Video

ORLANDO – Rates of diabetic peripheral neuropathy (DPN) in U.S. patients with type 1 diabetes (T1D) may have dipped, possibly because of improving clinical care, a new study suggests. Researchers also found evidence that nonglycemic factors may play important roles in the development of the condition.

There are differences between DPN in T1D and type 2 diabetes: Lifetime incidence in T1D is believed to be 45%, lower than in T2D. However, a 2016 report noted that, “whereas treating hyperglycemia in type 1 DM can significantly reduce the incidence of neuropathy by up to 60 to 70%, glucose control in type 2 DM has only a marginal 5 to 7% reduction in the development of neuropathy.” (F1000Research 2016, 5(F1000 Faculty Rev):738)

Still, DPN is believed to be very common in T1D. According to the new study, previous research has suggested that the DPN rate in this population could be as high as 35%.

For the new study, researchers examined self-reports of DPN from 5,058 patients across 62 sites via the T1D Exchange Registry. All patients were at least 18 years of age and had at least 5 years of T1D. Their mean age was 39 years, the duration of diabetes was 22 years, and their average hemoglobin A1c was 8.1. Over half (56%) were women, and most (88%) were white were white.

A preliminary analysis found that just 10% of the patients had signs of DPN, according to their self-reports. In part, the difference between this number and previous estimates of DPN prevalence may be because previous studies relied on symptoms, exams, and electrophysiologic testing, said study researcher Kara Mizokami-Stout, MD, of the University of Michigan, in an interview.

However, study researcher Rodica Pop-Busui, MD, PhD, noted in an interview that one strength of the new study is that it’s “a broad sample of patients with type 1 diabetes as they are currently treated in clinical care across the United States.”

Versus those without DPN, those with the condition were more likely to be older (mean 52 vs. 37 years), female (61% vs. 55%), and had T1D for a longer period (mean 32 vs. 21 years). They were also poorer and had less education. (All P less than .001)

The DPN group also had slightly higher systolic blood pressure (mean 126 vs. 123), higher triglycerides (117 vs. 95) and more than double the rate of tobacco use (9% vs. 4%), all P less than .001.

Also, cardiovascular disease was more common (26% vs. 6%) even though this group used statins (64% vs. 31%) and ACE inhibitors/ARBs (45% vs. 23%) at much higher levels, all P less than .001.

Researchers also found that this with DPN had higher HbA1c even after controlling for various confounders (8.4% vs. 8.1%, P less than .01).

SOURCE: Mizokami-Stout K, et al. ADA 2018, Abstract 62-OR.
 

ORLANDO – Rates of diabetic peripheral neuropathy (DPN) in U.S. patients with type 1 diabetes (T1D) may have dipped, possibly because of improving clinical care, a new study suggests. Researchers also found evidence that nonglycemic factors may play important roles in the development of the condition.

There are differences between DPN in T1D and type 2 diabetes: Lifetime incidence in T1D is believed to be 45%, lower than in T2D. However, a 2016 report noted that, “whereas treating hyperglycemia in type 1 DM can significantly reduce the incidence of neuropathy by up to 60 to 70%, glucose control in type 2 DM has only a marginal 5 to 7% reduction in the development of neuropathy.” (F1000Research 2016, 5(F1000 Faculty Rev):738)

Still, DPN is believed to be very common in T1D. According to the new study, previous research has suggested that the DPN rate in this population could be as high as 35%.

For the new study, researchers examined self-reports of DPN from 5,058 patients across 62 sites via the T1D Exchange Registry. All patients were at least 18 years of age and had at least 5 years of T1D. Their mean age was 39 years, the duration of diabetes was 22 years, and their average hemoglobin A1c was 8.1. Over half (56%) were women, and most (88%) were white were white.

A preliminary analysis found that just 10% of the patients had signs of DPN, according to their self-reports. In part, the difference between this number and previous estimates of DPN prevalence may be because previous studies relied on symptoms, exams, and electrophysiologic testing, said study researcher Kara Mizokami-Stout, MD, of the University of Michigan, in an interview.

However, study researcher Rodica Pop-Busui, MD, PhD, noted in an interview that one strength of the new study is that it’s “a broad sample of patients with type 1 diabetes as they are currently treated in clinical care across the United States.”

Versus those without DPN, those with the condition were more likely to be older (mean 52 vs. 37 years), female (61% vs. 55%), and had T1D for a longer period (mean 32 vs. 21 years). They were also poorer and had less education. (All P less than .001)

The DPN group also had slightly higher systolic blood pressure (mean 126 vs. 123), higher triglycerides (117 vs. 95) and more than double the rate of tobacco use (9% vs. 4%), all P less than .001.

Also, cardiovascular disease was more common (26% vs. 6%) even though this group used statins (64% vs. 31%) and ACE inhibitors/ARBs (45% vs. 23%) at much higher levels, all P less than .001.

Researchers also found that this with DPN had higher HbA1c even after controlling for various confounders (8.4% vs. 8.1%, P less than .01).

SOURCE: Mizokami-Stout K, et al. ADA 2018, Abstract 62-OR.
 

ORLANDO – Rates of diabetic peripheral neuropathy (DPN) in U.S. patients with type 1 diabetes (T1D) may have dipped, possibly because of improving clinical care, a new study suggests. Researchers also found evidence that nonglycemic factors may play important roles in the development of the condition.

There are differences between DPN in T1D and type 2 diabetes: Lifetime incidence in T1D is believed to be 45%, lower than in T2D. However, a 2016 report noted that, “whereas treating hyperglycemia in type 1 DM can significantly reduce the incidence of neuropathy by up to 60 to 70%, glucose control in type 2 DM has only a marginal 5 to 7% reduction in the development of neuropathy.” (F1000Research 2016, 5(F1000 Faculty Rev):738)

Still, DPN is believed to be very common in T1D. According to the new study, previous research has suggested that the DPN rate in this population could be as high as 35%.

For the new study, researchers examined self-reports of DPN from 5,058 patients across 62 sites via the T1D Exchange Registry. All patients were at least 18 years of age and had at least 5 years of T1D. Their mean age was 39 years, the duration of diabetes was 22 years, and their average hemoglobin A1c was 8.1. Over half (56%) were women, and most (88%) were white were white.

A preliminary analysis found that just 10% of the patients had signs of DPN, according to their self-reports. In part, the difference between this number and previous estimates of DPN prevalence may be because previous studies relied on symptoms, exams, and electrophysiologic testing, said study researcher Kara Mizokami-Stout, MD, of the University of Michigan, in an interview.

However, study researcher Rodica Pop-Busui, MD, PhD, noted in an interview that one strength of the new study is that it’s “a broad sample of patients with type 1 diabetes as they are currently treated in clinical care across the United States.”

