An amphetamine-based, extended-release, orally disintegrating tablet for patients age ≥6 diagnosed with attention-deficit/hyperactivity disorder (ADHD) won FDA approval on January 28, 2016 (Table).¹

Adzenys XR-ODT is the first extended-release, orally disintegrating tablet for ADHD, Neos Therapeutics, Inc. the drug’s manufacturer, said in a statement.² The newly approved agent is bioequivalent to Adderall XR (the capsule form of extended-release mixed amphetamine salts), and patients taking Adderall XR can be switched to the new drug. Equivalent dosages of the 2 drugs are outlined on the prescribing information.¹

“The novel features of an extended-release orally disintegrating tablet ... make Adzenys XR-ODT attractive for use in both children (6 and older) and adults,” Alice R. Mao, MD, Medical Director, Memorial Park Psychiatry, Houston, Texas, said in the statement.²

As a condition of the approval, Neos must annually report the status of 3 post-marketing studies of children diagnosed with ADHD taking Adzenys XR-ODT, according to the approval letter.² One is a single-dose, open-label study of children ages 4 and 5; the second is a randomized, double-blind, placebo-controlled titration study of children ages 4 and 5; and the third is a 1-year, open-label safety study of patients ages 4 and 5.

For patients age 6 to 17, the starting dosage is 6.3 mg once daily in the morning; for adults, it is 12.5 mg once daily in the morning, according to the label.¹ The medication will be available in 4 other dose strengths: 3.1 mg, 9.4 mg, 15.7 mg, and 18.8 mg.

The most common adverse reactions to the drug among pediatric patients include loss of appetite, insomnia, and abdominal pain. Among adult patients, adverse reactions include dry mouth, loss of appetite, and insomnia.

An amphetamine-based, extended-release, orally disintegrating tablet for patients age ≥6 diagnosed with attention-deficit/hyperactivity disorder (ADHD) won FDA approval on January 28, 2016 (Table).¹

Adzenys XR-ODT is the first extended-release, orally disintegrating tablet for ADHD, Neos Therapeutics, Inc. the drug’s manufacturer, said in a statement.² The newly approved agent is bioequivalent to Adderall XR (the capsule form of extended-release mixed amphetamine salts), and patients taking Adderall XR can be switched to the new drug. Equivalent dosages of the 2 drugs are outlined on the prescribing information.¹

“The novel features of an extended-release orally disintegrating tablet ... make Adzenys XR-ODT attractive for use in both children (6 and older) and adults,” Alice R. Mao, MD, Medical Director, Memorial Park Psychiatry, Houston, Texas, said in the statement.²

As a condition of the approval, Neos must annually report the status of 3 post-marketing studies of children diagnosed with ADHD taking Adzenys XR-ODT, according to the approval letter.² One is a single-dose, open-label study of children ages 4 and 5; the second is a randomized, double-blind, placebo-controlled titration study of children ages 4 and 5; and the third is a 1-year, open-label safety study of patients ages 4 and 5.

For patients age 6 to 17, the starting dosage is 6.3 mg once daily in the morning; for adults, it is 12.5 mg once daily in the morning, according to the label.¹ The medication will be available in 4 other dose strengths: 3.1 mg, 9.4 mg, 15.7 mg, and 18.8 mg.

The most common adverse reactions to the drug among pediatric patients include loss of appetite, insomnia, and abdominal pain. Among adult patients, adverse reactions include dry mouth, loss of appetite, and insomnia.

An amphetamine-based, extended-release, orally disintegrating tablet for patients age ≥6 diagnosed with attention-deficit/hyperactivity disorder (ADHD) won FDA approval on January 28, 2016 (Table).¹

Adzenys XR-ODT is the first extended-release, orally disintegrating tablet for ADHD, Neos Therapeutics, Inc. the drug’s manufacturer, said in a statement.² The newly approved agent is bioequivalent to Adderall XR (the capsule form of extended-release mixed amphetamine salts), and patients taking Adderall XR can be switched to the new drug. Equivalent dosages of the 2 drugs are outlined on the prescribing information.¹

“The novel features of an extended-release orally disintegrating tablet ... make Adzenys XR-ODT attractive for use in both children (6 and older) and adults,” Alice R. Mao, MD, Medical Director, Memorial Park Psychiatry, Houston, Texas, said in the statement.²

As a condition of the approval, Neos must annually report the status of 3 post-marketing studies of children diagnosed with ADHD taking Adzenys XR-ODT, according to the approval letter.² One is a single-dose, open-label study of children ages 4 and 5; the second is a randomized, double-blind, placebo-controlled titration study of children ages 4 and 5; and the third is a 1-year, open-label safety study of patients ages 4 and 5.

