Gout

VIENNA — To maintain gout in remission, nurses in a rheumatology service do better than doctors in implementing a straightforward treat-to-target (T2T) strategy, according to a randomized study that showed a consistent advantage across subgroups.

“Our study provides evidence that nurse-led therapy for gout leads to better uric acid control, which is an important consideration with the increasing incidence and the increasing costs of managing this condition,” said Jesper W. Larsen, a registered nurse affiliated with the Department of Rheumatology at North Denmark Regional Hospital, Hjørring, Denmark. He presented the study at the annual European Congress of Rheumatology.

The advantage of nurse-led care was seen across every subgroup evaluated. Moreover, more patients in the nurse-led group than in the usual care group remained on urate-lowering therapy at the end of the 2-year study.

The optimal management of gout is based on the treatment goal of lowering serum uric acid (sUA) to below the physiologic level of 0.36 mmol/L (6 mg/dL), a strategy called T2T that is endorsed by both EULAR and the American College of Rheumatology.

“This target can be reached in most patients with commonly used therapies, including allopurinol, which is relatively inexpensive,” Mr. Larsen said. Given that disease control and sustained remission are largely based on this target, he and his colleagues tested the hypothesis that nurses working in a rheumatology service could provide efficient and cost-effective care.

A total of 286 patients with gout defined by microscopy who were treated between 2015 and 2021 were enrolled in the study. Of these, 100 patients who had been enrolled before the introduction of nurse-led care received and were maintained on usual care, which generally included diagnosis by an orthopedist, an emergency room physician, or an internist, with subsequent treatment and follow-up with a general practitioner.

Of 186 patients treated after nurse-led care was implemented, 72 were transitioned to usual care, and the remaining 114 continued receiving nurse-led care over the next 2 years of follow-up. In the nurse-led care arm, nurses who specialized in rheumatology and were trained in gout management monitored a structured T2T strategy. They were available for consultation, provided patient education, and followed laboratory values, including sUA, which they used to adjust treatments.

Except in the case of complications, “there was no more contact with physicians” once care was transferred to the nurse, Mr. Larsen said. Most of the nurse management was based on sUA laboratory values and performed by telephone.

At 2 years, 112 patients in the nurse-led care group were compared with the 144 in the usual care group. Two of the 114 patients who entered the nurse-care cohort and 28 of the 172 in the usual care cohort died before the study ended.

At 2 years, the proportion of patients maintained at the target sUA was almost twice as great in the nurse-led arm (83% vs 44%). This was also true of patients aged 70 years or older (84% vs 45%), patients with tophi (60% vs 33%), and patients with sUA > 0.5 mmol/L at baseline (84% vs 44%). Nurse-led care also kept a greater proportion of patients at target who entered the study with an estimated glomerular filtration rate < 60 mL/min per 1.73 m² (84% vs 52%) or were taking diuretics (89% vs 52%). All differences reached statistical significance (P < .05).

The reason for the lower mortality at 2 years in the nurse-led group (4% vs 23%; P < .001) is unclear, according to Mr. Larsen. In addition to considering a selection bias that might have channeled patients with more severe disease to usual care, he and his coinvestigators are also considering whether the lower rates of sUA control in the usual care group might have led to a higher rate of cardiovascular events.

Because of some baseline imbalances, a selection bias cannot be ruled out, but the imbalances did not uniformly favor nurse-led care. For example, the proportion of patients with diabetes (23% vs 13%) or a baseline cancer diagnosis (11% vs 5%) was higher in the nurse-led care group. The proportion of patients with atrial fibrillation (45% vs 35%) or on diuretics (47% vs 33%) at baseline was higher in the usual care group.

The median age of 69 years was the same in the two groups, although the nurse-led group included a higher proportion of men to women (86% vs 76%).

Within a T2T strategy, nurses focused on reaching the target might do a better job than physicians in consistently monitoring and adjusting therapies as needed, but Mr. Larsen also speculated that nurses might offer a more collaborative approach and provide greater support through patient education and regular telephone contact.
 

Potential Advantages of Nurse-Led Care

Clinicians concerned about nurses missing nuances in disease progression or being slow to recognize complications might be surprised to learn about the advantage of nurse-led care, but Mwidimi Ndosi, PhD, an associate professor in rheumatology nursing at the University of the West of England, Bristol, England, was not.

“There is quite a large literature to show that nursing care is often superior to physician-led patient management in the appropriate circumstances,” Mr. Ndosi said. In this specific instance of gout management, he said that the treatment target is clear, and nurses are often able to devote more time to a specific goal, like T2T, than clinicians balancing more priorities.

trishudrebagici

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

VIENNA — To maintain gout in remission, nurses in a rheumatology service do better than doctors in implementing a straightforward treat-to-target (T2T) strategy, according to a randomized study that showed a consistent advantage across subgroups.

“Our study provides evidence that nurse-led therapy for gout leads to better uric acid control, which is an important consideration with the increasing incidence and the increasing costs of managing this condition,” said Jesper W. Larsen, a registered nurse affiliated with the Department of Rheumatology at North Denmark Regional Hospital, Hjørring, Denmark. He presented the study at the annual European Congress of Rheumatology.

The advantage of nurse-led care was seen across every subgroup evaluated. Moreover, more patients in the nurse-led group than in the usual care group remained on urate-lowering therapy at the end of the 2-year study.

The optimal management of gout is based on the treatment goal of lowering serum uric acid (sUA) to below the physiologic level of 0.36 mmol/L (6 mg/dL), a strategy called T2T that is endorsed by both EULAR and the American College of Rheumatology.

“This target can be reached in most patients with commonly used therapies, including allopurinol, which is relatively inexpensive,” Mr. Larsen said. Given that disease control and sustained remission are largely based on this target, he and his colleagues tested the hypothesis that nurses working in a rheumatology service could provide efficient and cost-effective care.

A total of 286 patients with gout defined by microscopy who were treated between 2015 and 2021 were enrolled in the study. Of these, 100 patients who had been enrolled before the introduction of nurse-led care received and were maintained on usual care, which generally included diagnosis by an orthopedist, an emergency room physician, or an internist, with subsequent treatment and follow-up with a general practitioner.

Of 186 patients treated after nurse-led care was implemented, 72 were transitioned to usual care, and the remaining 114 continued receiving nurse-led care over the next 2 years of follow-up. In the nurse-led care arm, nurses who specialized in rheumatology and were trained in gout management monitored a structured T2T strategy. They were available for consultation, provided patient education, and followed laboratory values, including sUA, which they used to adjust treatments.

Except in the case of complications, “there was no more contact with physicians” once care was transferred to the nurse, Mr. Larsen said. Most of the nurse management was based on sUA laboratory values and performed by telephone.

At 2 years, 112 patients in the nurse-led care group were compared with the 144 in the usual care group. Two of the 114 patients who entered the nurse-care cohort and 28 of the 172 in the usual care cohort died before the study ended.

At 2 years, the proportion of patients maintained at the target sUA was almost twice as great in the nurse-led arm (83% vs 44%). This was also true of patients aged 70 years or older (84% vs 45%), patients with tophi (60% vs 33%), and patients with sUA > 0.5 mmol/L at baseline (84% vs 44%). Nurse-led care also kept a greater proportion of patients at target who entered the study with an estimated glomerular filtration rate < 60 mL/min per 1.73 m² (84% vs 52%) or were taking diuretics (89% vs 52%). All differences reached statistical significance (P < .05).

The reason for the lower mortality at 2 years in the nurse-led group (4% vs 23%; P < .001) is unclear, according to Mr. Larsen. In addition to considering a selection bias that might have channeled patients with more severe disease to usual care, he and his coinvestigators are also considering whether the lower rates of sUA control in the usual care group might have led to a higher rate of cardiovascular events.

Because of some baseline imbalances, a selection bias cannot be ruled out, but the imbalances did not uniformly favor nurse-led care. For example, the proportion of patients with diabetes (23% vs 13%) or a baseline cancer diagnosis (11% vs 5%) was higher in the nurse-led care group. The proportion of patients with atrial fibrillation (45% vs 35%) or on diuretics (47% vs 33%) at baseline was higher in the usual care group.

The median age of 69 years was the same in the two groups, although the nurse-led group included a higher proportion of men to women (86% vs 76%).

Within a T2T strategy, nurses focused on reaching the target might do a better job than physicians in consistently monitoring and adjusting therapies as needed, but Mr. Larsen also speculated that nurses might offer a more collaborative approach and provide greater support through patient education and regular telephone contact.
 

Potential Advantages of Nurse-Led Care

Clinicians concerned about nurses missing nuances in disease progression or being slow to recognize complications might be surprised to learn about the advantage of nurse-led care, but Mwidimi Ndosi, PhD, an associate professor in rheumatology nursing at the University of the West of England, Bristol, England, was not.

“There is quite a large literature to show that nursing care is often superior to physician-led patient management in the appropriate circumstances,” Mr. Ndosi said. In this specific instance of gout management, he said that the treatment target is clear, and nurses are often able to devote more time to a specific goal, like T2T, than clinicians balancing more priorities.

trishudrebagici

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

VIENNA — To maintain gout in remission, nurses in a rheumatology service do better than doctors in implementing a straightforward treat-to-target (T2T) strategy, according to a randomized study that showed a consistent advantage across subgroups.

“Our study provides evidence that nurse-led therapy for gout leads to better uric acid control, which is an important consideration with the increasing incidence and the increasing costs of managing this condition,” said Jesper W. Larsen, a registered nurse affiliated with the Department of Rheumatology at North Denmark Regional Hospital, Hjørring, Denmark. He presented the study at the annual European Congress of Rheumatology.

The advantage of nurse-led care was seen across every subgroup evaluated. Moreover, more patients in the nurse-led group than in the usual care group remained on urate-lowering therapy at the end of the 2-year study.

The optimal management of gout is based on the treatment goal of lowering serum uric acid (sUA) to below the physiologic level of 0.36 mmol/L (6 mg/dL), a strategy called T2T that is endorsed by both EULAR and the American College of Rheumatology.

“This target can be reached in most patients with commonly used therapies, including allopurinol, which is relatively inexpensive,” Mr. Larsen said. Given that disease control and sustained remission are largely based on this target, he and his colleagues tested the hypothesis that nurses working in a rheumatology service could provide efficient and cost-effective care.

A total of 286 patients with gout defined by microscopy who were treated between 2015 and 2021 were enrolled in the study. Of these, 100 patients who had been enrolled before the introduction of nurse-led care received and were maintained on usual care, which generally included diagnosis by an orthopedist, an emergency room physician, or an internist, with subsequent treatment and follow-up with a general practitioner.

Of 186 patients treated after nurse-led care was implemented, 72 were transitioned to usual care, and the remaining 114 continued receiving nurse-led care over the next 2 years of follow-up. In the nurse-led care arm, nurses who specialized in rheumatology and were trained in gout management monitored a structured T2T strategy. They were available for consultation, provided patient education, and followed laboratory values, including sUA, which they used to adjust treatments.

Except in the case of complications, “there was no more contact with physicians” once care was transferred to the nurse, Mr. Larsen said. Most of the nurse management was based on sUA laboratory values and performed by telephone.

At 2 years, 112 patients in the nurse-led care group were compared with the 144 in the usual care group. Two of the 114 patients who entered the nurse-care cohort and 28 of the 172 in the usual care cohort died before the study ended.

At 2 years, the proportion of patients maintained at the target sUA was almost twice as great in the nurse-led arm (83% vs 44%). This was also true of patients aged 70 years or older (84% vs 45%), patients with tophi (60% vs 33%), and patients with sUA > 0.5 mmol/L at baseline (84% vs 44%). Nurse-led care also kept a greater proportion of patients at target who entered the study with an estimated glomerular filtration rate < 60 mL/min per 1.73 m² (84% vs 52%) or were taking diuretics (89% vs 52%). All differences reached statistical significance (P < .05).

The reason for the lower mortality at 2 years in the nurse-led group (4% vs 23%; P < .001) is unclear, according to Mr. Larsen. In addition to considering a selection bias that might have channeled patients with more severe disease to usual care, he and his coinvestigators are also considering whether the lower rates of sUA control in the usual care group might have led to a higher rate of cardiovascular events.

Because of some baseline imbalances, a selection bias cannot be ruled out, but the imbalances did not uniformly favor nurse-led care. For example, the proportion of patients with diabetes (23% vs 13%) or a baseline cancer diagnosis (11% vs 5%) was higher in the nurse-led care group. The proportion of patients with atrial fibrillation (45% vs 35%) or on diuretics (47% vs 33%) at baseline was higher in the usual care group.

The median age of 69 years was the same in the two groups, although the nurse-led group included a higher proportion of men to women (86% vs 76%).

Within a T2T strategy, nurses focused on reaching the target might do a better job than physicians in consistently monitoring and adjusting therapies as needed, but Mr. Larsen also speculated that nurses might offer a more collaborative approach and provide greater support through patient education and regular telephone contact.
 

Potential Advantages of Nurse-Led Care

Clinicians concerned about nurses missing nuances in disease progression or being slow to recognize complications might be surprised to learn about the advantage of nurse-led care, but Mwidimi Ndosi, PhD, an associate professor in rheumatology nursing at the University of the West of England, Bristol, England, was not.

“There is quite a large literature to show that nursing care is often superior to physician-led patient management in the appropriate circumstances,” Mr. Ndosi said. In this specific instance of gout management, he said that the treatment target is clear, and nurses are often able to devote more time to a specific goal, like T2T, than clinicians balancing more priorities.

trishudrebagici

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

VIENNA — The first multicenter randomized trial in gout to compare treat-to-target (T2T) and treat for symptom avoidance (T2S) strategies has finally generated data to make the guideline-recommended practice of T2T evidence-based.

The T2T strategy may be guideline-endorsed, but it has never been validated, contended Anusha Moses, MSc, a researcher and PhD candidate at the University of Twente, Enschede, the Netherlands. She argued that this controlled trial fills an evidence gap.

T2T is defined as maintaining a serum uric acid (sUA) level below the physiologic threshold level of 36 mmol/L (< 6 mg/dL). T2S, in contrast, is a strategy of symptom control, typically basing therapy on suppression of symptoms independent of sUA, Dr. Moses explained. 

bruchakoraspostevusufrogophogifracronobilaprelucerishachopiniclulecidreprerotruspapruspapihulesetresputrebriuibu

Both the American College of Rheumatology and European Alliance of Associations for Rheumatology (EULAR) have already endorsed T2T, but other organizations, such as the American College of Physicians (ACP), still accept symptom-based treatment in its gout clinical practice guideline, according to Dr. Moses.

The results of the trial were not surprising based on the pathophysiology of gout. Elevated sUA is considered the driver of both flares and the complications of gout. This well-established association led to endorsement of T2T in guidelines from organizations such as EULAR, but Dr. Moses said a controlled trial allows this to be declared as evidence based.

To provide proof that T2T is superior, 308 gout patients at eight centers were randomized to one of the two strategies in a trial called GO TEST OVERTURE. In the T2T arm, commonly used therapies, such as allopurinol, benzbromarone, and febuxostat were employed to achieve and maintain a target sUA of < 0.36 mmol/L. In the T2S comparator arm, the same drugs were offered to control symptoms and prevent recurrences, but sUA levels were not used to guide treatment. 

The 1-year results of a planned 2-year study were presented in an oral abstract session at the annual European Congress of Rheumatology. For this analysis, outcomes were compared in the last 6 months prior to the 1-year data analysis. When assessed at 2 years, the comparison will again be made in the prior 6 months of the study.

For the primary endpoint of flares defined by the validated Gallo criteria, the mean rates were 1.3 for T2T and 1.85 for T2S (P < .001), Dr. Moses reported.

The reduced risk for flares correlated with the greater proportion of patients with sUA < 0.36 mmol/L. These proportions were 72% and 26% (P < .001) for the T2T and T2S groups, respectively. The mean sUA levels were 0.31 mmol/L and 0.42 mmol/L (P < .001), respectively.

At the 1-year mark, none of the secondary endpoints reached statistical significance. These included mean numeric rating pain scale (2.46 vs 2.41), the proportion of patients in remission (8% vs 5.7%), and the mean Health Assessment Questionnaire-Disability Index score (0.65 vs 0.62), according to Dr. Moses, who said all of these endpoints will continue to be followed in the planned second year of the study.

At baseline, there were no differences in any of the variables evaluated, including age (about 62.5 years in both groups), proportion of patients with a body mass index > 30 kg/m2 (about 62%), sUA (about 0.5 mmol/L), or estimated glomerular filtration rate (about 70 mL/min/1.73 m2).
 

Nonspecialists Should Heed the Results

For those involved in the treatment of gout, this outcome was inevitable, according to Yael Klionsky, MD, a clinical assistant professor of rheumatology and immunology at Wake Forest University School of Medicine, Winston-Salem, North Carolina.

“We did not need a controlled trial to know that we should be focused on maintaining serum uric acid levels below physiological levels to improve outcomes,” Dr. Klionsky said. However, she conceded that objective data might have some value for nonspecialists.

“Primary care physicians often do not recognize the importance of controlling serum uric acid or the goals of treatment,” she told this news organization. For those who know this field, T2T does not need validation. She did not doubt that the ACP will change its position on T2T when its guidelines are updated.

However, she agreed with the principle that non-rheumatologists need to be reached with better guidance in regard to gout management. In a study she presented at this year’s EULAR, rheumatologists, nephrologists, and primary care physicians were surveyed about gout remission, which is an important clinical target even if there is no standard definition.

There was general agreement among the 151 rheumatologists, 150 nephrologists, and 102 primary care physicians that the absence of flares was among the top three criteria, but only 30% of primary care physicians and 35% of nephrologists vs 64% of rheumatologists identified the T2T target of < 0.36 mmol/L as one of the top three criteria.

Conversely, 58% of primary care physicians and 42% of nephrologists vs only 34% of rheumatologists considered absence of gout pain to be in the top three criteria.

In addition to the fact that primary care physicians differ from specialists in their goals for gout treatment, these data “highlight the need for the importance of a standardized definition of gout remission that includes serum uric acid control,” Dr. Klionsky said. She further thinks that this type of guidance should be disseminated to nonspecialists.

Dr. Moses reported no potential conflicts of interest. Dr. Klionsky reported financial relationships with Amgen, AstraZeneca, Eli Lilly, and MedIQ.

A version of this article appeared on Medscape.com.

VIENNA — The first multicenter randomized trial in gout to compare treat-to-target (T2T) and treat for symptom avoidance (T2S) strategies has finally generated data to make the guideline-recommended practice of T2T evidence-based.

The T2T strategy may be guideline-endorsed, but it has never been validated, contended Anusha Moses, MSc, a researcher and PhD candidate at the University of Twente, Enschede, the Netherlands. She argued that this controlled trial fills an evidence gap.

