SAN DIEGO – When the Food and Drug Administration gave the nod to a first-in-class tissue removal device in July of 2021, clearance was limited to the treatment of moderate to severe wrinkles in the mid to lower face.

But once the device – Ellacor– becomes available in late 2022, potential applications are likely to be wide-ranging, Jill S. Waibel, MD, a dermatologist with the Miami Dermatology and Laser Institute, predicted at the annual conference of the American Society for Laser Medicine and Surgery. “I’m using it in my practice more for laxity and jowls,” she said. Eventually, “I think it’s going to be preventative for 30- to 50-year-olds but that hasn’t been studied. I think it’s going to have a pre- and postrhytidectomy role, so I think the plastic surgeons are going to love this in their practice.”

Developed by Cytrellis, and based on research conducted by William G. Austen Jr., MD, chief of plastic and reconstructive surgery at Massachusetts General Hospital (MGH), Boston, and R. Rox Anderson, MD, director of the Wellman Center for Photomedicine at MGH, the company’s scientific founders, the device uses hollow needles contained in a handpiece to create thousands of microexcisions to physically remove small cores of skin – a process known as microcoring. Dr. Austin and Dr. Anderson were the senior authors, respectively, of seminal trials of the device in swine, published in 2013 and 2015.

This can result in immediate physical hole closures (mechanical closure), which may lead to skin tightening.

“We’re removing dermis and epidermis,” said Dr. Waibel, who noted that the technology has been studied mostly for skin laxity and rhytids. “There are no other devices that are doing this.”

The immediate closure of tiny holes in the skin results in a quantitative and directional reduction in the treated area of skin, she said, which leads to wrinkle improvement, tightening, and smoothing of lax skin. The device contains three 22-guage needles that are less than 500 micrometers in diameter. “Based on optical coherence tomography work we did, these channels of treated skin stay open for about 1.5 minutes,” she added, noting that the tunable depth of the device ranges from 0 to 4 mm. “I tend to treat only with the 4-mm depth,” said Dr. Waibel, who is subsection chief of dermatology at Baptist Hospital of Miami.

The device features a disposable tip that can remove up to 24,000 cores of skin, and the amount of skin removed in a treated area can be 1%, 3%, 5%, 7%, and 8%. “The more cores you do, the more wrinkle improvement we saw in pivotal trials,” she said. “A minimal core count of 12,000 per treatment is recommended for the mid and lower face. Interestingly, higher core counts do not result in more patient downtime.” In her office, she said that the treatment takes about 20 minutes. Recommended postoperative care involves application of petrolatum or Aquaphor over the treated area for 24 hours, or until the holes have closed. “There is very low postoperative downtime,” she noted.

According to pivotal clinical data from Cytrellis on 51 patients treated with Ellacor, patients experienced a mean 1.3-grade improvement on the Lemperle Rating Scale, 86% said that they were satisfied with the procedure, and investigators rated their Global Aesthetic Improvement as 90%.

To date, Dr. Waibel and her colleagues in Miami have treated 102 patients with Ellacor, mostly for wrinkles and skin laxity. In these patients, the minimal downtime experienced was 3.8 days, 75% of patients did not miss any work, and 46% did not miss any social activities. The worst part for patients is the preprocedure numbing, she said. “We do lidocaine injections. Some people do nerve blocks. Once you do the lidocaine injection, the average pain is about 0.36 on a scale of 1-10 during treatment and 0 for all subsequent time points.”

At the meeting, she presented a set of before and after photos that showed improvement of moderate facial wrinkles in a female patient 90 days after one treatment with Ellacor, which removed about 5% of skin in the area of the jowls. “It’s pretty incredible,” Dr. Waibel remarked.

“I don’t have anything in my practice that can help with that kind of laxity other than sending them to a plastic surgeon, and I have about 80 devices.”

Images courtesy Dr. Jill S. Waibel

At the 2019 meeting of the American Society for Dermatologic Surgery, Dr. Waibel and Roy G. Geronemus, MD, director of the Laser & Skin Surgery Center of New York, presented a small pilot study on the successful use of Ellacor for acne scars and striae. Dr. Waibel said that she and her colleagues in Miami have been using the device to treat skin laxity in several anatomical areas, including the neck, nose, inner thigh, above the knee, elbow, and the axillary region. They have used the device to treat tattoos, rhytidectomy scars, abdominal striae, acne and surgical scars, and idiopathic guttate hypomelanosis, she added.

“We do a lot of combinations with other devices on the same day, and I think this list will increase over the next few years,” she said. “Probably my favorite use in the past 5 months has been doing microcoring and, separated by a month, doing resurfacing.”

Clinical trials of Ellacor were conducted in patients with types I-IV skin, but she has treated several patients with types V-VI skin “with absolutely no safety issues,” which includes treatment of epidermal nevi.

Which variables are the most important for patient selection and procedural success remain unclear, she continued, including patient age, elastic recoil, body mass index, history of a prior procedure (such as radiofrequency or ultrasound), the amount of laxity and rhytids, and overall health, which have not been studied, Dr. Waibel said.

“We have patients that don’t have the same response as others. For the modest improvement seen in some patients, is that their elastic recoil or are we choosing the wrong patients? Do they need more treatments? We are also still learning about the ideal treatment for scars and other indications.”

The device is expected to launch in fourth quarter of 2022.

Dr. Waibel disclosed that she is an advisory board member for Cytrellis. She has conducted clinical trials for and is a consultant to many pharmaceutical and device companies.

SAN DIEGO – When the Food and Drug Administration gave the nod to a first-in-class tissue removal device in July of 2021, clearance was limited to the treatment of moderate to severe wrinkles in the mid to lower face.

But once the device – Ellacor– becomes available in late 2022, potential applications are likely to be wide-ranging, Jill S. Waibel, MD, a dermatologist with the Miami Dermatology and Laser Institute, predicted at the annual conference of the American Society for Laser Medicine and Surgery. “I’m using it in my practice more for laxity and jowls,” she said. Eventually, “I think it’s going to be preventative for 30- to 50-year-olds but that hasn’t been studied. I think it’s going to have a pre- and postrhytidectomy role, so I think the plastic surgeons are going to love this in their practice.”

Developed by Cytrellis, and based on research conducted by William G. Austen Jr., MD, chief of plastic and reconstructive surgery at Massachusetts General Hospital (MGH), Boston, and R. Rox Anderson, MD, director of the Wellman Center for Photomedicine at MGH, the company’s scientific founders, the device uses hollow needles contained in a handpiece to create thousands of microexcisions to physically remove small cores of skin – a process known as microcoring. Dr. Austin and Dr. Anderson were the senior authors, respectively, of seminal trials of the device in swine, published in 2013 and 2015.

This can result in immediate physical hole closures (mechanical closure), which may lead to skin tightening.

“We’re removing dermis and epidermis,” said Dr. Waibel, who noted that the technology has been studied mostly for skin laxity and rhytids. “There are no other devices that are doing this.”

The immediate closure of tiny holes in the skin results in a quantitative and directional reduction in the treated area of skin, she said, which leads to wrinkle improvement, tightening, and smoothing of lax skin. The device contains three 22-guage needles that are less than 500 micrometers in diameter. “Based on optical coherence tomography work we did, these channels of treated skin stay open for about 1.5 minutes,” she added, noting that the tunable depth of the device ranges from 0 to 4 mm. “I tend to treat only with the 4-mm depth,” said Dr. Waibel, who is subsection chief of dermatology at Baptist Hospital of Miami.

The device features a disposable tip that can remove up to 24,000 cores of skin, and the amount of skin removed in a treated area can be 1%, 3%, 5%, 7%, and 8%. “The more cores you do, the more wrinkle improvement we saw in pivotal trials,” she said. “A minimal core count of 12,000 per treatment is recommended for the mid and lower face. Interestingly, higher core counts do not result in more patient downtime.” In her office, she said that the treatment takes about 20 minutes. Recommended postoperative care involves application of petrolatum or Aquaphor over the treated area for 24 hours, or until the holes have closed. “There is very low postoperative downtime,” she noted.

According to pivotal clinical data from Cytrellis on 51 patients treated with Ellacor, patients experienced a mean 1.3-grade improvement on the Lemperle Rating Scale, 86% said that they were satisfied with the procedure, and investigators rated their Global Aesthetic Improvement as 90%.

To date, Dr. Waibel and her colleagues in Miami have treated 102 patients with Ellacor, mostly for wrinkles and skin laxity. In these patients, the minimal downtime experienced was 3.8 days, 75% of patients did not miss any work, and 46% did not miss any social activities. The worst part for patients is the preprocedure numbing, she said. “We do lidocaine injections. Some people do nerve blocks. Once you do the lidocaine injection, the average pain is about 0.36 on a scale of 1-10 during treatment and 0 for all subsequent time points.”

At the meeting, she presented a set of before and after photos that showed improvement of moderate facial wrinkles in a female patient 90 days after one treatment with Ellacor, which removed about 5% of skin in the area of the jowls. “It’s pretty incredible,” Dr. Waibel remarked.

“I don’t have anything in my practice that can help with that kind of laxity other than sending them to a plastic surgeon, and I have about 80 devices.”

Images courtesy Dr. Jill S. Waibel

At the 2019 meeting of the American Society for Dermatologic Surgery, Dr. Waibel and Roy G. Geronemus, MD, director of the Laser & Skin Surgery Center of New York, presented a small pilot study on the successful use of Ellacor for acne scars and striae. Dr. Waibel said that she and her colleagues in Miami have been using the device to treat skin laxity in several anatomical areas, including the neck, nose, inner thigh, above the knee, elbow, and the axillary region. They have used the device to treat tattoos, rhytidectomy scars, abdominal striae, acne and surgical scars, and idiopathic guttate hypomelanosis, she added.

“We do a lot of combinations with other devices on the same day, and I think this list will increase over the next few years,” she said. “Probably my favorite use in the past 5 months has been doing microcoring and, separated by a month, doing resurfacing.”

Clinical trials of Ellacor were conducted in patients with types I-IV skin, but she has treated several patients with types V-VI skin “with absolutely no safety issues,” which includes treatment of epidermal nevi.

Which variables are the most important for patient selection and procedural success remain unclear, she continued, including patient age, elastic recoil, body mass index, history of a prior procedure (such as radiofrequency or ultrasound), the amount of laxity and rhytids, and overall health, which have not been studied, Dr. Waibel said.

“We have patients that don’t have the same response as others. For the modest improvement seen in some patients, is that their elastic recoil or are we choosing the wrong patients? Do they need more treatments? We are also still learning about the ideal treatment for scars and other indications.”

The device is expected to launch in fourth quarter of 2022.

Dr. Waibel disclosed that she is an advisory board member for Cytrellis. She has conducted clinical trials for and is a consultant to many pharmaceutical and device companies.

SAN DIEGO – When the Food and Drug Administration gave the nod to a first-in-class tissue removal device in July of 2021, clearance was limited to the treatment of moderate to severe wrinkles in the mid to lower face.