For patients age 6 to 17, the starting dosage is 6.3 mg once daily in the morning; for adults, it is 12.5 mg once daily in the morning, according to the label.¹ The medication will be available in 4 other dose strengths: 3.1 mg, 9.4 mg, 15.7 mg, and 18.8 mg.

The most common adverse reactions to the drug among pediatric patients include loss of appetite, insomnia, and abdominal pain. Among adult patients, adverse reactions include dry mouth, loss of appetite, and insomnia.

JACKSONVILLE, FLA. – Over the past 30 years, transanal endoscopic microsurgery (TEM) has emerged as a technique for localized rectal cancer, but the need for expensive specialized equipment put it beyond the reach of most hospitals.

Now, early results with transanal minimally invasive surgery (TAMIS) may open the door to an option that achieves the benefits of TEM while using commonly available and less expensive equipment, according to a study presented at the Association for Academic Surgery/Society of University Surgeons Academic Surgical Congress.

Dr. John Costello, general surgery resident at Georgetown University, Washington, presented a poster summarizing the findings of a systematic literature review of TEM and TAMIS studies. The experience with TAMIS is more limited since Dr. Sam Atallah of Sebring, Fla., first introduced it in 2010. The review included the only head-to-head study of the technical aspects of TAMIS and TEM to date.

“Overall the results are very similar between the two approaches,” Dr. Costello said. “In many ways there are, at least anecdotally, some benefits potentially toward the TAMIS technique aside from cost: The perioperative morbidity may be a little lower and, particularly, there seemed to be fewer early problems with continence after surgery.”

The review found similar outcomes between the two approaches: low recurrence rates for small tumors (up to 3 cm) of 4% for TAMIS and 5% for TEM, although the study found that the recurrence rate for TEM increased with larger tumors. Surgery-related deaths with TAMIS ranged from 7.4% to19% and TEM from 6% to 31% across the studies reviewed.

The challenge with the systematic review was that the population of patients who had TAMIS was fewer than 500.

Dr. Costello elucidated the reasons that rectal cancer surgery has proved so challenging to surgeons over the years. The choice of operation was either limited to transabdominal or transanal excision, but the transanal approach had limitations anatomically and was found to be oncologically inferior for early stage cancer. Even with the evolution of the TEM approach, its adoption has been slow.

Either TEM or TAMIS would be a good option for patients too frail for the radical resection that low anterior resection or abdominal perineal resection demand, and would offer an option for palliation for advanced disease, Dr. Costello said. “You could locally resect patients in a way that they go home the same day or at most stay one day in the hospital,” he said.

“The challenge with TEM is that, although the oncologic outcomes are quite good with early-stage disease, the adoption has been very poor over 3 decades mainly because it requires specialized equipment with a very large upfront cost that is limited to use in the rectum,” Dr. Costello said. He estimated the initial capital investment cost for TEM equipment at up to $60,000 on average.

The TAMIS approach, on the other hand, carries a per-procedure equipment cost of about $500 over traditional laparoscopic surgery, he said. It can utilize the single-incision laparoscopic port (SILS) for the transanal approach. TAMIS sacrifices the three-dimensional view of TEM for two-dimensional, but it does provide 360-degree visualization. The surgeon must also be facile with the laparoscopic technique. “In the past that was a big challenge, but now all trainees are very familiar with laparoscopic surgery,” Dr. Costello said.

While the paucity of data on the TAMIS approach makes it difficult to make a strong case for the procedure, the path forward is clear, Dr. Costello said.