Versus those without DPN, those with the condition were more likely to be older (mean 52 vs. 37 years), female (61% vs. 55%), and had T1D for a longer period (mean 32 vs. 21 years). They were also poorer and had less education. (All P less than .001)

The DPN group also had slightly higher systolic blood pressure (mean 126 vs. 123), higher triglycerides (117 vs. 95) and more than double the rate of tobacco use (9% vs. 4%), all P less than .001.

Also, cardiovascular disease was more common (26% vs. 6%) even though this group used statins (64% vs. 31%) and ACE inhibitors/ARBs (45% vs. 23%) at much higher levels, all P less than .001.

Researchers also found that this with DPN had higher HbA1c even after controlling for various confounders (8.4% vs. 8.1%, P less than .01).

SOURCE: Mizokami-Stout K, et al. ADA 2018, Abstract 62-OR.
 

AMSTERDAM – The new systemic lupus erythematosus classification criteria of the American College of Rheumatology and the European League Against Rheumatism are based on a point system that will produce a “paradigm shift” in how the disease gets studied going forward, said Sindhu Johnson, MD, while presenting the latest version of the newly revised classification scheme at the European Congress of Rheumatology.

Until now, classification of systemic lupus erythematosus (SLE) was a yes-or-no decision, based on whether the patient had a minimum number of characteristic signs or symptoms. The new criteria, which are on track for formal endorsement before the end of 2018 by the two medical societies that sponsored the revision, instead use a point system that gives varying weight to each of the 22 criteria. A patient needs to score at least 10 points from these criteria, and all patients classified with SLE also must have an antinuclear antibody (ANA) titer of at least 1:80 on HEp-2 cells or an equivalent positive test. This means that the criteria also can define patients who just miss classification with SLE by meeting the ANA standard and by tallying 8 or 9 points, and the criteria also identify patients who far exceed the classification threshold by having the requisite ANA plus racking up as many as, perhaps, 20 or 30 points.

“This is a real research opportunity,” to follow patients who fall just short with 8 or 9 points to assess their longer-term prognosis, as well as to study whether “higher scores mean a higher risk for developing a bad outcome,” said Dr. Johnson, a rheumatologist at the University of Toronto and director of the Toronto Scleroderma Program. Other areas for future research with the new criteria include seeing how they work in various SLE subgroups, such as patients with renal-predominant disease or skin-predominant disease, and also seeing how they work in various ethnic populations.

That’s because “85% of our experts said that they would feel confident classifying a patient as having lupus based only on a renal biopsy” and ANA positivity, said Dr. Johnson, who served as the ACR-appointed cochair of the criteria-writing panel along with a cochair selected by EULAR, Martin Aringer, MD, PhD, of the Technical University of Dresden (Germany). She cautioned that other levels of lupus nephritis, class II or V, confer only 8 points to the classification and so by themselves are not enough to label a person as having lupus.

During her presentation, Dr. Johnson cited the high levels of sensitivity and specificity that the new classification criteria demonstrated in a validation cohort of more than 1,000 cases and controls. In the validation analysis, the new criteria had a sensitivity of 96.12% and specificity of 94.43% for classifying SLE, giving the new criteria a better result on both these measures than either the 1997 ACR criteria (Arthritis Rheum. 1997 Sept;40[9]:1725) or the 2012 Systemic Lupus International Collaborating Clinics criteria (Arthritis Rheum. 2012 Aug;64[8]:2677-86).

The 22 criteria cluster into seven separate clinical domains and three different immunologic domains. The point values assigned to each criterion range from 2 to 10 points.

Dr. Johnson had no disclosures.

[email protected]

AMSTERDAM – The new systemic lupus erythematosus classification criteria of the American College of Rheumatology and the European League Against Rheumatism are based on a point system that will produce a “paradigm shift” in how the disease gets studied going forward, said Sindhu Johnson, MD, while presenting the latest version of the newly revised classification scheme at the European Congress of Rheumatology.

Until now, classification of systemic lupus erythematosus (SLE) was a yes-or-no decision, based on whether the patient had a minimum number of characteristic signs or symptoms. The new criteria, which are on track for formal endorsement before the end of 2018 by the two medical societies that sponsored the revision, instead use a point system that gives varying weight to each of the 22 criteria. A patient needs to score at least 10 points from these criteria, and all patients classified with SLE also must have an antinuclear antibody (ANA) titer of at least 1:80 on HEp-2 cells or an equivalent positive test. This means that the criteria also can define patients who just miss classification with SLE by meeting the ANA standard and by tallying 8 or 9 points, and the criteria also identify patients who far exceed the classification threshold by having the requisite ANA plus racking up as many as, perhaps, 20 or 30 points.

“This is a real research opportunity,” to follow patients who fall just short with 8 or 9 points to assess their longer-term prognosis, as well as to study whether “higher scores mean a higher risk for developing a bad outcome,” said Dr. Johnson, a rheumatologist at the University of Toronto and director of the Toronto Scleroderma Program. Other areas for future research with the new criteria include seeing how they work in various SLE subgroups, such as patients with renal-predominant disease or skin-predominant disease, and also seeing how they work in various ethnic populations.

That’s because “85% of our experts said that they would feel confident classifying a patient as having lupus based only on a renal biopsy” and ANA positivity, said Dr. Johnson, who served as the ACR-appointed cochair of the criteria-writing panel along with a cochair selected by EULAR, Martin Aringer, MD, PhD, of the Technical University of Dresden (Germany). She cautioned that other levels of lupus nephritis, class II or V, confer only 8 points to the classification and so by themselves are not enough to label a person as having lupus.

During her presentation, Dr. Johnson cited the high levels of sensitivity and specificity that the new classification criteria demonstrated in a validation cohort of more than 1,000 cases and controls. In the validation analysis, the new criteria had a sensitivity of 96.12% and specificity of 94.43% for classifying SLE, giving the new criteria a better result on both these measures than either the 1997 ACR criteria (Arthritis Rheum. 1997 Sept;40[9]:1725) or the 2012 Systemic Lupus International Collaborating Clinics criteria (Arthritis Rheum. 2012 Aug;64[8]:2677-86).

The 22 criteria cluster into seven separate clinical domains and three different immunologic domains. The point values assigned to each criterion range from 2 to 10 points.

Dr. Johnson had no disclosures.

[email protected]

AMSTERDAM – The new systemic lupus erythematosus classification criteria of the American College of Rheumatology and the European League Against Rheumatism are based on a point system that will produce a “paradigm shift” in how the disease gets studied going forward, said Sindhu Johnson, MD, while presenting the latest version of the newly revised classification scheme at the European Congress of Rheumatology.

Until now, classification of systemic lupus erythematosus (SLE) was a yes-or-no decision, based on whether the patient had a minimum number of characteristic signs or symptoms. The new criteria, which are on track for formal endorsement before the end of 2018 by the two medical societies that sponsored the revision, instead use a point system that gives varying weight to each of the 22 criteria. A patient needs to score at least 10 points from these criteria, and all patients classified with SLE also must have an antinuclear antibody (ANA) titer of at least 1:80 on HEp-2 cells or an equivalent positive test. This means that the criteria also can define patients who just miss classification with SLE by meeting the ANA standard and by tallying 8 or 9 points, and the criteria also identify patients who far exceed the classification threshold by having the requisite ANA plus racking up as many as, perhaps, 20 or 30 points.

