Gout

Two relatively simple interventions — addressing high blood pressure (BP) and smoking cessation — could make a huge difference for patients with rheumatic disease. Patients with autoimmune disease are up to three times more likely to develop cardiovascular disease (CVD) than the general population. In addition to compounding CVD, smoking is tied to the development of certain autoimmune conditions, as well as worse outcomes. Christie Bartels, MD, chief of the Division of Rheumatology at the University of Wisconsin School of Medicine and Public Health, Madison, has focused her research on improving cardiac health in inflammatory diseases. This news organization spoke with Bartels about two short interventions she developed that tackle hypertension and smoking cessation during regular visits, each taking less than 3 minutes.

How Do These Programs Address Cardiac Disease Prevention?

The BP and Quit Connect programs help clinics systematically address the two most modifiable risk factors for CVD: high BP and smoking. There’s also evidence that addressing these two risk factors improves outcomes in rheumatic diseases. Hypertension predicts an increase in lupus damage. Particularly in lupus nephritis, hypertension will increase the risk for CVD and kidney failure. People who use tobacco have worse outcomes in diseases like rheumatoid arthritis, psoriatic arthritis, and lupus, as well as more CVD, and antirheumatic drugs may not work as well.

University of Wisconsin School of Medicine and Public Health

In 90 seconds to 3 minutes, staff can do protocol-based care, which we’ve done across 20,000-plus visits. We showed we can improve population level rates of high BP and BP control, as well as increase smoking quitting rates across different patient settings.
 

What Is the Quit Connect Program?

The Quit Connect program is a 10- to 90-second point of care intervention. During rooming, staff (medical assistants and nurses) ask patients: “A) Do you smoke? and B) Have you thought about cutting back or quitting in the next 30 days?”

It turns out, when you ask the question that way, between a third and a half of people say that they’ve thought about cutting back or quitting. Then, we can get patients connected directly to Quitline, a free public service across all 50 states that smokers can use to get cessation support.

If patients are ready, we ask if we can arrange for them to receive a call from a Quitline coach about setting a quit date or receiving free nicotine replacement therapy. The beautiful thing is when that all happens, A) it’s free to the patient, and B) the results from the Quitline can be recorded right back to the electronic health record.

In our most recent publication in Arthritis Care & Research, we documented bringing Quit Connect to Grady Hospital in downtown Atlanta. It’s a safety net hospital, where 80% patients are Black and 70%-80% patients are on public insurance or uninsured. Using this protocol, we improved Quitline referrals 20-fold.
 

What Is the BP Connect Program?

At least half of the encounters in United States happen in specialty clinics. Unfortunately, when patients get their BP measured in a specialty clinic that’s not a cardiology or a vascular clinic, often, even if the pressure is high, the clinic doesn’t give patients feedback on that. The problem is because we haven’t said anything, that gives people the false reassurance that their BP is okay.

We’ve developed a 3-minute protocol to ask, advise, and connect. The idea is that if we measure a high BP, then we remeasure and confirm that it’s high. Then, we advise why it matters in rheumatic disease: Patients with rheumatic diseases are already at an increased risk for heart disease, and controlling BP can make a big difference. Then, we connect patients with high BP back to primary care.

Specifically, a SmartSet — an electronic medical record feature — prompts different actions based on confirmed high BP readings:

• If systolic BP ≥ 140-159, the SmartSet directs scheduling a visit to a nurse or primary care provider.
• If systolic BP ≥ 160-179, the next primary care visit anticipates the need to see a prescriber.
• If systolic BP ≥ 180, then the medical assistant or nurse at the visit is instructed to notify the provider who can arrange a provider-to-provider handoff for safety to exclude a hypertensive emergency.

That order goes to the scheduler to call primary care to coordinate follow-up. BP Connect doubled the likelihood of a guideline-recommended follow-up in primary care within 30 days. All patients benefited, and disparities decreased. BP Connect has had 1100 downloads, and both BP and Quit Connect programs are endorsed by the Centers for Disease Control and Prevention and Million Hearts.
 

How Do These Programs Affect Clinical Practice?

We developed these interventions with a health system engineer, and we time stamped everything. Part of the sustainability of this model is that it fits within a regular workflow. As a practicing rheumatologist, I understand that time is a precious commodity.

The interventions are in partnership with frontline staff. We’ve received feedback that they feel pride participating in these initiatives. They can say, because of me, 30 patients followed up last month for high BP, or 10 patients took a referral to the Quitline last year. We celebrate these accomplishments with the staff.
 

What Are the Next Steps for These Programs?

Public-facing toolkits for both BP and Quit Connect programs are available online. We have implemented [these programs] in a rural setting, in an urban setting, in Milwaukee and in Atlanta, and we are looking in the future to do a larger, multistate implementation study. If folks are interested, we’d love to partner with them to look at disseminating this further.

A version of this article appeared on Medscape.com.

Two relatively simple interventions — addressing high blood pressure (BP) and smoking cessation — could make a huge difference for patients with rheumatic disease. Patients with autoimmune disease are up to three times more likely to develop cardiovascular disease (CVD) than the general population. In addition to compounding CVD, smoking is tied to the development of certain autoimmune conditions, as well as worse outcomes. Christie Bartels, MD, chief of the Division of Rheumatology at the University of Wisconsin School of Medicine and Public Health, Madison, has focused her research on improving cardiac health in inflammatory diseases. This news organization spoke with Bartels about two short interventions she developed that tackle hypertension and smoking cessation during regular visits, each taking less than 3 minutes.

How Do These Programs Address Cardiac Disease Prevention?

The BP and Quit Connect programs help clinics systematically address the two most modifiable risk factors for CVD: high BP and smoking. There’s also evidence that addressing these two risk factors improves outcomes in rheumatic diseases. Hypertension predicts an increase in lupus damage. Particularly in lupus nephritis, hypertension will increase the risk for CVD and kidney failure. People who use tobacco have worse outcomes in diseases like rheumatoid arthritis, psoriatic arthritis, and lupus, as well as more CVD, and antirheumatic drugs may not work as well.

University of Wisconsin School of Medicine and Public Health

In 90 seconds to 3 minutes, staff can do protocol-based care, which we’ve done across 20,000-plus visits. We showed we can improve population level rates of high BP and BP control, as well as increase smoking quitting rates across different patient settings.
 

What Is the Quit Connect Program?

The Quit Connect program is a 10- to 90-second point of care intervention. During rooming, staff (medical assistants and nurses) ask patients: “A) Do you smoke? and B) Have you thought about cutting back or quitting in the next 30 days?”

It turns out, when you ask the question that way, between a third and a half of people say that they’ve thought about cutting back or quitting. Then, we can get patients connected directly to Quitline, a free public service across all 50 states that smokers can use to get cessation support.

If patients are ready, we ask if we can arrange for them to receive a call from a Quitline coach about setting a quit date or receiving free nicotine replacement therapy. The beautiful thing is when that all happens, A) it’s free to the patient, and B) the results from the Quitline can be recorded right back to the electronic health record.

In our most recent publication in Arthritis Care & Research, we documented bringing Quit Connect to Grady Hospital in downtown Atlanta. It’s a safety net hospital, where 80% patients are Black and 70%-80% patients are on public insurance or uninsured. Using this protocol, we improved Quitline referrals 20-fold.
 

What Is the BP Connect Program?

At least half of the encounters in United States happen in specialty clinics. Unfortunately, when patients get their BP measured in a specialty clinic that’s not a cardiology or a vascular clinic, often, even if the pressure is high, the clinic doesn’t give patients feedback on that. The problem is because we haven’t said anything, that gives people the false reassurance that their BP is okay.

We’ve developed a 3-minute protocol to ask, advise, and connect. The idea is that if we measure a high BP, then we remeasure and confirm that it’s high. Then, we advise why it matters in rheumatic disease: Patients with rheumatic diseases are already at an increased risk for heart disease, and controlling BP can make a big difference. Then, we connect patients with high BP back to primary care.

Specifically, a SmartSet — an electronic medical record feature — prompts different actions based on confirmed high BP readings:

• If systolic BP ≥ 140-159, the SmartSet directs scheduling a visit to a nurse or primary care provider.
• If systolic BP ≥ 160-179, the next primary care visit anticipates the need to see a prescriber.
• If systolic BP ≥ 180, then the medical assistant or nurse at the visit is instructed to notify the provider who can arrange a provider-to-provider handoff for safety to exclude a hypertensive emergency.

That order goes to the scheduler to call primary care to coordinate follow-up. BP Connect doubled the likelihood of a guideline-recommended follow-up in primary care within 30 days. All patients benefited, and disparities decreased. BP Connect has had 1100 downloads, and both BP and Quit Connect programs are endorsed by the Centers for Disease Control and Prevention and Million Hearts.
 

How Do These Programs Affect Clinical Practice?

We developed these interventions with a health system engineer, and we time stamped everything. Part of the sustainability of this model is that it fits within a regular workflow. As a practicing rheumatologist, I understand that time is a precious commodity.

The interventions are in partnership with frontline staff. We’ve received feedback that they feel pride participating in these initiatives. They can say, because of me, 30 patients followed up last month for high BP, or 10 patients took a referral to the Quitline last year. We celebrate these accomplishments with the staff.
 

What Are the Next Steps for These Programs?

Public-facing toolkits for both BP and Quit Connect programs are available online. We have implemented [these programs] in a rural setting, in an urban setting, in Milwaukee and in Atlanta, and we are looking in the future to do a larger, multistate implementation study. If folks are interested, we’d love to partner with them to look at disseminating this further.

A version of this article appeared on Medscape.com.

Two relatively simple interventions — addressing high blood pressure (BP) and smoking cessation — could make a huge difference for patients with rheumatic disease. Patients with autoimmune disease are up to three times more likely to develop cardiovascular disease (CVD) than the general population. In addition to compounding CVD, smoking is tied to the development of certain autoimmune conditions, as well as worse outcomes. Christie Bartels, MD, chief of the Division of Rheumatology at the University of Wisconsin School of Medicine and Public Health, Madison, has focused her research on improving cardiac health in inflammatory diseases. This news organization spoke with Bartels about two short interventions she developed that tackle hypertension and smoking cessation during regular visits, each taking less than 3 minutes.

How Do These Programs Address Cardiac Disease Prevention?

The BP and Quit Connect programs help clinics systematically address the two most modifiable risk factors for CVD: high BP and smoking. There’s also evidence that addressing these two risk factors improves outcomes in rheumatic diseases. Hypertension predicts an increase in lupus damage. Particularly in lupus nephritis, hypertension will increase the risk for CVD and kidney failure. People who use tobacco have worse outcomes in diseases like rheumatoid arthritis, psoriatic arthritis, and lupus, as well as more CVD, and antirheumatic drugs may not work as well.

University of Wisconsin School of Medicine and Public Health

In 90 seconds to 3 minutes, staff can do protocol-based care, which we’ve done across 20,000-plus visits. We showed we can improve population level rates of high BP and BP control, as well as increase smoking quitting rates across different patient settings.
 

What Is the Quit Connect Program?

The Quit Connect program is a 10- to 90-second point of care intervention. During rooming, staff (medical assistants and nurses) ask patients: “A) Do you smoke? and B) Have you thought about cutting back or quitting in the next 30 days?”

It turns out, when you ask the question that way, between a third and a half of people say that they’ve thought about cutting back or quitting. Then, we can get patients connected directly to Quitline, a free public service across all 50 states that smokers can use to get cessation support.

If patients are ready, we ask if we can arrange for them to receive a call from a Quitline coach about setting a quit date or receiving free nicotine replacement therapy. The beautiful thing is when that all happens, A) it’s free to the patient, and B) the results from the Quitline can be recorded right back to the electronic health record.

In our most recent publication in Arthritis Care & Research, we documented bringing Quit Connect to Grady Hospital in downtown Atlanta. It’s a safety net hospital, where 80% patients are Black and 70%-80% patients are on public insurance or uninsured. Using this protocol, we improved Quitline referrals 20-fold.
 

What Is the BP Connect Program?

At least half of the encounters in United States happen in specialty clinics. Unfortunately, when patients get their BP measured in a specialty clinic that’s not a cardiology or a vascular clinic, often, even if the pressure is high, the clinic doesn’t give patients feedback on that. The problem is because we haven’t said anything, that gives people the false reassurance that their BP is okay.

We’ve developed a 3-minute protocol to ask, advise, and connect. The idea is that if we measure a high BP, then we remeasure and confirm that it’s high. Then, we advise why it matters in rheumatic disease: Patients with rheumatic diseases are already at an increased risk for heart disease, and controlling BP can make a big difference. Then, we connect patients with high BP back to primary care.