But once the device – Ellacor– becomes available in late 2022, potential applications are likely to be wide-ranging, Jill S. Waibel, MD, a dermatologist with the Miami Dermatology and Laser Institute, predicted at the annual conference of the American Society for Laser Medicine and Surgery. “I’m using it in my practice more for laxity and jowls,” she said. Eventually, “I think it’s going to be preventative for 30- to 50-year-olds but that hasn’t been studied. I think it’s going to have a pre- and postrhytidectomy role, so I think the plastic surgeons are going to love this in their practice.”

Developed by Cytrellis, and based on research conducted by William G. Austen Jr., MD, chief of plastic and reconstructive surgery at Massachusetts General Hospital (MGH), Boston, and R. Rox Anderson, MD, director of the Wellman Center for Photomedicine at MGH, the company’s scientific founders, the device uses hollow needles contained in a handpiece to create thousands of microexcisions to physically remove small cores of skin – a process known as microcoring. Dr. Austin and Dr. Anderson were the senior authors, respectively, of seminal trials of the device in swine, published in 2013 and 2015.

This can result in immediate physical hole closures (mechanical closure), which may lead to skin tightening.

“We’re removing dermis and epidermis,” said Dr. Waibel, who noted that the technology has been studied mostly for skin laxity and rhytids. “There are no other devices that are doing this.”

The immediate closure of tiny holes in the skin results in a quantitative and directional reduction in the treated area of skin, she said, which leads to wrinkle improvement, tightening, and smoothing of lax skin. The device contains three 22-guage needles that are less than 500 micrometers in diameter. “Based on optical coherence tomography work we did, these channels of treated skin stay open for about 1.5 minutes,” she added, noting that the tunable depth of the device ranges from 0 to 4 mm. “I tend to treat only with the 4-mm depth,” said Dr. Waibel, who is subsection chief of dermatology at Baptist Hospital of Miami.

The device features a disposable tip that can remove up to 24,000 cores of skin, and the amount of skin removed in a treated area can be 1%, 3%, 5%, 7%, and 8%. “The more cores you do, the more wrinkle improvement we saw in pivotal trials,” she said. “A minimal core count of 12,000 per treatment is recommended for the mid and lower face. Interestingly, higher core counts do not result in more patient downtime.” In her office, she said that the treatment takes about 20 minutes. Recommended postoperative care involves application of petrolatum or Aquaphor over the treated area for 24 hours, or until the holes have closed. “There is very low postoperative downtime,” she noted.

According to pivotal clinical data from Cytrellis on 51 patients treated with Ellacor, patients experienced a mean 1.3-grade improvement on the Lemperle Rating Scale, 86% said that they were satisfied with the procedure, and investigators rated their Global Aesthetic Improvement as 90%.

To date, Dr. Waibel and her colleagues in Miami have treated 102 patients with Ellacor, mostly for wrinkles and skin laxity. In these patients, the minimal downtime experienced was 3.8 days, 75% of patients did not miss any work, and 46% did not miss any social activities. The worst part for patients is the preprocedure numbing, she said. “We do lidocaine injections. Some people do nerve blocks. Once you do the lidocaine injection, the average pain is about 0.36 on a scale of 1-10 during treatment and 0 for all subsequent time points.”

At the meeting, she presented a set of before and after photos that showed improvement of moderate facial wrinkles in a female patient 90 days after one treatment with Ellacor, which removed about 5% of skin in the area of the jowls. “It’s pretty incredible,” Dr. Waibel remarked.

“I don’t have anything in my practice that can help with that kind of laxity other than sending them to a plastic surgeon, and I have about 80 devices.”

Images courtesy Dr. Jill S. Waibel

At the 2019 meeting of the American Society for Dermatologic Surgery, Dr. Waibel and Roy G. Geronemus, MD, director of the Laser & Skin Surgery Center of New York, presented a small pilot study on the successful use of Ellacor for acne scars and striae. Dr. Waibel said that she and her colleagues in Miami have been using the device to treat skin laxity in several anatomical areas, including the neck, nose, inner thigh, above the knee, elbow, and the axillary region. They have used the device to treat tattoos, rhytidectomy scars, abdominal striae, acne and surgical scars, and idiopathic guttate hypomelanosis, she added.

“We do a lot of combinations with other devices on the same day, and I think this list will increase over the next few years,” she said. “Probably my favorite use in the past 5 months has been doing microcoring and, separated by a month, doing resurfacing.”

Clinical trials of Ellacor were conducted in patients with types I-IV skin, but she has treated several patients with types V-VI skin “with absolutely no safety issues,” which includes treatment of epidermal nevi.

Which variables are the most important for patient selection and procedural success remain unclear, she continued, including patient age, elastic recoil, body mass index, history of a prior procedure (such as radiofrequency or ultrasound), the amount of laxity and rhytids, and overall health, which have not been studied, Dr. Waibel said.

“We have patients that don’t have the same response as others. For the modest improvement seen in some patients, is that their elastic recoil or are we choosing the wrong patients? Do they need more treatments? We are also still learning about the ideal treatment for scars and other indications.”

The device is expected to launch in fourth quarter of 2022.

Dr. Waibel disclosed that she is an advisory board member for Cytrellis. She has conducted clinical trials for and is a consultant to many pharmaceutical and device companies.

Although adolescents and young adults (AYAs) who survive leukemia are living much longer than ever before, their life spans are still shorter than those of the general population, a new study concludes.

The study found that the 10-year survival of AYA leukemia survivors was approximately 10% lower than that of the age-adjusted U.S. general population at large.

These differences persisted for up to 30 years of follow-up.

“We need to think about the long-term life span and the quality of life for our patients. Cure is not enough for our AYA cancer survivors,” said senior author Michael Roth, MD, associate professor of pediatric patient care and director of the Childhood Cancer Survivorship Clinic at the University of Texas MD Anderson Cancer Center, Houston.

“Once these patients reach the survivorship stage of their journey, they may encounter additional side effects as a result of intensive treatment, lack of access to quality health care, and other issues that may negatively impact their health and overall survival,” he said in a statement.

The study was published in Cancer Epidemiology, Biomarkers and Prevention.
 

Demographics play role in survival

AYAs were defined as those persons aged 15-39 years. For their study, Dr. Roth and colleagues used the Surveillance, Epidemiology, and End Results (SEER) registry to identify 1,938 AYA survivors of acute lymphoblastic leukemia (ALL) and 2,350 AYA survivors of acute myeloid leukemia (AML) who were diagnosed from 1980 to 2009. They were followed for a median of 12 years.

The median age at diagnosis was 23 years for ALL and 28 years for AML.

Among ALL survivors, 6% were Black, 7% were Asian or Pacific Islander, 29% were Hispanic, and 58% were White. Among AML survivors, 9% were Black, 10% were Asian or Pacific Islander, 22% were Hispanic, and 59% were White. Ten-year survival for ALL and AML survivors was 87% and 89%, respectively. For the general population, it was 99%.

For ALL survivors, the 10-year survival was 83% for those diagnosed in the 1980s; it was 88% for those diagnosed in the 1990s and in the 2000s. The pattern was similar for AML survivors: 82%, 90%, and 90%.

The most common cause of death during early survivorship was acute leukemia. Deaths plateaued approximately 10 years after the initial diagnosis.

“Some of these patients aren’t being fully cured of their initial cancer, so between 5 and 10 years post initial diagnosis, most of the deaths are due to disease progression or relapse, whereas after that, most of the deaths result from late side effects from treatment, including cardiovascular disease and secondary cancers,” Dr. Roth said. Mortality from other causes continued to rise during the survivorship period. Subsequent malignancies and cardiac disease were the most common causes of death for both ALL and AML survivors.

A recent study found that AYA cancer survivors face nearly a twofold higher risk of dying from a new primary cancer, compared with peers in the general population.

When looking at key demographics, the authors found that older age at diagnosis was significantly associated with differential long-term survival (P < .0001 for both ALL and AML). Each additional year older at diagnosis was associated with a 6% and 5% decrease in long-term survival for both types of leukemia.

The decade in which the diagnosis was made had a significant difference in long-term survival both for patients with ALL and those with AML. Long-term survival times for those diagnosed in the 1990s were more than twice those of patients diagnosed in the 1980s for ALL (unadjusted P = .008) and AML (unadjusted P = .0002). Survival times were also more than twice those of patients diagnosed in the 2000s versus the 1980s for ALL (unadjusted P = .009) and AML (unadjusted P = .0003).

No significant long-term survival differences were observed for those diagnosed in the 2000s, compared with the 1990s, for either leukemia.

“The data from the national registry used for this study gave us insights into some possible challenges AML and ALL patients may encounter throughout survivorship, but we need to more thoroughly survey their journey,” Dr. Roth said. “An examination of their socioeconomic status, comorbidities, access to quality health care, and other risk factors that may impact their survivorship is warranted.”

The research was supported by the National Cancer Institute at the National Institutes of Health, the Archer Charitable Foundation, and LyondellBasell. The authors disclosed no relevant financial relationships.

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

Although adolescents and young adults (AYAs) who survive leukemia are living much longer than ever before, their life spans are still shorter than those of the general population, a new study concludes.

The study found that the 10-year survival of AYA leukemia survivors was approximately 10% lower than that of the age-adjusted U.S. general population at large.

These differences persisted for up to 30 years of follow-up.

“We need to think about the long-term life span and the quality of life for our patients. Cure is not enough for our AYA cancer survivors,” said senior author Michael Roth, MD, associate professor of pediatric patient care and director of the Childhood Cancer Survivorship Clinic at the University of Texas MD Anderson Cancer Center, Houston.

“Once these patients reach the survivorship stage of their journey, they may encounter additional side effects as a result of intensive treatment, lack of access to quality health care, and other issues that may negatively impact their health and overall survival,” he said in a statement.

The study was published in Cancer Epidemiology, Biomarkers and Prevention.
 

Demographics play role in survival

AYAs were defined as those persons aged 15-39 years. For their study, Dr. Roth and colleagues used the Surveillance, Epidemiology, and End Results (SEER) registry to identify 1,938 AYA survivors of acute lymphoblastic leukemia (ALL) and 2,350 AYA survivors of acute myeloid leukemia (AML) who were diagnosed from 1980 to 2009. They were followed for a median of 12 years.

The median age at diagnosis was 23 years for ALL and 28 years for AML.

Among ALL survivors, 6% were Black, 7% were Asian or Pacific Islander, 29% were Hispanic, and 58% were White. Among AML survivors, 9% were Black, 10% were Asian or Pacific Islander, 22% were Hispanic, and 59% were White. Ten-year survival for ALL and AML survivors was 87% and 89%, respectively. For the general population, it was 99%.

For ALL survivors, the 10-year survival was 83% for those diagnosed in the 1980s; it was 88% for those diagnosed in the 1990s and in the 2000s. The pattern was similar for AML survivors: 82%, 90%, and 90%.

The most common cause of death during early survivorship was acute leukemia. Deaths plateaued approximately 10 years after the initial diagnosis.