T2T is defined as maintaining a serum uric acid (sUA) level below the physiologic threshold level of 36 mmol/L (< 6 mg/dL). T2S, in contrast, is a strategy of symptom control, typically basing therapy on suppression of symptoms independent of sUA, Dr. Moses explained. 

bruchakoraspostevusufrogophogifracronobilaprelucerishachopiniclulecidreprerotruspapruspapihulesetresputrebriuibu

Both the American College of Rheumatology and European Alliance of Associations for Rheumatology (EULAR) have already endorsed T2T, but other organizations, such as the American College of Physicians (ACP), still accept symptom-based treatment in its gout clinical practice guideline, according to Dr. Moses.

The results of the trial were not surprising based on the pathophysiology of gout. Elevated sUA is considered the driver of both flares and the complications of gout. This well-established association led to endorsement of T2T in guidelines from organizations such as EULAR, but Dr. Moses said a controlled trial allows this to be declared as evidence based.

To provide proof that T2T is superior, 308 gout patients at eight centers were randomized to one of the two strategies in a trial called GO TEST OVERTURE. In the T2T arm, commonly used therapies, such as allopurinol, benzbromarone, and febuxostat were employed to achieve and maintain a target sUA of < 0.36 mmol/L. In the T2S comparator arm, the same drugs were offered to control symptoms and prevent recurrences, but sUA levels were not used to guide treatment. 

The 1-year results of a planned 2-year study were presented in an oral abstract session at the annual European Congress of Rheumatology. For this analysis, outcomes were compared in the last 6 months prior to the 1-year data analysis. When assessed at 2 years, the comparison will again be made in the prior 6 months of the study.

For the primary endpoint of flares defined by the validated Gallo criteria, the mean rates were 1.3 for T2T and 1.85 for T2S (P < .001), Dr. Moses reported.

The reduced risk for flares correlated with the greater proportion of patients with sUA < 0.36 mmol/L. These proportions were 72% and 26% (P < .001) for the T2T and T2S groups, respectively. The mean sUA levels were 0.31 mmol/L and 0.42 mmol/L (P < .001), respectively.

At the 1-year mark, none of the secondary endpoints reached statistical significance. These included mean numeric rating pain scale (2.46 vs 2.41), the proportion of patients in remission (8% vs 5.7%), and the mean Health Assessment Questionnaire-Disability Index score (0.65 vs 0.62), according to Dr. Moses, who said all of these endpoints will continue to be followed in the planned second year of the study.

At baseline, there were no differences in any of the variables evaluated, including age (about 62.5 years in both groups), proportion of patients with a body mass index > 30 kg/m2 (about 62%), sUA (about 0.5 mmol/L), or estimated glomerular filtration rate (about 70 mL/min/1.73 m2).
 

Nonspecialists Should Heed the Results

For those involved in the treatment of gout, this outcome was inevitable, according to Yael Klionsky, MD, a clinical assistant professor of rheumatology and immunology at Wake Forest University School of Medicine, Winston-Salem, North Carolina.

“We did not need a controlled trial to know that we should be focused on maintaining serum uric acid levels below physiological levels to improve outcomes,” Dr. Klionsky said. However, she conceded that objective data might have some value for nonspecialists.

“Primary care physicians often do not recognize the importance of controlling serum uric acid or the goals of treatment,” she told this news organization. For those who know this field, T2T does not need validation. She did not doubt that the ACP will change its position on T2T when its guidelines are updated.

However, she agreed with the principle that non-rheumatologists need to be reached with better guidance in regard to gout management. In a study she presented at this year’s EULAR, rheumatologists, nephrologists, and primary care physicians were surveyed about gout remission, which is an important clinical target even if there is no standard definition.

There was general agreement among the 151 rheumatologists, 150 nephrologists, and 102 primary care physicians that the absence of flares was among the top three criteria, but only 30% of primary care physicians and 35% of nephrologists vs 64% of rheumatologists identified the T2T target of < 0.36 mmol/L as one of the top three criteria.

Conversely, 58% of primary care physicians and 42% of nephrologists vs only 34% of rheumatologists considered absence of gout pain to be in the top three criteria.

In addition to the fact that primary care physicians differ from specialists in their goals for gout treatment, these data “highlight the need for the importance of a standardized definition of gout remission that includes serum uric acid control,” Dr. Klionsky said. She further thinks that this type of guidance should be disseminated to nonspecialists.

Dr. Moses reported no potential conflicts of interest. Dr. Klionsky reported financial relationships with Amgen, AstraZeneca, Eli Lilly, and MedIQ.

A version of this article appeared on Medscape.com.

VIENNA — The first multicenter randomized trial in gout to compare treat-to-target (T2T) and treat for symptom avoidance (T2S) strategies has finally generated data to make the guideline-recommended practice of T2T evidence-based.

The T2T strategy may be guideline-endorsed, but it has never been validated, contended Anusha Moses, MSc, a researcher and PhD candidate at the University of Twente, Enschede, the Netherlands. She argued that this controlled trial fills an evidence gap.

T2T is defined as maintaining a serum uric acid (sUA) level below the physiologic threshold level of 36 mmol/L (< 6 mg/dL). T2S, in contrast, is a strategy of symptom control, typically basing therapy on suppression of symptoms independent of sUA, Dr. Moses explained. 

bruchakoraspostevusufrogophogifracronobilaprelucerishachopiniclulecidreprerotruspapruspapihulesetresputrebriuibu

Both the American College of Rheumatology and European Alliance of Associations for Rheumatology (EULAR) have already endorsed T2T, but other organizations, such as the American College of Physicians (ACP), still accept symptom-based treatment in its gout clinical practice guideline, according to Dr. Moses.

The results of the trial were not surprising based on the pathophysiology of gout. Elevated sUA is considered the driver of both flares and the complications of gout. This well-established association led to endorsement of T2T in guidelines from organizations such as EULAR, but Dr. Moses said a controlled trial allows this to be declared as evidence based.

To provide proof that T2T is superior, 308 gout patients at eight centers were randomized to one of the two strategies in a trial called GO TEST OVERTURE. In the T2T arm, commonly used therapies, such as allopurinol, benzbromarone, and febuxostat were employed to achieve and maintain a target sUA of < 0.36 mmol/L. In the T2S comparator arm, the same drugs were offered to control symptoms and prevent recurrences, but sUA levels were not used to guide treatment. 

The 1-year results of a planned 2-year study were presented in an oral abstract session at the annual European Congress of Rheumatology. For this analysis, outcomes were compared in the last 6 months prior to the 1-year data analysis. When assessed at 2 years, the comparison will again be made in the prior 6 months of the study.

For the primary endpoint of flares defined by the validated Gallo criteria, the mean rates were 1.3 for T2T and 1.85 for T2S (P < .001), Dr. Moses reported.

The reduced risk for flares correlated with the greater proportion of patients with sUA < 0.36 mmol/L. These proportions were 72% and 26% (P < .001) for the T2T and T2S groups, respectively. The mean sUA levels were 0.31 mmol/L and 0.42 mmol/L (P < .001), respectively.

At the 1-year mark, none of the secondary endpoints reached statistical significance. These included mean numeric rating pain scale (2.46 vs 2.41), the proportion of patients in remission (8% vs 5.7%), and the mean Health Assessment Questionnaire-Disability Index score (0.65 vs 0.62), according to Dr. Moses, who said all of these endpoints will continue to be followed in the planned second year of the study.

At baseline, there were no differences in any of the variables evaluated, including age (about 62.5 years in both groups), proportion of patients with a body mass index > 30 kg/m2 (about 62%), sUA (about 0.5 mmol/L), or estimated glomerular filtration rate (about 70 mL/min/1.73 m2).
 

Nonspecialists Should Heed the Results

For those involved in the treatment of gout, this outcome was inevitable, according to Yael Klionsky, MD, a clinical assistant professor of rheumatology and immunology at Wake Forest University School of Medicine, Winston-Salem, North Carolina.

“We did not need a controlled trial to know that we should be focused on maintaining serum uric acid levels below physiological levels to improve outcomes,” Dr. Klionsky said. However, she conceded that objective data might have some value for nonspecialists.

“Primary care physicians often do not recognize the importance of controlling serum uric acid or the goals of treatment,” she told this news organization. For those who know this field, T2T does not need validation. She did not doubt that the ACP will change its position on T2T when its guidelines are updated.

However, she agreed with the principle that non-rheumatologists need to be reached with better guidance in regard to gout management. In a study she presented at this year’s EULAR, rheumatologists, nephrologists, and primary care physicians were surveyed about gout remission, which is an important clinical target even if there is no standard definition.

There was general agreement among the 151 rheumatologists, 150 nephrologists, and 102 primary care physicians that the absence of flares was among the top three criteria, but only 30% of primary care physicians and 35% of nephrologists vs 64% of rheumatologists identified the T2T target of < 0.36 mmol/L as one of the top three criteria.

Conversely, 58% of primary care physicians and 42% of nephrologists vs only 34% of rheumatologists considered absence of gout pain to be in the top three criteria.

In addition to the fact that primary care physicians differ from specialists in their goals for gout treatment, these data “highlight the need for the importance of a standardized definition of gout remission that includes serum uric acid control,” Dr. Klionsky said. She further thinks that this type of guidance should be disseminated to nonspecialists.

Dr. Moses reported no potential conflicts of interest. Dr. Klionsky reported financial relationships with Amgen, AstraZeneca, Eli Lilly, and MedIQ.

A version of this article appeared on Medscape.com.

BASEL, SWITZERLAND — The anti-inflammatory agent colchicine failed to show significant benefit in the treatment of patients with non-cardioembolic ischemic stroke in the primary analysis of the CONVINCE trial. However, the results did reveal a significant reduction in recurrent stroke and cardiovascular events in the per-protocol analysis and in the subgroup of patients with coronary artery disease.

“Although the primary endpoint was neutral, the CONVINCE results support the hypothesis that long-term anti-inflammatory therapy with colchicine may reduce recurrent stroke and cardiovascular events, specifically in stroke patients with atherosclerosis,” lead investigator Peter Kelly, MD, University College Dublin School of Medicine, Dublin, Ireland, concluded.

The results were presented at the European Stroke Organization Conference (ESOC) 2024.

Inflammation, Dr. Kelly said, plays an important role in the pathophysiology of atherosclerotic plaque, a major cause of cardiovascular events and ischemic strokes.

Colchicine, an established, widely available, low-cost drug that reduces inflammatory response, has been shown to reduce recurrent vascular events in patients with coronary artery disease.

The CONVINCE trial was conducted to see whether colchicine could show similar benefits in patients with non-severe, non-cardioembolic stroke or transient ischemic attack.

Conducted in 16 European countries and Canada, the CONVINCE trial included 3154 patients with a recent non-cardioembolic nondisabling ischemic stroke or high-risk transient ischemic attack. They were randomly assigned to receive colchicine (0.5 mg/d) or placebo.

Key exclusion criteria included evidence of atrial fibrillation or other source of cardioembolism, a defined cause of stroke other than atherosclerosis or small vessel disease, a glomerular filtration rate below 50 mL/min, and the use of drugs that interact with colchicine.

The primary endpoint was a composite of first recurrent ischemic stroke, myocardial infarction, cardiac arrest, or hospitalization for unstable angina. Study participants were followed-up over 36 months.

Results of the primary intention-to-treat analysis showed that the primary endpoint occurred in 153 patients randomized to low-dose colchicine (9.8%) versus 185 in the placebo group (11.8%). This translated into a hazard ratio (HR) of 0.84 (95% CI, 0.68-1.05; P = .12) — a nonsignificant result.

Reduced levels of C-reactive protein in the colchicine group showed the anti-inflammatory effect of treatment with colchicine, Dr. Kelly reported.

In a prespecified on-treatment analysis (excluding patients with major protocol violations), colchicine did show a significant benefit in the primary endpoint (HR, 0.80; 95% CI, 0.63-0.99).
 

A Novel Target for Stroke Treatment

In addition, significantly reduced rates of recurrent stroke or cardiovascular events were observed in the subgroup of patients with a history of coronary artery disease.

In an updated meta-analysis of existing colchicine studies including CONVINCE, there was a significant reduction in the risk for ischemic stroke (risk ratio, 0.73; 95% CI, 0.58-0.90).

“The signals of benefit of colchicine in secondary analyses are in line with findings from previous trials and indicate the potential of colchicine in prevention after stroke,” Dr. Kelly said.

He pointed out that the COVID pandemic reduced the planned follow-up time in the CONVINCE trial, which led to the study being underpowered for the primary analysis.

“Further trials are needed in all stroke subtypes, but with particular focus on patients with objective evidence of atherosclerosis,” he said.

Commenting on the findings, Mira Katan, MD, University Hospital of Basel, Switzerland, noted that inflammation represents a novel target for stroke treatment.

“We have never before looked at treating inflammation in stroke. Although the primary endpoint was not reached in the CONVINCE study, the on-treatment analysis and meta-analysis showed a risk reduction, and we know colchicine works in cardiology. I think this is a fantastic trial, giving us a new target for stroke therapy,” Dr. Katan said.

“I think we have a new tool, but of course we need further trials to confirm that,” she added.

The CONVINCE trial was supported by Health Research Board Ireland, Deutsche Forschungsgesellschaft, Fonds Wetenschappelijk Onderzoek (FWO), and the Irish Heart Foundation. Dr. Kelly received funding from the Irish Heart Foundation. Dr. Katan reported no relevant disclosures.
 

A version of this article appeared on Medscape.com.

BASEL, SWITZERLAND — The anti-inflammatory agent colchicine failed to show significant benefit in the treatment of patients with non-cardioembolic ischemic stroke in the primary analysis of the CONVINCE trial. However, the results did reveal a significant reduction in recurrent stroke and cardiovascular events in the per-protocol analysis and in the subgroup of patients with coronary artery disease.

“Although the primary endpoint was neutral, the CONVINCE results support the hypothesis that long-term anti-inflammatory therapy with colchicine may reduce recurrent stroke and cardiovascular events, specifically in stroke patients with atherosclerosis,” lead investigator Peter Kelly, MD, University College Dublin School of Medicine, Dublin, Ireland, concluded.

The results were presented at the European Stroke Organization Conference (ESOC) 2024.

Inflammation, Dr. Kelly said, plays an important role in the pathophysiology of atherosclerotic plaque, a major cause of cardiovascular events and ischemic strokes.

Colchicine, an established, widely available, low-cost drug that reduces inflammatory response, has been shown to reduce recurrent vascular events in patients with coronary artery disease.

The CONVINCE trial was conducted to see whether colchicine could show similar benefits in patients with non-severe, non-cardioembolic stroke or transient ischemic attack.

Conducted in 16 European countries and Canada, the CONVINCE trial included 3154 patients with a recent non-cardioembolic nondisabling ischemic stroke or high-risk transient ischemic attack. They were randomly assigned to receive colchicine (0.5 mg/d) or placebo.

Key exclusion criteria included evidence of atrial fibrillation or other source of cardioembolism, a defined cause of stroke other than atherosclerosis or small vessel disease, a glomerular filtration rate below 50 mL/min, and the use of drugs that interact with colchicine.

The primary endpoint was a composite of first recurrent ischemic stroke, myocardial infarction, cardiac arrest, or hospitalization for unstable angina. Study participants were followed-up over 36 months.

Results of the primary intention-to-treat analysis showed that the primary endpoint occurred in 153 patients randomized to low-dose colchicine (9.8%) versus 185 in the placebo group (11.8%). This translated into a hazard ratio (HR) of 0.84 (95% CI, 0.68-1.05; P = .12) — a nonsignificant result.

Reduced levels of C-reactive protein in the colchicine group showed the anti-inflammatory effect of treatment with colchicine, Dr. Kelly reported.

In a prespecified on-treatment analysis (excluding patients with major protocol violations), colchicine did show a significant benefit in the primary endpoint (HR, 0.80; 95% CI, 0.63-0.99).
 

A Novel Target for Stroke Treatment

In addition, significantly reduced rates of recurrent stroke or cardiovascular events were observed in the subgroup of patients with a history of coronary artery disease.

In an updated meta-analysis of existing colchicine studies including CONVINCE, there was a significant reduction in the risk for ischemic stroke (risk ratio, 0.73; 95% CI, 0.58-0.90).

“The signals of benefit of colchicine in secondary analyses are in line with findings from previous trials and indicate the potential of colchicine in prevention after stroke,” Dr. Kelly said.

He pointed out that the COVID pandemic reduced the planned follow-up time in the CONVINCE trial, which led to the study being underpowered for the primary analysis.

“Further trials are needed in all stroke subtypes, but with particular focus on patients with objective evidence of atherosclerosis,” he said.

Commenting on the findings, Mira Katan, MD, University Hospital of Basel, Switzerland, noted that inflammation represents a novel target for stroke treatment.

“We have never before looked at treating inflammation in stroke. Although the primary endpoint was not reached in the CONVINCE study, the on-treatment analysis and meta-analysis showed a risk reduction, and we know colchicine works in cardiology. I think this is a fantastic trial, giving us a new target for stroke therapy,” Dr. Katan said.

“I think we have a new tool, but of course we need further trials to confirm that,” she added.

The CONVINCE trial was supported by Health Research Board Ireland, Deutsche Forschungsgesellschaft, Fonds Wetenschappelijk Onderzoek (FWO), and the Irish Heart Foundation. Dr. Kelly received funding from the Irish Heart Foundation. Dr. Katan reported no relevant disclosures.
 

A version of this article appeared on Medscape.com.

BASEL, SWITZERLAND — The anti-inflammatory agent colchicine failed to show significant benefit in the treatment of patients with non-cardioembolic ischemic stroke in the primary analysis of the CONVINCE trial. However, the results did reveal a significant reduction in recurrent stroke and cardiovascular events in the per-protocol analysis and in the subgroup of patients with coronary artery disease.

“Although the primary endpoint was neutral, the CONVINCE results support the hypothesis that long-term anti-inflammatory therapy with colchicine may reduce recurrent stroke and cardiovascular events, specifically in stroke patients with atherosclerosis,” lead investigator Peter Kelly, MD, University College Dublin School of Medicine, Dublin, Ireland, concluded.

The results were presented at the European Stroke Organization Conference (ESOC) 2024.

Inflammation, Dr. Kelly said, plays an important role in the pathophysiology of atherosclerotic plaque, a major cause of cardiovascular events and ischemic strokes.

Colchicine, an established, widely available, low-cost drug that reduces inflammatory response, has been shown to reduce recurrent vascular events in patients with coronary artery disease.

The CONVINCE trial was conducted to see whether colchicine could show similar benefits in patients with non-severe, non-cardioembolic stroke or transient ischemic attack.