Specifically, a SmartSet — an electronic medical record feature — prompts different actions based on confirmed high BP readings:

• If systolic BP ≥ 140-159, the SmartSet directs scheduling a visit to a nurse or primary care provider.
• If systolic BP ≥ 160-179, the next primary care visit anticipates the need to see a prescriber.
• If systolic BP ≥ 180, then the medical assistant or nurse at the visit is instructed to notify the provider who can arrange a provider-to-provider handoff for safety to exclude a hypertensive emergency.

That order goes to the scheduler to call primary care to coordinate follow-up. BP Connect doubled the likelihood of a guideline-recommended follow-up in primary care within 30 days. All patients benefited, and disparities decreased. BP Connect has had 1100 downloads, and both BP and Quit Connect programs are endorsed by the Centers for Disease Control and Prevention and Million Hearts.
 

How Do These Programs Affect Clinical Practice?

We developed these interventions with a health system engineer, and we time stamped everything. Part of the sustainability of this model is that it fits within a regular workflow. As a practicing rheumatologist, I understand that time is a precious commodity.

The interventions are in partnership with frontline staff. We’ve received feedback that they feel pride participating in these initiatives. They can say, because of me, 30 patients followed up last month for high BP, or 10 patients took a referral to the Quitline last year. We celebrate these accomplishments with the staff.
 

What Are the Next Steps for These Programs?

Public-facing toolkits for both BP and Quit Connect programs are available online. We have implemented [these programs] in a rural setting, in an urban setting, in Milwaukee and in Atlanta, and we are looking in the future to do a larger, multistate implementation study. If folks are interested, we’d love to partner with them to look at disseminating this further.

A version of this article appeared on Medscape.com.

TOPLINE:

A higher alcohol consumption is associated with an increased risk for gout, more strongly in men than in women. This sex-specific difference may be attributed to the different types of alcohol consumed by men and women, rather than biologic variations.

METHODOLOGY:

• This prospective cohort study investigated the association between total and specific alcohol consumption and the long-term risk for incident gout in 179,828 men (mean age, 56.0 years) and 221,300 women (mean age, 56.0 years) from the UK Biobank who did not have gout at baseline.
• Alcohol consumption was assessed using a computer-assisted touch screen system. Among men, 2.9%, 3.6%, and 93.6% were identified as never, former, and current drinkers, respectively. Among women, 5.9%, 3.6%, and 90.5% were identified as never, former, and current drinkers, respectively.
• Participants were also required to share details about their weekly alcohol intake and the types of alcoholic beverages they consumed (red wine, champagne or white wine, beer or cider, spirits, or fortified wine).
• The median follow-up duration of this study was 12.7 years.
• Cases of incident gout during the follow-up period were identified using hospital records and the International Classification of Diseases codes.

TAKEAWAY:

• The risk for gout was 69% higher in men who were current drinkers than in those who were never drinkers (hazard ratio [HR], 1.69; 95% CI, 1.30-2.18), while an inverse association was observed in women who were current drinkers, although it was not statistically significant. A significant interaction was observed between drinking status and sex (P < .001 for interaction).
• Among current drinkers, more frequent alcohol consumption was associated with a higher risk for gout among both sexes, with the association being stronger in men (HR, 2.05; 95% CI, 1.84-2.30) than in women (HR, 1.34; 95% CI, 1.12-1.61).
• The consumption of beer or cider was higher in men than in women (4.2 vs 0.4 pints/wk).
• Among all alcoholic beverages, the consumption of beer or cider (per 1 pint/d) showed the strongest association with the risk for gout in both men (HR, 1.60; 95% CI, 1.53-1.67) and women (HR, 1.62; 95% CI, 1.02-2.57).

IN PRACTICE:

“The observed sex-specific difference in the association of total alcohol consumption with incident gout may be owing to differences between men and women in the types of alcohol consumed rather than biological differences,” the authors wrote.

SOURCE:

The study was led by Jie-Qiong Lyu, MPH, Department of Nutrition and Food Hygiene, School of Public Health, Suzhou Medical College of Soochow University in China. It was published online in JAMA Network Open.

LIMITATIONS:

The frequency of alcohol consumption was self-reported, leading to potential misclassification. Incident cases of gout were identified from hospital records, which may have caused some undiagnosed cases or those diagnosed only in primary care settings to be missed. Most participants were of European descent and relatively healthier than the general population, limiting generalizability.

DISCLOSURES:

This work was supported by the Gusu Leading Talent Plan for Scientific and Technological Innovation and Entrepreneurship. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

A higher alcohol consumption is associated with an increased risk for gout, more strongly in men than in women. This sex-specific difference may be attributed to the different types of alcohol consumed by men and women, rather than biologic variations.

METHODOLOGY:

• This prospective cohort study investigated the association between total and specific alcohol consumption and the long-term risk for incident gout in 179,828 men (mean age, 56.0 years) and 221,300 women (mean age, 56.0 years) from the UK Biobank who did not have gout at baseline.
• Alcohol consumption was assessed using a computer-assisted touch screen system. Among men, 2.9%, 3.6%, and 93.6% were identified as never, former, and current drinkers, respectively. Among women, 5.9%, 3.6%, and 90.5% were identified as never, former, and current drinkers, respectively.
• Participants were also required to share details about their weekly alcohol intake and the types of alcoholic beverages they consumed (red wine, champagne or white wine, beer or cider, spirits, or fortified wine).
• The median follow-up duration of this study was 12.7 years.
• Cases of incident gout during the follow-up period were identified using hospital records and the International Classification of Diseases codes.

TAKEAWAY:

• The risk for gout was 69% higher in men who were current drinkers than in those who were never drinkers (hazard ratio [HR], 1.69; 95% CI, 1.30-2.18), while an inverse association was observed in women who were current drinkers, although it was not statistically significant. A significant interaction was observed between drinking status and sex (P < .001 for interaction).
• Among current drinkers, more frequent alcohol consumption was associated with a higher risk for gout among both sexes, with the association being stronger in men (HR, 2.05; 95% CI, 1.84-2.30) than in women (HR, 1.34; 95% CI, 1.12-1.61).
• The consumption of beer or cider was higher in men than in women (4.2 vs 0.4 pints/wk).
• Among all alcoholic beverages, the consumption of beer or cider (per 1 pint/d) showed the strongest association with the risk for gout in both men (HR, 1.60; 95% CI, 1.53-1.67) and women (HR, 1.62; 95% CI, 1.02-2.57).

IN PRACTICE:

“The observed sex-specific difference in the association of total alcohol consumption with incident gout may be owing to differences between men and women in the types of alcohol consumed rather than biological differences,” the authors wrote.

SOURCE:

The study was led by Jie-Qiong Lyu, MPH, Department of Nutrition and Food Hygiene, School of Public Health, Suzhou Medical College of Soochow University in China. It was published online in JAMA Network Open.

LIMITATIONS:

The frequency of alcohol consumption was self-reported, leading to potential misclassification. Incident cases of gout were identified from hospital records, which may have caused some undiagnosed cases or those diagnosed only in primary care settings to be missed. Most participants were of European descent and relatively healthier than the general population, limiting generalizability.

DISCLOSURES:

This work was supported by the Gusu Leading Talent Plan for Scientific and Technological Innovation and Entrepreneurship. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

A higher alcohol consumption is associated with an increased risk for gout, more strongly in men than in women. This sex-specific difference may be attributed to the different types of alcohol consumed by men and women, rather than biologic variations.

METHODOLOGY:

• This prospective cohort study investigated the association between total and specific alcohol consumption and the long-term risk for incident gout in 179,828 men (mean age, 56.0 years) and 221,300 women (mean age, 56.0 years) from the UK Biobank who did not have gout at baseline.
• Alcohol consumption was assessed using a computer-assisted touch screen system. Among men, 2.9%, 3.6%, and 93.6% were identified as never, former, and current drinkers, respectively. Among women, 5.9%, 3.6%, and 90.5% were identified as never, former, and current drinkers, respectively.
• Participants were also required to share details about their weekly alcohol intake and the types of alcoholic beverages they consumed (red wine, champagne or white wine, beer or cider, spirits, or fortified wine).
• The median follow-up duration of this study was 12.7 years.
• Cases of incident gout during the follow-up period were identified using hospital records and the International Classification of Diseases codes.

TAKEAWAY:

• The risk for gout was 69% higher in men who were current drinkers than in those who were never drinkers (hazard ratio [HR], 1.69; 95% CI, 1.30-2.18), while an inverse association was observed in women who were current drinkers, although it was not statistically significant. A significant interaction was observed between drinking status and sex (P < .001 for interaction).
• Among current drinkers, more frequent alcohol consumption was associated with a higher risk for gout among both sexes, with the association being stronger in men (HR, 2.05; 95% CI, 1.84-2.30) than in women (HR, 1.34; 95% CI, 1.12-1.61).
• The consumption of beer or cider was higher in men than in women (4.2 vs 0.4 pints/wk).
• Among all alcoholic beverages, the consumption of beer or cider (per 1 pint/d) showed the strongest association with the risk for gout in both men (HR, 1.60; 95% CI, 1.53-1.67) and women (HR, 1.62; 95% CI, 1.02-2.57).

IN PRACTICE:

“The observed sex-specific difference in the association of total alcohol consumption with incident gout may be owing to differences between men and women in the types of alcohol consumed rather than biological differences,” the authors wrote.

SOURCE:

The study was led by Jie-Qiong Lyu, MPH, Department of Nutrition and Food Hygiene, School of Public Health, Suzhou Medical College of Soochow University in China. It was published online in JAMA Network Open.

LIMITATIONS:

The frequency of alcohol consumption was self-reported, leading to potential misclassification. Incident cases of gout were identified from hospital records, which may have caused some undiagnosed cases or those diagnosed only in primary care settings to be missed. Most participants were of European descent and relatively healthier than the general population, limiting generalizability.

DISCLOSURES:

This work was supported by the Gusu Leading Talent Plan for Scientific and Technological Innovation and Entrepreneurship. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The presence of an operational classification of drug interactions (ORCA) class 3 or 4 drug-drug interactions (DDIs) did not increase the risk for colchicine-related gastrointestinal adverse events or modify the effect of colchicine on death or hospitalization caused by COVID-19 infection in ambulatory patients.

METHODOLOGY:

• This secondary analysis of the COLCORONA trial aimed to evaluate if a potential DDI of colchicine was associated with changes in its pharmacokinetics or modified its clinical safety and efficacy in patients with COVID-19.
• Overall, 4432 ambulatory patients with COVID-19 (median age, 54 years; 54% women) were randomly assigned to receive colchicine 0.5 mg twice daily for 3 days and then 0.5 mg once daily for 27 days (n = 2205) or a placebo (n = 2227).
• All the participants had at least one high-risk criterion such as age ≥ 70 years, diabetes, heart failure, systolic blood pressure ≥ 150 mm Hg, respiratory disease, coronary disease, body temperature ≥ 38.4 °C within the last 48 hours, dyspnea, bicytopenia, pancytopenia, or high neutrophil count with low lymphocyte count.
• The medications that could interact with colchicine were determined and categorized under ORCA classes 1 (contraindicated), 2 (provisionally contraindicated), 3 (conditional use), or 4 (minimal risk).
• The primary outcome was any gastrointestinal adverse event assessed over a 30-day follow-up period.

TAKEAWAY:

• Among all the participants, 1% received medications with an ORCA class 2 interaction, 14% with a class 3 interaction, and 13% with a class 4 interaction; rosuvastatin (12%) and atorvastatin (10%) were the most common interacting medications.
• The odds of any gastrointestinal adverse event were 1.80 times and 1.68 times higher in the colchicine arm than in the placebo arm among those without and with a DDI, respectively, with the effect of colchicine being consistent regardless of the presence of drug interactions (P = .69 for interaction).
• Similarly, DDIs did not influence the effect of colchicine on combined risk for COVID-19 hospitalization or mortality (P = .80 for interaction).

IN PRACTICE:

“Once potential DDIs have been identified through screening, they must be tested,” Hemalkumar B. Mehta, PhD, and G. Caleb Alexander, MD, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, wrote in an invited commentary published online in JAMA Network Open. “Theoretical DDIs may not translate into real-world harms,” they added.

SOURCE:

The study was led by Lama S. Alfehaid, PharmD, of Brigham and Women’s Hospital, Boston. It was published online in JAMA Network Open.

LIMITATIONS:

This study focused on the medications used by participants at baseline, which may not have captured all potential DDIs. The findings did not provide information on rare adverse events, such as rhabdomyolysis, which usually occur months after initiating drug therapy. Furthermore, all the study participants had confirmed SARS-CoV-2 infection, which may have increased their susceptibility to adverse reactions associated with the use of colchicine.

DISCLOSURES:

Some authors were supported by grants from the National Institutes of Health/National Heart, Lung, and Blood Institute, American Heart Association, and other sources. The authors also declared serving on advisory boards or on the board of directors; receiving personal fees, grants, research support, or speaking fees; or having other ties with many pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The presence of an operational classification of drug interactions (ORCA) class 3 or 4 drug-drug interactions (DDIs) did not increase the risk for colchicine-related gastrointestinal adverse events or modify the effect of colchicine on death or hospitalization caused by COVID-19 infection in ambulatory patients.