“This is a real research opportunity,” to follow patients who fall just short with 8 or 9 points to assess their longer-term prognosis, as well as to study whether “higher scores mean a higher risk for developing a bad outcome,” said Dr. Johnson, a rheumatologist at the University of Toronto and director of the Toronto Scleroderma Program. Other areas for future research with the new criteria include seeing how they work in various SLE subgroups, such as patients with renal-predominant disease or skin-predominant disease, and also seeing how they work in various ethnic populations.

That’s because “85% of our experts said that they would feel confident classifying a patient as having lupus based only on a renal biopsy” and ANA positivity, said Dr. Johnson, who served as the ACR-appointed cochair of the criteria-writing panel along with a cochair selected by EULAR, Martin Aringer, MD, PhD, of the Technical University of Dresden (Germany). She cautioned that other levels of lupus nephritis, class II or V, confer only 8 points to the classification and so by themselves are not enough to label a person as having lupus.

During her presentation, Dr. Johnson cited the high levels of sensitivity and specificity that the new classification criteria demonstrated in a validation cohort of more than 1,000 cases and controls. In the validation analysis, the new criteria had a sensitivity of 96.12% and specificity of 94.43% for classifying SLE, giving the new criteria a better result on both these measures than either the 1997 ACR criteria (Arthritis Rheum. 1997 Sept;40[9]:1725) or the 2012 Systemic Lupus International Collaborating Clinics criteria (Arthritis Rheum. 2012 Aug;64[8]:2677-86).

The 22 criteria cluster into seven separate clinical domains and three different immunologic domains. The point values assigned to each criterion range from 2 to 10 points.

Dr. Johnson had no disclosures.

[email protected]

AMSTERDAM – The first European League Against Rheumatism and American College of Rheumatology joint criteria for classifying systemic lupus erythematosus have a sensitivity and a specificity of more than 90%.

This is important because they improve upon the existing ACR and Systemic Lupus International Collaborating Clinics (SLICC) criteria, said Martin Aringer, MD, PhD, who cochaired the Steering Committee that produced the new classification criteria.

Most clinicians working with lupus are familiar with the 1997 ACR criteria for the classification of systemic lupus erythematosus (SLE), which “had a relatively simple structure,” Dr. Aringer said during the opening plenary abstract session at the European Congress of Rheumatology. These considered items such as the presence of malar or discoid rash, photosensitivity, oral ulcers and arthritis, among others. These had a high specificity but a lower sensitivity. The development of the SLICC criteria in 2012 improved upon the sensitivity of the ACR criteria (92%-99% vs. 77%-91%), but at a loss in specificity (74%–88% vs. 91%-96%).

The SLICC criteria introduced two novel ideas, said Dr. Aringer, professor of medicine and chief of the division of rheumatology at the Technical University of Dresden (Germany). The first was that there had to be at least one immunologic criterion met, and the second was that biopsy-proven lupus nephritis had to be present with antinuclear antibodies (ANA) and anti-DNA antibodies detected.

One of the goals in developing the joint EULAR/ACR criteria therefore was to try to maintain the respective sensitivity and specificity achieved with the SLICC and ACR criteria. One of the key things that the new criteria looked at was to see if ANA could be used as an entry criterion. Investigations involving more than 13,000 patients with SLE showed that it could, with a antibody titer threshold of 1:80, exhibit a sensitivity of 98% (Arthritis Care Res. 2018;70[3]:428-38). Another goal was to see if histology-proven nephritis was a stronger predictor of SLE than clinical factors, such as oral ulcers, and to identify items that would only be included if there was no other more likely explanation (Lupus. 2016;25[8]:805-11).

Draft SLE classification criteria were developed based on an expert Delphi process and included ANA as an entry criterion and weighted items according to the likelihood of being associated with lupus. Items considered included the presence and severity of lupus nephritis, serology and other antibody tests, skin and central nervous system involvement, and hematologic and immunologic criteria such as the presence of thrombocytopenia and low complement (C3 and/or C4).

Sara Freeman/MDedge News

SOURCE: Aringer M et al. Ann Rheum Dis. 2018;77(Suppl 2):60. Abstract OP0020.

AMSTERDAM – The first European League Against Rheumatism and American College of Rheumatology joint criteria for classifying systemic lupus erythematosus have a sensitivity and a specificity of more than 90%.

This is important because they improve upon the existing ACR and Systemic Lupus International Collaborating Clinics (SLICC) criteria, said Martin Aringer, MD, PhD, who cochaired the Steering Committee that produced the new classification criteria.

Most clinicians working with lupus are familiar with the 1997 ACR criteria for the classification of systemic lupus erythematosus (SLE), which “had a relatively simple structure,” Dr. Aringer said during the opening plenary abstract session at the European Congress of Rheumatology. These considered items such as the presence of malar or discoid rash, photosensitivity, oral ulcers and arthritis, among others. These had a high specificity but a lower sensitivity. The development of the SLICC criteria in 2012 improved upon the sensitivity of the ACR criteria (92%-99% vs. 77%-91%), but at a loss in specificity (74%–88% vs. 91%-96%).

The SLICC criteria introduced two novel ideas, said Dr. Aringer, professor of medicine and chief of the division of rheumatology at the Technical University of Dresden (Germany). The first was that there had to be at least one immunologic criterion met, and the second was that biopsy-proven lupus nephritis had to be present with antinuclear antibodies (ANA) and anti-DNA antibodies detected.

One of the goals in developing the joint EULAR/ACR criteria therefore was to try to maintain the respective sensitivity and specificity achieved with the SLICC and ACR criteria. One of the key things that the new criteria looked at was to see if ANA could be used as an entry criterion. Investigations involving more than 13,000 patients with SLE showed that it could, with a antibody titer threshold of 1:80, exhibit a sensitivity of 98% (Arthritis Care Res. 2018;70[3]:428-38). Another goal was to see if histology-proven nephritis was a stronger predictor of SLE than clinical factors, such as oral ulcers, and to identify items that would only be included if there was no other more likely explanation (Lupus. 2016;25[8]:805-11).

Draft SLE classification criteria were developed based on an expert Delphi process and included ANA as an entry criterion and weighted items according to the likelihood of being associated with lupus. Items considered included the presence and severity of lupus nephritis, serology and other antibody tests, skin and central nervous system involvement, and hematologic and immunologic criteria such as the presence of thrombocytopenia and low complement (C3 and/or C4).

Sara Freeman/MDedge News

SOURCE: Aringer M et al. Ann Rheum Dis. 2018;77(Suppl 2):60. Abstract OP0020.

