Randy Dotinga

SAN DIEGO – A Food and Drug Administration official told diabetes educators that her agency is carefully monitoring the growth of an unusual development in diabetes care: the do-it-yourself artificial pancreas.

While the homemade insulin pumps are serving a need that has been unmet by manufacturers, the unregulated devices can be dangerous, according to Courtney Lias, PhD, director of the FDA’s Division of Chemistry and Toxicology Devices, who spoke at the annual meeting of the American Association of Diabetes Educators. “As they go toward a larger community, we see that the risk is raised.”

Still, “people are doing this because they feel this is the best way for them to help themselves or their children. We understand why people are doing it, but we want to make sure they do it safely,” Dr. Lias said.

At issue: The need for a “closed loop” artificial pancreas that needs little or no human intervention to measure blood sugar levels and deliver insulin as needed.

While current insulin pumps can deliver basal insulin continuously, users must program them to deliver an insulin bolus after meals or to address high blood sugar. Manufacturers are trying to develop a closed-loop artificial pancreas (also known as a bionic pancreas) that will simplify the process.

On their own, computer experts have been experimenting with jury-rigged homemade do-it-yourself (DIY) systems. “We recognize that for many PWDs [people with diabetes] the available help is not yet enough, so we are not waiting,” according to Dana Lewis and Scott Leibrand, two bloggers on a site called DIYPS.org.

In May 2016, The Wall Street Journal profiled a San Diego third-grader who uses a homemade “robotic pancreas” designed by his software engineer father. “More than 50 people have soldered, tinkered, and written software to make such devices for themselves or their children,” according to the Wall Street Journal report.

In her talk at the American Association of Diabetes Educators meeting, Dr. Lias noted that “there are a lot of questions about whether this is something that should be done.”

The algorithm behind a homemade device is one of area of concern, she said. “Who developed it and who’s responsible for having developed it? You may not understand how the algorithm is developed and what information is behind it. If something goes wrong, there’s no recourse.”

There are also questions about quality control, she noted: “Is there a responsible party for understanding things, for collecting information and making corrections?”

Dr. Lias said physicians should ask these questions if patients say they are using a DIY artificial pancreas: Do you understand exactly what algorithm is being used? Is it right for you? Have you checked the code to ensure it implements the algorithm correctly? Have you double-checked? When new, modified versions of code are shared, have you re-validated your entire system before implementing it?

It’s also important, she said, to note that these devices have not been determined to be safe and effective.

As the FDA monitors these DIY devices, Dr. Lias said, it’s also working to be ready to consider the work of manufacturers who are trying to develop the first commercial artificial pancreas device.

“Artificial pancreas devices do not have to be perfect with zero risk to be beneficial,” she says. “The approval decision is a benefit/risk decision. We make this decision in the context of the high risks that people with diabetes face every day.”

For now, she says, one focus is to make it easier for companies to work together to create the components of an artificial pancreas device.

The FDA is also concerned about what newly diagnosed people with diabetes will do if their devices break down, and they don’t know how to give themselves an insulin injection. “That’s a scenario that we will need to work out,” she said. “We’re talking with manufacturers about how they plan to work with that.”

SAN DIEGO – A Food and Drug Administration official told diabetes educators that her agency is carefully monitoring the growth of an unusual development in diabetes care: the do-it-yourself artificial pancreas.

While the homemade insulin pumps are serving a need that has been unmet by manufacturers, the unregulated devices can be dangerous, according to Courtney Lias, PhD, director of the FDA’s Division of Chemistry and Toxicology Devices, who spoke at the annual meeting of the American Association of Diabetes Educators. “As they go toward a larger community, we see that the risk is raised.”

Still, “people are doing this because they feel this is the best way for them to help themselves or their children. We understand why people are doing it, but we want to make sure they do it safely,” Dr. Lias said.

At issue: The need for a “closed loop” artificial pancreas that needs little or no human intervention to measure blood sugar levels and deliver insulin as needed.

While current insulin pumps can deliver basal insulin continuously, users must program them to deliver an insulin bolus after meals or to address high blood sugar. Manufacturers are trying to develop a closed-loop artificial pancreas (also known as a bionic pancreas) that will simplify the process.

On their own, computer experts have been experimenting with jury-rigged homemade do-it-yourself (DIY) systems. “We recognize that for many PWDs [people with diabetes] the available help is not yet enough, so we are not waiting,” according to Dana Lewis and Scott Leibrand, two bloggers on a site called DIYPS.org.

In May 2016, The Wall Street Journal profiled a San Diego third-grader who uses a homemade “robotic pancreas” designed by his software engineer father. “More than 50 people have soldered, tinkered, and written software to make such devices for themselves or their children,” according to the Wall Street Journal report.

In her talk at the American Association of Diabetes Educators meeting, Dr. Lias noted that “there are a lot of questions about whether this is something that should be done.”

The algorithm behind a homemade device is one of area of concern, she said. “Who developed it and who’s responsible for having developed it? You may not understand how the algorithm is developed and what information is behind it. If something goes wrong, there’s no recourse.”

There are also questions about quality control, she noted: “Is there a responsible party for understanding things, for collecting information and making corrections?”

Dr. Lias said physicians should ask these questions if patients say they are using a DIY artificial pancreas: Do you understand exactly what algorithm is being used? Is it right for you? Have you checked the code to ensure it implements the algorithm correctly? Have you double-checked? When new, modified versions of code are shared, have you re-validated your entire system before implementing it?

It’s also important, she said, to note that these devices have not been determined to be safe and effective.

As the FDA monitors these DIY devices, Dr. Lias said, it’s also working to be ready to consider the work of manufacturers who are trying to develop the first commercial artificial pancreas device.

“Artificial pancreas devices do not have to be perfect with zero risk to be beneficial,” she says. “The approval decision is a benefit/risk decision. We make this decision in the context of the high risks that people with diabetes face every day.”

For now, she says, one focus is to make it easier for companies to work together to create the components of an artificial pancreas device.

The FDA is also concerned about what newly diagnosed people with diabetes will do if their devices break down, and they don’t know how to give themselves an insulin injection. “That’s a scenario that we will need to work out,” she said. “We’re talking with manufacturers about how they plan to work with that.”

SAN DIEGO – A Food and Drug Administration official told diabetes educators that her agency is carefully monitoring the growth of an unusual development in diabetes care: the do-it-yourself artificial pancreas.

While the homemade insulin pumps are serving a need that has been unmet by manufacturers, the unregulated devices can be dangerous, according to Courtney Lias, PhD, director of the FDA’s Division of Chemistry and Toxicology Devices, who spoke at the annual meeting of the American Association of Diabetes Educators. “As they go toward a larger community, we see that the risk is raised.”

Still, “people are doing this because they feel this is the best way for them to help themselves or their children. We understand why people are doing it, but we want to make sure they do it safely,” Dr. Lias said.

At issue: The need for a “closed loop” artificial pancreas that needs little or no human intervention to measure blood sugar levels and deliver insulin as needed.

While current insulin pumps can deliver basal insulin continuously, users must program them to deliver an insulin bolus after meals or to address high blood sugar. Manufacturers are trying to develop a closed-loop artificial pancreas (also known as a bionic pancreas) that will simplify the process.

On their own, computer experts have been experimenting with jury-rigged homemade do-it-yourself (DIY) systems. “We recognize that for many PWDs [people with diabetes] the available help is not yet enough, so we are not waiting,” according to Dana Lewis and Scott Leibrand, two bloggers on a site called DIYPS.org.

In May 2016, The Wall Street Journal profiled a San Diego third-grader who uses a homemade “robotic pancreas” designed by his software engineer father. “More than 50 people have soldered, tinkered, and written software to make such devices for themselves or their children,” according to the Wall Street Journal report.