METHODOLOGY:

• This secondary analysis of the COLCORONA trial aimed to evaluate if a potential DDI of colchicine was associated with changes in its pharmacokinetics or modified its clinical safety and efficacy in patients with COVID-19.
• Overall, 4432 ambulatory patients with COVID-19 (median age, 54 years; 54% women) were randomly assigned to receive colchicine 0.5 mg twice daily for 3 days and then 0.5 mg once daily for 27 days (n = 2205) or a placebo (n = 2227).
• All the participants had at least one high-risk criterion such as age ≥ 70 years, diabetes, heart failure, systolic blood pressure ≥ 150 mm Hg, respiratory disease, coronary disease, body temperature ≥ 38.4 °C within the last 48 hours, dyspnea, bicytopenia, pancytopenia, or high neutrophil count with low lymphocyte count.
• The medications that could interact with colchicine were determined and categorized under ORCA classes 1 (contraindicated), 2 (provisionally contraindicated), 3 (conditional use), or 4 (minimal risk).
• The primary outcome was any gastrointestinal adverse event assessed over a 30-day follow-up period.

TAKEAWAY:

• Among all the participants, 1% received medications with an ORCA class 2 interaction, 14% with a class 3 interaction, and 13% with a class 4 interaction; rosuvastatin (12%) and atorvastatin (10%) were the most common interacting medications.
• The odds of any gastrointestinal adverse event were 1.80 times and 1.68 times higher in the colchicine arm than in the placebo arm among those without and with a DDI, respectively, with the effect of colchicine being consistent regardless of the presence of drug interactions (P = .69 for interaction).
• Similarly, DDIs did not influence the effect of colchicine on combined risk for COVID-19 hospitalization or mortality (P = .80 for interaction).

IN PRACTICE:

“Once potential DDIs have been identified through screening, they must be tested,” Hemalkumar B. Mehta, PhD, and G. Caleb Alexander, MD, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, wrote in an invited commentary published online in JAMA Network Open. “Theoretical DDIs may not translate into real-world harms,” they added.

SOURCE:

The study was led by Lama S. Alfehaid, PharmD, of Brigham and Women’s Hospital, Boston. It was published online in JAMA Network Open.

LIMITATIONS:

This study focused on the medications used by participants at baseline, which may not have captured all potential DDIs. The findings did not provide information on rare adverse events, such as rhabdomyolysis, which usually occur months after initiating drug therapy. Furthermore, all the study participants had confirmed SARS-CoV-2 infection, which may have increased their susceptibility to adverse reactions associated with the use of colchicine.

DISCLOSURES:

Some authors were supported by grants from the National Institutes of Health/National Heart, Lung, and Blood Institute, American Heart Association, and other sources. The authors also declared serving on advisory boards or on the board of directors; receiving personal fees, grants, research support, or speaking fees; or having other ties with many pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The presence of an operational classification of drug interactions (ORCA) class 3 or 4 drug-drug interactions (DDIs) did not increase the risk for colchicine-related gastrointestinal adverse events or modify the effect of colchicine on death or hospitalization caused by COVID-19 infection in ambulatory patients.

METHODOLOGY:

• This secondary analysis of the COLCORONA trial aimed to evaluate if a potential DDI of colchicine was associated with changes in its pharmacokinetics or modified its clinical safety and efficacy in patients with COVID-19.
• Overall, 4432 ambulatory patients with COVID-19 (median age, 54 years; 54% women) were randomly assigned to receive colchicine 0.5 mg twice daily for 3 days and then 0.5 mg once daily for 27 days (n = 2205) or a placebo (n = 2227).
• All the participants had at least one high-risk criterion such as age ≥ 70 years, diabetes, heart failure, systolic blood pressure ≥ 150 mm Hg, respiratory disease, coronary disease, body temperature ≥ 38.4 °C within the last 48 hours, dyspnea, bicytopenia, pancytopenia, or high neutrophil count with low lymphocyte count.
• The medications that could interact with colchicine were determined and categorized under ORCA classes 1 (contraindicated), 2 (provisionally contraindicated), 3 (conditional use), or 4 (minimal risk).
• The primary outcome was any gastrointestinal adverse event assessed over a 30-day follow-up period.

TAKEAWAY:

• Among all the participants, 1% received medications with an ORCA class 2 interaction, 14% with a class 3 interaction, and 13% with a class 4 interaction; rosuvastatin (12%) and atorvastatin (10%) were the most common interacting medications.
• The odds of any gastrointestinal adverse event were 1.80 times and 1.68 times higher in the colchicine arm than in the placebo arm among those without and with a DDI, respectively, with the effect of colchicine being consistent regardless of the presence of drug interactions (P = .69 for interaction).
• Similarly, DDIs did not influence the effect of colchicine on combined risk for COVID-19 hospitalization or mortality (P = .80 for interaction).

IN PRACTICE:

“Once potential DDIs have been identified through screening, they must be tested,” Hemalkumar B. Mehta, PhD, and G. Caleb Alexander, MD, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, wrote in an invited commentary published online in JAMA Network Open. “Theoretical DDIs may not translate into real-world harms,” they added.

SOURCE:

The study was led by Lama S. Alfehaid, PharmD, of Brigham and Women’s Hospital, Boston. It was published online in JAMA Network Open.

LIMITATIONS:

This study focused on the medications used by participants at baseline, which may not have captured all potential DDIs. The findings did not provide information on rare adverse events, such as rhabdomyolysis, which usually occur months after initiating drug therapy. Furthermore, all the study participants had confirmed SARS-CoV-2 infection, which may have increased their susceptibility to adverse reactions associated with the use of colchicine.

DISCLOSURES:

Some authors were supported by grants from the National Institutes of Health/National Heart, Lung, and Blood Institute, American Heart Association, and other sources. The authors also declared serving on advisory boards or on the board of directors; receiving personal fees, grants, research support, or speaking fees; or having other ties with many pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

The global dietary supplement industry generates more than $400 billion a year. Supplements are alleged to treat many health concerns, from immune conditions and cognition to sexual dysfunction and premature wrinkles. Although some supplements have been proven to be helpful, others have no scientific basis.

I can preach all day that a healthy diet rarely needs supplementation. But even as a dietitian, I find it difficult to consistently eat a diet that is both sufficiently varied and adequate to provide for all my nutrition needs. Our patients with kidney disease, surely, are not immune to this plight. They may even be more inclined to nutrient deficiencies, as poor diet is linked to increased incidence and progression of chronic kidney disease (CKD).

I find that patients with kidney disease often have an interest in dietary supplementation, even those with a well-rounded diet. Though we can discourage the use of supplements, or at the very least encourage patient transparency regarding supplement use, many will continue dietary supplementation at the suggestion of their friends, family, or even their preferred daytime talk show host. 

What these patients truly require is education on using supplements that are most beneficial to them. By recommending supplements that address patients’ pain points like inflammation, dyslipidemia, cardiovascular health, and reduced progression to end-stage renal disease (ESRD), we can improve patient health and, hopefully, decrease use of questionable supplements.
 

Probiotics

Although probiotics have been used in the treatment of digestive issues for many years, the gut-kidney axis is only recently being explored. Studies show that the microbiota of patients with CKD is altered, even in the early stages of disease, producing additional inflammation and metabolic dysfunction. This can be remedied, or at least alleviated, by introducing a probiotic supplement.

Some probiotics have been shown to decrease inflammation, decrease fasting blood glucose, decrease low-density lipoprotein cholesterol, triglycerides, and total cholesterol, increase estimated glomerular filtration rate (eGFR), decrease blood urea nitrogen and urea, and decrease uric acid

Probiotic-rich foods like kimchi or fermented pickles may not be appropriate because of excessive sodium content or simply because of patient preference — kombucha isn’t for everyone. However, adding a probiotic supplement can improve gut microbiota without undermining dietary concerns. 

When recommending probiotics, patients should be educated to ensure that their probiotic has strains that have been proven to be beneficial for kidney health. Lactobacillus acidophilus, Lactobacillus casei, ^{Bifidobacterium} species, and Streptococcus thermophilus have been shown to have a positive effect on kidney health and decreasing progression of CKD at a dosage of 109 colony-forming units per day.
 

Fish Oil

Though nephrology and cardiology are separate fields, it cannot be overstated that kidney patients are also heart patients. 

Patients with CKD and an eGFR < 60 mL/min per 1.73 m²are most likely to die from cardiovascular causes, and this likelihood increases as eGFR decreases. CKD-associated dyslipidemia results in elevated triglycerides and reduced high-density lipoprotein cholesterol often accompanied by proteinuria, and has been linked to an increase in atherosclerosis.

A simple fish oil supplement can work to decrease oxidative stress, relieve inflammation, and improve serum lipids, leading to improved kidney and cardiovascular health. One meta-analysis found that high-dose fish oil supplementation, though it had no effect on serum creatinine or eGFR, was associated with a lower risk for proteinuria and progression to ESRD. 

Fish oil’s popularity in recent years bodes well for the kidney patient. It is now easily obtained over the counter in high doses to meet the recommended adequate intake of omega-3s, which is 1100 mg/d for women and 1600 mg/d for men. There are also more burpless varieties of these supplements to increase compliance. 
 

Vitamin D

Patients with renal disease are prone to vitamin D deficiency through inadequate intake and limited sunlight, which is exacerbated by the diseased kidney’s inability to effectively convert calcidiol to calcitriol. Vitamin D deficiency is linked to poor bone health, fatigue, muscle pain, impaired wound healing, and depression. Low vitamin D status has also been linked to poor outcomes in cancer, multiple sclerosis, cardiovascular disease, type 2 diabetes, and weight loss.

A meta-analysis of over 6000 patients with CKD found that high levels of 25-hydroxy vitamin D (25[OH]D) are associated with significantly improved survival rates regardless of CKD or ESRD status. 

Kidney Disease: Improving Global Outcomes guidelines recommend supplementing with ergocalciferol or cholecalciferol to correct (OH)D deficiency. This ensures adequate supply for conversion to calcitriol, but it cannot affect bone and mineral metabolism without further intervention in the form of calcitriol supplementation. By supplementing with ergocalciferol or cholecalciferol to meet the recommended daily allowance of 15 µg (600 IU) for adults under 70 years and 20 µg (800 IU) for adults over 70 years, the primary care team can ensure that the body has all the building blocks required for the nephrology team to then address mineral and bone disorder in CKD without the fear of promoting hypercalcemia. 
 

Safe Purchasing Practices

Patients should be reminded to purchase dietary supplements from reputable dealers, especially when purchasing online. Retailers like Amazon are increasing the barriers required to sell supplements to improve the quality of products sold on the site. But other online retailers may sell products from outside of the United States that fall outside of the Food and Drug Administration’s jurisdiction. 

Patients should also be reminded that “more is not always better” and counseled on appropriate dosages for individual needs. 
 

In Summary

Patients will probably continue to lean on dietary supplements, regardless of our approval. Transparency and education are important when working with patients with CKD, especially in regard to dietary supplements. 

When recommended appropriately, however, the supplements discussed can lead to better outcomes with improvements in kidney health by addressing inflammation, serum lipids, glycemic control, and cardiovascular health.

Ms. Winfree Root is a renal dietitian in private practice in Mary Esther, Florida. She disclosed no relevant conflicts of interest.

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

The global dietary supplement industry generates more than $400 billion a year. Supplements are alleged to treat many health concerns, from immune conditions and cognition to sexual dysfunction and premature wrinkles. Although some supplements have been proven to be helpful, others have no scientific basis.

I can preach all day that a healthy diet rarely needs supplementation. But even as a dietitian, I find it difficult to consistently eat a diet that is both sufficiently varied and adequate to provide for all my nutrition needs. Our patients with kidney disease, surely, are not immune to this plight. They may even be more inclined to nutrient deficiencies, as poor diet is linked to increased incidence and progression of chronic kidney disease (CKD).

I find that patients with kidney disease often have an interest in dietary supplementation, even those with a well-rounded diet. Though we can discourage the use of supplements, or at the very least encourage patient transparency regarding supplement use, many will continue dietary supplementation at the suggestion of their friends, family, or even their preferred daytime talk show host. 

What these patients truly require is education on using supplements that are most beneficial to them. By recommending supplements that address patients’ pain points like inflammation, dyslipidemia, cardiovascular health, and reduced progression to end-stage renal disease (ESRD), we can improve patient health and, hopefully, decrease use of questionable supplements.
 

Probiotics

Although probiotics have been used in the treatment of digestive issues for many years, the gut-kidney axis is only recently being explored. Studies show that the microbiota of patients with CKD is altered, even in the early stages of disease, producing additional inflammation and metabolic dysfunction. This can be remedied, or at least alleviated, by introducing a probiotic supplement.

