BERLIN – Spinal cord volume deficits in patients with multiple sclerosis may contribute to clinical disability that appears out of proportion to lesion load on brain imaging, according to new research.

Kari Oakes/MDedge News

In a pool of 362 patients with mild to moderate MS-related disability but identical white matter lesion load identified by MRI, those with higher disability had significantly lower spinal cord volumes when compared against those with disability scores in the mild range (P less than .001).

Though brain MRI is a key tool used to track disease severity and progression in MS, some patients have relatively high disability but a low burden of white matter intracerebral lesions on MRI. Little is known about spinal cord volume in MS patients with pronounced dissociation between intracerebral lesion load and disability, Michaela Andelova, MD, said in an interview during a poster session at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Dr. Andelova, of Charles University, Prague, said that she and her colleagues hypothesized that spinal cord volume would differ between patients who had varying levels of disability, despite identical white matter lesion load.

To test this, she and her colleagues looked at records of 1,245 patients with relapsing-remitting MS. They divided them into three groups by severity of clinical disability, and also by extent of cerebral T2 hyperintense lesion load. The investigators identified a group of patients (n = 53) whose total volume of T2-weighted hyperintense lesions was less than 3 mL, but whose Expanded Disability Status Scale (EDSS) scores were at least 3.5; this was the low lesion load/high disability (LLHD) group.

Dr. Andelova and her colleagues then identified another group of patients (n = 71) who had a volume of T2-weighted hyperintensities that was greater than 9 mL, but whose EDSS score was less than 1.5. This was the high lesion load/low disability (HLLD) group.

The remaining patients (n = 1,121), who did not have these paradoxical associations, were analyzed separately.

For all patients, mean upper cervical cord area (MUCCA) was also measured. Using images acquired by a 3 T MRI scanner, MUCCA was calculated as the mean sum of spinal cord area in 21 slices centered at the C3/4 intervertebral disk, using an in-house, semiautomated method.

“Despite higher disability, LLHD patients demonstrated significantly higher normalized total brain volume, higher normalized volumes of thalamus and callosum, and smaller lateral ventricles than [the] HLLD group,” wrote Dr. Andelova and her collaborators.

However, the LLHD patients had MUCCA values that were significantly lower than the other groups: The nonparadoxical group’s mean MUCCA was 84.02 mm², while the HLLD group had a mean MUCCA of 85.75 mm². This difference was not statistically significant. By contrast, the LLHD group’s mean MUCCA was significantly smaller, at 80.40 mm² (P = .023 versus nonparadoxical patients, and P = .007 versus HLLD patients).

Looking at the data another way, Dr. Andelova and her colleagues compared 362 evenly divided patients with moderate disability (EDSS 3.5-6.5) with matched patients who had mild MS-related disability (EDSS less than 3) and identical cerebral lesion loads. They found that MUCCA was significantly smaller in the moderate disability group (78.86 versus 84.44 mm²; P less than .001).

In addition to having identical lesions loads, the mild and moderate disability groups didn’t differ significantly in normalized total brain volume or regional brain volumes. The group with moderate disability did have slightly less white matter volume (P = .039), Dr. Andelova pointed out.

All differences found between groups retained statistical significance even after adjustment for such potential confounders as age, sex, and duration of disease, Dr. Andelova said.

“Reduced spinal cord volume may explain part of the clinical-radiological paradox in patients who have high disability despite low intracranial lesion load,” Dr. Andelova and her collaborators wrote. “In line with this finding, relatively preserved spinal cord volume may be associated with functional reserve and less physical disability in patients with low disability despite high cerebral lesion load.”

Further work looking more precisely at cerebral lesion distribution and quantitative MRI investigation of lesion distribution is in the works for Dr. Andelova and her collaborators. They are hoping to see some association between various distribution patterns and accelerated spinal atrophy.

The research was supported by the Czech government. Dr. Andelova and several of her collaborators reported financial relationships with pharmaceutical companies.

[email protected]

SOURCE: Andelova M et al. Mult Scler. 2018;24(Suppl 2):211, Abstract P477.

BERLIN – Spinal cord volume deficits in patients with multiple sclerosis may contribute to clinical disability that appears out of proportion to lesion load on brain imaging, according to new research.

Kari Oakes/MDedge News

In a pool of 362 patients with mild to moderate MS-related disability but identical white matter lesion load identified by MRI, those with higher disability had significantly lower spinal cord volumes when compared against those with disability scores in the mild range (P less than .001).

Though brain MRI is a key tool used to track disease severity and progression in MS, some patients have relatively high disability but a low burden of white matter intracerebral lesions on MRI. Little is known about spinal cord volume in MS patients with pronounced dissociation between intracerebral lesion load and disability, Michaela Andelova, MD, said in an interview during a poster session at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Dr. Andelova, of Charles University, Prague, said that she and her colleagues hypothesized that spinal cord volume would differ between patients who had varying levels of disability, despite identical white matter lesion load.

To test this, she and her colleagues looked at records of 1,245 patients with relapsing-remitting MS. They divided them into three groups by severity of clinical disability, and also by extent of cerebral T2 hyperintense lesion load. The investigators identified a group of patients (n = 53) whose total volume of T2-weighted hyperintense lesions was less than 3 mL, but whose Expanded Disability Status Scale (EDSS) scores were at least 3.5; this was the low lesion load/high disability (LLHD) group.

Dr. Andelova and her colleagues then identified another group of patients (n = 71) who had a volume of T2-weighted hyperintensities that was greater than 9 mL, but whose EDSS score was less than 1.5. This was the high lesion load/low disability (HLLD) group.

The remaining patients (n = 1,121), who did not have these paradoxical associations, were analyzed separately.

For all patients, mean upper cervical cord area (MUCCA) was also measured. Using images acquired by a 3 T MRI scanner, MUCCA was calculated as the mean sum of spinal cord area in 21 slices centered at the C3/4 intervertebral disk, using an in-house, semiautomated method.

“Despite higher disability, LLHD patients demonstrated significantly higher normalized total brain volume, higher normalized volumes of thalamus and callosum, and smaller lateral ventricles than [the] HLLD group,” wrote Dr. Andelova and her collaborators.

However, the LLHD patients had MUCCA values that were significantly lower than the other groups: The nonparadoxical group’s mean MUCCA was 84.02 mm², while the HLLD group had a mean MUCCA of 85.75 mm². This difference was not statistically significant. By contrast, the LLHD group’s mean MUCCA was significantly smaller, at 80.40 mm² (P = .023 versus nonparadoxical patients, and P = .007 versus HLLD patients).

Looking at the data another way, Dr. Andelova and her colleagues compared 362 evenly divided patients with moderate disability (EDSS 3.5-6.5) with matched patients who had mild MS-related disability (EDSS less than 3) and identical cerebral lesion loads. They found that MUCCA was significantly smaller in the moderate disability group (78.86 versus 84.44 mm²; P less than .001).

In addition to having identical lesions loads, the mild and moderate disability groups didn’t differ significantly in normalized total brain volume or regional brain volumes. The group with moderate disability did have slightly less white matter volume (P = .039), Dr. Andelova pointed out.

All differences found between groups retained statistical significance even after adjustment for such potential confounders as age, sex, and duration of disease, Dr. Andelova said.

“Reduced spinal cord volume may explain part of the clinical-radiological paradox in patients who have high disability despite low intracranial lesion load,” Dr. Andelova and her collaborators wrote. “In line with this finding, relatively preserved spinal cord volume may be associated with functional reserve and less physical disability in patients with low disability despite high cerebral lesion load.”

Further work looking more precisely at cerebral lesion distribution and quantitative MRI investigation of lesion distribution is in the works for Dr. Andelova and her collaborators. They are hoping to see some association between various distribution patterns and accelerated spinal atrophy.

The research was supported by the Czech government. Dr. Andelova and several of her collaborators reported financial relationships with pharmaceutical companies.

[email protected]

SOURCE: Andelova M et al. Mult Scler. 2018;24(Suppl 2):211, Abstract P477.

BERLIN – Spinal cord volume deficits in patients with multiple sclerosis may contribute to clinical disability that appears out of proportion to lesion load on brain imaging, according to new research.

Kari Oakes/MDedge News

In a pool of 362 patients with mild to moderate MS-related disability but identical white matter lesion load identified by MRI, those with higher disability had significantly lower spinal cord volumes when compared against those with disability scores in the mild range (P less than .001).

Though brain MRI is a key tool used to track disease severity and progression in MS, some patients have relatively high disability but a low burden of white matter intracerebral lesions on MRI. Little is known about spinal cord volume in MS patients with pronounced dissociation between intracerebral lesion load and disability, Michaela Andelova, MD, said in an interview during a poster session at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Dr. Andelova, of Charles University, Prague, said that she and her colleagues hypothesized that spinal cord volume would differ between patients who had varying levels of disability, despite identical white matter lesion load.

To test this, she and her colleagues looked at records of 1,245 patients with relapsing-remitting MS. They divided them into three groups by severity of clinical disability, and also by extent of cerebral T2 hyperintense lesion load. The investigators identified a group of patients (n = 53) whose total volume of T2-weighted hyperintense lesions was less than 3 mL, but whose Expanded Disability Status Scale (EDSS) scores were at least 3.5; this was the low lesion load/high disability (LLHD) group.

Dr. Andelova and her colleagues then identified another group of patients (n = 71) who had a volume of T2-weighted hyperintensities that was greater than 9 mL, but whose EDSS score was less than 1.5. This was the high lesion load/low disability (HLLD) group.

The remaining patients (n = 1,121), who did not have these paradoxical associations, were analyzed separately.

For all patients, mean upper cervical cord area (MUCCA) was also measured. Using images acquired by a 3 T MRI scanner, MUCCA was calculated as the mean sum of spinal cord area in 21 slices centered at the C3/4 intervertebral disk, using an in-house, semiautomated method.

“Despite higher disability, LLHD patients demonstrated significantly higher normalized total brain volume, higher normalized volumes of thalamus and callosum, and smaller lateral ventricles than [the] HLLD group,” wrote Dr. Andelova and her collaborators.