AMSTERDAM – The first European League Against Rheumatism and American College of Rheumatology joint criteria for classifying systemic lupus erythematosus have a sensitivity and a specificity of more than 90%.

This is important because they improve upon the existing ACR and Systemic Lupus International Collaborating Clinics (SLICC) criteria, said Martin Aringer, MD, PhD, who cochaired the Steering Committee that produced the new classification criteria.

Most clinicians working with lupus are familiar with the 1997 ACR criteria for the classification of systemic lupus erythematosus (SLE), which “had a relatively simple structure,” Dr. Aringer said during the opening plenary abstract session at the European Congress of Rheumatology. These considered items such as the presence of malar or discoid rash, photosensitivity, oral ulcers and arthritis, among others. These had a high specificity but a lower sensitivity. The development of the SLICC criteria in 2012 improved upon the sensitivity of the ACR criteria (92%-99% vs. 77%-91%), but at a loss in specificity (74%–88% vs. 91%-96%).

The SLICC criteria introduced two novel ideas, said Dr. Aringer, professor of medicine and chief of the division of rheumatology at the Technical University of Dresden (Germany). The first was that there had to be at least one immunologic criterion met, and the second was that biopsy-proven lupus nephritis had to be present with antinuclear antibodies (ANA) and anti-DNA antibodies detected.

One of the goals in developing the joint EULAR/ACR criteria therefore was to try to maintain the respective sensitivity and specificity achieved with the SLICC and ACR criteria. One of the key things that the new criteria looked at was to see if ANA could be used as an entry criterion. Investigations involving more than 13,000 patients with SLE showed that it could, with a antibody titer threshold of 1:80, exhibit a sensitivity of 98% (Arthritis Care Res. 2018;70[3]:428-38). Another goal was to see if histology-proven nephritis was a stronger predictor of SLE than clinical factors, such as oral ulcers, and to identify items that would only be included if there was no other more likely explanation (Lupus. 2016;25[8]:805-11).

Draft SLE classification criteria were developed based on an expert Delphi process and included ANA as an entry criterion and weighted items according to the likelihood of being associated with lupus. Items considered included the presence and severity of lupus nephritis, serology and other antibody tests, skin and central nervous system involvement, and hematologic and immunologic criteria such as the presence of thrombocytopenia and low complement (C3 and/or C4).

Sara Freeman/MDedge News

SOURCE: Aringer M et al. Ann Rheum Dis. 2018;77(Suppl 2):60. Abstract OP0020.

AMSTERDAM – Treatment with the anti-inflammatory, interleukin-1 blocking drug canakinumab roughly halves gout attacks in an exploratory, post hoc analysis of data collected from more than 10,000 patients in the CANTOS multicenter, randomized trial.

While this result is only a hypothesis-generating suggestion that blocking interleukin (IL)-1 beta can have a significant impact on the frequency of gout flares, it serves as a proof-of-concept that IL-1 beta blockade is a potentially clinically meaningful strategy for future efforts to block gout attacks, Daniel H. Solomon, MD, said at the European Congress of Rheumatology.

“IL-1 beta is incredibly important in the inflammation associated with gout. Gout is considered by many to be the canonical IL-1 beta disease,” and hence it was important to examine the impact that treatment with the IL-1 beta blocker canakinumab had on gout in the CANTOS trial, Dr. Solomon explained in a video interview.

The answer was that treatment with canakinumab was linked with a roughly 50% reduction in gout flares in the total study group. The same reduction was seen in both the subgroups of patients with and without a history of gout. The effect was seen across all three subgroups of patients, based on their baseline serum urate levels including those with normal, elevated, or very elevated levels and across all the other prespecified subgroups including divisions based on sex, age, baseline body mass index, and baseline level of high-sensitivity C-reactive protein (hsCRP).

It’s also unclear that canakinumab (Ilaris) is the best type of IL-1 beta blocking drug to use for prevention of gout flares. In CANTOS, this expensive drug was administered subcutaneously every 3 months. A more appropriate agent might be an oral, small-molecule drug that blocks IL-1 beta. Several examples of this type of agent are currently in clinical development, said Dr. Solomon, a professor of medicine at Harvard Medical School and a rheumatologist at Brigham and Women’s Hospital, both in Boston.

CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study) randomized 10,061 patients with a history of MI and a hsCRP level of at least 2 mg/L at centers in 39 countries. The study’s primary endpoint was the combined rate of cardiovascular death, MI, or stroke, and canakinumab treatment at the 150-mg dosage level linked with a 15% relative reduction in this endpoint, compared with placebo in this secondary-prevention study (N Engl J Med. 2017 Sept 21;377[12]:1119-31). The study also randomized patients to either of two other canakinumab dosages, 50 mg or 300 mg, administered every 3 months, and, while each of these produced reductions in the primary endpoint relative to placebo, the 150-mg dosage had the largest effect. In the gout analysis reported by Dr. Solomon, the three different canakinumab dosages produced somewhat different levels of gout-flare reductions, but, generally, the effect was similar across the three treatment groups.

In the total study population, regardless of gout history, treatment with 50 mg, 150 mg, and 300 mg canakinumab every 3 months was linked with a reduction in gout attacks of 46%, 57%, and 53%, respectively, compared with placebo-treated patients, Dr. Solomon reported. The three dosages also uniformly produced significantly drops in serum levels of hsCRP, compared with placebo, but canakinumab treatment had no impact on serum urate levels, indicating that the gout-reducing effects of the drug did not occur via a mechanism that involved serum urate.

Because CANTOS exclusively enrolled patients with established coronary disease, the new analysis could not address whether IL-1 beta blockade would also be an effective strategy for reducing gout flares in people without cardiovascular disease, Dr. Solomon cautioned. Although it probably would, he said. He also stressed that treatment with an IL-1 blocking drug should not be seen as a substitute for appropriate urate-lowering treatment in patients with elevated levels of serum urate.

[email protected]

SOURCE: Solomon DH et al. Ann Rheum Dis. 2018;77(Suppl 2):56. Abstract OP0014.

AMSTERDAM – Treatment with the anti-inflammatory, interleukin-1 blocking drug canakinumab roughly halves gout attacks in an exploratory, post hoc analysis of data collected from more than 10,000 patients in the CANTOS multicenter, randomized trial.

While this result is only a hypothesis-generating suggestion that blocking interleukin (IL)-1 beta can have a significant impact on the frequency of gout flares, it serves as a proof-of-concept that IL-1 beta blockade is a potentially clinically meaningful strategy for future efforts to block gout attacks, Daniel H. Solomon, MD, said at the European Congress of Rheumatology.

“IL-1 beta is incredibly important in the inflammation associated with gout. Gout is considered by many to be the canonical IL-1 beta disease,” and hence it was important to examine the impact that treatment with the IL-1 beta blocker canakinumab had on gout in the CANTOS trial, Dr. Solomon explained in a video interview.

