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Uric Acid Levels, Gout Symptoms Improved With Plant-Based Diet in Pilot Trial
A Mediterranean-inspired plant-based diet improved self-reported measures of gout as well as uric acid levels, a pilot study has found.
There hasn’t been a lot of research on diet in gout, according to Anna Kretova, RD, who presented the study at the annual research symposium of the Gout Hyperuricemia and Crystal-Associated Disease Network. She noted that a 2019 systematic review of low-calorie diets, low-purine diets, and Mediterranean diets found that uric acid levels below 0.6 mmol/L were achieved only in those on the Mediterranean diet (Nutrients. 2019 Dec 4;11[12]:2955). A 2020 study compared a low-fat, high-carbohydrate, plant-based diet vs an animal-based, ketogenic diet in healthy individuals. After 2 weeks, uric acid levels increased in those on the animal-based, low-carb diet and decreased in those on the plant-based diet.
Some foods are considered to be proinflammatory and generally come from animal origins, including saturated fats and animal protein in addition to ultraprocessed foods. Foods that have anti-inflammatory properties are mostly plant based and unprocessed and often rich in fiber. “From recent interventional studies, we also know that the whole-foods plant-based diet has shown to be effective as treatments of the main comorbidities of gout, such as obesity, cardiovascular disease, or [osteoarthritis],” said Kretova, who is a registered dietitian and a researcher at the Reade Rehabilitation and Rheumatology Center, Amsterdam, the Netherlands.
Those findings led the researchers to develop a whole-foods, plant-based diet and test its effect on serum uric acid in patients with gout, as well as gout disease activity and cardiovascular disease risk. Participants could not eat meat, fish, eggs, or dairy.
The trial included 33 individuals with gout who were randomized to a 16-week intervention with five consultations with a registered dietitian (n = 18) or a wait-list control group (n = 15) who received standard care. The mean age overall was 52 years, and 91% were men. The mean body mass index (BMI) was 32.6 kg/m2, and the median uric acid level was 0.50 mmol/L (8.4 mg/dL).
Among gout-related outcomes, the researchers noted improvements in gout severity as measured by visual analog scale (VAS; between group difference, –2.0; P =.01), pain as measured by VAS (between group difference, –2.0; P =.04), and uric acid levels after adjustment for age, sex, and BMI (between group difference, –0.05 mmol/L, P =.004). There were also improvements in the intervention group in weight loss (between group difference, –5.3 kg; P <.0001), BMI (between group difference, –1.7; P < .0001), waist circumference (between group difference, –3.9 cm; P = .004), and low-density lipoprotein (LDL) cholesterol (between group difference, –0.5; P = .007).
At 16 weeks, “we concluded that a Mediterranean-inspired whole-foods, plant-based diet significantly lowers serum uric acid in patients with gout and abdominal obesity, and additionally, the diet reduces gout-related pain and disease activity, promotes substantial weight loss, decreases weight circumference, and improves LDL cholesterol levels, and thus decreases [cardiovascular disease] risk in these patients,” Kretova said.
She added that some might question whether a uric acid reduction of –0.05 mmol/L is clinically relevant. “We would argue it is because of the strong decrease in disease activity and pain in the intervention group,” Kretova said.
The study is limited by its small size, the fact that it was not blinded, and the 4-month duration, which might be too short to capture potential indirect effects of diet on hyperuricemia and chronic inflammation, Kretova said. The group is planning to follow participants out to 12 months in an extension study.
During the Q&A session after the presentation, an audience member asked if the participants were vegetarians before they entered the study, and whether the dietary change could be sustained. “It’s a very good proof-of-concept study, but whether an intervention based entirely on plant-based therapy will be something that patients will be able to adhere to long term [is uncertain],” Kretova said.
She was optimistic, even though the participants generally enjoyed food and ate a lot of red meat. “I think there will be a gradation of people who can sustain and who cannot sustain [the diet]. From what we saw, people actually found it easier to follow than they expected, and a lot of participants changed their diet permanently for the better. Not everyone became [entirely] plant-based, but they became much more plant-based than they expected from themselves. So, it is definitely feasible,” she said.
Kretova reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
A Mediterranean-inspired plant-based diet improved self-reported measures of gout as well as uric acid levels, a pilot study has found.
There hasn’t been a lot of research on diet in gout, according to Anna Kretova, RD, who presented the study at the annual research symposium of the Gout Hyperuricemia and Crystal-Associated Disease Network. She noted that a 2019 systematic review of low-calorie diets, low-purine diets, and Mediterranean diets found that uric acid levels below 0.6 mmol/L were achieved only in those on the Mediterranean diet (Nutrients. 2019 Dec 4;11[12]:2955). A 2020 study compared a low-fat, high-carbohydrate, plant-based diet vs an animal-based, ketogenic diet in healthy individuals. After 2 weeks, uric acid levels increased in those on the animal-based, low-carb diet and decreased in those on the plant-based diet.
Some foods are considered to be proinflammatory and generally come from animal origins, including saturated fats and animal protein in addition to ultraprocessed foods. Foods that have anti-inflammatory properties are mostly plant based and unprocessed and often rich in fiber. “From recent interventional studies, we also know that the whole-foods plant-based diet has shown to be effective as treatments of the main comorbidities of gout, such as obesity, cardiovascular disease, or [osteoarthritis],” said Kretova, who is a registered dietitian and a researcher at the Reade Rehabilitation and Rheumatology Center, Amsterdam, the Netherlands.
Those findings led the researchers to develop a whole-foods, plant-based diet and test its effect on serum uric acid in patients with gout, as well as gout disease activity and cardiovascular disease risk. Participants could not eat meat, fish, eggs, or dairy.
The trial included 33 individuals with gout who were randomized to a 16-week intervention with five consultations with a registered dietitian (n = 18) or a wait-list control group (n = 15) who received standard care. The mean age overall was 52 years, and 91% were men. The mean body mass index (BMI) was 32.6 kg/m2, and the median uric acid level was 0.50 mmol/L (8.4 mg/dL).
Among gout-related outcomes, the researchers noted improvements in gout severity as measured by visual analog scale (VAS; between group difference, –2.0; P =.01), pain as measured by VAS (between group difference, –2.0; P =.04), and uric acid levels after adjustment for age, sex, and BMI (between group difference, –0.05 mmol/L, P =.004). There were also improvements in the intervention group in weight loss (between group difference, –5.3 kg; P <.0001), BMI (between group difference, –1.7; P < .0001), waist circumference (between group difference, –3.9 cm; P = .004), and low-density lipoprotein (LDL) cholesterol (between group difference, –0.5; P = .007).
At 16 weeks, “we concluded that a Mediterranean-inspired whole-foods, plant-based diet significantly lowers serum uric acid in patients with gout and abdominal obesity, and additionally, the diet reduces gout-related pain and disease activity, promotes substantial weight loss, decreases weight circumference, and improves LDL cholesterol levels, and thus decreases [cardiovascular disease] risk in these patients,” Kretova said.
She added that some might question whether a uric acid reduction of –0.05 mmol/L is clinically relevant. “We would argue it is because of the strong decrease in disease activity and pain in the intervention group,” Kretova said.
The study is limited by its small size, the fact that it was not blinded, and the 4-month duration, which might be too short to capture potential indirect effects of diet on hyperuricemia and chronic inflammation, Kretova said. The group is planning to follow participants out to 12 months in an extension study.
During the Q&A session after the presentation, an audience member asked if the participants were vegetarians before they entered the study, and whether the dietary change could be sustained. “It’s a very good proof-of-concept study, but whether an intervention based entirely on plant-based therapy will be something that patients will be able to adhere to long term [is uncertain],” Kretova said.
She was optimistic, even though the participants generally enjoyed food and ate a lot of red meat. “I think there will be a gradation of people who can sustain and who cannot sustain [the diet]. From what we saw, people actually found it easier to follow than they expected, and a lot of participants changed their diet permanently for the better. Not everyone became [entirely] plant-based, but they became much more plant-based than they expected from themselves. So, it is definitely feasible,” she said.
Kretova reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
A Mediterranean-inspired plant-based diet improved self-reported measures of gout as well as uric acid levels, a pilot study has found.
There hasn’t been a lot of research on diet in gout, according to Anna Kretova, RD, who presented the study at the annual research symposium of the Gout Hyperuricemia and Crystal-Associated Disease Network. She noted that a 2019 systematic review of low-calorie diets, low-purine diets, and Mediterranean diets found that uric acid levels below 0.6 mmol/L were achieved only in those on the Mediterranean diet (Nutrients. 2019 Dec 4;11[12]:2955). A 2020 study compared a low-fat, high-carbohydrate, plant-based diet vs an animal-based, ketogenic diet in healthy individuals. After 2 weeks, uric acid levels increased in those on the animal-based, low-carb diet and decreased in those on the plant-based diet.