However, the LLHD patients had MUCCA values that were significantly lower than the other groups: The nonparadoxical group’s mean MUCCA was 84.02 mm², while the HLLD group had a mean MUCCA of 85.75 mm². This difference was not statistically significant. By contrast, the LLHD group’s mean MUCCA was significantly smaller, at 80.40 mm² (P = .023 versus nonparadoxical patients, and P = .007 versus HLLD patients).

Looking at the data another way, Dr. Andelova and her colleagues compared 362 evenly divided patients with moderate disability (EDSS 3.5-6.5) with matched patients who had mild MS-related disability (EDSS less than 3) and identical cerebral lesion loads. They found that MUCCA was significantly smaller in the moderate disability group (78.86 versus 84.44 mm²; P less than .001).

In addition to having identical lesions loads, the mild and moderate disability groups didn’t differ significantly in normalized total brain volume or regional brain volumes. The group with moderate disability did have slightly less white matter volume (P = .039), Dr. Andelova pointed out.

All differences found between groups retained statistical significance even after adjustment for such potential confounders as age, sex, and duration of disease, Dr. Andelova said.

“Reduced spinal cord volume may explain part of the clinical-radiological paradox in patients who have high disability despite low intracranial lesion load,” Dr. Andelova and her collaborators wrote. “In line with this finding, relatively preserved spinal cord volume may be associated with functional reserve and less physical disability in patients with low disability despite high cerebral lesion load.”

Further work looking more precisely at cerebral lesion distribution and quantitative MRI investigation of lesion distribution is in the works for Dr. Andelova and her collaborators. They are hoping to see some association between various distribution patterns and accelerated spinal atrophy.

The research was supported by the Czech government. Dr. Andelova and several of her collaborators reported financial relationships with pharmaceutical companies.

[email protected]

SOURCE: Andelova M et al. Mult Scler. 2018;24(Suppl 2):211, Abstract P477.

The Food and Drug Administration has approved ID CORE XT, a molecular-based assay that uses DNA to test for non-ABO red blood cell types for use in transfusion.

It’s the second molecular test for blood compatibility but the first to report genotype in its results, according to an announcement from the agency.

The test is important because it evaluates patients – especially those who receive repeated blood transfusions for conditions such as sickle cell anemia – for non-ABO antigens, but it does so without using antisera, which is sometimes unavailable.

A study found comparable performance between the ID CORE XT, licensed serologic reagents, and DNA sequencing tests, according to the FDA.

The ID CORE XT test is marketed by Progenika Biopharma, a Grifols company.

More information can be found in the full FDA press announcement.

[email protected]

The Food and Drug Administration has approved ID CORE XT, a molecular-based assay that uses DNA to test for non-ABO red blood cell types for use in transfusion.

It’s the second molecular test for blood compatibility but the first to report genotype in its results, according to an announcement from the agency.

The test is important because it evaluates patients – especially those who receive repeated blood transfusions for conditions such as sickle cell anemia – for non-ABO antigens, but it does so without using antisera, which is sometimes unavailable.

A study found comparable performance between the ID CORE XT, licensed serologic reagents, and DNA sequencing tests, according to the FDA.

The ID CORE XT test is marketed by Progenika Biopharma, a Grifols company.

More information can be found in the full FDA press announcement.

[email protected]

The Food and Drug Administration has approved ID CORE XT, a molecular-based assay that uses DNA to test for non-ABO red blood cell types for use in transfusion.

It’s the second molecular test for blood compatibility but the first to report genotype in its results, according to an announcement from the agency.

The test is important because it evaluates patients – especially those who receive repeated blood transfusions for conditions such as sickle cell anemia – for non-ABO antigens, but it does so without using antisera, which is sometimes unavailable.

A study found comparable performance between the ID CORE XT, licensed serologic reagents, and DNA sequencing tests, according to the FDA.

The ID CORE XT test is marketed by Progenika Biopharma, a Grifols company.

More information can be found in the full FDA press announcement.

[email protected]

BERLIN – Children with acute disseminated encephalomyelitis have a significantly increased risk of subsequent epilepsy when it occurs with oligoclonal bands in cerebrospinal fluid and seizures at presentation, Thomas Rossor, MD, reported at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Michele G. Sullivan/MDedge News

But fortunately, the seizures of postacute disseminated encephalomyelitis (post-ADEM) epilepsy are relatively easy to control and not clinically devastating, said Dr. Rossor of Great Ormond Street Hospital, London.

Of the 12 who developed epilepsy in Dr. Rossor’s retrospective, multicenter review of 74 children with ADEM, 11 were well controlled on one drug and 1 on two drugs.

Pediatric ADEM is usually monophasic with good clinical outcome, he said. But a benign course is not set in stone: Up to 40% of children experience seizures during the acute presentation. “In contrast,” Dr. Rossor said, “adult patients with relapsing-remitting multiple sclerosis have the same risk of developing epilepsy as the general population.” Among adults with cortical encephalitis, antibodies against myelin oligodendrocyte glycoprotein (MOG) have been associated with seizures and the need for antiepileptic medications, he added.

That finding was part of what spurred Dr. Rossor’s study, which aimed to identify predictors of relapse and post-ADEM epilepsy in children. The patients in the review had a median age of 4.5 years. All were tested for anti-MOG antibodies, and most (about 68%) were positive. Oligoclonal bands in cerebrospinal fluid (CSF) occurred in 22%. The median follow-up period was 5 years.

A total of 41% (n = 31) relapsed after the initial acute phase. Among these, the final diagnosis included multiphasic disseminated encephalomyelitis (n = 19); ADEM-optic neuritis (n = 3); and neuromyelitis optica spectrum disorder (n = 6).

Of the 74 patients, 16 (22%) had seizures during the acute phase, and 12 (16%) developed post-ADEM epilepsy at a median of 3 months. The most common clinical characteristics with post-ADEM epilepsy included oligoclonal bands (57% vs. 13%), anti-MOG antibodies (92% vs. 16%), and seizures at presentation (50% vs. 16%). When these were entered into a regression model, oligoclonal bands and initial seizures significantly predicted epilepsy, increasing the risk by 20.7 and 13.5 times, respectively.

Since relapse is known to be associated with post-ADEM epilepsy, Dr. Rossor first looked at relapse risk. He conducted a multivariate analysis that included several clinical characteristics: age, prodrome, increased CSF white cells and protein, oligoclonal bands, anti-MOG antibodies, and seizures both at presentation and after the acute phase.

Anti-MOG antibodies were significantly more common among the relapsed patients than among the monophasic patients (87% vs. 53%). Seizures at presentation also were more common among the relapsed patients (32% vs. 14%). These two factors were entered into a binary regression analysis; only anti-MOG antibodies remained significantly associated with relapse, increasing the risk fivefold (odds ratio = 5.4; P = .007).

Anti-MOG antibodies also were associated with both earlier and more relapses. Overall, 40% of anti–MOG-antibody–positive patients relapsed by 24 months. In contrast, only 20% of anti–MOG-antibody–negative patients had relapsed by 24 months, and this number remained steady throughout the follow-up period.

By 96 months, almost all the anti–MOG-antibody–positive patients had relapsed, and some experienced many relapses. “In the antibody-negative group, four patients did relapse, but they had relatively few relapses. In the antibody-positive group, some had relatively few relapses, but several had 15, 20, or 25 clinical relapses in the follow-up period,” he said.

Dr. Rossor and his coauthors had no financial disclosures.

[email protected]

SOURCE: Rossor T et al. Mult Scler. 2018;24(Suppl 2):27. Abstract 62.

BERLIN – Children with acute disseminated encephalomyelitis have a significantly increased risk of subsequent epilepsy when it occurs with oligoclonal bands in cerebrospinal fluid and seizures at presentation, Thomas Rossor, MD, reported at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Michele G. Sullivan/MDedge News

But fortunately, the seizures of postacute disseminated encephalomyelitis (post-ADEM) epilepsy are relatively easy to control and not clinically devastating, said Dr. Rossor of Great Ormond Street Hospital, London.

Of the 12 who developed epilepsy in Dr. Rossor’s retrospective, multicenter review of 74 children with ADEM, 11 were well controlled on one drug and 1 on two drugs.

Pediatric ADEM is usually monophasic with good clinical outcome, he said. But a benign course is not set in stone: Up to 40% of children experience seizures during the acute presentation. “In contrast,” Dr. Rossor said, “adult patients with relapsing-remitting multiple sclerosis have the same risk of developing epilepsy as the general population.” Among adults with cortical encephalitis, antibodies against myelin oligodendrocyte glycoprotein (MOG) have been associated with seizures and the need for antiepileptic medications, he added.

That finding was part of what spurred Dr. Rossor’s study, which aimed to identify predictors of relapse and post-ADEM epilepsy in children. The patients in the review had a median age of 4.5 years. All were tested for anti-MOG antibodies, and most (about 68%) were positive. Oligoclonal bands in cerebrospinal fluid (CSF) occurred in 22%. The median follow-up period was 5 years.

A total of 41% (n = 31) relapsed after the initial acute phase. Among these, the final diagnosis included multiphasic disseminated encephalomyelitis (n = 19); ADEM-optic neuritis (n = 3); and neuromyelitis optica spectrum disorder (n = 6).

Of the 74 patients, 16 (22%) had seizures during the acute phase, and 12 (16%) developed post-ADEM epilepsy at a median of 3 months. The most common clinical characteristics with post-ADEM epilepsy included oligoclonal bands (57% vs. 13%), anti-MOG antibodies (92% vs. 16%), and seizures at presentation (50% vs. 16%). When these were entered into a regression model, oligoclonal bands and initial seizures significantly predicted epilepsy, increasing the risk by 20.7 and 13.5 times, respectively.

Since relapse is known to be associated with post-ADEM epilepsy, Dr. Rossor first looked at relapse risk. He conducted a multivariate analysis that included several clinical characteristics: age, prodrome, increased CSF white cells and protein, oligoclonal bands, anti-MOG antibodies, and seizures both at presentation and after the acute phase.

