Diabetes

In a striking convergence of veterinary biology and medical science, researchers from the University of Sheffield (England) have unveiled findings that could potentially advance the treatment of diabetic foot ulcers, a condition affecting an estimated 18.6 million people worldwide. The unexpected ingredient in this potentially transformative therapy? Feces from endangered species, sourced from Yorkshire Wildlife Park, Doncaster, England.

The scourge of antibiotic resistance

Diabetic foot ulcers are a significant challenge in health care, not only because of their prevalence but also because of the alarming rise of antibiotic-resistant bacterial infections. Current antibiotic treatments frequently fail, leading to life-altering consequences like amputations and significant health care costs – estimated at one-third of the total direct costs of diabetes care. The critical need for alternative therapies has propelled scientists into a pressing search for novel antimicrobial agents.

A pioneering approach: zoo poo as bioactive goldmine

Led by Professor Graham Stafford, chair of molecular microbiology at the University of Sheffield, the research team began to explore a rather unorthodox resource: the fecal matter of endangered animals like Guinea baboons, lemurs, and Visayan pigs. While such a source might seem surprising at first glance, the rationale becomes clear when considering the nature of bacteriophages.

What are bacteriophages?

Bacteriophages, commonly known as phages, are viruses that selectively target and kill bacteria. Despite being the most prevalent biological entities on Earth, their therapeutic potential has remained largely untapped. What makes bacteriophages particularly interesting is their ability to kill antibiotic-resistant bacteria – a feature making them prime candidates for treating otherwise unmanageable diabetic foot ulcers. (Armstrong DG, et al; Fish R, et al).

Findings and future directions

Professor Stafford and his team discovered that the feces of several endangered animals harbored bacteriophages capable of killing bacterial strains resistant to antibiotics. The findings not only hold promise for a groundbreaking treatment but also provide another compelling reason to conserve endangered species: Their inherent biodiversity might contain cures for a range of infectious diseases.

While research is ongoing and clinical trials have not yet begun, the preliminary results are overwhelmingly promising. Phages isolated from the feces could potentially be incorporated into dressings for ulcers, creating a novel treatment modality that is both effective and cost-saving.

We often look to complex technologies and synthetic materials for medical science breakthroughs, yet sometimes the most innovative solutions can be found in the most overlooked places. In this case, the feces of endangered species could turn out to be a vital asset in battling antibiotic resistance, thus affecting diabetic foot care in ways we never imagined possible.

The research conducted at the University of Sheffield also serves as a powerful argument for a One Health approach – a multidisciplinary field focusing on the interconnectedness of human, animal, and environmental health.

This intriguing work reaffirms the need for an interdisciplinary approach in tackling the world’s pressing health care challenges. The collaborative efforts between the University of Sheffield and Yorkshire Wildlife Park exemplify how academic research and conservation can come together to yield solutions for some of the most devastating and costly health conditions, while also underscoring the invaluable role that biodiversity plays in our collective well-being. Here’s to teaming up to act against amputation worldwide.

Dr. Armstrong is professor of surgery and director of limb preservation at University of Southern California, Los Angeles. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

In a striking convergence of veterinary biology and medical science, researchers from the University of Sheffield (England) have unveiled findings that could potentially advance the treatment of diabetic foot ulcers, a condition affecting an estimated 18.6 million people worldwide. The unexpected ingredient in this potentially transformative therapy? Feces from endangered species, sourced from Yorkshire Wildlife Park, Doncaster, England.

The scourge of antibiotic resistance

Diabetic foot ulcers are a significant challenge in health care, not only because of their prevalence but also because of the alarming rise of antibiotic-resistant bacterial infections. Current antibiotic treatments frequently fail, leading to life-altering consequences like amputations and significant health care costs – estimated at one-third of the total direct costs of diabetes care. The critical need for alternative therapies has propelled scientists into a pressing search for novel antimicrobial agents.

A pioneering approach: zoo poo as bioactive goldmine

Led by Professor Graham Stafford, chair of molecular microbiology at the University of Sheffield, the research team began to explore a rather unorthodox resource: the fecal matter of endangered animals like Guinea baboons, lemurs, and Visayan pigs. While such a source might seem surprising at first glance, the rationale becomes clear when considering the nature of bacteriophages.

What are bacteriophages?

Bacteriophages, commonly known as phages, are viruses that selectively target and kill bacteria. Despite being the most prevalent biological entities on Earth, their therapeutic potential has remained largely untapped. What makes bacteriophages particularly interesting is their ability to kill antibiotic-resistant bacteria – a feature making them prime candidates for treating otherwise unmanageable diabetic foot ulcers. (Armstrong DG, et al; Fish R, et al).

Findings and future directions

Professor Stafford and his team discovered that the feces of several endangered animals harbored bacteriophages capable of killing bacterial strains resistant to antibiotics. The findings not only hold promise for a groundbreaking treatment but also provide another compelling reason to conserve endangered species: Their inherent biodiversity might contain cures for a range of infectious diseases.

While research is ongoing and clinical trials have not yet begun, the preliminary results are overwhelmingly promising. Phages isolated from the feces could potentially be incorporated into dressings for ulcers, creating a novel treatment modality that is both effective and cost-saving.

We often look to complex technologies and synthetic materials for medical science breakthroughs, yet sometimes the most innovative solutions can be found in the most overlooked places. In this case, the feces of endangered species could turn out to be a vital asset in battling antibiotic resistance, thus affecting diabetic foot care in ways we never imagined possible.

The research conducted at the University of Sheffield also serves as a powerful argument for a One Health approach – a multidisciplinary field focusing on the interconnectedness of human, animal, and environmental health.

This intriguing work reaffirms the need for an interdisciplinary approach in tackling the world’s pressing health care challenges. The collaborative efforts between the University of Sheffield and Yorkshire Wildlife Park exemplify how academic research and conservation can come together to yield solutions for some of the most devastating and costly health conditions, while also underscoring the invaluable role that biodiversity plays in our collective well-being. Here’s to teaming up to act against amputation worldwide.

Dr. Armstrong is professor of surgery and director of limb preservation at University of Southern California, Los Angeles. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

In a striking convergence of veterinary biology and medical science, researchers from the University of Sheffield (England) have unveiled findings that could potentially advance the treatment of diabetic foot ulcers, a condition affecting an estimated 18.6 million people worldwide. The unexpected ingredient in this potentially transformative therapy? Feces from endangered species, sourced from Yorkshire Wildlife Park, Doncaster, England.

The scourge of antibiotic resistance

Diabetic foot ulcers are a significant challenge in health care, not only because of their prevalence but also because of the alarming rise of antibiotic-resistant bacterial infections. Current antibiotic treatments frequently fail, leading to life-altering consequences like amputations and significant health care costs – estimated at one-third of the total direct costs of diabetes care. The critical need for alternative therapies has propelled scientists into a pressing search for novel antimicrobial agents.

A pioneering approach: zoo poo as bioactive goldmine

Led by Professor Graham Stafford, chair of molecular microbiology at the University of Sheffield, the research team began to explore a rather unorthodox resource: the fecal matter of endangered animals like Guinea baboons, lemurs, and Visayan pigs. While such a source might seem surprising at first glance, the rationale becomes clear when considering the nature of bacteriophages.

What are bacteriophages?

Bacteriophages, commonly known as phages, are viruses that selectively target and kill bacteria. Despite being the most prevalent biological entities on Earth, their therapeutic potential has remained largely untapped. What makes bacteriophages particularly interesting is their ability to kill antibiotic-resistant bacteria – a feature making them prime candidates for treating otherwise unmanageable diabetic foot ulcers. (Armstrong DG, et al; Fish R, et al).

Findings and future directions

Professor Stafford and his team discovered that the feces of several endangered animals harbored bacteriophages capable of killing bacterial strains resistant to antibiotics. The findings not only hold promise for a groundbreaking treatment but also provide another compelling reason to conserve endangered species: Their inherent biodiversity might contain cures for a range of infectious diseases.

While research is ongoing and clinical trials have not yet begun, the preliminary results are overwhelmingly promising. Phages isolated from the feces could potentially be incorporated into dressings for ulcers, creating a novel treatment modality that is both effective and cost-saving.

We often look to complex technologies and synthetic materials for medical science breakthroughs, yet sometimes the most innovative solutions can be found in the most overlooked places. In this case, the feces of endangered species could turn out to be a vital asset in battling antibiotic resistance, thus affecting diabetic foot care in ways we never imagined possible.

The research conducted at the University of Sheffield also serves as a powerful argument for a One Health approach – a multidisciplinary field focusing on the interconnectedness of human, animal, and environmental health.

This intriguing work reaffirms the need for an interdisciplinary approach in tackling the world’s pressing health care challenges. The collaborative efforts between the University of Sheffield and Yorkshire Wildlife Park exemplify how academic research and conservation can come together to yield solutions for some of the most devastating and costly health conditions, while also underscoring the invaluable role that biodiversity plays in our collective well-being. Here’s to teaming up to act against amputation worldwide.

Dr. Armstrong is professor of surgery and director of limb preservation at University of Southern California, Los Angeles. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

A 36-year-old woman presents to your office for assistance with weight loss. She usually weighs around 150 lb, but she had two pregnancies in the past 4 years and has gained 70 lb. Her current weight is 220 lb with a body mass index (BMI) of 36.6 kg/m2, and she has been unable to lose any weight despite diet and exercise. She reports back pain and generalized fatigue but is primarily worried about developing type 2 diabetes, which runs in her family. Her insurance covers weight loss medications, but she is asking if she can take “Ozempic off-label” or “compounded semaglutide” instead because Wegovy isn’t available at her local pharmacy.

More and more people are turning to “medical weight management” to drop pounds and improve their health. This is a strategy that adds pharmacotherapy to lifestyle modifications to treat the chronic disease of obesity, and it is analogous to the treatment of high blood pressure or high cholesterol with medications.

This patient meets the criteria set forth by the American Heart Association, American College of Cardiology, and The Obesity Society for the management of obesity with antiobesity medications:

• BMI ≥ 30 or BMI ≥ 27 with weight-related comorbidities and
• Has been unable to achieve ≥ 5% weight loss with lifestyle changes alone.

Several U.S. Food and Drug Administration–approved antiobesity medications have been proven to cause clinically significant weight loss:

• orlistat (Alli or Xenical).
• phentermine/topiramate (Qsymia).
• naltrexone/bupropion (Contrave).
• liraglutide 3.0 mg subcutaneously daily (Saxenda).
• semaglutide 2.4 mg subcutaneously weekly (Wegovy).

When considering an antiobesity medication for a patient, it’s important to discuss efficacy, side-effect profile, contraindications, cost and coverage, and long-term use.

In this commentary, we’ll specifically focus on semaglutide (Wegovy) as it is currently the most effective FDA-approved medication for weight loss.
 

Efficacy

In a phase 3 clinical trial, patients on semaglutide 2.4 mg weekly lost an average of 15% of their body weight at 68 weeks, or approximately 33 lb. It is important to note that there is variability in treatment response to semaglutide 2.4 mg, just like with any other medication. About 1 in 3 individuals lost ≥ 20% of their weight, but about 1 in every 10 patients did not lose any weight.

In this patient, who has a family history of type 2 diabetes, weight loss with semaglutide 2.4 mg will probably reduce her risk of developing diabetes. With just 5%-10% weight loss, she will see improvements in her blood glucose, blood pressure, and cholesterol. Even greater weight loss (≥ 10%) has been associated with resolution of fatty liver and sleep apnea.
 

Side effects

Before starting semaglutide, patients should be counseled about potential gastrointestinal side effects, including nausea, upset stomach, diarrhea, constipation, and reflux.

Side effects can be managed with dietary modifications, over-the-counter treatments, and slow dose escalation. Some common tips include:

• Eat slowly.
• Eat a bland diet.
• Avoid fatty or fried foods.
• Avoid lying down immediately after eating.
• Prioritize water and fiber intake to mitigate constipation.
• Use over-the-counter treatments as needed (for example, laxative for constipation).

Most of these side effects are present only during dose escalation and resolve once the patient is on a stable dose.

Patients should be counseled about the less than 1% risk for gallbladder issues or pancreatitis. They should be instructed to go to an urgent care or emergency room if they develop severe abdominal pain, recurrent vomiting, or the inability to eat or drink.
 

Contraindications

We don’t prescribe GLP-1 receptor agonists, including semaglutide 2.4 mg, in patients with a personal or family history of medullary thyroid cancer. GLP-1 agonists are contraindicated in patients with a history of pancreatitis or gastroparesis. All FDA-approved antiobesity medications are contraindicated in women who are breastfeeding or trying for pregnancy. If this patient would like to pursue pregnancy again, semaglutide 2.4 mg should be stopped 2 months prior to conception.