Some foods are considered to be proinflammatory and generally come from animal origins, including saturated fats and animal protein in addition to ultraprocessed foods. Foods that have anti-inflammatory properties are mostly plant based and unprocessed and often rich in fiber. “From recent interventional studies, we also know that the whole-foods plant-based diet has shown to be effective as treatments of the main comorbidities of gout, such as obesity, cardiovascular disease, or [osteoarthritis],” said Kretova, who is a registered dietitian and a researcher at the Reade Rehabilitation and Rheumatology Center, Amsterdam, the Netherlands.
Those findings led the researchers to develop a whole-foods, plant-based diet and test its effect on serum uric acid in patients with gout, as well as gout disease activity and cardiovascular disease risk. Participants could not eat meat, fish, eggs, or dairy.
The trial included 33 individuals with gout who were randomized to a 16-week intervention with five consultations with a registered dietitian (n = 18) or a wait-list control group (n = 15) who received standard care. The mean age overall was 52 years, and 91% were men. The mean body mass index (BMI) was 32.6 kg/m2, and the median uric acid level was 0.50 mmol/L (8.4 mg/dL).
Among gout-related outcomes, the researchers noted improvements in gout severity as measured by visual analog scale (VAS; between group difference, –2.0; P =.01), pain as measured by VAS (between group difference, –2.0; P =.04), and uric acid levels after adjustment for age, sex, and BMI (between group difference, –0.05 mmol/L, P =.004). There were also improvements in the intervention group in weight loss (between group difference, –5.3 kg; P <.0001), BMI (between group difference, –1.7; P < .0001), waist circumference (between group difference, –3.9 cm; P = .004), and low-density lipoprotein (LDL) cholesterol (between group difference, –0.5; P = .007).
At 16 weeks, “we concluded that a Mediterranean-inspired whole-foods, plant-based diet significantly lowers serum uric acid in patients with gout and abdominal obesity, and additionally, the diet reduces gout-related pain and disease activity, promotes substantial weight loss, decreases weight circumference, and improves LDL cholesterol levels, and thus decreases [cardiovascular disease] risk in these patients,” Kretova said.
She added that some might question whether a uric acid reduction of –0.05 mmol/L is clinically relevant. “We would argue it is because of the strong decrease in disease activity and pain in the intervention group,” Kretova said.
The study is limited by its small size, the fact that it was not blinded, and the 4-month duration, which might be too short to capture potential indirect effects of diet on hyperuricemia and chronic inflammation, Kretova said. The group is planning to follow participants out to 12 months in an extension study.
During the Q&A session after the presentation, an audience member asked if the participants were vegetarians before they entered the study, and whether the dietary change could be sustained. “It’s a very good proof-of-concept study, but whether an intervention based entirely on plant-based therapy will be something that patients will be able to adhere to long term [is uncertain],” Kretova said.
She was optimistic, even though the participants generally enjoyed food and ate a lot of red meat. “I think there will be a gradation of people who can sustain and who cannot sustain [the diet]. From what we saw, people actually found it easier to follow than they expected, and a lot of participants changed their diet permanently for the better. Not everyone became [entirely] plant-based, but they became much more plant-based than they expected from themselves. So, it is definitely feasible,” she said.
Kretova reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
FROM G-CAN 2024
New Gout Remission Criteria Approved
In a nearly unanimous vote at the annual research symposium of the Gout Hyperuricemia and Crystal-Associated Disease Network (G-CAN), members approved a revision to gout remission criteria first established in 2016. The new version simplifies the definition in response to patient comments that the earlier version was redundant in some areas.
The previous version was developed following deliberations by 49 clinicians and researchers with experience in gout. They settled on a definition of gout remission that included five criteria:
- Serum urate levels lower than 0.36 mmol/L measured at least twice over 12 months, with no intervening values of 0.36 mmol/L or higher
- No gout flares over 12 months
- No tophi
- Pain score due to gout < 2 at least twice over 12 months on a 10-point Likert scale or 10-cm visual analog scale, with no intervening values ≥ 2
- Patient global assessment of gout disease activity < 2 on a 10-point Likert scale or 10-cm visual analog scale, with no intervening values of ≥ 2.
Some participants reported that patients sometimes misattributed pain from other sources while using patient-reported outcomes (PROs). The argument for keeping PROs was that they are validated measures and endorsed by Outcome Measures in Rheumatology. Nevertheless, there was no direct patient involvement in the development of the 2016 criteria.
Researchers later interviewed 20 individuals with well-controlled gout to get their feedback on the 2016 criteria. Those individuals endorsed the existing criteria and did not suggest any new ones, but they suggested that the pain due to gout and the absence of gout flares were redundant measures. One said: “If you have no flare-ups, you’ve got no pain; it sort of answers itself.”
“That was a bit challenging for us because it wasn’t quite what we expected, but I think it did make us look again at the definition and think about whether we could simplify the definition further,” Nicola Dalbeth, MBChB, said during a presentation at G-CAN. Dalbeth is an academic rheumatologist at the University of Auckland, in New Zealand, who was also the lead author of the original criteria.
Simplified Version Created With Only Three Criteria
In response to these points, researchers produced a revised version with only three criteria, including the serum urate, absence of gout flares, and absence of subcutaneous tophi at the time of assessment.
To determine if the simplified criteria performed well, they compared the original and revised remission criteria in the context of the CARES trial, the Nottingham nurse-led trial, and randomized controlled trials in patients with gout that were conducted in New Zealand (here and here).
Dansoa Tabi-Amponsah, a PhD candidate at the University of Auckland, presented results of a study comparing the two versions in the Nottingham trial, which included 517 participants who received nurse-led or usual general practitioner care. The nurse-led care included education, regular follow-up and serum urate testing, individualized advice on gout flare management, and escalation of urate-lowering therapy with a treat-to-target strategy.
Both definitions demonstrated a link between the nurse-led strategy and increased rates of remission at year 1 and year 2, although the simplified definition found that more patients were in remission (17.6% vs 9.9% at year 1 and 42.7% vs 28.4% at year 2, both P < .001). “This is something we’ve seen across all of our analyses,” said Tabi-Amponsah.
Both criteria also found significant differences in remission rates between the nurse-led group in year 2 vs year 1 but not in the usual care group.
Participants who achieved remission had better gout impact scale scores in areas like worrying that a gout attack will occur, fears of worsening gout, and concerns about the impact of gout on future activities. “This is important because during that qualitative study, a key aspect of being in remission was no longer being worried about their gout, no longer feeling anxious about having constant gout flares, and having control over their gout. So, it’s important to note that despite the absence of PROs in that simplified definition, it’s still able to align with the patients’ perspectives of their disease state,” said Tabi-Amponsah.
During the Q&A period after her talk, an audience member asked whether the higher rate of remission found by the simplified criteria is actually a good thing. “If I compare that to rheumatoid arthritis, when you use DAS28 you have a lot more remission, but still progression. So, are we missing some people? Are we including people in remission that still have disease?” she asked.
Tabi-Amponsah responded that the pain and patient global assessment domains seem to be quite difficult to achieve. In a separate analysis, the researchers examined tender and swollen joint counts and found that those achieving remission no longer had tender or swollen joints. “So, we don’t think the simplified definition is heavily misclassifying anyone as being in remission,” she said.
During the Q&A following Dalbeth’s talk, an audience member asked about patients with what he described as “mountains of tophi,” despite responding well to uricase therapy. “They may take months or even a year to really resolve that burden. They may be doing very well, yet they’re not going to be in remission because they’ve still got visible tophi. So, are we underselling them, and do we need a different definition for them doing well that this doesn’t capture?” he asked.
Dalbeth suggested that patients with large amounts of tophi aren’t really in remission. “I think we do need to be thinking about the disease, not just in terms of just crystals or just inflammation, but actually trying to integrate both of those, and I think this is where these composite measures might work quite well. I think we need to be aiming for holistic disease control, which is essentially what this is,” she said.
Tabi-Amponsah and Dalbeth did not disclose any financial relationships.
A version of this article appeared on Medscape.com.
In a nearly unanimous vote at the annual research symposium of the Gout Hyperuricemia and Crystal-Associated Disease Network (G-CAN), members approved a revision to gout remission criteria first established in 2016. The new version simplifies the definition in response to patient comments that the earlier version was redundant in some areas.
The previous version was developed following deliberations by 49 clinicians and researchers with experience in gout. They settled on a definition of gout remission that included five criteria:
- Serum urate levels lower than 0.36 mmol/L measured at least twice over 12 months, with no intervening values of 0.36 mmol/L or higher
- No gout flares over 12 months
- No tophi
- Pain score due to gout < 2 at least twice over 12 months on a 10-point Likert scale or 10-cm visual analog scale, with no intervening values ≥ 2
- Patient global assessment of gout disease activity < 2 on a 10-point Likert scale or 10-cm visual analog scale, with no intervening values of ≥ 2.