Anti-MOG antibodies were significantly more common among the relapsed patients than among the monophasic patients (87% vs. 53%). Seizures at presentation also were more common among the relapsed patients (32% vs. 14%). These two factors were entered into a binary regression analysis; only anti-MOG antibodies remained significantly associated with relapse, increasing the risk fivefold (odds ratio = 5.4; P = .007).

Anti-MOG antibodies also were associated with both earlier and more relapses. Overall, 40% of anti–MOG-antibody–positive patients relapsed by 24 months. In contrast, only 20% of anti–MOG-antibody–negative patients had relapsed by 24 months, and this number remained steady throughout the follow-up period.

By 96 months, almost all the anti–MOG-antibody–positive patients had relapsed, and some experienced many relapses. “In the antibody-negative group, four patients did relapse, but they had relatively few relapses. In the antibody-positive group, some had relatively few relapses, but several had 15, 20, or 25 clinical relapses in the follow-up period,” he said.

Dr. Rossor and his coauthors had no financial disclosures.

[email protected]

SOURCE: Rossor T et al. Mult Scler. 2018;24(Suppl 2):27. Abstract 62.

BERLIN – Children with acute disseminated encephalomyelitis have a significantly increased risk of subsequent epilepsy when it occurs with oligoclonal bands in cerebrospinal fluid and seizures at presentation, Thomas Rossor, MD, reported at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Michele G. Sullivan/MDedge News

But fortunately, the seizures of postacute disseminated encephalomyelitis (post-ADEM) epilepsy are relatively easy to control and not clinically devastating, said Dr. Rossor of Great Ormond Street Hospital, London.

Of the 12 who developed epilepsy in Dr. Rossor’s retrospective, multicenter review of 74 children with ADEM, 11 were well controlled on one drug and 1 on two drugs.

Pediatric ADEM is usually monophasic with good clinical outcome, he said. But a benign course is not set in stone: Up to 40% of children experience seizures during the acute presentation. “In contrast,” Dr. Rossor said, “adult patients with relapsing-remitting multiple sclerosis have the same risk of developing epilepsy as the general population.” Among adults with cortical encephalitis, antibodies against myelin oligodendrocyte glycoprotein (MOG) have been associated with seizures and the need for antiepileptic medications, he added.

That finding was part of what spurred Dr. Rossor’s study, which aimed to identify predictors of relapse and post-ADEM epilepsy in children. The patients in the review had a median age of 4.5 years. All were tested for anti-MOG antibodies, and most (about 68%) were positive. Oligoclonal bands in cerebrospinal fluid (CSF) occurred in 22%. The median follow-up period was 5 years.

A total of 41% (n = 31) relapsed after the initial acute phase. Among these, the final diagnosis included multiphasic disseminated encephalomyelitis (n = 19); ADEM-optic neuritis (n = 3); and neuromyelitis optica spectrum disorder (n = 6).

Of the 74 patients, 16 (22%) had seizures during the acute phase, and 12 (16%) developed post-ADEM epilepsy at a median of 3 months. The most common clinical characteristics with post-ADEM epilepsy included oligoclonal bands (57% vs. 13%), anti-MOG antibodies (92% vs. 16%), and seizures at presentation (50% vs. 16%). When these were entered into a regression model, oligoclonal bands and initial seizures significantly predicted epilepsy, increasing the risk by 20.7 and 13.5 times, respectively.

Since relapse is known to be associated with post-ADEM epilepsy, Dr. Rossor first looked at relapse risk. He conducted a multivariate analysis that included several clinical characteristics: age, prodrome, increased CSF white cells and protein, oligoclonal bands, anti-MOG antibodies, and seizures both at presentation and after the acute phase.

Anti-MOG antibodies were significantly more common among the relapsed patients than among the monophasic patients (87% vs. 53%). Seizures at presentation also were more common among the relapsed patients (32% vs. 14%). These two factors were entered into a binary regression analysis; only anti-MOG antibodies remained significantly associated with relapse, increasing the risk fivefold (odds ratio = 5.4; P = .007).

Anti-MOG antibodies also were associated with both earlier and more relapses. Overall, 40% of anti–MOG-antibody–positive patients relapsed by 24 months. In contrast, only 20% of anti–MOG-antibody–negative patients had relapsed by 24 months, and this number remained steady throughout the follow-up period.

By 96 months, almost all the anti–MOG-antibody–positive patients had relapsed, and some experienced many relapses. “In the antibody-negative group, four patients did relapse, but they had relatively few relapses. In the antibody-positive group, some had relatively few relapses, but several had 15, 20, or 25 clinical relapses in the follow-up period,” he said.

Dr. Rossor and his coauthors had no financial disclosures.

[email protected]

SOURCE: Rossor T et al. Mult Scler. 2018;24(Suppl 2):27. Abstract 62.

A comparison of the genomic landscapes of both primary and metastatic clear cell renal cell carcinoma (ccRCC) found no significant differences in gene expression or mutational burden between the disease states, suggesting that there is no single genetic driver of metastases, investigators reported.

An analysis of targeted next-generation sequencing of both primary tumors and metastases in two independent patient cohorts showed that only the gene encoding for the tumor suppressor TP53 was significantly more frequently mutated in metastases, compared with primary tumors, but this finding did not pass a false positive test (false discovery rate), noted Toni K. Choueiri, MD, from the Dana-Farber Cancer Institute in Boston, and his colleagues, in the British Journal of Cancer.

“No other gene had significant difference in the cohort frequency of mutations between the metastases and primary tumors. Mutation burden was not significantly different between the metastases and primary tumors or between metastatic sites,” they wrote.

Frequently mutated genes in ccRCC include VHL, the gene encoding for von Hippel–Lindau syndrome, as well as tumor suppressor genes such as PBRM1, SEDT2, BAP1 and KDM5C, but few mutations are clinically actionable, the investigators noted. “However, the value of genomic alterations will be determined by understanding the interactions between acquired genetic alterations, treatments received, heterogeneity, and the dynamics of mutations during evolution of disease.”

To see whether they could improve understanding of the genomic differences between primary and metastatic ccRCC and potentially develop personalized therapies, the investigators studied targeted next-generation sequencing data from two separate cohorts.

The first cohort included data on 349 ccRCC primary tumors and 229 unmatched cases of metastatic ccRCC from the Foundation Medicine database. The second, a validation cohort, included data on 177 ccRCC primary tumors and 80 metastases from patients treated at Dana-Farber. In each cohort, sequencing was performed on 275 genes and intronic regions in 30 genes for a total of 282 unique genes.

In cohort 1, which included tumor samples from 417 men and 169 women with a median age of 58 years, the frequency of mutations was similar in primary tumors and metastases. As noted before, mutations in TP53 were significantly more frequent in metastases than in primary tumors, detected in 14.85% versus 8.90% of samples, respectively (P = .031). This difference did not, however, pass the false discovery rate test (q = 0.21). Two other tumor suppressor genes, PBRM1 and KDM5C, were numerically but not significantly more frequent in metastases.

There were no differences in median tumor mutational burden between primary and metastatic samples and no difference in either mutations or mutational burden across different metastatic sites.

In cohort 2 there were no significantly different mutational frequencies between primary and metastatic samples for any gene and no differences in median tumor mutational burden.

An analysis comparing the frequency of gene mutations in primary tumors of patients in this cohort who went on to develop metastatic disease versus those of patients with only localized disease showed that, after a median follow-up of 21.9 months, there were no significant differences in either mutational frequency or tumor mutational burden.

“It is currently unknown if cohortwide genomic alterations in RCC metastases have a different genomic profile, including potential actionable mutations, compared to samples derived from the primary site. To our knowledge, our analysis is the largest genomic ccRCC study that compares cohortwide mutational differences between metastases and primary tumors,” the investigators wrote.

They acknowledged that because they did not match primary tumors with metastatic tumors in the same patients they were unable to evaluate how individual tumors evolve over time or how systemic therapies may alter the tumor genomic landscape.

Dr. Choueri is supported in part by the Dana-Farber/Harvard Cancer Center Kidney SPORE, the Kohlberg Chair at Harvard Medical School and the Trust Family, Michael Brigham, and Loker Pinard Funds for Kidney Cancer Research at the Dana-Farber Cancer Institute. Six of the study’s coauthors are employed by Foundation Medicine. The remaining authors declared no competing interests.

SOURCE: Choueiri TK et al. Br J Cancer. 2018 May;118(9):1238-42.

A comparison of the genomic landscapes of both primary and metastatic clear cell renal cell carcinoma (ccRCC) found no significant differences in gene expression or mutational burden between the disease states, suggesting that there is no single genetic driver of metastases, investigators reported.

An analysis of targeted next-generation sequencing of both primary tumors and metastases in two independent patient cohorts showed that only the gene encoding for the tumor suppressor TP53 was significantly more frequently mutated in metastases, compared with primary tumors, but this finding did not pass a false positive test (false discovery rate), noted Toni K. Choueiri, MD, from the Dana-Farber Cancer Institute in Boston, and his colleagues, in the British Journal of Cancer.

“No other gene had significant difference in the cohort frequency of mutations between the metastases and primary tumors. Mutation burden was not significantly different between the metastases and primary tumors or between metastatic sites,” they wrote.

Frequently mutated genes in ccRCC include VHL, the gene encoding for von Hippel–Lindau syndrome, as well as tumor suppressor genes such as PBRM1, SEDT2, BAP1 and KDM5C, but few mutations are clinically actionable, the investigators noted. “However, the value of genomic alterations will be determined by understanding the interactions between acquired genetic alterations, treatments received, heterogeneity, and the dynamics of mutations during evolution of disease.”

To see whether they could improve understanding of the genomic differences between primary and metastatic ccRCC and potentially develop personalized therapies, the investigators studied targeted next-generation sequencing data from two separate cohorts.