In her talk at the American Association of Diabetes Educators meeting, Dr. Lias noted that “there are a lot of questions about whether this is something that should be done.”

The algorithm behind a homemade device is one of area of concern, she said. “Who developed it and who’s responsible for having developed it? You may not understand how the algorithm is developed and what information is behind it. If something goes wrong, there’s no recourse.”

There are also questions about quality control, she noted: “Is there a responsible party for understanding things, for collecting information and making corrections?”

Dr. Lias said physicians should ask these questions if patients say they are using a DIY artificial pancreas: Do you understand exactly what algorithm is being used? Is it right for you? Have you checked the code to ensure it implements the algorithm correctly? Have you double-checked? When new, modified versions of code are shared, have you re-validated your entire system before implementing it?

It’s also important, she said, to note that these devices have not been determined to be safe and effective.

As the FDA monitors these DIY devices, Dr. Lias said, it’s also working to be ready to consider the work of manufacturers who are trying to develop the first commercial artificial pancreas device.

“Artificial pancreas devices do not have to be perfect with zero risk to be beneficial,” she says. “The approval decision is a benefit/risk decision. We make this decision in the context of the high risks that people with diabetes face every day.”

For now, she says, one focus is to make it easier for companies to work together to create the components of an artificial pancreas device.

The FDA is also concerned about what newly diagnosed people with diabetes will do if their devices break down, and they don’t know how to give themselves an insulin injection. “That’s a scenario that we will need to work out,” she said. “We’re talking with manufacturers about how they plan to work with that.”

SAN DIEGO – Weight loss isn’t always a top priority for people with diabetes. Patients can figure out their proper carb intake. And don’t fret over an optimal percentage mix of carbs, fat and proteins.

A nutrition consultant gave this advice to colleagues at the annual meeting of the American Association of Diabetes Educators, startling some of those in the audience. And no wonder: A few years ago, these kinds of tips would have surprised the educator herself, Mary Ann Hodorowicz, RN, MBA, a licensed registered dietitian and certified diabetes educator based in the Chicago area.

For instance, she was taught that specific percentages of our diets must come from carbohydrates, protein, and fat. “If you didn’t do it that way, you committed the most major mortal sin,” she said. “You’ll go to diabetes jail, and you’ll probably be fired from your job, and the patient will die.”

In fact, “there’s no evidence to support those percentages,” she said. “They don’t mean anything in terms of blood glucose control, although we do have percentages of fat to control lipids and percentages of protein for health and well-being.”

So how many carbs should diabetics eat? She acknowledges to patients that she doesn’t know: “I don’t have a clue.” Instead, she urges them to figure it out themselves: “How many can you get away with and reach your 2-hour post-meal target? My job is to teach you what how to measure, whether it’s by handfuls, exchanges, servings, or grams. Here’s a log sheet, go home and write about how many carbs you’re eating, and test your blood sugar 2 hours later. You’ll find out really quickly how many carbs you can eat to reach that post-meal target.”

Ms. Hodorowicz provided other “evidence-based” tips about nutrition for diabetes patients:

• Assess the need for weight loss in overweight and obese patients, and don’t assume that weight loss is always the top priority.

In new patients with type 2 diabetes, weight loss of 7% is optimal and can typically be achieved with an energy deficit of 500-750 calories a day: a limit of 1,200-1,500 calories for women and 1,500-1,800 for men.

However, “studies of sustained weight loss at 1 or more years have shown inconsistent effects on hemoglobin A1c, even though modest weight loss is shown to improve insulin resistance in overweight and obese insulin-resistant persons. This blows out what we’ve been taught in our careers,” she said.

Why? Weight reduction does improve blood glucose in these type 2 patients at first, she said, but they’ll go into insulin deficiency if they live long enough.

After that happens, she said, “weight loss is not that effective in controlling blood glucose. At that point, the gurus are saying that we really want to prevent weight gain and seek blood glucose control.”

• Don’t go overboard on the glycemic index.

Ms. Hodorowicz advises patients to substitute low-glycemic foods for high-glycemic foods. However, “the evidence does not support the glycemic index as the best meal planning strategy for a patient with diabetes. It doesn’t do better than controlling carbs.”

In addition, she said, teaching patients about the confusing glycemic index is a drag: “Good luck!” But, she said, “substituting foods is a good thing.”

• Be aware of the limited evidence supporting supplements for glucose control.

On the supplement front, chromium, cinnamon, herbs and vitamin D haven’t been clearly demonstrated to control glucose, she says.

• Encourage consumption – even via supplementation – of fiber and plant stanols and sterols.

Ms. Hodorowicz encourages patients to consume 1.6-3.0 grams a day in plant stanols and sterols, which can be purchased in over-the-counter capsules and via fortified foods like certain Minute Maid and Benecol products.

“You’re fooling the body into thinking it’s cholesterol,” she said, “but it’s innocuous.”

She also advises patients to boost viscous soluble fiber to 7-13 g/day. Since it’s not feasible to do this through food, she recommends supplements: “You really need to supplement your diet with psyllium fiber that you get in a bottle.”

Ms. Hodorowicz reported having no relevant financial disclosures.

SAN DIEGO – Weight loss isn’t always a top priority for people with diabetes. Patients can figure out their proper carb intake. And don’t fret over an optimal percentage mix of carbs, fat and proteins.

A nutrition consultant gave this advice to colleagues at the annual meeting of the American Association of Diabetes Educators, startling some of those in the audience. And no wonder: A few years ago, these kinds of tips would have surprised the educator herself, Mary Ann Hodorowicz, RN, MBA, a licensed registered dietitian and certified diabetes educator based in the Chicago area.

For instance, she was taught that specific percentages of our diets must come from carbohydrates, protein, and fat. “If you didn’t do it that way, you committed the most major mortal sin,” she said. “You’ll go to diabetes jail, and you’ll probably be fired from your job, and the patient will die.”

In fact, “there’s no evidence to support those percentages,” she said. “They don’t mean anything in terms of blood glucose control, although we do have percentages of fat to control lipids and percentages of protein for health and well-being.”

So how many carbs should diabetics eat? She acknowledges to patients that she doesn’t know: “I don’t have a clue.” Instead, she urges them to figure it out themselves: “How many can you get away with and reach your 2-hour post-meal target? My job is to teach you what how to measure, whether it’s by handfuls, exchanges, servings, or grams. Here’s a log sheet, go home and write about how many carbs you’re eating, and test your blood sugar 2 hours later. You’ll find out really quickly how many carbs you can eat to reach that post-meal target.”

Ms. Hodorowicz provided other “evidence-based” tips about nutrition for diabetes patients:

• Assess the need for weight loss in overweight and obese patients, and don’t assume that weight loss is always the top priority.

In new patients with type 2 diabetes, weight loss of 7% is optimal and can typically be achieved with an energy deficit of 500-750 calories a day: a limit of 1,200-1,500 calories for women and 1,500-1,800 for men.

However, “studies of sustained weight loss at 1 or more years have shown inconsistent effects on hemoglobin A1c, even though modest weight loss is shown to improve insulin resistance in overweight and obese insulin-resistant persons. This blows out what we’ve been taught in our careers,” she said.

Why? Weight reduction does improve blood glucose in these type 2 patients at first, she said, but they’ll go into insulin deficiency if they live long enough.

After that happens, she said, “weight loss is not that effective in controlling blood glucose. At that point, the gurus are saying that we really want to prevent weight gain and seek blood glucose control.”

• Don’t go overboard on the glycemic index.

Ms. Hodorowicz advises patients to substitute low-glycemic foods for high-glycemic foods. However, “the evidence does not support the glycemic index as the best meal planning strategy for a patient with diabetes. It doesn’t do better than controlling carbs.”