Access

In this case, the patient’s insurance covered semaglutide 2.4 mg with a copay of $25 per month. Without insurance, semaglutide 2.4 mg (Wegovy) costs about $1,400 per month, and semaglutide 2.0 mg (Ozempic), the formulation approved for type 2 diabetes, costs up to $1,000 per month. These price ranges are often cost-prohibitive and unsustainable, especially because these medications are intended for long-term use.

Currently, Medicare does not cover antiobesity medications nor do most state Medicaid plans. Therefore, these medications are usually not considered by patients who have Medicare or Medicaid insurance.

Because insurance coverage varies and out-of-pocket costs can be prohibitive, many individuals seek other ways of acquiring semaglutide. The off-label use of semaglutide 2.0 mg (Ozempic) for obesity is scientifically supported and safe, whereas the use of compounded semaglutide is risky due to lack of regulation.

Compounded semaglutide should be avoided, given that these products are not controlled by the FDA, and adverse events have been reported in connection with compounded semaglutide.

In our clinical practice, patients have reported advertisements for “generic semaglutide” compounded with vitamins like vitamin B12 or B6. This is a significant area of concern because some vitamins (for instance, vitamin B6) are toxic at high doses.

We discussed the dangers of compounded semaglutide with our patient and told her that this isn’t something we recommend prescribing. If the patient didn’t want to wait for semaglutide 2.4 mg to be available at her pharmacy, we discussed alternative medications used for the management of obesity, such as other FDA-approved GLP-1 agonists (that is, liraglutide 3.0 mg) and off-label medications. In this case, the patient opted to wait for semaglutide 2.4 mg because she preferred a weekly injectable medication, given her busy lifestyle as a new mom.

Dr. Schmitz, of Weill Cornell Medicine, New York, disclosed no relevant financial relationships. Dr. Tchang, of Weill Cornell Medicine and the Iris Cantor Women's Health Center, both in New York, serves or has served as a director, officer, partner, employee, advisor, consultant, or trustee for Gelesis and Novo Nordisk, and has received income from Gelesis.

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

A 36-year-old woman presents to your office for assistance with weight loss. She usually weighs around 150 lb, but she had two pregnancies in the past 4 years and has gained 70 lb. Her current weight is 220 lb with a body mass index (BMI) of 36.6 kg/m2, and she has been unable to lose any weight despite diet and exercise. She reports back pain and generalized fatigue but is primarily worried about developing type 2 diabetes, which runs in her family. Her insurance covers weight loss medications, but she is asking if she can take “Ozempic off-label” or “compounded semaglutide” instead because Wegovy isn’t available at her local pharmacy.

More and more people are turning to “medical weight management” to drop pounds and improve their health. This is a strategy that adds pharmacotherapy to lifestyle modifications to treat the chronic disease of obesity, and it is analogous to the treatment of high blood pressure or high cholesterol with medications.

This patient meets the criteria set forth by the American Heart Association, American College of Cardiology, and The Obesity Society for the management of obesity with antiobesity medications:

• BMI ≥ 30 or BMI ≥ 27 with weight-related comorbidities and
• Has been unable to achieve ≥ 5% weight loss with lifestyle changes alone.

Several U.S. Food and Drug Administration–approved antiobesity medications have been proven to cause clinically significant weight loss:

• orlistat (Alli or Xenical).
• phentermine/topiramate (Qsymia).
• naltrexone/bupropion (Contrave).
• liraglutide 3.0 mg subcutaneously daily (Saxenda).
• semaglutide 2.4 mg subcutaneously weekly (Wegovy).

When considering an antiobesity medication for a patient, it’s important to discuss efficacy, side-effect profile, contraindications, cost and coverage, and long-term use.

In this commentary, we’ll specifically focus on semaglutide (Wegovy) as it is currently the most effective FDA-approved medication for weight loss.
 

Efficacy

In a phase 3 clinical trial, patients on semaglutide 2.4 mg weekly lost an average of 15% of their body weight at 68 weeks, or approximately 33 lb. It is important to note that there is variability in treatment response to semaglutide 2.4 mg, just like with any other medication. About 1 in 3 individuals lost ≥ 20% of their weight, but about 1 in every 10 patients did not lose any weight.

In this patient, who has a family history of type 2 diabetes, weight loss with semaglutide 2.4 mg will probably reduce her risk of developing diabetes. With just 5%-10% weight loss, she will see improvements in her blood glucose, blood pressure, and cholesterol. Even greater weight loss (≥ 10%) has been associated with resolution of fatty liver and sleep apnea.
 

Side effects

Before starting semaglutide, patients should be counseled about potential gastrointestinal side effects, including nausea, upset stomach, diarrhea, constipation, and reflux.

Side effects can be managed with dietary modifications, over-the-counter treatments, and slow dose escalation. Some common tips include:

• Eat slowly.
• Eat a bland diet.
• Avoid fatty or fried foods.
• Avoid lying down immediately after eating.
• Prioritize water and fiber intake to mitigate constipation.
• Use over-the-counter treatments as needed (for example, laxative for constipation).

Most of these side effects are present only during dose escalation and resolve once the patient is on a stable dose.

Patients should be counseled about the less than 1% risk for gallbladder issues or pancreatitis. They should be instructed to go to an urgent care or emergency room if they develop severe abdominal pain, recurrent vomiting, or the inability to eat or drink.
 

Contraindications

We don’t prescribe GLP-1 receptor agonists, including semaglutide 2.4 mg, in patients with a personal or family history of medullary thyroid cancer. GLP-1 agonists are contraindicated in patients with a history of pancreatitis or gastroparesis. All FDA-approved antiobesity medications are contraindicated in women who are breastfeeding or trying for pregnancy. If this patient would like to pursue pregnancy again, semaglutide 2.4 mg should be stopped 2 months prior to conception.

Access

In this case, the patient’s insurance covered semaglutide 2.4 mg with a copay of $25 per month. Without insurance, semaglutide 2.4 mg (Wegovy) costs about $1,400 per month, and semaglutide 2.0 mg (Ozempic), the formulation approved for type 2 diabetes, costs up to $1,000 per month. These price ranges are often cost-prohibitive and unsustainable, especially because these medications are intended for long-term use.

Currently, Medicare does not cover antiobesity medications nor do most state Medicaid plans. Therefore, these medications are usually not considered by patients who have Medicare or Medicaid insurance.

Because insurance coverage varies and out-of-pocket costs can be prohibitive, many individuals seek other ways of acquiring semaglutide. The off-label use of semaglutide 2.0 mg (Ozempic) for obesity is scientifically supported and safe, whereas the use of compounded semaglutide is risky due to lack of regulation.

Compounded semaglutide should be avoided, given that these products are not controlled by the FDA, and adverse events have been reported in connection with compounded semaglutide.

In our clinical practice, patients have reported advertisements for “generic semaglutide” compounded with vitamins like vitamin B12 or B6. This is a significant area of concern because some vitamins (for instance, vitamin B6) are toxic at high doses.

We discussed the dangers of compounded semaglutide with our patient and told her that this isn’t something we recommend prescribing. If the patient didn’t want to wait for semaglutide 2.4 mg to be available at her pharmacy, we discussed alternative medications used for the management of obesity, such as other FDA-approved GLP-1 agonists (that is, liraglutide 3.0 mg) and off-label medications. In this case, the patient opted to wait for semaglutide 2.4 mg because she preferred a weekly injectable medication, given her busy lifestyle as a new mom.

Dr. Schmitz, of Weill Cornell Medicine, New York, disclosed no relevant financial relationships. Dr. Tchang, of Weill Cornell Medicine and the Iris Cantor Women's Health Center, both in New York, serves or has served as a director, officer, partner, employee, advisor, consultant, or trustee for Gelesis and Novo Nordisk, and has received income from Gelesis.

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

A 36-year-old woman presents to your office for assistance with weight loss. She usually weighs around 150 lb, but she had two pregnancies in the past 4 years and has gained 70 lb. Her current weight is 220 lb with a body mass index (BMI) of 36.6 kg/m2, and she has been unable to lose any weight despite diet and exercise. She reports back pain and generalized fatigue but is primarily worried about developing type 2 diabetes, which runs in her family. Her insurance covers weight loss medications, but she is asking if she can take “Ozempic off-label” or “compounded semaglutide” instead because Wegovy isn’t available at her local pharmacy.

More and more people are turning to “medical weight management” to drop pounds and improve their health. This is a strategy that adds pharmacotherapy to lifestyle modifications to treat the chronic disease of obesity, and it is analogous to the treatment of high blood pressure or high cholesterol with medications.

This patient meets the criteria set forth by the American Heart Association, American College of Cardiology, and The Obesity Society for the management of obesity with antiobesity medications:

• BMI ≥ 30 or BMI ≥ 27 with weight-related comorbidities and
• Has been unable to achieve ≥ 5% weight loss with lifestyle changes alone.

Several U.S. Food and Drug Administration–approved antiobesity medications have been proven to cause clinically significant weight loss:

• orlistat (Alli or Xenical).
• phentermine/topiramate (Qsymia).
• naltrexone/bupropion (Contrave).
• liraglutide 3.0 mg subcutaneously daily (Saxenda).
• semaglutide 2.4 mg subcutaneously weekly (Wegovy).

When considering an antiobesity medication for a patient, it’s important to discuss efficacy, side-effect profile, contraindications, cost and coverage, and long-term use.

In this commentary, we’ll specifically focus on semaglutide (Wegovy) as it is currently the most effective FDA-approved medication for weight loss.
 

Efficacy

In a phase 3 clinical trial, patients on semaglutide 2.4 mg weekly lost an average of 15% of their body weight at 68 weeks, or approximately 33 lb. It is important to note that there is variability in treatment response to semaglutide 2.4 mg, just like with any other medication. About 1 in 3 individuals lost ≥ 20% of their weight, but about 1 in every 10 patients did not lose any weight.

In this patient, who has a family history of type 2 diabetes, weight loss with semaglutide 2.4 mg will probably reduce her risk of developing diabetes. With just 5%-10% weight loss, she will see improvements in her blood glucose, blood pressure, and cholesterol. Even greater weight loss (≥ 10%) has been associated with resolution of fatty liver and sleep apnea.
 

Side effects

Before starting semaglutide, patients should be counseled about potential gastrointestinal side effects, including nausea, upset stomach, diarrhea, constipation, and reflux.

Side effects can be managed with dietary modifications, over-the-counter treatments, and slow dose escalation. Some common tips include:

• Eat slowly.
• Eat a bland diet.
• Avoid fatty or fried foods.
• Avoid lying down immediately after eating.
• Prioritize water and fiber intake to mitigate constipation.
• Use over-the-counter treatments as needed (for example, laxative for constipation).

Most of these side effects are present only during dose escalation and resolve once the patient is on a stable dose.

Patients should be counseled about the less than 1% risk for gallbladder issues or pancreatitis. They should be instructed to go to an urgent care or emergency room if they develop severe abdominal pain, recurrent vomiting, or the inability to eat or drink.
 

Contraindications

We don’t prescribe GLP-1 receptor agonists, including semaglutide 2.4 mg, in patients with a personal or family history of medullary thyroid cancer. GLP-1 agonists are contraindicated in patients with a history of pancreatitis or gastroparesis. All FDA-approved antiobesity medications are contraindicated in women who are breastfeeding or trying for pregnancy. If this patient would like to pursue pregnancy again, semaglutide 2.4 mg should be stopped 2 months prior to conception.

Access

In this case, the patient’s insurance covered semaglutide 2.4 mg with a copay of $25 per month. Without insurance, semaglutide 2.4 mg (Wegovy) costs about $1,400 per month, and semaglutide 2.0 mg (Ozempic), the formulation approved for type 2 diabetes, costs up to $1,000 per month. These price ranges are often cost-prohibitive and unsustainable, especially because these medications are intended for long-term use.

Currently, Medicare does not cover antiobesity medications nor do most state Medicaid plans. Therefore, these medications are usually not considered by patients who have Medicare or Medicaid insurance.

Because insurance coverage varies and out-of-pocket costs can be prohibitive, many individuals seek other ways of acquiring semaglutide. The off-label use of semaglutide 2.0 mg (Ozempic) for obesity is scientifically supported and safe, whereas the use of compounded semaglutide is risky due to lack of regulation.

Compounded semaglutide should be avoided, given that these products are not controlled by the FDA, and adverse events have been reported in connection with compounded semaglutide.

In our clinical practice, patients have reported advertisements for “generic semaglutide” compounded with vitamins like vitamin B12 or B6. This is a significant area of concern because some vitamins (for instance, vitamin B6) are toxic at high doses.