The first cohort included data on 349 ccRCC primary tumors and 229 unmatched cases of metastatic ccRCC from the Foundation Medicine database. The second, a validation cohort, included data on 177 ccRCC primary tumors and 80 metastases from patients treated at Dana-Farber. In each cohort, sequencing was performed on 275 genes and intronic regions in 30 genes for a total of 282 unique genes.

In cohort 1, which included tumor samples from 417 men and 169 women with a median age of 58 years, the frequency of mutations was similar in primary tumors and metastases. As noted before, mutations in TP53 were significantly more frequent in metastases than in primary tumors, detected in 14.85% versus 8.90% of samples, respectively (P = .031). This difference did not, however, pass the false discovery rate test (q = 0.21). Two other tumor suppressor genes, PBRM1 and KDM5C, were numerically but not significantly more frequent in metastases.

There were no differences in median tumor mutational burden between primary and metastatic samples and no difference in either mutations or mutational burden across different metastatic sites.

In cohort 2 there were no significantly different mutational frequencies between primary and metastatic samples for any gene and no differences in median tumor mutational burden.

An analysis comparing the frequency of gene mutations in primary tumors of patients in this cohort who went on to develop metastatic disease versus those of patients with only localized disease showed that, after a median follow-up of 21.9 months, there were no significant differences in either mutational frequency or tumor mutational burden.

“It is currently unknown if cohortwide genomic alterations in RCC metastases have a different genomic profile, including potential actionable mutations, compared to samples derived from the primary site. To our knowledge, our analysis is the largest genomic ccRCC study that compares cohortwide mutational differences between metastases and primary tumors,” the investigators wrote.

They acknowledged that because they did not match primary tumors with metastatic tumors in the same patients they were unable to evaluate how individual tumors evolve over time or how systemic therapies may alter the tumor genomic landscape.

Dr. Choueri is supported in part by the Dana-Farber/Harvard Cancer Center Kidney SPORE, the Kohlberg Chair at Harvard Medical School and the Trust Family, Michael Brigham, and Loker Pinard Funds for Kidney Cancer Research at the Dana-Farber Cancer Institute. Six of the study’s coauthors are employed by Foundation Medicine. The remaining authors declared no competing interests.

SOURCE: Choueiri TK et al. Br J Cancer. 2018 May;118(9):1238-42.

A comparison of the genomic landscapes of both primary and metastatic clear cell renal cell carcinoma (ccRCC) found no significant differences in gene expression or mutational burden between the disease states, suggesting that there is no single genetic driver of metastases, investigators reported.

An analysis of targeted next-generation sequencing of both primary tumors and metastases in two independent patient cohorts showed that only the gene encoding for the tumor suppressor TP53 was significantly more frequently mutated in metastases, compared with primary tumors, but this finding did not pass a false positive test (false discovery rate), noted Toni K. Choueiri, MD, from the Dana-Farber Cancer Institute in Boston, and his colleagues, in the British Journal of Cancer.

“No other gene had significant difference in the cohort frequency of mutations between the metastases and primary tumors. Mutation burden was not significantly different between the metastases and primary tumors or between metastatic sites,” they wrote.

Frequently mutated genes in ccRCC include VHL, the gene encoding for von Hippel–Lindau syndrome, as well as tumor suppressor genes such as PBRM1, SEDT2, BAP1 and KDM5C, but few mutations are clinically actionable, the investigators noted. “However, the value of genomic alterations will be determined by understanding the interactions between acquired genetic alterations, treatments received, heterogeneity, and the dynamics of mutations during evolution of disease.”

To see whether they could improve understanding of the genomic differences between primary and metastatic ccRCC and potentially develop personalized therapies, the investigators studied targeted next-generation sequencing data from two separate cohorts.

The first cohort included data on 349 ccRCC primary tumors and 229 unmatched cases of metastatic ccRCC from the Foundation Medicine database. The second, a validation cohort, included data on 177 ccRCC primary tumors and 80 metastases from patients treated at Dana-Farber. In each cohort, sequencing was performed on 275 genes and intronic regions in 30 genes for a total of 282 unique genes.

In cohort 1, which included tumor samples from 417 men and 169 women with a median age of 58 years, the frequency of mutations was similar in primary tumors and metastases. As noted before, mutations in TP53 were significantly more frequent in metastases than in primary tumors, detected in 14.85% versus 8.90% of samples, respectively (P = .031). This difference did not, however, pass the false discovery rate test (q = 0.21). Two other tumor suppressor genes, PBRM1 and KDM5C, were numerically but not significantly more frequent in metastases.

There were no differences in median tumor mutational burden between primary and metastatic samples and no difference in either mutations or mutational burden across different metastatic sites.

In cohort 2 there were no significantly different mutational frequencies between primary and metastatic samples for any gene and no differences in median tumor mutational burden.

An analysis comparing the frequency of gene mutations in primary tumors of patients in this cohort who went on to develop metastatic disease versus those of patients with only localized disease showed that, after a median follow-up of 21.9 months, there were no significant differences in either mutational frequency or tumor mutational burden.

“It is currently unknown if cohortwide genomic alterations in RCC metastases have a different genomic profile, including potential actionable mutations, compared to samples derived from the primary site. To our knowledge, our analysis is the largest genomic ccRCC study that compares cohortwide mutational differences between metastases and primary tumors,” the investigators wrote.

They acknowledged that because they did not match primary tumors with metastatic tumors in the same patients they were unable to evaluate how individual tumors evolve over time or how systemic therapies may alter the tumor genomic landscape.

Dr. Choueri is supported in part by the Dana-Farber/Harvard Cancer Center Kidney SPORE, the Kohlberg Chair at Harvard Medical School and the Trust Family, Michael Brigham, and Loker Pinard Funds for Kidney Cancer Research at the Dana-Farber Cancer Institute. Six of the study’s coauthors are employed by Foundation Medicine. The remaining authors declared no competing interests.

SOURCE: Choueiri TK et al. Br J Cancer. 2018 May;118(9):1238-42.

BERLIN—Dimethyl fumarate and teriflunomide have similar efficacy in terms of risk of relapse and worsening of Expanded Disability Status Scale (EDSS) score after one and two years of treatment, according to data presented at ECTRIMS 2018. Significantly more patients have new T2 lesions after two years of teriflunomide, however, compared with dimethyl fumarate, and this outcome may explain an increased treatment withdrawal for lack of efficacy among patients receiving teriflunomide.

Teriflunomide and dimethyl fumarate have been approved as first-line treatments for patients with relapsing-remitting multiple sclerosis (MS). To date, no randomized controlled nor observational studies have compared their relative efficacies. David A. Laplaud, MD, PhD, a team leader at the Center of Research in Transplantation and Immunology in Nantes, France, and colleagues conducted a study to compare the effects of teriflunomide and dimethyl fumarate on clinical and MRI outcomes in patients with relapsing-remitting MS from 34 MS centers participating in the French prospective national cohort of MS patients.

The investigators included 1,770 patients with relapsing-remitting MS in the study. In all, 713 participants received teriflunomide, and 1,057 received dimethyl fumarate. Participants were aged 18 to 65 and had an EDSS score of 0 to 5.5 and an available brain MRI performed within six months before treatment initiation. The outcomes under investigation were the proportion of patients with at least one relapse in the year and the two years following teriflunomide or dimethyl fumarate initiation, the proportion of patients with at least one new T2 lesion at one and two years, the number of patients with an increased EDSS score at one and two years, and reasons for treatment cessation at one and two years. For statistical analyses, the outcomes were modeled with propensity scores and logistic regressions by using weighted likelihood maximization and a robust variance estimator.

The confounder-adjusted proportion of patients with at least one relapse at one and two years of treatment was similar in the teriflunomide group and the dimethyl fumarate group (21.6% vs 20.2% for the first year, 30.4% vs 29.5% at two years). Likewise, a similar percentage of patients had an increase of EDSS score at one and two years in the teriflunomide group (27.4% and 41.6%, respectively) and the dimethyl fumarate group (27.1% and 40.6%, respectively). MRI comparisons, however, revealed that the confounder-adjusted proportion of patients with at least one new T2 lesion at two years was significantly lower in patients treated with dimethyl fumarate, compared with teriflunomide (60.8% vs 72.2%; odds ratio [OR], 0.6). The reason for treatment withdrawal at two years was lack of efficacy in 8.5% of patients who received dimethyl fumarate versus 14.5% of patients who received teriflunomide (OR, 0.54).

BERLIN—Dimethyl fumarate and teriflunomide have similar efficacy in terms of risk of relapse and worsening of Expanded Disability Status Scale (EDSS) score after one and two years of treatment, according to data presented at ECTRIMS 2018. Significantly more patients have new T2 lesions after two years of teriflunomide, however, compared with dimethyl fumarate, and this outcome may explain an increased treatment withdrawal for lack of efficacy among patients receiving teriflunomide.

Teriflunomide and dimethyl fumarate have been approved as first-line treatments for patients with relapsing-remitting multiple sclerosis (MS). To date, no randomized controlled nor observational studies have compared their relative efficacies. David A. Laplaud, MD, PhD, a team leader at the Center of Research in Transplantation and Immunology in Nantes, France, and colleagues conducted a study to compare the effects of teriflunomide and dimethyl fumarate on clinical and MRI outcomes in patients with relapsing-remitting MS from 34 MS centers participating in the French prospective national cohort of MS patients.

The investigators included 1,770 patients with relapsing-remitting MS in the study. In all, 713 participants received teriflunomide, and 1,057 received dimethyl fumarate. Participants were aged 18 to 65 and had an EDSS score of 0 to 5.5 and an available brain MRI performed within six months before treatment initiation. The outcomes under investigation were the proportion of patients with at least one relapse in the year and the two years following teriflunomide or dimethyl fumarate initiation, the proportion of patients with at least one new T2 lesion at one and two years, the number of patients with an increased EDSS score at one and two years, and reasons for treatment cessation at one and two years. For statistical analyses, the outcomes were modeled with propensity scores and logistic regressions by using weighted likelihood maximization and a robust variance estimator.