Conducted in 16 European countries and Canada, the CONVINCE trial included 3154 patients with a recent non-cardioembolic nondisabling ischemic stroke or high-risk transient ischemic attack. They were randomly assigned to receive colchicine (0.5 mg/d) or placebo.

Key exclusion criteria included evidence of atrial fibrillation or other source of cardioembolism, a defined cause of stroke other than atherosclerosis or small vessel disease, a glomerular filtration rate below 50 mL/min, and the use of drugs that interact with colchicine.

The primary endpoint was a composite of first recurrent ischemic stroke, myocardial infarction, cardiac arrest, or hospitalization for unstable angina. Study participants were followed-up over 36 months.

Results of the primary intention-to-treat analysis showed that the primary endpoint occurred in 153 patients randomized to low-dose colchicine (9.8%) versus 185 in the placebo group (11.8%). This translated into a hazard ratio (HR) of 0.84 (95% CI, 0.68-1.05; P = .12) — a nonsignificant result.

Reduced levels of C-reactive protein in the colchicine group showed the anti-inflammatory effect of treatment with colchicine, Dr. Kelly reported.

In a prespecified on-treatment analysis (excluding patients with major protocol violations), colchicine did show a significant benefit in the primary endpoint (HR, 0.80; 95% CI, 0.63-0.99).
 

A Novel Target for Stroke Treatment

In addition, significantly reduced rates of recurrent stroke or cardiovascular events were observed in the subgroup of patients with a history of coronary artery disease.

In an updated meta-analysis of existing colchicine studies including CONVINCE, there was a significant reduction in the risk for ischemic stroke (risk ratio, 0.73; 95% CI, 0.58-0.90).

“The signals of benefit of colchicine in secondary analyses are in line with findings from previous trials and indicate the potential of colchicine in prevention after stroke,” Dr. Kelly said.

He pointed out that the COVID pandemic reduced the planned follow-up time in the CONVINCE trial, which led to the study being underpowered for the primary analysis.

“Further trials are needed in all stroke subtypes, but with particular focus on patients with objective evidence of atherosclerosis,” he said.

Commenting on the findings, Mira Katan, MD, University Hospital of Basel, Switzerland, noted that inflammation represents a novel target for stroke treatment.

“We have never before looked at treating inflammation in stroke. Although the primary endpoint was not reached in the CONVINCE study, the on-treatment analysis and meta-analysis showed a risk reduction, and we know colchicine works in cardiology. I think this is a fantastic trial, giving us a new target for stroke therapy,” Dr. Katan said.

“I think we have a new tool, but of course we need further trials to confirm that,” she added.

The CONVINCE trial was supported by Health Research Board Ireland, Deutsche Forschungsgesellschaft, Fonds Wetenschappelijk Onderzoek (FWO), and the Irish Heart Foundation. Dr. Kelly received funding from the Irish Heart Foundation. Dr. Katan reported no relevant disclosures.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Metformin use lowers the risk for gout by 32% in individuals with prediabetes; however, the treatment doesn’t change serum urate or C-reactive protein levels.

METHODOLOGY:

• Individuals with prediabetes not only are at an elevated risk for diabetes but also face an increased risk for incident gout. Many previous reports have demonstrated the efficacy of antidiabetic medications in reducing the risk for gout in adults with diabetes.
• This study assessed the gout-lowering properties of metformin in 25,064 individuals with prediabetes (age ≥ 18 years; A1c levels, 5.7%-6.4%) who had never reported A1c levels > 6.4%.
• Patients who were initiated on metformin within 18 months after the diagnosis of prediabetes (n = 1154) were propensity score–matched with those who did not initiate metformin or other antidiabetic medications in this period (n = 13,877) and were followed for a median of 3.9 years for the primary outcome of incident gout.

TAKEAWAY:

• Initiation vs no initiation of metformin resulted in 2.4 fewer cases of gout per 1000 person-years and a 32% reduced relative risk for incident gout (hazard ratio, 0.68; 95% CI, 0.48-0.96).
• The results were consistent across different subgroups stratified on the basis of sex, age (≤ 60 vs > 60 years), estimated glomerular filtration rate (≥ 90 vs < 90 mL/min/1.73 m²), and baseline diuretic use.
• Metformin initiation was not associated with significant changes in serum urate or C-reactive protein levels.
• Metformin use was associated with a reduction in A1c levels and body mass index.

IN PRACTICE:

The authors suggested that “metformin may be important in lowering gout risk in individuals with prediabetes.”

SOURCE:

Javier Marrugo, MD, Department of Medicine, Brigham and Women’s Hospital, Boston, led this study, which was published online in Annals of the Rheumatic Diseases.

LIMITATIONS:

Although gout is more commonly observed in men, around 60% of the study population consisted of women. Owing to the observational nature of this study, exposure misclassifications might have occurred. Misclassification of the outcome is also possible due to the presence of two or more diagnostic codes for gout and/or the combination of urate-lowering therapies or colchicine with at least one diagnostic code.

DISCLOSURES:

This work was supported by the National Institutes of Health. Some authors declared serving as consultants or receiving salary support or consulting fees from various sources.

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

TOPLINE:

Metformin use lowers the risk for gout by 32% in individuals with prediabetes; however, the treatment doesn’t change serum urate or C-reactive protein levels.

METHODOLOGY:

• Individuals with prediabetes not only are at an elevated risk for diabetes but also face an increased risk for incident gout. Many previous reports have demonstrated the efficacy of antidiabetic medications in reducing the risk for gout in adults with diabetes.
• This study assessed the gout-lowering properties of metformin in 25,064 individuals with prediabetes (age ≥ 18 years; A1c levels, 5.7%-6.4%) who had never reported A1c levels > 6.4%.
• Patients who were initiated on metformin within 18 months after the diagnosis of prediabetes (n = 1154) were propensity score–matched with those who did not initiate metformin or other antidiabetic medications in this period (n = 13,877) and were followed for a median of 3.9 years for the primary outcome of incident gout.

TAKEAWAY:

• Initiation vs no initiation of metformin resulted in 2.4 fewer cases of gout per 1000 person-years and a 32% reduced relative risk for incident gout (hazard ratio, 0.68; 95% CI, 0.48-0.96).
• The results were consistent across different subgroups stratified on the basis of sex, age (≤ 60 vs > 60 years), estimated glomerular filtration rate (≥ 90 vs < 90 mL/min/1.73 m²), and baseline diuretic use.
• Metformin initiation was not associated with significant changes in serum urate or C-reactive protein levels.
• Metformin use was associated with a reduction in A1c levels and body mass index.

IN PRACTICE:

The authors suggested that “metformin may be important in lowering gout risk in individuals with prediabetes.”

SOURCE:

Javier Marrugo, MD, Department of Medicine, Brigham and Women’s Hospital, Boston, led this study, which was published online in Annals of the Rheumatic Diseases.

LIMITATIONS:

Although gout is more commonly observed in men, around 60% of the study population consisted of women. Owing to the observational nature of this study, exposure misclassifications might have occurred. Misclassification of the outcome is also possible due to the presence of two or more diagnostic codes for gout and/or the combination of urate-lowering therapies or colchicine with at least one diagnostic code.

DISCLOSURES:

This work was supported by the National Institutes of Health. Some authors declared serving as consultants or receiving salary support or consulting fees from various sources.

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

TOPLINE:

Metformin use lowers the risk for gout by 32% in individuals with prediabetes; however, the treatment doesn’t change serum urate or C-reactive protein levels.

METHODOLOGY:

• Individuals with prediabetes not only are at an elevated risk for diabetes but also face an increased risk for incident gout. Many previous reports have demonstrated the efficacy of antidiabetic medications in reducing the risk for gout in adults with diabetes.
• This study assessed the gout-lowering properties of metformin in 25,064 individuals with prediabetes (age ≥ 18 years; A1c levels, 5.7%-6.4%) who had never reported A1c levels > 6.4%.
• Patients who were initiated on metformin within 18 months after the diagnosis of prediabetes (n = 1154) were propensity score–matched with those who did not initiate metformin or other antidiabetic medications in this period (n = 13,877) and were followed for a median of 3.9 years for the primary outcome of incident gout.

TAKEAWAY:

• Initiation vs no initiation of metformin resulted in 2.4 fewer cases of gout per 1000 person-years and a 32% reduced relative risk for incident gout (hazard ratio, 0.68; 95% CI, 0.48-0.96).
• The results were consistent across different subgroups stratified on the basis of sex, age (≤ 60 vs > 60 years), estimated glomerular filtration rate (≥ 90 vs < 90 mL/min/1.73 m²), and baseline diuretic use.
• Metformin initiation was not associated with significant changes in serum urate or C-reactive protein levels.
• Metformin use was associated with a reduction in A1c levels and body mass index.

IN PRACTICE:

The authors suggested that “metformin may be important in lowering gout risk in individuals with prediabetes.”

SOURCE:

Javier Marrugo, MD, Department of Medicine, Brigham and Women’s Hospital, Boston, led this study, which was published online in Annals of the Rheumatic Diseases.

LIMITATIONS:

Although gout is more commonly observed in men, around 60% of the study population consisted of women. Owing to the observational nature of this study, exposure misclassifications might have occurred. Misclassification of the outcome is also possible due to the presence of two or more diagnostic codes for gout and/or the combination of urate-lowering therapies or colchicine with at least one diagnostic code.

DISCLOSURES:

This work was supported by the National Institutes of Health. Some authors declared serving as consultants or receiving salary support or consulting fees from various sources.

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

NEW YORK — Urate, the culprit of gout, affects the vasculature in multiple ways that can raise cardiovascular risk (CV) in an individual with gout, and following guidelines for gout treatment, including the use of colchicine, can be the key to reducing those risks.

“Guideline-concordant gout treatment, which is essentially an anti-inflammatory urate-lowering strategy, at least improves arterial physiology and likely reduces cardiovascular risk,” Michael H. Pillinger, MD, told attendees at the 4th Annual Cardiometabolic Risk in Inflammatory Conditions conference. Dr. Pillinger is professor of medicine and biochemistry and molecular pharmacology at New York University Grossman School of Medicine, New York City, who has published multiple studies on gout.

brojideclewrapricrewronicrauodespeposaprelarewrinochatinestubolephiuuclegesposhutihibrotimathorakichalerucluceneswuvugapishifrabraswajurespasorulobrumuresp

He cited evidence that has shown soluble urate stimulates the production of C-reactive protein (CRP), which is a predictor of cardiovascular disease (CVD). Another study, in which Dr. Pillinger participated, demonstrated that gout patients have impaired vascular endothelial function associated with a chronic, low-level inflammatory state, he said.

“There’s good evidence that urate itself affects the vasculature in multiple ways, and I suspect this may be a model for other metabolic effects on vasculature,” Dr. Pillinger said. “Patients with gout have abnormal endothelium in ways that really convey vascular risk.”
 

Gout, Inflammation, and CVD

However, for rheumatologists to study the association between gout-related inflammation and CVD is “very, very hard,” Dr. Pillinger added. “But I do think that the mechanisms by which gout induces biological changes in the vasculature may provide insights into cardiovascular disease in general.”

One way to evaluate the effects of gout on the endothelium in the clinic is to measure flow-mediated dilation. This technique involves placing an ultrasound probe over the brachial artery and measuring the baseline artery diameter. Then, with the blood pressure cuff over the forearm, inflate it to reduce flow, then release the cuff and measure the brachial artery diameter after the endothelium releases vasodilators.

Dr. Pillinger and colleagues evaluated this technique in 34 patients with gout and 64 controls and found that patients with gout had an almost 50% decrease in flow-mediated dilation, he said. “Interestingly, the higher the urate, the worse the flow; the more the inflammation, the worse the flow, so seemingly corresponding with the severity of the gout,” he said. That raised an obvious question, Dr. Pillinger continued: “If you can treat the gout, can you improve the flow-mediated dilation?”

His group answered that question with a study in 38 previously untreated patients with gout, giving them colchicine 0.6 mg twice daily for a month plus a urate-lowering xanthine oxidase inhibitor (allopurinol or febuxostat) to treat them to a target urate level of < 6 mg/dL. “We saw an increase in endothelial function, and it normalized,” Dr. Pillinger said.

However, some study participants didn’t respond. “They were people with well-established other cardiovascular comorbidities — hypertension, hyperlipidemia,” he said. “I think some people just have vessels that are too damaged to get at them just by fixing their gout problem or their inflammation.”

That means patients with gout need to be treated with colchicine early on to avoid CV problems, Dr. Pillinger added. “We ought to get to them before they have the other problems,” he said.

Managing gout, and the concomitant CV problems, requires vigilance both during and in between flares, Dr. Pillinger said after his presentation.

“We have always taught that patients between flares basically look like people with no gout, but we do know now that patients with gout between flares tend to have what you might call ‘subclinical’ inflammation: CRPs and ESRs [erythrocyte sedimentation rates] that are higher than those of the general population, though not so excessive that they might grab attention,” he said. “We also know that many, if not all, patients between flares have urate deposited in or around their joints, but how these two relate is not fully established.”

Better treatment within 3 months of an acute gout flare may reduce the risk for CV events, he said, but that’s based on speculation more so than clinical data.
 

Potential Benefits of Targeting Inflammation

“More chronically, we know from the cardiologists’ studies that anti-inflammatory therapy should reduce risk in the high-risk general population,” Dr. Pillinger said. “There are no prospective studies confirming that this approach will work among gout patients, but there is no reason why it shouldn’t work — except perhaps that gout patients may have higher inflammation than the general population and also have more comorbidities, so they could perhaps be more resistant.”

Dr. Pillinger said that his group’s studies and another led by Daniel Solomon, MD, at Brigham and Women’s Hospital in Boston, have indicated that anti-inflammatory strategies in gout will lower CV risk.

“And interestingly,” he added, “our data suggest that colchicine use may lower risk not only in high-risk gout patients but also in gout patients who start with no CAD [coronary artery disease] but who seem to have less incident CAD on colchicine. I see this as identifying that gout patients are intrinsically at high risk for CAD, even if they don’t actually have any, so they represent a population for whom lowering chronic inflammation may help prevent incident disease.”

Dr. Pillinger provided more evidence that the understanding of the relationship between gout, gout flares, and CV risk is evolving, said Michael S. Garshick, MD, who attended the conference and is head of the Cardio-Rheumatology Program at NYU Langone, New York City.

Garshick_Michael_NY_web.JPG

“There’s epidemiologic evidence supporting the association,” Dr. Garshick told this news organization after the conference. “We think that most conditions with immune system activation do tend to have an increased risk of some form of cardiovascular disease, but I think the relationship with gout has been highly underpublicized.”

Many patients with gout tend to have a higher prevalence of traditional cardiometabolic issues, which may compound the relationship, Dr. Garshick added. “However, I would argue that with this patient subset that it doesn’t matter because gout patients have a higher risk of traditional risk factors, and you have to [treat-to-target] those traditional risk factors.”

While the clinical evidence of a link between gout and atherosclerosis may not be conclusive, enough circumstantial evidence exists to believe that treating gout will reduce CV risks, he said. “Some of the imaging techniques do suggest that gouty crystals [are] in the atherosclerotic plaque of gout patients,” Dr. Garshick added. Dr. Pillinger’s work, he said, “is showing us that there are different pathways to develop atherosclerosis.”

Dr. Pillinger disclosed relationships with Federation Bio, Fortress Biotech, Amgen, Scilex, Hikma Pharmaceuticals, LG Chem, and Olatec Therapeutics. Dr. Garshick disclosed relationships with Kiniksa Pharmaceuticals, Agepha Pharma, Bristol Myers Squibb, and Horizon Therapeutics.
 

A version of this article appeared on Medscape.com.

NEW YORK — Urate, the culprit of gout, affects the vasculature in multiple ways that can raise cardiovascular risk (CV) in an individual with gout, and following guidelines for gout treatment, including the use of colchicine, can be the key to reducing those risks.

“Guideline-concordant gout treatment, which is essentially an anti-inflammatory urate-lowering strategy, at least improves arterial physiology and likely reduces cardiovascular risk,” Michael H. Pillinger, MD, told attendees at the 4th Annual Cardiometabolic Risk in Inflammatory Conditions conference. Dr. Pillinger is professor of medicine and biochemistry and molecular pharmacology at New York University Grossman School of Medicine, New York City, who has published multiple studies on gout.

brojideclewrapricrewronicrauodespeposaprelarewrinochatinestubolephiuuclegesposhutihibrotimathorakichalerucluceneswuvugapishifrabraswajurespasorulobrumuresp

He cited evidence that has shown soluble urate stimulates the production of C-reactive protein (CRP), which is a predictor of cardiovascular disease (CVD). Another study, in which Dr. Pillinger participated, demonstrated that gout patients have impaired vascular endothelial function associated with a chronic, low-level inflammatory state, he said.

“There’s good evidence that urate itself affects the vasculature in multiple ways, and I suspect this may be a model for other metabolic effects on vasculature,” Dr. Pillinger said. “Patients with gout have abnormal endothelium in ways that really convey vascular risk.”
 

Gout, Inflammation, and CVD

However, for rheumatologists to study the association between gout-related inflammation and CVD is “very, very hard,” Dr. Pillinger added. “But I do think that the mechanisms by which gout induces biological changes in the vasculature may provide insights into cardiovascular disease in general.”

One way to evaluate the effects of gout on the endothelium in the clinic is to measure flow-mediated dilation. This technique involves placing an ultrasound probe over the brachial artery and measuring the baseline artery diameter. Then, with the blood pressure cuff over the forearm, inflate it to reduce flow, then release the cuff and measure the brachial artery diameter after the endothelium releases vasodilators.

Dr. Pillinger and colleagues evaluated this technique in 34 patients with gout and 64 controls and found that patients with gout had an almost 50% decrease in flow-mediated dilation, he said. “Interestingly, the higher the urate, the worse the flow; the more the inflammation, the worse the flow, so seemingly corresponding with the severity of the gout,” he said. That raised an obvious question, Dr. Pillinger continued: “If you can treat the gout, can you improve the flow-mediated dilation?”

His group answered that question with a study in 38 previously untreated patients with gout, giving them colchicine 0.6 mg twice daily for a month plus a urate-lowering xanthine oxidase inhibitor (allopurinol or febuxostat) to treat them to a target urate level of < 6 mg/dL. “We saw an increase in endothelial function, and it normalized,” Dr. Pillinger said.

However, some study participants didn’t respond. “They were people with well-established other cardiovascular comorbidities — hypertension, hyperlipidemia,” he said. “I think some people just have vessels that are too damaged to get at them just by fixing their gout problem or their inflammation.”

That means patients with gout need to be treated with colchicine early on to avoid CV problems, Dr. Pillinger added. “We ought to get to them before they have the other problems,” he said.