The answer was that treatment with canakinumab was linked with a roughly 50% reduction in gout flares in the total study group. The same reduction was seen in both the subgroups of patients with and without a history of gout. The effect was seen across all three subgroups of patients, based on their baseline serum urate levels including those with normal, elevated, or very elevated levels and across all the other prespecified subgroups including divisions based on sex, age, baseline body mass index, and baseline level of high-sensitivity C-reactive protein (hsCRP).

It’s also unclear that canakinumab (Ilaris) is the best type of IL-1 beta blocking drug to use for prevention of gout flares. In CANTOS, this expensive drug was administered subcutaneously every 3 months. A more appropriate agent might be an oral, small-molecule drug that blocks IL-1 beta. Several examples of this type of agent are currently in clinical development, said Dr. Solomon, a professor of medicine at Harvard Medical School and a rheumatologist at Brigham and Women’s Hospital, both in Boston.

CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study) randomized 10,061 patients with a history of MI and a hsCRP level of at least 2 mg/L at centers in 39 countries. The study’s primary endpoint was the combined rate of cardiovascular death, MI, or stroke, and canakinumab treatment at the 150-mg dosage level linked with a 15% relative reduction in this endpoint, compared with placebo in this secondary-prevention study (N Engl J Med. 2017 Sept 21;377[12]:1119-31). The study also randomized patients to either of two other canakinumab dosages, 50 mg or 300 mg, administered every 3 months, and, while each of these produced reductions in the primary endpoint relative to placebo, the 150-mg dosage had the largest effect. In the gout analysis reported by Dr. Solomon, the three different canakinumab dosages produced somewhat different levels of gout-flare reductions, but, generally, the effect was similar across the three treatment groups.

In the total study population, regardless of gout history, treatment with 50 mg, 150 mg, and 300 mg canakinumab every 3 months was linked with a reduction in gout attacks of 46%, 57%, and 53%, respectively, compared with placebo-treated patients, Dr. Solomon reported. The three dosages also uniformly produced significantly drops in serum levels of hsCRP, compared with placebo, but canakinumab treatment had no impact on serum urate levels, indicating that the gout-reducing effects of the drug did not occur via a mechanism that involved serum urate.

Because CANTOS exclusively enrolled patients with established coronary disease, the new analysis could not address whether IL-1 beta blockade would also be an effective strategy for reducing gout flares in people without cardiovascular disease, Dr. Solomon cautioned. Although it probably would, he said. He also stressed that treatment with an IL-1 blocking drug should not be seen as a substitute for appropriate urate-lowering treatment in patients with elevated levels of serum urate.

[email protected]

SOURCE: Solomon DH et al. Ann Rheum Dis. 2018;77(Suppl 2):56. Abstract OP0014.

AMSTERDAM – Treatment with the anti-inflammatory, interleukin-1 blocking drug canakinumab roughly halves gout attacks in an exploratory, post hoc analysis of data collected from more than 10,000 patients in the CANTOS multicenter, randomized trial.

While this result is only a hypothesis-generating suggestion that blocking interleukin (IL)-1 beta can have a significant impact on the frequency of gout flares, it serves as a proof-of-concept that IL-1 beta blockade is a potentially clinically meaningful strategy for future efforts to block gout attacks, Daniel H. Solomon, MD, said at the European Congress of Rheumatology.

“IL-1 beta is incredibly important in the inflammation associated with gout. Gout is considered by many to be the canonical IL-1 beta disease,” and hence it was important to examine the impact that treatment with the IL-1 beta blocker canakinumab had on gout in the CANTOS trial, Dr. Solomon explained in a video interview.

The answer was that treatment with canakinumab was linked with a roughly 50% reduction in gout flares in the total study group. The same reduction was seen in both the subgroups of patients with and without a history of gout. The effect was seen across all three subgroups of patients, based on their baseline serum urate levels including those with normal, elevated, or very elevated levels and across all the other prespecified subgroups including divisions based on sex, age, baseline body mass index, and baseline level of high-sensitivity C-reactive protein (hsCRP).

It’s also unclear that canakinumab (Ilaris) is the best type of IL-1 beta blocking drug to use for prevention of gout flares. In CANTOS, this expensive drug was administered subcutaneously every 3 months. A more appropriate agent might be an oral, small-molecule drug that blocks IL-1 beta. Several examples of this type of agent are currently in clinical development, said Dr. Solomon, a professor of medicine at Harvard Medical School and a rheumatologist at Brigham and Women’s Hospital, both in Boston.

CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study) randomized 10,061 patients with a history of MI and a hsCRP level of at least 2 mg/L at centers in 39 countries. The study’s primary endpoint was the combined rate of cardiovascular death, MI, or stroke, and canakinumab treatment at the 150-mg dosage level linked with a 15% relative reduction in this endpoint, compared with placebo in this secondary-prevention study (N Engl J Med. 2017 Sept 21;377[12]:1119-31). The study also randomized patients to either of two other canakinumab dosages, 50 mg or 300 mg, administered every 3 months, and, while each of these produced reductions in the primary endpoint relative to placebo, the 150-mg dosage had the largest effect. In the gout analysis reported by Dr. Solomon, the three different canakinumab dosages produced somewhat different levels of gout-flare reductions, but, generally, the effect was similar across the three treatment groups.

In the total study population, regardless of gout history, treatment with 50 mg, 150 mg, and 300 mg canakinumab every 3 months was linked with a reduction in gout attacks of 46%, 57%, and 53%, respectively, compared with placebo-treated patients, Dr. Solomon reported. The three dosages also uniformly produced significantly drops in serum levels of hsCRP, compared with placebo, but canakinumab treatment had no impact on serum urate levels, indicating that the gout-reducing effects of the drug did not occur via a mechanism that involved serum urate.

Because CANTOS exclusively enrolled patients with established coronary disease, the new analysis could not address whether IL-1 beta blockade would also be an effective strategy for reducing gout flares in people without cardiovascular disease, Dr. Solomon cautioned. Although it probably would, he said. He also stressed that treatment with an IL-1 blocking drug should not be seen as a substitute for appropriate urate-lowering treatment in patients with elevated levels of serum urate.

[email protected]

SOURCE: Solomon DH et al. Ann Rheum Dis. 2018;77(Suppl 2):56. Abstract OP0014.

AMSTERDAM – The attempt to determine whether biologics such as tumor necrosis factor inhibitors (TNFi) inhibit progression of ankylosing spondylitis has been pursued with observational studies, but these types of studies will never definitively answer the question, according to Robert B.M. Landewé, MD, PhD, professor of rheumatology at the University of Amsterdam.

“The methodology is sensitive to a lot of measurement error, making the results spurious,” Dr. Landewé said in an interview, recapping remarks he made in a presentation at the European Congress of Rheumatology.

This was disappointing to many investigators, including several speaking in the same symposium where Dr. Landewé made his remarks. Randomized, controlled trials that employ serial radiographs to document changes in ankylosing spondylitis are expensive, making observational studies an attractive surrogate, but Dr. Landewé said such studies are associated with an inherent risk of residual confounding.