In addition, she said, teaching patients about the confusing glycemic index is a drag: “Good luck!” But, she said, “substituting foods is a good thing.”

• Be aware of the limited evidence supporting supplements for glucose control.

On the supplement front, chromium, cinnamon, herbs and vitamin D haven’t been clearly demonstrated to control glucose, she says.

• Encourage consumption – even via supplementation – of fiber and plant stanols and sterols.

Ms. Hodorowicz encourages patients to consume 1.6-3.0 grams a day in plant stanols and sterols, which can be purchased in over-the-counter capsules and via fortified foods like certain Minute Maid and Benecol products.

“You’re fooling the body into thinking it’s cholesterol,” she said, “but it’s innocuous.”

She also advises patients to boost viscous soluble fiber to 7-13 g/day. Since it’s not feasible to do this through food, she recommends supplements: “You really need to supplement your diet with psyllium fiber that you get in a bottle.”

Ms. Hodorowicz reported having no relevant financial disclosures.

SAN DIEGO – Weight loss isn’t always a top priority for people with diabetes. Patients can figure out their proper carb intake. And don’t fret over an optimal percentage mix of carbs, fat and proteins.

A nutrition consultant gave this advice to colleagues at the annual meeting of the American Association of Diabetes Educators, startling some of those in the audience. And no wonder: A few years ago, these kinds of tips would have surprised the educator herself, Mary Ann Hodorowicz, RN, MBA, a licensed registered dietitian and certified diabetes educator based in the Chicago area.

For instance, she was taught that specific percentages of our diets must come from carbohydrates, protein, and fat. “If you didn’t do it that way, you committed the most major mortal sin,” she said. “You’ll go to diabetes jail, and you’ll probably be fired from your job, and the patient will die.”

In fact, “there’s no evidence to support those percentages,” she said. “They don’t mean anything in terms of blood glucose control, although we do have percentages of fat to control lipids and percentages of protein for health and well-being.”

So how many carbs should diabetics eat? She acknowledges to patients that she doesn’t know: “I don’t have a clue.” Instead, she urges them to figure it out themselves: “How many can you get away with and reach your 2-hour post-meal target? My job is to teach you what how to measure, whether it’s by handfuls, exchanges, servings, or grams. Here’s a log sheet, go home and write about how many carbs you’re eating, and test your blood sugar 2 hours later. You’ll find out really quickly how many carbs you can eat to reach that post-meal target.”

Ms. Hodorowicz provided other “evidence-based” tips about nutrition for diabetes patients:

• Assess the need for weight loss in overweight and obese patients, and don’t assume that weight loss is always the top priority.

In new patients with type 2 diabetes, weight loss of 7% is optimal and can typically be achieved with an energy deficit of 500-750 calories a day: a limit of 1,200-1,500 calories for women and 1,500-1,800 for men.

However, “studies of sustained weight loss at 1 or more years have shown inconsistent effects on hemoglobin A1c, even though modest weight loss is shown to improve insulin resistance in overweight and obese insulin-resistant persons. This blows out what we’ve been taught in our careers,” she said.

Why? Weight reduction does improve blood glucose in these type 2 patients at first, she said, but they’ll go into insulin deficiency if they live long enough.

After that happens, she said, “weight loss is not that effective in controlling blood glucose. At that point, the gurus are saying that we really want to prevent weight gain and seek blood glucose control.”

• Don’t go overboard on the glycemic index.

Ms. Hodorowicz advises patients to substitute low-glycemic foods for high-glycemic foods. However, “the evidence does not support the glycemic index as the best meal planning strategy for a patient with diabetes. It doesn’t do better than controlling carbs.”

In addition, she said, teaching patients about the confusing glycemic index is a drag: “Good luck!” But, she said, “substituting foods is a good thing.”

• Be aware of the limited evidence supporting supplements for glucose control.

On the supplement front, chromium, cinnamon, herbs and vitamin D haven’t been clearly demonstrated to control glucose, she says.

• Encourage consumption – even via supplementation – of fiber and plant stanols and sterols.

Ms. Hodorowicz encourages patients to consume 1.6-3.0 grams a day in plant stanols and sterols, which can be purchased in over-the-counter capsules and via fortified foods like certain Minute Maid and Benecol products.

“You’re fooling the body into thinking it’s cholesterol,” she said, “but it’s innocuous.”

She also advises patients to boost viscous soluble fiber to 7-13 g/day. Since it’s not feasible to do this through food, she recommends supplements: “You really need to supplement your diet with psyllium fiber that you get in a bottle.”

Ms. Hodorowicz reported having no relevant financial disclosures.

SAN DIEGO – The former president of the Endocrine Society told diabetes educators that it’s time to replace the much-used hemoglobin A_1c level with a measurement that better reflects how diabetes patients are faring.

The problem is that the HbA_1c is “woefully inadequate,” said Robert Vigersky, MD, the medical director of Medtronic Diabetes and president of the Endocrine Society in 2009-2010. “It doesn’t tell you about time-in-range or the frequency, duration, and severity of hypoglycemia or hyperglycemia. And there’s nothing about glycemic variability.”

These measurements are important, he told an audience at the annual meeting of the American Association of Diabetes Educators. For example, “there are several new classes of medication and new technologies. Some decrease HbA_1c with no effect on hypoglycemia. Some affect hypoglycemia with no effect on HbA_1c. How do we think about these globally and compare them to one another?”

To shed more light on the true condition of patients, he said, it’s time to “change the conversation from HbA_1c alone to one that is more glucose-centric. It’s about thinking about glucose as a vital sign, not HbA_1c. This may help health care providers, regulators, and payers better understand what is best for patients.”

He is also thinking about going beyond sugar levels. “Maybe a future composite metric will have more than just glucose numbers,” he said.

Indeed, last hear Dr. Vigersky proposed a composite metric known as “the hypoglycemia-A1C score” that can also take factors like weight, quality of life and costs into account (J Diabetes Sci Technol. 2015 Feb 19;9[5]:1148-51).

But he acknowledged there are challenges. For one, there are at least a dozen different ways to measure hypoglycemia, he said, “and every paper cherry-picks the method they want to show their data in the best light.”

It’s also not clear how best to represent the data once researchers figure out which statistics should be included. Should the overall measurement be a single number? Or should there be multiple numbers? In that case, should the numbers be represented graphically?

Dr. Vigersky said he is working on an approach that illustrates various measurements through a pentagon shape. Its appearance reflects measurements such as mean glucose and duration of high glucose.

However, he predicted the future will produce a simpler measurement: “a multicomponent single value.”

What’s next? “We need to educate the payers about how we can’t stay with HbA_1c. This will take an effort with professional societies. Once everyone agrees, we need to get some consensus about what the elements of the composite metric are.”

Dr. Vigersky is hopeful that the HbA_1c is on its way out, although he acknowledges that it won’t be a rapid process. “It took 20 or more years for everyone to buy into A1C and understand what it represented,” he said. “Changing the conversation isn’t going to happen overnight. But unless we start to address it, it will never happen.”

Dr. Vigersky reported having no relevant financial disclosures.

SAN DIEGO – The former president of the Endocrine Society told diabetes educators that it’s time to replace the much-used hemoglobin A_1c level with a measurement that better reflects how diabetes patients are faring.

The problem is that the HbA_1c is “woefully inadequate,” said Robert Vigersky, MD, the medical director of Medtronic Diabetes and president of the Endocrine Society in 2009-2010. “It doesn’t tell you about time-in-range or the frequency, duration, and severity of hypoglycemia or hyperglycemia. And there’s nothing about glycemic variability.”

These measurements are important, he told an audience at the annual meeting of the American Association of Diabetes Educators. For example, “there are several new classes of medication and new technologies. Some decrease HbA_1c with no effect on hypoglycemia. Some affect hypoglycemia with no effect on HbA_1c. How do we think about these globally and compare them to one another?”