Some participants reported that patients sometimes misattributed pain from other sources while using patient-reported outcomes (PROs). The argument for keeping PROs was that they are validated measures and endorsed by Outcome Measures in Rheumatology. Nevertheless, there was no direct patient involvement in the development of the 2016 criteria.
Researchers later interviewed 20 individuals with well-controlled gout to get their feedback on the 2016 criteria. Those individuals endorsed the existing criteria and did not suggest any new ones, but they suggested that the pain due to gout and the absence of gout flares were redundant measures. One said: “If you have no flare-ups, you’ve got no pain; it sort of answers itself.”
“That was a bit challenging for us because it wasn’t quite what we expected, but I think it did make us look again at the definition and think about whether we could simplify the definition further,” Nicola Dalbeth, MBChB, said during a presentation at G-CAN. Dalbeth is an academic rheumatologist at the University of Auckland, in New Zealand, who was also the lead author of the original criteria.
Simplified Version Created With Only Three Criteria
In response to these points, researchers produced a revised version with only three criteria, including the serum urate, absence of gout flares, and absence of subcutaneous tophi at the time of assessment.
To determine if the simplified criteria performed well, they compared the original and revised remission criteria in the context of the CARES trial, the Nottingham nurse-led trial, and randomized controlled trials in patients with gout that were conducted in New Zealand (here and here).
Dansoa Tabi-Amponsah, a PhD candidate at the University of Auckland, presented results of a study comparing the two versions in the Nottingham trial, which included 517 participants who received nurse-led or usual general practitioner care. The nurse-led care included education, regular follow-up and serum urate testing, individualized advice on gout flare management, and escalation of urate-lowering therapy with a treat-to-target strategy.
Both definitions demonstrated a link between the nurse-led strategy and increased rates of remission at year 1 and year 2, although the simplified definition found that more patients were in remission (17.6% vs 9.9% at year 1 and 42.7% vs 28.4% at year 2, both P < .001). “This is something we’ve seen across all of our analyses,” said Tabi-Amponsah.
Both criteria also found significant differences in remission rates between the nurse-led group in year 2 vs year 1 but not in the usual care group.
Participants who achieved remission had better gout impact scale scores in areas like worrying that a gout attack will occur, fears of worsening gout, and concerns about the impact of gout on future activities. “This is important because during that qualitative study, a key aspect of being in remission was no longer being worried about their gout, no longer feeling anxious about having constant gout flares, and having control over their gout. So, it’s important to note that despite the absence of PROs in that simplified definition, it’s still able to align with the patients’ perspectives of their disease state,” said Tabi-Amponsah.
During the Q&A period after her talk, an audience member asked whether the higher rate of remission found by the simplified criteria is actually a good thing. “If I compare that to rheumatoid arthritis, when you use DAS28 you have a lot more remission, but still progression. So, are we missing some people? Are we including people in remission that still have disease?” she asked.
Tabi-Amponsah responded that the pain and patient global assessment domains seem to be quite difficult to achieve. In a separate analysis, the researchers examined tender and swollen joint counts and found that those achieving remission no longer had tender or swollen joints. “So, we don’t think the simplified definition is heavily misclassifying anyone as being in remission,” she said.
During the Q&A following Dalbeth’s talk, an audience member asked about patients with what he described as “mountains of tophi,” despite responding well to uricase therapy. “They may take months or even a year to really resolve that burden. They may be doing very well, yet they’re not going to be in remission because they’ve still got visible tophi. So, are we underselling them, and do we need a different definition for them doing well that this doesn’t capture?” he asked.
Dalbeth suggested that patients with large amounts of tophi aren’t really in remission. “I think we do need to be thinking about the disease, not just in terms of just crystals or just inflammation, but actually trying to integrate both of those, and I think this is where these composite measures might work quite well. I think we need to be aiming for holistic disease control, which is essentially what this is,” she said.
Tabi-Amponsah and Dalbeth did not disclose any financial relationships.
A version of this article appeared on Medscape.com.
In a nearly unanimous vote at the annual research symposium of the Gout Hyperuricemia and Crystal-Associated Disease Network (G-CAN), members approved a revision to gout remission criteria first established in 2016. The new version simplifies the definition in response to patient comments that the earlier version was redundant in some areas.
The previous version was developed following deliberations by 49 clinicians and researchers with experience in gout. They settled on a definition of gout remission that included five criteria:
- Serum urate levels lower than 0.36 mmol/L measured at least twice over 12 months, with no intervening values of 0.36 mmol/L or higher
- No gout flares over 12 months
- No tophi
- Pain score due to gout < 2 at least twice over 12 months on a 10-point Likert scale or 10-cm visual analog scale, with no intervening values ≥ 2
- Patient global assessment of gout disease activity < 2 on a 10-point Likert scale or 10-cm visual analog scale, with no intervening values of ≥ 2.
Some participants reported that patients sometimes misattributed pain from other sources while using patient-reported outcomes (PROs). The argument for keeping PROs was that they are validated measures and endorsed by Outcome Measures in Rheumatology. Nevertheless, there was no direct patient involvement in the development of the 2016 criteria.
Researchers later interviewed 20 individuals with well-controlled gout to get their feedback on the 2016 criteria. Those individuals endorsed the existing criteria and did not suggest any new ones, but they suggested that the pain due to gout and the absence of gout flares were redundant measures. One said: “If you have no flare-ups, you’ve got no pain; it sort of answers itself.”
“That was a bit challenging for us because it wasn’t quite what we expected, but I think it did make us look again at the definition and think about whether we could simplify the definition further,” Nicola Dalbeth, MBChB, said during a presentation at G-CAN. Dalbeth is an academic rheumatologist at the University of Auckland, in New Zealand, who was also the lead author of the original criteria.
Simplified Version Created With Only Three Criteria
In response to these points, researchers produced a revised version with only three criteria, including the serum urate, absence of gout flares, and absence of subcutaneous tophi at the time of assessment.
To determine if the simplified criteria performed well, they compared the original and revised remission criteria in the context of the CARES trial, the Nottingham nurse-led trial, and randomized controlled trials in patients with gout that were conducted in New Zealand (here and here).
Dansoa Tabi-Amponsah, a PhD candidate at the University of Auckland, presented results of a study comparing the two versions in the Nottingham trial, which included 517 participants who received nurse-led or usual general practitioner care. The nurse-led care included education, regular follow-up and serum urate testing, individualized advice on gout flare management, and escalation of urate-lowering therapy with a treat-to-target strategy.
Both definitions demonstrated a link between the nurse-led strategy and increased rates of remission at year 1 and year 2, although the simplified definition found that more patients were in remission (17.6% vs 9.9% at year 1 and 42.7% vs 28.4% at year 2, both P < .001). “This is something we’ve seen across all of our analyses,” said Tabi-Amponsah.
Both criteria also found significant differences in remission rates between the nurse-led group in year 2 vs year 1 but not in the usual care group.
Participants who achieved remission had better gout impact scale scores in areas like worrying that a gout attack will occur, fears of worsening gout, and concerns about the impact of gout on future activities. “This is important because during that qualitative study, a key aspect of being in remission was no longer being worried about their gout, no longer feeling anxious about having constant gout flares, and having control over their gout. So, it’s important to note that despite the absence of PROs in that simplified definition, it’s still able to align with the patients’ perspectives of their disease state,” said Tabi-Amponsah.
During the Q&A period after her talk, an audience member asked whether the higher rate of remission found by the simplified criteria is actually a good thing. “If I compare that to rheumatoid arthritis, when you use DAS28 you have a lot more remission, but still progression. So, are we missing some people? Are we including people in remission that still have disease?” she asked.
Tabi-Amponsah responded that the pain and patient global assessment domains seem to be quite difficult to achieve. In a separate analysis, the researchers examined tender and swollen joint counts and found that those achieving remission no longer had tender or swollen joints. “So, we don’t think the simplified definition is heavily misclassifying anyone as being in remission,” she said.
During the Q&A following Dalbeth’s talk, an audience member asked about patients with what he described as “mountains of tophi,” despite responding well to uricase therapy. “They may take months or even a year to really resolve that burden. They may be doing very well, yet they’re not going to be in remission because they’ve still got visible tophi. So, are we underselling them, and do we need a different definition for them doing well that this doesn’t capture?” he asked.
Dalbeth suggested that patients with large amounts of tophi aren’t really in remission. “I think we do need to be thinking about the disease, not just in terms of just crystals or just inflammation, but actually trying to integrate both of those, and I think this is where these composite measures might work quite well. I think we need to be aiming for holistic disease control, which is essentially what this is,” she said.
Tabi-Amponsah and Dalbeth did not disclose any financial relationships.