In addition, he believes the effect size of biologics on progression, if it exists at all, is likely to be subtle. In the observational studies that have concluded that there is protection, complicated statistical analyses have been typically employed to produce a significant finding.

Observational studies do have hypothesis-generating value, according to Dr. Landewé, but he cautioned that they produce “more questions than answers.” He also emphasized that the inflammation-related progression that leads to bone growth in ankylosing spondylitis is different than it is in the destructive inflammatory diseases, such as rheumatoid arthritis, where the issue is bone loss.

It is rational to assume that effective anti-inflammatory therapy would prevent progression of inflammatory diseases, but Dr. Landewé said in his presentation that this is the type of bias that undermines the value of observational studies for reaching objective conclusions. Unlike the results of a registered randomized, controlled trial, which will be known to be consistent or not with the underlying hypothesis, there is a strong risk that data in an observational study will be reworked until they produce the desired result.

AMSTERDAM – The attempt to determine whether biologics such as tumor necrosis factor inhibitors (TNFi) inhibit progression of ankylosing spondylitis has been pursued with observational studies, but these types of studies will never definitively answer the question, according to Robert B.M. Landewé, MD, PhD, professor of rheumatology at the University of Amsterdam.

“The methodology is sensitive to a lot of measurement error, making the results spurious,” Dr. Landewé said in an interview, recapping remarks he made in a presentation at the European Congress of Rheumatology.

This was disappointing to many investigators, including several speaking in the same symposium where Dr. Landewé made his remarks. Randomized, controlled trials that employ serial radiographs to document changes in ankylosing spondylitis are expensive, making observational studies an attractive surrogate, but Dr. Landewé said such studies are associated with an inherent risk of residual confounding.

In addition, he believes the effect size of biologics on progression, if it exists at all, is likely to be subtle. In the observational studies that have concluded that there is protection, complicated statistical analyses have been typically employed to produce a significant finding.

Observational studies do have hypothesis-generating value, according to Dr. Landewé, but he cautioned that they produce “more questions than answers.” He also emphasized that the inflammation-related progression that leads to bone growth in ankylosing spondylitis is different than it is in the destructive inflammatory diseases, such as rheumatoid arthritis, where the issue is bone loss.

It is rational to assume that effective anti-inflammatory therapy would prevent progression of inflammatory diseases, but Dr. Landewé said in his presentation that this is the type of bias that undermines the value of observational studies for reaching objective conclusions. Unlike the results of a registered randomized, controlled trial, which will be known to be consistent or not with the underlying hypothesis, there is a strong risk that data in an observational study will be reworked until they produce the desired result.

AMSTERDAM – The attempt to determine whether biologics such as tumor necrosis factor inhibitors (TNFi) inhibit progression of ankylosing spondylitis has been pursued with observational studies, but these types of studies will never definitively answer the question, according to Robert B.M. Landewé, MD, PhD, professor of rheumatology at the University of Amsterdam.

“The methodology is sensitive to a lot of measurement error, making the results spurious,” Dr. Landewé said in an interview, recapping remarks he made in a presentation at the European Congress of Rheumatology.

This was disappointing to many investigators, including several speaking in the same symposium where Dr. Landewé made his remarks. Randomized, controlled trials that employ serial radiographs to document changes in ankylosing spondylitis are expensive, making observational studies an attractive surrogate, but Dr. Landewé said such studies are associated with an inherent risk of residual confounding.

In addition, he believes the effect size of biologics on progression, if it exists at all, is likely to be subtle. In the observational studies that have concluded that there is protection, complicated statistical analyses have been typically employed to produce a significant finding.

Observational studies do have hypothesis-generating value, according to Dr. Landewé, but he cautioned that they produce “more questions than answers.” He also emphasized that the inflammation-related progression that leads to bone growth in ankylosing spondylitis is different than it is in the destructive inflammatory diseases, such as rheumatoid arthritis, where the issue is bone loss.

It is rational to assume that effective anti-inflammatory therapy would prevent progression of inflammatory diseases, but Dr. Landewé said in his presentation that this is the type of bias that undermines the value of observational studies for reaching objective conclusions. Unlike the results of a registered randomized, controlled trial, which will be known to be consistent or not with the underlying hypothesis, there is a strong risk that data in an observational study will be reworked until they produce the desired result.

AMSTERDAM – There is an increased relative risk of deliberate self-harm that results in emergency treatment among individuals newly diagnosed with ankylosing spondylitis, according to the results of a large, Canadian population-based study.

A diagnosis of ankylosing spondylitis was associated with a 59% increased risk of deliberate self-harm, compared with no diagnosis (HR = 1.59, 95% CI, 1.16-2.21). While the risk of deliberate self-harm in patients diagnosed with rheumatoid arthritis (RA) was initially elevated, the association was not significant after adjustment for confounding factors (HR = 1.08, 95% CI, 0.87-1.34).

These findings call for heightened awareness among clinicians, study investigator Nigil Haroon, MD, PhD, said in an interview at the European Congress of Rheumatology. “Depression is generally well known to be increased in patients with chronic diseases, especially so with chronic inflammatory rheumatic diseases like ankylosing spondylitis and rheumatoid arthritis,” he said. This may in turn be linked to increased cases of deliberate self-harm, but there have been few studies to determine if this is the case, he said, which may be because it is a relatively rare event in routine clinical practice.

Dr. Haroon, who runs a specialist clinic in ankylosing spondylitis in Toronto, has seen the long-term effects of chronic pain, lack of social support, and inability to sleep on patients’ mood first hand. This is what drove him and other colleagues at the University of Toronto and University Health Network to look at the possibility that this could be linked to an increased risk for depression and perhaps deliberate self-harm among newly diagnosed patients.

To try to estimate the risk, they obtained administrative data on more than 100,000 individuals diagnosed with ankylosing spondylitis or RA in the province of Ontario, Canada, between 2002 and 2014. Excluding those with a history of mental illness or a prior self-harm attempt resulted in the creation of two cohorts of patients – 13,964 with ankylosing spondylitis and 53,240 with RA. Indviduals in these two cohorts were then matched, 4:1, to similar controls in the general population.

The average age of those diagnosed with ankylosing spondylitis was 46 years and of those with RA was 57 years, with more males than females in the ankylosing spondylitis group (57% vs. 43%) and more females than males in the RA group (67% vs. 33%).

The main outcome assessed was the first episode of intentional self-injury or self-poisoning that required emergency treatment that occurred after the diagnosis of ankylosing spondylitis or RA.

Overall, there were 69 deliberate self-harm attempts recorded in the ankylosing spondylitis patient group, compared with 131 attempts in the non-ankylosing spondylitis group. In the RA patient group, there were 129 attempts, and 372 attempts in the non-RA group.