“We feel, as do a number of authors of the most papers, that the time truly is now for an actual prospective randomized trial to compare these techniques head-to-head, because colorectal surgeons now have the skill set to be facile at both,” Dr. Costello said.

The investigators had no financial relationships to disclose.

JACKSONVILLE, FLA. – Over the past 30 years, transanal endoscopic microsurgery (TEM) has emerged as a technique for localized rectal cancer, but the need for expensive specialized equipment put it beyond the reach of most hospitals.

Now, early results with transanal minimally invasive surgery (TAMIS) may open the door to an option that achieves the benefits of TEM while using commonly available and less expensive equipment, according to a study presented at the Association for Academic Surgery/Society of University Surgeons Academic Surgical Congress.

Dr. John Costello, general surgery resident at Georgetown University, Washington, presented a poster summarizing the findings of a systematic literature review of TEM and TAMIS studies. The experience with TAMIS is more limited since Dr. Sam Atallah of Sebring, Fla., first introduced it in 2010. The review included the only head-to-head study of the technical aspects of TAMIS and TEM to date.

“Overall the results are very similar between the two approaches,” Dr. Costello said. “In many ways there are, at least anecdotally, some benefits potentially toward the TAMIS technique aside from cost: The perioperative morbidity may be a little lower and, particularly, there seemed to be fewer early problems with continence after surgery.”

The review found similar outcomes between the two approaches: low recurrence rates for small tumors (up to 3 cm) of 4% for TAMIS and 5% for TEM, although the study found that the recurrence rate for TEM increased with larger tumors. Surgery-related deaths with TAMIS ranged from 7.4% to19% and TEM from 6% to 31% across the studies reviewed.

The challenge with the systematic review was that the population of patients who had TAMIS was fewer than 500.

Dr. Costello elucidated the reasons that rectal cancer surgery has proved so challenging to surgeons over the years. The choice of operation was either limited to transabdominal or transanal excision, but the transanal approach had limitations anatomically and was found to be oncologically inferior for early stage cancer. Even with the evolution of the TEM approach, its adoption has been slow.

Either TEM or TAMIS would be a good option for patients too frail for the radical resection that low anterior resection or abdominal perineal resection demand, and would offer an option for palliation for advanced disease, Dr. Costello said. “You could locally resect patients in a way that they go home the same day or at most stay one day in the hospital,” he said.

“The challenge with TEM is that, although the oncologic outcomes are quite good with early-stage disease, the adoption has been very poor over 3 decades mainly because it requires specialized equipment with a very large upfront cost that is limited to use in the rectum,” Dr. Costello said. He estimated the initial capital investment cost for TEM equipment at up to $60,000 on average.

The TAMIS approach, on the other hand, carries a per-procedure equipment cost of about $500 over traditional laparoscopic surgery, he said. It can utilize the single-incision laparoscopic port (SILS) for the transanal approach. TAMIS sacrifices the three-dimensional view of TEM for two-dimensional, but it does provide 360-degree visualization. The surgeon must also be facile with the laparoscopic technique. “In the past that was a big challenge, but now all trainees are very familiar with laparoscopic surgery,” Dr. Costello said.

While the paucity of data on the TAMIS approach makes it difficult to make a strong case for the procedure, the path forward is clear, Dr. Costello said.

“We feel, as do a number of authors of the most papers, that the time truly is now for an actual prospective randomized trial to compare these techniques head-to-head, because colorectal surgeons now have the skill set to be facile at both,” Dr. Costello said.

The investigators had no financial relationships to disclose.

JACKSONVILLE, FLA. – Over the past 30 years, transanal endoscopic microsurgery (TEM) has emerged as a technique for localized rectal cancer, but the need for expensive specialized equipment put it beyond the reach of most hospitals.

Now, early results with transanal minimally invasive surgery (TAMIS) may open the door to an option that achieves the benefits of TEM while using commonly available and less expensive equipment, according to a study presented at the Association for Academic Surgery/Society of University Surgeons Academic Surgical Congress.