A version of this article appeared on Medscape.com.
FROM G-CAN 2024
Could Probiotics Tuned to Reduce Intestinal Urate Counter Gout?
Efforts to combat hyperuricemia may find help from gut microbes, according to Dylan Dodd, MD, PhD, who spoke at the annual research symposium of the Gout, Hyperuricemia, and Crystal-Associated Disease Network.
Dodd is an assistant professor of pathology and microbiology and immunology at Stanford University, Palo Alto, California, where he studies novel metabolic pathways in microbes. “The idea is that we can leverage these novel pathways that microbes have as therapeutics to promote human health, and in particular for this meeting today, we’re focused on hyperuricemia and how microbes that break down purines may actually have a role as urate-lowering therapies,” Dodd said during his presentation.
Specifically, he highlighted the fact that some microbes found in the gut break down purines as a food source, producing both energy and molecular building blocks for their own use. Dietary purines, left intact, can otherwise be absorbed and metabolized by the body to produce urate.
Nucleic acids like DNA and RNA in the diet are first broken down by enzymes produced in the pancreas, resulting in purine nucleosides, which in turn are believed to be the source of purines absorbed in the small intestine and eventually into circulation, according to Dodd. “I really view urate in the intestine as being in equilibrium between being secreted into the lumen but also being reabsorbed, and specifically, as it pertains to microbes in the gut. If the microbes degrade the urate, then it will limit its reabsorption, and that could increase net excretion,” Dodd said.
There is evidence that some strains of Lactobacillus species, which are the most important group in the human gut, can metabolize purine nucleosides, he said. In recent years, researchers have screened for Lactobacillus species capable of metabolizing purine nucleosides. The research shows some strain-to-strain variation, but most are proprietary, making it impossible to conduct follow-up research. A small number of human trials have suggested efficacy, but they have generally been conducted in few patients with mixed results. “Overall, I think it’s promising that these lactobacilli probiotics could potentially be used as urate-lowering therapies,” Dodd said.
Aside from direct metabolism of purines, Dodd’s group has identified an additional pathway that some microbes can use to break down urate into short-chain fatty acids. His group cultured various purine nucleosides with various bacterial strains, including two Lactobacillus strains, under anaerobic conditions. The Lactobacillus strains did not degrade urate, but some bacterial species did. The group also found that Lactobacillus could convert nucleosides, including those derived from purines, into the smaller nucleobase compounds, but they did not consume the resultant purines. Some other types of bacteria consumed all purines “voraciously,” according to Dodd, and his team is working to identify the bacterial genetic pathways that drive the metabolic pathways.
Such studies may open up various therapeutic pathways, he said. One is to employ Lactobacillus probiotics to convert purine nucleosides to their nucleobases, which could reduce absorption in the small intestine. Other bacteria could potentially be used to convert urate produced by paracellular reabsorption to short-chain fatty acids, which have potential benefits through their anti-inflammatory properties. Finally, probiotics could be engineered to degrade urate produced in the intestine.
Dodd noted that probiotics would have the advantage of high patient acceptance and are generally regarded as safe. Some existing products might have purine-degrading capabilities but haven’t been tested, he said. However, there is strain-to-strain variation and the probiotic formulas would likely need to be optimized to reduce nucleobases. On the other hand, bacteria that degrade urate are likely safe since they have been found in the guts of healthy individuals. However, there are still potential safety concerns, and it is unknown if they could withstand the harsh conditions of the upper gastrointestinal tract or if they would remain active even in the presence of oxygen found in the small intestine, he said.
During the Q&A period after his talk, Dodd was asked whether fructose consumption could suppress the function of anaerobic bacteria that naturally degrade purine. “When people talk about fructose-induced hyperuricemia, they talk about the ATP degradation in fructose metabolism in the liver or small intestine, [but] they never talk about this potential pathway in the gut,” the questioner said.
Dodd responded that his group found that some carbohydrates suppress urate degradation in some bacterial strains. “It’s certainly a possible mechanism that increased fructose intake could suppress microbial urate degradation in the gut, and that could contribute to hyperuricemia, but obviously more studies need to be done,” he said.
Another audience member wondered if antibiotic use could be tied to gout risk and whether serum urate levels might rise after antibiotic use. “Do you have any data on serum urate before and after antibiotic use, where you might expect to see changes which might support your hypothesis?” she asked. Dodd said that the group had done a retrospective analysis of data from Stanford’s medical records and did not find a change in serum urate after antibiotic exposure. However, a controlled feeding study of healthy individuals who later received antibiotics showed a large increase in urate levels, but the study did not include plasma samples. “It’s a really good question, and we hope to be able to follow that up,” he said.
Dodd disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Efforts to combat hyperuricemia may find help from gut microbes, according to Dylan Dodd, MD, PhD, who spoke at the annual research symposium of the Gout, Hyperuricemia, and Crystal-Associated Disease Network.
Dodd is an assistant professor of pathology and microbiology and immunology at Stanford University, Palo Alto, California, where he studies novel metabolic pathways in microbes. “The idea is that we can leverage these novel pathways that microbes have as therapeutics to promote human health, and in particular for this meeting today, we’re focused on hyperuricemia and how microbes that break down purines may actually have a role as urate-lowering therapies,” Dodd said during his presentation.
Specifically, he highlighted the fact that some microbes found in the gut break down purines as a food source, producing both energy and molecular building blocks for their own use. Dietary purines, left intact, can otherwise be absorbed and metabolized by the body to produce urate.
Nucleic acids like DNA and RNA in the diet are first broken down by enzymes produced in the pancreas, resulting in purine nucleosides, which in turn are believed to be the source of purines absorbed in the small intestine and eventually into circulation, according to Dodd. “I really view urate in the intestine as being in equilibrium between being secreted into the lumen but also being reabsorbed, and specifically, as it pertains to microbes in the gut. If the microbes degrade the urate, then it will limit its reabsorption, and that could increase net excretion,” Dodd said.
There is evidence that some strains of Lactobacillus species, which are the most important group in the human gut, can metabolize purine nucleosides, he said. In recent years, researchers have screened for Lactobacillus species capable of metabolizing purine nucleosides. The research shows some strain-to-strain variation, but most are proprietary, making it impossible to conduct follow-up research. A small number of human trials have suggested efficacy, but they have generally been conducted in few patients with mixed results. “Overall, I think it’s promising that these lactobacilli probiotics could potentially be used as urate-lowering therapies,” Dodd said.
Aside from direct metabolism of purines, Dodd’s group has identified an additional pathway that some microbes can use to break down urate into short-chain fatty acids. His group cultured various purine nucleosides with various bacterial strains, including two Lactobacillus strains, under anaerobic conditions. The Lactobacillus strains did not degrade urate, but some bacterial species did. The group also found that Lactobacillus could convert nucleosides, including those derived from purines, into the smaller nucleobase compounds, but they did not consume the resultant purines. Some other types of bacteria consumed all purines “voraciously,” according to Dodd, and his team is working to identify the bacterial genetic pathways that drive the metabolic pathways.
Such studies may open up various therapeutic pathways, he said. One is to employ Lactobacillus probiotics to convert purine nucleosides to their nucleobases, which could reduce absorption in the small intestine. Other bacteria could potentially be used to convert urate produced by paracellular reabsorption to short-chain fatty acids, which have potential benefits through their anti-inflammatory properties. Finally, probiotics could be engineered to degrade urate produced in the intestine.
Dodd noted that probiotics would have the advantage of high patient acceptance and are generally regarded as safe. Some existing products might have purine-degrading capabilities but haven’t been tested, he said. However, there is strain-to-strain variation and the probiotic formulas would likely need to be optimized to reduce nucleobases. On the other hand, bacteria that degrade urate are likely safe since they have been found in the guts of healthy individuals. However, there are still potential safety concerns, and it is unknown if they could withstand the harsh conditions of the upper gastrointestinal tract or if they would remain active even in the presence of oxygen found in the small intestine, he said.
During the Q&A period after his talk, Dodd was asked whether fructose consumption could suppress the function of anaerobic bacteria that naturally degrade purine. “When people talk about fructose-induced hyperuricemia, they talk about the ATP degradation in fructose metabolism in the liver or small intestine, [but] they never talk about this potential pathway in the gut,” the questioner said.
Dodd responded that his group found that some carbohydrates suppress urate degradation in some bacterial strains. “It’s certainly a possible mechanism that increased fructose intake could suppress microbial urate degradation in the gut, and that could contribute to hyperuricemia, but obviously more studies need to be done,” he said.