The confounder-adjusted proportion of patients with at least one relapse at one and two years of treatment was similar in the teriflunomide group and the dimethyl fumarate group (21.6% vs 20.2% for the first year, 30.4% vs 29.5% at two years). Likewise, a similar percentage of patients had an increase of EDSS score at one and two years in the teriflunomide group (27.4% and 41.6%, respectively) and the dimethyl fumarate group (27.1% and 40.6%, respectively). MRI comparisons, however, revealed that the confounder-adjusted proportion of patients with at least one new T2 lesion at two years was significantly lower in patients treated with dimethyl fumarate, compared with teriflunomide (60.8% vs 72.2%; odds ratio [OR], 0.6). The reason for treatment withdrawal at two years was lack of efficacy in 8.5% of patients who received dimethyl fumarate versus 14.5% of patients who received teriflunomide (OR, 0.54).

BERLIN—Dimethyl fumarate and teriflunomide have similar efficacy in terms of risk of relapse and worsening of Expanded Disability Status Scale (EDSS) score after one and two years of treatment, according to data presented at ECTRIMS 2018. Significantly more patients have new T2 lesions after two years of teriflunomide, however, compared with dimethyl fumarate, and this outcome may explain an increased treatment withdrawal for lack of efficacy among patients receiving teriflunomide.

Teriflunomide and dimethyl fumarate have been approved as first-line treatments for patients with relapsing-remitting multiple sclerosis (MS). To date, no randomized controlled nor observational studies have compared their relative efficacies. David A. Laplaud, MD, PhD, a team leader at the Center of Research in Transplantation and Immunology in Nantes, France, and colleagues conducted a study to compare the effects of teriflunomide and dimethyl fumarate on clinical and MRI outcomes in patients with relapsing-remitting MS from 34 MS centers participating in the French prospective national cohort of MS patients.

The investigators included 1,770 patients with relapsing-remitting MS in the study. In all, 713 participants received teriflunomide, and 1,057 received dimethyl fumarate. Participants were aged 18 to 65 and had an EDSS score of 0 to 5.5 and an available brain MRI performed within six months before treatment initiation. The outcomes under investigation were the proportion of patients with at least one relapse in the year and the two years following teriflunomide or dimethyl fumarate initiation, the proportion of patients with at least one new T2 lesion at one and two years, the number of patients with an increased EDSS score at one and two years, and reasons for treatment cessation at one and two years. For statistical analyses, the outcomes were modeled with propensity scores and logistic regressions by using weighted likelihood maximization and a robust variance estimator.

The confounder-adjusted proportion of patients with at least one relapse at one and two years of treatment was similar in the teriflunomide group and the dimethyl fumarate group (21.6% vs 20.2% for the first year, 30.4% vs 29.5% at two years). Likewise, a similar percentage of patients had an increase of EDSS score at one and two years in the teriflunomide group (27.4% and 41.6%, respectively) and the dimethyl fumarate group (27.1% and 40.6%, respectively). MRI comparisons, however, revealed that the confounder-adjusted proportion of patients with at least one new T2 lesion at two years was significantly lower in patients treated with dimethyl fumarate, compared with teriflunomide (60.8% vs 72.2%; odds ratio [OR], 0.6). The reason for treatment withdrawal at two years was lack of efficacy in 8.5% of patients who received dimethyl fumarate versus 14.5% of patients who received teriflunomide (OR, 0.54).

The U.S. Preventive Services Task Force advises clinicians to refer or offer intensive behavioral weight-loss interventions to obese adults, according to an updated recommendation statement published in JAMA.

Top Photo Group/ThinkStock

Obesity affects more than one-third of U.S. adults, according to federal statistics. It carries increased risk for comorbidities including heart disease, diabetes, and various cancers, as well as increased risk of death among adults younger than 65 years, noted lead author Susan J. Curry, PhD, of the University of Iowa, Iowa City, and members of the Task Force.

The B recommendation applies to obese adults; obesity was defined as a body mass index of 30 kg/m² or higher. The evidence review focused on interventions for weight loss and weight maintenance that could be provided in primary care or referred from primary care, such as nutrition counseling, exercise strategies, and goal setting.

The Task Force found adequate evidence that behavior-based weight-loss interventions improved weight, reduced incidence of type 2 diabetes, and helped maintain weight loss after interventions ended.

The Task Force found small to no evidence of harm associated with any of the behavioral weight-loss interventions, which included group sessions, personal sessions, print-based interventions, and technology-based interventions (such as text messages). Although interventions that combined drug therapy with behavioral intervention resulted in greater weight loss over 12-18 months, compared with behavioral interventions alone, the attrition rates were high and data on weight-loss maintenance after discontinuation of the drugs were limited, the Task Force noted.

“As a result, the USPSTF encourages clinicians to promote behavioral interventions as the primary focus of effective interventions for weight loss in adults,” they wrote.

The Task Force acknowledged the need for future research in subgroups and to explore whether factors such as genetics and untreated conditions are barriers to behavior-based weight loss interventions.

In the evidence review published in JAMA, Erin S. LeBlanc, MD, of Kaiser Permanente in Portland, Ore., and her colleagues reviewed data from 122 randomized, controlled trials including more than 62,000 persons and 2 observational studies including more than 209,000 persons.

The researchers found behavioral interventions were associated with greater weight loss and less risk of developing diabetes, compared with control interventions.

Intensive behavioral interventions included counseling patients about healthy eating, encouraging physical activity, setting weight and health goals, and assisting with weight monitoring. The interventions ranged from text messaging to in-person sessions for individuals or groups. The average absolute weight loss in the trials included in the review ranged from –0.5 kg to –9.3 kg (–1.1 lb to –20.5 lb) for intervention patients and from +1.4 kg to –5.6 kg (+3.1 lb to –12.3 lb) in controls.

Limitations of the review included a lack of data on population subgroups and a lack of long-term data on weight and health outcomes, the researchers noted. However, the results support the value of behavior-based therapy for obesity treatment.

The final recommendation is consistent with the 2018 draft recommendation and updates the 2012 final recommendation on obesity management.

The researchers and Task Force members had no relevant financial conflicts to disclose.

SOURCE: U.S. Preventive Services Task Force. JAMA. 2018;320(11):1163-71. doi: 10.1001/jama.2018.13022.

The U.S. Preventive Services Task Force advises clinicians to refer or offer intensive behavioral weight-loss interventions to obese adults, according to an updated recommendation statement published in JAMA.

Top Photo Group/ThinkStock

Obesity affects more than one-third of U.S. adults, according to federal statistics. It carries increased risk for comorbidities including heart disease, diabetes, and various cancers, as well as increased risk of death among adults younger than 65 years, noted lead author Susan J. Curry, PhD, of the University of Iowa, Iowa City, and members of the Task Force.

The B recommendation applies to obese adults; obesity was defined as a body mass index of 30 kg/m² or higher. The evidence review focused on interventions for weight loss and weight maintenance that could be provided in primary care or referred from primary care, such as nutrition counseling, exercise strategies, and goal setting.

The Task Force found adequate evidence that behavior-based weight-loss interventions improved weight, reduced incidence of type 2 diabetes, and helped maintain weight loss after interventions ended.

The Task Force found small to no evidence of harm associated with any of the behavioral weight-loss interventions, which included group sessions, personal sessions, print-based interventions, and technology-based interventions (such as text messages). Although interventions that combined drug therapy with behavioral intervention resulted in greater weight loss over 12-18 months, compared with behavioral interventions alone, the attrition rates were high and data on weight-loss maintenance after discontinuation of the drugs were limited, the Task Force noted.

“As a result, the USPSTF encourages clinicians to promote behavioral interventions as the primary focus of effective interventions for weight loss in adults,” they wrote.

The Task Force acknowledged the need for future research in subgroups and to explore whether factors such as genetics and untreated conditions are barriers to behavior-based weight loss interventions.

In the evidence review published in JAMA, Erin S. LeBlanc, MD, of Kaiser Permanente in Portland, Ore., and her colleagues reviewed data from 122 randomized, controlled trials including more than 62,000 persons and 2 observational studies including more than 209,000 persons.

The researchers found behavioral interventions were associated with greater weight loss and less risk of developing diabetes, compared with control interventions.

Intensive behavioral interventions included counseling patients about healthy eating, encouraging physical activity, setting weight and health goals, and assisting with weight monitoring. The interventions ranged from text messaging to in-person sessions for individuals or groups. The average absolute weight loss in the trials included in the review ranged from –0.5 kg to –9.3 kg (–1.1 lb to –20.5 lb) for intervention patients and from +1.4 kg to –5.6 kg (+3.1 lb to –12.3 lb) in controls.

Limitations of the review included a lack of data on population subgroups and a lack of long-term data on weight and health outcomes, the researchers noted. However, the results support the value of behavior-based therapy for obesity treatment.

The final recommendation is consistent with the 2018 draft recommendation and updates the 2012 final recommendation on obesity management.

The researchers and Task Force members had no relevant financial conflicts to disclose.

SOURCE: U.S. Preventive Services Task Force. JAMA. 2018;320(11):1163-71. doi: 10.1001/jama.2018.13022.

The U.S. Preventive Services Task Force advises clinicians to refer or offer intensive behavioral weight-loss interventions to obese adults, according to an updated recommendation statement published in JAMA.

Top Photo Group/ThinkStock

Obesity affects more than one-third of U.S. adults, according to federal statistics. It carries increased risk for comorbidities including heart disease, diabetes, and various cancers, as well as increased risk of death among adults younger than 65 years, noted lead author Susan J. Curry, PhD, of the University of Iowa, Iowa City, and members of the Task Force.

The B recommendation applies to obese adults; obesity was defined as a body mass index of 30 kg/m² or higher. The evidence review focused on interventions for weight loss and weight maintenance that could be provided in primary care or referred from primary care, such as nutrition counseling, exercise strategies, and goal setting.

The Task Force found adequate evidence that behavior-based weight-loss interventions improved weight, reduced incidence of type 2 diabetes, and helped maintain weight loss after interventions ended.