To shed more light on the true condition of patients, he said, it’s time to “change the conversation from HbA_1c alone to one that is more glucose-centric. It’s about thinking about glucose as a vital sign, not HbA_1c. This may help health care providers, regulators, and payers better understand what is best for patients.”

He is also thinking about going beyond sugar levels. “Maybe a future composite metric will have more than just glucose numbers,” he said.

Indeed, last hear Dr. Vigersky proposed a composite metric known as “the hypoglycemia-A1C score” that can also take factors like weight, quality of life and costs into account (J Diabetes Sci Technol. 2015 Feb 19;9[5]:1148-51).

But he acknowledged there are challenges. For one, there are at least a dozen different ways to measure hypoglycemia, he said, “and every paper cherry-picks the method they want to show their data in the best light.”

It’s also not clear how best to represent the data once researchers figure out which statistics should be included. Should the overall measurement be a single number? Or should there be multiple numbers? In that case, should the numbers be represented graphically?

Dr. Vigersky said he is working on an approach that illustrates various measurements through a pentagon shape. Its appearance reflects measurements such as mean glucose and duration of high glucose.

However, he predicted the future will produce a simpler measurement: “a multicomponent single value.”

What’s next? “We need to educate the payers about how we can’t stay with HbA_1c. This will take an effort with professional societies. Once everyone agrees, we need to get some consensus about what the elements of the composite metric are.”

Dr. Vigersky is hopeful that the HbA_1c is on its way out, although he acknowledges that it won’t be a rapid process. “It took 20 or more years for everyone to buy into A1C and understand what it represented,” he said. “Changing the conversation isn’t going to happen overnight. But unless we start to address it, it will never happen.”

Dr. Vigersky reported having no relevant financial disclosures.

SAN DIEGO – The former president of the Endocrine Society told diabetes educators that it’s time to replace the much-used hemoglobin A_1c level with a measurement that better reflects how diabetes patients are faring.

The problem is that the HbA_1c is “woefully inadequate,” said Robert Vigersky, MD, the medical director of Medtronic Diabetes and president of the Endocrine Society in 2009-2010. “It doesn’t tell you about time-in-range or the frequency, duration, and severity of hypoglycemia or hyperglycemia. And there’s nothing about glycemic variability.”

These measurements are important, he told an audience at the annual meeting of the American Association of Diabetes Educators. For example, “there are several new classes of medication and new technologies. Some decrease HbA_1c with no effect on hypoglycemia. Some affect hypoglycemia with no effect on HbA_1c. How do we think about these globally and compare them to one another?”

To shed more light on the true condition of patients, he said, it’s time to “change the conversation from HbA_1c alone to one that is more glucose-centric. It’s about thinking about glucose as a vital sign, not HbA_1c. This may help health care providers, regulators, and payers better understand what is best for patients.”

He is also thinking about going beyond sugar levels. “Maybe a future composite metric will have more than just glucose numbers,” he said.

Indeed, last hear Dr. Vigersky proposed a composite metric known as “the hypoglycemia-A1C score” that can also take factors like weight, quality of life and costs into account (J Diabetes Sci Technol. 2015 Feb 19;9[5]:1148-51).

But he acknowledged there are challenges. For one, there are at least a dozen different ways to measure hypoglycemia, he said, “and every paper cherry-picks the method they want to show their data in the best light.”

It’s also not clear how best to represent the data once researchers figure out which statistics should be included. Should the overall measurement be a single number? Or should there be multiple numbers? In that case, should the numbers be represented graphically?

Dr. Vigersky said he is working on an approach that illustrates various measurements through a pentagon shape. Its appearance reflects measurements such as mean glucose and duration of high glucose.

However, he predicted the future will produce a simpler measurement: “a multicomponent single value.”

What’s next? “We need to educate the payers about how we can’t stay with HbA_1c. This will take an effort with professional societies. Once everyone agrees, we need to get some consensus about what the elements of the composite metric are.”

Dr. Vigersky is hopeful that the HbA_1c is on its way out, although he acknowledges that it won’t be a rapid process. “It took 20 or more years for everyone to buy into A1C and understand what it represented,” he said. “Changing the conversation isn’t going to happen overnight. But unless we start to address it, it will never happen.”

Dr. Vigersky reported having no relevant financial disclosures.

SAN DIEGO – New research suggests histamine-2 receptor antagonists aren’t a viable alternative to proton pump inhibitors to prevent recurrence of bleeding peptic ulcers in clopidogrel users.

U.S. and European agencies have warned of interactions between proton pump inhibitors (PPIs) and clopidogrel. But a study presented at the annual Digestive Disease Week finds significant upper GI events were much more common in patients who took famotidine (Protonix), a histamine-2 receptor antagonist (H₂RA), compared with those who took pantoprazole (Pepcid), a PPI, as a preventive treatment.

“The findings will change the practice of some physicians who prescribe H₂RA to prevent UGI [upper GI] events in clopidogrel users,” said study lead author Dr. Ping-I Hsu, chief of gastroenterology at Kaohsiung Veterans General Hospital and professor of medicine at National Yang-Ming University, both in Taiwan.

Currently, Dr. Hsu said, “physicians often use PPIs to prevent ulcer complications in clopidogrel users because it is the only drug proven useful in the prevention of peptic ulcers and ulcer complications in clopidogrel users.”

But “both the U.S. Food & Drug Administration and the European Medicines Agency have posted safety warnings and discourage the use of PPIs with clopidogrel unless absolutely necessary,” he said.

Enter the prospect of H₂RA medications as an alternative. The new study, Dr. Hsu said, is the first to explore the GI protection effect and safety of H₂RAs in patients on clopidogrel monotherapy.

The randomized prospective study followed 120 patients with a history of peptic ulcer bleeding (but not at initial endoscopy) and atherosclerosis. All long-term users of ADP receptor antagonists, they were assigned to pantoprazole (40 mg daily) or famotidine (40 mg daily) for 48 weeks.

Patients were examined via endoscopy when they experienced events like severe epigastric discomfort.

The famotidine group had more significant upper GI events (13.3%) than the pantoprazole group (1.7%). Diarrhea was equal in both groups (1.7%). Pneumonia was comparable (0% and 1.7% for pantoprazole and famotidine, respectively), as was fracture (1.7% and 0%).

Wider differences were found in acute myocardial infarction (1.5% and 4.5%), and cerebral vascular accident (0% and 3.4%) for pantoprazole and famotidine, respectively.

According to Dr. Hsu, three earlier studies linked concurrent use of PPIs and clopidogrel to significant increases in cardiovascular events. But this study linked a higher cardiac risk to the H₂RA medication.

The researchers found no differences between the drugs in sequential changes of serum magnesium levels and bone mineral densities.

Dr. Hsu made this recommendation to physicians: “Please don’t use H₂RAs to prevent peptic ulcer or ulcer complications in clopidogrel users. It is ineffective to prevent UGI [upper GI] events in clopidogrel users who have a history of ulcer bleeding. PPIs can effectively prevent UGI events in clopidogrel users with a history of ulcer bleeding.”

In addition, he said, the risk of thrombotic events is lower on a PPI.

SAN DIEGO – New research suggests histamine-2 receptor antagonists aren’t a viable alternative to proton pump inhibitors to prevent recurrence of bleeding peptic ulcers in clopidogrel users.

U.S. and European agencies have warned of interactions between proton pump inhibitors (PPIs) and clopidogrel. But a study presented at the annual Digestive Disease Week finds significant upper GI events were much more common in patients who took famotidine (Protonix), a histamine-2 receptor antagonist (H₂RA), compared with those who took pantoprazole (Pepcid), a PPI, as a preventive treatment.