Dr. John Costello, general surgery resident at Georgetown University, Washington, presented a poster summarizing the findings of a systematic literature review of TEM and TAMIS studies. The experience with TAMIS is more limited since Dr. Sam Atallah of Sebring, Fla., first introduced it in 2010. The review included the only head-to-head study of the technical aspects of TAMIS and TEM to date.

“Overall the results are very similar between the two approaches,” Dr. Costello said. “In many ways there are, at least anecdotally, some benefits potentially toward the TAMIS technique aside from cost: The perioperative morbidity may be a little lower and, particularly, there seemed to be fewer early problems with continence after surgery.”

The review found similar outcomes between the two approaches: low recurrence rates for small tumors (up to 3 cm) of 4% for TAMIS and 5% for TEM, although the study found that the recurrence rate for TEM increased with larger tumors. Surgery-related deaths with TAMIS ranged from 7.4% to19% and TEM from 6% to 31% across the studies reviewed.

The challenge with the systematic review was that the population of patients who had TAMIS was fewer than 500.

Dr. Costello elucidated the reasons that rectal cancer surgery has proved so challenging to surgeons over the years. The choice of operation was either limited to transabdominal or transanal excision, but the transanal approach had limitations anatomically and was found to be oncologically inferior for early stage cancer. Even with the evolution of the TEM approach, its adoption has been slow.

Either TEM or TAMIS would be a good option for patients too frail for the radical resection that low anterior resection or abdominal perineal resection demand, and would offer an option for palliation for advanced disease, Dr. Costello said. “You could locally resect patients in a way that they go home the same day or at most stay one day in the hospital,” he said.

“The challenge with TEM is that, although the oncologic outcomes are quite good with early-stage disease, the adoption has been very poor over 3 decades mainly because it requires specialized equipment with a very large upfront cost that is limited to use in the rectum,” Dr. Costello said. He estimated the initial capital investment cost for TEM equipment at up to $60,000 on average.

The TAMIS approach, on the other hand, carries a per-procedure equipment cost of about $500 over traditional laparoscopic surgery, he said. It can utilize the single-incision laparoscopic port (SILS) for the transanal approach. TAMIS sacrifices the three-dimensional view of TEM for two-dimensional, but it does provide 360-degree visualization. The surgeon must also be facile with the laparoscopic technique. “In the past that was a big challenge, but now all trainees are very familiar with laparoscopic surgery,” Dr. Costello said.

While the paucity of data on the TAMIS approach makes it difficult to make a strong case for the procedure, the path forward is clear, Dr. Costello said.

“We feel, as do a number of authors of the most papers, that the time truly is now for an actual prospective randomized trial to compare these techniques head-to-head, because colorectal surgeons now have the skill set to be facile at both,” Dr. Costello said.

The investigators had no financial relationships to disclose.

New Orleans – A “Lessons from the Bench” session at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis addressed the ongoing debate regarding the relative importance of neurodegeneration vs. inflammation in progressive multiple sclerosis.

In an interview, session chair Dr. Benjamin Segal discussed the research presented – on topics ranging from immunological biomarkers that could also prove to be therapeutic targets, to immune- and central nervous system–related susceptibility alleles identified in genome wide association studies – and how the findings could lead to new and improved treatments.

“These types of studies give us insights into the immune pathways that are dysregulated in the different diseases and how they may be similar or different from one another. Ultimately all of these scientific studies hopefully will translate into treatments in the future,” said Dr. Segal of the University of Michigan, Ann Arbor.

New Orleans – A “Lessons from the Bench” session at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis addressed the ongoing debate regarding the relative importance of neurodegeneration vs. inflammation in progressive multiple sclerosis.

In an interview, session chair Dr. Benjamin Segal discussed the research presented – on topics ranging from immunological biomarkers that could also prove to be therapeutic targets, to immune- and central nervous system–related susceptibility alleles identified in genome wide association studies – and how the findings could lead to new and improved treatments.

“These types of studies give us insights into the immune pathways that are dysregulated in the different diseases and how they may be similar or different from one another. Ultimately all of these scientific studies hopefully will translate into treatments in the future,” said Dr. Segal of the University of Michigan, Ann Arbor.