The Task Force found small to no evidence of harm associated with any of the behavioral weight-loss interventions, which included group sessions, personal sessions, print-based interventions, and technology-based interventions (such as text messages). Although interventions that combined drug therapy with behavioral intervention resulted in greater weight loss over 12-18 months, compared with behavioral interventions alone, the attrition rates were high and data on weight-loss maintenance after discontinuation of the drugs were limited, the Task Force noted.

“As a result, the USPSTF encourages clinicians to promote behavioral interventions as the primary focus of effective interventions for weight loss in adults,” they wrote.

The Task Force acknowledged the need for future research in subgroups and to explore whether factors such as genetics and untreated conditions are barriers to behavior-based weight loss interventions.

In the evidence review published in JAMA, Erin S. LeBlanc, MD, of Kaiser Permanente in Portland, Ore., and her colleagues reviewed data from 122 randomized, controlled trials including more than 62,000 persons and 2 observational studies including more than 209,000 persons.

The researchers found behavioral interventions were associated with greater weight loss and less risk of developing diabetes, compared with control interventions.

Intensive behavioral interventions included counseling patients about healthy eating, encouraging physical activity, setting weight and health goals, and assisting with weight monitoring. The interventions ranged from text messaging to in-person sessions for individuals or groups. The average absolute weight loss in the trials included in the review ranged from –0.5 kg to –9.3 kg (–1.1 lb to –20.5 lb) for intervention patients and from +1.4 kg to –5.6 kg (+3.1 lb to –12.3 lb) in controls.

Limitations of the review included a lack of data on population subgroups and a lack of long-term data on weight and health outcomes, the researchers noted. However, the results support the value of behavior-based therapy for obesity treatment.

The final recommendation is consistent with the 2018 draft recommendation and updates the 2012 final recommendation on obesity management.

The researchers and Task Force members had no relevant financial conflicts to disclose.

SOURCE: U.S. Preventive Services Task Force. JAMA. 2018;320(11):1163-71. doi: 10.1001/jama.2018.13022.

BERLIN—Widespread focal cortical damage at multiple sclerosis (MS) onset identifies patients likely to have frequent early relapses and a rapid development of progressive disease, which results from worsening global cortical pathology over time, according to a study presented at ECTRIMS 2018. The results provide a basis for patient stratification with the goal of therapeutic optimization. In addition, the data “highlight the importance of elucidating mechanisms involved in early cortical pathology,” according to the investigators.

Following Patients With Relapsing-Remitting MS

Among patients with relapsing-remitting MS, a high frequency of early relapses is associated with increased risk of developing severe disability, which suggests that early biologic mechanisms influence long-term disease evolution. Antonio Scalfari, MD, PhD, a consultant neurologist at Imperial College Healthcare in London, and colleagues sought to investigate the relationship between early cortical pathology, early relapses, and the risk of converting to secondary progressive MS.

Dr. Scalfari and colleagues examined 219 patients with relapsing-remitting MS. Participants had one (n = 116), two (n = 53), or three or more (n = 50) relapses during the first two years. Follow-up lasted for a mean of 7.9 years. The researchers assessed the number of cortical lesions and white matter lesions and the rate of cortical thinning using 3D double inversion recovery, 3D T1-weighted imaging, and Freesurfer analysis.

Cortical Lesions Predicted Cortical Thinning

During the observation period, 59 (27%) patients converted to secondary progressive MS in a mean of 6.1 years. At disease onset, the investigators detected 674 cortical lesions in 166 (76%) patients. A larger number of cortical lesions was associated with a significantly higher risk of secondary progressive MS. The hazard ratios (HR) for secondary progressive MS were 2.16 for patients with two lesions, 4.79 for patients with five lesions, and 12.3 for patients with seven lesions. A large number of cortical lesions also was associated with shorter latency to secondary progressive MS and a faster rate of global cortical thinning. The mean loss per year was 0.93% for patients with no lesions, 0.99% for patients with one to three lesions, 1.13% for patients with four to six lesions, and 1.33% for patients with seven or more lesions. In the group with no cortical lesions (n = 53), no patients entered the secondary progressive phase, and four reached an Expanded Disability Status Scale score of 4.

Patients with a high number of early relapses, compared with those with low and moderate numbers, had a larger volume of white matter lesions and cortical lesions at onset. The mean volumes of cortical lesions were 181.6 mm³, 386.8 mm³, and 544.0 mm³ for patients with one, two, and three or more early relapses, respectively. Patients with a high number of early relapses also accrued more cortical lesions (mean cortical lesion volumes were 118.8 mm³, 138.8 mm³, and 790.5 mm³ for patients with one, two, and three or more early relapses, respectively), had a faster rate of cortical atrophy (mean loss/year was 0.47%, 0.79%, and 0.94% for patients with one, two, and three or more early relapses, respectively), and entered the secondary progressive phase more rapidly.

In the multivariate model, older age at onset (HR, 1.97), a larger baseline cortical lesion (HR, 2.21) and white matter lesion (HR, 1.32) volume, early changes of global cortical thickness (HR, 1.36), and three or more early relapses (HR, 6.08) independently predicted a higher probability of secondary progressive MS.

BERLIN—Widespread focal cortical damage at multiple sclerosis (MS) onset identifies patients likely to have frequent early relapses and a rapid development of progressive disease, which results from worsening global cortical pathology over time, according to a study presented at ECTRIMS 2018. The results provide a basis for patient stratification with the goal of therapeutic optimization. In addition, the data “highlight the importance of elucidating mechanisms involved in early cortical pathology,” according to the investigators.

Following Patients With Relapsing-Remitting MS

Among patients with relapsing-remitting MS, a high frequency of early relapses is associated with increased risk of developing severe disability, which suggests that early biologic mechanisms influence long-term disease evolution. Antonio Scalfari, MD, PhD, a consultant neurologist at Imperial College Healthcare in London, and colleagues sought to investigate the relationship between early cortical pathology, early relapses, and the risk of converting to secondary progressive MS.

Dr. Scalfari and colleagues examined 219 patients with relapsing-remitting MS. Participants had one (n = 116), two (n = 53), or three or more (n = 50) relapses during the first two years. Follow-up lasted for a mean of 7.9 years. The researchers assessed the number of cortical lesions and white matter lesions and the rate of cortical thinning using 3D double inversion recovery, 3D T1-weighted imaging, and Freesurfer analysis.

Cortical Lesions Predicted Cortical Thinning

During the observation period, 59 (27%) patients converted to secondary progressive MS in a mean of 6.1 years. At disease onset, the investigators detected 674 cortical lesions in 166 (76%) patients. A larger number of cortical lesions was associated with a significantly higher risk of secondary progressive MS. The hazard ratios (HR) for secondary progressive MS were 2.16 for patients with two lesions, 4.79 for patients with five lesions, and 12.3 for patients with seven lesions. A large number of cortical lesions also was associated with shorter latency to secondary progressive MS and a faster rate of global cortical thinning. The mean loss per year was 0.93% for patients with no lesions, 0.99% for patients with one to three lesions, 1.13% for patients with four to six lesions, and 1.33% for patients with seven or more lesions. In the group with no cortical lesions (n = 53), no patients entered the secondary progressive phase, and four reached an Expanded Disability Status Scale score of 4.

Patients with a high number of early relapses, compared with those with low and moderate numbers, had a larger volume of white matter lesions and cortical lesions at onset. The mean volumes of cortical lesions were 181.6 mm³, 386.8 mm³, and 544.0 mm³ for patients with one, two, and three or more early relapses, respectively. Patients with a high number of early relapses also accrued more cortical lesions (mean cortical lesion volumes were 118.8 mm³, 138.8 mm³, and 790.5 mm³ for patients with one, two, and three or more early relapses, respectively), had a faster rate of cortical atrophy (mean loss/year was 0.47%, 0.79%, and 0.94% for patients with one, two, and three or more early relapses, respectively), and entered the secondary progressive phase more rapidly.

In the multivariate model, older age at onset (HR, 1.97), a larger baseline cortical lesion (HR, 2.21) and white matter lesion (HR, 1.32) volume, early changes of global cortical thickness (HR, 1.36), and three or more early relapses (HR, 6.08) independently predicted a higher probability of secondary progressive MS.

BERLIN—Widespread focal cortical damage at multiple sclerosis (MS) onset identifies patients likely to have frequent early relapses and a rapid development of progressive disease, which results from worsening global cortical pathology over time, according to a study presented at ECTRIMS 2018. The results provide a basis for patient stratification with the goal of therapeutic optimization. In addition, the data “highlight the importance of elucidating mechanisms involved in early cortical pathology,” according to the investigators.

Following Patients With Relapsing-Remitting MS

Among patients with relapsing-remitting MS, a high frequency of early relapses is associated with increased risk of developing severe disability, which suggests that early biologic mechanisms influence long-term disease evolution. Antonio Scalfari, MD, PhD, a consultant neurologist at Imperial College Healthcare in London, and colleagues sought to investigate the relationship between early cortical pathology, early relapses, and the risk of converting to secondary progressive MS.

Dr. Scalfari and colleagues examined 219 patients with relapsing-remitting MS. Participants had one (n = 116), two (n = 53), or three or more (n = 50) relapses during the first two years. Follow-up lasted for a mean of 7.9 years. The researchers assessed the number of cortical lesions and white matter lesions and the rate of cortical thinning using 3D double inversion recovery, 3D T1-weighted imaging, and Freesurfer analysis.

Cortical Lesions Predicted Cortical Thinning

During the observation period, 59 (27%) patients converted to secondary progressive MS in a mean of 6.1 years. At disease onset, the investigators detected 674 cortical lesions in 166 (76%) patients. A larger number of cortical lesions was associated with a significantly higher risk of secondary progressive MS. The hazard ratios (HR) for secondary progressive MS were 2.16 for patients with two lesions, 4.79 for patients with five lesions, and 12.3 for patients with seven lesions. A large number of cortical lesions also was associated with shorter latency to secondary progressive MS and a faster rate of global cortical thinning. The mean loss per year was 0.93% for patients with no lesions, 0.99% for patients with one to three lesions, 1.13% for patients with four to six lesions, and 1.33% for patients with seven or more lesions. In the group with no cortical lesions (n = 53), no patients entered the secondary progressive phase, and four reached an Expanded Disability Status Scale score of 4.