Some probiotics have been shown to decrease inflammation, decrease fasting blood glucose, decrease low-density lipoprotein cholesterol, triglycerides, and total cholesterol, increase estimated glomerular filtration rate (eGFR), decrease blood urea nitrogen and urea, and decrease uric acid

Probiotic-rich foods like kimchi or fermented pickles may not be appropriate because of excessive sodium content or simply because of patient preference — kombucha isn’t for everyone. However, adding a probiotic supplement can improve gut microbiota without undermining dietary concerns. 

When recommending probiotics, patients should be educated to ensure that their probiotic has strains that have been proven to be beneficial for kidney health. Lactobacillus acidophilus, Lactobacillus casei, ^{Bifidobacterium} species, and Streptococcus thermophilus have been shown to have a positive effect on kidney health and decreasing progression of CKD at a dosage of 109 colony-forming units per day.
 

Fish Oil

Though nephrology and cardiology are separate fields, it cannot be overstated that kidney patients are also heart patients. 

Patients with CKD and an eGFR < 60 mL/min per 1.73 m²are most likely to die from cardiovascular causes, and this likelihood increases as eGFR decreases. CKD-associated dyslipidemia results in elevated triglycerides and reduced high-density lipoprotein cholesterol often accompanied by proteinuria, and has been linked to an increase in atherosclerosis.

A simple fish oil supplement can work to decrease oxidative stress, relieve inflammation, and improve serum lipids, leading to improved kidney and cardiovascular health. One meta-analysis found that high-dose fish oil supplementation, though it had no effect on serum creatinine or eGFR, was associated with a lower risk for proteinuria and progression to ESRD. 

Fish oil’s popularity in recent years bodes well for the kidney patient. It is now easily obtained over the counter in high doses to meet the recommended adequate intake of omega-3s, which is 1100 mg/d for women and 1600 mg/d for men. There are also more burpless varieties of these supplements to increase compliance. 
 

Vitamin D

Patients with renal disease are prone to vitamin D deficiency through inadequate intake and limited sunlight, which is exacerbated by the diseased kidney’s inability to effectively convert calcidiol to calcitriol. Vitamin D deficiency is linked to poor bone health, fatigue, muscle pain, impaired wound healing, and depression. Low vitamin D status has also been linked to poor outcomes in cancer, multiple sclerosis, cardiovascular disease, type 2 diabetes, and weight loss.

A meta-analysis of over 6000 patients with CKD found that high levels of 25-hydroxy vitamin D (25[OH]D) are associated with significantly improved survival rates regardless of CKD or ESRD status. 

Kidney Disease: Improving Global Outcomes guidelines recommend supplementing with ergocalciferol or cholecalciferol to correct (OH)D deficiency. This ensures adequate supply for conversion to calcitriol, but it cannot affect bone and mineral metabolism without further intervention in the form of calcitriol supplementation. By supplementing with ergocalciferol or cholecalciferol to meet the recommended daily allowance of 15 µg (600 IU) for adults under 70 years and 20 µg (800 IU) for adults over 70 years, the primary care team can ensure that the body has all the building blocks required for the nephrology team to then address mineral and bone disorder in CKD without the fear of promoting hypercalcemia. 
 

Safe Purchasing Practices

Patients should be reminded to purchase dietary supplements from reputable dealers, especially when purchasing online. Retailers like Amazon are increasing the barriers required to sell supplements to improve the quality of products sold on the site. But other online retailers may sell products from outside of the United States that fall outside of the Food and Drug Administration’s jurisdiction. 

Patients should also be reminded that “more is not always better” and counseled on appropriate dosages for individual needs. 
 

In Summary

Patients will probably continue to lean on dietary supplements, regardless of our approval. Transparency and education are important when working with patients with CKD, especially in regard to dietary supplements. 

When recommended appropriately, however, the supplements discussed can lead to better outcomes with improvements in kidney health by addressing inflammation, serum lipids, glycemic control, and cardiovascular health.

Ms. Winfree Root is a renal dietitian in private practice in Mary Esther, Florida. She disclosed no relevant conflicts of interest.

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

The global dietary supplement industry generates more than $400 billion a year. Supplements are alleged to treat many health concerns, from immune conditions and cognition to sexual dysfunction and premature wrinkles. Although some supplements have been proven to be helpful, others have no scientific basis.

I can preach all day that a healthy diet rarely needs supplementation. But even as a dietitian, I find it difficult to consistently eat a diet that is both sufficiently varied and adequate to provide for all my nutrition needs. Our patients with kidney disease, surely, are not immune to this plight. They may even be more inclined to nutrient deficiencies, as poor diet is linked to increased incidence and progression of chronic kidney disease (CKD).

I find that patients with kidney disease often have an interest in dietary supplementation, even those with a well-rounded diet. Though we can discourage the use of supplements, or at the very least encourage patient transparency regarding supplement use, many will continue dietary supplementation at the suggestion of their friends, family, or even their preferred daytime talk show host. 

What these patients truly require is education on using supplements that are most beneficial to them. By recommending supplements that address patients’ pain points like inflammation, dyslipidemia, cardiovascular health, and reduced progression to end-stage renal disease (ESRD), we can improve patient health and, hopefully, decrease use of questionable supplements.
 

Probiotics

Although probiotics have been used in the treatment of digestive issues for many years, the gut-kidney axis is only recently being explored. Studies show that the microbiota of patients with CKD is altered, even in the early stages of disease, producing additional inflammation and metabolic dysfunction. This can be remedied, or at least alleviated, by introducing a probiotic supplement.

Some probiotics have been shown to decrease inflammation, decrease fasting blood glucose, decrease low-density lipoprotein cholesterol, triglycerides, and total cholesterol, increase estimated glomerular filtration rate (eGFR), decrease blood urea nitrogen and urea, and decrease uric acid

Probiotic-rich foods like kimchi or fermented pickles may not be appropriate because of excessive sodium content or simply because of patient preference — kombucha isn’t for everyone. However, adding a probiotic supplement can improve gut microbiota without undermining dietary concerns. 

When recommending probiotics, patients should be educated to ensure that their probiotic has strains that have been proven to be beneficial for kidney health. Lactobacillus acidophilus, Lactobacillus casei, ^{Bifidobacterium} species, and Streptococcus thermophilus have been shown to have a positive effect on kidney health and decreasing progression of CKD at a dosage of 109 colony-forming units per day.
 

Fish Oil

Though nephrology and cardiology are separate fields, it cannot be overstated that kidney patients are also heart patients. 

Patients with CKD and an eGFR < 60 mL/min per 1.73 m²are most likely to die from cardiovascular causes, and this likelihood increases as eGFR decreases. CKD-associated dyslipidemia results in elevated triglycerides and reduced high-density lipoprotein cholesterol often accompanied by proteinuria, and has been linked to an increase in atherosclerosis.

A simple fish oil supplement can work to decrease oxidative stress, relieve inflammation, and improve serum lipids, leading to improved kidney and cardiovascular health. One meta-analysis found that high-dose fish oil supplementation, though it had no effect on serum creatinine or eGFR, was associated with a lower risk for proteinuria and progression to ESRD. 

Fish oil’s popularity in recent years bodes well for the kidney patient. It is now easily obtained over the counter in high doses to meet the recommended adequate intake of omega-3s, which is 1100 mg/d for women and 1600 mg/d for men. There are also more burpless varieties of these supplements to increase compliance. 
 

Vitamin D

Patients with renal disease are prone to vitamin D deficiency through inadequate intake and limited sunlight, which is exacerbated by the diseased kidney’s inability to effectively convert calcidiol to calcitriol. Vitamin D deficiency is linked to poor bone health, fatigue, muscle pain, impaired wound healing, and depression. Low vitamin D status has also been linked to poor outcomes in cancer, multiple sclerosis, cardiovascular disease, type 2 diabetes, and weight loss.

A meta-analysis of over 6000 patients with CKD found that high levels of 25-hydroxy vitamin D (25[OH]D) are associated with significantly improved survival rates regardless of CKD or ESRD status. 

Kidney Disease: Improving Global Outcomes guidelines recommend supplementing with ergocalciferol or cholecalciferol to correct (OH)D deficiency. This ensures adequate supply for conversion to calcitriol, but it cannot affect bone and mineral metabolism without further intervention in the form of calcitriol supplementation. By supplementing with ergocalciferol or cholecalciferol to meet the recommended daily allowance of 15 µg (600 IU) for adults under 70 years and 20 µg (800 IU) for adults over 70 years, the primary care team can ensure that the body has all the building blocks required for the nephrology team to then address mineral and bone disorder in CKD without the fear of promoting hypercalcemia. 
 

Safe Purchasing Practices

Patients should be reminded to purchase dietary supplements from reputable dealers, especially when purchasing online. Retailers like Amazon are increasing the barriers required to sell supplements to improve the quality of products sold on the site. But other online retailers may sell products from outside of the United States that fall outside of the Food and Drug Administration’s jurisdiction. 

Patients should also be reminded that “more is not always better” and counseled on appropriate dosages for individual needs. 
 

In Summary

Patients will probably continue to lean on dietary supplements, regardless of our approval. Transparency and education are important when working with patients with CKD, especially in regard to dietary supplements. 

When recommended appropriately, however, the supplements discussed can lead to better outcomes with improvements in kidney health by addressing inflammation, serum lipids, glycemic control, and cardiovascular health.

Ms. Winfree Root is a renal dietitian in private practice in Mary Esther, Florida. She disclosed no relevant conflicts of interest.

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

Many patients struggle with healthcare costs and basic expenses, according to new research.

People with rheumatologic diseases often experience a hidden symptom: financial toxicity or significant economic strain from out-of-pocket costs. A new study of 41,502 patients published in JCR: Journal of Clinical Rheumatology showed that 20% of those with rheumatologic diseases faced financial hardship from medical expenses, with 55% of those unable to pay their bills. 

Compared with patients who do not have rheumatologic diseases, and after clinical and sociodemographic factors were controlled for, patients with rheumatologic diseases were:

• 29% more likely to have high levels of financial hardship — difficulty paying; needing to pay over time; or inability to pay bills for doctors, dentists, hospitals, therapists, medication, equipment, nursing homes, or home care.
• 53% more likely to have high levels of financial distress — significant worry about having enough money for retirement, paying medical costs in the event of a serious illness or accident, maintaining their standard of living, paying their usual healthcare costs, and affording their normal monthly bills and housing costs.
• 29% more likely to experience food insecurity, defined as limited or uncertain access to adequate food.
• 58% more likely to report cost-related medication nonadherence — skipping doses, taking less medication, or delaying filling a prescription to save money.

People who were younger than 64 years, male, Black, or uninsured had higher odds of experiencing financial hardship, financial distress, food insecurity, and cost-related medication nonadherence. 

This study highlights “just how costly everyday rheumatologic conditions can be for your average American,” said lead study author Troy Amen, MD, MBA, an orthopedic surgery resident at the Hospital for Special Surgery in New York City. These diseases can be disabling, limiting a patient’s ability to work at the very time when expensive medications are needed. 

“It’s critical for clinicians to recognize how common the financial burden from healthcare costs can be, and only then can they take steps to better support patients,” said G. Caleb Alexander, MD, MS, professor of epidemiology at Johns Hopkins University in Baltimore, who was not involved in the study. 

Here’s how healthcare providers can help. 

Consider skipped medication a red flag. It’s often the first sign of a financial concern. “Sometimes with these problems, it looks like simple medication noncompliance, but it’s really a more complex form of nonadherence,” said Susan M. Goodman, MD, professor of clinical medicine at Weill Cornell Medicine in New York City and a coauthor of the study. “And I think if someone’s not taking the medication that had been very helpful, it does behoove the physician to try and figure out why that is.”

Normalize the issue to help patients open up. “I will often say, ‘You know, many, many patients don’t take their medicines exactly as prescribed. About how many days a week do you take this medicine?’” said Dr. Alexander. “If you ask in a nonconfrontational, supportive manner, I’ve found that patients are quite candid.” 

Don’t assume insurance has it covered. If patients are uninsured, help them enroll in (or renew) insurance coverage. But don’t assume insurance will solve the whole problem. “There are many people who, although they do have coverage, still can’t afford their medications,” said Dr. Goodman.

For products on high formulary tiers, the patient’s monthly cost can be hundreds to thousands of dollars. “Over the past 10-20 years, we’ve seen remarkable technological innovation in the types of medicines being brought to market, and here, I’m referring primarily to biologics and medicines made from living cells,” said Dr. Alexander, “but many of these have a price tag that is simply astronomical, and insurers aren’t going to bear the brunt of these costs alone.” 