“The findings will change the practice of some physicians who prescribe H₂RA to prevent UGI [upper GI] events in clopidogrel users,” said study lead author Dr. Ping-I Hsu, chief of gastroenterology at Kaohsiung Veterans General Hospital and professor of medicine at National Yang-Ming University, both in Taiwan.

Currently, Dr. Hsu said, “physicians often use PPIs to prevent ulcer complications in clopidogrel users because it is the only drug proven useful in the prevention of peptic ulcers and ulcer complications in clopidogrel users.”

But “both the U.S. Food & Drug Administration and the European Medicines Agency have posted safety warnings and discourage the use of PPIs with clopidogrel unless absolutely necessary,” he said.

Enter the prospect of H₂RA medications as an alternative. The new study, Dr. Hsu said, is the first to explore the GI protection effect and safety of H₂RAs in patients on clopidogrel monotherapy.

The randomized prospective study followed 120 patients with a history of peptic ulcer bleeding (but not at initial endoscopy) and atherosclerosis. All long-term users of ADP receptor antagonists, they were assigned to pantoprazole (40 mg daily) or famotidine (40 mg daily) for 48 weeks.

Patients were examined via endoscopy when they experienced events like severe epigastric discomfort.

The famotidine group had more significant upper GI events (13.3%) than the pantoprazole group (1.7%). Diarrhea was equal in both groups (1.7%). Pneumonia was comparable (0% and 1.7% for pantoprazole and famotidine, respectively), as was fracture (1.7% and 0%).

Wider differences were found in acute myocardial infarction (1.5% and 4.5%), and cerebral vascular accident (0% and 3.4%) for pantoprazole and famotidine, respectively.

According to Dr. Hsu, three earlier studies linked concurrent use of PPIs and clopidogrel to significant increases in cardiovascular events. But this study linked a higher cardiac risk to the H₂RA medication.

The researchers found no differences between the drugs in sequential changes of serum magnesium levels and bone mineral densities.

Dr. Hsu made this recommendation to physicians: “Please don’t use H₂RAs to prevent peptic ulcer or ulcer complications in clopidogrel users. It is ineffective to prevent UGI [upper GI] events in clopidogrel users who have a history of ulcer bleeding. PPIs can effectively prevent UGI events in clopidogrel users with a history of ulcer bleeding.”

In addition, he said, the risk of thrombotic events is lower on a PPI.

SAN DIEGO – New research suggests histamine-2 receptor antagonists aren’t a viable alternative to proton pump inhibitors to prevent recurrence of bleeding peptic ulcers in clopidogrel users.

U.S. and European agencies have warned of interactions between proton pump inhibitors (PPIs) and clopidogrel. But a study presented at the annual Digestive Disease Week finds significant upper GI events were much more common in patients who took famotidine (Protonix), a histamine-2 receptor antagonist (H₂RA), compared with those who took pantoprazole (Pepcid), a PPI, as a preventive treatment.

“The findings will change the practice of some physicians who prescribe H₂RA to prevent UGI [upper GI] events in clopidogrel users,” said study lead author Dr. Ping-I Hsu, chief of gastroenterology at Kaohsiung Veterans General Hospital and professor of medicine at National Yang-Ming University, both in Taiwan.

Currently, Dr. Hsu said, “physicians often use PPIs to prevent ulcer complications in clopidogrel users because it is the only drug proven useful in the prevention of peptic ulcers and ulcer complications in clopidogrel users.”

But “both the U.S. Food & Drug Administration and the European Medicines Agency have posted safety warnings and discourage the use of PPIs with clopidogrel unless absolutely necessary,” he said.

Enter the prospect of H₂RA medications as an alternative. The new study, Dr. Hsu said, is the first to explore the GI protection effect and safety of H₂RAs in patients on clopidogrel monotherapy.

The randomized prospective study followed 120 patients with a history of peptic ulcer bleeding (but not at initial endoscopy) and atherosclerosis. All long-term users of ADP receptor antagonists, they were assigned to pantoprazole (40 mg daily) or famotidine (40 mg daily) for 48 weeks.

Patients were examined via endoscopy when they experienced events like severe epigastric discomfort.

The famotidine group had more significant upper GI events (13.3%) than the pantoprazole group (1.7%). Diarrhea was equal in both groups (1.7%). Pneumonia was comparable (0% and 1.7% for pantoprazole and famotidine, respectively), as was fracture (1.7% and 0%).

Wider differences were found in acute myocardial infarction (1.5% and 4.5%), and cerebral vascular accident (0% and 3.4%) for pantoprazole and famotidine, respectively.

According to Dr. Hsu, three earlier studies linked concurrent use of PPIs and clopidogrel to significant increases in cardiovascular events. But this study linked a higher cardiac risk to the H₂RA medication.

The researchers found no differences between the drugs in sequential changes of serum magnesium levels and bone mineral densities.

Dr. Hsu made this recommendation to physicians: “Please don’t use H₂RAs to prevent peptic ulcer or ulcer complications in clopidogrel users. It is ineffective to prevent UGI [upper GI] events in clopidogrel users who have a history of ulcer bleeding. PPIs can effectively prevent UGI events in clopidogrel users with a history of ulcer bleeding.”

In addition, he said, the risk of thrombotic events is lower on a PPI.

SAN DIEGO – Despite an increase in women entering the gastroenterology field, a new study finds that they are severely underrepresented in academia as fellowship program directors and division chiefs.

In addition, most female program directors have lower academic ranks than did their male counterparts.

“A lack of female leadership can detract future women from entering the field,” said study lead author Dr. Sonali Paul, a gastroenterologist and research fellow in medicine at Massachusetts General Hospital in Boston. “Further research is needed to understand these barriers, whether they’re due to personal choice or more systemic issues. Understanding the challenges women face in academic promotions will allow for policy changes.”

According to statistics quoted in the study, women made up more than a third of gastroenterology fellowship positions and 18% of the academic workforce in 2013. At the same time, more than half of medical graduates are women.

“The role of women in GI is important, especially given that studies have shown that women prefer female endoscopists,” Dr. Paul said. And women make up significant portions of the patient load in GI clinical practices, she said.

But it hasn’t been clear if the increase in fellowship positions has corresponded to a higher number of women in positions of academic leadership.

To better understand the situation, Dr. Paul and her associates analyzed the gender and academic rank of GI fellowship program directors and division chiefs in 2015. The researchers analyzed websites and social media to gather the data and also made direct contacts, Dr. Paul said.

At 165 academic GI programs, 85% of these positions were held by men. Of program directors, 81% were male; 89% of division chiefs were male.

Of the men who hold these positions, half were program directors and half were division chiefs. Among women, however, 67% were program directors and 33% were division chiefs.

There was also a disparity in terms of academic experience. Female division chiefs were less likely to be professors (46%), compared with male division chiefs (82%).

Why the disparity? One possible explanation is a “leaky pipeline,” Dr. Paul said. This refers to the fact that women leave academic medicine at higher rates than men do.

Family obligations are one explanation, she said, “but I don’t think that explains everything in the process. A lot of women have felt that promotion was of no benefit to them and that there was a lack of encouragement.”

Dr. Paul notes that the study has limitations. It’s cross sectional, and misclassification errors are possible.

During a discussion period, a questioner noted that it takes time for an academic physician to move up: “Shouldn’t we look at the fraction of graduates in 1996 who were female and now are professors? It’s unusual for someone at less than a professor rank to be division chief, as compared with program director.” Dr. Paul agreed that this would be a good avenue of research.

In addition, she said, “it will be important to examine if these gender disparities are unique to gastroenterology or if they extend into other specialties that are more female dominant, such as rheumatology or geriatrics.”

SAN DIEGO – Despite an increase in women entering the gastroenterology field, a new study finds that they are severely underrepresented in academia as fellowship program directors and division chiefs.