We discussed the dangers of compounded semaglutide with our patient and told her that this isn’t something we recommend prescribing. If the patient didn’t want to wait for semaglutide 2.4 mg to be available at her pharmacy, we discussed alternative medications used for the management of obesity, such as other FDA-approved GLP-1 agonists (that is, liraglutide 3.0 mg) and off-label medications. In this case, the patient opted to wait for semaglutide 2.4 mg because she preferred a weekly injectable medication, given her busy lifestyle as a new mom.

Dr. Schmitz, of Weill Cornell Medicine, New York, disclosed no relevant financial relationships. Dr. Tchang, of Weill Cornell Medicine and the Iris Cantor Women's Health Center, both in New York, serves or has served as a director, officer, partner, employee, advisor, consultant, or trustee for Gelesis and Novo Nordisk, and has received income from Gelesis.

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

TOPLINE:

Use of a novel clinical-decision support tool and shared decision-making in elderly patients with type 2 diabetes managed in a primary care practice and at high risk for hypoglycemic episodes led to a 46% decrease in the number of at-risk patients and discontinuation of hypoglycemic agents in 20% in a prospective, 6-month, single-arm study with 94 patients.

METHODOLOGY:

• The HypoPrevent study enrolled 94 people from a Pennsylvania primary care practice who were at least 65 years old with type 2 diabetes and at risk for hypoglycemia because of treatment with insulin or sulfonylureas, and having a hemoglobin A1c of less than 7.0%.
• Clinicians and patients used a newly devised hypoglycemia reduction clinical-decision support tool developed by the Endocrine Society and a health care consulting company to help guide shared decision-making for a goal A1c level, potential changes to treatment, and other steps to reduce the risk of hypoglycemia.
• Primary outcomes during 6-month follow-up were impact of the intervention on A1c, changes in use of insulin or sulfonylureas, change in the number of study patients at risk for hypoglycemia, and impact on the incidence of nonsevere hypoglycemic events (NSHEs) measured with the Treatment-Related Impact Measure–Non-severe Hypoglycemic Events (TRIM-HYPO) survey.

TAKEAWAY:

• Patients averaged 74 years old, 57% were women, 95% were White, 61% had diabetes for more than 10 years, 48% had chronic kidney disease, 51% were on insulin, 47% on a sulfonylurea, and 80 of the 94 enrolled patients completed all three study visits.
• Nineteen patients (20%) reduced their dose of or discontinued insulin or sulfonylurea.
• In patients with both baseline and follow-up A1c measures, A1c rose from 6.29% at baseline to 6.82%.
• Fifty patients set an A1c goal and had a timely follow-up A1c measurement, and in this subgroup the number of patients at risk for hypoglycemia decreased by 46%, a significant change.
• Patients who reported at least one NSHE at baseline had a significant reduction between the baseline survey and follow-up visits in both the total score as well as each of the five scored domains.

IN PRACTICE:

The HypoPrevent study results “show the potential of a decision support tool and shared decision making to reduce the risk of hypoglycemia in older persons with type 2 diabetes,” and that “the tested decision tool can be effectively used by a busy primary care practice with positive results,” concluded the researchers in their report.

SOURCE:

The HypoPrevent study was funded and organized by the Endocrine Society in collaboration with a multicenter team of researchers. The report appeared in the Journal of the American Geriatrics Society.

LIMITATIONS:

Lack of a control group makes it impossible to conclusively determine whether the intervention led to the observed increases in A1c levels, nor can the study exclude regression to the mean as the cause for lowered A1c levels.

DISCLOSURES:

The study received funding from Abbott, Lilly, Merck, Novo Nordisk, and Sanofi. Two coauthors had individual disclosures listed in the report; the other six coauthors had no disclosures.

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

TOPLINE:

Use of a novel clinical-decision support tool and shared decision-making in elderly patients with type 2 diabetes managed in a primary care practice and at high risk for hypoglycemic episodes led to a 46% decrease in the number of at-risk patients and discontinuation of hypoglycemic agents in 20% in a prospective, 6-month, single-arm study with 94 patients.

METHODOLOGY:

• The HypoPrevent study enrolled 94 people from a Pennsylvania primary care practice who were at least 65 years old with type 2 diabetes and at risk for hypoglycemia because of treatment with insulin or sulfonylureas, and having a hemoglobin A1c of less than 7.0%.
• Clinicians and patients used a newly devised hypoglycemia reduction clinical-decision support tool developed by the Endocrine Society and a health care consulting company to help guide shared decision-making for a goal A1c level, potential changes to treatment, and other steps to reduce the risk of hypoglycemia.
• Primary outcomes during 6-month follow-up were impact of the intervention on A1c, changes in use of insulin or sulfonylureas, change in the number of study patients at risk for hypoglycemia, and impact on the incidence of nonsevere hypoglycemic events (NSHEs) measured with the Treatment-Related Impact Measure–Non-severe Hypoglycemic Events (TRIM-HYPO) survey.

TAKEAWAY:

• Patients averaged 74 years old, 57% were women, 95% were White, 61% had diabetes for more than 10 years, 48% had chronic kidney disease, 51% were on insulin, 47% on a sulfonylurea, and 80 of the 94 enrolled patients completed all three study visits.
• Nineteen patients (20%) reduced their dose of or discontinued insulin or sulfonylurea.
• In patients with both baseline and follow-up A1c measures, A1c rose from 6.29% at baseline to 6.82%.
• Fifty patients set an A1c goal and had a timely follow-up A1c measurement, and in this subgroup the number of patients at risk for hypoglycemia decreased by 46%, a significant change.
• Patients who reported at least one NSHE at baseline had a significant reduction between the baseline survey and follow-up visits in both the total score as well as each of the five scored domains.

IN PRACTICE:

The HypoPrevent study results “show the potential of a decision support tool and shared decision making to reduce the risk of hypoglycemia in older persons with type 2 diabetes,” and that “the tested decision tool can be effectively used by a busy primary care practice with positive results,” concluded the researchers in their report.

SOURCE:

The HypoPrevent study was funded and organized by the Endocrine Society in collaboration with a multicenter team of researchers. The report appeared in the Journal of the American Geriatrics Society.

LIMITATIONS:

Lack of a control group makes it impossible to conclusively determine whether the intervention led to the observed increases in A1c levels, nor can the study exclude regression to the mean as the cause for lowered A1c levels.

DISCLOSURES:

The study received funding from Abbott, Lilly, Merck, Novo Nordisk, and Sanofi. Two coauthors had individual disclosures listed in the report; the other six coauthors had no disclosures.

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

TOPLINE:

Use of a novel clinical-decision support tool and shared decision-making in elderly patients with type 2 diabetes managed in a primary care practice and at high risk for hypoglycemic episodes led to a 46% decrease in the number of at-risk patients and discontinuation of hypoglycemic agents in 20% in a prospective, 6-month, single-arm study with 94 patients.

METHODOLOGY:

• The HypoPrevent study enrolled 94 people from a Pennsylvania primary care practice who were at least 65 years old with type 2 diabetes and at risk for hypoglycemia because of treatment with insulin or sulfonylureas, and having a hemoglobin A1c of less than 7.0%.
• Clinicians and patients used a newly devised hypoglycemia reduction clinical-decision support tool developed by the Endocrine Society and a health care consulting company to help guide shared decision-making for a goal A1c level, potential changes to treatment, and other steps to reduce the risk of hypoglycemia.
• Primary outcomes during 6-month follow-up were impact of the intervention on A1c, changes in use of insulin or sulfonylureas, change in the number of study patients at risk for hypoglycemia, and impact on the incidence of nonsevere hypoglycemic events (NSHEs) measured with the Treatment-Related Impact Measure–Non-severe Hypoglycemic Events (TRIM-HYPO) survey.

TAKEAWAY:

• Patients averaged 74 years old, 57% were women, 95% were White, 61% had diabetes for more than 10 years, 48% had chronic kidney disease, 51% were on insulin, 47% on a sulfonylurea, and 80 of the 94 enrolled patients completed all three study visits.
• Nineteen patients (20%) reduced their dose of or discontinued insulin or sulfonylurea.
• In patients with both baseline and follow-up A1c measures, A1c rose from 6.29% at baseline to 6.82%.
• Fifty patients set an A1c goal and had a timely follow-up A1c measurement, and in this subgroup the number of patients at risk for hypoglycemia decreased by 46%, a significant change.
• Patients who reported at least one NSHE at baseline had a significant reduction between the baseline survey and follow-up visits in both the total score as well as each of the five scored domains.

IN PRACTICE:

The HypoPrevent study results “show the potential of a decision support tool and shared decision making to reduce the risk of hypoglycemia in older persons with type 2 diabetes,” and that “the tested decision tool can be effectively used by a busy primary care practice with positive results,” concluded the researchers in their report.

SOURCE:

The HypoPrevent study was funded and organized by the Endocrine Society in collaboration with a multicenter team of researchers. The report appeared in the Journal of the American Geriatrics Society.

LIMITATIONS:

Lack of a control group makes it impossible to conclusively determine whether the intervention led to the observed increases in A1c levels, nor can the study exclude regression to the mean as the cause for lowered A1c levels.

DISCLOSURES:

The study received funding from Abbott, Lilly, Merck, Novo Nordisk, and Sanofi. Two coauthors had individual disclosures listed in the report; the other six coauthors had no disclosures.

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

The hugely popular weight loss agent semaglutide (approved as Wegovy for weight loss; Ozempic for type 2 diabetes; Novo Nordisk) received a pair of drug safety–related labeling additions from the Food and Drug Administration in late September for the Ozempic formulation.

The FDA added a warning to the drug-interaction section of the Ozempic label that reiterates a warning that is already in place in other label sections, reinforcing the message that the glucagon-like peptide-1 (GLP-1) receptor agonist Ozempic can potentially interact with the action of certain other agents to increase a person’s risk for hypoglycemia.

The added text says: “Ozempic stimulates insulin release in the presence of elevated blood glucose concentrations. Patients receiving Ozempic in combination with an insulin secretagogue (for instance, sulfonylurea) or insulin may have an increased risk of hypoglycemia, including severe hypoglycemia.”

This text was already included in both the “Warning and Precautions” and the “Adverse Reactions” sections of the label. The warning also advises, “The risk of hypoglycemia may be lowered by a reduction in the dose of sulfonylurea (or other concomitantly administered insulin secretagogue) or insulin. Inform patients using these concomitant medications of the risk of hypoglycemia and educate them on the signs and symptoms of hypoglycemia.”

Reports of ileus episodes after approval

The second addition concerns a new adverse reaction that was identified during the postmarketing experience.

The FDA has received more than 8,500 reports of gastrointestinal issues among patients prescribed glucagon-like peptide-1 (GLP-1) receptor agonists. Ileus is mentioned in 33 cases, including two deaths, associated with semaglutide. The FDA stopped short of saying there is a direct link between the drug and intestinal blockages.

“Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure,” the FDA stated in its approval of the label update.

The same warning for the risk of intestinal blockages is already listed on the labels for tirzepatide (Mounjaro, Lilly) and semaglutide injection 2.4 mg (Wegovy, Novo Nordisk).

The label change comes after a Louisiana woman filed a lawsuit in August that claims she was “severely injured” after using Mounjaro and Ozempic. She claimed the drug makers failed to disclose risks of vomiting and diarrhea due to inflammation of the stomach lining, as well as the risk of gastroparesis.

*Correction, 10/3/23: An earlier version of this article misstated the semaglutide formulation that received the updates. 

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

The hugely popular weight loss agent semaglutide (approved as Wegovy for weight loss; Ozempic for type 2 diabetes; Novo Nordisk) received a pair of drug safety–related labeling additions from the Food and Drug Administration in late September for the Ozempic formulation.

The FDA added a warning to the drug-interaction section of the Ozempic label that reiterates a warning that is already in place in other label sections, reinforcing the message that the glucagon-like peptide-1 (GLP-1) receptor agonist Ozempic can potentially interact with the action of certain other agents to increase a person’s risk for hypoglycemia.

The added text says: “Ozempic stimulates insulin release in the presence of elevated blood glucose concentrations. Patients receiving Ozempic in combination with an insulin secretagogue (for instance, sulfonylurea) or insulin may have an increased risk of hypoglycemia, including severe hypoglycemia.”

This text was already included in both the “Warning and Precautions” and the “Adverse Reactions” sections of the label. The warning also advises, “The risk of hypoglycemia may be lowered by a reduction in the dose of sulfonylurea (or other concomitantly administered insulin secretagogue) or insulin. Inform patients using these concomitant medications of the risk of hypoglycemia and educate them on the signs and symptoms of hypoglycemia.”