Biosimilars can be a bit more affordable, but “the dirty little secret of biosimilars is that they’re not really very much less expensive,” said Dr. Goodman. “If your patient is doing well on a drug that gets dropped from their insurance plan’s formulary, or if they switch to a plan that doesn’t cover it, try calling and advocating for an exception. It’s an uphill battle, but it sometimes works,” she said.

If not? Help your patients apply for a patient assistance program. Many drug manufacturers offer copay assistance through their websites, and nonprofit patient assistance organizations such as the PAN Foundation, the Patient Advocate Foundation’s Co-Pay Relief Program, or The Assistance Fund can also help fill the gaps. One study published in the Journal of Managed Care and Specialty Pharmacy showed that in patients with rheumatoid arthritis, copay assistance was associated with 79% lower odds of prescription abandonment (failure to fill within 30 days of health plan approval).

Beware of “shiny penny syndrome.” It’s easy to get excited about new, innovative medications, especially when sales reps provide plenty of free samples. “There is a tendency to treat every new medicine as if it’s a bright shiny object in the streambed, and you know that’s not always the case,” said Dr. Alexander. “So, I think we have to be careful, especially in settings when we’re talking about ultra–high-cost medicines, that we’re aware of the burden these medicines may place on patients and that we’re navigating that with patients together, and not simply leaving that as a conversation that never happens in the exam room.”

Maybe there’s an older, time-tested drug that works just as well as the newer, more expensive one. Perhaps there is a slightly less effective medicine that costs a lot less. “These are cost–quality trade-offs that clinicians and patients should be navigating together,” said Dr. Alexander. For example, in a patient with rheumatoid arthritis, a tumor necrosis factor alpha inhibitor might work similarly to or almost as well as an interleukin inhibitor, the newer and typically more expensive choice. 

“Some clinicians may find it quite unpalatable to be potentially compromising on safety or efficacy in the interest of reducing the cost of therapies, but as former Surgeon General C. Everett Koop said, ‘Drugs don’t work in patients who don’t take them,’ ” said Dr. Alexander. “So, if the choice is for someone not to be taking a treatment, or to be taking one that may be a little bit less good, I’ll take the latter.”

Consider the patient’s broader care team. Encourage patients to discuss costs with their other healthcare providers. For patients taking multiple medications, a few adjustments could make a big impact on their wallets. Primary care providers or other specialists might recommend some older and less expensive, but still effective, drugs, such as thiazides for hypertension or metformin for type 2 diabetes. Another option might be to simplify the patient’s regimen or include some fixed-dose combination pills in place of two others.

And if no one has referred the patient to a medical social worker, make the connection. A social worker can put patients in touch with local agencies that can help them with food, housing, and other nonmedical costs. 

Talk about this problem with anyone who will listen. One of the best ways to help patients with rheumatologic diseases is to ensure that decision-makers don’t overlook them. Professional societies such as the American College of Rheumatology can be great resources for advocacy in Washington, DC. Political movements can make drugs more affordable — for example, insulin prices have dropped in recent years because of political pressure, said Dr. Goodman.

“A lot of our national policy now focuses on aiding patients with single high-cost events, but we hope studies like these can really get policymakers to think through how to better support patients with chronic conditions that may have been historically ignored, such as patients with rheumatologic disease,” said Dr. Amen. 

The first step is raising awareness and telling your story. “As providers, we are often [at the] forefront in witnessing how chronic conditions and their associated costs can negatively affect patients’ lives and even alter clinical outcomes,” Dr. Amen added. “By publishing data and sharing meaningful patient stories and clinical vignettes, we can begin to advocate and humanize these patients to policymakers.” 

Information on study funding was not available. All authors reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

Many patients struggle with healthcare costs and basic expenses, according to new research.

People with rheumatologic diseases often experience a hidden symptom: financial toxicity or significant economic strain from out-of-pocket costs. A new study of 41,502 patients published in JCR: Journal of Clinical Rheumatology showed that 20% of those with rheumatologic diseases faced financial hardship from medical expenses, with 55% of those unable to pay their bills. 

Compared with patients who do not have rheumatologic diseases, and after clinical and sociodemographic factors were controlled for, patients with rheumatologic diseases were:

• 29% more likely to have high levels of financial hardship — difficulty paying; needing to pay over time; or inability to pay bills for doctors, dentists, hospitals, therapists, medication, equipment, nursing homes, or home care.
• 53% more likely to have high levels of financial distress — significant worry about having enough money for retirement, paying medical costs in the event of a serious illness or accident, maintaining their standard of living, paying their usual healthcare costs, and affording their normal monthly bills and housing costs.
• 29% more likely to experience food insecurity, defined as limited or uncertain access to adequate food.
• 58% more likely to report cost-related medication nonadherence — skipping doses, taking less medication, or delaying filling a prescription to save money.

People who were younger than 64 years, male, Black, or uninsured had higher odds of experiencing financial hardship, financial distress, food insecurity, and cost-related medication nonadherence. 

This study highlights “just how costly everyday rheumatologic conditions can be for your average American,” said lead study author Troy Amen, MD, MBA, an orthopedic surgery resident at the Hospital for Special Surgery in New York City. These diseases can be disabling, limiting a patient’s ability to work at the very time when expensive medications are needed. 

“It’s critical for clinicians to recognize how common the financial burden from healthcare costs can be, and only then can they take steps to better support patients,” said G. Caleb Alexander, MD, MS, professor of epidemiology at Johns Hopkins University in Baltimore, who was not involved in the study. 

Here’s how healthcare providers can help. 

Consider skipped medication a red flag. It’s often the first sign of a financial concern. “Sometimes with these problems, it looks like simple medication noncompliance, but it’s really a more complex form of nonadherence,” said Susan M. Goodman, MD, professor of clinical medicine at Weill Cornell Medicine in New York City and a coauthor of the study. “And I think if someone’s not taking the medication that had been very helpful, it does behoove the physician to try and figure out why that is.”

Normalize the issue to help patients open up. “I will often say, ‘You know, many, many patients don’t take their medicines exactly as prescribed. About how many days a week do you take this medicine?’” said Dr. Alexander. “If you ask in a nonconfrontational, supportive manner, I’ve found that patients are quite candid.” 

Don’t assume insurance has it covered. If patients are uninsured, help them enroll in (or renew) insurance coverage. But don’t assume insurance will solve the whole problem. “There are many people who, although they do have coverage, still can’t afford their medications,” said Dr. Goodman.

For products on high formulary tiers, the patient’s monthly cost can be hundreds to thousands of dollars. “Over the past 10-20 years, we’ve seen remarkable technological innovation in the types of medicines being brought to market, and here, I’m referring primarily to biologics and medicines made from living cells,” said Dr. Alexander, “but many of these have a price tag that is simply astronomical, and insurers aren’t going to bear the brunt of these costs alone.” 

Biosimilars can be a bit more affordable, but “the dirty little secret of biosimilars is that they’re not really very much less expensive,” said Dr. Goodman. “If your patient is doing well on a drug that gets dropped from their insurance plan’s formulary, or if they switch to a plan that doesn’t cover it, try calling and advocating for an exception. It’s an uphill battle, but it sometimes works,” she said.

If not? Help your patients apply for a patient assistance program. Many drug manufacturers offer copay assistance through their websites, and nonprofit patient assistance organizations such as the PAN Foundation, the Patient Advocate Foundation’s Co-Pay Relief Program, or The Assistance Fund can also help fill the gaps. One study published in the Journal of Managed Care and Specialty Pharmacy showed that in patients with rheumatoid arthritis, copay assistance was associated with 79% lower odds of prescription abandonment (failure to fill within 30 days of health plan approval).

Beware of “shiny penny syndrome.” It’s easy to get excited about new, innovative medications, especially when sales reps provide plenty of free samples. “There is a tendency to treat every new medicine as if it’s a bright shiny object in the streambed, and you know that’s not always the case,” said Dr. Alexander. “So, I think we have to be careful, especially in settings when we’re talking about ultra–high-cost medicines, that we’re aware of the burden these medicines may place on patients and that we’re navigating that with patients together, and not simply leaving that as a conversation that never happens in the exam room.”

Maybe there’s an older, time-tested drug that works just as well as the newer, more expensive one. Perhaps there is a slightly less effective medicine that costs a lot less. “These are cost–quality trade-offs that clinicians and patients should be navigating together,” said Dr. Alexander. For example, in a patient with rheumatoid arthritis, a tumor necrosis factor alpha inhibitor might work similarly to or almost as well as an interleukin inhibitor, the newer and typically more expensive choice. 

“Some clinicians may find it quite unpalatable to be potentially compromising on safety or efficacy in the interest of reducing the cost of therapies, but as former Surgeon General C. Everett Koop said, ‘Drugs don’t work in patients who don’t take them,’ ” said Dr. Alexander. “So, if the choice is for someone not to be taking a treatment, or to be taking one that may be a little bit less good, I’ll take the latter.”

Consider the patient’s broader care team. Encourage patients to discuss costs with their other healthcare providers. For patients taking multiple medications, a few adjustments could make a big impact on their wallets. Primary care providers or other specialists might recommend some older and less expensive, but still effective, drugs, such as thiazides for hypertension or metformin for type 2 diabetes. Another option might be to simplify the patient’s regimen or include some fixed-dose combination pills in place of two others.

And if no one has referred the patient to a medical social worker, make the connection. A social worker can put patients in touch with local agencies that can help them with food, housing, and other nonmedical costs. 

Talk about this problem with anyone who will listen. One of the best ways to help patients with rheumatologic diseases is to ensure that decision-makers don’t overlook them. Professional societies such as the American College of Rheumatology can be great resources for advocacy in Washington, DC. Political movements can make drugs more affordable — for example, insulin prices have dropped in recent years because of political pressure, said Dr. Goodman.

“A lot of our national policy now focuses on aiding patients with single high-cost events, but we hope studies like these can really get policymakers to think through how to better support patients with chronic conditions that may have been historically ignored, such as patients with rheumatologic disease,” said Dr. Amen. 

The first step is raising awareness and telling your story. “As providers, we are often [at the] forefront in witnessing how chronic conditions and their associated costs can negatively affect patients’ lives and even alter clinical outcomes,” Dr. Amen added. “By publishing data and sharing meaningful patient stories and clinical vignettes, we can begin to advocate and humanize these patients to policymakers.” 

Information on study funding was not available. All authors reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

Many patients struggle with healthcare costs and basic expenses, according to new research.

People with rheumatologic diseases often experience a hidden symptom: financial toxicity or significant economic strain from out-of-pocket costs. A new study of 41,502 patients published in JCR: Journal of Clinical Rheumatology showed that 20% of those with rheumatologic diseases faced financial hardship from medical expenses, with 55% of those unable to pay their bills. 

Compared with patients who do not have rheumatologic diseases, and after clinical and sociodemographic factors were controlled for, patients with rheumatologic diseases were:

• 29% more likely to have high levels of financial hardship — difficulty paying; needing to pay over time; or inability to pay bills for doctors, dentists, hospitals, therapists, medication, equipment, nursing homes, or home care.
• 53% more likely to have high levels of financial distress — significant worry about having enough money for retirement, paying medical costs in the event of a serious illness or accident, maintaining their standard of living, paying their usual healthcare costs, and affording their normal monthly bills and housing costs.
• 29% more likely to experience food insecurity, defined as limited or uncertain access to adequate food.
• 58% more likely to report cost-related medication nonadherence — skipping doses, taking less medication, or delaying filling a prescription to save money.

People who were younger than 64 years, male, Black, or uninsured had higher odds of experiencing financial hardship, financial distress, food insecurity, and cost-related medication nonadherence. 

This study highlights “just how costly everyday rheumatologic conditions can be for your average American,” said lead study author Troy Amen, MD, MBA, an orthopedic surgery resident at the Hospital for Special Surgery in New York City. These diseases can be disabling, limiting a patient’s ability to work at the very time when expensive medications are needed. 

“It’s critical for clinicians to recognize how common the financial burden from healthcare costs can be, and only then can they take steps to better support patients,” said G. Caleb Alexander, MD, MS, professor of epidemiology at Johns Hopkins University in Baltimore, who was not involved in the study. 

Here’s how healthcare providers can help. 

Consider skipped medication a red flag. It’s often the first sign of a financial concern. “Sometimes with these problems, it looks like simple medication noncompliance, but it’s really a more complex form of nonadherence,” said Susan M. Goodman, MD, professor of clinical medicine at Weill Cornell Medicine in New York City and a coauthor of the study. “And I think if someone’s not taking the medication that had been very helpful, it does behoove the physician to try and figure out why that is.”

Normalize the issue to help patients open up. “I will often say, ‘You know, many, many patients don’t take their medicines exactly as prescribed. About how many days a week do you take this medicine?’” said Dr. Alexander. “If you ask in a nonconfrontational, supportive manner, I’ve found that patients are quite candid.” 