Another audience member wondered if antibiotic use could be tied to gout risk and whether serum urate levels might rise after antibiotic use. “Do you have any data on serum urate before and after antibiotic use, where you might expect to see changes which might support your hypothesis?” she asked. Dodd said that the group had done a retrospective analysis of data from Stanford’s medical records and did not find a change in serum urate after antibiotic exposure. However, a controlled feeding study of healthy individuals who later received antibiotics showed a large increase in urate levels, but the study did not include plasma samples. “It’s a really good question, and we hope to be able to follow that up,” he said.
Dodd disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Efforts to combat hyperuricemia may find help from gut microbes, according to Dylan Dodd, MD, PhD, who spoke at the annual research symposium of the Gout, Hyperuricemia, and Crystal-Associated Disease Network.
Dodd is an assistant professor of pathology and microbiology and immunology at Stanford University, Palo Alto, California, where he studies novel metabolic pathways in microbes. “The idea is that we can leverage these novel pathways that microbes have as therapeutics to promote human health, and in particular for this meeting today, we’re focused on hyperuricemia and how microbes that break down purines may actually have a role as urate-lowering therapies,” Dodd said during his presentation.
Specifically, he highlighted the fact that some microbes found in the gut break down purines as a food source, producing both energy and molecular building blocks for their own use. Dietary purines, left intact, can otherwise be absorbed and metabolized by the body to produce urate.
Nucleic acids like DNA and RNA in the diet are first broken down by enzymes produced in the pancreas, resulting in purine nucleosides, which in turn are believed to be the source of purines absorbed in the small intestine and eventually into circulation, according to Dodd. “I really view urate in the intestine as being in equilibrium between being secreted into the lumen but also being reabsorbed, and specifically, as it pertains to microbes in the gut. If the microbes degrade the urate, then it will limit its reabsorption, and that could increase net excretion,” Dodd said.
There is evidence that some strains of Lactobacillus species, which are the most important group in the human gut, can metabolize purine nucleosides, he said. In recent years, researchers have screened for Lactobacillus species capable of metabolizing purine nucleosides. The research shows some strain-to-strain variation, but most are proprietary, making it impossible to conduct follow-up research. A small number of human trials have suggested efficacy, but they have generally been conducted in few patients with mixed results. “Overall, I think it’s promising that these lactobacilli probiotics could potentially be used as urate-lowering therapies,” Dodd said.
Aside from direct metabolism of purines, Dodd’s group has identified an additional pathway that some microbes can use to break down urate into short-chain fatty acids. His group cultured various purine nucleosides with various bacterial strains, including two Lactobacillus strains, under anaerobic conditions. The Lactobacillus strains did not degrade urate, but some bacterial species did. The group also found that Lactobacillus could convert nucleosides, including those derived from purines, into the smaller nucleobase compounds, but they did not consume the resultant purines. Some other types of bacteria consumed all purines “voraciously,” according to Dodd, and his team is working to identify the bacterial genetic pathways that drive the metabolic pathways.
Such studies may open up various therapeutic pathways, he said. One is to employ Lactobacillus probiotics to convert purine nucleosides to their nucleobases, which could reduce absorption in the small intestine. Other bacteria could potentially be used to convert urate produced by paracellular reabsorption to short-chain fatty acids, which have potential benefits through their anti-inflammatory properties. Finally, probiotics could be engineered to degrade urate produced in the intestine.
Dodd noted that probiotics would have the advantage of high patient acceptance and are generally regarded as safe. Some existing products might have purine-degrading capabilities but haven’t been tested, he said. However, there is strain-to-strain variation and the probiotic formulas would likely need to be optimized to reduce nucleobases. On the other hand, bacteria that degrade urate are likely safe since they have been found in the guts of healthy individuals. However, there are still potential safety concerns, and it is unknown if they could withstand the harsh conditions of the upper gastrointestinal tract or if they would remain active even in the presence of oxygen found in the small intestine, he said.
During the Q&A period after his talk, Dodd was asked whether fructose consumption could suppress the function of anaerobic bacteria that naturally degrade purine. “When people talk about fructose-induced hyperuricemia, they talk about the ATP degradation in fructose metabolism in the liver or small intestine, [but] they never talk about this potential pathway in the gut,” the questioner said.
Dodd responded that his group found that some carbohydrates suppress urate degradation in some bacterial strains. “It’s certainly a possible mechanism that increased fructose intake could suppress microbial urate degradation in the gut, and that could contribute to hyperuricemia, but obviously more studies need to be done,” he said.
Another audience member wondered if antibiotic use could be tied to gout risk and whether serum urate levels might rise after antibiotic use. “Do you have any data on serum urate before and after antibiotic use, where you might expect to see changes which might support your hypothesis?” she asked. Dodd said that the group had done a retrospective analysis of data from Stanford’s medical records and did not find a change in serum urate after antibiotic exposure. However, a controlled feeding study of healthy individuals who later received antibiotics showed a large increase in urate levels, but the study did not include plasma samples. “It’s a really good question, and we hope to be able to follow that up,” he said.
Dodd disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
FROM G-CAN 2024
Gout and SGLT2 Inhibitors: Evidence Points to Reduced Need for ULT, Flare Drugs
WASHINGTON — Use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) reduced the need for urate-lowering therapy (ULT) and gout flare therapies in people who had both type 2 diabetes (T2D) and gout, new research has found.
Data from a large US claims database showed that SGLT2i use was associated with a 31% lower rate of initiation of ULT. “This provides further support for the use of SLGT2i therapy in patients with gout, particularly those with high-risk multimorbidity and polypharmacy,” Greg Challener, MD, a postdoctoral fellow at the Rheumatology and Allergy Clinical Epidemiology Research Center, Massachusetts General Hospital, Boston, said in his presentation of the data at the annual meeting of the American College of Rheumatology.
The first agent of the SGLT2i class, dapagliflozin, was initially approved in the United States a decade ago for treating T2D. Since then, several other “flozins” have become available, and some have also received additional indications for heart failure and albuminuric chronic kidney disease. Several prior studies have linked SGLT2i use with lower rates of gout flares as well as lower likelihood of developing gout in the first place, although not all studies have found this benefit.
Asked about the clinical implications of the new data, Challener said in an interview that “I don’t think we’re quite at the point where this is changing gout management per se, but this just helps us understand that [SGT2is] may have a role at some point, maybe as a combination on top of another agent. Or, in some patients, it really may be enough if they’re already on an SGLT2i where we don’t need to jump to adding allopurinol. Maybe they have tophi, but they were just started on an SGLT2i and they’re not flaring. Typically, you would start those patients on allopurinol, but you could potentially just monitor them if they were just started on one of those [SGLT2i] agents.”
Asked to comment, session moderator J. Antonio Aviña-Zubieta, MD, PhD, head of the Division of Rheumatology at the University of British Columbia, Vancouver, Canada, and senior scientist at Arthritis Research Canada, said in an interview: “What I can see possibly happening when there’s more evidence is that SGLT2is may be used or even become standard of care as an adjuvant therapy to decrease flares, and by that, decrease the risk of complications.”
Reductions in ULT, Flares, and Healthcare Visits
The new study used administrative health data from the multicenter TriNetX Diamond network of electronic medical record and claims data from 92 healthcare sites with 212 million patients. Among those with both T2D and gout who were not taking ULT at baseline, a total of 16,104 initiated SGLT2is and 16,046 initiated glucagon-like peptide 1 receptor agonists (GLP-1 RA).
Propensity score matching was conducted for demographics including age, race, and sex; comorbidities; use of emergency, inpatient, and critical care services; medications; labs; and body mass index. That yielded 11,800 individuals each in the SGLT2i and GLP-1 RA groups.
Over 5 years, 9.9% of the SGLT2i group vs 13.4% of those using GLP-1 RA had initiated ULT, a significant difference with a hazard ratio (HR) of 0.69 (95% CI, 0.64-0.75). The risk for initiation of colchicine for gout flares was 4.7% with SGLT2i vs 6.0% for GLP-1 RA — also a significant difference with an HR of 0.74 (0.65-0.83).
Medical visits for gout occurred in 28.0% vs 28.4% of patients, which also reached statistical significance (HR, 0.94; 95% CI, 0.89-0.99).
Aviña-Zubieta, an author of one of the previous studies finding a reduction in gout flares with SGLT2i, said, “many patients do not want to start gout therapy until they start having more acute attacks. ... So, for a lot of people, it’s a burden taking another pill to prevent one attack. But, if you don’t treat it over time, the attacks come more often. So, can we still delay the initiation of therapy? If you’re not having that many flares, you’re decreasing the burden of the disease and polypharmacy, which I think is the potential benefit in the long run if you already have an indication for the therapy for diabetes. ... These data are supporting that.”
Indeed, Challener said these data can help in counseling patients. “Taking your SGLT2i for your heart failure and your diabetes is also providing some benefit for your gout, and we know that there is also cardiac benefit when gout is controlled.”
Challener and Aviña-Zubieta had no disclosures.