Reports of ileus episodes after approval

The second addition concerns a new adverse reaction that was identified during the postmarketing experience.

The FDA has received more than 8,500 reports of gastrointestinal issues among patients prescribed glucagon-like peptide-1 (GLP-1) receptor agonists. Ileus is mentioned in 33 cases, including two deaths, associated with semaglutide. The FDA stopped short of saying there is a direct link between the drug and intestinal blockages.

“Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure,” the FDA stated in its approval of the label update.

The same warning for the risk of intestinal blockages is already listed on the labels for tirzepatide (Mounjaro, Lilly) and semaglutide injection 2.4 mg (Wegovy, Novo Nordisk).

The label change comes after a Louisiana woman filed a lawsuit in August that claims she was “severely injured” after using Mounjaro and Ozempic. She claimed the drug makers failed to disclose risks of vomiting and diarrhea due to inflammation of the stomach lining, as well as the risk of gastroparesis.

*Correction, 10/3/23: An earlier version of this article misstated the semaglutide formulation that received the updates. 

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

The hugely popular weight loss agent semaglutide (approved as Wegovy for weight loss; Ozempic for type 2 diabetes; Novo Nordisk) received a pair of drug safety–related labeling additions from the Food and Drug Administration in late September for the Ozempic formulation.

The FDA added a warning to the drug-interaction section of the Ozempic label that reiterates a warning that is already in place in other label sections, reinforcing the message that the glucagon-like peptide-1 (GLP-1) receptor agonist Ozempic can potentially interact with the action of certain other agents to increase a person’s risk for hypoglycemia.

The added text says: “Ozempic stimulates insulin release in the presence of elevated blood glucose concentrations. Patients receiving Ozempic in combination with an insulin secretagogue (for instance, sulfonylurea) or insulin may have an increased risk of hypoglycemia, including severe hypoglycemia.”

This text was already included in both the “Warning and Precautions” and the “Adverse Reactions” sections of the label. The warning also advises, “The risk of hypoglycemia may be lowered by a reduction in the dose of sulfonylurea (or other concomitantly administered insulin secretagogue) or insulin. Inform patients using these concomitant medications of the risk of hypoglycemia and educate them on the signs and symptoms of hypoglycemia.”

Reports of ileus episodes after approval

The second addition concerns a new adverse reaction that was identified during the postmarketing experience.

The FDA has received more than 8,500 reports of gastrointestinal issues among patients prescribed glucagon-like peptide-1 (GLP-1) receptor agonists. Ileus is mentioned in 33 cases, including two deaths, associated with semaglutide. The FDA stopped short of saying there is a direct link between the drug and intestinal blockages.

“Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure,” the FDA stated in its approval of the label update.

The same warning for the risk of intestinal blockages is already listed on the labels for tirzepatide (Mounjaro, Lilly) and semaglutide injection 2.4 mg (Wegovy, Novo Nordisk).

The label change comes after a Louisiana woman filed a lawsuit in August that claims she was “severely injured” after using Mounjaro and Ozempic. She claimed the drug makers failed to disclose risks of vomiting and diarrhea due to inflammation of the stomach lining, as well as the risk of gastroparesis.

*Correction, 10/3/23: An earlier version of this article misstated the semaglutide formulation that received the updates. 

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

This year’s annual meeting of the European Association for the Study of Diabetes offers an in-depth look into “disease-modifying and disrupting therapies” in both type 1 and type 2 diabetes.

Noteworthy at the meeting, taking place Oct. 3-6, in Hamburg, Germany, will be final detailed data from the SURMOUNT-4 trial of the “twincretin” tirzepatide (Mounjaro, Lilly) on obesity. The top-line results, announced by the company in July, showed an average 21.1% weight loss at 36 weeks with tirzepatide injections once weekly among adults with overweight or obesity. The drug is approved in the United States and Europe for treating type 2 diabetes, and approval for obesity is expected in the United States later this year.

In addition, a symposium will present a new EASD/American Diabetes Association (ADA) consensus report, Hyperglycaemic Crisis in Adult Patients with Diabetes, scheduled to be simultaneously published in Diabetologia and Diabetes Care on Oct. 6.  

Aside from those, much of the EASD meeting content will feature smaller studies on both type 2 and type 1 diabetes, along with award lectures, symposia, debates, and lots of discussion on hot topics in diabetes and clinical challenges including complications. In essence, it will provide a forum for in-depth follow-up to the jam-packed clinical trial–filled agenda at the ADA meeting in June, said EASD Honorary Secretary Tina Vilsbøll, MD, clinical professor and head of clinic at the Steno Diabetes Center, Copenhagen.

“There were so many large trials at ADA that we just took them in without really having a chance to discuss them. ... There’s so much to discuss with all these new treatments, how do we place them in obesity and diabetes? ... All the data that we have from ADA will make good discussions at EASD,” Dr. Vilsbøll said in an interview.

Indeed, said EASD President Chantal Mathieu, MD, PhD, chair of endocrinology at University Hospital Gasthuisberg Leuven, Belgium, “We always come after ADA. That puts us in a position where we can take deeper dives into the data. ... EASD is a calmer meeting where you can really look at the details.”
 

Type 2 diabetes: Disease modifying in many ways

Dr. Mathieu told this news organization that a unifying theme for much of the EASD meeting’s content is “We are now entering the era of disease-modifying and disease-disrupting therapies” in both diabetes types.

In type 2, this means “getting to the root, which is obesity, so you’ll see a lot of presentations on the incretin system, but you also don’t get type 2 diabetes if you have an iron-clad beta cell. ... So, we also gave a lot of attention to basic translational research that helps us to understand the role of the beta cell in type 2 diabetes.”

In addition to SURMOUNT-4, there will be oral abstract sessions with follow-up data from the SURPASS series of studies of tirzepatide in type 2 diabetes, other abstract sessions, symposia about incretins and obesity, and an oral abstract session on beta cell function in both diabetes types.

Three debates will address controversial questions in the type 2 diabetes arena. In one, speakers will take opposite sides on “Initial combined therapy for type 2 diabetes: Should diabetes follow hypertension?”

In another, speakers will argue over “Is lasting remission of type 2 diabetes feasible in the real-world setting?” That’s an important question, Dr. Vilsbøll said.

“A person might be able to have a remission but go back if they regain the weight. Do we really have remission? How do we define it? Now, suddenly, we have tools to help people go in the right direction. Now we’re in a place where we can actually help our patients with their cravings and their body weight and all that. It’s more fun to discuss when we have the tools.”

A third debate will tackle the question of whether all people with type 2 diabetes and chronic kidney disease should be on [sodium-glucose co-transporter 2] (SGLT2) inhibitors “by default.”

The Minkowski Prize Lecture will address the regulation of energy and glucose metabolism by the dual incretin receptor agonists, while the EASD-Lilly Anniversary Prize Lecture will be about the role of ectopic lipid in insulin resistance and cardiometabolic disease.
 

Type 1 diabetes: Both disease modifying and disruptive

For type 1 diabetes, “disease-modifying” and “disruptive” approaches on the meeting agenda include new data on immune modulation for people in early stages in order to prevent or delay insulin dependence, islet transplantation including the use of stem cell–derived beta cells, and the latest in technology including automated insulin delivery systems, also known colloquially as the “artificial pancreas.”

Prize lectures about type 1 diabetes will include the Claude Bernard Lecture, on etiologies of autoimmune diabetes, the Albert Renold Lecture, on “disrupted RNA editing as a path to type 1 diabetes,” and the EASD/Novo Nordisk Foundation Diabetes Prize for Excellence Lecture on automated insulin delivery.

Focus on complications: The known and the emerging

The meeting also will focus a great deal on complications of diabetes, including the well-studied cardiovascular disease, neuropathy, nephropathy, retinopathy, and fatty liver disease as well as others that typically receive less attention, such as gastrointestinal problems and cardiomyopathy.

Another debate will address the question “Is it time to reclassify diabetes complications because microvascular and macrovascular classification is no longer sufficient?” And, the Camillo Golgi Lecture will cover “Diabetes Complications: From Classical to Emerging.”

As always, there’s much more on the agenda including pregnancy and diabetes, cystic fibrosis–derived diabetes, mental health in diabetes, COVID-19 and diabetes, hypoglycemia, and hypoglycemia unawareness.  

According to Dr. Vilsbøll, “Clinicians should come and enjoy all the great science we have, interact, and be inspired.”

Dr. Vilsbøll has served on scientific advisory panels, been part of speaker bureaus, and served as a consultant to and/or received research support from Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, Gilead, GSK, Mundipharma, Novo Nordisk, Sanofi, and Sun Pharmaceuticals. Dr. Mathieu serves or has served on the advisory panel for Novo Nordisk, Sanofi, Merck Sharp and Dohme Ltd., Eli Lilly and Company, Novartis, AstraZeneca, Boehringer Ingelheim, Roche, Medtronic, ActoBio Therapeutics, Pfizer, Imcyse, Insulet, Zealand Pharma, Avotres, Mannkind, Sandoz, and Vertex. She has served on the speakers bureau for Novo Nordisk, Sanofi, Eli Lilly and Company, Boehringer Ingelheim, AstraZeneca, and Novartis. Financial compensation for these activities has been received by KU Leuven.
 

A version of this article appeared on Medscape.com.

This year’s annual meeting of the European Association for the Study of Diabetes offers an in-depth look into “disease-modifying and disrupting therapies” in both type 1 and type 2 diabetes.

Noteworthy at the meeting, taking place Oct. 3-6, in Hamburg, Germany, will be final detailed data from the SURMOUNT-4 trial of the “twincretin” tirzepatide (Mounjaro, Lilly) on obesity. The top-line results, announced by the company in July, showed an average 21.1% weight loss at 36 weeks with tirzepatide injections once weekly among adults with overweight or obesity. The drug is approved in the United States and Europe for treating type 2 diabetes, and approval for obesity is expected in the United States later this year.

In addition, a symposium will present a new EASD/American Diabetes Association (ADA) consensus report, Hyperglycaemic Crisis in Adult Patients with Diabetes, scheduled to be simultaneously published in Diabetologia and Diabetes Care on Oct. 6.  

Aside from those, much of the EASD meeting content will feature smaller studies on both type 2 and type 1 diabetes, along with award lectures, symposia, debates, and lots of discussion on hot topics in diabetes and clinical challenges including complications. In essence, it will provide a forum for in-depth follow-up to the jam-packed clinical trial–filled agenda at the ADA meeting in June, said EASD Honorary Secretary Tina Vilsbøll, MD, clinical professor and head of clinic at the Steno Diabetes Center, Copenhagen.

“There were so many large trials at ADA that we just took them in without really having a chance to discuss them. ... There’s so much to discuss with all these new treatments, how do we place them in obesity and diabetes? ... All the data that we have from ADA will make good discussions at EASD,” Dr. Vilsbøll said in an interview.

Indeed, said EASD President Chantal Mathieu, MD, PhD, chair of endocrinology at University Hospital Gasthuisberg Leuven, Belgium, “We always come after ADA. That puts us in a position where we can take deeper dives into the data. ... EASD is a calmer meeting where you can really look at the details.”
 

Type 2 diabetes: Disease modifying in many ways

Dr. Mathieu told this news organization that a unifying theme for much of the EASD meeting’s content is “We are now entering the era of disease-modifying and disease-disrupting therapies” in both diabetes types.

In type 2, this means “getting to the root, which is obesity, so you’ll see a lot of presentations on the incretin system, but you also don’t get type 2 diabetes if you have an iron-clad beta cell. ... So, we also gave a lot of attention to basic translational research that helps us to understand the role of the beta cell in type 2 diabetes.”

In addition to SURMOUNT-4, there will be oral abstract sessions with follow-up data from the SURPASS series of studies of tirzepatide in type 2 diabetes, other abstract sessions, symposia about incretins and obesity, and an oral abstract session on beta cell function in both diabetes types.

Three debates will address controversial questions in the type 2 diabetes arena. In one, speakers will take opposite sides on “Initial combined therapy for type 2 diabetes: Should diabetes follow hypertension?”

In another, speakers will argue over “Is lasting remission of type 2 diabetes feasible in the real-world setting?” That’s an important question, Dr. Vilsbøll said.

“A person might be able to have a remission but go back if they regain the weight. Do we really have remission? How do we define it? Now, suddenly, we have tools to help people go in the right direction. Now we’re in a place where we can actually help our patients with their cravings and their body weight and all that. It’s more fun to discuss when we have the tools.”

A third debate will tackle the question of whether all people with type 2 diabetes and chronic kidney disease should be on [sodium-glucose co-transporter 2] (SGLT2) inhibitors “by default.”