In addition, most female program directors have lower academic ranks than did their male counterparts.

“A lack of female leadership can detract future women from entering the field,” said study lead author Dr. Sonali Paul, a gastroenterologist and research fellow in medicine at Massachusetts General Hospital in Boston. “Further research is needed to understand these barriers, whether they’re due to personal choice or more systemic issues. Understanding the challenges women face in academic promotions will allow for policy changes.”

According to statistics quoted in the study, women made up more than a third of gastroenterology fellowship positions and 18% of the academic workforce in 2013. At the same time, more than half of medical graduates are women.

“The role of women in GI is important, especially given that studies have shown that women prefer female endoscopists,” Dr. Paul said. And women make up significant portions of the patient load in GI clinical practices, she said.

But it hasn’t been clear if the increase in fellowship positions has corresponded to a higher number of women in positions of academic leadership.

To better understand the situation, Dr. Paul and her associates analyzed the gender and academic rank of GI fellowship program directors and division chiefs in 2015. The researchers analyzed websites and social media to gather the data and also made direct contacts, Dr. Paul said.

At 165 academic GI programs, 85% of these positions were held by men. Of program directors, 81% were male; 89% of division chiefs were male.

Of the men who hold these positions, half were program directors and half were division chiefs. Among women, however, 67% were program directors and 33% were division chiefs.

There was also a disparity in terms of academic experience. Female division chiefs were less likely to be professors (46%), compared with male division chiefs (82%).

Why the disparity? One possible explanation is a “leaky pipeline,” Dr. Paul said. This refers to the fact that women leave academic medicine at higher rates than men do.

Family obligations are one explanation, she said, “but I don’t think that explains everything in the process. A lot of women have felt that promotion was of no benefit to them and that there was a lack of encouragement.”

Dr. Paul notes that the study has limitations. It’s cross sectional, and misclassification errors are possible.

During a discussion period, a questioner noted that it takes time for an academic physician to move up: “Shouldn’t we look at the fraction of graduates in 1996 who were female and now are professors? It’s unusual for someone at less than a professor rank to be division chief, as compared with program director.” Dr. Paul agreed that this would be a good avenue of research.

In addition, she said, “it will be important to examine if these gender disparities are unique to gastroenterology or if they extend into other specialties that are more female dominant, such as rheumatology or geriatrics.”

SAN DIEGO – Despite an increase in women entering the gastroenterology field, a new study finds that they are severely underrepresented in academia as fellowship program directors and division chiefs.

In addition, most female program directors have lower academic ranks than did their male counterparts.

“A lack of female leadership can detract future women from entering the field,” said study lead author Dr. Sonali Paul, a gastroenterologist and research fellow in medicine at Massachusetts General Hospital in Boston. “Further research is needed to understand these barriers, whether they’re due to personal choice or more systemic issues. Understanding the challenges women face in academic promotions will allow for policy changes.”

According to statistics quoted in the study, women made up more than a third of gastroenterology fellowship positions and 18% of the academic workforce in 2013. At the same time, more than half of medical graduates are women.

“The role of women in GI is important, especially given that studies have shown that women prefer female endoscopists,” Dr. Paul said. And women make up significant portions of the patient load in GI clinical practices, she said.

But it hasn’t been clear if the increase in fellowship positions has corresponded to a higher number of women in positions of academic leadership.

To better understand the situation, Dr. Paul and her associates analyzed the gender and academic rank of GI fellowship program directors and division chiefs in 2015. The researchers analyzed websites and social media to gather the data and also made direct contacts, Dr. Paul said.

At 165 academic GI programs, 85% of these positions were held by men. Of program directors, 81% were male; 89% of division chiefs were male.

Of the men who hold these positions, half were program directors and half were division chiefs. Among women, however, 67% were program directors and 33% were division chiefs.

There was also a disparity in terms of academic experience. Female division chiefs were less likely to be professors (46%), compared with male division chiefs (82%).

Why the disparity? One possible explanation is a “leaky pipeline,” Dr. Paul said. This refers to the fact that women leave academic medicine at higher rates than men do.

Family obligations are one explanation, she said, “but I don’t think that explains everything in the process. A lot of women have felt that promotion was of no benefit to them and that there was a lack of encouragement.”

Dr. Paul notes that the study has limitations. It’s cross sectional, and misclassification errors are possible.

During a discussion period, a questioner noted that it takes time for an academic physician to move up: “Shouldn’t we look at the fraction of graduates in 1996 who were female and now are professors? It’s unusual for someone at less than a professor rank to be division chief, as compared with program director.” Dr. Paul agreed that this would be a good avenue of research.

In addition, she said, “it will be important to examine if these gender disparities are unique to gastroenterology or if they extend into other specialties that are more female dominant, such as rheumatology or geriatrics.”

SAN DIEGO – A new analysis of phase II research finds that the experimental drug ozanimod prompted histologic healing in ulcerative colitis patients at 8 and 32 weeks.

“Ozanimod both induces and maintains remissions in a proportion of patients with refractory ulcerative colitis,” said study coauthor Dr. Stephen B. Hanauer, professor of medicine and medical director of the Digestive Health Center at Northwestern University, Chicago. “It’s a safe and effective oral drug for ulcerative colitis and possibly Crohn’s disease.”

Ozanimod, an experimental drug developed by Celgene and its subsidiary Receptos, has been undergoing review as a treatment for both multiple sclerosis and ulcerative colitis.

“Ozanimod impacts lymphocyte trafficking by retaining lymphocytes in lymph nodes and prevents recirculation. The mechanism of action is impairing S1P [sphingosine-1-phosphate] that ‘traps’ lymphocytes in lymph nodes.” Dr. Hanauer said.

“Other mechanisms by which lymphocyte trafficking has been inhibited have been effective in treating multiple sclerosis and Crohn’s disease (natalizumab) and both ulcerative colitis and Crohn’s disease (vedolizumab),” he said. However, he said, natalizumab has been linked to a risk of progressive multifocal leukoencephalopathy, a rare and mostly fatal brain disease.

Vedolizumab, meanwhile, “is a biologic that requires IV infusions.” By contrast, he says, ozanimod is an oral drug.

In a recent issue of the New England Journal of Medicine, researchers published findings from a phase II randomized, double-blind, placebo-controlled trial of ozanimod in 197 patients with moderate to severe ulcerative colitis. Patients were assigned to high dose (n = 67), low dose (n = 65), or placebo (n = 65) (N Engl J Med. 2016 May;374:1754-62).

At 8 weeks, clinical remission (Mayo Clinic score less than or equal to 2, with no subscore over 1) occurred in 16% of patients who received 1-mg doses (P = .048) and 14% of those who received the 0.5-mg doses (P = .14); the remission rate was 6% for placebo.

The new analysis examined histologic improvement from baseline to 8 and 32 weeks. (Those who reached clinical response continued through 32 weeks.) Improvement was greater in the high-dose group than in the placebo group at week 8 (Geboes score [–4.37 vs. –2.20; P = .0345]) and week 32 (Geboes score [–5.50 vs. –2.24; P = .0033]); low-dose improvement was greater than placebo but didn’t reach statistical significance.

Histologic remission (Geboes score less than 2) occurred in 15/67 (22.4%) for high dose (P = .0705, compared with placebo), 9/65 (13.8%) for low dose (P = .6294, compared with placebo) and 7/65 (10.8%) for placebo at week 8. At week 32, remission was 21/67 (31.3%) for high dose (P = 0.0006, compared with placebo), 15/65 (23.1%) for low dose (P = .0164, compared with placebo) and 5/65 (7.7%) for placebo.

Adverse events were “minor, without significant cardiotoxicity or risk of infections,” Dr. Hanauer said. The events affected 26/67 (38.8%) patients on the high dose, 26/65 (40.0%) on the low dose, and 26/65 (40.0%) on placebo; worsening of ulcerative colitis and anemia were most common, especially in the placebo group.