“Some of these patients aren’t being fully cured of their initial cancer, so between 5 and 10 years post initial diagnosis, most of the deaths are due to disease progression or relapse, whereas after that, most of the deaths result from late side effects from treatment, including cardiovascular disease and secondary cancers,” Dr. Roth said. Mortality from other causes continued to rise during the survivorship period. Subsequent malignancies and cardiac disease were the most common causes of death for both ALL and AML survivors.

A recent study found that AYA cancer survivors face nearly a twofold higher risk of dying from a new primary cancer, compared with peers in the general population.

When looking at key demographics, the authors found that older age at diagnosis was significantly associated with differential long-term survival (P < .0001 for both ALL and AML). Each additional year older at diagnosis was associated with a 6% and 5% decrease in long-term survival for both types of leukemia.

The decade in which the diagnosis was made had a significant difference in long-term survival both for patients with ALL and those with AML. Long-term survival times for those diagnosed in the 1990s were more than twice those of patients diagnosed in the 1980s for ALL (unadjusted P = .008) and AML (unadjusted P = .0002). Survival times were also more than twice those of patients diagnosed in the 2000s versus the 1980s for ALL (unadjusted P = .009) and AML (unadjusted P = .0003).

No significant long-term survival differences were observed for those diagnosed in the 2000s, compared with the 1990s, for either leukemia.

“The data from the national registry used for this study gave us insights into some possible challenges AML and ALL patients may encounter throughout survivorship, but we need to more thoroughly survey their journey,” Dr. Roth said. “An examination of their socioeconomic status, comorbidities, access to quality health care, and other risk factors that may impact their survivorship is warranted.”

The research was supported by the National Cancer Institute at the National Institutes of Health, the Archer Charitable Foundation, and LyondellBasell. The authors disclosed no relevant financial relationships.

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

Although adolescents and young adults (AYAs) who survive leukemia are living much longer than ever before, their life spans are still shorter than those of the general population, a new study concludes.

The study found that the 10-year survival of AYA leukemia survivors was approximately 10% lower than that of the age-adjusted U.S. general population at large.

These differences persisted for up to 30 years of follow-up.

“We need to think about the long-term life span and the quality of life for our patients. Cure is not enough for our AYA cancer survivors,” said senior author Michael Roth, MD, associate professor of pediatric patient care and director of the Childhood Cancer Survivorship Clinic at the University of Texas MD Anderson Cancer Center, Houston.

“Once these patients reach the survivorship stage of their journey, they may encounter additional side effects as a result of intensive treatment, lack of access to quality health care, and other issues that may negatively impact their health and overall survival,” he said in a statement.

The study was published in Cancer Epidemiology, Biomarkers and Prevention.
 

Demographics play role in survival

AYAs were defined as those persons aged 15-39 years. For their study, Dr. Roth and colleagues used the Surveillance, Epidemiology, and End Results (SEER) registry to identify 1,938 AYA survivors of acute lymphoblastic leukemia (ALL) and 2,350 AYA survivors of acute myeloid leukemia (AML) who were diagnosed from 1980 to 2009. They were followed for a median of 12 years.

The median age at diagnosis was 23 years for ALL and 28 years for AML.

Among ALL survivors, 6% were Black, 7% were Asian or Pacific Islander, 29% were Hispanic, and 58% were White. Among AML survivors, 9% were Black, 10% were Asian or Pacific Islander, 22% were Hispanic, and 59% were White. Ten-year survival for ALL and AML survivors was 87% and 89%, respectively. For the general population, it was 99%.

For ALL survivors, the 10-year survival was 83% for those diagnosed in the 1980s; it was 88% for those diagnosed in the 1990s and in the 2000s. The pattern was similar for AML survivors: 82%, 90%, and 90%.

The most common cause of death during early survivorship was acute leukemia. Deaths plateaued approximately 10 years after the initial diagnosis.

“Some of these patients aren’t being fully cured of their initial cancer, so between 5 and 10 years post initial diagnosis, most of the deaths are due to disease progression or relapse, whereas after that, most of the deaths result from late side effects from treatment, including cardiovascular disease and secondary cancers,” Dr. Roth said. Mortality from other causes continued to rise during the survivorship period. Subsequent malignancies and cardiac disease were the most common causes of death for both ALL and AML survivors.

A recent study found that AYA cancer survivors face nearly a twofold higher risk of dying from a new primary cancer, compared with peers in the general population.

When looking at key demographics, the authors found that older age at diagnosis was significantly associated with differential long-term survival (P < .0001 for both ALL and AML). Each additional year older at diagnosis was associated with a 6% and 5% decrease in long-term survival for both types of leukemia.

The decade in which the diagnosis was made had a significant difference in long-term survival both for patients with ALL and those with AML. Long-term survival times for those diagnosed in the 1990s were more than twice those of patients diagnosed in the 1980s for ALL (unadjusted P = .008) and AML (unadjusted P = .0002). Survival times were also more than twice those of patients diagnosed in the 2000s versus the 1980s for ALL (unadjusted P = .009) and AML (unadjusted P = .0003).

No significant long-term survival differences were observed for those diagnosed in the 2000s, compared with the 1990s, for either leukemia.

“The data from the national registry used for this study gave us insights into some possible challenges AML and ALL patients may encounter throughout survivorship, but we need to more thoroughly survey their journey,” Dr. Roth said. “An examination of their socioeconomic status, comorbidities, access to quality health care, and other risk factors that may impact their survivorship is warranted.”

The research was supported by the National Cancer Institute at the National Institutes of Health, the Archer Charitable Foundation, and LyondellBasell. The authors disclosed no relevant financial relationships.

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

A clinical practice guideline for the diagnosis and management of gastrointestinal hamartomatous polyposis syndromes has just been published by the U.S. Multi-Society Task Force on Colorectal Cancer, which is comprised of experts representing the American College of Gastroenterology, the American Gastroenterological Association, and the American Society for Gastrointestinal Endoscopy.

Gastrointestinal hamartomatous polyposis syndromes are rare, autosomal dominant disorders associated with intestinal and extraintestinal tumors. Expert consensus statements have previously offered some recommendations for managing these syndromes, but clinical data are scarce, so the present review “is intended to establish a starting point for future research,” lead author C. Richard Boland, MD, of the University of California, San Diego, and colleagues reported.

According to the investigators, “there are essentially no long-term prospective controlled studies of comparative effectiveness of management strategies for these syndromes.” As a result, their recommendations are based on “low-quality” evidence according to GRADE criteria.

Still, Dr. Boland and colleagues highlighted that “there has been tremendous progress in recent years, both in understanding the underlying genetics that underpin these disorders and in elucidating the biology of associated premalignant and malignant conditions.”

The guideline was published online in Gastroenterology .
 

Four syndromes reviewed

The investigators gathered these data to provide an overview of genetic and clinical features for each syndrome, as well as management strategies. Four disorders are included: juvenile polyposis syndrome; Peutz-Jeghers syndrome; hereditary mixed polyposis syndrome; and PTEN-hamartoma tumor syndrome, encompassing Bannayan-Riley-Ruvalcaba syndrome and Cowden’s syndrome.

Although all gastrointestinal hamartomatous polyposis syndromes are caused by germline alterations, Dr. Boland and colleagues pointed out that diagnoses are typically made based on clinical criteria, with germline results serving as confirmatory evidence.

The guideline recommends that any patient with a family history of hamartomatous polyps, or with a history of at least two hamartomatous polyps, should undergo genetic testing. The guideline also provides more nuanced genetic testing algorithms for each syndrome.

Among all the hamartomatous polyp disorders, Peutz-Jeghers syndrome is most understood, according to the investigators. It is caused by aberrations in the STK11 gene, and is characterized by polyps with “branching bands of smooth muscle covered by hyperplastic glandular mucosa” that may occur in the stomach, small intestine, and colon. Patients are also at risk of extraintestinal neoplasia.

For management of Peutz-Jeghers syndrome, the guideline advises frequent endoscopic surveillance to prevent mechanical obstruction and bleeding, as well as multidisciplinary surveillance of the breasts, pancreas, ovaries, testes, and lungs.

Juvenile polyposis syndrome is most often characterized by solitary, sporadic polyps in the colorectum (98% of patients affected), followed distantly by polyps in the stomach (14%), ileum (7%), jejunum (7%), and duodenum (7%). The condition is linked with abnormalities in BMPR1A or SMAD4 genes, with SMAD4 germline abnormalities more often leading to “massive” gastric polyps, gastrointestinal bleeding, protein-losing enteropathy, and a higher incidence of gastric cancer in adulthood. Most patients with SMAD4 mutations also have hereditary hemorrhagic telangiectasia, characterized by gastrointestinal bleeding from mucocutaneous telangiectasias, arteriovenous malformations, and epistaxis.

Management of juvenile polyposis syndrome depends on frequent colonoscopies with polypectomies beginning at 12-15 years.

“The goal of surveillance in juvenile polyposis syndrome is to mitigate symptoms related to the disorder and decrease the risk of complications from the manifestations, including cancer,” Dr. Boland and colleagues wrote.

PTEN-hamartoma tumor syndrome, which includes both Bannayan-Riley-Ruvalcaba syndrome and Cowden’s syndrome, is caused by abnormalities in the eponymous PTEN gene. Patients with the condition have an increased risk of colon cancer and polyposis, as well as extraintestinal cancers.

Diagnosis of PTEN-hamartoma tumor syndrome may be complex, involving “clinical examination, mammography and breast MRI, thyroid ultrasound, transvaginal ultrasound, upper gastrointestinal endoscopy, colonoscopy, and renal ultrasound,” according to the guideline.

After diagnosis, frequent colonoscopies are recommended, typically starting at age 35 years, as well as continued surveillance of other organs.

Hereditary mixed polyposis syndrome, which involves attenuated colonic polyposis, is the rarest of the four disorders, having been reported in only “a few families,” according to the guideline. The condition has been linked with “large duplications of the promoter region or entire GREM1 gene.”

Onset is typically in the late 20s, “which is when colonoscopic surveillance should begin,” the investigators wrote. More data are needed to determine appropriate surveillance intervals and if the condition is associated with increased risk of extraintestinal neoplasia.

This call for more research into gastrointestinal hamartomatous polyposis syndromes carried through to the conclusion of the guideline.

“Long-term prospective studies of mutation carriers are still needed to further clarify the risk of cancer and the role of surveillance in these syndromes,” Dr. Boland and colleagues wrote. “With increases in genetic testing and evaluation, future studies will be conducted with more robust cohorts of genetically characterized, less heterogeneous populations. However, there is also a need to study patients and families with unusual phenotypes where no genotype can be found.”

The investigators disclosed no conflicts of interest with the current guideline; however, they provided a list of industry relationships, including Salix Pharmaceuticals, Ferring Pharmaceuticals, and Pfizer, among others.

A clinical practice guideline for the diagnosis and management of gastrointestinal hamartomatous polyposis syndromes has just been published by the U.S. Multi-Society Task Force on Colorectal Cancer, which is comprised of experts representing the American College of Gastroenterology, the American Gastroenterological Association, and the American Society for Gastrointestinal Endoscopy.