Patients with a high number of early relapses, compared with those with low and moderate numbers, had a larger volume of white matter lesions and cortical lesions at onset. The mean volumes of cortical lesions were 181.6 mm³, 386.8 mm³, and 544.0 mm³ for patients with one, two, and three or more early relapses, respectively. Patients with a high number of early relapses also accrued more cortical lesions (mean cortical lesion volumes were 118.8 mm³, 138.8 mm³, and 790.5 mm³ for patients with one, two, and three or more early relapses, respectively), had a faster rate of cortical atrophy (mean loss/year was 0.47%, 0.79%, and 0.94% for patients with one, two, and three or more early relapses, respectively), and entered the secondary progressive phase more rapidly.

In the multivariate model, older age at onset (HR, 1.97), a larger baseline cortical lesion (HR, 2.21) and white matter lesion (HR, 1.32) volume, early changes of global cortical thickness (HR, 1.36), and three or more early relapses (HR, 6.08) independently predicted a higher probability of secondary progressive MS.

BERLIN—Data from the Big Multiple Sclerosis Data (BMSD) Network indicate that the optimal time to start disease-modifying therapy in patients with multiple sclerosis (MS) to prevent the long-term accumulation of disability is within six months of disease onset. This finding was presented by Pietro Iaffaldano, MD, and colleagues at ECTRIMS 2018. Dr. Iaffaldano is Assistant Professor of Neurology at the University of Bari, Italy.

Many randomized clinical trials support the early start of disease-modifying therapies in MS. However, there is still an ongoing discussion on the optimal timing of treatment. For insight into this and other questions, the Danish, Italian, and Swedish national MS registries, MSBase, and the OFSEP of France pooled data for specific research projects in the BMSD Network. One question they sought to answer with this large, real-world data set was the optimal time to start disease-modifying therapy to prevent long-term disability accumulation in MS.

A cohort of patients with relapsing-remitting MS who had 10 or more years of follow-up, three or more years of cumulative disease-modifying therapy exposure, and three or more Expanded Disability Status Scale (EDSS) score evaluations was selected from the pooled cohort of the BMSD Network. The researchers conducted a set of pairwise (1:1) propensity score matching analyses with 10 different cut-offs for early versus delayed treatment (> 0.5 year up to > 5.0 years, using 0.5-year intervals) to allow an unbiased comparison between groups. The logistic model to predict propensity score included the following covariates: age at onset of the disease, sex, baseline EDSS, number of relapses in the two years before disease-modifying therapy start, number of EDSS evaluations, decade of birth, and registry source. To estimate the risk of reaching 12 months-confirmed EDSS progression (EDSSpr), a set of Cox models, adjusted for disease duration and relapses after disease-modifying therapy start as time-dependent covariates, was calculated.

A cohort of 11,871 patients with relapsing-remitting MS (71.0% female) was retrieved from the pooled BMSD Network database. The median (interquartile range) age at onset was 27.7 (22.3–34.6), median follow-up was 13.2 (11.4–15.4) years, and median time to the first disease-modifying therapy start was 3.8 (1.5–8.5) years. During the follow-up, an EDSSpr was reached by 4,138 (34.9%) patients. The lowest hazard ratio (HR) with relative 95% confidence interval (CI) for the propensity score matched models was obtained by a cutoff of treatment start within six months from disease onset (n = 873 per group). Early treatment significantly reduced the risk of reaching an EDSSpr (HR, 0.72 ). All subsequent comparisons between early and delayed treatment were not statistically significant.

This project was supported by Biogen International (Zug, Switzerland) on the basis of a sponsored research agreement with the BMSD Network.

BERLIN—Data from the Big Multiple Sclerosis Data (BMSD) Network indicate that the optimal time to start disease-modifying therapy in patients with multiple sclerosis (MS) to prevent the long-term accumulation of disability is within six months of disease onset. This finding was presented by Pietro Iaffaldano, MD, and colleagues at ECTRIMS 2018. Dr. Iaffaldano is Assistant Professor of Neurology at the University of Bari, Italy.

Many randomized clinical trials support the early start of disease-modifying therapies in MS. However, there is still an ongoing discussion on the optimal timing of treatment. For insight into this and other questions, the Danish, Italian, and Swedish national MS registries, MSBase, and the OFSEP of France pooled data for specific research projects in the BMSD Network. One question they sought to answer with this large, real-world data set was the optimal time to start disease-modifying therapy to prevent long-term disability accumulation in MS.

A cohort of patients with relapsing-remitting MS who had 10 or more years of follow-up, three or more years of cumulative disease-modifying therapy exposure, and three or more Expanded Disability Status Scale (EDSS) score evaluations was selected from the pooled cohort of the BMSD Network. The researchers conducted a set of pairwise (1:1) propensity score matching analyses with 10 different cut-offs for early versus delayed treatment (> 0.5 year up to > 5.0 years, using 0.5-year intervals) to allow an unbiased comparison between groups. The logistic model to predict propensity score included the following covariates: age at onset of the disease, sex, baseline EDSS, number of relapses in the two years before disease-modifying therapy start, number of EDSS evaluations, decade of birth, and registry source. To estimate the risk of reaching 12 months-confirmed EDSS progression (EDSSpr), a set of Cox models, adjusted for disease duration and relapses after disease-modifying therapy start as time-dependent covariates, was calculated.

A cohort of 11,871 patients with relapsing-remitting MS (71.0% female) was retrieved from the pooled BMSD Network database. The median (interquartile range) age at onset was 27.7 (22.3–34.6), median follow-up was 13.2 (11.4–15.4) years, and median time to the first disease-modifying therapy start was 3.8 (1.5–8.5) years. During the follow-up, an EDSSpr was reached by 4,138 (34.9%) patients. The lowest hazard ratio (HR) with relative 95% confidence interval (CI) for the propensity score matched models was obtained by a cutoff of treatment start within six months from disease onset (n = 873 per group). Early treatment significantly reduced the risk of reaching an EDSSpr (HR, 0.72 ). All subsequent comparisons between early and delayed treatment were not statistically significant.

This project was supported by Biogen International (Zug, Switzerland) on the basis of a sponsored research agreement with the BMSD Network.

BERLIN—Data from the Big Multiple Sclerosis Data (BMSD) Network indicate that the optimal time to start disease-modifying therapy in patients with multiple sclerosis (MS) to prevent the long-term accumulation of disability is within six months of disease onset. This finding was presented by Pietro Iaffaldano, MD, and colleagues at ECTRIMS 2018. Dr. Iaffaldano is Assistant Professor of Neurology at the University of Bari, Italy.

Many randomized clinical trials support the early start of disease-modifying therapies in MS. However, there is still an ongoing discussion on the optimal timing of treatment. For insight into this and other questions, the Danish, Italian, and Swedish national MS registries, MSBase, and the OFSEP of France pooled data for specific research projects in the BMSD Network. One question they sought to answer with this large, real-world data set was the optimal time to start disease-modifying therapy to prevent long-term disability accumulation in MS.

A cohort of patients with relapsing-remitting MS who had 10 or more years of follow-up, three or more years of cumulative disease-modifying therapy exposure, and three or more Expanded Disability Status Scale (EDSS) score evaluations was selected from the pooled cohort of the BMSD Network. The researchers conducted a set of pairwise (1:1) propensity score matching analyses with 10 different cut-offs for early versus delayed treatment (> 0.5 year up to > 5.0 years, using 0.5-year intervals) to allow an unbiased comparison between groups. The logistic model to predict propensity score included the following covariates: age at onset of the disease, sex, baseline EDSS, number of relapses in the two years before disease-modifying therapy start, number of EDSS evaluations, decade of birth, and registry source. To estimate the risk of reaching 12 months-confirmed EDSS progression (EDSSpr), a set of Cox models, adjusted for disease duration and relapses after disease-modifying therapy start as time-dependent covariates, was calculated.

A cohort of 11,871 patients with relapsing-remitting MS (71.0% female) was retrieved from the pooled BMSD Network database. The median (interquartile range) age at onset was 27.7 (22.3–34.6), median follow-up was 13.2 (11.4–15.4) years, and median time to the first disease-modifying therapy start was 3.8 (1.5–8.5) years. During the follow-up, an EDSSpr was reached by 4,138 (34.9%) patients. The lowest hazard ratio (HR) with relative 95% confidence interval (CI) for the propensity score matched models was obtained by a cutoff of treatment start within six months from disease onset (n = 873 per group). Early treatment significantly reduced the risk of reaching an EDSSpr (HR, 0.72 ). All subsequent comparisons between early and delayed treatment were not statistically significant.

This project was supported by Biogen International (Zug, Switzerland) on the basis of a sponsored research agreement with the BMSD Network.

The direct oral anticoagulant rivaroxaban is now approved for prevention of major cardiovascular events in patients with chronic coronary or peripheral artery disease when taken with aspirin, Janssen Pharmaceuticals announced on October 11.

Wikimedia Commons/FitzColinGerald/Creative Commons License

The Food and Drug Administration’s approval was based on a review of the 27,000-patient COMPASS trial, which showed last year that a low dosage of rivaroxaban (Xarelto) plus aspirin reduced the combined rate of cardiovascular disease events by 24% in patients with coronary artery disease and by 28% in participants with peripheral artery disease, compared with aspirin alone. (N Engl J Med. 2017 Oct 5;377[14]:1319-30)

The flip side to the reduction in COMPASS’s combined primary endpoint was a 51% increase in major bleeding. However, that bump did not translate to increases in fatal bleeds, intracerebral bleeds, or bleeding in other critical organs.

COMPASS (Cardiovascular Outcomes for People Using Anticoagulation Strategies) studied two dosages of rivaroxaban, 2.5 mg and 5 mg twice daily, and it was the lower dosage that did the trick. Until this approval, that formulation wasn’t available; Janssen announced the coming of the 2.5-mg pill in its release.