The cost of the drug is unclear, Dr. Hanauer said.

The patients are now in open-label follow-up, he said.

The study is industry funded by Receptos. Dr. Hanauer is on the ozanimod steering committee and consults for Celgene and its subsidiary research division, Receptos.

SAN DIEGO – A new analysis of phase II research finds that the experimental drug ozanimod prompted histologic healing in ulcerative colitis patients at 8 and 32 weeks.

“Ozanimod both induces and maintains remissions in a proportion of patients with refractory ulcerative colitis,” said study coauthor Dr. Stephen B. Hanauer, professor of medicine and medical director of the Digestive Health Center at Northwestern University, Chicago. “It’s a safe and effective oral drug for ulcerative colitis and possibly Crohn’s disease.”

Ozanimod, an experimental drug developed by Celgene and its subsidiary Receptos, has been undergoing review as a treatment for both multiple sclerosis and ulcerative colitis.

“Ozanimod impacts lymphocyte trafficking by retaining lymphocytes in lymph nodes and prevents recirculation. The mechanism of action is impairing S1P [sphingosine-1-phosphate] that ‘traps’ lymphocytes in lymph nodes.” Dr. Hanauer said.

“Other mechanisms by which lymphocyte trafficking has been inhibited have been effective in treating multiple sclerosis and Crohn’s disease (natalizumab) and both ulcerative colitis and Crohn’s disease (vedolizumab),” he said. However, he said, natalizumab has been linked to a risk of progressive multifocal leukoencephalopathy, a rare and mostly fatal brain disease.

Vedolizumab, meanwhile, “is a biologic that requires IV infusions.” By contrast, he says, ozanimod is an oral drug.

In a recent issue of the New England Journal of Medicine, researchers published findings from a phase II randomized, double-blind, placebo-controlled trial of ozanimod in 197 patients with moderate to severe ulcerative colitis. Patients were assigned to high dose (n = 67), low dose (n = 65), or placebo (n = 65) (N Engl J Med. 2016 May;374:1754-62).

At 8 weeks, clinical remission (Mayo Clinic score less than or equal to 2, with no subscore over 1) occurred in 16% of patients who received 1-mg doses (P = .048) and 14% of those who received the 0.5-mg doses (P = .14); the remission rate was 6% for placebo.

The new analysis examined histologic improvement from baseline to 8 and 32 weeks. (Those who reached clinical response continued through 32 weeks.) Improvement was greater in the high-dose group than in the placebo group at week 8 (Geboes score [–4.37 vs. –2.20; P = .0345]) and week 32 (Geboes score [–5.50 vs. –2.24; P = .0033]); low-dose improvement was greater than placebo but didn’t reach statistical significance.

Histologic remission (Geboes score less than 2) occurred in 15/67 (22.4%) for high dose (P = .0705, compared with placebo), 9/65 (13.8%) for low dose (P = .6294, compared with placebo) and 7/65 (10.8%) for placebo at week 8. At week 32, remission was 21/67 (31.3%) for high dose (P = 0.0006, compared with placebo), 15/65 (23.1%) for low dose (P = .0164, compared with placebo) and 5/65 (7.7%) for placebo.

Adverse events were “minor, without significant cardiotoxicity or risk of infections,” Dr. Hanauer said. The events affected 26/67 (38.8%) patients on the high dose, 26/65 (40.0%) on the low dose, and 26/65 (40.0%) on placebo; worsening of ulcerative colitis and anemia were most common, especially in the placebo group.

The cost of the drug is unclear, Dr. Hanauer said.

The patients are now in open-label follow-up, he said.

The study is industry funded by Receptos. Dr. Hanauer is on the ozanimod steering committee and consults for Celgene and its subsidiary research division, Receptos.

SAN DIEGO – A new analysis of phase II research finds that the experimental drug ozanimod prompted histologic healing in ulcerative colitis patients at 8 and 32 weeks.

“Ozanimod both induces and maintains remissions in a proportion of patients with refractory ulcerative colitis,” said study coauthor Dr. Stephen B. Hanauer, professor of medicine and medical director of the Digestive Health Center at Northwestern University, Chicago. “It’s a safe and effective oral drug for ulcerative colitis and possibly Crohn’s disease.”

Ozanimod, an experimental drug developed by Celgene and its subsidiary Receptos, has been undergoing review as a treatment for both multiple sclerosis and ulcerative colitis.

“Ozanimod impacts lymphocyte trafficking by retaining lymphocytes in lymph nodes and prevents recirculation. The mechanism of action is impairing S1P [sphingosine-1-phosphate] that ‘traps’ lymphocytes in lymph nodes.” Dr. Hanauer said.

“Other mechanisms by which lymphocyte trafficking has been inhibited have been effective in treating multiple sclerosis and Crohn’s disease (natalizumab) and both ulcerative colitis and Crohn’s disease (vedolizumab),” he said. However, he said, natalizumab has been linked to a risk of progressive multifocal leukoencephalopathy, a rare and mostly fatal brain disease.

Vedolizumab, meanwhile, “is a biologic that requires IV infusions.” By contrast, he says, ozanimod is an oral drug.

In a recent issue of the New England Journal of Medicine, researchers published findings from a phase II randomized, double-blind, placebo-controlled trial of ozanimod in 197 patients with moderate to severe ulcerative colitis. Patients were assigned to high dose (n = 67), low dose (n = 65), or placebo (n = 65) (N Engl J Med. 2016 May;374:1754-62).

At 8 weeks, clinical remission (Mayo Clinic score less than or equal to 2, with no subscore over 1) occurred in 16% of patients who received 1-mg doses (P = .048) and 14% of those who received the 0.5-mg doses (P = .14); the remission rate was 6% for placebo.

The new analysis examined histologic improvement from baseline to 8 and 32 weeks. (Those who reached clinical response continued through 32 weeks.) Improvement was greater in the high-dose group than in the placebo group at week 8 (Geboes score [–4.37 vs. –2.20; P = .0345]) and week 32 (Geboes score [–5.50 vs. –2.24; P = .0033]); low-dose improvement was greater than placebo but didn’t reach statistical significance.

Histologic remission (Geboes score less than 2) occurred in 15/67 (22.4%) for high dose (P = .0705, compared with placebo), 9/65 (13.8%) for low dose (P = .6294, compared with placebo) and 7/65 (10.8%) for placebo at week 8. At week 32, remission was 21/67 (31.3%) for high dose (P = 0.0006, compared with placebo), 15/65 (23.1%) for low dose (P = .0164, compared with placebo) and 5/65 (7.7%) for placebo.

Adverse events were “minor, without significant cardiotoxicity or risk of infections,” Dr. Hanauer said. The events affected 26/67 (38.8%) patients on the high dose, 26/65 (40.0%) on the low dose, and 26/65 (40.0%) on placebo; worsening of ulcerative colitis and anemia were most common, especially in the placebo group.

The cost of the drug is unclear, Dr. Hanauer said.

The patients are now in open-label follow-up, he said.

The study is industry funded by Receptos. Dr. Hanauer is on the ozanimod steering committee and consults for Celgene and its subsidiary research division, Receptos.

SAN DIEGO – Taking selective serotonin reuptake inhibitors (SSRIs) was not associated with an increased risk of endoscopy-refractory bleeding, rebleeding, or in-hospital mortality among 14,343 consecutive patients admitted with bleeding peptic ulcer in Denmark.

The study suggests that patients with bleeding peptic ulcers can “continue SSRI treatment if the treatment is well indicated,” and that these patients can otherwise receive treatment similar to that of other patients with peptic ulcer bleeding, Dr. Stig B. Laursen reported at the annual Digestive Disease Week.