The Minkowski Prize Lecture will address the regulation of energy and glucose metabolism by the dual incretin receptor agonists, while the EASD-Lilly Anniversary Prize Lecture will be about the role of ectopic lipid in insulin resistance and cardiometabolic disease.
 

Type 1 diabetes: Both disease modifying and disruptive

For type 1 diabetes, “disease-modifying” and “disruptive” approaches on the meeting agenda include new data on immune modulation for people in early stages in order to prevent or delay insulin dependence, islet transplantation including the use of stem cell–derived beta cells, and the latest in technology including automated insulin delivery systems, also known colloquially as the “artificial pancreas.”

Prize lectures about type 1 diabetes will include the Claude Bernard Lecture, on etiologies of autoimmune diabetes, the Albert Renold Lecture, on “disrupted RNA editing as a path to type 1 diabetes,” and the EASD/Novo Nordisk Foundation Diabetes Prize for Excellence Lecture on automated insulin delivery.

Focus on complications: The known and the emerging

The meeting also will focus a great deal on complications of diabetes, including the well-studied cardiovascular disease, neuropathy, nephropathy, retinopathy, and fatty liver disease as well as others that typically receive less attention, such as gastrointestinal problems and cardiomyopathy.

Another debate will address the question “Is it time to reclassify diabetes complications because microvascular and macrovascular classification is no longer sufficient?” And, the Camillo Golgi Lecture will cover “Diabetes Complications: From Classical to Emerging.”

As always, there’s much more on the agenda including pregnancy and diabetes, cystic fibrosis–derived diabetes, mental health in diabetes, COVID-19 and diabetes, hypoglycemia, and hypoglycemia unawareness.  

According to Dr. Vilsbøll, “Clinicians should come and enjoy all the great science we have, interact, and be inspired.”

Dr. Vilsbøll has served on scientific advisory panels, been part of speaker bureaus, and served as a consultant to and/or received research support from Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, Gilead, GSK, Mundipharma, Novo Nordisk, Sanofi, and Sun Pharmaceuticals. Dr. Mathieu serves or has served on the advisory panel for Novo Nordisk, Sanofi, Merck Sharp and Dohme Ltd., Eli Lilly and Company, Novartis, AstraZeneca, Boehringer Ingelheim, Roche, Medtronic, ActoBio Therapeutics, Pfizer, Imcyse, Insulet, Zealand Pharma, Avotres, Mannkind, Sandoz, and Vertex. She has served on the speakers bureau for Novo Nordisk, Sanofi, Eli Lilly and Company, Boehringer Ingelheim, AstraZeneca, and Novartis. Financial compensation for these activities has been received by KU Leuven.
 

A version of this article appeared on Medscape.com.

This year’s annual meeting of the European Association for the Study of Diabetes offers an in-depth look into “disease-modifying and disrupting therapies” in both type 1 and type 2 diabetes.

Noteworthy at the meeting, taking place Oct. 3-6, in Hamburg, Germany, will be final detailed data from the SURMOUNT-4 trial of the “twincretin” tirzepatide (Mounjaro, Lilly) on obesity. The top-line results, announced by the company in July, showed an average 21.1% weight loss at 36 weeks with tirzepatide injections once weekly among adults with overweight or obesity. The drug is approved in the United States and Europe for treating type 2 diabetes, and approval for obesity is expected in the United States later this year.

In addition, a symposium will present a new EASD/American Diabetes Association (ADA) consensus report, Hyperglycaemic Crisis in Adult Patients with Diabetes, scheduled to be simultaneously published in Diabetologia and Diabetes Care on Oct. 6.  

Aside from those, much of the EASD meeting content will feature smaller studies on both type 2 and type 1 diabetes, along with award lectures, symposia, debates, and lots of discussion on hot topics in diabetes and clinical challenges including complications. In essence, it will provide a forum for in-depth follow-up to the jam-packed clinical trial–filled agenda at the ADA meeting in June, said EASD Honorary Secretary Tina Vilsbøll, MD, clinical professor and head of clinic at the Steno Diabetes Center, Copenhagen.

“There were so many large trials at ADA that we just took them in without really having a chance to discuss them. ... There’s so much to discuss with all these new treatments, how do we place them in obesity and diabetes? ... All the data that we have from ADA will make good discussions at EASD,” Dr. Vilsbøll said in an interview.

Indeed, said EASD President Chantal Mathieu, MD, PhD, chair of endocrinology at University Hospital Gasthuisberg Leuven, Belgium, “We always come after ADA. That puts us in a position where we can take deeper dives into the data. ... EASD is a calmer meeting where you can really look at the details.”
 

Type 2 diabetes: Disease modifying in many ways

Dr. Mathieu told this news organization that a unifying theme for much of the EASD meeting’s content is “We are now entering the era of disease-modifying and disease-disrupting therapies” in both diabetes types.

In type 2, this means “getting to the root, which is obesity, so you’ll see a lot of presentations on the incretin system, but you also don’t get type 2 diabetes if you have an iron-clad beta cell. ... So, we also gave a lot of attention to basic translational research that helps us to understand the role of the beta cell in type 2 diabetes.”

In addition to SURMOUNT-4, there will be oral abstract sessions with follow-up data from the SURPASS series of studies of tirzepatide in type 2 diabetes, other abstract sessions, symposia about incretins and obesity, and an oral abstract session on beta cell function in both diabetes types.

Three debates will address controversial questions in the type 2 diabetes arena. In one, speakers will take opposite sides on “Initial combined therapy for type 2 diabetes: Should diabetes follow hypertension?”

In another, speakers will argue over “Is lasting remission of type 2 diabetes feasible in the real-world setting?” That’s an important question, Dr. Vilsbøll said.

“A person might be able to have a remission but go back if they regain the weight. Do we really have remission? How do we define it? Now, suddenly, we have tools to help people go in the right direction. Now we’re in a place where we can actually help our patients with their cravings and their body weight and all that. It’s more fun to discuss when we have the tools.”

A third debate will tackle the question of whether all people with type 2 diabetes and chronic kidney disease should be on [sodium-glucose co-transporter 2] (SGLT2) inhibitors “by default.”

The Minkowski Prize Lecture will address the regulation of energy and glucose metabolism by the dual incretin receptor agonists, while the EASD-Lilly Anniversary Prize Lecture will be about the role of ectopic lipid in insulin resistance and cardiometabolic disease.
 

Type 1 diabetes: Both disease modifying and disruptive

For type 1 diabetes, “disease-modifying” and “disruptive” approaches on the meeting agenda include new data on immune modulation for people in early stages in order to prevent or delay insulin dependence, islet transplantation including the use of stem cell–derived beta cells, and the latest in technology including automated insulin delivery systems, also known colloquially as the “artificial pancreas.”

Prize lectures about type 1 diabetes will include the Claude Bernard Lecture, on etiologies of autoimmune diabetes, the Albert Renold Lecture, on “disrupted RNA editing as a path to type 1 diabetes,” and the EASD/Novo Nordisk Foundation Diabetes Prize for Excellence Lecture on automated insulin delivery.

Focus on complications: The known and the emerging

The meeting also will focus a great deal on complications of diabetes, including the well-studied cardiovascular disease, neuropathy, nephropathy, retinopathy, and fatty liver disease as well as others that typically receive less attention, such as gastrointestinal problems and cardiomyopathy.

Another debate will address the question “Is it time to reclassify diabetes complications because microvascular and macrovascular classification is no longer sufficient?” And, the Camillo Golgi Lecture will cover “Diabetes Complications: From Classical to Emerging.”

As always, there’s much more on the agenda including pregnancy and diabetes, cystic fibrosis–derived diabetes, mental health in diabetes, COVID-19 and diabetes, hypoglycemia, and hypoglycemia unawareness.  

According to Dr. Vilsbøll, “Clinicians should come and enjoy all the great science we have, interact, and be inspired.”

Dr. Vilsbøll has served on scientific advisory panels, been part of speaker bureaus, and served as a consultant to and/or received research support from Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, Gilead, GSK, Mundipharma, Novo Nordisk, Sanofi, and Sun Pharmaceuticals. Dr. Mathieu serves or has served on the advisory panel for Novo Nordisk, Sanofi, Merck Sharp and Dohme Ltd., Eli Lilly and Company, Novartis, AstraZeneca, Boehringer Ingelheim, Roche, Medtronic, ActoBio Therapeutics, Pfizer, Imcyse, Insulet, Zealand Pharma, Avotres, Mannkind, Sandoz, and Vertex. She has served on the speakers bureau for Novo Nordisk, Sanofi, Eli Lilly and Company, Boehringer Ingelheim, AstraZeneca, and Novartis. Financial compensation for these activities has been received by KU Leuven.
 

A version of this article appeared on Medscape.com.

TOPLINE:

In insulin-naive people with type 2 diabetes, once-weekly icodec titrated with a dosing guide app was both noninferior and superior to daily basal analogs in reducing A1c levels, with improved treatment satisfaction and compliance scores and similarly low hypoglycemia rates.

METHODOLOGY:

• A 52-week, randomized, open-label, parallel-group, phase 3a trial with real-world elements was conducted at 176 sites in seven countries.
• A total of 1,085 insulin-naive patients with type 2 diabetes were randomly assigned to receive icodec with a dosing guide app or daily analogs (U100 glargine, U300 glargine, or icodec).

TAKEAWAY:

• A1c levels dropped from 8.96% at baseline to 7.24% at week 52 with icodec and from 8.88% to 7.61% with the daily analog, a treatment difference of 0.37 percentage point (P < .001 for noninferiority and P = .009 for superiority in favor of icodec plus the app).
• Patient-reported outcomes were more favorable with icodec plus the app vs. daily analogs, with estimated treatment differences that were significant for the Treatment Related Impact Measure for Diabetes (3.04) but not the Diabetes Treatment Satisfaction Questionnaire (0.78).
• Observed rates of combined clinically significant or severe hypoglycemia were low (0.19 event per patient-year of exposure for icodec plus the app vs. 0.14 for daily analogs; estimated rate ratio, 1.17).

IN PRACTICE:

“Once-weekly icodec with a dosing guide app could conceivably address several challenges seen in everyday practice, including inadequate dose titration and nonadherence to prescribed treatment regimens.”

SOURCE:

The study was conducted by Harpreet S. Bajaj, MD, MPH, of LMC Diabetes and Endocrinology, Brampton, Ontario, and colleagues. It was published online in Annals of Internal Medicine.

LIMITATIONS:

The research could not differentiate between the effects of icodec and those of the dosing guide app. The study had an open-label design. A 1-year duration is insufficient to assess long-term diabetes- and cardiovascular-related outcomes.

DISCLOSURES:

The study was funded by Novo Nordisk A/S.
 

A version of this article appeared on Medscape.com.

TOPLINE:

In insulin-naive people with type 2 diabetes, once-weekly icodec titrated with a dosing guide app was both noninferior and superior to daily basal analogs in reducing A1c levels, with improved treatment satisfaction and compliance scores and similarly low hypoglycemia rates.

METHODOLOGY:

• A 52-week, randomized, open-label, parallel-group, phase 3a trial with real-world elements was conducted at 176 sites in seven countries.
• A total of 1,085 insulin-naive patients with type 2 diabetes were randomly assigned to receive icodec with a dosing guide app or daily analogs (U100 glargine, U300 glargine, or icodec).

TAKEAWAY:

• A1c levels dropped from 8.96% at baseline to 7.24% at week 52 with icodec and from 8.88% to 7.61% with the daily analog, a treatment difference of 0.37 percentage point (P < .001 for noninferiority and P = .009 for superiority in favor of icodec plus the app).
• Patient-reported outcomes were more favorable with icodec plus the app vs. daily analogs, with estimated treatment differences that were significant for the Treatment Related Impact Measure for Diabetes (3.04) but not the Diabetes Treatment Satisfaction Questionnaire (0.78).
• Observed rates of combined clinically significant or severe hypoglycemia were low (0.19 event per patient-year of exposure for icodec plus the app vs. 0.14 for daily analogs; estimated rate ratio, 1.17).

IN PRACTICE:

“Once-weekly icodec with a dosing guide app could conceivably address several challenges seen in everyday practice, including inadequate dose titration and nonadherence to prescribed treatment regimens.”

SOURCE:

The study was conducted by Harpreet S. Bajaj, MD, MPH, of LMC Diabetes and Endocrinology, Brampton, Ontario, and colleagues. It was published online in Annals of Internal Medicine.

LIMITATIONS:

The research could not differentiate between the effects of icodec and those of the dosing guide app. The study had an open-label design. A 1-year duration is insufficient to assess long-term diabetes- and cardiovascular-related outcomes.