Managing gout, and the concomitant CV problems, requires vigilance both during and in between flares, Dr. Pillinger said after his presentation.

“We have always taught that patients between flares basically look like people with no gout, but we do know now that patients with gout between flares tend to have what you might call ‘subclinical’ inflammation: CRPs and ESRs [erythrocyte sedimentation rates] that are higher than those of the general population, though not so excessive that they might grab attention,” he said. “We also know that many, if not all, patients between flares have urate deposited in or around their joints, but how these two relate is not fully established.”

Better treatment within 3 months of an acute gout flare may reduce the risk for CV events, he said, but that’s based on speculation more so than clinical data.
 

Potential Benefits of Targeting Inflammation

“More chronically, we know from the cardiologists’ studies that anti-inflammatory therapy should reduce risk in the high-risk general population,” Dr. Pillinger said. “There are no prospective studies confirming that this approach will work among gout patients, but there is no reason why it shouldn’t work — except perhaps that gout patients may have higher inflammation than the general population and also have more comorbidities, so they could perhaps be more resistant.”

Dr. Pillinger said that his group’s studies and another led by Daniel Solomon, MD, at Brigham and Women’s Hospital in Boston, have indicated that anti-inflammatory strategies in gout will lower CV risk.

“And interestingly,” he added, “our data suggest that colchicine use may lower risk not only in high-risk gout patients but also in gout patients who start with no CAD [coronary artery disease] but who seem to have less incident CAD on colchicine. I see this as identifying that gout patients are intrinsically at high risk for CAD, even if they don’t actually have any, so they represent a population for whom lowering chronic inflammation may help prevent incident disease.”

Dr. Pillinger provided more evidence that the understanding of the relationship between gout, gout flares, and CV risk is evolving, said Michael S. Garshick, MD, who attended the conference and is head of the Cardio-Rheumatology Program at NYU Langone, New York City.

Garshick_Michael_NY_web.JPG

“There’s epidemiologic evidence supporting the association,” Dr. Garshick told this news organization after the conference. “We think that most conditions with immune system activation do tend to have an increased risk of some form of cardiovascular disease, but I think the relationship with gout has been highly underpublicized.”

Many patients with gout tend to have a higher prevalence of traditional cardiometabolic issues, which may compound the relationship, Dr. Garshick added. “However, I would argue that with this patient subset that it doesn’t matter because gout patients have a higher risk of traditional risk factors, and you have to [treat-to-target] those traditional risk factors.”

While the clinical evidence of a link between gout and atherosclerosis may not be conclusive, enough circumstantial evidence exists to believe that treating gout will reduce CV risks, he said. “Some of the imaging techniques do suggest that gouty crystals [are] in the atherosclerotic plaque of gout patients,” Dr. Garshick added. Dr. Pillinger’s work, he said, “is showing us that there are different pathways to develop atherosclerosis.”

Dr. Pillinger disclosed relationships with Federation Bio, Fortress Biotech, Amgen, Scilex, Hikma Pharmaceuticals, LG Chem, and Olatec Therapeutics. Dr. Garshick disclosed relationships with Kiniksa Pharmaceuticals, Agepha Pharma, Bristol Myers Squibb, and Horizon Therapeutics.
 

A version of this article appeared on Medscape.com.

NEW YORK — Urate, the culprit of gout, affects the vasculature in multiple ways that can raise cardiovascular risk (CV) in an individual with gout, and following guidelines for gout treatment, including the use of colchicine, can be the key to reducing those risks.

“Guideline-concordant gout treatment, which is essentially an anti-inflammatory urate-lowering strategy, at least improves arterial physiology and likely reduces cardiovascular risk,” Michael H. Pillinger, MD, told attendees at the 4th Annual Cardiometabolic Risk in Inflammatory Conditions conference. Dr. Pillinger is professor of medicine and biochemistry and molecular pharmacology at New York University Grossman School of Medicine, New York City, who has published multiple studies on gout.

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He cited evidence that has shown soluble urate stimulates the production of C-reactive protein (CRP), which is a predictor of cardiovascular disease (CVD). Another study, in which Dr. Pillinger participated, demonstrated that gout patients have impaired vascular endothelial function associated with a chronic, low-level inflammatory state, he said.

“There’s good evidence that urate itself affects the vasculature in multiple ways, and I suspect this may be a model for other metabolic effects on vasculature,” Dr. Pillinger said. “Patients with gout have abnormal endothelium in ways that really convey vascular risk.”
 

Gout, Inflammation, and CVD

However, for rheumatologists to study the association between gout-related inflammation and CVD is “very, very hard,” Dr. Pillinger added. “But I do think that the mechanisms by which gout induces biological changes in the vasculature may provide insights into cardiovascular disease in general.”

One way to evaluate the effects of gout on the endothelium in the clinic is to measure flow-mediated dilation. This technique involves placing an ultrasound probe over the brachial artery and measuring the baseline artery diameter. Then, with the blood pressure cuff over the forearm, inflate it to reduce flow, then release the cuff and measure the brachial artery diameter after the endothelium releases vasodilators.

Dr. Pillinger and colleagues evaluated this technique in 34 patients with gout and 64 controls and found that patients with gout had an almost 50% decrease in flow-mediated dilation, he said. “Interestingly, the higher the urate, the worse the flow; the more the inflammation, the worse the flow, so seemingly corresponding with the severity of the gout,” he said. That raised an obvious question, Dr. Pillinger continued: “If you can treat the gout, can you improve the flow-mediated dilation?”

His group answered that question with a study in 38 previously untreated patients with gout, giving them colchicine 0.6 mg twice daily for a month plus a urate-lowering xanthine oxidase inhibitor (allopurinol or febuxostat) to treat them to a target urate level of < 6 mg/dL. “We saw an increase in endothelial function, and it normalized,” Dr. Pillinger said.

However, some study participants didn’t respond. “They were people with well-established other cardiovascular comorbidities — hypertension, hyperlipidemia,” he said. “I think some people just have vessels that are too damaged to get at them just by fixing their gout problem or their inflammation.”

That means patients with gout need to be treated with colchicine early on to avoid CV problems, Dr. Pillinger added. “We ought to get to them before they have the other problems,” he said.

Managing gout, and the concomitant CV problems, requires vigilance both during and in between flares, Dr. Pillinger said after his presentation.

“We have always taught that patients between flares basically look like people with no gout, but we do know now that patients with gout between flares tend to have what you might call ‘subclinical’ inflammation: CRPs and ESRs [erythrocyte sedimentation rates] that are higher than those of the general population, though not so excessive that they might grab attention,” he said. “We also know that many, if not all, patients between flares have urate deposited in or around their joints, but how these two relate is not fully established.”

Better treatment within 3 months of an acute gout flare may reduce the risk for CV events, he said, but that’s based on speculation more so than clinical data.
 

Potential Benefits of Targeting Inflammation

“More chronically, we know from the cardiologists’ studies that anti-inflammatory therapy should reduce risk in the high-risk general population,” Dr. Pillinger said. “There are no prospective studies confirming that this approach will work among gout patients, but there is no reason why it shouldn’t work — except perhaps that gout patients may have higher inflammation than the general population and also have more comorbidities, so they could perhaps be more resistant.”

Dr. Pillinger said that his group’s studies and another led by Daniel Solomon, MD, at Brigham and Women’s Hospital in Boston, have indicated that anti-inflammatory strategies in gout will lower CV risk.

“And interestingly,” he added, “our data suggest that colchicine use may lower risk not only in high-risk gout patients but also in gout patients who start with no CAD [coronary artery disease] but who seem to have less incident CAD on colchicine. I see this as identifying that gout patients are intrinsically at high risk for CAD, even if they don’t actually have any, so they represent a population for whom lowering chronic inflammation may help prevent incident disease.”

Dr. Pillinger provided more evidence that the understanding of the relationship between gout, gout flares, and CV risk is evolving, said Michael S. Garshick, MD, who attended the conference and is head of the Cardio-Rheumatology Program at NYU Langone, New York City.

Garshick_Michael_NY_web.JPG

“There’s epidemiologic evidence supporting the association,” Dr. Garshick told this news organization after the conference. “We think that most conditions with immune system activation do tend to have an increased risk of some form of cardiovascular disease, but I think the relationship with gout has been highly underpublicized.”

Many patients with gout tend to have a higher prevalence of traditional cardiometabolic issues, which may compound the relationship, Dr. Garshick added. “However, I would argue that with this patient subset that it doesn’t matter because gout patients have a higher risk of traditional risk factors, and you have to [treat-to-target] those traditional risk factors.”

While the clinical evidence of a link between gout and atherosclerosis may not be conclusive, enough circumstantial evidence exists to believe that treating gout will reduce CV risks, he said. “Some of the imaging techniques do suggest that gouty crystals [are] in the atherosclerotic plaque of gout patients,” Dr. Garshick added. Dr. Pillinger’s work, he said, “is showing us that there are different pathways to develop atherosclerosis.”

Dr. Pillinger disclosed relationships with Federation Bio, Fortress Biotech, Amgen, Scilex, Hikma Pharmaceuticals, LG Chem, and Olatec Therapeutics. Dr. Garshick disclosed relationships with Kiniksa Pharmaceuticals, Agepha Pharma, Bristol Myers Squibb, and Horizon Therapeutics.
 

A version of this article appeared on Medscape.com.

NEW YORK — New insights into colchicine’s disruption of the pathway that contributes to arterial inflammation and new clinical studies of the drug could pave the way toward greater use of the anti-inflammatory drug in patients with or at risk for atherosclerotic cardiovascular disease (ASCVD), researchers said at the 4th Annual Cardiometabolic Risk in Inflammatory Conditions conference.

Colchicine was approved by the US Food and Drug Administration (FDA) in June 2023 in a once-daily 0.5-mg formulation under the brand name Lodoco to reduce the risk for major adverse cardiovascular events (MACE) in patients with established atherosclerotic disease or with multiple risk factors for CVD. The Lodoco formulation is slightly smaller than the 0.6-mg formulation that’s taken twice daily for the prophylaxis and treatment of acute gout flares.

In a presentation at the conference, Binita Shah, MD, one of the principal investigators in trials of Lodoco, explained how the inflammatory pathway contributes to atherosclerosis and provided an update on how colchicine disrupts the pathway. Dr. Shah is an associate professor of medicine at New York University in New York City and director of research at NYU Langone Health Interventional Cardiology.

“Colchicine dampens inflammatory markers on neutrophils so that they are less likely to be attracted to inflamed or injured endothelium, which would be the site of where plaque is building up or where the plaque has ruptured in the setting of a heart attack,” Shah told this news organization after her presentation.

Shah_Binita_NY_web.jpg

The Inflammatory Pathway

Dr. Shah explained that normal coronary endothelium resists adhesion by circulating leukocytes, but inflamed or injured coronary endothelium attracts those neutrophils via two types of selectins: L-selectins on neutrophils and E-selectins on endothelial cells. Those neutrophils then release inflammatory cytokines including interleukin-1 beta (IL-1ß), which then triggers production of IL-6 and, subsequently, high-sensitivity C-reactive protein (hsCRP), which contributes to plaque formation, she said.

“Colchicine affects these pathways with a balance for safety and effect on clinical outcomes, particularly to reduce recurrent myocardial infarction [MI],” Dr. Shah said during her presentation. 

Results from the CIRT trial demonstrated that methotrexate is ineffective in blocking the adenosine-mediated anti-inflammatory pathway, Dr. Shah said, so focusing on the IL-1ß–IL-6–hsCRP pathway, which is known to work based on the results of the CANTOS trial, could pay dividends.

“This is where colchicine can potentially play a role,” she said. 

Dr. Shah cited a secondary analysis of the CANTOS trial in which the magnitude of hsCRP reduction correlated with a reduction in MI, stroke, or cardiovascular death. The secondary analysis showed that patients who received canakinumab and achieved hsCRP ≥ 2 mg/L had a nonsignificant 5% lower risk and those who reached < 2 mg/L had a statistically significant 25% lower risk than those who received placebo.

The COPE-PCI Pilot trial demonstrated the benefit of targeting the interleukin pathways, she noted. 

Further clarification of the role of colchicine in managing patients with acute coronary syndrome may come from two other randomized trials now underway, Dr. Shah said: POPCORN is evaluating colchicine to reduce MACE after noncardiac surgery, and CLEAR SYNERGY is evaluating the best timing for colchicine therapy after an acute MI.

Dr. Shah presented preliminary data from her group from a neutrophil biomarker substudy of CLEAR SYNERGY that isolated neutrophils from patients who had an acute MI. “We treated them with various doses of colchicine and showed that the interaction between those treated neutrophils [and] the endothelial cells were a lot lower; they were less sticky to endothelial cells as colchicine was administered,” she said in her presentation. She added that colchicine also reduced neutrophil chemotaxis and neutrophil activation and potentially inhibited inflammasomes, decreasing IL-1ß production.

What’s more, colchicine has been shown to not affect platelets alone but rather platelets at the site of inflammation or plaque rupture, Dr. Shah added. “At currently used doses, colchicine does not inhibit platelet activity [by] itself, so we’ve never seen increased bleeding events, but it will dampen neutrophils’ ability to latch onto a platelet that could contribute to a clot,” she later told this news organization.

“There are multiple studies, both retrospective studies in gout cohorts as well as prospective studies in the cardiovascular cohort, that all show consistently one thing, which is that colchicine continues to reduce the risk of having a recurrent MI in patients who either have cardiovascular disease or are at high risk of having cardiovascular disease,” she said.

“I think that’s very helpful to know that it’s not just one study — it’s not just a fluke, potentially a play of chance — but multiple studies consistently showing the same thing: That there’s a reduced risk of acute MI.”
 

Slow to Embrace Colchicine

Despite this evidence, cardiologists and rheumatologists have been slow to embrace colchicine for patients at risk for cardiovascular events, said Michael S. Garshick, MD, who attended the conference and is head of the Cardio-Rheumatology Program at NYU Langone. “What [Shah] really highlighted was that for a number of years now, we’ve had several clinical trials showing the benefit of low-dose colchicine to prevent atherosclerotic cardiovascular events, and yet despite these and that there’s now an indication to use low-dose colchicine to reduce cardiovascular disease, we’re still struggling for this medication to be taken up by the general cardiology community to treat high-risk patients.

Garshick_Michael_NY_web.JPG

“There’s still some work to do to prove that we need to break those barriers,” Dr. Garshick added. Some of the confusion surrounding the use of colchicine for ASCVD may be attributed to the 0.5-mg dose approved for CVD as opposed to the long-approved 0.6-mg dose for gout, he said. “People are generally confused: Is it OK to use the 0.6-mg dose?” Dr. Garshick said.

Potential gastrointestinal side effects may be another concerning factor, although, he added, “we didn’t see any major complications.” Another issue could be polypharmacy in many of these patients, he said.

Dr. Garshick concurred with Shah that the existing evidence supporting the use of colchicine to reduce risk for cardiovascular events is strong, but more will come out. “I think there’s going to be evolving data supporting it,” he said.

Dr. Shah disclosed financial relationships with Philips Volcano and Novo Nordisk. She is a principal investigator of the CLEAR SYNERGY biomarker substudy and the POPCORN trial. Dr. Garshick disclosed relationships with Kiniksa Pharmaceuticals, Agepha Pharma, Bristol Myers Squibb, and Horizon Therapeutics.

A version of this article appeared on Medscape.com .

NEW YORK — New insights into colchicine’s disruption of the pathway that contributes to arterial inflammation and new clinical studies of the drug could pave the way toward greater use of the anti-inflammatory drug in patients with or at risk for atherosclerotic cardiovascular disease (ASCVD), researchers said at the 4th Annual Cardiometabolic Risk in Inflammatory Conditions conference.

Colchicine was approved by the US Food and Drug Administration (FDA) in June 2023 in a once-daily 0.5-mg formulation under the brand name Lodoco to reduce the risk for major adverse cardiovascular events (MACE) in patients with established atherosclerotic disease or with multiple risk factors for CVD. The Lodoco formulation is slightly smaller than the 0.6-mg formulation that’s taken twice daily for the prophylaxis and treatment of acute gout flares.

In a presentation at the conference, Binita Shah, MD, one of the principal investigators in trials of Lodoco, explained how the inflammatory pathway contributes to atherosclerosis and provided an update on how colchicine disrupts the pathway. Dr. Shah is an associate professor of medicine at New York University in New York City and director of research at NYU Langone Health Interventional Cardiology.

“Colchicine dampens inflammatory markers on neutrophils so that they are less likely to be attracted to inflamed or injured endothelium, which would be the site of where plaque is building up or where the plaque has ruptured in the setting of a heart attack,” Shah told this news organization after her presentation.

Shah_Binita_NY_web.jpg

The Inflammatory Pathway

Dr. Shah explained that normal coronary endothelium resists adhesion by circulating leukocytes, but inflamed or injured coronary endothelium attracts those neutrophils via two types of selectins: L-selectins on neutrophils and E-selectins on endothelial cells. Those neutrophils then release inflammatory cytokines including interleukin-1 beta (IL-1ß), which then triggers production of IL-6 and, subsequently, high-sensitivity C-reactive protein (hsCRP), which contributes to plaque formation, she said.

“Colchicine affects these pathways with a balance for safety and effect on clinical outcomes, particularly to reduce recurrent myocardial infarction [MI],” Dr. Shah said during her presentation. 

Results from the CIRT trial demonstrated that methotrexate is ineffective in blocking the adenosine-mediated anti-inflammatory pathway, Dr. Shah said, so focusing on the IL-1ß–IL-6–hsCRP pathway, which is known to work based on the results of the CANTOS trial, could pay dividends.

“This is where colchicine can potentially play a role,” she said. 

Dr. Shah cited a secondary analysis of the CANTOS trial in which the magnitude of hsCRP reduction correlated with a reduction in MI, stroke, or cardiovascular death. The secondary analysis showed that patients who received canakinumab and achieved hsCRP ≥ 2 mg/L had a nonsignificant 5% lower risk and those who reached < 2 mg/L had a statistically significant 25% lower risk than those who received placebo.

The COPE-PCI Pilot trial demonstrated the benefit of targeting the interleukin pathways, she noted. 

Further clarification of the role of colchicine in managing patients with acute coronary syndrome may come from two other randomized trials now underway, Dr. Shah said: POPCORN is evaluating colchicine to reduce MACE after noncardiac surgery, and CLEAR SYNERGY is evaluating the best timing for colchicine therapy after an acute MI.

Dr. Shah presented preliminary data from her group from a neutrophil biomarker substudy of CLEAR SYNERGY that isolated neutrophils from patients who had an acute MI. “We treated them with various doses of colchicine and showed that the interaction between those treated neutrophils [and] the endothelial cells were a lot lower; they were less sticky to endothelial cells as colchicine was administered,” she said in her presentation. She added that colchicine also reduced neutrophil chemotaxis and neutrophil activation and potentially inhibited inflammasomes, decreasing IL-1ß production.