Don’t assume insurance has it covered. If patients are uninsured, help them enroll in (or renew) insurance coverage. But don’t assume insurance will solve the whole problem. “There are many people who, although they do have coverage, still can’t afford their medications,” said Dr. Goodman.

For products on high formulary tiers, the patient’s monthly cost can be hundreds to thousands of dollars. “Over the past 10-20 years, we’ve seen remarkable technological innovation in the types of medicines being brought to market, and here, I’m referring primarily to biologics and medicines made from living cells,” said Dr. Alexander, “but many of these have a price tag that is simply astronomical, and insurers aren’t going to bear the brunt of these costs alone.” 

Biosimilars can be a bit more affordable, but “the dirty little secret of biosimilars is that they’re not really very much less expensive,” said Dr. Goodman. “If your patient is doing well on a drug that gets dropped from their insurance plan’s formulary, or if they switch to a plan that doesn’t cover it, try calling and advocating for an exception. It’s an uphill battle, but it sometimes works,” she said.

If not? Help your patients apply for a patient assistance program. Many drug manufacturers offer copay assistance through their websites, and nonprofit patient assistance organizations such as the PAN Foundation, the Patient Advocate Foundation’s Co-Pay Relief Program, or The Assistance Fund can also help fill the gaps. One study published in the Journal of Managed Care and Specialty Pharmacy showed that in patients with rheumatoid arthritis, copay assistance was associated with 79% lower odds of prescription abandonment (failure to fill within 30 days of health plan approval).

Beware of “shiny penny syndrome.” It’s easy to get excited about new, innovative medications, especially when sales reps provide plenty of free samples. “There is a tendency to treat every new medicine as if it’s a bright shiny object in the streambed, and you know that’s not always the case,” said Dr. Alexander. “So, I think we have to be careful, especially in settings when we’re talking about ultra–high-cost medicines, that we’re aware of the burden these medicines may place on patients and that we’re navigating that with patients together, and not simply leaving that as a conversation that never happens in the exam room.”

Maybe there’s an older, time-tested drug that works just as well as the newer, more expensive one. Perhaps there is a slightly less effective medicine that costs a lot less. “These are cost–quality trade-offs that clinicians and patients should be navigating together,” said Dr. Alexander. For example, in a patient with rheumatoid arthritis, a tumor necrosis factor alpha inhibitor might work similarly to or almost as well as an interleukin inhibitor, the newer and typically more expensive choice. 

“Some clinicians may find it quite unpalatable to be potentially compromising on safety or efficacy in the interest of reducing the cost of therapies, but as former Surgeon General C. Everett Koop said, ‘Drugs don’t work in patients who don’t take them,’ ” said Dr. Alexander. “So, if the choice is for someone not to be taking a treatment, or to be taking one that may be a little bit less good, I’ll take the latter.”

Consider the patient’s broader care team. Encourage patients to discuss costs with their other healthcare providers. For patients taking multiple medications, a few adjustments could make a big impact on their wallets. Primary care providers or other specialists might recommend some older and less expensive, but still effective, drugs, such as thiazides for hypertension or metformin for type 2 diabetes. Another option might be to simplify the patient’s regimen or include some fixed-dose combination pills in place of two others.

And if no one has referred the patient to a medical social worker, make the connection. A social worker can put patients in touch with local agencies that can help them with food, housing, and other nonmedical costs. 

Talk about this problem with anyone who will listen. One of the best ways to help patients with rheumatologic diseases is to ensure that decision-makers don’t overlook them. Professional societies such as the American College of Rheumatology can be great resources for advocacy in Washington, DC. Political movements can make drugs more affordable — for example, insulin prices have dropped in recent years because of political pressure, said Dr. Goodman.

“A lot of our national policy now focuses on aiding patients with single high-cost events, but we hope studies like these can really get policymakers to think through how to better support patients with chronic conditions that may have been historically ignored, such as patients with rheumatologic disease,” said Dr. Amen. 

The first step is raising awareness and telling your story. “As providers, we are often [at the] forefront in witnessing how chronic conditions and their associated costs can negatively affect patients’ lives and even alter clinical outcomes,” Dr. Amen added. “By publishing data and sharing meaningful patient stories and clinical vignettes, we can begin to advocate and humanize these patients to policymakers.” 

Information on study funding was not available. All authors reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

VIENNA — Safe and effective options for lowering serum uric acid (sUA) in patients with gout who are refractory to conventional therapies appear to be near, judging from phase 2 and 3 trials that produced positive results at the annual European Congress of Rheumatology.

Reports from the meeting included two phase 2 studies with novel urate anion transporter 1 (URAT1) inhibitors for patients with refractory gout, in addition to extension data from the phase 3 trial program for SEL-212. In all cases, efficacy appeared to be on the same order of currently available drugs with potentially better tolerability, an important unmet need for patients with gout refractory to traditional therapies.
 

12-Month Outcomes With SEL-212

The extension data with SEL-212 follow the 6-month results presented from the DISSOLVE I and II trials at EULAR 2023. Now at 12 months, the benefits have proven to be generally sustained with no new safety signals, according to Herbert S.B. Baraf, MD, The Center for Rheumatology and Bone Research, Wheaton, Maryland.

Arthritis Foundation

SEL-212 is a drug platform involving two components delivered by intravenous infusion once monthly in sequence. The first, SEL-110, consists of tolerogenic nanoparticles containing sirolimus. The second, SEL-037, is the pegylated uricase pegadricase.

On the 1-month dosing schedule, most patients who had responded at 6 months were still responding at 12 months, and both of the two study doses of SEL-212 in the DISSOLVE trials were well tolerated over the extension, Dr. Baraf reported.

On the basis of the data so far, “this will be an effective and well tolerated therapy for refractory gout over a period of at least 12 months,” Dr. Baraf said.

The DISSOLVE I and II trials were identically designed. Patients with refractory gout, defined as failure to normalize sUA or control symptoms with a xanthine oxidase inhibitor, were randomly assigned to receive 0.15 mg SEL-212, 1.0 mg SEL-212, or placebo.

There was a stopping rule for patients who reached a sUA level < 2 mg/dL 1 hour after the infusion.

The primary endpoint was sUA level < 6 mg/dL for at least 80% of the sixth month of the 6-month trial. About 50% of patients on either dose of SEL-212 met this endpoint (vs 4% of those receiving placebo; P < .0001). There was a numerical advantage for the higher dose in both studies.

Patients who completed the 6-month trial were eligible for a 6-month extension, during which they remained on their assigned therapy, including placebo. This phase was also blinded. Patients who met the stopping rule in either the main study or extension did not take the study drug but remained in the study for final analysis.

Of the 265 patients who participated in the main phase of the study, 143 (54%) completed the 6-month extension. Most discontinuations were the result of the stopping rule. Reasons for other patients discontinuing the study included withdrawal of consent in about 10% of each treatment arm and adverse events in 13.8%, 6.8%, and 2.2% of the high-dose, low-dose, and placebo groups, respectively.

At 12 months, when the data from the two trials were pooled, the proportion of patients on therapy and responding remained at about 50% in the high-dose group and 43% in the low-dose group on an intention-to-treat analysis. Relative to the 8% response rate for placebo, the advantage for either dose was highly significant (P < .0001).

In the subgroup of patients with tophi at baseline, representing about half the study group, responses were low at 12 months, whether on high- (41%) or low-dose (43%) SEL-212. The rate of response among placebo patients with baseline tophi was 9%.
 

Safety of SEL-212

The safety over the 6-month extension did not differ substantially from that observed during the first 6 months, according to Dr. Baraf. This was reiterated in more detail by Alan Kivitz, MD, Altoona Center for Clinical Research, Duncansville, Pennsylvania. He delivered a separate safety presentation focused on DISSOLVE I.

Specifically, there were no serious adverse events thought to be related to treatment. Besides gout flares, which affected approximately 27% of patients regardless of active treatment or placebo assignment, the most common adverse effect was hypertriglyceridemia, which was observed in 5.4% of patients on active treatment vs 0% of those receiving placebo. Independent of the treatment arm, less than 5% of patients developed stomatitis or cellulitis during the 6-month extension period.

In the 6-month extension phase, there were no infusion reactions observed within 1 hour after SEL-212 administration and just two overall that occurred with low-dose SEL-212, according to Kivitz.

New Selective URAT1 Inhibitors

The other potential advance in the treatment of refractory gout is coming from newer selective URAT1 inhibitors. According to the lead investigators of two phase 2 trials evaluating a novel URAT1 inhibitor, the urate transporter protein has long been considered the most promising target for gout treatment. As this protein regulates the absorption of uric acid from the renal tubule, it has a direct uric acid–lowering effect. However, the adverse events of current agents, such as probenecid, benzbromarone, and sulfinpyrazone, have created a need for drugs with a better benefit-to-risk ratio.

In one of two multicenter phase 2 studies on refractory gout, the experimental agent ruzinurad was tested as an adjunct to the xanthine oxidase inhibitor febuxostat. In the other, the objective was to evaluate whether the experimental agent AR882 or AR882 plus allopurinol is better than allopurinol alone for reducing tophi at 12 months.
 

Ruzinurad Plus Febuxostat

In the ruzinurad trial, 151 patients with symptomatic gout and elevated sUA (> 6 mg/dL) for at least 6 weeks on stable doses of febuxostat were randomized to receive 5 mg ruzinurad, 10 mg ruzinurad, or placebo. All remained on febuxostat. In the active treatment arms, the starting ruzinurad dose was 1 mg before titrating up to the assigned target.

For the primary endpoint of sUA < 6 mg/dL at 12 weeks, the rates were 56.9%, 53.1%, and 13.7% in the high-dose, low-dose, and placebo groups, respectively (P < .0001 for both ruzinurad arms), reported Huihua Ding, MD, a clinician and researcher at Shanghai Jiao Tong University, Shanghai, China.

“Consistently, subgroup analyses based on baseline eGFR [estimated glomerular filtration rate], sUA, and tophus demonstrated superior effective of ruzinurad plus febuxostat over placebo plus febuxostat,” reported Dr. Ding, who noted that previous clinical studies suggested the potential for synergism between ruzinurad and febuxostat.

The proportion of patients achieving the more rigorous target of < 0.5 mg/dL was also higher with the higher and lower doses of ruzinurad vs placebo (43.1% and 38.8% vs 9.8%, respectively).

The proportion of patients with treatment-emergent side effects did not differ between the three groups. The most common were gout flares, which were observed in 39.2%, 49.0%, and 45.1% in the high-dose, low-dose, and placebo groups, respectively. Most adverse events were mild or moderate, and none led to treatment discontinuation.

The favorable benefit-to-risk profile of ruzinurad was attributed by Dr. Ding to its high relative selectivity and potent inhibition of URAT1, an advantage that might be relevant to avoiding side effects at higher doses.

AR882 in Patients With Tophi

In the trial with AR882, 42 patients with refractory gout and at least one subcutaneous tophus were randomized to receive 75 mg AR882, 50 mg AR882 plus allopurinol, or allopurinol alone. All drugs were taken once daily. Doses of allopurinol of up to 300 mg were permitted.

The changes in the target tophus area and crystal volume at month 6 were compared, and patients who completed this phase were invited into a 6-month extension. In the 6-month extension, 75 mg AR882 was additionally provided to those who had been in the single-agent allopurinol arm. The other arms were unchanged.

Tophi measurements were performed with calipers at regular intervals. Change from baseline in sUA levels was also an efficacy measure, according to Robert Keenan, MD, chief medical officer of Arthrosi Therapeutics, which is developing AR882.

From average baseline sUA levels of > 9 mg/dL, all three treatments reduced sUA levels by an average of at least 4.5 mg by month 3. At month 6, complete resolution of at least one target tophus was observed in 29% of the group randomized to receive 75 mg AR882 alone, 8% of those randomized to receive 50 mg AR882 plus allopurinol, and 8% of those on allopurinol alone.

At month 12, the average sUA levels were 4.3 mg/dL for 75 mg AR882, 3.7 mg/dL for 50 mg AR882 plus allopurinol, and 2.9 mg/dL for the 75 mg AR882 plus allopurinol extension-switch arm.

At the 12-month mark, the proportions of patients with complete resolution of any tophus were 50.0% for 75 mg AR882, 12.5% for 50 mg AR882 plus allopurinol, and 36.4% for the 75 mg AR882 plus allopurinol extension-switch arm, according to Dr. Keenan.

Compared with allopurinol alone at 6 months, 75 mg AR882 led to a reduction in total urate crystal volume, and this reduction was sustained at 12 months, he added.

Alone or in combination with allopurinol, AR882 was well tolerated. Gout flares were the most common adverse events, but they declined with continued AR882 treatment, according to Dr. Keenan. Diarrhea, headache, and upper respiratory infections were reported but were of mild or moderate severity.

Again, the take-home message from this study, like the other phase 2 study of a novel URAT1 inhibitor, is that these newer drugs might offer a better benefit-to-risk ratio, particularly in those with refractory disease.