Gastrointestinal hamartomatous polyposis syndromes are rare, autosomal dominant disorders associated with intestinal and extraintestinal tumors. Expert consensus statements have previously offered some recommendations for managing these syndromes, but clinical data are scarce, so the present review “is intended to establish a starting point for future research,” lead author C. Richard Boland, MD, of the University of California, San Diego, and colleagues reported.

According to the investigators, “there are essentially no long-term prospective controlled studies of comparative effectiveness of management strategies for these syndromes.” As a result, their recommendations are based on “low-quality” evidence according to GRADE criteria.

Still, Dr. Boland and colleagues highlighted that “there has been tremendous progress in recent years, both in understanding the underlying genetics that underpin these disorders and in elucidating the biology of associated premalignant and malignant conditions.”

The guideline was published online in Gastroenterology .
 

Four syndromes reviewed

The investigators gathered these data to provide an overview of genetic and clinical features for each syndrome, as well as management strategies. Four disorders are included: juvenile polyposis syndrome; Peutz-Jeghers syndrome; hereditary mixed polyposis syndrome; and PTEN-hamartoma tumor syndrome, encompassing Bannayan-Riley-Ruvalcaba syndrome and Cowden’s syndrome.

Although all gastrointestinal hamartomatous polyposis syndromes are caused by germline alterations, Dr. Boland and colleagues pointed out that diagnoses are typically made based on clinical criteria, with germline results serving as confirmatory evidence.

The guideline recommends that any patient with a family history of hamartomatous polyps, or with a history of at least two hamartomatous polyps, should undergo genetic testing. The guideline also provides more nuanced genetic testing algorithms for each syndrome.

Among all the hamartomatous polyp disorders, Peutz-Jeghers syndrome is most understood, according to the investigators. It is caused by aberrations in the STK11 gene, and is characterized by polyps with “branching bands of smooth muscle covered by hyperplastic glandular mucosa” that may occur in the stomach, small intestine, and colon. Patients are also at risk of extraintestinal neoplasia.

For management of Peutz-Jeghers syndrome, the guideline advises frequent endoscopic surveillance to prevent mechanical obstruction and bleeding, as well as multidisciplinary surveillance of the breasts, pancreas, ovaries, testes, and lungs.

Juvenile polyposis syndrome is most often characterized by solitary, sporadic polyps in the colorectum (98% of patients affected), followed distantly by polyps in the stomach (14%), ileum (7%), jejunum (7%), and duodenum (7%). The condition is linked with abnormalities in BMPR1A or SMAD4 genes, with SMAD4 germline abnormalities more often leading to “massive” gastric polyps, gastrointestinal bleeding, protein-losing enteropathy, and a higher incidence of gastric cancer in adulthood. Most patients with SMAD4 mutations also have hereditary hemorrhagic telangiectasia, characterized by gastrointestinal bleeding from mucocutaneous telangiectasias, arteriovenous malformations, and epistaxis.

Management of juvenile polyposis syndrome depends on frequent colonoscopies with polypectomies beginning at 12-15 years.

“The goal of surveillance in juvenile polyposis syndrome is to mitigate symptoms related to the disorder and decrease the risk of complications from the manifestations, including cancer,” Dr. Boland and colleagues wrote.

PTEN-hamartoma tumor syndrome, which includes both Bannayan-Riley-Ruvalcaba syndrome and Cowden’s syndrome, is caused by abnormalities in the eponymous PTEN gene. Patients with the condition have an increased risk of colon cancer and polyposis, as well as extraintestinal cancers.

Diagnosis of PTEN-hamartoma tumor syndrome may be complex, involving “clinical examination, mammography and breast MRI, thyroid ultrasound, transvaginal ultrasound, upper gastrointestinal endoscopy, colonoscopy, and renal ultrasound,” according to the guideline.

After diagnosis, frequent colonoscopies are recommended, typically starting at age 35 years, as well as continued surveillance of other organs.

Hereditary mixed polyposis syndrome, which involves attenuated colonic polyposis, is the rarest of the four disorders, having been reported in only “a few families,” according to the guideline. The condition has been linked with “large duplications of the promoter region or entire GREM1 gene.”

Onset is typically in the late 20s, “which is when colonoscopic surveillance should begin,” the investigators wrote. More data are needed to determine appropriate surveillance intervals and if the condition is associated with increased risk of extraintestinal neoplasia.

This call for more research into gastrointestinal hamartomatous polyposis syndromes carried through to the conclusion of the guideline.

“Long-term prospective studies of mutation carriers are still needed to further clarify the risk of cancer and the role of surveillance in these syndromes,” Dr. Boland and colleagues wrote. “With increases in genetic testing and evaluation, future studies will be conducted with more robust cohorts of genetically characterized, less heterogeneous populations. However, there is also a need to study patients and families with unusual phenotypes where no genotype can be found.”

The investigators disclosed no conflicts of interest with the current guideline; however, they provided a list of industry relationships, including Salix Pharmaceuticals, Ferring Pharmaceuticals, and Pfizer, among others.

A clinical practice guideline for the diagnosis and management of gastrointestinal hamartomatous polyposis syndromes has just been published by the U.S. Multi-Society Task Force on Colorectal Cancer, which is comprised of experts representing the American College of Gastroenterology, the American Gastroenterological Association, and the American Society for Gastrointestinal Endoscopy.

Gastrointestinal hamartomatous polyposis syndromes are rare, autosomal dominant disorders associated with intestinal and extraintestinal tumors. Expert consensus statements have previously offered some recommendations for managing these syndromes, but clinical data are scarce, so the present review “is intended to establish a starting point for future research,” lead author C. Richard Boland, MD, of the University of California, San Diego, and colleagues reported.

According to the investigators, “there are essentially no long-term prospective controlled studies of comparative effectiveness of management strategies for these syndromes.” As a result, their recommendations are based on “low-quality” evidence according to GRADE criteria.

Still, Dr. Boland and colleagues highlighted that “there has been tremendous progress in recent years, both in understanding the underlying genetics that underpin these disorders and in elucidating the biology of associated premalignant and malignant conditions.”

The guideline was published online in Gastroenterology .
 

Four syndromes reviewed

The investigators gathered these data to provide an overview of genetic and clinical features for each syndrome, as well as management strategies. Four disorders are included: juvenile polyposis syndrome; Peutz-Jeghers syndrome; hereditary mixed polyposis syndrome; and PTEN-hamartoma tumor syndrome, encompassing Bannayan-Riley-Ruvalcaba syndrome and Cowden’s syndrome.

Although all gastrointestinal hamartomatous polyposis syndromes are caused by germline alterations, Dr. Boland and colleagues pointed out that diagnoses are typically made based on clinical criteria, with germline results serving as confirmatory evidence.

The guideline recommends that any patient with a family history of hamartomatous polyps, or with a history of at least two hamartomatous polyps, should undergo genetic testing. The guideline also provides more nuanced genetic testing algorithms for each syndrome.

Among all the hamartomatous polyp disorders, Peutz-Jeghers syndrome is most understood, according to the investigators. It is caused by aberrations in the STK11 gene, and is characterized by polyps with “branching bands of smooth muscle covered by hyperplastic glandular mucosa” that may occur in the stomach, small intestine, and colon. Patients are also at risk of extraintestinal neoplasia.

For management of Peutz-Jeghers syndrome, the guideline advises frequent endoscopic surveillance to prevent mechanical obstruction and bleeding, as well as multidisciplinary surveillance of the breasts, pancreas, ovaries, testes, and lungs.

Juvenile polyposis syndrome is most often characterized by solitary, sporadic polyps in the colorectum (98% of patients affected), followed distantly by polyps in the stomach (14%), ileum (7%), jejunum (7%), and duodenum (7%). The condition is linked with abnormalities in BMPR1A or SMAD4 genes, with SMAD4 germline abnormalities more often leading to “massive” gastric polyps, gastrointestinal bleeding, protein-losing enteropathy, and a higher incidence of gastric cancer in adulthood. Most patients with SMAD4 mutations also have hereditary hemorrhagic telangiectasia, characterized by gastrointestinal bleeding from mucocutaneous telangiectasias, arteriovenous malformations, and epistaxis.

Management of juvenile polyposis syndrome depends on frequent colonoscopies with polypectomies beginning at 12-15 years.

“The goal of surveillance in juvenile polyposis syndrome is to mitigate symptoms related to the disorder and decrease the risk of complications from the manifestations, including cancer,” Dr. Boland and colleagues wrote.

PTEN-hamartoma tumor syndrome, which includes both Bannayan-Riley-Ruvalcaba syndrome and Cowden’s syndrome, is caused by abnormalities in the eponymous PTEN gene. Patients with the condition have an increased risk of colon cancer and polyposis, as well as extraintestinal cancers.

Diagnosis of PTEN-hamartoma tumor syndrome may be complex, involving “clinical examination, mammography and breast MRI, thyroid ultrasound, transvaginal ultrasound, upper gastrointestinal endoscopy, colonoscopy, and renal ultrasound,” according to the guideline.

After diagnosis, frequent colonoscopies are recommended, typically starting at age 35 years, as well as continued surveillance of other organs.

Hereditary mixed polyposis syndrome, which involves attenuated colonic polyposis, is the rarest of the four disorders, having been reported in only “a few families,” according to the guideline. The condition has been linked with “large duplications of the promoter region or entire GREM1 gene.”

Onset is typically in the late 20s, “which is when colonoscopic surveillance should begin,” the investigators wrote. More data are needed to determine appropriate surveillance intervals and if the condition is associated with increased risk of extraintestinal neoplasia.

This call for more research into gastrointestinal hamartomatous polyposis syndromes carried through to the conclusion of the guideline.

“Long-term prospective studies of mutation carriers are still needed to further clarify the risk of cancer and the role of surveillance in these syndromes,” Dr. Boland and colleagues wrote. “With increases in genetic testing and evaluation, future studies will be conducted with more robust cohorts of genetically characterized, less heterogeneous populations. However, there is also a need to study patients and families with unusual phenotypes where no genotype can be found.”

The investigators disclosed no conflicts of interest with the current guideline; however, they provided a list of industry relationships, including Salix Pharmaceuticals, Ferring Pharmaceuticals, and Pfizer, among others.

This transcript has been edited for clarity.

Does having had a COVID-19 infection increase your risk for the development of diabetes subsequently? Some data say yes and other data say no. No matter what, it’s obviously important to screen people for diabetes routinely, pandemic or not. Remember, screening should start at age 35.

For over a decade, we have known that SARS-type viruses bind to beta cells. This could cause either direct damage to the beta cell or in some way trigger beta cell autoimmunity. We also know that COVID-19 infection increases the levels of inflammatory mediators, which could cause damage to beta cells and potentially to insulin receptors. There is a potential that having had a COVID-19 infection could increase rates of developing type 1 and/or type 2 diabetes.

However, there are other possible causes for people to develop diabetes after having a COVID-19 infection. A COVID-19 infection could cause one to seek medical care, unmasking latent type 1 and/or type 2 diabetes by causing infection-related insulin resistance and worsening preexisting mild hypoglycemia. In addition, people could have sought more medical care in the years since the pandemic has been ebbing, which may make it look like cases have increased.