What’s more, colchicine has been shown to not affect platelets alone but rather platelets at the site of inflammation or plaque rupture, Dr. Shah added. “At currently used doses, colchicine does not inhibit platelet activity [by] itself, so we’ve never seen increased bleeding events, but it will dampen neutrophils’ ability to latch onto a platelet that could contribute to a clot,” she later told this news organization.

“There are multiple studies, both retrospective studies in gout cohorts as well as prospective studies in the cardiovascular cohort, that all show consistently one thing, which is that colchicine continues to reduce the risk of having a recurrent MI in patients who either have cardiovascular disease or are at high risk of having cardiovascular disease,” she said.

“I think that’s very helpful to know that it’s not just one study — it’s not just a fluke, potentially a play of chance — but multiple studies consistently showing the same thing: That there’s a reduced risk of acute MI.”
 

Slow to Embrace Colchicine

Despite this evidence, cardiologists and rheumatologists have been slow to embrace colchicine for patients at risk for cardiovascular events, said Michael S. Garshick, MD, who attended the conference and is head of the Cardio-Rheumatology Program at NYU Langone. “What [Shah] really highlighted was that for a number of years now, we’ve had several clinical trials showing the benefit of low-dose colchicine to prevent atherosclerotic cardiovascular events, and yet despite these and that there’s now an indication to use low-dose colchicine to reduce cardiovascular disease, we’re still struggling for this medication to be taken up by the general cardiology community to treat high-risk patients.

Garshick_Michael_NY_web.JPG

“There’s still some work to do to prove that we need to break those barriers,” Dr. Garshick added. Some of the confusion surrounding the use of colchicine for ASCVD may be attributed to the 0.5-mg dose approved for CVD as opposed to the long-approved 0.6-mg dose for gout, he said. “People are generally confused: Is it OK to use the 0.6-mg dose?” Dr. Garshick said.

Potential gastrointestinal side effects may be another concerning factor, although, he added, “we didn’t see any major complications.” Another issue could be polypharmacy in many of these patients, he said.

Dr. Garshick concurred with Shah that the existing evidence supporting the use of colchicine to reduce risk for cardiovascular events is strong, but more will come out. “I think there’s going to be evolving data supporting it,” he said.

Dr. Shah disclosed financial relationships with Philips Volcano and Novo Nordisk. She is a principal investigator of the CLEAR SYNERGY biomarker substudy and the POPCORN trial. Dr. Garshick disclosed relationships with Kiniksa Pharmaceuticals, Agepha Pharma, Bristol Myers Squibb, and Horizon Therapeutics.

A version of this article appeared on Medscape.com .

NEW YORK — New insights into colchicine’s disruption of the pathway that contributes to arterial inflammation and new clinical studies of the drug could pave the way toward greater use of the anti-inflammatory drug in patients with or at risk for atherosclerotic cardiovascular disease (ASCVD), researchers said at the 4th Annual Cardiometabolic Risk in Inflammatory Conditions conference.

Colchicine was approved by the US Food and Drug Administration (FDA) in June 2023 in a once-daily 0.5-mg formulation under the brand name Lodoco to reduce the risk for major adverse cardiovascular events (MACE) in patients with established atherosclerotic disease or with multiple risk factors for CVD. The Lodoco formulation is slightly smaller than the 0.6-mg formulation that’s taken twice daily for the prophylaxis and treatment of acute gout flares.

In a presentation at the conference, Binita Shah, MD, one of the principal investigators in trials of Lodoco, explained how the inflammatory pathway contributes to atherosclerosis and provided an update on how colchicine disrupts the pathway. Dr. Shah is an associate professor of medicine at New York University in New York City and director of research at NYU Langone Health Interventional Cardiology.

“Colchicine dampens inflammatory markers on neutrophils so that they are less likely to be attracted to inflamed or injured endothelium, which would be the site of where plaque is building up or where the plaque has ruptured in the setting of a heart attack,” Shah told this news organization after her presentation.

Shah_Binita_NY_web.jpg

The Inflammatory Pathway

Dr. Shah explained that normal coronary endothelium resists adhesion by circulating leukocytes, but inflamed or injured coronary endothelium attracts those neutrophils via two types of selectins: L-selectins on neutrophils and E-selectins on endothelial cells. Those neutrophils then release inflammatory cytokines including interleukin-1 beta (IL-1ß), which then triggers production of IL-6 and, subsequently, high-sensitivity C-reactive protein (hsCRP), which contributes to plaque formation, she said.

“Colchicine affects these pathways with a balance for safety and effect on clinical outcomes, particularly to reduce recurrent myocardial infarction [MI],” Dr. Shah said during her presentation. 

Results from the CIRT trial demonstrated that methotrexate is ineffective in blocking the adenosine-mediated anti-inflammatory pathway, Dr. Shah said, so focusing on the IL-1ß–IL-6–hsCRP pathway, which is known to work based on the results of the CANTOS trial, could pay dividends.

“This is where colchicine can potentially play a role,” she said. 

Dr. Shah cited a secondary analysis of the CANTOS trial in which the magnitude of hsCRP reduction correlated with a reduction in MI, stroke, or cardiovascular death. The secondary analysis showed that patients who received canakinumab and achieved hsCRP ≥ 2 mg/L had a nonsignificant 5% lower risk and those who reached < 2 mg/L had a statistically significant 25% lower risk than those who received placebo.

The COPE-PCI Pilot trial demonstrated the benefit of targeting the interleukin pathways, she noted. 

Further clarification of the role of colchicine in managing patients with acute coronary syndrome may come from two other randomized trials now underway, Dr. Shah said: POPCORN is evaluating colchicine to reduce MACE after noncardiac surgery, and CLEAR SYNERGY is evaluating the best timing for colchicine therapy after an acute MI.

Dr. Shah presented preliminary data from her group from a neutrophil biomarker substudy of CLEAR SYNERGY that isolated neutrophils from patients who had an acute MI. “We treated them with various doses of colchicine and showed that the interaction between those treated neutrophils [and] the endothelial cells were a lot lower; they were less sticky to endothelial cells as colchicine was administered,” she said in her presentation. She added that colchicine also reduced neutrophil chemotaxis and neutrophil activation and potentially inhibited inflammasomes, decreasing IL-1ß production.

What’s more, colchicine has been shown to not affect platelets alone but rather platelets at the site of inflammation or plaque rupture, Dr. Shah added. “At currently used doses, colchicine does not inhibit platelet activity [by] itself, so we’ve never seen increased bleeding events, but it will dampen neutrophils’ ability to latch onto a platelet that could contribute to a clot,” she later told this news organization.

“There are multiple studies, both retrospective studies in gout cohorts as well as prospective studies in the cardiovascular cohort, that all show consistently one thing, which is that colchicine continues to reduce the risk of having a recurrent MI in patients who either have cardiovascular disease or are at high risk of having cardiovascular disease,” she said.

“I think that’s very helpful to know that it’s not just one study — it’s not just a fluke, potentially a play of chance — but multiple studies consistently showing the same thing: That there’s a reduced risk of acute MI.”
 

Slow to Embrace Colchicine

Despite this evidence, cardiologists and rheumatologists have been slow to embrace colchicine for patients at risk for cardiovascular events, said Michael S. Garshick, MD, who attended the conference and is head of the Cardio-Rheumatology Program at NYU Langone. “What [Shah] really highlighted was that for a number of years now, we’ve had several clinical trials showing the benefit of low-dose colchicine to prevent atherosclerotic cardiovascular events, and yet despite these and that there’s now an indication to use low-dose colchicine to reduce cardiovascular disease, we’re still struggling for this medication to be taken up by the general cardiology community to treat high-risk patients.

Garshick_Michael_NY_web.JPG

“There’s still some work to do to prove that we need to break those barriers,” Dr. Garshick added. Some of the confusion surrounding the use of colchicine for ASCVD may be attributed to the 0.5-mg dose approved for CVD as opposed to the long-approved 0.6-mg dose for gout, he said. “People are generally confused: Is it OK to use the 0.6-mg dose?” Dr. Garshick said.

Potential gastrointestinal side effects may be another concerning factor, although, he added, “we didn’t see any major complications.” Another issue could be polypharmacy in many of these patients, he said.

Dr. Garshick concurred with Shah that the existing evidence supporting the use of colchicine to reduce risk for cardiovascular events is strong, but more will come out. “I think there’s going to be evolving data supporting it,” he said.

Dr. Shah disclosed financial relationships with Philips Volcano and Novo Nordisk. She is a principal investigator of the CLEAR SYNERGY biomarker substudy and the POPCORN trial. Dr. Garshick disclosed relationships with Kiniksa Pharmaceuticals, Agepha Pharma, Bristol Myers Squibb, and Horizon Therapeutics.

A version of this article appeared on Medscape.com .

LIVERPOOL, ENGLAND — Optimizing how people experiencing a gout flare are managed in hospital and then followed-up afterwards can substantially increase the uptake of guideline-recommended urate-lowering therapy (ULT), researchers reported at the annual meeting of the British Society for Rheumatology (BSR).

In a prospective study, 92% of 97 people admitted to hospital for gout flares were using ULT within 6 months of discharge after a multifaceted intervention was introduced. By comparison, 49% of 94 people admitted for gout flares before the introduction of the intervention were taking ULT within the same postdischarge time frame. 

Moreover, a higher proportion of individuals had urate blood tests done at least once within the 6-month postdischarge period after the intervention’s introduction (58% vs 32%) and fewer (9% vs 15%) needed repeated hospital treatment. 

“Gout is the most common inflammatory arthritis affecting one in 30 adults in the United Kingdom, yet it’s one of the most poorly managed,” study investigator Mark D. Russell, MB, BChir, pointed out during a poster presentation. 

“There are very effective treatments,” added Dr. Russell, a rheumatology registrar and postdoctoral research fellow at King’s College London in London, England. “Urate-lowering therapies such as allopurinol, which when taken at the correct dose, in the long term, effectively cures patients of their symptoms and prevents complications.” 

Dr. Russell said in an interview that there was still work to be done as the rate of people achieving urate levels below the recommended threshold of 360 micromol/L (6 mg/dL) within 6 months was still low, at 27%, even it if was still better than the 11% seen before the intervention was introduced.
 

Improving the In- and Post-Hospital Pathway

“We developed and implemented an in-hospital management pathway which encouraged urate-lowering therapy initiation prior to discharge, followed by a post-discharge nurse-led review,” Dr. Russell explained. 

The in-hospital pathway was based upon BSR, European Alliance of Associations for Rheumatology, and American College of Rheumatology guidelines and involved diagnosing and managing the gout flare appropriately. This may have been via early joint aspiration, medication, or both, as directed by the rheumatology team. Affected individuals also received education and were directed where to obtain further information on the use of ULT. Outpatient follow-up was considered if an individual had severe or tophaceous gout, recurrent episodes, or contraindications or intolerances to ULT. Otherwise, a rheumatology nurse telephoned the individual 2 weeks later to review symptoms and discuss next steps.

The researchers recorded improvements in in-hospital outcomes. The frequency of in-hospital serum urate level measurements rose from 66% in the 12-month preimplementation period to 93% in the 12-month period after the intervention’s introduction. Almost two thirds (62%) of patients were discharged on ULT compared with 18% preimplementation. And gout-specific recommendations were given 86% of the time compared with 59% before the intervention.
 

Related Work on Gout Incidence

Separately, Dr. Russell also presented data from a nationwide, population-level cohort study that used data from OpenSAFELY, the secure data analytics platform used by the National Health Service in England. 

“We did an analysis previously using the CPRD [Clinical Research Practice Datalink], which is another good primary care database, showing that only a third of people with gout in the UK get urate-lowering drugs, when really it should be the vast majority,” he said in the interview.

“And then we wanted to look at, on top of that, what was the impact of the [COVID-19] pandemic,” Russell added. Specifically, the aim was to look at how the pandemic had affected the incidence, management, and prevalence of gout.

Between March 2015 and February 2023, 246,695 new cases of gout were identified among 17.9 million adults, seen in primary and secondary care. 
 

COVID-19 Pandemic Affected Cases

“The number of new cases of gout dropped by about one third in the first year of the pandemic,” Dr. Russell said. Incidence declined from 1.78 to 1.23 per 1000 adults. “Whether that was through people not feeling comfortable going to their GP [general practitioner] or not being able to get an appointment, we don’t know.”

While there was a subsequent increase in new cases of gout since this time, the rates still haven’t reached what they were before the pandemic. This implies that there could be a substantial number of people who may be undiagnosed because of the pandemic, Dr. Russell suggested. 

Moreover, he reported that in 2022-2023, the prevalence of gout was 3.21%, up slightly from the 3.07% recorded 7 years earlier in 2015-2016.
 

ULT Treatment Rates Low

“If you did see a GP, however, so as long as you saw someone, the treatment wasn’t any worse,” Dr. Russell said. Just under 30% of people with incident gout for whom follow-up data were available had initiated ULT within 6 months of their diagnosis. And, of these new starters, around a quarter had a serum urate level below a target of 360 micromol/L. 

“This doesn’t detract from the fact that this is pretty low. Despite guidelines, we’re still not getting the majority of people on these very effective urate-lowering drugs,” Dr. Russell said.

There is perhaps too much reliance on modifying diet and lifestyle, he added, which are important for many reasons but will not do much to lower blood urate levels. 

As a final word, Dr. Russell said, “It’s not just a case of preventing a bit of joint pain. People get lots of complications when they’re undertreated — erosive joint damage, work disability, impaired quality of life — and yet we’ve got very cheap, well-tolerated drugs.”

The work was independently funded. Dr. Russell acknowledged grant or research support from Eli Lilly, Janssen, Pfizer, and UCB and receipt of honoraria from AbbVie, Biogen, Eli Lilly, Galapagos, and Menarini. 

A version of this article appeared on Medscape.com.

LIVERPOOL, ENGLAND — Optimizing how people experiencing a gout flare are managed in hospital and then followed-up afterwards can substantially increase the uptake of guideline-recommended urate-lowering therapy (ULT), researchers reported at the annual meeting of the British Society for Rheumatology (BSR).

In a prospective study, 92% of 97 people admitted to hospital for gout flares were using ULT within 6 months of discharge after a multifaceted intervention was introduced. By comparison, 49% of 94 people admitted for gout flares before the introduction of the intervention were taking ULT within the same postdischarge time frame. 

Moreover, a higher proportion of individuals had urate blood tests done at least once within the 6-month postdischarge period after the intervention’s introduction (58% vs 32%) and fewer (9% vs 15%) needed repeated hospital treatment. 

“Gout is the most common inflammatory arthritis affecting one in 30 adults in the United Kingdom, yet it’s one of the most poorly managed,” study investigator Mark D. Russell, MB, BChir, pointed out during a poster presentation. 

“There are very effective treatments,” added Dr. Russell, a rheumatology registrar and postdoctoral research fellow at King’s College London in London, England. “Urate-lowering therapies such as allopurinol, which when taken at the correct dose, in the long term, effectively cures patients of their symptoms and prevents complications.” 

Dr. Russell said in an interview that there was still work to be done as the rate of people achieving urate levels below the recommended threshold of 360 micromol/L (6 mg/dL) within 6 months was still low, at 27%, even it if was still better than the 11% seen before the intervention was introduced.
 

Improving the In- and Post-Hospital Pathway

“We developed and implemented an in-hospital management pathway which encouraged urate-lowering therapy initiation prior to discharge, followed by a post-discharge nurse-led review,” Dr. Russell explained. 

The in-hospital pathway was based upon BSR, European Alliance of Associations for Rheumatology, and American College of Rheumatology guidelines and involved diagnosing and managing the gout flare appropriately. This may have been via early joint aspiration, medication, or both, as directed by the rheumatology team. Affected individuals also received education and were directed where to obtain further information on the use of ULT. Outpatient follow-up was considered if an individual had severe or tophaceous gout, recurrent episodes, or contraindications or intolerances to ULT. Otherwise, a rheumatology nurse telephoned the individual 2 weeks later to review symptoms and discuss next steps.

The researchers recorded improvements in in-hospital outcomes. The frequency of in-hospital serum urate level measurements rose from 66% in the 12-month preimplementation period to 93% in the 12-month period after the intervention’s introduction. Almost two thirds (62%) of patients were discharged on ULT compared with 18% preimplementation. And gout-specific recommendations were given 86% of the time compared with 59% before the intervention.
 

Related Work on Gout Incidence

Separately, Dr. Russell also presented data from a nationwide, population-level cohort study that used data from OpenSAFELY, the secure data analytics platform used by the National Health Service in England. 

“We did an analysis previously using the CPRD [Clinical Research Practice Datalink], which is another good primary care database, showing that only a third of people with gout in the UK get urate-lowering drugs, when really it should be the vast majority,” he said in the interview.

“And then we wanted to look at, on top of that, what was the impact of the [COVID-19] pandemic,” Russell added. Specifically, the aim was to look at how the pandemic had affected the incidence, management, and prevalence of gout.

Between March 2015 and February 2023, 246,695 new cases of gout were identified among 17.9 million adults, seen in primary and secondary care. 
 

COVID-19 Pandemic Affected Cases

“The number of new cases of gout dropped by about one third in the first year of the pandemic,” Dr. Russell said. Incidence declined from 1.78 to 1.23 per 1000 adults. “Whether that was through people not feeling comfortable going to their GP [general practitioner] or not being able to get an appointment, we don’t know.”

While there was a subsequent increase in new cases of gout since this time, the rates still haven’t reached what they were before the pandemic. This implies that there could be a substantial number of people who may be undiagnosed because of the pandemic, Dr. Russell suggested. 

Moreover, he reported that in 2022-2023, the prevalence of gout was 3.21%, up slightly from the 3.07% recorded 7 years earlier in 2015-2016.
 

ULT Treatment Rates Low

“If you did see a GP, however, so as long as you saw someone, the treatment wasn’t any worse,” Dr. Russell said. Just under 30% of people with incident gout for whom follow-up data were available had initiated ULT within 6 months of their diagnosis. And, of these new starters, around a quarter had a serum urate level below a target of 360 micromol/L. 

“This doesn’t detract from the fact that this is pretty low. Despite guidelines, we’re still not getting the majority of people on these very effective urate-lowering drugs,” Dr. Russell said.

There is perhaps too much reliance on modifying diet and lifestyle, he added, which are important for many reasons but will not do much to lower blood urate levels. 

As a final word, Dr. Russell said, “It’s not just a case of preventing a bit of joint pain. People get lots of complications when they’re undertreated — erosive joint damage, work disability, impaired quality of life — and yet we’ve got very cheap, well-tolerated drugs.”