DISCLOSURES:

The study was funded by Novo Nordisk A/S.
 

A version of this article appeared on Medscape.com.

TOPLINE:

In insulin-naive people with type 2 diabetes, once-weekly icodec titrated with a dosing guide app was both noninferior and superior to daily basal analogs in reducing A1c levels, with improved treatment satisfaction and compliance scores and similarly low hypoglycemia rates.

METHODOLOGY:

• A 52-week, randomized, open-label, parallel-group, phase 3a trial with real-world elements was conducted at 176 sites in seven countries.
• A total of 1,085 insulin-naive patients with type 2 diabetes were randomly assigned to receive icodec with a dosing guide app or daily analogs (U100 glargine, U300 glargine, or icodec).

TAKEAWAY:

• A1c levels dropped from 8.96% at baseline to 7.24% at week 52 with icodec and from 8.88% to 7.61% with the daily analog, a treatment difference of 0.37 percentage point (P < .001 for noninferiority and P = .009 for superiority in favor of icodec plus the app).
• Patient-reported outcomes were more favorable with icodec plus the app vs. daily analogs, with estimated treatment differences that were significant for the Treatment Related Impact Measure for Diabetes (3.04) but not the Diabetes Treatment Satisfaction Questionnaire (0.78).
• Observed rates of combined clinically significant or severe hypoglycemia were low (0.19 event per patient-year of exposure for icodec plus the app vs. 0.14 for daily analogs; estimated rate ratio, 1.17).

IN PRACTICE:

“Once-weekly icodec with a dosing guide app could conceivably address several challenges seen in everyday practice, including inadequate dose titration and nonadherence to prescribed treatment regimens.”

SOURCE:

The study was conducted by Harpreet S. Bajaj, MD, MPH, of LMC Diabetes and Endocrinology, Brampton, Ontario, and colleagues. It was published online in Annals of Internal Medicine.

LIMITATIONS:

The research could not differentiate between the effects of icodec and those of the dosing guide app. The study had an open-label design. A 1-year duration is insufficient to assess long-term diabetes- and cardiovascular-related outcomes.

DISCLOSURES:

The study was funded by Novo Nordisk A/S.
 

A version of this article appeared on Medscape.com.

Approximately 4 in 10 cases of type 1 diabetes in adults are diagnosed at age 30 years and older, based on data from nearly 1,000 individuals.

New-onset type 1 diabetes in adults is often misdiagnosed as type 2 diabetes, which may lead to inappropriate care, wrote Michael Fang, PhD, of Johns Hopkins University, Baltimore, and colleagues.

Previous research suggests that more than half of type 1 diabetes cases develop in adults, but data on variations in clinical characteristics and age at diagnosis are limited, the researchers said. “Clarifying the burden of adult-onset type 1 diabetes in the general population may help reduce misdiagnosis.”

In a study published in Annals of Internal Medicine, the researchers identified 947 adults aged 18 years and older with newly diagnosed type 1 diabetes, by using data from the National Health Interview Survey between 2016 and 2022. The subjects’ mean age at the time of the survey was 49 years and 48% were women. The racial/ethnic distribution was 73% non-Hispanic White, 10% non-Hispanic Black, 12% Hispanic, 3%, non-Hispanic Asian, and 3% other race/ethnicity.

Overall, 37% of participants were diagnosed with type 1 diabetes after age 30 years, with an overall median age at diagnosis of 24 years.

Type 1 diabetes was diagnosed later in men than in women, at a median age of 27 years vs. 22 years, respectively, and later in racial/ethnic minorities than in non-Hispanic Whites, with a median age of 26-30 years versus 21 years, respectively.

Autoantibody and C-peptide tests are recommended to confirm type 1 diabetes in adults with a suspected diagnosis, but the best method to identify high-risk adults remains unclear, the researchers wrote in their discussion.

“Traditional markers used to differentiate type 1 and type 2 diabetes, such as body mass index, may have limited utility, especially because obesity is now common in the type 1 diabetes population,” they said. New tools combining clinical features and biomarkers may improve accuracy of diagnosis of type 1 diabetes in the adult population, but more research is needed.

The findings were limited by several factors including misclassification based on self-reports of diagnosis and age, the researchers noted. Other limitations included lack of data on diagnostic measures such as levels of autoantibodies, C-peptides, and other indicators of diabetes, as well as inexact subgroup estimates because of small sample sizes.

“We extended existing research by characterizing the age at diagnosis in a nationally representative sample and by documenting variation across race/ethnicity and clinical characteristics,” they said.

The study was supported by grants from the National Heart, Lung, and Blood Institute. The lead authors had no financial conflicts to disclose. Corresponding author Elizabeth Selvin, PhD, disclosed grants from NIH and FNIH, personal fees from Novo Nordisk, other financial relationships with Wolters Kluwer, and nonfinancial support from many pharmaceutical companies outside the current study; she also serves as deputy editor of Diabetes Care and a member of the editorial board of Diabetologia.

Approximately 4 in 10 cases of type 1 diabetes in adults are diagnosed at age 30 years and older, based on data from nearly 1,000 individuals.

New-onset type 1 diabetes in adults is often misdiagnosed as type 2 diabetes, which may lead to inappropriate care, wrote Michael Fang, PhD, of Johns Hopkins University, Baltimore, and colleagues.

Previous research suggests that more than half of type 1 diabetes cases develop in adults, but data on variations in clinical characteristics and age at diagnosis are limited, the researchers said. “Clarifying the burden of adult-onset type 1 diabetes in the general population may help reduce misdiagnosis.”

In a study published in Annals of Internal Medicine, the researchers identified 947 adults aged 18 years and older with newly diagnosed type 1 diabetes, by using data from the National Health Interview Survey between 2016 and 2022. The subjects’ mean age at the time of the survey was 49 years and 48% were women. The racial/ethnic distribution was 73% non-Hispanic White, 10% non-Hispanic Black, 12% Hispanic, 3%, non-Hispanic Asian, and 3% other race/ethnicity.

Overall, 37% of participants were diagnosed with type 1 diabetes after age 30 years, with an overall median age at diagnosis of 24 years.

Type 1 diabetes was diagnosed later in men than in women, at a median age of 27 years vs. 22 years, respectively, and later in racial/ethnic minorities than in non-Hispanic Whites, with a median age of 26-30 years versus 21 years, respectively.

Autoantibody and C-peptide tests are recommended to confirm type 1 diabetes in adults with a suspected diagnosis, but the best method to identify high-risk adults remains unclear, the researchers wrote in their discussion.

“Traditional markers used to differentiate type 1 and type 2 diabetes, such as body mass index, may have limited utility, especially because obesity is now common in the type 1 diabetes population,” they said. New tools combining clinical features and biomarkers may improve accuracy of diagnosis of type 1 diabetes in the adult population, but more research is needed.

The findings were limited by several factors including misclassification based on self-reports of diagnosis and age, the researchers noted. Other limitations included lack of data on diagnostic measures such as levels of autoantibodies, C-peptides, and other indicators of diabetes, as well as inexact subgroup estimates because of small sample sizes.

“We extended existing research by characterizing the age at diagnosis in a nationally representative sample and by documenting variation across race/ethnicity and clinical characteristics,” they said.

The study was supported by grants from the National Heart, Lung, and Blood Institute. The lead authors had no financial conflicts to disclose. Corresponding author Elizabeth Selvin, PhD, disclosed grants from NIH and FNIH, personal fees from Novo Nordisk, other financial relationships with Wolters Kluwer, and nonfinancial support from many pharmaceutical companies outside the current study; she also serves as deputy editor of Diabetes Care and a member of the editorial board of Diabetologia.

Approximately 4 in 10 cases of type 1 diabetes in adults are diagnosed at age 30 years and older, based on data from nearly 1,000 individuals.

New-onset type 1 diabetes in adults is often misdiagnosed as type 2 diabetes, which may lead to inappropriate care, wrote Michael Fang, PhD, of Johns Hopkins University, Baltimore, and colleagues.

Previous research suggests that more than half of type 1 diabetes cases develop in adults, but data on variations in clinical characteristics and age at diagnosis are limited, the researchers said. “Clarifying the burden of adult-onset type 1 diabetes in the general population may help reduce misdiagnosis.”

In a study published in Annals of Internal Medicine, the researchers identified 947 adults aged 18 years and older with newly diagnosed type 1 diabetes, by using data from the National Health Interview Survey between 2016 and 2022. The subjects’ mean age at the time of the survey was 49 years and 48% were women. The racial/ethnic distribution was 73% non-Hispanic White, 10% non-Hispanic Black, 12% Hispanic, 3%, non-Hispanic Asian, and 3% other race/ethnicity.

Overall, 37% of participants were diagnosed with type 1 diabetes after age 30 years, with an overall median age at diagnosis of 24 years.

Type 1 diabetes was diagnosed later in men than in women, at a median age of 27 years vs. 22 years, respectively, and later in racial/ethnic minorities than in non-Hispanic Whites, with a median age of 26-30 years versus 21 years, respectively.

Autoantibody and C-peptide tests are recommended to confirm type 1 diabetes in adults with a suspected diagnosis, but the best method to identify high-risk adults remains unclear, the researchers wrote in their discussion.

“Traditional markers used to differentiate type 1 and type 2 diabetes, such as body mass index, may have limited utility, especially because obesity is now common in the type 1 diabetes population,” they said. New tools combining clinical features and biomarkers may improve accuracy of diagnosis of type 1 diabetes in the adult population, but more research is needed.

The findings were limited by several factors including misclassification based on self-reports of diagnosis and age, the researchers noted. Other limitations included lack of data on diagnostic measures such as levels of autoantibodies, C-peptides, and other indicators of diabetes, as well as inexact subgroup estimates because of small sample sizes.

“We extended existing research by characterizing the age at diagnosis in a nationally representative sample and by documenting variation across race/ethnicity and clinical characteristics,” they said.

The study was supported by grants from the National Heart, Lung, and Blood Institute. The lead authors had no financial conflicts to disclose. Corresponding author Elizabeth Selvin, PhD, disclosed grants from NIH and FNIH, personal fees from Novo Nordisk, other financial relationships with Wolters Kluwer, and nonfinancial support from many pharmaceutical companies outside the current study; she also serves as deputy editor of Diabetes Care and a member of the editorial board of Diabetologia.

Vitamin D deficiency appears to render people more vulnerable to canagliflozin’s adverse effects on bone health, whereas vitamin D3 supplementation appears protective of individuals with vitamin D deficiency.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are beneficial for treating type 2 diabetes and reducing cardiovascular and kidney disease risk. However, some, but not all, trial data have linked the SLGT2 inhibitor canagliflozin to increased fracture risk. That particular agent has been reported to accelerate loss of bone mineral density, which could contribute to fracture risk. Other drugs in the class have also been implicated in worsening markers of bone health.

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

Vitamin D deficiency appears to render people more vulnerable to canagliflozin’s adverse effects on bone health, whereas vitamin D3 supplementation appears protective of individuals with vitamin D deficiency.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are beneficial for treating type 2 diabetes and reducing cardiovascular and kidney disease risk. However, some, but not all, trial data have linked the SLGT2 inhibitor canagliflozin to increased fracture risk. That particular agent has been reported to accelerate loss of bone mineral density, which could contribute to fracture risk. Other drugs in the class have also been implicated in worsening markers of bone health.

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

Vitamin D deficiency appears to render people more vulnerable to canagliflozin’s adverse effects on bone health, whereas vitamin D3 supplementation appears protective of individuals with vitamin D deficiency.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are beneficial for treating type 2 diabetes and reducing cardiovascular and kidney disease risk. However, some, but not all, trial data have linked the SLGT2 inhibitor canagliflozin to increased fracture risk. That particular agent has been reported to accelerate loss of bone mineral density, which could contribute to fracture risk. Other drugs in the class have also been implicated in worsening markers of bone health.

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

Antidiabetic drug tirzepatide (Mounjaro) shows superiority over semaglutide (Ozempic, Wegovy, and Rybelsus) in controlling blood glucose as well as in the amount of weight lost, results from a meta-analysis of 22 randomized controlled trials show.

“The results indicate tirzepatide’s superior performance over subcutaneous semaglutide in managing blood sugar and achieving weight loss, making it a promising option in the pharmaceutical management of type 2 diabetes,” first author Thomas Karagiannis, MD, PhD, Aristotle University of Thessaloniki, Greece, said in an interview.

“In clinical context, the most potent doses of each drug revealed a clear difference regarding weight loss, with tirzepatide resulting in an average weight reduction that exceeded that of semaglutide by 5.7 kg (12.6 pounds),” he said.