A version of this article first appeared on Medscape.com.
WASHINGTON — Use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) reduced the need for urate-lowering therapy (ULT) and gout flare therapies in people who had both type 2 diabetes (T2D) and gout, new research has found.
Data from a large US claims database showed that SGLT2i use was associated with a 31% lower rate of initiation of ULT. “This provides further support for the use of SLGT2i therapy in patients with gout, particularly those with high-risk multimorbidity and polypharmacy,” Greg Challener, MD, a postdoctoral fellow at the Rheumatology and Allergy Clinical Epidemiology Research Center, Massachusetts General Hospital, Boston, said in his presentation of the data at the annual meeting of the American College of Rheumatology.
The first agent of the SGLT2i class, dapagliflozin, was initially approved in the United States a decade ago for treating T2D. Since then, several other “flozins” have become available, and some have also received additional indications for heart failure and albuminuric chronic kidney disease. Several prior studies have linked SGLT2i use with lower rates of gout flares as well as lower likelihood of developing gout in the first place, although not all studies have found this benefit.
Asked about the clinical implications of the new data, Challener said in an interview that “I don’t think we’re quite at the point where this is changing gout management per se, but this just helps us understand that [SGT2is] may have a role at some point, maybe as a combination on top of another agent. Or, in some patients, it really may be enough if they’re already on an SGLT2i where we don’t need to jump to adding allopurinol. Maybe they have tophi, but they were just started on an SGLT2i and they’re not flaring. Typically, you would start those patients on allopurinol, but you could potentially just monitor them if they were just started on one of those [SGLT2i] agents.”
Asked to comment, session moderator J. Antonio Aviña-Zubieta, MD, PhD, head of the Division of Rheumatology at the University of British Columbia, Vancouver, Canada, and senior scientist at Arthritis Research Canada, said in an interview: “What I can see possibly happening when there’s more evidence is that SGLT2is may be used or even become standard of care as an adjuvant therapy to decrease flares, and by that, decrease the risk of complications.”
Reductions in ULT, Flares, and Healthcare Visits
The new study used administrative health data from the multicenter TriNetX Diamond network of electronic medical record and claims data from 92 healthcare sites with 212 million patients. Among those with both T2D and gout who were not taking ULT at baseline, a total of 16,104 initiated SGLT2is and 16,046 initiated glucagon-like peptide 1 receptor agonists (GLP-1 RA).
Propensity score matching was conducted for demographics including age, race, and sex; comorbidities; use of emergency, inpatient, and critical care services; medications; labs; and body mass index. That yielded 11,800 individuals each in the SGLT2i and GLP-1 RA groups.
Over 5 years, 9.9% of the SGLT2i group vs 13.4% of those using GLP-1 RA had initiated ULT, a significant difference with a hazard ratio (HR) of 0.69 (95% CI, 0.64-0.75). The risk for initiation of colchicine for gout flares was 4.7% with SGLT2i vs 6.0% for GLP-1 RA — also a significant difference with an HR of 0.74 (0.65-0.83).
Medical visits for gout occurred in 28.0% vs 28.4% of patients, which also reached statistical significance (HR, 0.94; 95% CI, 0.89-0.99).
Aviña-Zubieta, an author of one of the previous studies finding a reduction in gout flares with SGLT2i, said, “many patients do not want to start gout therapy until they start having more acute attacks. ... So, for a lot of people, it’s a burden taking another pill to prevent one attack. But, if you don’t treat it over time, the attacks come more often. So, can we still delay the initiation of therapy? If you’re not having that many flares, you’re decreasing the burden of the disease and polypharmacy, which I think is the potential benefit in the long run if you already have an indication for the therapy for diabetes. ... These data are supporting that.”
Indeed, Challener said these data can help in counseling patients. “Taking your SGLT2i for your heart failure and your diabetes is also providing some benefit for your gout, and we know that there is also cardiac benefit when gout is controlled.”
Challener and Aviña-Zubieta had no disclosures.
A version of this article first appeared on Medscape.com.
WASHINGTON — Use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) reduced the need for urate-lowering therapy (ULT) and gout flare therapies in people who had both type 2 diabetes (T2D) and gout, new research has found.
Data from a large US claims database showed that SGLT2i use was associated with a 31% lower rate of initiation of ULT. “This provides further support for the use of SLGT2i therapy in patients with gout, particularly those with high-risk multimorbidity and polypharmacy,” Greg Challener, MD, a postdoctoral fellow at the Rheumatology and Allergy Clinical Epidemiology Research Center, Massachusetts General Hospital, Boston, said in his presentation of the data at the annual meeting of the American College of Rheumatology.
The first agent of the SGLT2i class, dapagliflozin, was initially approved in the United States a decade ago for treating T2D. Since then, several other “flozins” have become available, and some have also received additional indications for heart failure and albuminuric chronic kidney disease. Several prior studies have linked SGLT2i use with lower rates of gout flares as well as lower likelihood of developing gout in the first place, although not all studies have found this benefit.
Asked about the clinical implications of the new data, Challener said in an interview that “I don’t think we’re quite at the point where this is changing gout management per se, but this just helps us understand that [SGT2is] may have a role at some point, maybe as a combination on top of another agent. Or, in some patients, it really may be enough if they’re already on an SGLT2i where we don’t need to jump to adding allopurinol. Maybe they have tophi, but they were just started on an SGLT2i and they’re not flaring. Typically, you would start those patients on allopurinol, but you could potentially just monitor them if they were just started on one of those [SGLT2i] agents.”
Asked to comment, session moderator J. Antonio Aviña-Zubieta, MD, PhD, head of the Division of Rheumatology at the University of British Columbia, Vancouver, Canada, and senior scientist at Arthritis Research Canada, said in an interview: “What I can see possibly happening when there’s more evidence is that SGLT2is may be used or even become standard of care as an adjuvant therapy to decrease flares, and by that, decrease the risk of complications.”
Reductions in ULT, Flares, and Healthcare Visits
The new study used administrative health data from the multicenter TriNetX Diamond network of electronic medical record and claims data from 92 healthcare sites with 212 million patients. Among those with both T2D and gout who were not taking ULT at baseline, a total of 16,104 initiated SGLT2is and 16,046 initiated glucagon-like peptide 1 receptor agonists (GLP-1 RA).
Propensity score matching was conducted for demographics including age, race, and sex; comorbidities; use of emergency, inpatient, and critical care services; medications; labs; and body mass index. That yielded 11,800 individuals each in the SGLT2i and GLP-1 RA groups.
Over 5 years, 9.9% of the SGLT2i group vs 13.4% of those using GLP-1 RA had initiated ULT, a significant difference with a hazard ratio (HR) of 0.69 (95% CI, 0.64-0.75). The risk for initiation of colchicine for gout flares was 4.7% with SGLT2i vs 6.0% for GLP-1 RA — also a significant difference with an HR of 0.74 (0.65-0.83).
Medical visits for gout occurred in 28.0% vs 28.4% of patients, which also reached statistical significance (HR, 0.94; 95% CI, 0.89-0.99).
Aviña-Zubieta, an author of one of the previous studies finding a reduction in gout flares with SGLT2i, said, “many patients do not want to start gout therapy until they start having more acute attacks. ... So, for a lot of people, it’s a burden taking another pill to prevent one attack. But, if you don’t treat it over time, the attacks come more often. So, can we still delay the initiation of therapy? If you’re not having that many flares, you’re decreasing the burden of the disease and polypharmacy, which I think is the potential benefit in the long run if you already have an indication for the therapy for diabetes. ... These data are supporting that.”
Indeed, Challener said these data can help in counseling patients. “Taking your SGLT2i for your heart failure and your diabetes is also providing some benefit for your gout, and we know that there is also cardiac benefit when gout is controlled.”
Challener and Aviña-Zubieta had no disclosures.
A version of this article first appeared on Medscape.com.
FROM ACR 2024
Genetic Risk for Gout Raises Risk for Cardiovascular Disease Independent of Urate Level
TOPLINE:
Genetic predisposition to gout, unfavorable lifestyle habits, and poor metabolic health are associated with an increased risk for cardiovascular disease (CVD); however, adherence to a healthy lifestyle can reduce this risk by up to 62%, even in individuals with high genetic risk.
METHODOLOGY:
- Researchers investigated the association between genetic predisposition to gout, combined with lifestyle habits, and the risk for CVD in two diverse prospective cohorts from different ancestral backgrounds.
- They analyzed the data of 224,689 participants of European descent from the UK Biobank (mean age, 57.0 years; 56.1% women) and 50,364 participants of East Asian descent from the Korean Genome and Epidemiology Study (KoGES; mean age, 53.7 years; 66.0% women).
- The genetic predisposition to gout was evaluated using a polygenic risk score (PRS) derived from a metagenome-wide association study, and the participants were categorized into low, intermediate, and high genetic risk groups based on their PRS for gout.