The new prescribing information states specifically that Xarelto 2.5 mg is indicated, in combination with aspirin, to reduce the risk of major cardiovascular events, cardiovascular death, MI, and stroke in patients with chronic coronary artery disease or peripheral artery disease.

This is the sixth indication for rivaroxaban, a factor Xa inhibitor that was first approved in 2011. It is also the first indication for cardiovascular prevention for any factor Xa inhibitor. Others on the U.S. market are apixaban (Eliquis), edoxaban (Savaysa), and betrixaban (Bevyxxa).

COMPASS was presented at the 2017 annual congress of the European Society of Cardiology. At that time, Eugene Braunwald, MD, of Harvard Medical School and Brigham and Women’s Hospital in Boston, commented that the trial produced “unambiguous results that should change guidelines and the management of stable coronary artery disease.” He added that the results are “an important step for thrombocardiology.”

[email protected]

The direct oral anticoagulant rivaroxaban is now approved for prevention of major cardiovascular events in patients with chronic coronary or peripheral artery disease when taken with aspirin, Janssen Pharmaceuticals announced on October 11.

Wikimedia Commons/FitzColinGerald/Creative Commons License

The Food and Drug Administration’s approval was based on a review of the 27,000-patient COMPASS trial, which showed last year that a low dosage of rivaroxaban (Xarelto) plus aspirin reduced the combined rate of cardiovascular disease events by 24% in patients with coronary artery disease and by 28% in participants with peripheral artery disease, compared with aspirin alone. (N Engl J Med. 2017 Oct 5;377[14]:1319-30)

The flip side to the reduction in COMPASS’s combined primary endpoint was a 51% increase in major bleeding. However, that bump did not translate to increases in fatal bleeds, intracerebral bleeds, or bleeding in other critical organs.

COMPASS (Cardiovascular Outcomes for People Using Anticoagulation Strategies) studied two dosages of rivaroxaban, 2.5 mg and 5 mg twice daily, and it was the lower dosage that did the trick. Until this approval, that formulation wasn’t available; Janssen announced the coming of the 2.5-mg pill in its release.

The new prescribing information states specifically that Xarelto 2.5 mg is indicated, in combination with aspirin, to reduce the risk of major cardiovascular events, cardiovascular death, MI, and stroke in patients with chronic coronary artery disease or peripheral artery disease.

This is the sixth indication for rivaroxaban, a factor Xa inhibitor that was first approved in 2011. It is also the first indication for cardiovascular prevention for any factor Xa inhibitor. Others on the U.S. market are apixaban (Eliquis), edoxaban (Savaysa), and betrixaban (Bevyxxa).

COMPASS was presented at the 2017 annual congress of the European Society of Cardiology. At that time, Eugene Braunwald, MD, of Harvard Medical School and Brigham and Women’s Hospital in Boston, commented that the trial produced “unambiguous results that should change guidelines and the management of stable coronary artery disease.” He added that the results are “an important step for thrombocardiology.”

[email protected]

The direct oral anticoagulant rivaroxaban is now approved for prevention of major cardiovascular events in patients with chronic coronary or peripheral artery disease when taken with aspirin, Janssen Pharmaceuticals announced on October 11.

Wikimedia Commons/FitzColinGerald/Creative Commons License

The Food and Drug Administration’s approval was based on a review of the 27,000-patient COMPASS trial, which showed last year that a low dosage of rivaroxaban (Xarelto) plus aspirin reduced the combined rate of cardiovascular disease events by 24% in patients with coronary artery disease and by 28% in participants with peripheral artery disease, compared with aspirin alone. (N Engl J Med. 2017 Oct 5;377[14]:1319-30)

The flip side to the reduction in COMPASS’s combined primary endpoint was a 51% increase in major bleeding. However, that bump did not translate to increases in fatal bleeds, intracerebral bleeds, or bleeding in other critical organs.

COMPASS (Cardiovascular Outcomes for People Using Anticoagulation Strategies) studied two dosages of rivaroxaban, 2.5 mg and 5 mg twice daily, and it was the lower dosage that did the trick. Until this approval, that formulation wasn’t available; Janssen announced the coming of the 2.5-mg pill in its release.

The new prescribing information states specifically that Xarelto 2.5 mg is indicated, in combination with aspirin, to reduce the risk of major cardiovascular events, cardiovascular death, MI, and stroke in patients with chronic coronary artery disease or peripheral artery disease.

This is the sixth indication for rivaroxaban, a factor Xa inhibitor that was first approved in 2011. It is also the first indication for cardiovascular prevention for any factor Xa inhibitor. Others on the U.S. market are apixaban (Eliquis), edoxaban (Savaysa), and betrixaban (Bevyxxa).

COMPASS was presented at the 2017 annual congress of the European Society of Cardiology. At that time, Eugene Braunwald, MD, of Harvard Medical School and Brigham and Women’s Hospital in Boston, commented that the trial produced “unambiguous results that should change guidelines and the management of stable coronary artery disease.” He added that the results are “an important step for thrombocardiology.”

[email protected]

SAN ANTONIO – Physicians and other health care providers may harbor implicit, or unconscious, biases that contribute to health care disparities, patient communication researcher Stacey Passalacqua, PhD, said here at the annual meeting of the American College of Chest Physicians.

Implicit biases are beliefs or attitudes, for example, about certain social groups, that exist outside of a health care provider’s conscious awareness, said Dr. Passalacqua of the department of communication at the University of Texas, San Antonio. If bias is implicit, it can be difficult self-assess.

Patients at risk for biased treatment include African Americans, women, Native Americans, LGBT patients, disabled patients, and patients with substance abuse disorders, among other social, ethnic, and racial groups, Dr. Passalacqua told attendees in workshops at the meeting.

“If a health care provider has negative biases toward a particular patient – maybe they think that these patients doesn’t care that much about their health or that they really have no interest in participating – then obviously that health care provider is far less likely to engage that patient in shared decision making,” she said in a video interview.

Diagnosis and treatment are subject to influence by the bias that physicians have toward certain patient groups, according to Dr. Passalacqua. For example, she said women with heart disease are less likely to be accurately diagnosed.

The bias in the medical setting might be mitigated by the presence of more individuals from the at-risk groups in the health care workforce, she added. In one recent retrospective study, investigators found that after an MI, a woman treated by a male physician was associated with higher mortality, while women and men had similar outcomes when treated by female physicians.

“That is one of the reasons why it is so important to have a diverse workforce, to have health care providers of different ethnicities, of different genders, or different backgrounds, because they are less subject to some of these implicit biases that we know are highly problematic in health care,” she said in the interview.

Dr. Passalacqua had no disclosures related to her presentation.

SAN ANTONIO – Physicians and other health care providers may harbor implicit, or unconscious, biases that contribute to health care disparities, patient communication researcher Stacey Passalacqua, PhD, said here at the annual meeting of the American College of Chest Physicians.

Implicit biases are beliefs or attitudes, for example, about certain social groups, that exist outside of a health care provider’s conscious awareness, said Dr. Passalacqua of the department of communication at the University of Texas, San Antonio. If bias is implicit, it can be difficult self-assess.

Patients at risk for biased treatment include African Americans, women, Native Americans, LGBT patients, disabled patients, and patients with substance abuse disorders, among other social, ethnic, and racial groups, Dr. Passalacqua told attendees in workshops at the meeting.

“If a health care provider has negative biases toward a particular patient – maybe they think that these patients doesn’t care that much about their health or that they really have no interest in participating – then obviously that health care provider is far less likely to engage that patient in shared decision making,” she said in a video interview.

Diagnosis and treatment are subject to influence by the bias that physicians have toward certain patient groups, according to Dr. Passalacqua. For example, she said women with heart disease are less likely to be accurately diagnosed.

The bias in the medical setting might be mitigated by the presence of more individuals from the at-risk groups in the health care workforce, she added. In one recent retrospective study, investigators found that after an MI, a woman treated by a male physician was associated with higher mortality, while women and men had similar outcomes when treated by female physicians.

“That is one of the reasons why it is so important to have a diverse workforce, to have health care providers of different ethnicities, of different genders, or different backgrounds, because they are less subject to some of these implicit biases that we know are highly problematic in health care,” she said in the interview.

Dr. Passalacqua had no disclosures related to her presentation.

SAN ANTONIO – Physicians and other health care providers may harbor implicit, or unconscious, biases that contribute to health care disparities, patient communication researcher Stacey Passalacqua, PhD, said here at the annual meeting of the American College of Chest Physicians.

Implicit biases are beliefs or attitudes, for example, about certain social groups, that exist outside of a health care provider’s conscious awareness, said Dr. Passalacqua of the department of communication at the University of Texas, San Antonio. If bias is implicit, it can be difficult self-assess.

Patients at risk for biased treatment include African Americans, women, Native Americans, LGBT patients, disabled patients, and patients with substance abuse disorders, among other social, ethnic, and racial groups, Dr. Passalacqua told attendees in workshops at the meeting.

“If a health care provider has negative biases toward a particular patient – maybe they think that these patients doesn’t care that much about their health or that they really have no interest in participating – then obviously that health care provider is far less likely to engage that patient in shared decision making,” she said in a video interview.

Diagnosis and treatment are subject to influence by the bias that physicians have toward certain patient groups, according to Dr. Passalacqua. For example, she said women with heart disease are less likely to be accurately diagnosed.

The bias in the medical setting might be mitigated by the presence of more individuals from the at-risk groups in the health care workforce, she added. In one recent retrospective study, investigators found that after an MI, a woman treated by a male physician was associated with higher mortality, while women and men had similar outcomes when treated by female physicians.

“That is one of the reasons why it is so important to have a diverse workforce, to have health care providers of different ethnicities, of different genders, or different backgrounds, because they are less subject to some of these implicit biases that we know are highly problematic in health care,” she said in the interview.

Dr. Passalacqua had no disclosures related to her presentation.