believe that burnout is just another case of “they-don’t-make-’em-like-they-used-to” and would claim that young physicians just don’t have the same grit that we had a generation ago. I guess it is possible that the shift away from the owner/operator model toward one in which a physician has become a cog in the wheel of a large corporation has selected for physicians who are less resilient by nature. But I suspect that the number of resilient physicians is unchanged over the last hundred years. It is more likely that even those blessed with a resilient nature enter their training challenged by a burden of debt significantly greater than my peers and I faced 50 years ago.
The problem isn’t the resiliency deficit. Burnout is the result of a job that has evolved into one with challenges that even the more resilient physicians struggle to tolerate. Under a litigious cloud, hunched over a computer for half the day, the modern physician must struggle to find relevance in a situation in which he has relinquished control to a system that may not share his values.
Refining the selection process to find even more resilient candidates for medical school might lower the burnout rate by a point or two. However, the real answer requires a major overhaul of medical delivery system so that providers can once again feel that every hour they invest is meaningful. The privilege to practice medicine always has required sacrifices on the part of the physician. However, without a sense of purpose, these sacrifices can become intolerable.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@frontlinemedcom.com.
Even if you have never experienced a symptom of burnout, you probably have at least one colleague who has. In the last decade, collateral damage from physician burnout has earned it a place on the agenda of the American Academy of Pediatrics and most other physician organizations.
When one steps back and takes a longer view, burnout is simply a poor fit between physicians and their roles. An increasing number of physicians are finding themselves in jobs in which – for a variety of reasons – they feel uncomfortable. Eventually, the discomfort resulting from that poor fit becomes so unbearable the only solution is to change jobs or retire.
However, an article in Pediatrics entitled “Seeking professional resilience” addresses burnout from the perspective that physician vulnerability is a major contributor to the problem (Pediatrics. 2018, Feb 1. doi: 10.1542/peds.2017-2388). The author, Abby R. Rosenberg, MD, suggests that one solution to burnout is helping physicians learn how “to maintain physical and emotional well-being in the face of adversity,” that is, “resilience.”
It turns out that the recent buzz surrounding “resilience” has drawn a throng of theorists. I guess if we can have chaos theory, we can have resilience theories. Dr. Rosenberg sorts these theories into three categories based on whether they consider resilience an intrinsic trait, a process of adaptation, or an outcome. She offers an alternative description in which resilience is conceived as “a process of harnessing the resources we need to sustain well-being.” Dr. Rosenberg’s suggestions of how this harnessing process can be achieved are certainly worth reading, but I fear that most physicians threatened with burnout won’t have the time or the composure to follow her recommendations. Fifty years of watching physicians both thrive and flame out has convinced me that in most cases, resilience is an intrinsic trait gifted to the recipient at birth.
I am sure there are older physicians who believe that burnout is just another case of “they-don’t-make-’em-like-they-used-to” and would claim that young physicians just don’t have the same grit that we had a generation ago. I guess it is possible that the shift away from the owner/operator model toward one in which a physician has become a cog in the wheel of a large corporation has selected for physicians who are less resilient by nature. But I suspect that the number of resilient physicians is unchanged over the last hundred years. It is more likely that even those blessed with a resilient nature enter their training challenged by a burden of debt significantly greater than my peers and I faced 50 years ago.
The problem isn’t the resiliency deficit. Burnout is the result of a job that has evolved into one with challenges that even the more resilient physicians struggle to tolerate. Under a litigious cloud, hunched over a computer for half the day, the modern physician must struggle to find relevance in a situation in which he has relinquished control to a system that may not share his values.
Refining the selection process to find even more resilient candidates for medical school might lower the burnout rate by a point or two. However, the real answer requires a major overhaul of medical delivery system so that providers can once again feel that every hour they invest is meaningful. The privilege to practice medicine always has required sacrifices on the part of the physician. However, without a sense of purpose, these sacrifices can become intolerable.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@frontlinemedcom.com.
Even if you have never experienced a symptom of burnout, you probably have at least one colleague who has. In the last decade, collateral damage from physician burnout has earned it a place on the agenda of the American Academy of Pediatrics and most other physician organizations.
When one steps back and takes a longer view, burnout is simply a poor fit between physicians and their roles. An increasing number of physicians are finding themselves in jobs in which – for a variety of reasons – they feel uncomfortable. Eventually, the discomfort resulting from that poor fit becomes so unbearable the only solution is to change jobs or retire.
However, an article in Pediatrics entitled “Seeking professional resilience” addresses burnout from the perspective that physician vulnerability is a major contributor to the problem (Pediatrics. 2018, Feb 1. doi: 10.1542/peds.2017-2388). The author, Abby R. Rosenberg, MD, suggests that one solution to burnout is helping physicians learn how “to maintain physical and emotional well-being in the face of adversity,” that is, “resilience.”
It turns out that the recent buzz surrounding “resilience” has drawn a throng of theorists. I guess if we can have chaos theory, we can have resilience theories. Dr. Rosenberg sorts these theories into three categories based on whether they consider resilience an intrinsic trait, a process of adaptation, or an outcome. She offers an alternative description in which resilience is conceived as “a process of harnessing the resources we need to sustain well-being.” Dr. Rosenberg’s suggestions of how this harnessing process can be achieved are certainly worth reading, but I fear that most physicians threatened with burnout won’t have the time or the composure to follow her recommendations. Fifty years of watching physicians both thrive and flame out has convinced me that in most cases, resilience is an intrinsic trait gifted to the recipient at birth.
I am sure there are older physicians who believe that burnout is just another case of “they-don’t-make-’em-like-they-used-to” and would claim that young physicians just don’t have the same grit that we had a generation ago. I guess it is possible that the shift away from the owner/operator model toward one in which a physician has become a cog in the wheel of a large corporation has selected for physicians who are less resilient by nature. But I suspect that the number of resilient physicians is unchanged over the last hundred years. It is more likely that even those blessed with a resilient nature enter their training challenged by a burden of debt significantly greater than my peers and I faced 50 years ago.
The problem isn’t the resiliency deficit. Burnout is the result of a job that has evolved into one with challenges that even the more resilient physicians struggle to tolerate. Under a litigious cloud, hunched over a computer for half the day, the modern physician must struggle to find relevance in a situation in which he has relinquished control to a system that may not share his values.
Refining the selection process to find even more resilient candidates for medical school might lower the burnout rate by a point or two. However, the real answer requires a major overhaul of medical delivery system so that providers can once again feel that every hour they invest is meaningful. The privilege to practice medicine always has required sacrifices on the part of the physician. However, without a sense of purpose, these sacrifices can become intolerable.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@frontlinemedcom.com.