For example, during the worst of the pandemic, I had multiple referrals for “COVID-19–caused new-onset diabetes” only to find that the patient had an A1c level above 10% and a history of mildly elevated blood glucose levels. This suggests to me that COVID-19 did not cause the diabetes per se but rather worsened an underlying glucose abnormality.

Since the pandemic has improved, I have also seen people diagnosed with type 2 diabetes that I think is associated with pandemic-related weight gain and inactivity.

The bigger issue is what is happening to people after COVID-19 infection who lack risk factors. What about those who we didn’t think were at high risk to get diabetes to begin with and didn’t have prediabetes?

An article by Xie and Al-Aly in The Lancet Diabetes & Endocrinology showed an increase in rates of diabetes in a large VA cohort among those who had a COVID-19 infection compared with both a contemporaneous control who did not have COVID-19 and a historical control. The researchers looked at the patient data 1 year after they’d had COVID-19, so it wasn’t the immediate post–COVID-19 phase but several months later.

They found that the risk for incident type 2 diabetes development was increased by 40% after adjusting for many risk factors. This included individuals who didn’t have traditional risk factors before they developed type 2 diabetes.

What does this mean clinically? First, pandemic or not, people need screening for diabetes and encouragement to have a healthy lifestyle. There may be an increased risk for the diagnosis of type 2 diabetes after COVID-19 infection due to a variety of different mechanisms.

As for people with type 1 diabetes, we also don’t know if having a COVID-19 infection increases their risk. We do know that there was an increase in the severity of diabetic ketoacidosis presentation during the pandemic, so we need to be sure that we reinforce sick-day rules with our patients with type 1 diabetes and that all individuals with type 1 diabetes have the ability to test their ketone levels at home.

In people with new-onset diabetes, whether type 1 or type 2, caused by COVID-19 or not, we need to treat appropriately based on their clinical situation.

Data from registries started during the pandemic will provide more definitive answers and help us find out if there is a relationship between having had COVID-19 infection and developing diabetes.

Perhaps that can help us better understand the mechanisms behind the development of diabetes overall.

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Does having had a COVID-19 infection increase your risk for the development of diabetes subsequently? Some data say yes and other data say no. No matter what, it’s obviously important to screen people for diabetes routinely, pandemic or not. Remember, screening should start at age 35.

For over a decade, we have known that SARS-type viruses bind to beta cells. This could cause either direct damage to the beta cell or in some way trigger beta cell autoimmunity. We also know that COVID-19 infection increases the levels of inflammatory mediators, which could cause damage to beta cells and potentially to insulin receptors. There is a potential that having had a COVID-19 infection could increase rates of developing type 1 and/or type 2 diabetes.

However, there are other possible causes for people to develop diabetes after having a COVID-19 infection. A COVID-19 infection could cause one to seek medical care, unmasking latent type 1 and/or type 2 diabetes by causing infection-related insulin resistance and worsening preexisting mild hypoglycemia. In addition, people could have sought more medical care in the years since the pandemic has been ebbing, which may make it look like cases have increased.

For example, during the worst of the pandemic, I had multiple referrals for “COVID-19–caused new-onset diabetes” only to find that the patient had an A1c level above 10% and a history of mildly elevated blood glucose levels. This suggests to me that COVID-19 did not cause the diabetes per se but rather worsened an underlying glucose abnormality.

Since the pandemic has improved, I have also seen people diagnosed with type 2 diabetes that I think is associated with pandemic-related weight gain and inactivity.

The bigger issue is what is happening to people after COVID-19 infection who lack risk factors. What about those who we didn’t think were at high risk to get diabetes to begin with and didn’t have prediabetes?

An article by Xie and Al-Aly in The Lancet Diabetes & Endocrinology showed an increase in rates of diabetes in a large VA cohort among those who had a COVID-19 infection compared with both a contemporaneous control who did not have COVID-19 and a historical control. The researchers looked at the patient data 1 year after they’d had COVID-19, so it wasn’t the immediate post–COVID-19 phase but several months later.

They found that the risk for incident type 2 diabetes development was increased by 40% after adjusting for many risk factors. This included individuals who didn’t have traditional risk factors before they developed type 2 diabetes.

What does this mean clinically? First, pandemic or not, people need screening for diabetes and encouragement to have a healthy lifestyle. There may be an increased risk for the diagnosis of type 2 diabetes after COVID-19 infection due to a variety of different mechanisms.

As for people with type 1 diabetes, we also don’t know if having a COVID-19 infection increases their risk. We do know that there was an increase in the severity of diabetic ketoacidosis presentation during the pandemic, so we need to be sure that we reinforce sick-day rules with our patients with type 1 diabetes and that all individuals with type 1 diabetes have the ability to test their ketone levels at home.

In people with new-onset diabetes, whether type 1 or type 2, caused by COVID-19 or not, we need to treat appropriately based on their clinical situation.

Data from registries started during the pandemic will provide more definitive answers and help us find out if there is a relationship between having had COVID-19 infection and developing diabetes.

Perhaps that can help us better understand the mechanisms behind the development of diabetes overall.

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Does having had a COVID-19 infection increase your risk for the development of diabetes subsequently? Some data say yes and other data say no. No matter what, it’s obviously important to screen people for diabetes routinely, pandemic or not. Remember, screening should start at age 35.

For over a decade, we have known that SARS-type viruses bind to beta cells. This could cause either direct damage to the beta cell or in some way trigger beta cell autoimmunity. We also know that COVID-19 infection increases the levels of inflammatory mediators, which could cause damage to beta cells and potentially to insulin receptors. There is a potential that having had a COVID-19 infection could increase rates of developing type 1 and/or type 2 diabetes.

However, there are other possible causes for people to develop diabetes after having a COVID-19 infection. A COVID-19 infection could cause one to seek medical care, unmasking latent type 1 and/or type 2 diabetes by causing infection-related insulin resistance and worsening preexisting mild hypoglycemia. In addition, people could have sought more medical care in the years since the pandemic has been ebbing, which may make it look like cases have increased.

For example, during the worst of the pandemic, I had multiple referrals for “COVID-19–caused new-onset diabetes” only to find that the patient had an A1c level above 10% and a history of mildly elevated blood glucose levels. This suggests to me that COVID-19 did not cause the diabetes per se but rather worsened an underlying glucose abnormality.

Since the pandemic has improved, I have also seen people diagnosed with type 2 diabetes that I think is associated with pandemic-related weight gain and inactivity.

The bigger issue is what is happening to people after COVID-19 infection who lack risk factors. What about those who we didn’t think were at high risk to get diabetes to begin with and didn’t have prediabetes?

An article by Xie and Al-Aly in The Lancet Diabetes & Endocrinology showed an increase in rates of diabetes in a large VA cohort among those who had a COVID-19 infection compared with both a contemporaneous control who did not have COVID-19 and a historical control. The researchers looked at the patient data 1 year after they’d had COVID-19, so it wasn’t the immediate post–COVID-19 phase but several months later.

They found that the risk for incident type 2 diabetes development was increased by 40% after adjusting for many risk factors. This included individuals who didn’t have traditional risk factors before they developed type 2 diabetes.

What does this mean clinically? First, pandemic or not, people need screening for diabetes and encouragement to have a healthy lifestyle. There may be an increased risk for the diagnosis of type 2 diabetes after COVID-19 infection due to a variety of different mechanisms.

As for people with type 1 diabetes, we also don’t know if having a COVID-19 infection increases their risk. We do know that there was an increase in the severity of diabetic ketoacidosis presentation during the pandemic, so we need to be sure that we reinforce sick-day rules with our patients with type 1 diabetes and that all individuals with type 1 diabetes have the ability to test their ketone levels at home.

In people with new-onset diabetes, whether type 1 or type 2, caused by COVID-19 or not, we need to treat appropriately based on their clinical situation.

Data from registries started during the pandemic will provide more definitive answers and help us find out if there is a relationship between having had COVID-19 infection and developing diabetes.

Perhaps that can help us better understand the mechanisms behind the development of diabetes overall.

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article first appeared on Medscape.com.

Davida F. Kruger, MSN, APN-BC, BC-ADM
Ms. Kruger has been a certified nurse practitioner in diabetes at Henry Ford Health System in Detroit, MI, for more than 35 years. Ms. Kruger has been a co-investigator on numerous studies of diabetes interventions and care, including the National Institutes of Health–funded multicenter EDIC and ACCORD trials.

She is a past Chair of the American Diabetes Association (ADA) Research Foundation and has served on the ADA Research Policy Committee. She is also an ADA Past President (Health Care and Education). She has also served as editor-in-chief of 2 American Diabetes Association (ADA) journals, Diabetes Spectrum and Clinical Diabetes.

Our diabetes clinic in Detroit is ground zero for diabetes care and education.

High-risk obstetrician gynecologists, cardiologists, nephrologists, and primary care providers, which are all specialties seeing more patients with type 2 diabetes (T2D) comorbidities, are coming to us or sharing patient cases to learn more about diabetes care, newer medications, and the technology needed to help disease management. Considering the complexity of the disease, its comorbidities, the long list of medications, and the human skills required to help these individuals, our clinic has long considered that patients are better served by a team of providers with experience in the intricacies and nuances of this chronic disease.

With over 40 years in the trenches, I can write without equivocation that the treatment of patients with diabetes requires a team approach involving diabetes educators, nurse practitioners, physician assistants, pharmacists, physicians, and nutritionists, who have long known that diabetes is a serious, deadly disease. 

Some facts to prove my point: 
When I started treating people with  diabetes, 4% of the US population had the disease. Life expectancy was about 74 years. Today, 11% of the population has diabetes, and life expectancy is closer to 78 years. Longer life, for someone with diabetes, means more time with kidney disease, cardiovascular problems, neuropathy, macular degeneration, and more.T2D is no longer just an adult disease. We are treating T2D in a much younger population. The Centers for Disease Control and Prevention says from 2002 to 2015, the incidence rate for people <20 years rose 4.8% per year. 
In 2019, the World Health Organization said that 16,300 people < 25 years old died from diabetes, and most of these deaths were from type 1 diabetes.
If we maintain the status quo, between now and 2050, 33% of the adult population in this country could have this disease. 
Our clinic has enrolled  at least 3500 patients with some type of diabetes. 

The list of therapies ─ and more importantly the different classes of therapies ─ has grown significantly since the time when sulfonylureas, metformin, and insulin were the only therapies available. Today, there are at least 9 classes of medications to treat type 2 diabetes. 

Considering that patients with T2D, most of whom are overweight or obese, also have heart disease, kidney disease, and more, the collective input from various kinds of healthcare providers to discuss how these medications can work together, or not, is beyond beneficial. The literature shows that a multidisciplinary team improves patient outcomes in the T2D population. The literature also shows that despite therapeutic advances, most of these patients have disease that is not well controlled, for a variety of reasons.