Poisoning was “by far the most common modality” used to intentionally self-harm, used by 67% of patients with ankylosing spondylitis and by 81% of those with RA, Dr. Haroon reported. Contact with a sharp object was the second most common method used to deliberately self-harm by 30% of ankylosing spondylitis patients and 16% of RA patients.

Most (70%) patients were discharged following emergency treatment for a deliberate self-harm attempt, with around 15% of ankylosing spondylitis and 22% of RA patients requiring hospital admission.

“For any chronic disease there is a potential for depression to settle, and we should identify [patients] early, even at the primary care levels itself and try to address it,” Dr. Haroon advised. It’s important to spend time and to develop a good rapport with your patients, he added, which can help them open up and talk about their mood.

The work was funded by the Division of Rheumatology Pfizer Research Chair, University of Toronto. Dr. Haroon reported having no relevant financial disclosures.

SOURCE: Kuriya B et al. Ann Rheum Dis. 2018;77(Suppl 2):195. Abstract OP0296.
 

AMSTERDAM – There is an increased relative risk of deliberate self-harm that results in emergency treatment among individuals newly diagnosed with ankylosing spondylitis, according to the results of a large, Canadian population-based study.

A diagnosis of ankylosing spondylitis was associated with a 59% increased risk of deliberate self-harm, compared with no diagnosis (HR = 1.59, 95% CI, 1.16-2.21). While the risk of deliberate self-harm in patients diagnosed with rheumatoid arthritis (RA) was initially elevated, the association was not significant after adjustment for confounding factors (HR = 1.08, 95% CI, 0.87-1.34).

These findings call for heightened awareness among clinicians, study investigator Nigil Haroon, MD, PhD, said in an interview at the European Congress of Rheumatology. “Depression is generally well known to be increased in patients with chronic diseases, especially so with chronic inflammatory rheumatic diseases like ankylosing spondylitis and rheumatoid arthritis,” he said. This may in turn be linked to increased cases of deliberate self-harm, but there have been few studies to determine if this is the case, he said, which may be because it is a relatively rare event in routine clinical practice.

Dr. Haroon, who runs a specialist clinic in ankylosing spondylitis in Toronto, has seen the long-term effects of chronic pain, lack of social support, and inability to sleep on patients’ mood first hand. This is what drove him and other colleagues at the University of Toronto and University Health Network to look at the possibility that this could be linked to an increased risk for depression and perhaps deliberate self-harm among newly diagnosed patients.

To try to estimate the risk, they obtained administrative data on more than 100,000 individuals diagnosed with ankylosing spondylitis or RA in the province of Ontario, Canada, between 2002 and 2014. Excluding those with a history of mental illness or a prior self-harm attempt resulted in the creation of two cohorts of patients – 13,964 with ankylosing spondylitis and 53,240 with RA. Indviduals in these two cohorts were then matched, 4:1, to similar controls in the general population.

The average age of those diagnosed with ankylosing spondylitis was 46 years and of those with RA was 57 years, with more males than females in the ankylosing spondylitis group (57% vs. 43%) and more females than males in the RA group (67% vs. 33%).

The main outcome assessed was the first episode of intentional self-injury or self-poisoning that required emergency treatment that occurred after the diagnosis of ankylosing spondylitis or RA.

Overall, there were 69 deliberate self-harm attempts recorded in the ankylosing spondylitis patient group, compared with 131 attempts in the non-ankylosing spondylitis group. In the RA patient group, there were 129 attempts, and 372 attempts in the non-RA group.

Poisoning was “by far the most common modality” used to intentionally self-harm, used by 67% of patients with ankylosing spondylitis and by 81% of those with RA, Dr. Haroon reported. Contact with a sharp object was the second most common method used to deliberately self-harm by 30% of ankylosing spondylitis patients and 16% of RA patients.

Most (70%) patients were discharged following emergency treatment for a deliberate self-harm attempt, with around 15% of ankylosing spondylitis and 22% of RA patients requiring hospital admission.

“For any chronic disease there is a potential for depression to settle, and we should identify [patients] early, even at the primary care levels itself and try to address it,” Dr. Haroon advised. It’s important to spend time and to develop a good rapport with your patients, he added, which can help them open up and talk about their mood.

The work was funded by the Division of Rheumatology Pfizer Research Chair, University of Toronto. Dr. Haroon reported having no relevant financial disclosures.

SOURCE: Kuriya B et al. Ann Rheum Dis. 2018;77(Suppl 2):195. Abstract OP0296.
 

AMSTERDAM – There is an increased relative risk of deliberate self-harm that results in emergency treatment among individuals newly diagnosed with ankylosing spondylitis, according to the results of a large, Canadian population-based study.

A diagnosis of ankylosing spondylitis was associated with a 59% increased risk of deliberate self-harm, compared with no diagnosis (HR = 1.59, 95% CI, 1.16-2.21). While the risk of deliberate self-harm in patients diagnosed with rheumatoid arthritis (RA) was initially elevated, the association was not significant after adjustment for confounding factors (HR = 1.08, 95% CI, 0.87-1.34).

These findings call for heightened awareness among clinicians, study investigator Nigil Haroon, MD, PhD, said in an interview at the European Congress of Rheumatology. “Depression is generally well known to be increased in patients with chronic diseases, especially so with chronic inflammatory rheumatic diseases like ankylosing spondylitis and rheumatoid arthritis,” he said. This may in turn be linked to increased cases of deliberate self-harm, but there have been few studies to determine if this is the case, he said, which may be because it is a relatively rare event in routine clinical practice.

Dr. Haroon, who runs a specialist clinic in ankylosing spondylitis in Toronto, has seen the long-term effects of chronic pain, lack of social support, and inability to sleep on patients’ mood first hand. This is what drove him and other colleagues at the University of Toronto and University Health Network to look at the possibility that this could be linked to an increased risk for depression and perhaps deliberate self-harm among newly diagnosed patients.

To try to estimate the risk, they obtained administrative data on more than 100,000 individuals diagnosed with ankylosing spondylitis or RA in the province of Ontario, Canada, between 2002 and 2014. Excluding those with a history of mental illness or a prior self-harm attempt resulted in the creation of two cohorts of patients – 13,964 with ankylosing spondylitis and 53,240 with RA. Indviduals in these two cohorts were then matched, 4:1, to similar controls in the general population.

The average age of those diagnosed with ankylosing spondylitis was 46 years and of those with RA was 57 years, with more males than females in the ankylosing spondylitis group (57% vs. 43%) and more females than males in the RA group (67% vs. 33%).

The main outcome assessed was the first episode of intentional self-injury or self-poisoning that required emergency treatment that occurred after the diagnosis of ankylosing spondylitis or RA.

Overall, there were 69 deliberate self-harm attempts recorded in the ankylosing spondylitis patient group, compared with 131 attempts in the non-ankylosing spondylitis group. In the RA patient group, there were 129 attempts, and 372 attempts in the non-RA group.