“AR882 may offer improved efficacy and better safety compared to existing therapies in the treatment of patients with gout, including those with both clinically visible and subclinical crystal deposition,” Dr. Keenan said.

Dr. Baraf reported financial relationships with Horizon Therapeutics, Fresenius Kabi, Grünenthal, Olatec, Selecta Biosciences, and Sobi, which provided funding for the trials he discussed. Dr. Kivitz also reported a financial relationship with Sobi, which funded the DISSOLVE trials, along with AbbVie, Amgen, Eli Lilly, Flexion, GlaxoSmithKline, and Sanofi Regeneron. Dr. Ding reported no potential conflicts. The study she discussed was funded by Jiangsu Hengrui Pharmaceuticals. Dr. Keenan is an employee of Arthrosi Therapeutics, which provided funding for the trial he presented.

August 1, 2024 — Editor's note: This article has been updated to reflect the correct number of infusion reactions reported in the 6-month extension phase of the DISSOLVE I trial.

A version of this article appeared on Medscape.com.

VIENNA — Safe and effective options for lowering serum uric acid (sUA) in patients with gout who are refractory to conventional therapies appear to be near, judging from phase 2 and 3 trials that produced positive results at the annual European Congress of Rheumatology.

Reports from the meeting included two phase 2 studies with novel urate anion transporter 1 (URAT1) inhibitors for patients with refractory gout, in addition to extension data from the phase 3 trial program for SEL-212. In all cases, efficacy appeared to be on the same order of currently available drugs with potentially better tolerability, an important unmet need for patients with gout refractory to traditional therapies.
 

12-Month Outcomes With SEL-212

The extension data with SEL-212 follow the 6-month results presented from the DISSOLVE I and II trials at EULAR 2023. Now at 12 months, the benefits have proven to be generally sustained with no new safety signals, according to Herbert S.B. Baraf, MD, The Center for Rheumatology and Bone Research, Wheaton, Maryland.

Arthritis Foundation

SEL-212 is a drug platform involving two components delivered by intravenous infusion once monthly in sequence. The first, SEL-110, consists of tolerogenic nanoparticles containing sirolimus. The second, SEL-037, is the pegylated uricase pegadricase.

On the 1-month dosing schedule, most patients who had responded at 6 months were still responding at 12 months, and both of the two study doses of SEL-212 in the DISSOLVE trials were well tolerated over the extension, Dr. Baraf reported.

On the basis of the data so far, “this will be an effective and well tolerated therapy for refractory gout over a period of at least 12 months,” Dr. Baraf said.

The DISSOLVE I and II trials were identically designed. Patients with refractory gout, defined as failure to normalize sUA or control symptoms with a xanthine oxidase inhibitor, were randomly assigned to receive 0.15 mg SEL-212, 1.0 mg SEL-212, or placebo.

There was a stopping rule for patients who reached a sUA level < 2 mg/dL 1 hour after the infusion.

The primary endpoint was sUA level < 6 mg/dL for at least 80% of the sixth month of the 6-month trial. About 50% of patients on either dose of SEL-212 met this endpoint (vs 4% of those receiving placebo; P < .0001). There was a numerical advantage for the higher dose in both studies.

Patients who completed the 6-month trial were eligible for a 6-month extension, during which they remained on their assigned therapy, including placebo. This phase was also blinded. Patients who met the stopping rule in either the main study or extension did not take the study drug but remained in the study for final analysis.

Of the 265 patients who participated in the main phase of the study, 143 (54%) completed the 6-month extension. Most discontinuations were the result of the stopping rule. Reasons for other patients discontinuing the study included withdrawal of consent in about 10% of each treatment arm and adverse events in 13.8%, 6.8%, and 2.2% of the high-dose, low-dose, and placebo groups, respectively.

At 12 months, when the data from the two trials were pooled, the proportion of patients on therapy and responding remained at about 50% in the high-dose group and 43% in the low-dose group on an intention-to-treat analysis. Relative to the 8% response rate for placebo, the advantage for either dose was highly significant (P < .0001).

In the subgroup of patients with tophi at baseline, representing about half the study group, responses were low at 12 months, whether on high- (41%) or low-dose (43%) SEL-212. The rate of response among placebo patients with baseline tophi was 9%.
 

Safety of SEL-212

The safety over the 6-month extension did not differ substantially from that observed during the first 6 months, according to Dr. Baraf. This was reiterated in more detail by Alan Kivitz, MD, Altoona Center for Clinical Research, Duncansville, Pennsylvania. He delivered a separate safety presentation focused on DISSOLVE I.

Specifically, there were no serious adverse events thought to be related to treatment. Besides gout flares, which affected approximately 27% of patients regardless of active treatment or placebo assignment, the most common adverse effect was hypertriglyceridemia, which was observed in 5.4% of patients on active treatment vs 0% of those receiving placebo. Independent of the treatment arm, less than 5% of patients developed stomatitis or cellulitis during the 6-month extension period.

In the 6-month extension phase, there were no infusion reactions observed within 1 hour after SEL-212 administration and just two overall that occurred with low-dose SEL-212, according to Kivitz.

New Selective URAT1 Inhibitors

The other potential advance in the treatment of refractory gout is coming from newer selective URAT1 inhibitors. According to the lead investigators of two phase 2 trials evaluating a novel URAT1 inhibitor, the urate transporter protein has long been considered the most promising target for gout treatment. As this protein regulates the absorption of uric acid from the renal tubule, it has a direct uric acid–lowering effect. However, the adverse events of current agents, such as probenecid, benzbromarone, and sulfinpyrazone, have created a need for drugs with a better benefit-to-risk ratio.

In one of two multicenter phase 2 studies on refractory gout, the experimental agent ruzinurad was tested as an adjunct to the xanthine oxidase inhibitor febuxostat. In the other, the objective was to evaluate whether the experimental agent AR882 or AR882 plus allopurinol is better than allopurinol alone for reducing tophi at 12 months.
 

Ruzinurad Plus Febuxostat

In the ruzinurad trial, 151 patients with symptomatic gout and elevated sUA (> 6 mg/dL) for at least 6 weeks on stable doses of febuxostat were randomized to receive 5 mg ruzinurad, 10 mg ruzinurad, or placebo. All remained on febuxostat. In the active treatment arms, the starting ruzinurad dose was 1 mg before titrating up to the assigned target.

For the primary endpoint of sUA < 6 mg/dL at 12 weeks, the rates were 56.9%, 53.1%, and 13.7% in the high-dose, low-dose, and placebo groups, respectively (P < .0001 for both ruzinurad arms), reported Huihua Ding, MD, a clinician and researcher at Shanghai Jiao Tong University, Shanghai, China.

“Consistently, subgroup analyses based on baseline eGFR [estimated glomerular filtration rate], sUA, and tophus demonstrated superior effective of ruzinurad plus febuxostat over placebo plus febuxostat,” reported Dr. Ding, who noted that previous clinical studies suggested the potential for synergism between ruzinurad and febuxostat.

The proportion of patients achieving the more rigorous target of < 0.5 mg/dL was also higher with the higher and lower doses of ruzinurad vs placebo (43.1% and 38.8% vs 9.8%, respectively).

The proportion of patients with treatment-emergent side effects did not differ between the three groups. The most common were gout flares, which were observed in 39.2%, 49.0%, and 45.1% in the high-dose, low-dose, and placebo groups, respectively. Most adverse events were mild or moderate, and none led to treatment discontinuation.

The favorable benefit-to-risk profile of ruzinurad was attributed by Dr. Ding to its high relative selectivity and potent inhibition of URAT1, an advantage that might be relevant to avoiding side effects at higher doses.

AR882 in Patients With Tophi

In the trial with AR882, 42 patients with refractory gout and at least one subcutaneous tophus were randomized to receive 75 mg AR882, 50 mg AR882 plus allopurinol, or allopurinol alone. All drugs were taken once daily. Doses of allopurinol of up to 300 mg were permitted.

The changes in the target tophus area and crystal volume at month 6 were compared, and patients who completed this phase were invited into a 6-month extension. In the 6-month extension, 75 mg AR882 was additionally provided to those who had been in the single-agent allopurinol arm. The other arms were unchanged.

Tophi measurements were performed with calipers at regular intervals. Change from baseline in sUA levels was also an efficacy measure, according to Robert Keenan, MD, chief medical officer of Arthrosi Therapeutics, which is developing AR882.

From average baseline sUA levels of > 9 mg/dL, all three treatments reduced sUA levels by an average of at least 4.5 mg by month 3. At month 6, complete resolution of at least one target tophus was observed in 29% of the group randomized to receive 75 mg AR882 alone, 8% of those randomized to receive 50 mg AR882 plus allopurinol, and 8% of those on allopurinol alone.

At month 12, the average sUA levels were 4.3 mg/dL for 75 mg AR882, 3.7 mg/dL for 50 mg AR882 plus allopurinol, and 2.9 mg/dL for the 75 mg AR882 plus allopurinol extension-switch arm.

At the 12-month mark, the proportions of patients with complete resolution of any tophus were 50.0% for 75 mg AR882, 12.5% for 50 mg AR882 plus allopurinol, and 36.4% for the 75 mg AR882 plus allopurinol extension-switch arm, according to Dr. Keenan.

Compared with allopurinol alone at 6 months, 75 mg AR882 led to a reduction in total urate crystal volume, and this reduction was sustained at 12 months, he added.

Alone or in combination with allopurinol, AR882 was well tolerated. Gout flares were the most common adverse events, but they declined with continued AR882 treatment, according to Dr. Keenan. Diarrhea, headache, and upper respiratory infections were reported but were of mild or moderate severity.

Again, the take-home message from this study, like the other phase 2 study of a novel URAT1 inhibitor, is that these newer drugs might offer a better benefit-to-risk ratio, particularly in those with refractory disease.

“AR882 may offer improved efficacy and better safety compared to existing therapies in the treatment of patients with gout, including those with both clinically visible and subclinical crystal deposition,” Dr. Keenan said.

Dr. Baraf reported financial relationships with Horizon Therapeutics, Fresenius Kabi, Grünenthal, Olatec, Selecta Biosciences, and Sobi, which provided funding for the trials he discussed. Dr. Kivitz also reported a financial relationship with Sobi, which funded the DISSOLVE trials, along with AbbVie, Amgen, Eli Lilly, Flexion, GlaxoSmithKline, and Sanofi Regeneron. Dr. Ding reported no potential conflicts. The study she discussed was funded by Jiangsu Hengrui Pharmaceuticals. Dr. Keenan is an employee of Arthrosi Therapeutics, which provided funding for the trial he presented.

August 1, 2024 — Editor's note: This article has been updated to reflect the correct number of infusion reactions reported in the 6-month extension phase of the DISSOLVE I trial.

A version of this article appeared on Medscape.com.

VIENNA — Safe and effective options for lowering serum uric acid (sUA) in patients with gout who are refractory to conventional therapies appear to be near, judging from phase 2 and 3 trials that produced positive results at the annual European Congress of Rheumatology.

Reports from the meeting included two phase 2 studies with novel urate anion transporter 1 (URAT1) inhibitors for patients with refractory gout, in addition to extension data from the phase 3 trial program for SEL-212. In all cases, efficacy appeared to be on the same order of currently available drugs with potentially better tolerability, an important unmet need for patients with gout refractory to traditional therapies.
 

12-Month Outcomes With SEL-212

The extension data with SEL-212 follow the 6-month results presented from the DISSOLVE I and II trials at EULAR 2023. Now at 12 months, the benefits have proven to be generally sustained with no new safety signals, according to Herbert S.B. Baraf, MD, The Center for Rheumatology and Bone Research, Wheaton, Maryland.

Arthritis Foundation

SEL-212 is a drug platform involving two components delivered by intravenous infusion once monthly in sequence. The first, SEL-110, consists of tolerogenic nanoparticles containing sirolimus. The second, SEL-037, is the pegylated uricase pegadricase.

On the 1-month dosing schedule, most patients who had responded at 6 months were still responding at 12 months, and both of the two study doses of SEL-212 in the DISSOLVE trials were well tolerated over the extension, Dr. Baraf reported.

On the basis of the data so far, “this will be an effective and well tolerated therapy for refractory gout over a period of at least 12 months,” Dr. Baraf said.

The DISSOLVE I and II trials were identically designed. Patients with refractory gout, defined as failure to normalize sUA or control symptoms with a xanthine oxidase inhibitor, were randomly assigned to receive 0.15 mg SEL-212, 1.0 mg SEL-212, or placebo.

There was a stopping rule for patients who reached a sUA level < 2 mg/dL 1 hour after the infusion.

The primary endpoint was sUA level < 6 mg/dL for at least 80% of the sixth month of the 6-month trial. About 50% of patients on either dose of SEL-212 met this endpoint (vs 4% of those receiving placebo; P < .0001). There was a numerical advantage for the higher dose in both studies.