Patients and Attitudes
I was riding in an elevator with a rheumatologist a few years ago. He told me that my patients were all “fat” and “responsible for their situation.” I told him an elevator ride could not cover the amount of education he needed, so I invited him to call me. There are many reasons why people develop T2D and carrying too much weight is a significant one. We tell our patients that this extra weight puts stress on the natural production of insulin. The result is that less organic insulin is produced so more manufactured insulin is prescribed, and this puts weight on the patient. 

Patients have busy lives, and those with diabetes are no different; their lives get in the way of managing their disease. Some need to remember to take 3 or 4 injections a day. They forget an injection at lunch because their routine has been disrupted; they forget at bedtime because they fell asleep on the sofa. Or they had to feed their children dinner quickly to make it to a teacher’s meeting, so they forgot their medication. But it is vital that they maintain their insulin injection schedule. Research says missing 2.1 meal-related injections a week increases glycated hemoglobin (A1c) by 0.3% to 0.4%.

Most people with T2D will eventually need insulin. For someone with diabetes – and for their family members – hypoglycemia is a real fear. Hypoglycemia has significant physical (eg, irregular heartbeat, shakiness) and mental (eg, anxiety, irritability) effects. In response, patients can treat themselves with glucose tablets or simple carbohydrates (between 15 and 30 g). If the patient is unconscious, the family may need to use injectable glucagon. This is where the benefits of a continuous glucose monitor come in.
Patients can see the hypoglycemic state they are approaching so they can treat a low blood glucose level on their own before others need to. 

Our clinic members focus on having open, honest conversations with our patients about how their lives affect their diabetes. We encourage them to choose a nutrition plan or see our dietitian. Some do phenomenally well with plans like Weight Watchers, but others do not. Whatever they choose, our dietitians aim to help them stay on it, with weekly check-ins, teleconferences, and appointments.

Communication goes both ways. Our patients tell us constantly that they do not want another medication. Diabetes is an expensive disease, and most of our patients take at least 5 medications, prescribed by nephrologists, cardiologists, endocrinologists, and family physicians. Our clinical pharmacists and other team members try to find ways to bring those costs down; sometimes we cannot.

Some Pointers
It is not a bad idea to keep a flowchart on your phone that details which diabetes drug is applicable under which circumstances, and when it is not applicable. While most are complementary, a list would detail how each of the new medications work, how they work together and how they benefit patients.

Some wisdom learned in the trenches: 

• Do not shy away from starting a newly diagnosed patient on metformin and a second agent. The American Diabetes Association guidelines say that more intensive initial treatment can be beneficial. If the patient’s  A1c is elevated, consider using 2 medications upon diagnosis. 
• Using a sulfonylurea, which stimulates insulin secretion, as a second-line therapy alone can increase risk of myocardial infarction, all-cause mortality, and severe hypoglycemia (hazard ratios, 1.26, 1.28, and 7.60, respectively); these medications also cause weight gain. The sulfonylureas put pressure on the beta cells to work harder. More importantly, we do not know what these medications do to the cardiovascular system in the long term.
• If the patient has cardiovascular disease, then, in combination with metformin, use a glucagon-like peptide 1 receptor agonist (GLP-1) or a sodium-glucose cotransporter 2 (SGLT2) inhibitor. If the patient has kidney disease, start with an SGLT2 inhibitor. And yes, you can prescribe both at the same time. 
• SGLT2 inhibitors lower glucose levels by preventing the kidneys from reabsorbing glucose. The GLP-1 agonists encourage insulin production and inhibit glucagon secretion  after meals. Neither of these medications are known to add weight; they are linked with weight loss. 
• If your patient is on a dipeptidyl peptidase 4 (DPP-4) inhibitor and is moving to a GLP-1 receptor agonist, stop the DDP-4 before starting the GLP-1 since both target the incretin system to control blood glucose levels.

While years in the making, new medications and technologies now available for T2D have given healthcare providers more options for their patients, and patients have better opportunities to achieve their treatment goals. 
 

Davida F. Kruger, MSN, APN-BC, BC-ADM
Ms. Kruger has been a certified nurse practitioner in diabetes at Henry Ford Health System in Detroit, MI, for more than 35 years. Ms. Kruger has been a co-investigator on numerous studies of diabetes interventions and care, including the National Institutes of Health–funded multicenter EDIC and ACCORD trials.

She is a past Chair of the American Diabetes Association (ADA) Research Foundation and has served on the ADA Research Policy Committee. She is also an ADA Past President (Health Care and Education). She has also served as editor-in-chief of 2 American Diabetes Association (ADA) journals, Diabetes Spectrum and Clinical Diabetes.

Our diabetes clinic in Detroit is ground zero for diabetes care and education.

High-risk obstetrician gynecologists, cardiologists, nephrologists, and primary care providers, which are all specialties seeing more patients with type 2 diabetes (T2D) comorbidities, are coming to us or sharing patient cases to learn more about diabetes care, newer medications, and the technology needed to help disease management. Considering the complexity of the disease, its comorbidities, the long list of medications, and the human skills required to help these individuals, our clinic has long considered that patients are better served by a team of providers with experience in the intricacies and nuances of this chronic disease.

With over 40 years in the trenches, I can write without equivocation that the treatment of patients with diabetes requires a team approach involving diabetes educators, nurse practitioners, physician assistants, pharmacists, physicians, and nutritionists, who have long known that diabetes is a serious, deadly disease. 

Some facts to prove my point: 
When I started treating people with  diabetes, 4% of the US population had the disease. Life expectancy was about 74 years. Today, 11% of the population has diabetes, and life expectancy is closer to 78 years. Longer life, for someone with diabetes, means more time with kidney disease, cardiovascular problems, neuropathy, macular degeneration, and more.T2D is no longer just an adult disease. We are treating T2D in a much younger population. The Centers for Disease Control and Prevention says from 2002 to 2015, the incidence rate for people <20 years rose 4.8% per year. 
In 2019, the World Health Organization said that 16,300 people < 25 years old died from diabetes, and most of these deaths were from type 1 diabetes.
If we maintain the status quo, between now and 2050, 33% of the adult population in this country could have this disease. 
Our clinic has enrolled  at least 3500 patients with some type of diabetes. 

The list of therapies ─ and more importantly the different classes of therapies ─ has grown significantly since the time when sulfonylureas, metformin, and insulin were the only therapies available. Today, there are at least 9 classes of medications to treat type 2 diabetes. 

Considering that patients with T2D, most of whom are overweight or obese, also have heart disease, kidney disease, and more, the collective input from various kinds of healthcare providers to discuss how these medications can work together, or not, is beyond beneficial. The literature shows that a multidisciplinary team improves patient outcomes in the T2D population. The literature also shows that despite therapeutic advances, most of these patients have disease that is not well controlled, for a variety of reasons.

Patients and Attitudes
I was riding in an elevator with a rheumatologist a few years ago. He told me that my patients were all “fat” and “responsible for their situation.” I told him an elevator ride could not cover the amount of education he needed, so I invited him to call me. There are many reasons why people develop T2D and carrying too much weight is a significant one. We tell our patients that this extra weight puts stress on the natural production of insulin. The result is that less organic insulin is produced so more manufactured insulin is prescribed, and this puts weight on the patient. 

Patients have busy lives, and those with diabetes are no different; their lives get in the way of managing their disease. Some need to remember to take 3 or 4 injections a day. They forget an injection at lunch because their routine has been disrupted; they forget at bedtime because they fell asleep on the sofa. Or they had to feed their children dinner quickly to make it to a teacher’s meeting, so they forgot their medication. But it is vital that they maintain their insulin injection schedule. Research says missing 2.1 meal-related injections a week increases glycated hemoglobin (A1c) by 0.3% to 0.4%.

Most people with T2D will eventually need insulin. For someone with diabetes – and for their family members – hypoglycemia is a real fear. Hypoglycemia has significant physical (eg, irregular heartbeat, shakiness) and mental (eg, anxiety, irritability) effects. In response, patients can treat themselves with glucose tablets or simple carbohydrates (between 15 and 30 g). If the patient is unconscious, the family may need to use injectable glucagon. This is where the benefits of a continuous glucose monitor come in.
Patients can see the hypoglycemic state they are approaching so they can treat a low blood glucose level on their own before others need to. 

Our clinic members focus on having open, honest conversations with our patients about how their lives affect their diabetes. We encourage them to choose a nutrition plan or see our dietitian. Some do phenomenally well with plans like Weight Watchers, but others do not. Whatever they choose, our dietitians aim to help them stay on it, with weekly check-ins, teleconferences, and appointments.

Communication goes both ways. Our patients tell us constantly that they do not want another medication. Diabetes is an expensive disease, and most of our patients take at least 5 medications, prescribed by nephrologists, cardiologists, endocrinologists, and family physicians. Our clinical pharmacists and other team members try to find ways to bring those costs down; sometimes we cannot.

Some Pointers
It is not a bad idea to keep a flowchart on your phone that details which diabetes drug is applicable under which circumstances, and when it is not applicable. While most are complementary, a list would detail how each of the new medications work, how they work together and how they benefit patients.

Some wisdom learned in the trenches: 

• Do not shy away from starting a newly diagnosed patient on metformin and a second agent. The American Diabetes Association guidelines say that more intensive initial treatment can be beneficial. If the patient’s  A1c is elevated, consider using 2 medications upon diagnosis. 
• Using a sulfonylurea, which stimulates insulin secretion, as a second-line therapy alone can increase risk of myocardial infarction, all-cause mortality, and severe hypoglycemia (hazard ratios, 1.26, 1.28, and 7.60, respectively); these medications also cause weight gain. The sulfonylureas put pressure on the beta cells to work harder. More importantly, we do not know what these medications do to the cardiovascular system in the long term.
• If the patient has cardiovascular disease, then, in combination with metformin, use a glucagon-like peptide 1 receptor agonist (GLP-1) or a sodium-glucose cotransporter 2 (SGLT2) inhibitor. If the patient has kidney disease, start with an SGLT2 inhibitor. And yes, you can prescribe both at the same time. 
• SGLT2 inhibitors lower glucose levels by preventing the kidneys from reabsorbing glucose. The GLP-1 agonists encourage insulin production and inhibit glucagon secretion  after meals. Neither of these medications are known to add weight; they are linked with weight loss. 
• If your patient is on a dipeptidyl peptidase 4 (DPP-4) inhibitor and is moving to a GLP-1 receptor agonist, stop the DDP-4 before starting the GLP-1 since both target the incretin system to control blood glucose levels.

While years in the making, new medications and technologies now available for T2D have given healthcare providers more options for their patients, and patients have better opportunities to achieve their treatment goals. 
 

Davida F. Kruger, MSN, APN-BC, BC-ADM
Ms. Kruger has been a certified nurse practitioner in diabetes at Henry Ford Health System in Detroit, MI, for more than 35 years. Ms. Kruger has been a co-investigator on numerous studies of diabetes interventions and care, including the National Institutes of Health–funded multicenter EDIC and ACCORD trials.

She is a past Chair of the American Diabetes Association (ADA) Research Foundation and has served on the ADA Research Policy Committee. She is also an ADA Past President (Health Care and Education). She has also served as editor-in-chief of 2 American Diabetes Association (ADA) journals, Diabetes Spectrum and Clinical Diabetes.