Poisoning was “by far the most common modality” used to intentionally self-harm, used by 67% of patients with ankylosing spondylitis and by 81% of those with RA, Dr. Haroon reported. Contact with a sharp object was the second most common method used to deliberately self-harm by 30% of ankylosing spondylitis patients and 16% of RA patients.

Most (70%) patients were discharged following emergency treatment for a deliberate self-harm attempt, with around 15% of ankylosing spondylitis and 22% of RA patients requiring hospital admission.

“For any chronic disease there is a potential for depression to settle, and we should identify [patients] early, even at the primary care levels itself and try to address it,” Dr. Haroon advised. It’s important to spend time and to develop a good rapport with your patients, he added, which can help them open up and talk about their mood.

The work was funded by the Division of Rheumatology Pfizer Research Chair, University of Toronto. Dr. Haroon reported having no relevant financial disclosures.

SOURCE: Kuriya B et al. Ann Rheum Dis. 2018;77(Suppl 2):195. Abstract OP0296.
 

AMSTERDAM – A significantly higher proportion of patients with lupus experienced improvements in joint and skin symptoms if they were treated with baricitinib (Olumiant) than if they received placebo in a phase 2 trial.

The primary endpoint of arthritis or rash resolution as measured by the Systemic Lupus Erythematosus (SLE) Disease Activity Index 2000 (SLEDAI-2K) was met by approximately 67% of patients who were treated with 4 mg baricitinib once daily and by around 53% of patients given a matching placebo (P less than .05).

SOURCE: Wallace DJ et al. Ann Rheum Dis. 2018;77(Suppl 2):59. Abstract OP0019.

AMSTERDAM – A significantly higher proportion of patients with lupus experienced improvements in joint and skin symptoms if they were treated with baricitinib (Olumiant) than if they received placebo in a phase 2 trial.

The primary endpoint of arthritis or rash resolution as measured by the Systemic Lupus Erythematosus (SLE) Disease Activity Index 2000 (SLEDAI-2K) was met by approximately 67% of patients who were treated with 4 mg baricitinib once daily and by around 53% of patients given a matching placebo (P less than .05).

SOURCE: Wallace DJ et al. Ann Rheum Dis. 2018;77(Suppl 2):59. Abstract OP0019.

AMSTERDAM – A significantly higher proportion of patients with lupus experienced improvements in joint and skin symptoms if they were treated with baricitinib (Olumiant) than if they received placebo in a phase 2 trial.

The primary endpoint of arthritis or rash resolution as measured by the Systemic Lupus Erythematosus (SLE) Disease Activity Index 2000 (SLEDAI-2K) was met by approximately 67% of patients who were treated with 4 mg baricitinib once daily and by around 53% of patients given a matching placebo (P less than .05).

SOURCE: Wallace DJ et al. Ann Rheum Dis. 2018;77(Suppl 2):59. Abstract OP0019.

CHICAGO – Preoperative chemotherapy improves outcomes in patients with resectable or borderline resectable pancreatic cancer, preliminary findings from the phase 3 PREOPANC-1 trial suggest.

Overall survival in 127 patients randomized to immediate surgery followed by adjuvant chemotherapy was 13.7 months vs. 17.1 months in 119 patients randomized to receive preoperative chemoradiotherapy and postoperative adjuvant chemotherapy, Geertjan van Tienhoven, MD, PhD, reported at the annual meeting of the American Society of Clinical Oncology.

The difference did not quite reach statistical significance, but final analysis requires an additional 26 events, Dr. van Tienhoven of Academic Medical Center, Amsterdam explained in a video interview at the meeting.

Other differences between the groups, which included disease-free survival, local control, and metastasis-free survival, did differ significantly in favor of preoperative chemotherapy, he said.

Of note, 72% and 62% of patients in the immediate surgery and preoperative chemoradiotherapy groups, respectively, underwent resection and a greater proportion of patients in the latter group achieved microscopically complete resection, he said (63% vs. 31%).

Should these results hold up in the final analysis, particularly if the difference in overall survival reaches statistical significance, “then this is a proof of principle and practice-changing trial,” Dr. van Tienhoven said.

Dr. van Tienhoven reported having no disclosures.

SOURCE: van Tienhoven et al. ASCO 2108, Abstract LBA4002.

CHICAGO – Preoperative chemotherapy improves outcomes in patients with resectable or borderline resectable pancreatic cancer, preliminary findings from the phase 3 PREOPANC-1 trial suggest.

Overall survival in 127 patients randomized to immediate surgery followed by adjuvant chemotherapy was 13.7 months vs. 17.1 months in 119 patients randomized to receive preoperative chemoradiotherapy and postoperative adjuvant chemotherapy, Geertjan van Tienhoven, MD, PhD, reported at the annual meeting of the American Society of Clinical Oncology.

The difference did not quite reach statistical significance, but final analysis requires an additional 26 events, Dr. van Tienhoven of Academic Medical Center, Amsterdam explained in a video interview at the meeting.

Other differences between the groups, which included disease-free survival, local control, and metastasis-free survival, did differ significantly in favor of preoperative chemotherapy, he said.

Of note, 72% and 62% of patients in the immediate surgery and preoperative chemoradiotherapy groups, respectively, underwent resection and a greater proportion of patients in the latter group achieved microscopically complete resection, he said (63% vs. 31%).

Should these results hold up in the final analysis, particularly if the difference in overall survival reaches statistical significance, “then this is a proof of principle and practice-changing trial,” Dr. van Tienhoven said.

Dr. van Tienhoven reported having no disclosures.

SOURCE: van Tienhoven et al. ASCO 2108, Abstract LBA4002.

CHICAGO – Preoperative chemotherapy improves outcomes in patients with resectable or borderline resectable pancreatic cancer, preliminary findings from the phase 3 PREOPANC-1 trial suggest.

Overall survival in 127 patients randomized to immediate surgery followed by adjuvant chemotherapy was 13.7 months vs. 17.1 months in 119 patients randomized to receive preoperative chemoradiotherapy and postoperative adjuvant chemotherapy, Geertjan van Tienhoven, MD, PhD, reported at the annual meeting of the American Society of Clinical Oncology.

The difference did not quite reach statistical significance, but final analysis requires an additional 26 events, Dr. van Tienhoven of Academic Medical Center, Amsterdam explained in a video interview at the meeting.

Other differences between the groups, which included disease-free survival, local control, and metastasis-free survival, did differ significantly in favor of preoperative chemotherapy, he said.

Of note, 72% and 62% of patients in the immediate surgery and preoperative chemoradiotherapy groups, respectively, underwent resection and a greater proportion of patients in the latter group achieved microscopically complete resection, he said (63% vs. 31%).

Should these results hold up in the final analysis, particularly if the difference in overall survival reaches statistical significance, “then this is a proof of principle and practice-changing trial,” Dr. van Tienhoven said.

Dr. van Tienhoven reported having no disclosures.

SOURCE: van Tienhoven et al. ASCO 2108, Abstract LBA4002.