Observational research has linked use of SSRI antidepressants to an approximately 1.5-fold increase in upper GI bleeding in peptic ulcer bleeding cases, said Dr. Laursen of Odense (Denmark) University Hospital. Studies, mostly in vitro ones, indicate SSRIs decrease the function of thrombocytes and fibrin formation via lowered levels of serotonin. Therefore, it has been suggested that temporarily discontinuing SSRIs may benefit patients with bleeding peptic ulcers.

However, sudden cessation of SSRIs can be associated with withdrawal symptoms, which have been reported in up to one-third of such patients.

Dr. Laursen and his associates prospectively analyzed data for 14,343 consecutive patients admitted with bleeding peptic ulcers in Denmark from 2006 to 2014. They investigated associations between SSRI use and several outcomes, adjusted for confounding factors including age, sex, comorbidity, anemia, medication use, circulatory failure at hospital admission, location of ulcer, stigmata of bleeding, and weekend admission.

After adjustment for confounding risk factors, SSRIs were not associated with increased risk of endoscopy-refractory bleeding (odds ratio [OR] 95% confidence interval [CI]: 1.01 [0.78-1.30]), rebleeding (OR [95% CI]: 0.94 [0.81-1.10]), or in-hospital mortality (hazard ratio [95% CI]: 0.84 [0.68-1.05]).

“Patients taking SSRIs have the same outcomes following peptic ulcer bleeding as non-SSRI users. This suggests that there is no clinically significant impairment of hemostatic function,” Dr. Laursen said. “Therefore, it seems safe to continue SSRI treatment in patients developing peptic ulcer bleeding and thereby avoid development of withdrawal symptoms.”

Dr. Laursen noted that the study has several limitations. It’s not a randomized controlled trial, he said, and there’s no information about the types of SSRIs that the patients were taking. Also, there’s a lack of information about possible discontinuation of SSRIs during hospitalization. However, he said, “that doesn’t seem to be a major confounder.”

During the question-and-answer session following his presentation, Dr. Laursen said the increased risk of poor outcome is quite low, but “there may be a small risk that we haven’t found yet. But if it’s small, maybe it doesn’t have an impact in day-to-day practice.”

The research is hospital-funded. Dr. Laursen had no financial disclosures to report.

SAN DIEGO – Taking selective serotonin reuptake inhibitors (SSRIs) was not associated with an increased risk of endoscopy-refractory bleeding, rebleeding, or in-hospital mortality among 14,343 consecutive patients admitted with bleeding peptic ulcer in Denmark.

The study suggests that patients with bleeding peptic ulcers can “continue SSRI treatment if the treatment is well indicated,” and that these patients can otherwise receive treatment similar to that of other patients with peptic ulcer bleeding, Dr. Stig B. Laursen reported at the annual Digestive Disease Week.

Observational research has linked use of SSRI antidepressants to an approximately 1.5-fold increase in upper GI bleeding in peptic ulcer bleeding cases, said Dr. Laursen of Odense (Denmark) University Hospital. Studies, mostly in vitro ones, indicate SSRIs decrease the function of thrombocytes and fibrin formation via lowered levels of serotonin. Therefore, it has been suggested that temporarily discontinuing SSRIs may benefit patients with bleeding peptic ulcers.

However, sudden cessation of SSRIs can be associated with withdrawal symptoms, which have been reported in up to one-third of such patients.

Dr. Laursen and his associates prospectively analyzed data for 14,343 consecutive patients admitted with bleeding peptic ulcers in Denmark from 2006 to 2014. They investigated associations between SSRI use and several outcomes, adjusted for confounding factors including age, sex, comorbidity, anemia, medication use, circulatory failure at hospital admission, location of ulcer, stigmata of bleeding, and weekend admission.

After adjustment for confounding risk factors, SSRIs were not associated with increased risk of endoscopy-refractory bleeding (odds ratio [OR] 95% confidence interval [CI]: 1.01 [0.78-1.30]), rebleeding (OR [95% CI]: 0.94 [0.81-1.10]), or in-hospital mortality (hazard ratio [95% CI]: 0.84 [0.68-1.05]).

“Patients taking SSRIs have the same outcomes following peptic ulcer bleeding as non-SSRI users. This suggests that there is no clinically significant impairment of hemostatic function,” Dr. Laursen said. “Therefore, it seems safe to continue SSRI treatment in patients developing peptic ulcer bleeding and thereby avoid development of withdrawal symptoms.”

Dr. Laursen noted that the study has several limitations. It’s not a randomized controlled trial, he said, and there’s no information about the types of SSRIs that the patients were taking. Also, there’s a lack of information about possible discontinuation of SSRIs during hospitalization. However, he said, “that doesn’t seem to be a major confounder.”

During the question-and-answer session following his presentation, Dr. Laursen said the increased risk of poor outcome is quite low, but “there may be a small risk that we haven’t found yet. But if it’s small, maybe it doesn’t have an impact in day-to-day practice.”

The research is hospital-funded. Dr. Laursen had no financial disclosures to report.

SAN DIEGO – Taking selective serotonin reuptake inhibitors (SSRIs) was not associated with an increased risk of endoscopy-refractory bleeding, rebleeding, or in-hospital mortality among 14,343 consecutive patients admitted with bleeding peptic ulcer in Denmark.

The study suggests that patients with bleeding peptic ulcers can “continue SSRI treatment if the treatment is well indicated,” and that these patients can otherwise receive treatment similar to that of other patients with peptic ulcer bleeding, Dr. Stig B. Laursen reported at the annual Digestive Disease Week.

Observational research has linked use of SSRI antidepressants to an approximately 1.5-fold increase in upper GI bleeding in peptic ulcer bleeding cases, said Dr. Laursen of Odense (Denmark) University Hospital. Studies, mostly in vitro ones, indicate SSRIs decrease the function of thrombocytes and fibrin formation via lowered levels of serotonin. Therefore, it has been suggested that temporarily discontinuing SSRIs may benefit patients with bleeding peptic ulcers.

However, sudden cessation of SSRIs can be associated with withdrawal symptoms, which have been reported in up to one-third of such patients.

Dr. Laursen and his associates prospectively analyzed data for 14,343 consecutive patients admitted with bleeding peptic ulcers in Denmark from 2006 to 2014. They investigated associations between SSRI use and several outcomes, adjusted for confounding factors including age, sex, comorbidity, anemia, medication use, circulatory failure at hospital admission, location of ulcer, stigmata of bleeding, and weekend admission.

After adjustment for confounding risk factors, SSRIs were not associated with increased risk of endoscopy-refractory bleeding (odds ratio [OR] 95% confidence interval [CI]: 1.01 [0.78-1.30]), rebleeding (OR [95% CI]: 0.94 [0.81-1.10]), or in-hospital mortality (hazard ratio [95% CI]: 0.84 [0.68-1.05]).

“Patients taking SSRIs have the same outcomes following peptic ulcer bleeding as non-SSRI users. This suggests that there is no clinically significant impairment of hemostatic function,” Dr. Laursen said. “Therefore, it seems safe to continue SSRI treatment in patients developing peptic ulcer bleeding and thereby avoid development of withdrawal symptoms.”

Dr. Laursen noted that the study has several limitations. It’s not a randomized controlled trial, he said, and there’s no information about the types of SSRIs that the patients were taking. Also, there’s a lack of information about possible discontinuation of SSRIs during hospitalization. However, he said, “that doesn’t seem to be a major confounder.”

During the question-and-answer session following his presentation, Dr. Laursen said the increased risk of poor outcome is quite low, but “there may be a small risk that we haven’t found yet. But if it’s small, maybe it doesn’t have an impact in day-to-day practice.”

The research is hospital-funded. Dr. Laursen had no financial disclosures to report.