- A favorable lifestyle was defined as having ≥ 3 healthy lifestyle factors, and 0-1 metabolic syndrome factor defined the ideal metabolic health status.
- The incident CVD risk was evaluated according to genetic risk, lifestyle habits, and metabolic syndrome.
TAKEAWAY:
- Individuals in the high genetic risk group had a higher risk for CVD than those in the low genetic risk group in both the UK Biobank (adjusted hazard ratio [aHR], 1.10; P < .001) and KoGES (aHR, 1.31; P = .024) cohorts.
- In the UK Biobank cohort, individuals with a high genetic risk for gout and unfavorable lifestyle choices had a 1.99 times higher risk for incident CVD than those with low genetic risk (aHR, 1.99; P < .001); similar outcomes were observed in the KoGES cohort.
- Similarly, individuals with a high genetic risk for gout and poor metabolic health in the UK Biobank cohort had a 2.16 times higher risk for CVD than those with low genetic risk (aHR, 2.16; P < .001 for both); outcomes were no different in the KoGES cohort.
- Improving metabolic health and adhering to a healthy lifestyle reduced the risk for CVD by 62% in individuals with high genetic risk and by 46% in those with low genetic risk (P < .001 for both).
IN PRACTICE:
“PRS for gout can be used for preventing not only gout but also CVD. It is possible to identify individuals with high genetic risk for gout and strongly recommend modifying lifestyle habits. Weight reduction, smoking cessation, regular exercise, and eating healthy food are effective strategies to prevent gout and CVD,” the authors wrote.
SOURCE:
This study was led by Ki Won Moon, MD, PhD, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, Republic of Korea, and SangHyuk Jung, PhD, University of Pennsylvania, Philadelphia, and was published online on October 8, 2024, in RMD Open.
LIMITATIONS:
The definitions of lifestyle and metabolic syndrome were different in each cohort, which may have affected the findings. Data on lifestyle behaviors and metabolic health statuses were collected at enrollment, but these variables may have changed during the follow-up period, which potentially introduced bias into the results. This study was not able to establish causality between genetic predisposition to gout and the incident risk for CVD.
DISCLOSURES:
This study was supported by the National Institute of General Medical Sciences and the National Research Foundation of Korea. The authors declared no competing interests.
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:
Genetic predisposition to gout, unfavorable lifestyle habits, and poor metabolic health are associated with an increased risk for cardiovascular disease (CVD); however, adherence to a healthy lifestyle can reduce this risk by up to 62%, even in individuals with high genetic risk.
METHODOLOGY:
- Researchers investigated the association between genetic predisposition to gout, combined with lifestyle habits, and the risk for CVD in two diverse prospective cohorts from different ancestral backgrounds.
- They analyzed the data of 224,689 participants of European descent from the UK Biobank (mean age, 57.0 years; 56.1% women) and 50,364 participants of East Asian descent from the Korean Genome and Epidemiology Study (KoGES; mean age, 53.7 years; 66.0% women).
- The genetic predisposition to gout was evaluated using a polygenic risk score (PRS) derived from a metagenome-wide association study, and the participants were categorized into low, intermediate, and high genetic risk groups based on their PRS for gout.
- A favorable lifestyle was defined as having ≥ 3 healthy lifestyle factors, and 0-1 metabolic syndrome factor defined the ideal metabolic health status.
- The incident CVD risk was evaluated according to genetic risk, lifestyle habits, and metabolic syndrome.
TAKEAWAY:
- Individuals in the high genetic risk group had a higher risk for CVD than those in the low genetic risk group in both the UK Biobank (adjusted hazard ratio [aHR], 1.10; P < .001) and KoGES (aHR, 1.31; P = .024) cohorts.
- In the UK Biobank cohort, individuals with a high genetic risk for gout and unfavorable lifestyle choices had a 1.99 times higher risk for incident CVD than those with low genetic risk (aHR, 1.99; P < .001); similar outcomes were observed in the KoGES cohort.
- Similarly, individuals with a high genetic risk for gout and poor metabolic health in the UK Biobank cohort had a 2.16 times higher risk for CVD than those with low genetic risk (aHR, 2.16; P < .001 for both); outcomes were no different in the KoGES cohort.
- Improving metabolic health and adhering to a healthy lifestyle reduced the risk for CVD by 62% in individuals with high genetic risk and by 46% in those with low genetic risk (P < .001 for both).
IN PRACTICE:
“PRS for gout can be used for preventing not only gout but also CVD. It is possible to identify individuals with high genetic risk for gout and strongly recommend modifying lifestyle habits. Weight reduction, smoking cessation, regular exercise, and eating healthy food are effective strategies to prevent gout and CVD,” the authors wrote.
SOURCE:
This study was led by Ki Won Moon, MD, PhD, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, Republic of Korea, and SangHyuk Jung, PhD, University of Pennsylvania, Philadelphia, and was published online on October 8, 2024, in RMD Open.
LIMITATIONS:
The definitions of lifestyle and metabolic syndrome were different in each cohort, which may have affected the findings. Data on lifestyle behaviors and metabolic health statuses were collected at enrollment, but these variables may have changed during the follow-up period, which potentially introduced bias into the results. This study was not able to establish causality between genetic predisposition to gout and the incident risk for CVD.
DISCLOSURES:
This study was supported by the National Institute of General Medical Sciences and the National Research Foundation of Korea. The authors declared no competing interests.
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:
Genetic predisposition to gout, unfavorable lifestyle habits, and poor metabolic health are associated with an increased risk for cardiovascular disease (CVD); however, adherence to a healthy lifestyle can reduce this risk by up to 62%, even in individuals with high genetic risk.
METHODOLOGY:
- Researchers investigated the association between genetic predisposition to gout, combined with lifestyle habits, and the risk for CVD in two diverse prospective cohorts from different ancestral backgrounds.
- They analyzed the data of 224,689 participants of European descent from the UK Biobank (mean age, 57.0 years; 56.1% women) and 50,364 participants of East Asian descent from the Korean Genome and Epidemiology Study (KoGES; mean age, 53.7 years; 66.0% women).
- The genetic predisposition to gout was evaluated using a polygenic risk score (PRS) derived from a metagenome-wide association study, and the participants were categorized into low, intermediate, and high genetic risk groups based on their PRS for gout.
- A favorable lifestyle was defined as having ≥ 3 healthy lifestyle factors, and 0-1 metabolic syndrome factor defined the ideal metabolic health status.
- The incident CVD risk was evaluated according to genetic risk, lifestyle habits, and metabolic syndrome.
TAKEAWAY:
- Individuals in the high genetic risk group had a higher risk for CVD than those in the low genetic risk group in both the UK Biobank (adjusted hazard ratio [aHR], 1.10; P < .001) and KoGES (aHR, 1.31; P = .024) cohorts.
- In the UK Biobank cohort, individuals with a high genetic risk for gout and unfavorable lifestyle choices had a 1.99 times higher risk for incident CVD than those with low genetic risk (aHR, 1.99; P < .001); similar outcomes were observed in the KoGES cohort.
- Similarly, individuals with a high genetic risk for gout and poor metabolic health in the UK Biobank cohort had a 2.16 times higher risk for CVD than those with low genetic risk (aHR, 2.16; P < .001 for both); outcomes were no different in the KoGES cohort.
- Improving metabolic health and adhering to a healthy lifestyle reduced the risk for CVD by 62% in individuals with high genetic risk and by 46% in those with low genetic risk (P < .001 for both).
IN PRACTICE:
“PRS for gout can be used for preventing not only gout but also CVD. It is possible to identify individuals with high genetic risk for gout and strongly recommend modifying lifestyle habits. Weight reduction, smoking cessation, regular exercise, and eating healthy food are effective strategies to prevent gout and CVD,” the authors wrote.
SOURCE:
This study was led by Ki Won Moon, MD, PhD, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, Republic of Korea, and SangHyuk Jung, PhD, University of Pennsylvania, Philadelphia, and was published online on October 8, 2024, in RMD Open.
LIMITATIONS:
The definitions of lifestyle and metabolic syndrome were different in each cohort, which may have affected the findings. Data on lifestyle behaviors and metabolic health statuses were collected at enrollment, but these variables may have changed during the follow-up period, which potentially introduced bias into the results. This study was not able to establish causality between genetic predisposition to gout and the incident risk for CVD.
DISCLOSURES:
This study was supported by the National Institute of General Medical Sciences and the National Research Foundation of Korea. The authors declared no competing interests.
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.
Weight Loss After Anti-Obesity Medications Linked to Reduced Gout Risk
TOPLINE:
A higher rate of weight loss within 1 year of initiating orlistat is associated with lower risks for incident gout and recurrent gout flares in individuals with body mass index (BMI) > 25, particularly if they have obesity or high baseline serum urate levels.