The study is scheduled to be presented at the annual meeting of the European Association for the Study of Diabetes (EASD) in early October.

While a multitude of studies have been conducted for tirzepatide, a dual glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 (GLP-1) receptor agonist, and semaglutide, a selective GLP-1 agonist, studies comparing the two drugs directly are lacking.

For a more comprehensive understanding of how the drugs compare, Dr. Karagiannis and colleagues conducted the meta-analysis of 22 trials, including two direct comparisons, the SURPASS-2 trial and a smaller trial, and 20 other studies comparing either semaglutide or tirzepatide with a common comparator, such as placebo, basal insulin, or other GLP-RA-1 drugs.

Overall, 18,472 participants were included in the studies.

All included studies had assessed a maintenance dose of tirzepatide of either 5, 10, or 15 mg once weekly or semaglutide at doses of 0.5, 1.0, or 2.0 mg once weekly for at least 12 weeks. All comparisons were for subcutaneous injection formulations (semaglutide can also be taken orally).
 

Blood glucose reduction

Tirzepatide at 15 mg was found to have the highest efficacy in the reduction of A1c compared with placebo, with a mean difference of –2.00%, followed by tirzepatide 10 mg (–1.86%) and semaglutide 2.0 mg (–1.62%).

All three of the tirzepatide doses had greater reductions in A1c compared with the respective low, medium, and high doses of semaglutide.

Dr. Karagiannis noted that the differences are significant: “An A1c reduction even by 0.5% is often deemed clinically important,” he said.
 

Body weight reduction comparisons

The reductions in body weight across the three drug doses were greater with tirzepatide (–10.96 kg [24.2 pounds], –8.75 kg [19.3 pounds], and –6.16 kg [13.6 pounds] for 15, 10, and 5 mg, respectively) compared with semaglutide (–5.24 kg [11.6 pounds], –4.44 kg [9.8 pounds], and –2.72 kg [6 pounds] for semaglutide 2.0, 1.0, and 0.5 mg, respectively).

In terms of drug-to-drug comparisons, tirzepatide 15 mg had a mean of 5.72 kg (12.6 pounds) greater reduction in body weight vs. semaglutide 2.0 mg; tirzepatide 10 mg had a mean of 3.52 kg (7.8 pounds) reduction vs. semaglutide 2.0 mg; and tirzepatide 5 mg had a mean of a 1.72 kg (3.8 pounds) greater reduction vs. semaglutide 1.0 mg.
 

Adverse events: Increased GI events with highest tirzepatide dose

Regarding the gastrointestinal adverse events associated with the drugs, tirzepatide 15 mg had the highest rate of the two drugs at their various doses, with a risk ratio (RR) of 3.57 compared with placebo for nausea, an RR of 4.35 for vomiting, and 2.04 for diarrhea.

There were no significant differences between the two drugs for the gastrointestinal events, with the exception of the highest dose of tirzepatide, 15 mg, which had a higher risk of vomiting vs. semaglutide 1.0 (RR 1.39) and semaglutide 0.5 mg (RR 1.85).

In addition, tirzepatide 15 mg had a higher risk vs. semaglutide 0.5 mg for nausea (RR 1.45).

There were no significant differences between the two drugs and placebo in the risk of serious adverse events.
 

Real-world applications, comparisons

Dr. Karagiannis noted that the results indicate that benefits of the efficacy of the higher tirzepatide dose need to be balanced with those potential side effects.

“Although the efficacy of the high tirzepatide dose might make it a favorable choice, its real-world application can be affected on an individual’s ability to tolerate these side effects in case they occur,” he explained.

Ultimately, “some patients may prioritize tolerability over enhanced efficacy,” he added.

Furthermore, while all three maintenance doses of tirzepatide analyzed have received marketing authorization, “to get a clearer picture of the real-world tolerance to these doses outside the context of randomized controlled trials, well-designed observational studies would be necessary,” Dr. Karagiannis said.

Among other issues of comparison with the two drugs is cost.

In a recent analysis, the cost per 1% of body weight reduction was reported to be $1,197 for high-dose tirzepatide (15 mg) vs. $1,511 for semaglutide 2.4 mg, with an overall cost of 72 weeks of therapy with tirzepatide at $17,527 compared with $22,878 for semaglutide.

Overall, patients and clinicians should consider the full range of differences and similarities between the medications, “from [their] efficacy and side effects to cost-effectiveness, long-term safety, and cardiovascular profile,” Dr. Karagiannis said.

Semaglutide is currently approved by the Food and Drug Administration for treatment of type 2 diabetes and obesity/weight loss management.

Tirzepatide has also received approval for the treatment of type 2 diabetes and its manufacturers have submitted applications for its approval for obesity/weight loss management.

Dr. Karagiannis reports no relevant financial relationships.

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

Antidiabetic drug tirzepatide (Mounjaro) shows superiority over semaglutide (Ozempic, Wegovy, and Rybelsus) in controlling blood glucose as well as in the amount of weight lost, results from a meta-analysis of 22 randomized controlled trials show.

“The results indicate tirzepatide’s superior performance over subcutaneous semaglutide in managing blood sugar and achieving weight loss, making it a promising option in the pharmaceutical management of type 2 diabetes,” first author Thomas Karagiannis, MD, PhD, Aristotle University of Thessaloniki, Greece, said in an interview.

“In clinical context, the most potent doses of each drug revealed a clear difference regarding weight loss, with tirzepatide resulting in an average weight reduction that exceeded that of semaglutide by 5.7 kg (12.6 pounds),” he said.

The study is scheduled to be presented at the annual meeting of the European Association for the Study of Diabetes (EASD) in early October.

While a multitude of studies have been conducted for tirzepatide, a dual glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 (GLP-1) receptor agonist, and semaglutide, a selective GLP-1 agonist, studies comparing the two drugs directly are lacking.

For a more comprehensive understanding of how the drugs compare, Dr. Karagiannis and colleagues conducted the meta-analysis of 22 trials, including two direct comparisons, the SURPASS-2 trial and a smaller trial, and 20 other studies comparing either semaglutide or tirzepatide with a common comparator, such as placebo, basal insulin, or other GLP-RA-1 drugs.

Overall, 18,472 participants were included in the studies.

All included studies had assessed a maintenance dose of tirzepatide of either 5, 10, or 15 mg once weekly or semaglutide at doses of 0.5, 1.0, or 2.0 mg once weekly for at least 12 weeks. All comparisons were for subcutaneous injection formulations (semaglutide can also be taken orally).
 

Blood glucose reduction

Tirzepatide at 15 mg was found to have the highest efficacy in the reduction of A1c compared with placebo, with a mean difference of –2.00%, followed by tirzepatide 10 mg (–1.86%) and semaglutide 2.0 mg (–1.62%).

All three of the tirzepatide doses had greater reductions in A1c compared with the respective low, medium, and high doses of semaglutide.

Dr. Karagiannis noted that the differences are significant: “An A1c reduction even by 0.5% is often deemed clinically important,” he said.
 

Body weight reduction comparisons

The reductions in body weight across the three drug doses were greater with tirzepatide (–10.96 kg [24.2 pounds], –8.75 kg [19.3 pounds], and –6.16 kg [13.6 pounds] for 15, 10, and 5 mg, respectively) compared with semaglutide (–5.24 kg [11.6 pounds], –4.44 kg [9.8 pounds], and –2.72 kg [6 pounds] for semaglutide 2.0, 1.0, and 0.5 mg, respectively).

In terms of drug-to-drug comparisons, tirzepatide 15 mg had a mean of 5.72 kg (12.6 pounds) greater reduction in body weight vs. semaglutide 2.0 mg; tirzepatide 10 mg had a mean of 3.52 kg (7.8 pounds) reduction vs. semaglutide 2.0 mg; and tirzepatide 5 mg had a mean of a 1.72 kg (3.8 pounds) greater reduction vs. semaglutide 1.0 mg.
 

Adverse events: Increased GI events with highest tirzepatide dose

Regarding the gastrointestinal adverse events associated with the drugs, tirzepatide 15 mg had the highest rate of the two drugs at their various doses, with a risk ratio (RR) of 3.57 compared with placebo for nausea, an RR of 4.35 for vomiting, and 2.04 for diarrhea.

There were no significant differences between the two drugs for the gastrointestinal events, with the exception of the highest dose of tirzepatide, 15 mg, which had a higher risk of vomiting vs. semaglutide 1.0 (RR 1.39) and semaglutide 0.5 mg (RR 1.85).

In addition, tirzepatide 15 mg had a higher risk vs. semaglutide 0.5 mg for nausea (RR 1.45).

There were no significant differences between the two drugs and placebo in the risk of serious adverse events.
 

Real-world applications, comparisons

Dr. Karagiannis noted that the results indicate that benefits of the efficacy of the higher tirzepatide dose need to be balanced with those potential side effects.

“Although the efficacy of the high tirzepatide dose might make it a favorable choice, its real-world application can be affected on an individual’s ability to tolerate these side effects in case they occur,” he explained.

Ultimately, “some patients may prioritize tolerability over enhanced efficacy,” he added.

Furthermore, while all three maintenance doses of tirzepatide analyzed have received marketing authorization, “to get a clearer picture of the real-world tolerance to these doses outside the context of randomized controlled trials, well-designed observational studies would be necessary,” Dr. Karagiannis said.

Among other issues of comparison with the two drugs is cost.

In a recent analysis, the cost per 1% of body weight reduction was reported to be $1,197 for high-dose tirzepatide (15 mg) vs. $1,511 for semaglutide 2.4 mg, with an overall cost of 72 weeks of therapy with tirzepatide at $17,527 compared with $22,878 for semaglutide.

Overall, patients and clinicians should consider the full range of differences and similarities between the medications, “from [their] efficacy and side effects to cost-effectiveness, long-term safety, and cardiovascular profile,” Dr. Karagiannis said.

Semaglutide is currently approved by the Food and Drug Administration for treatment of type 2 diabetes and obesity/weight loss management.

Tirzepatide has also received approval for the treatment of type 2 diabetes and its manufacturers have submitted applications for its approval for obesity/weight loss management.

Dr. Karagiannis reports no relevant financial relationships.

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

Antidiabetic drug tirzepatide (Mounjaro) shows superiority over semaglutide (Ozempic, Wegovy, and Rybelsus) in controlling blood glucose as well as in the amount of weight lost, results from a meta-analysis of 22 randomized controlled trials show.

“The results indicate tirzepatide’s superior performance over subcutaneous semaglutide in managing blood sugar and achieving weight loss, making it a promising option in the pharmaceutical management of type 2 diabetes,” first author Thomas Karagiannis, MD, PhD, Aristotle University of Thessaloniki, Greece, said in an interview.

“In clinical context, the most potent doses of each drug revealed a clear difference regarding weight loss, with tirzepatide resulting in an average weight reduction that exceeded that of semaglutide by 5.7 kg (12.6 pounds),” he said.

The study is scheduled to be presented at the annual meeting of the European Association for the Study of Diabetes (EASD) in early October.

While a multitude of studies have been conducted for tirzepatide, a dual glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 (GLP-1) receptor agonist, and semaglutide, a selective GLP-1 agonist, studies comparing the two drugs directly are lacking.

For a more comprehensive understanding of how the drugs compare, Dr. Karagiannis and colleagues conducted the meta-analysis of 22 trials, including two direct comparisons, the SURPASS-2 trial and a smaller trial, and 20 other studies comparing either semaglutide or tirzepatide with a common comparator, such as placebo, basal insulin, or other GLP-RA-1 drugs.

Overall, 18,472 participants were included in the studies.

All included studies had assessed a maintenance dose of tirzepatide of either 5, 10, or 15 mg once weekly or semaglutide at doses of 0.5, 1.0, or 2.0 mg once weekly for at least 12 weeks. All comparisons were for subcutaneous injection formulations (semaglutide can also be taken orally).
 

Blood glucose reduction

Tirzepatide at 15 mg was found to have the highest efficacy in the reduction of A1c compared with placebo, with a mean difference of –2.00%, followed by tirzepatide 10 mg (–1.86%) and semaglutide 2.0 mg (–1.62%).

All three of the tirzepatide doses had greater reductions in A1c compared with the respective low, medium, and high doses of semaglutide.

Dr. Karagiannis noted that the differences are significant: “An A1c reduction even by 0.5% is often deemed clinically important,” he said.
 

Body weight reduction comparisons

The reductions in body weight across the three drug doses were greater with tirzepatide (–10.96 kg [24.2 pounds], –8.75 kg [19.3 pounds], and –6.16 kg [13.6 pounds] for 15, 10, and 5 mg, respectively) compared with semaglutide (–5.24 kg [11.6 pounds], –4.44 kg [9.8 pounds], and –2.72 kg [6 pounds] for semaglutide 2.0, 1.0, and 0.5 mg, respectively).