The work was independently funded. Dr. Russell acknowledged grant or research support from Eli Lilly, Janssen, Pfizer, and UCB and receipt of honoraria from AbbVie, Biogen, Eli Lilly, Galapagos, and Menarini. 

A version of this article appeared on Medscape.com.

LIVERPOOL, ENGLAND — Optimizing how people experiencing a gout flare are managed in hospital and then followed-up afterwards can substantially increase the uptake of guideline-recommended urate-lowering therapy (ULT), researchers reported at the annual meeting of the British Society for Rheumatology (BSR).

In a prospective study, 92% of 97 people admitted to hospital for gout flares were using ULT within 6 months of discharge after a multifaceted intervention was introduced. By comparison, 49% of 94 people admitted for gout flares before the introduction of the intervention were taking ULT within the same postdischarge time frame. 

Moreover, a higher proportion of individuals had urate blood tests done at least once within the 6-month postdischarge period after the intervention’s introduction (58% vs 32%) and fewer (9% vs 15%) needed repeated hospital treatment. 

“Gout is the most common inflammatory arthritis affecting one in 30 adults in the United Kingdom, yet it’s one of the most poorly managed,” study investigator Mark D. Russell, MB, BChir, pointed out during a poster presentation. 

“There are very effective treatments,” added Dr. Russell, a rheumatology registrar and postdoctoral research fellow at King’s College London in London, England. “Urate-lowering therapies such as allopurinol, which when taken at the correct dose, in the long term, effectively cures patients of their symptoms and prevents complications.” 

Dr. Russell said in an interview that there was still work to be done as the rate of people achieving urate levels below the recommended threshold of 360 micromol/L (6 mg/dL) within 6 months was still low, at 27%, even it if was still better than the 11% seen before the intervention was introduced.
 

Improving the In- and Post-Hospital Pathway

“We developed and implemented an in-hospital management pathway which encouraged urate-lowering therapy initiation prior to discharge, followed by a post-discharge nurse-led review,” Dr. Russell explained. 

The in-hospital pathway was based upon BSR, European Alliance of Associations for Rheumatology, and American College of Rheumatology guidelines and involved diagnosing and managing the gout flare appropriately. This may have been via early joint aspiration, medication, or both, as directed by the rheumatology team. Affected individuals also received education and were directed where to obtain further information on the use of ULT. Outpatient follow-up was considered if an individual had severe or tophaceous gout, recurrent episodes, or contraindications or intolerances to ULT. Otherwise, a rheumatology nurse telephoned the individual 2 weeks later to review symptoms and discuss next steps.

The researchers recorded improvements in in-hospital outcomes. The frequency of in-hospital serum urate level measurements rose from 66% in the 12-month preimplementation period to 93% in the 12-month period after the intervention’s introduction. Almost two thirds (62%) of patients were discharged on ULT compared with 18% preimplementation. And gout-specific recommendations were given 86% of the time compared with 59% before the intervention.
 

Related Work on Gout Incidence

Separately, Dr. Russell also presented data from a nationwide, population-level cohort study that used data from OpenSAFELY, the secure data analytics platform used by the National Health Service in England. 

“We did an analysis previously using the CPRD [Clinical Research Practice Datalink], which is another good primary care database, showing that only a third of people with gout in the UK get urate-lowering drugs, when really it should be the vast majority,” he said in the interview.

“And then we wanted to look at, on top of that, what was the impact of the [COVID-19] pandemic,” Russell added. Specifically, the aim was to look at how the pandemic had affected the incidence, management, and prevalence of gout.

Between March 2015 and February 2023, 246,695 new cases of gout were identified among 17.9 million adults, seen in primary and secondary care. 
 

COVID-19 Pandemic Affected Cases

“The number of new cases of gout dropped by about one third in the first year of the pandemic,” Dr. Russell said. Incidence declined from 1.78 to 1.23 per 1000 adults. “Whether that was through people not feeling comfortable going to their GP [general practitioner] or not being able to get an appointment, we don’t know.”

While there was a subsequent increase in new cases of gout since this time, the rates still haven’t reached what they were before the pandemic. This implies that there could be a substantial number of people who may be undiagnosed because of the pandemic, Dr. Russell suggested. 

Moreover, he reported that in 2022-2023, the prevalence of gout was 3.21%, up slightly from the 3.07% recorded 7 years earlier in 2015-2016.
 

ULT Treatment Rates Low

“If you did see a GP, however, so as long as you saw someone, the treatment wasn’t any worse,” Dr. Russell said. Just under 30% of people with incident gout for whom follow-up data were available had initiated ULT within 6 months of their diagnosis. And, of these new starters, around a quarter had a serum urate level below a target of 360 micromol/L. 

“This doesn’t detract from the fact that this is pretty low. Despite guidelines, we’re still not getting the majority of people on these very effective urate-lowering drugs,” Dr. Russell said.

There is perhaps too much reliance on modifying diet and lifestyle, he added, which are important for many reasons but will not do much to lower blood urate levels. 

As a final word, Dr. Russell said, “It’s not just a case of preventing a bit of joint pain. People get lots of complications when they’re undertreated — erosive joint damage, work disability, impaired quality of life — and yet we’ve got very cheap, well-tolerated drugs.”

The work was independently funded. Dr. Russell acknowledged grant or research support from Eli Lilly, Janssen, Pfizer, and UCB and receipt of honoraria from AbbVie, Biogen, Eli Lilly, Galapagos, and Menarini. 

A version of this article appeared on Medscape.com.

People with gout are 58% more likely to develop cardiovascular disease (CVD), according to a new analysis. This increased risk was observed across 12 different cardiovascular conditions, including heart failure, arrhythmias, and valve diseases.

“These findings suggest that the organ damage associated with gout is likely to be much broader than originally thought,” Nathalie Conrad, PhD, senior author of the research and cardiovascular epidemiologist at KU Leuven, Leuven, Belgium, said in an email. This could be useful for future research on underlying biological mechanisms driving CVD risk in gout, she added.

While previous research has tied gout to increased cardiovascular risk, these studies “largely focused on coronary heart disease, stroke, and thromboembolic outcomes,” she explained, and have been smaller in size.

This new study included more than 862,000 individuals, which permitted researchers to investigate rarer CVD outcomes such as myocarditis and pericarditis.

For the study, researchers used electronic health records from the UK Clinical Practice Research Datalink, a primary care database that contains anonymized health data for about 22 million individuals. Using these data, they identified more than 152,600 individuals with gout. Patients included in the analysis were diagnosed between 2000 and 2017, younger than 80 years at diagnosis, and free of CVD for at least 12 months after their gout diagnosis.

Patients with gout were compared with nearly 710,000 controls, matched on demographic factors such as age, sex, and geographic region.

Researchers then investigated the incidence of 12 CVDs, including atherosclerotic diseases, degenerative and thromboembolic diseases, and arrythmias, between the two groups from January 1, 2000, to June 30, 2019.

The findings were published in the March 2024 issue of The Lancet Rheumatology. Overall, patients with gout were 58% more likely to develop any CVD than their matched comparators without gout. There was a higher disease incidence among patients with gout for each of the 12 conditions. This association was more pronounced in women (hazard ratio [HR], 1.88) than in men (HR, 1.49), and gout amplified the risk for CVD in younger individuals to a greater extent.

Individuals younger than 45 years with gout were more than twice as likely to develop CVD compared with similarly aged individuals without gout. For comparison, individuals aged 45-54 years with gout were 84% more likely to develop CVD, and individuals aged 55-64 years were 57% more likely to develop CVD than matched controls.

Conduction system disease had the highest incident risk (HR, 1.88), followed by heart failure and valve disease (HR, 1.85 for both).

Individuals with gout had higher rates of comorbidities than the controls, including hypertension, obesity, and dyslipidemia. Overall, CVD risk was slightly attenuated after adjustment for traditional CVD risk factors such as smoking, blood pressure, and body mass index but still significant: Patients with gout had a 31% higher risk for CVD than comparators.

This shows “that known CVD risk factors only explain part of the CVD risks seen in patients with gout,” Dr. Conrad said. Other factors such as inflammation and other disease activity factors could be at play, she explained, which would need to be explored in future research.

The study “shows the whole landscape” of CVD and gout, Michael H. Pillinger, MD, rheumatologist and professor of medicine, biochemistry, and molecular pharmacology at NYU Grossman School of Medicine in New York City, said in an interview. He was not involved with the research.

“Every possible cardiovascular disease that they could think of was something that gout patients had more of than the non-gout patients,” he added. “I think this is going to be a paper that gets cited a lot, at minimum when describing the background of risk when we look at gout patients.”

The study had some limitations, including that researchers were unable to account for how medications such as nonsteroidal anti-inflammatory drugs, corticosteroids, colchicine, or allopurinol may have affected the association between gout and CVD.

“This is because analyses of nonrandomized treatment can be confounded by indication, wherein it is difficult to differentiate the effects of the treatment from underlying disease severity,” the authors wrote.

There was also a large amount of missing data on blood pressure, body mass index, smoking status, and other health information relevant to cardiovascular risk, so sensitivity analyses adjusting for these factors “should be interpreted with caution,” they added.

Dr. Pillinger also noted that the rates of comorbidities in the gout study population were lower than what have been found in US study populations. For example, about 40% of patients with gout in the analysis had hypertension, while other studies have suggested higher rates of 60%-70%, he said. However, it’s not clear if these differences could have affected outcomes. He added that these limitations do not “in any way weaken [the authors’] conclusion.”

The findings call for better strategies to reduce CVD risk in patients with gout, Dr. Conrad noted.

“Further improvements could come from better recognition and intervention on CVD risk factors (eg, through lifestyle changes or drug therapies where they are indicated), as well as proactive screening for heart disease in patients with gout, which could allow early diagnosis and interventions to delay more severe outcomes,” she added.

This study was funded by Research Foundation Flanders. Dr. Conrad was funded by a personal fellowship from the Research Foundation Flanders and a European Society of Cardiology research grant. She received royalties from Oxford University Innovation. Four of Dr. Conrad’s eight coauthors also reported financial relationships with pharmaceutical companies. Dr. Pillinger served as a consultant to Amgen, Federation Bio, Fortress Biotech, and Scilex, and he holds an investigator-initiated grant from Hikma.

A version of this article appeared on Medscape.com.

People with gout are 58% more likely to develop cardiovascular disease (CVD), according to a new analysis. This increased risk was observed across 12 different cardiovascular conditions, including heart failure, arrhythmias, and valve diseases.

“These findings suggest that the organ damage associated with gout is likely to be much broader than originally thought,” Nathalie Conrad, PhD, senior author of the research and cardiovascular epidemiologist at KU Leuven, Leuven, Belgium, said in an email. This could be useful for future research on underlying biological mechanisms driving CVD risk in gout, she added.

While previous research has tied gout to increased cardiovascular risk, these studies “largely focused on coronary heart disease, stroke, and thromboembolic outcomes,” she explained, and have been smaller in size.

This new study included more than 862,000 individuals, which permitted researchers to investigate rarer CVD outcomes such as myocarditis and pericarditis.

For the study, researchers used electronic health records from the UK Clinical Practice Research Datalink, a primary care database that contains anonymized health data for about 22 million individuals. Using these data, they identified more than 152,600 individuals with gout. Patients included in the analysis were diagnosed between 2000 and 2017, younger than 80 years at diagnosis, and free of CVD for at least 12 months after their gout diagnosis.

Patients with gout were compared with nearly 710,000 controls, matched on demographic factors such as age, sex, and geographic region.

Researchers then investigated the incidence of 12 CVDs, including atherosclerotic diseases, degenerative and thromboembolic diseases, and arrythmias, between the two groups from January 1, 2000, to June 30, 2019.

The findings were published in the March 2024 issue of The Lancet Rheumatology. Overall, patients with gout were 58% more likely to develop any CVD than their matched comparators without gout. There was a higher disease incidence among patients with gout for each of the 12 conditions. This association was more pronounced in women (hazard ratio [HR], 1.88) than in men (HR, 1.49), and gout amplified the risk for CVD in younger individuals to a greater extent.

Individuals younger than 45 years with gout were more than twice as likely to develop CVD compared with similarly aged individuals without gout. For comparison, individuals aged 45-54 years with gout were 84% more likely to develop CVD, and individuals aged 55-64 years were 57% more likely to develop CVD than matched controls.

Conduction system disease had the highest incident risk (HR, 1.88), followed by heart failure and valve disease (HR, 1.85 for both).

Individuals with gout had higher rates of comorbidities than the controls, including hypertension, obesity, and dyslipidemia. Overall, CVD risk was slightly attenuated after adjustment for traditional CVD risk factors such as smoking, blood pressure, and body mass index but still significant: Patients with gout had a 31% higher risk for CVD than comparators.

This shows “that known CVD risk factors only explain part of the CVD risks seen in patients with gout,” Dr. Conrad said. Other factors such as inflammation and other disease activity factors could be at play, she explained, which would need to be explored in future research.

The study “shows the whole landscape” of CVD and gout, Michael H. Pillinger, MD, rheumatologist and professor of medicine, biochemistry, and molecular pharmacology at NYU Grossman School of Medicine in New York City, said in an interview. He was not involved with the research.

“Every possible cardiovascular disease that they could think of was something that gout patients had more of than the non-gout patients,” he added. “I think this is going to be a paper that gets cited a lot, at minimum when describing the background of risk when we look at gout patients.”

The study had some limitations, including that researchers were unable to account for how medications such as nonsteroidal anti-inflammatory drugs, corticosteroids, colchicine, or allopurinol may have affected the association between gout and CVD.

“This is because analyses of nonrandomized treatment can be confounded by indication, wherein it is difficult to differentiate the effects of the treatment from underlying disease severity,” the authors wrote.

There was also a large amount of missing data on blood pressure, body mass index, smoking status, and other health information relevant to cardiovascular risk, so sensitivity analyses adjusting for these factors “should be interpreted with caution,” they added.

Dr. Pillinger also noted that the rates of comorbidities in the gout study population were lower than what have been found in US study populations. For example, about 40% of patients with gout in the analysis had hypertension, while other studies have suggested higher rates of 60%-70%, he said. However, it’s not clear if these differences could have affected outcomes. He added that these limitations do not “in any way weaken [the authors’] conclusion.”

The findings call for better strategies to reduce CVD risk in patients with gout, Dr. Conrad noted.

“Further improvements could come from better recognition and intervention on CVD risk factors (eg, through lifestyle changes or drug therapies where they are indicated), as well as proactive screening for heart disease in patients with gout, which could allow early diagnosis and interventions to delay more severe outcomes,” she added.

This study was funded by Research Foundation Flanders. Dr. Conrad was funded by a personal fellowship from the Research Foundation Flanders and a European Society of Cardiology research grant. She received royalties from Oxford University Innovation. Four of Dr. Conrad’s eight coauthors also reported financial relationships with pharmaceutical companies. Dr. Pillinger served as a consultant to Amgen, Federation Bio, Fortress Biotech, and Scilex, and he holds an investigator-initiated grant from Hikma.

A version of this article appeared on Medscape.com.

People with gout are 58% more likely to develop cardiovascular disease (CVD), according to a new analysis. This increased risk was observed across 12 different cardiovascular conditions, including heart failure, arrhythmias, and valve diseases.

“These findings suggest that the organ damage associated with gout is likely to be much broader than originally thought,” Nathalie Conrad, PhD, senior author of the research and cardiovascular epidemiologist at KU Leuven, Leuven, Belgium, said in an email. This could be useful for future research on underlying biological mechanisms driving CVD risk in gout, she added.

While previous research has tied gout to increased cardiovascular risk, these studies “largely focused on coronary heart disease, stroke, and thromboembolic outcomes,” she explained, and have been smaller in size.

This new study included more than 862,000 individuals, which permitted researchers to investigate rarer CVD outcomes such as myocarditis and pericarditis.

For the study, researchers used electronic health records from the UK Clinical Practice Research Datalink, a primary care database that contains anonymized health data for about 22 million individuals. Using these data, they identified more than 152,600 individuals with gout. Patients included in the analysis were diagnosed between 2000 and 2017, younger than 80 years at diagnosis, and free of CVD for at least 12 months after their gout diagnosis.

Patients with gout were compared with nearly 710,000 controls, matched on demographic factors such as age, sex, and geographic region.

Researchers then investigated the incidence of 12 CVDs, including atherosclerotic diseases, degenerative and thromboembolic diseases, and arrythmias, between the two groups from January 1, 2000, to June 30, 2019.

The findings were published in the March 2024 issue of The Lancet Rheumatology. Overall, patients with gout were 58% more likely to develop any CVD than their matched comparators without gout. There was a higher disease incidence among patients with gout for each of the 12 conditions. This association was more pronounced in women (hazard ratio [HR], 1.88) than in men (HR, 1.49), and gout amplified the risk for CVD in younger individuals to a greater extent.

Individuals younger than 45 years with gout were more than twice as likely to develop CVD compared with similarly aged individuals without gout. For comparison, individuals aged 45-54 years with gout were 84% more likely to develop CVD, and individuals aged 55-64 years were 57% more likely to develop CVD than matched controls.

Conduction system disease had the highest incident risk (HR, 1.88), followed by heart failure and valve disease (HR, 1.85 for both).

Individuals with gout had higher rates of comorbidities than the controls, including hypertension, obesity, and dyslipidemia. Overall, CVD risk was slightly attenuated after adjustment for traditional CVD risk factors such as smoking, blood pressure, and body mass index but still significant: Patients with gout had a 31% higher risk for CVD than comparators.

This shows “that known CVD risk factors only explain part of the CVD risks seen in patients with gout,” Dr. Conrad said. Other factors such as inflammation and other disease activity factors could be at play, she explained, which would need to be explored in future research.

The study “shows the whole landscape” of CVD and gout, Michael H. Pillinger, MD, rheumatologist and professor of medicine, biochemistry, and molecular pharmacology at NYU Grossman School of Medicine in New York City, said in an interview. He was not involved with the research.

“Every possible cardiovascular disease that they could think of was something that gout patients had more of than the non-gout patients,” he added. “I think this is going to be a paper that gets cited a lot, at minimum when describing the background of risk when we look at gout patients.”

The study had some limitations, including that researchers were unable to account for how medications such as nonsteroidal anti-inflammatory drugs, corticosteroids, colchicine, or allopurinol may have affected the association between gout and CVD.

“This is because analyses of nonrandomized treatment can be confounded by indication, wherein it is difficult to differentiate the effects of the treatment from underlying disease severity,” the authors wrote.

There was also a large amount of missing data on blood pressure, body mass index, smoking status, and other health information relevant to cardiovascular risk, so sensitivity analyses adjusting for these factors “should be interpreted with caution,” they added.