METHODOLOGY:
- Researchers conducted a population-based cohort study using data from The Health Improvement Network in the United Kingdom to examine the association between weight loss rates after the initiation of anti-obesity medication (orlistat) and the risk for incident gout and recurrent gout flares in patients with overweight or obesity.
- The risk for incident gout was analyzed in 131,000 patients with overweight or obesity (mean age, 45 years; 77.3% women; mean BMI, 37.2) who did not have gout before initiating orlistat.
- The risk for recurrent gout flares was evaluated in 3847 individuals with overweight or obesity (mean age, 56.6 years; 29.4% women; mean BMI, 38.5), who had gout before initiating orlistat.
- Participants were divided into four groups based on their rate of weight loss during the first year of orlistat use: Weight gain or stable (< 2%), slow (2% to < 5%), moderate (5% to < 10%), and fast (≥ 10%).
- The primary outcome was incident gout, and the secondary outcome was the rate of recurrent gout flares during the 5-year follow-up period after initiating orlistat.
TAKEAWAY:
- The 5-year risk for incident gout was the lowest among patients in the fast weight loss group (1.2%) and highest among those in the weight gain or stable weight group (1.6%).
- The risk for incident gout was lower in the fast (hazard ratio [HR], 0.73; 95% CI, 0.62-0.86) and moderate (HR, 0.82; 95% CI, 0.72-0.92) weight loss groups than in the weight gain or stable weight group.
- Similarly, faster weight loss rates were linked to lower rates of recurrent gout flares, with risk ratios of 0.71 (95% CI, 0.60-0.84) and 0.83 (95% CI, 0.71-0.96) in the fast and moderate weight loss groups, respectively.
- This study found that .
IN PRACTICE:
“Pharmacologic treatments, such as orlistat, present an alternative strategy for managing overweight and obesity. Our study provides empirical evidence of a dose-response effect of weight loss after initiating orlistat within 1 year lowers the risk of incident gout and recurrent gout flares,” the authors wrote.
SOURCE:
This study was led by Jie Wei, PhD, Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha, China, and was published online on September 19, 2024, in Arthritis & Rheumatology.
LIMITATIONS:
Despite adjustment for many variables, factors such as disease severity, exercise levels, and diet were not fully captured, which might have influenced the results. The lack of hospitalization data could have resulted in recurrent gout flares being underreported. The current study may have been subjected to bias due to potential exposure misclassification resulting from the timing of weight measurements and missing updated weight data.
DISCLOSURES:
This study was supported by the National Key Research and Development Plan, the National Natural Science Foundation of China, the Project Program of National Clinical Research Center for Geriatric Disorders, and other sources. No disclosures of interest were reported by the authors.
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 rate of weight loss within 1 year of initiating orlistat is associated with lower risks for incident gout and recurrent gout flares in individuals with body mass index (BMI) > 25, particularly if they have obesity or high baseline serum urate levels.
METHODOLOGY:
- Researchers conducted a population-based cohort study using data from The Health Improvement Network in the United Kingdom to examine the association between weight loss rates after the initiation of anti-obesity medication (orlistat) and the risk for incident gout and recurrent gout flares in patients with overweight or obesity.
- The risk for incident gout was analyzed in 131,000 patients with overweight or obesity (mean age, 45 years; 77.3% women; mean BMI, 37.2) who did not have gout before initiating orlistat.
- The risk for recurrent gout flares was evaluated in 3847 individuals with overweight or obesity (mean age, 56.6 years; 29.4% women; mean BMI, 38.5), who had gout before initiating orlistat.
- Participants were divided into four groups based on their rate of weight loss during the first year of orlistat use: Weight gain or stable (< 2%), slow (2% to < 5%), moderate (5% to < 10%), and fast (≥ 10%).
- The primary outcome was incident gout, and the secondary outcome was the rate of recurrent gout flares during the 5-year follow-up period after initiating orlistat.
TAKEAWAY:
- The 5-year risk for incident gout was the lowest among patients in the fast weight loss group (1.2%) and highest among those in the weight gain or stable weight group (1.6%).
- The risk for incident gout was lower in the fast (hazard ratio [HR], 0.73; 95% CI, 0.62-0.86) and moderate (HR, 0.82; 95% CI, 0.72-0.92) weight loss groups than in the weight gain or stable weight group.
- Similarly, faster weight loss rates were linked to lower rates of recurrent gout flares, with risk ratios of 0.71 (95% CI, 0.60-0.84) and 0.83 (95% CI, 0.71-0.96) in the fast and moderate weight loss groups, respectively.
- This study found that .
IN PRACTICE:
“Pharmacologic treatments, such as orlistat, present an alternative strategy for managing overweight and obesity. Our study provides empirical evidence of a dose-response effect of weight loss after initiating orlistat within 1 year lowers the risk of incident gout and recurrent gout flares,” the authors wrote.
SOURCE:
This study was led by Jie Wei, PhD, Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha, China, and was published online on September 19, 2024, in Arthritis & Rheumatology.
LIMITATIONS:
Despite adjustment for many variables, factors such as disease severity, exercise levels, and diet were not fully captured, which might have influenced the results. The lack of hospitalization data could have resulted in recurrent gout flares being underreported. The current study may have been subjected to bias due to potential exposure misclassification resulting from the timing of weight measurements and missing updated weight data.
DISCLOSURES:
This study was supported by the National Key Research and Development Plan, the National Natural Science Foundation of China, the Project Program of National Clinical Research Center for Geriatric Disorders, and other sources. No disclosures of interest were reported by the authors.
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 rate of weight loss within 1 year of initiating orlistat is associated with lower risks for incident gout and recurrent gout flares in individuals with body mass index (BMI) > 25, particularly if they have obesity or high baseline serum urate levels.
METHODOLOGY:
- Researchers conducted a population-based cohort study using data from The Health Improvement Network in the United Kingdom to examine the association between weight loss rates after the initiation of anti-obesity medication (orlistat) and the risk for incident gout and recurrent gout flares in patients with overweight or obesity.
- The risk for incident gout was analyzed in 131,000 patients with overweight or obesity (mean age, 45 years; 77.3% women; mean BMI, 37.2) who did not have gout before initiating orlistat.
- The risk for recurrent gout flares was evaluated in 3847 individuals with overweight or obesity (mean age, 56.6 years; 29.4% women; mean BMI, 38.5), who had gout before initiating orlistat.
- Participants were divided into four groups based on their rate of weight loss during the first year of orlistat use: Weight gain or stable (< 2%), slow (2% to < 5%), moderate (5% to < 10%), and fast (≥ 10%).
- The primary outcome was incident gout, and the secondary outcome was the rate of recurrent gout flares during the 5-year follow-up period after initiating orlistat.
TAKEAWAY:
- The 5-year risk for incident gout was the lowest among patients in the fast weight loss group (1.2%) and highest among those in the weight gain or stable weight group (1.6%).
- The risk for incident gout was lower in the fast (hazard ratio [HR], 0.73; 95% CI, 0.62-0.86) and moderate (HR, 0.82; 95% CI, 0.72-0.92) weight loss groups than in the weight gain or stable weight group.
- Similarly, faster weight loss rates were linked to lower rates of recurrent gout flares, with risk ratios of 0.71 (95% CI, 0.60-0.84) and 0.83 (95% CI, 0.71-0.96) in the fast and moderate weight loss groups, respectively.
- This study found that .
IN PRACTICE:
“Pharmacologic treatments, such as orlistat, present an alternative strategy for managing overweight and obesity. Our study provides empirical evidence of a dose-response effect of weight loss after initiating orlistat within 1 year lowers the risk of incident gout and recurrent gout flares,” the authors wrote.
SOURCE:
This study was led by Jie Wei, PhD, Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha, China, and was published online on September 19, 2024, in Arthritis & Rheumatology.
LIMITATIONS:
Despite adjustment for many variables, factors such as disease severity, exercise levels, and diet were not fully captured, which might have influenced the results. The lack of hospitalization data could have resulted in recurrent gout flares being underreported. The current study may have been subjected to bias due to potential exposure misclassification resulting from the timing of weight measurements and missing updated weight data.
DISCLOSURES:
This study was supported by the National Key Research and Development Plan, the National Natural Science Foundation of China, the Project Program of National Clinical Research Center for Geriatric Disorders, and other sources. No disclosures of interest were reported by the authors.
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.
Rheumatology Clinic Interventions for Smoking, Blood Pressure ‘Make a Big Difference’
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.
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.
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.
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.
Alcohol’s Effect on Gout Risk Strongest in Men But Present in Both Sexes
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.
Analysis of Colchicine’s Drug-Drug Interactions Finds Little Risk
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.
What Are the Best Supplements for Patients With Kidney Disease? A Few Stand Out
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.