Patients who completed the 6-month trial were eligible for a 6-month extension, during which they remained on their assigned therapy, including placebo. This phase was also blinded. Patients who met the stopping rule in either the main study or extension did not take the study drug but remained in the study for final analysis.

Of the 265 patients who participated in the main phase of the study, 143 (54%) completed the 6-month extension. Most discontinuations were the result of the stopping rule. Reasons for other patients discontinuing the study included withdrawal of consent in about 10% of each treatment arm and adverse events in 13.8%, 6.8%, and 2.2% of the high-dose, low-dose, and placebo groups, respectively.

At 12 months, when the data from the two trials were pooled, the proportion of patients on therapy and responding remained at about 50% in the high-dose group and 43% in the low-dose group on an intention-to-treat analysis. Relative to the 8% response rate for placebo, the advantage for either dose was highly significant (P < .0001).

In the subgroup of patients with tophi at baseline, representing about half the study group, responses were low at 12 months, whether on high- (41%) or low-dose (43%) SEL-212. The rate of response among placebo patients with baseline tophi was 9%.
 

Safety of SEL-212

The safety over the 6-month extension did not differ substantially from that observed during the first 6 months, according to Dr. Baraf. This was reiterated in more detail by Alan Kivitz, MD, Altoona Center for Clinical Research, Duncansville, Pennsylvania. He delivered a separate safety presentation focused on DISSOLVE I.

Specifically, there were no serious adverse events thought to be related to treatment. Besides gout flares, which affected approximately 27% of patients regardless of active treatment or placebo assignment, the most common adverse effect was hypertriglyceridemia, which was observed in 5.4% of patients on active treatment vs 0% of those receiving placebo. Independent of the treatment arm, less than 5% of patients developed stomatitis or cellulitis during the 6-month extension period.

In the 6-month extension phase, there were no infusion reactions observed within 1 hour after SEL-212 administration and just two overall that occurred with low-dose SEL-212, according to Kivitz.

New Selective URAT1 Inhibitors

The other potential advance in the treatment of refractory gout is coming from newer selective URAT1 inhibitors. According to the lead investigators of two phase 2 trials evaluating a novel URAT1 inhibitor, the urate transporter protein has long been considered the most promising target for gout treatment. As this protein regulates the absorption of uric acid from the renal tubule, it has a direct uric acid–lowering effect. However, the adverse events of current agents, such as probenecid, benzbromarone, and sulfinpyrazone, have created a need for drugs with a better benefit-to-risk ratio.

In one of two multicenter phase 2 studies on refractory gout, the experimental agent ruzinurad was tested as an adjunct to the xanthine oxidase inhibitor febuxostat. In the other, the objective was to evaluate whether the experimental agent AR882 or AR882 plus allopurinol is better than allopurinol alone for reducing tophi at 12 months.
 

Ruzinurad Plus Febuxostat

In the ruzinurad trial, 151 patients with symptomatic gout and elevated sUA (> 6 mg/dL) for at least 6 weeks on stable doses of febuxostat were randomized to receive 5 mg ruzinurad, 10 mg ruzinurad, or placebo. All remained on febuxostat. In the active treatment arms, the starting ruzinurad dose was 1 mg before titrating up to the assigned target.

For the primary endpoint of sUA < 6 mg/dL at 12 weeks, the rates were 56.9%, 53.1%, and 13.7% in the high-dose, low-dose, and placebo groups, respectively (P < .0001 for both ruzinurad arms), reported Huihua Ding, MD, a clinician and researcher at Shanghai Jiao Tong University, Shanghai, China.

“Consistently, subgroup analyses based on baseline eGFR [estimated glomerular filtration rate], sUA, and tophus demonstrated superior effective of ruzinurad plus febuxostat over placebo plus febuxostat,” reported Dr. Ding, who noted that previous clinical studies suggested the potential for synergism between ruzinurad and febuxostat.

The proportion of patients achieving the more rigorous target of < 0.5 mg/dL was also higher with the higher and lower doses of ruzinurad vs placebo (43.1% and 38.8% vs 9.8%, respectively).

The proportion of patients with treatment-emergent side effects did not differ between the three groups. The most common were gout flares, which were observed in 39.2%, 49.0%, and 45.1% in the high-dose, low-dose, and placebo groups, respectively. Most adverse events were mild or moderate, and none led to treatment discontinuation.

The favorable benefit-to-risk profile of ruzinurad was attributed by Dr. Ding to its high relative selectivity and potent inhibition of URAT1, an advantage that might be relevant to avoiding side effects at higher doses.

AR882 in Patients With Tophi

In the trial with AR882, 42 patients with refractory gout and at least one subcutaneous tophus were randomized to receive 75 mg AR882, 50 mg AR882 plus allopurinol, or allopurinol alone. All drugs were taken once daily. Doses of allopurinol of up to 300 mg were permitted.

The changes in the target tophus area and crystal volume at month 6 were compared, and patients who completed this phase were invited into a 6-month extension. In the 6-month extension, 75 mg AR882 was additionally provided to those who had been in the single-agent allopurinol arm. The other arms were unchanged.

Tophi measurements were performed with calipers at regular intervals. Change from baseline in sUA levels was also an efficacy measure, according to Robert Keenan, MD, chief medical officer of Arthrosi Therapeutics, which is developing AR882.

From average baseline sUA levels of > 9 mg/dL, all three treatments reduced sUA levels by an average of at least 4.5 mg by month 3. At month 6, complete resolution of at least one target tophus was observed in 29% of the group randomized to receive 75 mg AR882 alone, 8% of those randomized to receive 50 mg AR882 plus allopurinol, and 8% of those on allopurinol alone.

At month 12, the average sUA levels were 4.3 mg/dL for 75 mg AR882, 3.7 mg/dL for 50 mg AR882 plus allopurinol, and 2.9 mg/dL for the 75 mg AR882 plus allopurinol extension-switch arm.

At the 12-month mark, the proportions of patients with complete resolution of any tophus were 50.0% for 75 mg AR882, 12.5% for 50 mg AR882 plus allopurinol, and 36.4% for the 75 mg AR882 plus allopurinol extension-switch arm, according to Dr. Keenan.

Compared with allopurinol alone at 6 months, 75 mg AR882 led to a reduction in total urate crystal volume, and this reduction was sustained at 12 months, he added.

Alone or in combination with allopurinol, AR882 was well tolerated. Gout flares were the most common adverse events, but they declined with continued AR882 treatment, according to Dr. Keenan. Diarrhea, headache, and upper respiratory infections were reported but were of mild or moderate severity.

Again, the take-home message from this study, like the other phase 2 study of a novel URAT1 inhibitor, is that these newer drugs might offer a better benefit-to-risk ratio, particularly in those with refractory disease.

“AR882 may offer improved efficacy and better safety compared to existing therapies in the treatment of patients with gout, including those with both clinically visible and subclinical crystal deposition,” Dr. Keenan said.

Dr. Baraf reported financial relationships with Horizon Therapeutics, Fresenius Kabi, Grünenthal, Olatec, Selecta Biosciences, and Sobi, which provided funding for the trials he discussed. Dr. Kivitz also reported a financial relationship with Sobi, which funded the DISSOLVE trials, along with AbbVie, Amgen, Eli Lilly, Flexion, GlaxoSmithKline, and Sanofi Regeneron. Dr. Ding reported no potential conflicts. The study she discussed was funded by Jiangsu Hengrui Pharmaceuticals. Dr. Keenan is an employee of Arthrosi Therapeutics, which provided funding for the trial he presented.

August 1, 2024 — Editor's note: This article has been updated to reflect the correct number of infusion reactions reported in the 6-month extension phase of the DISSOLVE I trial.

A version of this article 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.

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.

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.

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

UPDATED July 8, 2024 // Editor's note: This article has been revised to give a more nuanced view from Yael Klionsky, MD, about the need for more accurate and consistent gout management guidelines for busy primary care clinicians who often rely on them in clinical practice.

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. 

Ted Bosworth/Medscape Medical News

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

According to Yael Klionsky, MD, a clinical assistant professor of rheumatology and immunology at Wake Forest University School of Medicine, Winston-Salem, North Carolina, these data are not a surprise. 

Even before this trial was completed, the message for clinicians is that they “should be focused on maintaining serum uric acid levels below physiological levels to improve outcomes” in patients with recurrent flares, said Klionsky, citing the validated EULAR and ACR guidelines.

While the ACP does still consider T2S acceptable as a strategy for chronic gout management, Klionsky pointed out that those guidelines have not been updated recently. Specialists in the treatment of gout do not need any more evidence that the T2T approach leads to better outcomes.

However, she agreed with the principle that non-rheumatologists need to be reached with better guidance in regard to gout management. While she expects the ACP to endorse T2T the next time their guidelines are updated, she hopes that primary care physicians recognize that T2T should now be a standard.

“In a 10- to 20-minute visit, managing multiple chronic conditions can be a challenge in primary care,” Klionsky said. “Many clinicians rely on guidelines so it is important to have consistent and accurate information.”

There is currently some distance between specialists and primary care physicians regarding the goals of gout management, according to a study that Klionsky presented at EULAR 2024. In a survey, nonspecialists and specialists did not perceive treatment priorities in the same way.

In this survey, which elicited responses from 151 rheumatologists, 150 nephrologists, and 102 primary care physicians, there was general agreement that preventing flares is a priority, 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 a key step in reaching this goal.

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.

UPDATED July 8, 2024 // Editor's note: This article has been revised to give a more nuanced view from Yael Klionsky, MD, about the need for more accurate and consistent gout management guidelines for busy primary care clinicians who often rely on them in clinical practice.

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. 

Ted Bosworth/Medscape Medical News

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

According to Yael Klionsky, MD, a clinical assistant professor of rheumatology and immunology at Wake Forest University School of Medicine, Winston-Salem, North Carolina, these data are not a surprise. 

Even before this trial was completed, the message for clinicians is that they “should be focused on maintaining serum uric acid levels below physiological levels to improve outcomes” in patients with recurrent flares, said Klionsky, citing the validated EULAR and ACR guidelines.

While the ACP does still consider T2S acceptable as a strategy for chronic gout management, Klionsky pointed out that those guidelines have not been updated recently. Specialists in the treatment of gout do not need any more evidence that the T2T approach leads to better outcomes.

However, she agreed with the principle that non-rheumatologists need to be reached with better guidance in regard to gout management. While she expects the ACP to endorse T2T the next time their guidelines are updated, she hopes that primary care physicians recognize that T2T should now be a standard.

“In a 10- to 20-minute visit, managing multiple chronic conditions can be a challenge in primary care,” Klionsky said. “Many clinicians rely on guidelines so it is important to have consistent and accurate information.”

There is currently some distance between specialists and primary care physicians regarding the goals of gout management, according to a study that Klionsky presented at EULAR 2024. In a survey, nonspecialists and specialists did not perceive treatment priorities in the same way.

In this survey, which elicited responses from 151 rheumatologists, 150 nephrologists, and 102 primary care physicians, there was general agreement that preventing flares is a priority, 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 a key step in reaching this goal.

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.

UPDATED July 8, 2024 // Editor's note: This article has been revised to give a more nuanced view from Yael Klionsky, MD, about the need for more accurate and consistent gout management guidelines for busy primary care clinicians who often rely on them in clinical practice.

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. 

Ted Bosworth/Medscape Medical News

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

According to Yael Klionsky, MD, a clinical assistant professor of rheumatology and immunology at Wake Forest University School of Medicine, Winston-Salem, North Carolina, these data are not a surprise. 

Even before this trial was completed, the message for clinicians is that they “should be focused on maintaining serum uric acid levels below physiological levels to improve outcomes” in patients with recurrent flares, said Klionsky, citing the validated EULAR and ACR guidelines.

While the ACP does still consider T2S acceptable as a strategy for chronic gout management, Klionsky pointed out that those guidelines have not been updated recently. Specialists in the treatment of gout do not need any more evidence that the T2T approach leads to better outcomes.

However, she agreed with the principle that non-rheumatologists need to be reached with better guidance in regard to gout management. While she expects the ACP to endorse T2T the next time their guidelines are updated, she hopes that primary care physicians recognize that T2T should now be a standard.

“In a 10- to 20-minute visit, managing multiple chronic conditions can be a challenge in primary care,” Klionsky said. “Many clinicians rely on guidelines so it is important to have consistent and accurate information.”

There is currently some distance between specialists and primary care physicians regarding the goals of gout management, according to a study that Klionsky presented at EULAR 2024. In a survey, nonspecialists and specialists did not perceive treatment priorities in the same way.

In this survey, which elicited responses from 151 rheumatologists, 150 nephrologists, and 102 primary care physicians, there was general agreement that preventing flares is a priority, 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 a key step in reaching this goal.

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.