In terms of drug-to-drug comparisons, tirzepatide 15 mg had a mean of 5.72 kg (12.6 pounds) greater reduction in body weight vs. semaglutide 2.0 mg; tirzepatide 10 mg had a mean of 3.52 kg (7.8 pounds) reduction vs. semaglutide 2.0 mg; and tirzepatide 5 mg had a mean of a 1.72 kg (3.8 pounds) greater reduction vs. semaglutide 1.0 mg.
 

Adverse events: Increased GI events with highest tirzepatide dose

Regarding the gastrointestinal adverse events associated with the drugs, tirzepatide 15 mg had the highest rate of the two drugs at their various doses, with a risk ratio (RR) of 3.57 compared with placebo for nausea, an RR of 4.35 for vomiting, and 2.04 for diarrhea.

There were no significant differences between the two drugs for the gastrointestinal events, with the exception of the highest dose of tirzepatide, 15 mg, which had a higher risk of vomiting vs. semaglutide 1.0 (RR 1.39) and semaglutide 0.5 mg (RR 1.85).

In addition, tirzepatide 15 mg had a higher risk vs. semaglutide 0.5 mg for nausea (RR 1.45).

There were no significant differences between the two drugs and placebo in the risk of serious adverse events.
 

Real-world applications, comparisons

Dr. Karagiannis noted that the results indicate that benefits of the efficacy of the higher tirzepatide dose need to be balanced with those potential side effects.

“Although the efficacy of the high tirzepatide dose might make it a favorable choice, its real-world application can be affected on an individual’s ability to tolerate these side effects in case they occur,” he explained.

Ultimately, “some patients may prioritize tolerability over enhanced efficacy,” he added.

Furthermore, while all three maintenance doses of tirzepatide analyzed have received marketing authorization, “to get a clearer picture of the real-world tolerance to these doses outside the context of randomized controlled trials, well-designed observational studies would be necessary,” Dr. Karagiannis said.

Among other issues of comparison with the two drugs is cost.

In a recent analysis, the cost per 1% of body weight reduction was reported to be $1,197 for high-dose tirzepatide (15 mg) vs. $1,511 for semaglutide 2.4 mg, with an overall cost of 72 weeks of therapy with tirzepatide at $17,527 compared with $22,878 for semaglutide.

Overall, patients and clinicians should consider the full range of differences and similarities between the medications, “from [their] efficacy and side effects to cost-effectiveness, long-term safety, and cardiovascular profile,” Dr. Karagiannis said.

Semaglutide is currently approved by the Food and Drug Administration for treatment of type 2 diabetes and obesity/weight loss management.

Tirzepatide has also received approval for the treatment of type 2 diabetes and its manufacturers have submitted applications for its approval for obesity/weight loss management.

Dr. Karagiannis reports no relevant financial relationships.

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

AMSTERDAM – Calculating a patient’s myocardial performance index (MPI) and adding it to a standard risk-prediction model significantly increased prognostic accuracy for major adverse cardiovascular events (MACE), especially heart failure, in people with type 1 but not type 2 diabetes, an analysis of data from about 2,000 Danish patients shows.

“MPI provides incremental prognostic information” in people with type 1 diabetes that “may enhance risk prediction” for their future risk of all-cause death, acute coronary syndrome, heart failure, or stroke, Hashmat S.Z. Bahrami, MD, said at the annual congress of the European Society of Cardiology.

The primary analysis he reported showed a significantly elevated adjusted hazard ratio of 1.2 among people with either type 1 or type 2 diabetes and an elevated MPI, compared with those with diabetes but a lower MPI value.

Further analysis divided the study cohort into the 1,093 people with type 1 diabetes and the 1,030 with type 2 diabetes and showed that the significant association of elevated MPI with increased MACE was entirely confined to the type 1 diabetes subgroup, again with a hazard ratio of 1.2, but without any significant association among those with type 2 diabetes, said Dr. Bahrami, a cardiology researcher at Copenhagen University Hospital.
 

‘Trying to figure out’ the type 1 diabetes link

“We’re still trying to figure out” the explanation for this difference based on diabetes type, Dr. Bahrami said. He speculated that it might relate to a higher incidence of heart failure among those with type 1 diabetes, or to longer duration of diabetes in the type 1 subgroup.

The ability of elevated MPI to predict an increased risk specifically for heart failure was apparent in another analysis he presented that divided MACE events into the individual components of this composite. Elevated MPI significantly linked with a 1.3-fold elevated risk for heart failure in those with type 1 diabetes, but high MPI had no significant association with any of the other event types included in the MACE composite.

The researchers also assessed the incremental impact from adding MPI data to an established cardiovascular disease (CVD) risk calculator for people with type 1 diabetes, the Steno Type 1 Risk Engine, which includes nine parameters such as age, sex, blood pressure, diabetes duration, and two different measures of renal function.

This analysis showed that adding MPI significantly boosted the attributable CVD risk from an area-under-the-curve of 0.77 to an AUC of 0.79. Including MPI also boosted the AUC for risk of future heart failure from 0.77 with the existing Steno Type 1 Risk Engine to 0.83, also a significant increase.

Simultaneously with his talk at the Congress, a report on the findings was published online in the European Heart Journal Cardiovascular Imaging.
 

MPI reflects left ventricular function

MPI is calculated by adding a person’s isovolumic cardiac relaxation time to their isovolumic cardiac contraction time and dividing this by their ejection time. These time measurements come from examination with tissue Doppler M-mode echocardiography, Dr. Bahrami explained, and when assessed together reflect left ventricular function during both systolic and diastolic phases.

“MPI has been around for many years, but our technique is rather novel” and has high intra- and inter-observer reproducibility, he said. “It’s highly reproducible and feasible.”

The study included data collected prospectively from Danish adults without any known CVD enrolled in the Thousand & 1 study of people with type 1 diabetes and the Thousand & 2 study of people with type 2 diabetes. The analyses that Dr. Bahrami reported included CVD events during a median 5.3 years of follow-up.

The study received funding from Novo Nordisk. Dr. Bahrami has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

AMSTERDAM – Calculating a patient’s myocardial performance index (MPI) and adding it to a standard risk-prediction model significantly increased prognostic accuracy for major adverse cardiovascular events (MACE), especially heart failure, in people with type 1 but not type 2 diabetes, an analysis of data from about 2,000 Danish patients shows.

“MPI provides incremental prognostic information” in people with type 1 diabetes that “may enhance risk prediction” for their future risk of all-cause death, acute coronary syndrome, heart failure, or stroke, Hashmat S.Z. Bahrami, MD, said at the annual congress of the European Society of Cardiology.

The primary analysis he reported showed a significantly elevated adjusted hazard ratio of 1.2 among people with either type 1 or type 2 diabetes and an elevated MPI, compared with those with diabetes but a lower MPI value.

Further analysis divided the study cohort into the 1,093 people with type 1 diabetes and the 1,030 with type 2 diabetes and showed that the significant association of elevated MPI with increased MACE was entirely confined to the type 1 diabetes subgroup, again with a hazard ratio of 1.2, but without any significant association among those with type 2 diabetes, said Dr. Bahrami, a cardiology researcher at Copenhagen University Hospital.
 

‘Trying to figure out’ the type 1 diabetes link

“We’re still trying to figure out” the explanation for this difference based on diabetes type, Dr. Bahrami said. He speculated that it might relate to a higher incidence of heart failure among those with type 1 diabetes, or to longer duration of diabetes in the type 1 subgroup.

The ability of elevated MPI to predict an increased risk specifically for heart failure was apparent in another analysis he presented that divided MACE events into the individual components of this composite. Elevated MPI significantly linked with a 1.3-fold elevated risk for heart failure in those with type 1 diabetes, but high MPI had no significant association with any of the other event types included in the MACE composite.

The researchers also assessed the incremental impact from adding MPI data to an established cardiovascular disease (CVD) risk calculator for people with type 1 diabetes, the Steno Type 1 Risk Engine, which includes nine parameters such as age, sex, blood pressure, diabetes duration, and two different measures of renal function.

This analysis showed that adding MPI significantly boosted the attributable CVD risk from an area-under-the-curve of 0.77 to an AUC of 0.79. Including MPI also boosted the AUC for risk of future heart failure from 0.77 with the existing Steno Type 1 Risk Engine to 0.83, also a significant increase.

Simultaneously with his talk at the Congress, a report on the findings was published online in the European Heart Journal Cardiovascular Imaging.
 

MPI reflects left ventricular function

MPI is calculated by adding a person’s isovolumic cardiac relaxation time to their isovolumic cardiac contraction time and dividing this by their ejection time. These time measurements come from examination with tissue Doppler M-mode echocardiography, Dr. Bahrami explained, and when assessed together reflect left ventricular function during both systolic and diastolic phases.

“MPI has been around for many years, but our technique is rather novel” and has high intra- and inter-observer reproducibility, he said. “It’s highly reproducible and feasible.”

The study included data collected prospectively from Danish adults without any known CVD enrolled in the Thousand & 1 study of people with type 1 diabetes and the Thousand & 2 study of people with type 2 diabetes. The analyses that Dr. Bahrami reported included CVD events during a median 5.3 years of follow-up.

The study received funding from Novo Nordisk. Dr. Bahrami has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

AMSTERDAM – Calculating a patient’s myocardial performance index (MPI) and adding it to a standard risk-prediction model significantly increased prognostic accuracy for major adverse cardiovascular events (MACE), especially heart failure, in people with type 1 but not type 2 diabetes, an analysis of data from about 2,000 Danish patients shows.

“MPI provides incremental prognostic information” in people with type 1 diabetes that “may enhance risk prediction” for their future risk of all-cause death, acute coronary syndrome, heart failure, or stroke, Hashmat S.Z. Bahrami, MD, said at the annual congress of the European Society of Cardiology.

The primary analysis he reported showed a significantly elevated adjusted hazard ratio of 1.2 among people with either type 1 or type 2 diabetes and an elevated MPI, compared with those with diabetes but a lower MPI value.

Further analysis divided the study cohort into the 1,093 people with type 1 diabetes and the 1,030 with type 2 diabetes and showed that the significant association of elevated MPI with increased MACE was entirely confined to the type 1 diabetes subgroup, again with a hazard ratio of 1.2, but without any significant association among those with type 2 diabetes, said Dr. Bahrami, a cardiology researcher at Copenhagen University Hospital.
 

‘Trying to figure out’ the type 1 diabetes link

“We’re still trying to figure out” the explanation for this difference based on diabetes type, Dr. Bahrami said. He speculated that it might relate to a higher incidence of heart failure among those with type 1 diabetes, or to longer duration of diabetes in the type 1 subgroup.

The ability of elevated MPI to predict an increased risk specifically for heart failure was apparent in another analysis he presented that divided MACE events into the individual components of this composite. Elevated MPI significantly linked with a 1.3-fold elevated risk for heart failure in those with type 1 diabetes, but high MPI had no significant association with any of the other event types included in the MACE composite.

The researchers also assessed the incremental impact from adding MPI data to an established cardiovascular disease (CVD) risk calculator for people with type 1 diabetes, the Steno Type 1 Risk Engine, which includes nine parameters such as age, sex, blood pressure, diabetes duration, and two different measures of renal function.

This analysis showed that adding MPI significantly boosted the attributable CVD risk from an area-under-the-curve of 0.77 to an AUC of 0.79. Including MPI also boosted the AUC for risk of future heart failure from 0.77 with the existing Steno Type 1 Risk Engine to 0.83, also a significant increase.

Simultaneously with his talk at the Congress, a report on the findings was published online in the European Heart Journal Cardiovascular Imaging.
 

MPI reflects left ventricular function

MPI is calculated by adding a person’s isovolumic cardiac relaxation time to their isovolumic cardiac contraction time and dividing this by their ejection time. These time measurements come from examination with tissue Doppler M-mode echocardiography, Dr. Bahrami explained, and when assessed together reflect left ventricular function during both systolic and diastolic phases.

“MPI has been around for many years, but our technique is rather novel” and has high intra- and inter-observer reproducibility, he said. “It’s highly reproducible and feasible.”

The study included data collected prospectively from Danish adults without any known CVD enrolled in the Thousand & 1 study of people with type 1 diabetes and the Thousand & 2 study of people with type 2 diabetes. The analyses that Dr. Bahrami reported included CVD events during a median 5.3 years of follow-up.

The study received funding from Novo Nordisk. Dr. Bahrami has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.