Our diabetes clinic in Detroit is ground zero for diabetes care and education.

High-risk obstetrician gynecologists, cardiologists, nephrologists, and primary care providers, which are all specialties seeing more patients with type 2 diabetes (T2D) comorbidities, are coming to us or sharing patient cases to learn more about diabetes care, newer medications, and the technology needed to help disease management. Considering the complexity of the disease, its comorbidities, the long list of medications, and the human skills required to help these individuals, our clinic has long considered that patients are better served by a team of providers with experience in the intricacies and nuances of this chronic disease.

With over 40 years in the trenches, I can write without equivocation that the treatment of patients with diabetes requires a team approach involving diabetes educators, nurse practitioners, physician assistants, pharmacists, physicians, and nutritionists, who have long known that diabetes is a serious, deadly disease. 

Some facts to prove my point: 
When I started treating people with  diabetes, 4% of the US population had the disease. Life expectancy was about 74 years. Today, 11% of the population has diabetes, and life expectancy is closer to 78 years. Longer life, for someone with diabetes, means more time with kidney disease, cardiovascular problems, neuropathy, macular degeneration, and more.T2D is no longer just an adult disease. We are treating T2D in a much younger population. The Centers for Disease Control and Prevention says from 2002 to 2015, the incidence rate for people <20 years rose 4.8% per year. 
In 2019, the World Health Organization said that 16,300 people < 25 years old died from diabetes, and most of these deaths were from type 1 diabetes.
If we maintain the status quo, between now and 2050, 33% of the adult population in this country could have this disease. 
Our clinic has enrolled  at least 3500 patients with some type of diabetes. 

The list of therapies ─ and more importantly the different classes of therapies ─ has grown significantly since the time when sulfonylureas, metformin, and insulin were the only therapies available. Today, there are at least 9 classes of medications to treat type 2 diabetes. 

Considering that patients with T2D, most of whom are overweight or obese, also have heart disease, kidney disease, and more, the collective input from various kinds of healthcare providers to discuss how these medications can work together, or not, is beyond beneficial. The literature shows that a multidisciplinary team improves patient outcomes in the T2D population. The literature also shows that despite therapeutic advances, most of these patients have disease that is not well controlled, for a variety of reasons.

Patients and Attitudes
I was riding in an elevator with a rheumatologist a few years ago. He told me that my patients were all “fat” and “responsible for their situation.” I told him an elevator ride could not cover the amount of education he needed, so I invited him to call me. There are many reasons why people develop T2D and carrying too much weight is a significant one. We tell our patients that this extra weight puts stress on the natural production of insulin. The result is that less organic insulin is produced so more manufactured insulin is prescribed, and this puts weight on the patient. 

Patients have busy lives, and those with diabetes are no different; their lives get in the way of managing their disease. Some need to remember to take 3 or 4 injections a day. They forget an injection at lunch because their routine has been disrupted; they forget at bedtime because they fell asleep on the sofa. Or they had to feed their children dinner quickly to make it to a teacher’s meeting, so they forgot their medication. But it is vital that they maintain their insulin injection schedule. Research says missing 2.1 meal-related injections a week increases glycated hemoglobin (A1c) by 0.3% to 0.4%.

Most people with T2D will eventually need insulin. For someone with diabetes – and for their family members – hypoglycemia is a real fear. Hypoglycemia has significant physical (eg, irregular heartbeat, shakiness) and mental (eg, anxiety, irritability) effects. In response, patients can treat themselves with glucose tablets or simple carbohydrates (between 15 and 30 g). If the patient is unconscious, the family may need to use injectable glucagon. This is where the benefits of a continuous glucose monitor come in.
Patients can see the hypoglycemic state they are approaching so they can treat a low blood glucose level on their own before others need to. 

Our clinic members focus on having open, honest conversations with our patients about how their lives affect their diabetes. We encourage them to choose a nutrition plan or see our dietitian. Some do phenomenally well with plans like Weight Watchers, but others do not. Whatever they choose, our dietitians aim to help them stay on it, with weekly check-ins, teleconferences, and appointments.

Communication goes both ways. Our patients tell us constantly that they do not want another medication. Diabetes is an expensive disease, and most of our patients take at least 5 medications, prescribed by nephrologists, cardiologists, endocrinologists, and family physicians. Our clinical pharmacists and other team members try to find ways to bring those costs down; sometimes we cannot.

Some Pointers
It is not a bad idea to keep a flowchart on your phone that details which diabetes drug is applicable under which circumstances, and when it is not applicable. While most are complementary, a list would detail how each of the new medications work, how they work together and how they benefit patients.

Some wisdom learned in the trenches: 

• Do not shy away from starting a newly diagnosed patient on metformin and a second agent. The American Diabetes Association guidelines say that more intensive initial treatment can be beneficial. If the patient’s  A1c is elevated, consider using 2 medications upon diagnosis. 
• Using a sulfonylurea, which stimulates insulin secretion, as a second-line therapy alone can increase risk of myocardial infarction, all-cause mortality, and severe hypoglycemia (hazard ratios, 1.26, 1.28, and 7.60, respectively); these medications also cause weight gain. The sulfonylureas put pressure on the beta cells to work harder. More importantly, we do not know what these medications do to the cardiovascular system in the long term.
• If the patient has cardiovascular disease, then, in combination with metformin, use a glucagon-like peptide 1 receptor agonist (GLP-1) or a sodium-glucose cotransporter 2 (SGLT2) inhibitor. If the patient has kidney disease, start with an SGLT2 inhibitor. And yes, you can prescribe both at the same time. 
• SGLT2 inhibitors lower glucose levels by preventing the kidneys from reabsorbing glucose. The GLP-1 agonists encourage insulin production and inhibit glucagon secretion  after meals. Neither of these medications are known to add weight; they are linked with weight loss. 
• If your patient is on a dipeptidyl peptidase 4 (DPP-4) inhibitor and is moving to a GLP-1 receptor agonist, stop the DDP-4 before starting the GLP-1 since both target the incretin system to control blood glucose levels.

While years in the making, new medications and technologies now available for T2D have given healthcare providers more options for their patients, and patients have better opportunities to achieve their treatment goals. 
 

Key clinical point: The prevalence of migraine is higher in children and adolescents with attention deficit hyperactivity disorder (ADHD) vs those without.

Major finding: The risk of developing migraine was significantly higher in patients with ADHD than in matched controls (adjusted hazard ratio [aHR] 1.92; 95% CI 1.64-2.31) with the risk being prominent in children (aHR 2.01; 95% CI 1.63-2.49) and adolescents (aHR 1.94; 95% CI 1.35-2.79) but not in young adults with ADHD.

Study details: This was a nationwide longitudinal case-cohort study including 81,441 patients (including children, adolescents, and young adults aged 3-11, 12-17, and 18-29 years, respectively) with ADHD and 81,441 matched controls without ADHD.

Disclosures: The study was supported by grants from Taipei Veterans General Hospital; Kaohsiung Veterans General Hospital; Yen Tjing Ling Medical Foundation; and the Ministry of Science and Technology, Taiwan. The authors declared no conflicts of interest.

Source: Hsu T-W et al. Attention deficit hyperactivity disorder and risk of migraine: A nationwide longitudinal study. Headache. 2022 (May 6). Doi:  10.1111/head.14306

Key clinical point: The prevalence of migraine is higher in children and adolescents with attention deficit hyperactivity disorder (ADHD) vs those without.

Major finding: The risk of developing migraine was significantly higher in patients with ADHD than in matched controls (adjusted hazard ratio [aHR] 1.92; 95% CI 1.64-2.31) with the risk being prominent in children (aHR 2.01; 95% CI 1.63-2.49) and adolescents (aHR 1.94; 95% CI 1.35-2.79) but not in young adults with ADHD.

Study details: This was a nationwide longitudinal case-cohort study including 81,441 patients (including children, adolescents, and young adults aged 3-11, 12-17, and 18-29 years, respectively) with ADHD and 81,441 matched controls without ADHD.

Disclosures: The study was supported by grants from Taipei Veterans General Hospital; Kaohsiung Veterans General Hospital; Yen Tjing Ling Medical Foundation; and the Ministry of Science and Technology, Taiwan. The authors declared no conflicts of interest.

Source: Hsu T-W et al. Attention deficit hyperactivity disorder and risk of migraine: A nationwide longitudinal study. Headache. 2022 (May 6). Doi:  10.1111/head.14306

Key clinical point: The prevalence of migraine is higher in children and adolescents with attention deficit hyperactivity disorder (ADHD) vs those without.

Major finding: The risk of developing migraine was significantly higher in patients with ADHD than in matched controls (adjusted hazard ratio [aHR] 1.92; 95% CI 1.64-2.31) with the risk being prominent in children (aHR 2.01; 95% CI 1.63-2.49) and adolescents (aHR 1.94; 95% CI 1.35-2.79) but not in young adults with ADHD.

Study details: This was a nationwide longitudinal case-cohort study including 81,441 patients (including children, adolescents, and young adults aged 3-11, 12-17, and 18-29 years, respectively) with ADHD and 81,441 matched controls without ADHD.

Disclosures: The study was supported by grants from Taipei Veterans General Hospital; Kaohsiung Veterans General Hospital; Yen Tjing Ling Medical Foundation; and the Ministry of Science and Technology, Taiwan. The authors declared no conflicts of interest.

Source: Hsu T-W et al. Attention deficit hyperactivity disorder and risk of migraine: A nationwide longitudinal study. Headache. 2022 (May 6). Doi:  10.1111/head.14306

Key clinical point: Interictal levels of plasma glutamate are elevated in patients with episodic migraine (EM) and chronic migraine (CM), thus qualifying it as a potential marker for both EM and CM.

Major finding: Plasma glutamate levels were significantly higher in patients with EM (49.73 μmol/L [95% CI 40.82-66.12] ) and CM (58.70 μmol/L [95% CI 44.64-72.46]) vs control participants (38.79 μmol/L [95% CI 29.50-53.60]; P < .001).

Study details: This single-center study included 240 women aged 19-65 years, of which 98 had EM, 92 had CM, and 50 were nonmigraine control participants.

Disclosures: The study was supported by a National Research Foundation of Korea (NRF) grant from the Korean government. MK Chu declared serving as a site investigator for a multicenter trial and an advisory member for and receiving lecture honoraria and grants from various organizations, including NRF.

Source: Park CG, Chu MK. Interictal plasma glutamate levels are elevated in individuals with episodic and chronic migraine. Sci Rep. 2022;12:6921 (Apr 28). Doi: 10.1038/s41598-022-10883-9

Key clinical point: Interictal levels of plasma glutamate are elevated in patients with episodic migraine (EM) and chronic migraine (CM), thus qualifying it as a potential marker for both EM and CM.

Major finding: Plasma glutamate levels were significantly higher in patients with EM (49.73 μmol/L [95% CI 40.82-66.12] ) and CM (58.70 μmol/L [95% CI 44.64-72.46]) vs control participants (38.79 μmol/L [95% CI 29.50-53.60]; P < .001).