Dr. Pillinger also noted that the rates of comorbidities in the gout study population were lower than what have been found in US study populations. For example, about 40% of patients with gout in the analysis had hypertension, while other studies have suggested higher rates of 60%-70%, he said. However, it’s not clear if these differences could have affected outcomes. He added that these limitations do not “in any way weaken [the authors’] conclusion.”

The findings call for better strategies to reduce CVD risk in patients with gout, Dr. Conrad noted.

“Further improvements could come from better recognition and intervention on CVD risk factors (eg, through lifestyle changes or drug therapies where they are indicated), as well as proactive screening for heart disease in patients with gout, which could allow early diagnosis and interventions to delay more severe outcomes,” she added.

This study was funded by Research Foundation Flanders. Dr. Conrad was funded by a personal fellowship from the Research Foundation Flanders and a European Society of Cardiology research grant. She received royalties from Oxford University Innovation. Four of Dr. Conrad’s eight coauthors also reported financial relationships with pharmaceutical companies. Dr. Pillinger served as a consultant to Amgen, Federation Bio, Fortress Biotech, and Scilex, and he holds an investigator-initiated grant from Hikma.

A version of this article appeared on Medscape.com.

Clinical efforts to get patients with a history of gout to reach specific target serum urate (SU) levels less than either 5 or 6 mg/dL could prevent the great majority of gout flares and hospitalizations for them, according to a new study that tracked patients for a mean of 8.3 years.

The findings, which appeared February 6 in JAMA, “support the value of target serum urate levels in gout flare prevention in primary care, where most gout patients are treated,” rheumatologist and study coauthor Hyon K. Choi, MD, DrPH, of Harvard Medical School and Massachusetts General Hospital, Boston, told this news organization. However, Dr. Choi noted that “the value of relying on target urate levels is not accepted in primary care practice,” and the author of an accompanying commentary said that the jury is still out about the best strategy to prevent flares.

Choi_Hyon_K_MA_web.jpg

Gout is caused by monosodium urate crystallization within the joints, which occurs when SU levels exceed the saturation point for uric acid crystallization in the body: approximately 6.8 mg/dL. “Studies have found strongly graded associations between serum urate levels above the saturation point and the risk of developing new cases of gout among individuals without gout at baseline,” Dr. Choi said. “However, associations between serum urate levels and the risk of recurrent flares among preexisting gout patients, which is relevant to clinical gout care practice, has not been established.”

Dr. Choi added that “despite the emphasis in US and European rheumatology guidelines on the use of urate-lowering therapy to treat-to-target serum urate level — eg, under 6 or 5 mg/dL — the proportions of flares associated with such target urate levels remained unknown.”
 

Study Shows Relationship Between SU Levels and Recurrent Flares

For the study, researchers tracked 3613 patients aged 40-69 with gout in the UK Biobank database from 2006-2010 to 2017 or 2020. The patients, 86% of whom were men, had a mean age of 60 years and about 96% were White.

Among the patients, 1773 new episodes of acute gout occurred in 27% of the patients (16% had one episode, 6% had two episodes, and 5% had at least three episodes). These were treated in primary care or required hospitalizations. The other 73% of patients had no new acute gout episodes.

Overall, 95% of flares occurred in those with baseline SU levels ≥ 6 mg/dL, and 98% occurred in those with levels ≥ 5 mg/dL.

Patients with baseline SU levels < 6.0 mg/dL had an acute gout flare rate of 10.6 per 1000 person-years. In comparison, relative risks for acute gout flares per 1000 person-years were 3.16 at baseline SU levels of 6.0-6.9 mg/dL, 6.20 for 7.0-7.9 mg/dL, 7.70 for 8.0-8.9 mg/dL, 9.80 for 9.0-9.9 mg/dL, and 11.26 for > 10 mg/dL after adjustment for various possible confounders (P < .001).

The researchers identified 64 hospitalizations with gout as the main discharge diagnosis, and 97% occurred in patients with baseline SU levels ≥ 6 mg/dL. All were in patients with baseline SU levels ≥ 5 mg/dL.

“An important feature of this study was that serum urate measurements were obtained from all gout patients at the study baseline, irrespective of clinical needs or flare status,” Dr. Choi said. “Prior studies failed to reveal the truly compelling nature of relations between serum urate levels and recurrent flares among preexisting gout patients.”

As for the cost of SU tests, Dr. Choi said they can run as low as $2. “Portable tests similar to home glucose measurement for diabetes patients are also being adopted by certain gout care practices,” he said.

The findings matter, Dr. Choi said, because SU is not tracked in the “vast majority of gout patients” in primary care. Instead, primary care doctors — as per the guidelines of the American College of Physicians — often adopt an approach that treats symptoms as needed instead of tracking and lowering SU levels, he said. In fact, “95% and 98% of gout flares can be potentially preventable at the population level if serum urate levels < 6 and < 5 mg/dL can be met, respectively, and 100% of hospitalizations for gout could be preventable with serum urate < 5 mg/dL,” he said.

As for limitations, the authors noted that participants in the UK Biobank “typically have a better socioeconomic status and are healthier than the UK general population,” and they added that “these data may underestimate the number of acute gout flares in the cohort.” Also, 55% of the total 502,490 patients in the UK Biobank were excluded owing to lack of primary care data.
 

Study ‘Offers the Kind of Evidence That We Need’

In an accompanying commentary, University of Alabama at Birmingham rheumatologist Angelo L. Gaffo, MD, MSPH, also noted that the study population was overwhelmingly White, had a low mean SU level (6.9 mg/dL), and had a low level of comorbidities, making the sample “poorly representative of the most commonly described gout populations.”

However, he also noted that there is “growing evidence linking serum urate levels with clinical outcomes,” with a pair of studies — one from 2021 and the other from 2022 — linking reductions in SU to < 6 md/dL to lower flare rates.

Gaffo_Angelo_AL_web.jpg

Dr. Gaffo told this news organization that although rheumatology guidelines support a treat-to-target strategy, “we haven›t generated a whole lot of important evidence to support it.”

The new study “offers the kind of evidence that we need,” he said, “but this is not going to be the ultimate answer.” That will only come from randomized clinical trials in the works that will pit the treat-to-target approach vs the primary care–favored strategy of titrating treatment until flares are controlled, he said.

Even though evidence is sparse, Dr. Gaffo said he still believes in the treat-to-target strategy: “I believe it is the best way to treat gout.”

What’s next? Researchers hope to understand how to better reach target SU goals in clinical practice, Dr. Choi said. “Involving nurses, pharmacists, or interactive online or app systems — as in other chronic treat-to-target care such as anticoagulation care, blood pressure, or lipid care — is actively being researched.”

He added that “we are trying to find the effective and safe medications and nonpharmacologic measures to reduce the urate burden, which can also simultaneously take care of gout’s frequent cardiovascular-kidney comorbidities.”

The US National Institutes of Health supported the study. Dr. Choi reports receiving grants from Horizon and serving on a board or committee for LG Chem, Shanton, and ANI Pharmaceuticals. Some other authors report an employment and stockholder relationship with Regeneron and support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, and Rheumatology Research Foundation. Dr. Gaffo reports personal fees from PK MED, SOBI/Selecta, Atom, and UpToDate.

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

Clinical efforts to get patients with a history of gout to reach specific target serum urate (SU) levels less than either 5 or 6 mg/dL could prevent the great majority of gout flares and hospitalizations for them, according to a new study that tracked patients for a mean of 8.3 years.

The findings, which appeared February 6 in JAMA, “support the value of target serum urate levels in gout flare prevention in primary care, where most gout patients are treated,” rheumatologist and study coauthor Hyon K. Choi, MD, DrPH, of Harvard Medical School and Massachusetts General Hospital, Boston, told this news organization. However, Dr. Choi noted that “the value of relying on target urate levels is not accepted in primary care practice,” and the author of an accompanying commentary said that the jury is still out about the best strategy to prevent flares.

Choi_Hyon_K_MA_web.jpg

Gout is caused by monosodium urate crystallization within the joints, which occurs when SU levels exceed the saturation point for uric acid crystallization in the body: approximately 6.8 mg/dL. “Studies have found strongly graded associations between serum urate levels above the saturation point and the risk of developing new cases of gout among individuals without gout at baseline,” Dr. Choi said. “However, associations between serum urate levels and the risk of recurrent flares among preexisting gout patients, which is relevant to clinical gout care practice, has not been established.”

Dr. Choi added that “despite the emphasis in US and European rheumatology guidelines on the use of urate-lowering therapy to treat-to-target serum urate level — eg, under 6 or 5 mg/dL — the proportions of flares associated with such target urate levels remained unknown.”
 

Study Shows Relationship Between SU Levels and Recurrent Flares

For the study, researchers tracked 3613 patients aged 40-69 with gout in the UK Biobank database from 2006-2010 to 2017 or 2020. The patients, 86% of whom were men, had a mean age of 60 years and about 96% were White.

Among the patients, 1773 new episodes of acute gout occurred in 27% of the patients (16% had one episode, 6% had two episodes, and 5% had at least three episodes). These were treated in primary care or required hospitalizations. The other 73% of patients had no new acute gout episodes.

Overall, 95% of flares occurred in those with baseline SU levels ≥ 6 mg/dL, and 98% occurred in those with levels ≥ 5 mg/dL.

Patients with baseline SU levels < 6.0 mg/dL had an acute gout flare rate of 10.6 per 1000 person-years. In comparison, relative risks for acute gout flares per 1000 person-years were 3.16 at baseline SU levels of 6.0-6.9 mg/dL, 6.20 for 7.0-7.9 mg/dL, 7.70 for 8.0-8.9 mg/dL, 9.80 for 9.0-9.9 mg/dL, and 11.26 for > 10 mg/dL after adjustment for various possible confounders (P < .001).

The researchers identified 64 hospitalizations with gout as the main discharge diagnosis, and 97% occurred in patients with baseline SU levels ≥ 6 mg/dL. All were in patients with baseline SU levels ≥ 5 mg/dL.

“An important feature of this study was that serum urate measurements were obtained from all gout patients at the study baseline, irrespective of clinical needs or flare status,” Dr. Choi said. “Prior studies failed to reveal the truly compelling nature of relations between serum urate levels and recurrent flares among preexisting gout patients.”

As for the cost of SU tests, Dr. Choi said they can run as low as $2. “Portable tests similar to home glucose measurement for diabetes patients are also being adopted by certain gout care practices,” he said.

The findings matter, Dr. Choi said, because SU is not tracked in the “vast majority of gout patients” in primary care. Instead, primary care doctors — as per the guidelines of the American College of Physicians — often adopt an approach that treats symptoms as needed instead of tracking and lowering SU levels, he said. In fact, “95% and 98% of gout flares can be potentially preventable at the population level if serum urate levels < 6 and < 5 mg/dL can be met, respectively, and 100% of hospitalizations for gout could be preventable with serum urate < 5 mg/dL,” he said.

As for limitations, the authors noted that participants in the UK Biobank “typically have a better socioeconomic status and are healthier than the UK general population,” and they added that “these data may underestimate the number of acute gout flares in the cohort.” Also, 55% of the total 502,490 patients in the UK Biobank were excluded owing to lack of primary care data.
 

Study ‘Offers the Kind of Evidence That We Need’

In an accompanying commentary, University of Alabama at Birmingham rheumatologist Angelo L. Gaffo, MD, MSPH, also noted that the study population was overwhelmingly White, had a low mean SU level (6.9 mg/dL), and had a low level of comorbidities, making the sample “poorly representative of the most commonly described gout populations.”

However, he also noted that there is “growing evidence linking serum urate levels with clinical outcomes,” with a pair of studies — one from 2021 and the other from 2022 — linking reductions in SU to < 6 md/dL to lower flare rates.

Gaffo_Angelo_AL_web.jpg

Dr. Gaffo told this news organization that although rheumatology guidelines support a treat-to-target strategy, “we haven›t generated a whole lot of important evidence to support it.”

The new study “offers the kind of evidence that we need,” he said, “but this is not going to be the ultimate answer.” That will only come from randomized clinical trials in the works that will pit the treat-to-target approach vs the primary care–favored strategy of titrating treatment until flares are controlled, he said.

Even though evidence is sparse, Dr. Gaffo said he still believes in the treat-to-target strategy: “I believe it is the best way to treat gout.”

What’s next? Researchers hope to understand how to better reach target SU goals in clinical practice, Dr. Choi said. “Involving nurses, pharmacists, or interactive online or app systems — as in other chronic treat-to-target care such as anticoagulation care, blood pressure, or lipid care — is actively being researched.”

He added that “we are trying to find the effective and safe medications and nonpharmacologic measures to reduce the urate burden, which can also simultaneously take care of gout’s frequent cardiovascular-kidney comorbidities.”

The US National Institutes of Health supported the study. Dr. Choi reports receiving grants from Horizon and serving on a board or committee for LG Chem, Shanton, and ANI Pharmaceuticals. Some other authors report an employment and stockholder relationship with Regeneron and support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, and Rheumatology Research Foundation. Dr. Gaffo reports personal fees from PK MED, SOBI/Selecta, Atom, and UpToDate.

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

Clinical efforts to get patients with a history of gout to reach specific target serum urate (SU) levels less than either 5 or 6 mg/dL could prevent the great majority of gout flares and hospitalizations for them, according to a new study that tracked patients for a mean of 8.3 years.

The findings, which appeared February 6 in JAMA, “support the value of target serum urate levels in gout flare prevention in primary care, where most gout patients are treated,” rheumatologist and study coauthor Hyon K. Choi, MD, DrPH, of Harvard Medical School and Massachusetts General Hospital, Boston, told this news organization. However, Dr. Choi noted that “the value of relying on target urate levels is not accepted in primary care practice,” and the author of an accompanying commentary said that the jury is still out about the best strategy to prevent flares.

Choi_Hyon_K_MA_web.jpg

Gout is caused by monosodium urate crystallization within the joints, which occurs when SU levels exceed the saturation point for uric acid crystallization in the body: approximately 6.8 mg/dL. “Studies have found strongly graded associations between serum urate levels above the saturation point and the risk of developing new cases of gout among individuals without gout at baseline,” Dr. Choi said. “However, associations between serum urate levels and the risk of recurrent flares among preexisting gout patients, which is relevant to clinical gout care practice, has not been established.”

Dr. Choi added that “despite the emphasis in US and European rheumatology guidelines on the use of urate-lowering therapy to treat-to-target serum urate level — eg, under 6 or 5 mg/dL — the proportions of flares associated with such target urate levels remained unknown.”
 

Study Shows Relationship Between SU Levels and Recurrent Flares

For the study, researchers tracked 3613 patients aged 40-69 with gout in the UK Biobank database from 2006-2010 to 2017 or 2020. The patients, 86% of whom were men, had a mean age of 60 years and about 96% were White.

Among the patients, 1773 new episodes of acute gout occurred in 27% of the patients (16% had one episode, 6% had two episodes, and 5% had at least three episodes). These were treated in primary care or required hospitalizations. The other 73% of patients had no new acute gout episodes.

Overall, 95% of flares occurred in those with baseline SU levels ≥ 6 mg/dL, and 98% occurred in those with levels ≥ 5 mg/dL.

Patients with baseline SU levels < 6.0 mg/dL had an acute gout flare rate of 10.6 per 1000 person-years. In comparison, relative risks for acute gout flares per 1000 person-years were 3.16 at baseline SU levels of 6.0-6.9 mg/dL, 6.20 for 7.0-7.9 mg/dL, 7.70 for 8.0-8.9 mg/dL, 9.80 for 9.0-9.9 mg/dL, and 11.26 for > 10 mg/dL after adjustment for various possible confounders (P < .001).

The researchers identified 64 hospitalizations with gout as the main discharge diagnosis, and 97% occurred in patients with baseline SU levels ≥ 6 mg/dL. All were in patients with baseline SU levels ≥ 5 mg/dL.

“An important feature of this study was that serum urate measurements were obtained from all gout patients at the study baseline, irrespective of clinical needs or flare status,” Dr. Choi said. “Prior studies failed to reveal the truly compelling nature of relations between serum urate levels and recurrent flares among preexisting gout patients.”

As for the cost of SU tests, Dr. Choi said they can run as low as $2. “Portable tests similar to home glucose measurement for diabetes patients are also being adopted by certain gout care practices,” he said.

The findings matter, Dr. Choi said, because SU is not tracked in the “vast majority of gout patients” in primary care. Instead, primary care doctors — as per the guidelines of the American College of Physicians — often adopt an approach that treats symptoms as needed instead of tracking and lowering SU levels, he said. In fact, “95% and 98% of gout flares can be potentially preventable at the population level if serum urate levels < 6 and < 5 mg/dL can be met, respectively, and 100% of hospitalizations for gout could be preventable with serum urate < 5 mg/dL,” he said.

As for limitations, the authors noted that participants in the UK Biobank “typically have a better socioeconomic status and are healthier than the UK general population,” and they added that “these data may underestimate the number of acute gout flares in the cohort.” Also, 55% of the total 502,490 patients in the UK Biobank were excluded owing to lack of primary care data.
 

Study ‘Offers the Kind of Evidence That We Need’

In an accompanying commentary, University of Alabama at Birmingham rheumatologist Angelo L. Gaffo, MD, MSPH, also noted that the study population was overwhelmingly White, had a low mean SU level (6.9 mg/dL), and had a low level of comorbidities, making the sample “poorly representative of the most commonly described gout populations.”

However, he also noted that there is “growing evidence linking serum urate levels with clinical outcomes,” with a pair of studies — one from 2021 and the other from 2022 — linking reductions in SU to < 6 md/dL to lower flare rates.

Gaffo_Angelo_AL_web.jpg

Dr. Gaffo told this news organization that although rheumatology guidelines support a treat-to-target strategy, “we haven›t generated a whole lot of important evidence to support it.”

The new study “offers the kind of evidence that we need,” he said, “but this is not going to be the ultimate answer.” That will only come from randomized clinical trials in the works that will pit the treat-to-target approach vs the primary care–favored strategy of titrating treatment until flares are controlled, he said.

Even though evidence is sparse, Dr. Gaffo said he still believes in the treat-to-target strategy: “I believe it is the best way to treat gout.”

What’s next? Researchers hope to understand how to better reach target SU goals in clinical practice, Dr. Choi said. “Involving nurses, pharmacists, or interactive online or app systems — as in other chronic treat-to-target care such as anticoagulation care, blood pressure, or lipid care — is actively being researched.”

He added that “we are trying to find the effective and safe medications and nonpharmacologic measures to reduce the urate burden, which can also simultaneously take care of gout’s frequent cardiovascular-kidney comorbidities.”

The US National Institutes of Health supported the study. Dr. Choi reports receiving grants from Horizon and serving on a board or committee for LG Chem, Shanton, and ANI Pharmaceuticals. Some other authors report an employment and stockholder relationship with Regeneron and support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, and Rheumatology Research Foundation. Dr. Gaffo reports personal fees from PK MED, SOBI/Selecta, Atom, and UpToDate.