Study details: This single-center study included 240 women aged 19-65 years, of which 98 had EM, 92 had CM, and 50 were nonmigraine control participants.

Disclosures: The study was supported by a National Research Foundation of Korea (NRF) grant from the Korean government. MK Chu declared serving as a site investigator for a multicenter trial and an advisory member for and receiving lecture honoraria and grants from various organizations, including NRF.

Source: Park CG, Chu MK. Interictal plasma glutamate levels are elevated in individuals with episodic and chronic migraine. Sci Rep. 2022;12:6921 (Apr 28). Doi: 10.1038/s41598-022-10883-9

Key clinical point: Interictal levels of plasma glutamate are elevated in patients with episodic migraine (EM) and chronic migraine (CM), thus qualifying it as a potential marker for both EM and CM.

Major finding: Plasma glutamate levels were significantly higher in patients with EM (49.73 μmol/L [95% CI 40.82-66.12] ) and CM (58.70 μmol/L [95% CI 44.64-72.46]) vs control participants (38.79 μmol/L [95% CI 29.50-53.60]; P < .001).

Study details: This single-center study included 240 women aged 19-65 years, of which 98 had EM, 92 had CM, and 50 were nonmigraine control participants.

Disclosures: The study was supported by a National Research Foundation of Korea (NRF) grant from the Korean government. MK Chu declared serving as a site investigator for a multicenter trial and an advisory member for and receiving lecture honoraria and grants from various organizations, including NRF.

Source: Park CG, Chu MK. Interictal plasma glutamate levels are elevated in individuals with episodic and chronic migraine. Sci Rep. 2022;12:6921 (Apr 28). Doi: 10.1038/s41598-022-10883-9

Key clinical point: Adherence and persistence to fremanezumab was high among patients with migraine, especially for quarterly vs monthly dosing.

Major finding: After 6 months of fremanezumab initiation, the mean proportion of days covered (PDC) and medication possession ratio (MPR) were 86.1% and 88.7% respectively, with 74.8% and 79.0% of patients being classified as higher adherers by PDC (≥80%) and MPR (≥80%), respectively. Quarterly vs monthly fremanezumab was associated with significantly higher adherence (P ≤ .006) and mean persistence rates (P = .011).

Study details: This was a retrospective study including 987 adult patients with ≥1 migraine diagnosis during the study period who received fremanezumab on or after diagnosis.

Disclosures: The study was sponsored by Teva Pharmaceuticals. Some authors reported being current orformer employees of Teva.

Source: Krasenbaum LJ et al. A real-world study of acute and preventive medication use, adherence, and persistence in patients prescribed fremanezumab in the United States. J Headache Pain. 2022;23:54 (May 4). Doi: 10.1186/s10194-022-01413-z

Key clinical point: Adherence and persistence to fremanezumab was high among patients with migraine, especially for quarterly vs monthly dosing.

Major finding: After 6 months of fremanezumab initiation, the mean proportion of days covered (PDC) and medication possession ratio (MPR) were 86.1% and 88.7% respectively, with 74.8% and 79.0% of patients being classified as higher adherers by PDC (≥80%) and MPR (≥80%), respectively. Quarterly vs monthly fremanezumab was associated with significantly higher adherence (P ≤ .006) and mean persistence rates (P = .011).

Study details: This was a retrospective study including 987 adult patients with ≥1 migraine diagnosis during the study period who received fremanezumab on or after diagnosis.

Disclosures: The study was sponsored by Teva Pharmaceuticals. Some authors reported being current orformer employees of Teva.

Source: Krasenbaum LJ et al. A real-world study of acute and preventive medication use, adherence, and persistence in patients prescribed fremanezumab in the United States. J Headache Pain. 2022;23:54 (May 4). Doi: 10.1186/s10194-022-01413-z

Key clinical point: Adherence and persistence to fremanezumab was high among patients with migraine, especially for quarterly vs monthly dosing.

Major finding: After 6 months of fremanezumab initiation, the mean proportion of days covered (PDC) and medication possession ratio (MPR) were 86.1% and 88.7% respectively, with 74.8% and 79.0% of patients being classified as higher adherers by PDC (≥80%) and MPR (≥80%), respectively. Quarterly vs monthly fremanezumab was associated with significantly higher adherence (P ≤ .006) and mean persistence rates (P = .011).

Study details: This was a retrospective study including 987 adult patients with ≥1 migraine diagnosis during the study period who received fremanezumab on or after diagnosis.

Disclosures: The study was sponsored by Teva Pharmaceuticals. Some authors reported being current orformer employees of Teva.

Source: Krasenbaum LJ et al. A real-world study of acute and preventive medication use, adherence, and persistence in patients prescribed fremanezumab in the United States. J Headache Pain. 2022;23:54 (May 4). Doi: 10.1186/s10194-022-01413-z

Key clinical point: With self-reported migraine being associated with 26% higher odds of adverse pregnancy outcomes (APO), it may be a significant risk factor for APO.

Major finding: After adjusting for confounding factors, women with migraine showed increased odds of any APO (adjusted odds ratio 1.26; 95% CI 1.12-1.41).

Study details: This was a multicenter prospective study, nuMoM2b, including 9450 nulliparous singleton pregnant women in early gestation, of which 1752 self-reported migraine at the first-trimester visit.

Disclosures: The nuMoM2b study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development, Case Western Reserve University, and Columbia University, among others. EC Miller and NA Bello declared receiving financial support from various sources.

Source: Miller EC et al. Migraine and adverse pregnancy outcomes: the nuMoM2b study. Am J Obstet Gynecol. 2022 (May 2). Doi: 10.1016/j.ajog.2022.04.049

Key clinical point: With self-reported migraine being associated with 26% higher odds of adverse pregnancy outcomes (APO), it may be a significant risk factor for APO.

Major finding: After adjusting for confounding factors, women with migraine showed increased odds of any APO (adjusted odds ratio 1.26; 95% CI 1.12-1.41).

Study details: This was a multicenter prospective study, nuMoM2b, including 9450 nulliparous singleton pregnant women in early gestation, of which 1752 self-reported migraine at the first-trimester visit.

Disclosures: The nuMoM2b study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development, Case Western Reserve University, and Columbia University, among others. EC Miller and NA Bello declared receiving financial support from various sources.

Source: Miller EC et al. Migraine and adverse pregnancy outcomes: the nuMoM2b study. Am J Obstet Gynecol. 2022 (May 2). Doi: 10.1016/j.ajog.2022.04.049

Key clinical point: With self-reported migraine being associated with 26% higher odds of adverse pregnancy outcomes (APO), it may be a significant risk factor for APO.

Major finding: After adjusting for confounding factors, women with migraine showed increased odds of any APO (adjusted odds ratio 1.26; 95% CI 1.12-1.41).

Study details: This was a multicenter prospective study, nuMoM2b, including 9450 nulliparous singleton pregnant women in early gestation, of which 1752 self-reported migraine at the first-trimester visit.

Disclosures: The nuMoM2b study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development, Case Western Reserve University, and Columbia University, among others. EC Miller and NA Bello declared receiving financial support from various sources.

Source: Miller EC et al. Migraine and adverse pregnancy outcomes: the nuMoM2b study. Am J Obstet Gynecol. 2022 (May 2). Doi: 10.1016/j.ajog.2022.04.049

Key clinical point: Self-administered single-dose subcutaneous (SC) injection of diclofenac sodium (50 mg/mL) complexed with hydroxypropyl-β-cyclodextrin (HPβCD) is safe and effective for the treatment of acute migraine attacks in patients with moderate-to-severe migraine pain.

Major finding: After 2 hours of injection, 46.7% of patients were pain-free in the 50 mg diclofenac/HPβCD group, with the percentage being significantly higher than that in the placebo group (16.1%; P = .01). Most treatment-emergent adverse events were mild.

Study details: The findings are from a multicenter, phase 2, dose-finding pilot study including 122 adult patients experiencing 2-8 migraine attacks/month with moderate-to-severe pain who were randomly assigned to receive diclofenac/HPβCD (25, 50, or 75 mg) or placebo.

Disclosures: The study was sponsored by IBSA Institut Biochimique S.A. (Switzerland). Some authors declared serving as advisory board members, consultants, or speakers, or receiving honoraria for clinical investigation studies, travel and research grants, or personal fees from various sources.

Source: Geppetti P et al. Self-administered subcutaneous diclofenac sodium in acute migraine attack: A randomized, double-blind, placebo-controlled dose-finding pilot study. Cephalalgia. 2022 (Apr 26). Doi: 10.1177/03331024221093712

Key clinical point: Self-administered single-dose subcutaneous (SC) injection of diclofenac sodium (50 mg/mL) complexed with hydroxypropyl-β-cyclodextrin (HPβCD) is safe and effective for the treatment of acute migraine attacks in patients with moderate-to-severe migraine pain.

Major finding: After 2 hours of injection, 46.7% of patients were pain-free in the 50 mg diclofenac/HPβCD group, with the percentage being significantly higher than that in the placebo group (16.1%; P = .01). Most treatment-emergent adverse events were mild.

Study details: The findings are from a multicenter, phase 2, dose-finding pilot study including 122 adult patients experiencing 2-8 migraine attacks/month with moderate-to-severe pain who were randomly assigned to receive diclofenac/HPβCD (25, 50, or 75 mg) or placebo.

Disclosures: The study was sponsored by IBSA Institut Biochimique S.A. (Switzerland). Some authors declared serving as advisory board members, consultants, or speakers, or receiving honoraria for clinical investigation studies, travel and research grants, or personal fees from various sources.

Source: Geppetti P et al. Self-administered subcutaneous diclofenac sodium in acute migraine attack: A randomized, double-blind, placebo-controlled dose-finding pilot study. Cephalalgia. 2022 (Apr 26). Doi: 10.1177/03331024221093712

Key clinical point: Self-administered single-dose subcutaneous (SC) injection of diclofenac sodium (50 mg/mL) complexed with hydroxypropyl-β-cyclodextrin (HPβCD) is safe and effective for the treatment of acute migraine attacks in patients with moderate-to-severe migraine pain.

Major finding: After 2 hours of injection, 46.7% of patients were pain-free in the 50 mg diclofenac/HPβCD group, with the percentage being significantly higher than that in the placebo group (16.1%; P = .01). Most treatment-emergent adverse events were mild.

Study details: The findings are from a multicenter, phase 2, dose-finding pilot study including 122 adult patients experiencing 2-8 migraine attacks/month with moderate-to-severe pain who were randomly assigned to receive diclofenac/HPβCD (25, 50, or 75 mg) or placebo.

Disclosures: The study was sponsored by IBSA Institut Biochimique S.A. (Switzerland). Some authors declared serving as advisory board members, consultants, or speakers, or receiving honoraria for clinical investigation studies, travel and research grants, or personal fees from various sources.

Source: Geppetti P et al. Self-administered subcutaneous diclofenac sodium in acute migraine attack: A randomized, double-blind, placebo-controlled dose-finding pilot study. Cephalalgia. 2022 (Apr 26). Doi: 10.1177/03331024221093712