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

A new diagnostic tool can effectively discriminate different rheumatologic conditions and could potentially aid in the diagnosis of early inflammatory arthritis.

The algorithm — called Genetic Probability tool (G-PROB) — uses genetic information to calculate the probability of certain diseases.

Bowes_John_UK_web.jpg

“At such an early stage of disease, it’s not always easy to determine what the final outcome will be with respect to final diagnosis,” said John Bowes, PhD, a senior lecturer in the division of musculoskeletal & dermatological sciences at the University of Manchester in the United Kingdom. He was a senior author of the newest study of G-PROB. “What we are hoping for here is that genetics can help [clinicians] with the decision-making process and hopefully accelerate the correct diagnosis and get individuals onto the correct treatment as early as possible.”
 

Creating the Algorithm

G-PROB was first developed by an international group of scientists with the goal of using genetic risk scores to predict the probabilities of common diagnoses for patients with early signs of arthritis, such as synovitis and joint swelling. According to the study authors, about 80% of these types of patients are eventually diagnosed with the following conditions: Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and gout.

The algorithm combines existing knowledge about single-nucleotide polymorphisms from prior genomic studies to create genetic risk scores — also called polygenic risk score (PRS) — for multiple diseases. Using these scores, the program then calculates the probabilities of certain diagnoses for a patient, based on the assumption that at least one disease was present.

In this first study, researchers trained the tool on simulated data and then tested it in three patient cohorts totaling about 1700 individuals from the Electronic Medical Records and Genomics database and Mass General Brigham Biobank. In the initial study, G-PROB identified a likely diagnosis in 45% of patients, with a positive predictive value (PPV) of 64%. Adding these genetic scores to clinical data improved diagnostic accuracy from 39% to 51%.
 

Validating G-PROB

But data from these biobanks may not necessarily be representative of early arthritis in patients appearing in outpatient clinics, noted Dr. Bowes. In this new study, researchers sought to independently validate the original study’s findings using data from the Norfolk Arthritis Register, a community-based, long-term observational study on inflammatory polyarthritis. The team applied G-PROB in this cohort and then compared the tool’s probabilities for common rheumatic conditions to the final clinician diagnosis.

The study ultimately included 1047 individuals with early inflammatory arthritis with genotype data. In the cohort, more than 70% (756 individuals) were diagnosed with RA. Of the remaining patients, 104 had PsA, 18 had SLE, 16 had AS, and 12 had gout. The research team also added an “other diseases” category to the algorithm. A total of 141 patients fell into this category and were diagnosed with diseases including chronic pain syndrome (52 individuals), polymyalgia rheumatica (29 individuals), and Sjögren’s syndrome (9 individuals).

G-PROB was best at excluding diagnoses: Probabilities under 5% for a single disease corresponded to a negative predictive value (NPV) of 96%. If probabilities for two diseases were both < 5%, the NPV was 94%.

For patients with a single probability above 50%, the tool had a PPV of 70.3%. In 55.7% of all patients, the disease with the highest probability ended up being the final diagnosis.

Generally, PRSs, as well as tests using biomarkers, were better at excluding diagnoses than affirming them, noted Matthew Brown, MBBS, MD, a professor of medicine at King’s College London, who was not involved with the research. If disease prevalence is low, then a test aimed at diagnosis of that disease would be better at excluding a diagnosis than affirming it, he explained.

Brown_Matthew_UK_web.jpg

Can G-PROB Improve Diagnosis?

The new study’s key contribution was that it independently validated findings from a previous study, noted Katherine Liao, MD, a rheumatologist at Brigham and Women’s Hospital in Boston, Massachusetts. She coauthored an accompanying editorial to the newest study and coauthored the original G-PROB paper.

Liao_Katherine_MA2_web.jpg

This new study also brought up an important question about G-PROB that has yet to be tested: Will this tool help clinicians make more efficient and accurate diagnoses in practice?

A prospective trial would be necessary to begin answering this question, both Dr. Bowes and Dr. Liao agreed. For example, one clinician group would have access to G-PROB data, while another would not, and “see if that helps [the first group] make the diagnosis faster or more accurately,” Dr. Liao said.

Dr. Bowes was also interested in exploring if combining G-PROB with other clinical data would improve diagnostic performance.

“Genetics isn’t the full story,” he said. Dr. Bowes saw genetics as one additional, complementary tool in a clinician’s toolbox.

Future studies were needed to understand the clinical utility of genetic information in conjunction with current diagnostic practices, such as imaging, physical exams, and lab results, Dr. Liao and her editorial coauthors argued. 

“For example, in cardiovascular disease, the clinical utility of polygenic risk scores has been defined by their ability to improve risk stratification beyond what is already achieved with more common risk factors and measures such as cholesterol levels, smoking status, and coronary calcium scores,” Dr. Liao and her coauthors wrote. “Similarly, a polygenic risk score for breast cancer would not be clinically implemented alone for risk prediction but rather as one risk factor among others, such as hormonal and reproductive factors and prior mammographic data.”
 

Future of Genetics in Rheumatology

An additional hurdle for using tools like G-PROB was that a patient must have undergone DNA sequencing, and these data must be available to clinicians. Even a decade ago, this type of testing may have seemed unrealistic to incorporate in daily practice, Dr. Liao noted, but technological advancements continue to make genetic sequencing more accessible to the public.

There are already efforts in the United Kingdom to incorporate genetics into healthcare, including trials for PRSs and heart disease, noted Dr. Bowes, as well as large-scale studies such as Our Future Health.

“As these population-based studies expand more, a high proportion of individuals should hopefully have access to this kind of data,” he said.

Brown added that genetic testing is already used to make rheumatology diagnoses.

“[HLA] B-27 testing, for example, is an extremely commonly used test to assist in the diagnosis of ankylosing spondylitis. Is it that different to change to a PRS as opposed to a straight HLA testing? I don’t think it is,” he said.

While there would need to be systematic training for clinicians to understand how to calculate and use PRSs in daily practice, Dr. Brown did not think this adjustment would be too difficult.

“There is a lot of exceptionalism about genetics, which is actually inappropriate,” he said. “This is actually just a quantitative score that should be easy for people to interpret.”

Dr. Bowes and Dr. Brown reported no relevant financial relationships. Dr. Liao worked as a consultant for UCB.

A version of this article appeared on Medscape.com.

A new diagnostic tool can effectively discriminate different rheumatologic conditions and could potentially aid in the diagnosis of early inflammatory arthritis.

The algorithm — called Genetic Probability tool (G-PROB) — uses genetic information to calculate the probability of certain diseases.

Bowes_John_UK_web.jpg

“At such an early stage of disease, it’s not always easy to determine what the final outcome will be with respect to final diagnosis,” said John Bowes, PhD, a senior lecturer in the division of musculoskeletal & dermatological sciences at the University of Manchester in the United Kingdom. He was a senior author of the newest study of G-PROB. “What we are hoping for here is that genetics can help [clinicians] with the decision-making process and hopefully accelerate the correct diagnosis and get individuals onto the correct treatment as early as possible.”
 

Creating the Algorithm

G-PROB was first developed by an international group of scientists with the goal of using genetic risk scores to predict the probabilities of common diagnoses for patients with early signs of arthritis, such as synovitis and joint swelling. According to the study authors, about 80% of these types of patients are eventually diagnosed with the following conditions: Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and gout.

The algorithm combines existing knowledge about single-nucleotide polymorphisms from prior genomic studies to create genetic risk scores — also called polygenic risk score (PRS) — for multiple diseases. Using these scores, the program then calculates the probabilities of certain diagnoses for a patient, based on the assumption that at least one disease was present.

In this first study, researchers trained the tool on simulated data and then tested it in three patient cohorts totaling about 1700 individuals from the Electronic Medical Records and Genomics database and Mass General Brigham Biobank. In the initial study, G-PROB identified a likely diagnosis in 45% of patients, with a positive predictive value (PPV) of 64%. Adding these genetic scores to clinical data improved diagnostic accuracy from 39% to 51%.
 

Validating G-PROB

But data from these biobanks may not necessarily be representative of early arthritis in patients appearing in outpatient clinics, noted Dr. Bowes. In this new study, researchers sought to independently validate the original study’s findings using data from the Norfolk Arthritis Register, a community-based, long-term observational study on inflammatory polyarthritis. The team applied G-PROB in this cohort and then compared the tool’s probabilities for common rheumatic conditions to the final clinician diagnosis.

The study ultimately included 1047 individuals with early inflammatory arthritis with genotype data. In the cohort, more than 70% (756 individuals) were diagnosed with RA. Of the remaining patients, 104 had PsA, 18 had SLE, 16 had AS, and 12 had gout. The research team also added an “other diseases” category to the algorithm. A total of 141 patients fell into this category and were diagnosed with diseases including chronic pain syndrome (52 individuals), polymyalgia rheumatica (29 individuals), and Sjögren’s syndrome (9 individuals).

G-PROB was best at excluding diagnoses: Probabilities under 5% for a single disease corresponded to a negative predictive value (NPV) of 96%. If probabilities for two diseases were both < 5%, the NPV was 94%.

For patients with a single probability above 50%, the tool had a PPV of 70.3%. In 55.7% of all patients, the disease with the highest probability ended up being the final diagnosis.

Generally, PRSs, as well as tests using biomarkers, were better at excluding diagnoses than affirming them, noted Matthew Brown, MBBS, MD, a professor of medicine at King’s College London, who was not involved with the research. If disease prevalence is low, then a test aimed at diagnosis of that disease would be better at excluding a diagnosis than affirming it, he explained.

Brown_Matthew_UK_web.jpg

Can G-PROB Improve Diagnosis?

The new study’s key contribution was that it independently validated findings from a previous study, noted Katherine Liao, MD, a rheumatologist at Brigham and Women’s Hospital in Boston, Massachusetts. She coauthored an accompanying editorial to the newest study and coauthored the original G-PROB paper.

Liao_Katherine_MA2_web.jpg

This new study also brought up an important question about G-PROB that has yet to be tested: Will this tool help clinicians make more efficient and accurate diagnoses in practice?

A prospective trial would be necessary to begin answering this question, both Dr. Bowes and Dr. Liao agreed. For example, one clinician group would have access to G-PROB data, while another would not, and “see if that helps [the first group] make the diagnosis faster or more accurately,” Dr. Liao said.

Dr. Bowes was also interested in exploring if combining G-PROB with other clinical data would improve diagnostic performance.

“Genetics isn’t the full story,” he said. Dr. Bowes saw genetics as one additional, complementary tool in a clinician’s toolbox.

Future studies were needed to understand the clinical utility of genetic information in conjunction with current diagnostic practices, such as imaging, physical exams, and lab results, Dr. Liao and her editorial coauthors argued. 

“For example, in cardiovascular disease, the clinical utility of polygenic risk scores has been defined by their ability to improve risk stratification beyond what is already achieved with more common risk factors and measures such as cholesterol levels, smoking status, and coronary calcium scores,” Dr. Liao and her coauthors wrote. “Similarly, a polygenic risk score for breast cancer would not be clinically implemented alone for risk prediction but rather as one risk factor among others, such as hormonal and reproductive factors and prior mammographic data.”
 

Future of Genetics in Rheumatology

An additional hurdle for using tools like G-PROB was that a patient must have undergone DNA sequencing, and these data must be available to clinicians. Even a decade ago, this type of testing may have seemed unrealistic to incorporate in daily practice, Dr. Liao noted, but technological advancements continue to make genetic sequencing more accessible to the public.

There are already efforts in the United Kingdom to incorporate genetics into healthcare, including trials for PRSs and heart disease, noted Dr. Bowes, as well as large-scale studies such as Our Future Health.

“As these population-based studies expand more, a high proportion of individuals should hopefully have access to this kind of data,” he said.

Brown added that genetic testing is already used to make rheumatology diagnoses.

“[HLA] B-27 testing, for example, is an extremely commonly used test to assist in the diagnosis of ankylosing spondylitis. Is it that different to change to a PRS as opposed to a straight HLA testing? I don’t think it is,” he said.

While there would need to be systematic training for clinicians to understand how to calculate and use PRSs in daily practice, Dr. Brown did not think this adjustment would be too difficult.

“There is a lot of exceptionalism about genetics, which is actually inappropriate,” he said. “This is actually just a quantitative score that should be easy for people to interpret.”

Dr. Bowes and Dr. Brown reported no relevant financial relationships. Dr. Liao worked as a consultant for UCB.

A version of this article appeared on Medscape.com.

A new diagnostic tool can effectively discriminate different rheumatologic conditions and could potentially aid in the diagnosis of early inflammatory arthritis.

The algorithm — called Genetic Probability tool (G-PROB) — uses genetic information to calculate the probability of certain diseases.

Bowes_John_UK_web.jpg

“At such an early stage of disease, it’s not always easy to determine what the final outcome will be with respect to final diagnosis,” said John Bowes, PhD, a senior lecturer in the division of musculoskeletal & dermatological sciences at the University of Manchester in the United Kingdom. He was a senior author of the newest study of G-PROB. “What we are hoping for here is that genetics can help [clinicians] with the decision-making process and hopefully accelerate the correct diagnosis and get individuals onto the correct treatment as early as possible.”
 

Creating the Algorithm

G-PROB was first developed by an international group of scientists with the goal of using genetic risk scores to predict the probabilities of common diagnoses for patients with early signs of arthritis, such as synovitis and joint swelling. According to the study authors, about 80% of these types of patients are eventually diagnosed with the following conditions: Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and gout.

The algorithm combines existing knowledge about single-nucleotide polymorphisms from prior genomic studies to create genetic risk scores — also called polygenic risk score (PRS) — for multiple diseases. Using these scores, the program then calculates the probabilities of certain diagnoses for a patient, based on the assumption that at least one disease was present.

In this first study, researchers trained the tool on simulated data and then tested it in three patient cohorts totaling about 1700 individuals from the Electronic Medical Records and Genomics database and Mass General Brigham Biobank. In the initial study, G-PROB identified a likely diagnosis in 45% of patients, with a positive predictive value (PPV) of 64%. Adding these genetic scores to clinical data improved diagnostic accuracy from 39% to 51%.
 

Validating G-PROB

But data from these biobanks may not necessarily be representative of early arthritis in patients appearing in outpatient clinics, noted Dr. Bowes. In this new study, researchers sought to independently validate the original study’s findings using data from the Norfolk Arthritis Register, a community-based, long-term observational study on inflammatory polyarthritis. The team applied G-PROB in this cohort and then compared the tool’s probabilities for common rheumatic conditions to the final clinician diagnosis.

The study ultimately included 1047 individuals with early inflammatory arthritis with genotype data. In the cohort, more than 70% (756 individuals) were diagnosed with RA. Of the remaining patients, 104 had PsA, 18 had SLE, 16 had AS, and 12 had gout. The research team also added an “other diseases” category to the algorithm. A total of 141 patients fell into this category and were diagnosed with diseases including chronic pain syndrome (52 individuals), polymyalgia rheumatica (29 individuals), and Sjögren’s syndrome (9 individuals).

G-PROB was best at excluding diagnoses: Probabilities under 5% for a single disease corresponded to a negative predictive value (NPV) of 96%. If probabilities for two diseases were both < 5%, the NPV was 94%.

For patients with a single probability above 50%, the tool had a PPV of 70.3%. In 55.7% of all patients, the disease with the highest probability ended up being the final diagnosis.

Generally, PRSs, as well as tests using biomarkers, were better at excluding diagnoses than affirming them, noted Matthew Brown, MBBS, MD, a professor of medicine at King’s College London, who was not involved with the research. If disease prevalence is low, then a test aimed at diagnosis of that disease would be better at excluding a diagnosis than affirming it, he explained.

Brown_Matthew_UK_web.jpg

Can G-PROB Improve Diagnosis?

The new study’s key contribution was that it independently validated findings from a previous study, noted Katherine Liao, MD, a rheumatologist at Brigham and Women’s Hospital in Boston, Massachusetts. She coauthored an accompanying editorial to the newest study and coauthored the original G-PROB paper.

Liao_Katherine_MA2_web.jpg

This new study also brought up an important question about G-PROB that has yet to be tested: Will this tool help clinicians make more efficient and accurate diagnoses in practice?

A prospective trial would be necessary to begin answering this question, both Dr. Bowes and Dr. Liao agreed. For example, one clinician group would have access to G-PROB data, while another would not, and “see if that helps [the first group] make the diagnosis faster or more accurately,” Dr. Liao said.

Dr. Bowes was also interested in exploring if combining G-PROB with other clinical data would improve diagnostic performance.

“Genetics isn’t the full story,” he said. Dr. Bowes saw genetics as one additional, complementary tool in a clinician’s toolbox.

Future studies were needed to understand the clinical utility of genetic information in conjunction with current diagnostic practices, such as imaging, physical exams, and lab results, Dr. Liao and her editorial coauthors argued. 

“For example, in cardiovascular disease, the clinical utility of polygenic risk scores has been defined by their ability to improve risk stratification beyond what is already achieved with more common risk factors and measures such as cholesterol levels, smoking status, and coronary calcium scores,” Dr. Liao and her coauthors wrote. “Similarly, a polygenic risk score for breast cancer would not be clinically implemented alone for risk prediction but rather as one risk factor among others, such as hormonal and reproductive factors and prior mammographic data.”
 

Future of Genetics in Rheumatology

An additional hurdle for using tools like G-PROB was that a patient must have undergone DNA sequencing, and these data must be available to clinicians. Even a decade ago, this type of testing may have seemed unrealistic to incorporate in daily practice, Dr. Liao noted, but technological advancements continue to make genetic sequencing more accessible to the public.

There are already efforts in the United Kingdom to incorporate genetics into healthcare, including trials for PRSs and heart disease, noted Dr. Bowes, as well as large-scale studies such as Our Future Health.

“As these population-based studies expand more, a high proportion of individuals should hopefully have access to this kind of data,” he said.

Brown added that genetic testing is already used to make rheumatology diagnoses.

“[HLA] B-27 testing, for example, is an extremely commonly used test to assist in the diagnosis of ankylosing spondylitis. Is it that different to change to a PRS as opposed to a straight HLA testing? I don’t think it is,” he said.

While there would need to be systematic training for clinicians to understand how to calculate and use PRSs in daily practice, Dr. Brown did not think this adjustment would be too difficult.

“There is a lot of exceptionalism about genetics, which is actually inappropriate,” he said. “This is actually just a quantitative score that should be easy for people to interpret.”

Dr. Bowes and Dr. Brown reported no relevant financial relationships. Dr. Liao worked as a consultant for UCB.

A version of this article appeared on Medscape.com.