New Orleans – A “Lessons from the Bench” session at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis addressed the ongoing debate regarding the relative importance of neurodegeneration vs. inflammation in progressive multiple sclerosis.

In an interview, session chair Dr. Benjamin Segal discussed the research presented – on topics ranging from immunological biomarkers that could also prove to be therapeutic targets, to immune- and central nervous system–related susceptibility alleles identified in genome wide association studies – and how the findings could lead to new and improved treatments.

“These types of studies give us insights into the immune pathways that are dysregulated in the different diseases and how they may be similar or different from one another. Ultimately all of these scientific studies hopefully will translate into treatments in the future,” said Dr. Segal of the University of Michigan, Ann Arbor.

NEW ORLEANS—Contrary to researchers’ hypothesis, fatigue did not result in worsening of spasticity in patients with multiple sclerosis (MS), resulting instead in a nonsignificant decrease. “Clinically, this suggests that the worsening of gait seen over time in persons with MS may be due to reasons other than spasticity,” reported Herbert Karpatkin, PT, DSc, NCS, MSCS, an Assistant Professor at Hunter College in New York, NY, and colleagues at the ACTRIMS 2016 Forum.

Herbert Karpatkin, PT, DSc, NCS, MSCS

Disturbance of gait is known to occur in approximately 80% of patients with MS. Fatigue and spasticity are among the most common and debilitating symptoms in this patient population and both have been known to worsen with physical performance. Anecdotal reports claim that spasticity is associated with worsening fatigue, but the literature provides little information regarding this relationship.

Dr. Karpatkin and colleagues sought to determine whether, as they hypothecized, increases in fatigue in patients with MS result in increases in lower extremity spasticity. If correct, this would mean that physical therapists who perform gait-training activities in patients with MS would need to take the interaction between fatigue and spasticity into account as a factor that may impact outcomes and help determine an appropriate course of treatment.

A convenience sample of 16 ambulatory subjects with MS was recruited from New York City physical therapy practices that specialize in MS. Demographic and subject characteristics including MS type, years since diagnosis, age, gender, Expanded Disability Status Scale (EDSS) score, medications, and use of assistive devices were recorded and analyzed. The Fatigue Severity Scale (FSS), the MS Impact Scale–29 (MSIS–29), and the MS Severity Scale–88 (MSSS–88) were completed for baseline analysis.

Subjects were randomized into walking and resting groups. All subjects received spasticity testing using the Modified Ashworth Scale (MAS). Subjects in the walking group then underwent a six-minute walk to induce fatigue, while subjects in the resting group lay supine for six minutes to minimize fatigue. Immediately following either six-minute condition, MAS testing was repeated. This was performed on three separate trials during a five-day period, followed by a two-week detraining period. Subjects then crossed over to the opposite condition. Fatigue was measured using the Visual Analog Scale of Fatigue (VAS–F) before and after each six-minute condition.

Sixteen subjects (mean EDSS, 3.59) completed the study. Mean MAS scores decreased nonsignificantly following the six-minute walk from 1.054 to 0.827. MAS scores also decreased nonsignificantly in the nonfatigued condition from 0.841 to 0.839. Mean VAS–F scores increased 29.5 mm following the six-minute walk, indicating that MAS testing was performed in a fatigued condition.

NEW ORLEANS—Contrary to researchers’ hypothesis, fatigue did not result in worsening of spasticity in patients with multiple sclerosis (MS), resulting instead in a nonsignificant decrease. “Clinically, this suggests that the worsening of gait seen over time in persons with MS may be due to reasons other than spasticity,” reported Herbert Karpatkin, PT, DSc, NCS, MSCS, an Assistant Professor at Hunter College in New York, NY, and colleagues at the ACTRIMS 2016 Forum.

Herbert Karpatkin, PT, DSc, NCS, MSCS

Disturbance of gait is known to occur in approximately 80% of patients with MS. Fatigue and spasticity are among the most common and debilitating symptoms in this patient population and both have been known to worsen with physical performance. Anecdotal reports claim that spasticity is associated with worsening fatigue, but the literature provides little information regarding this relationship.

Dr. Karpatkin and colleagues sought to determine whether, as they hypothecized, increases in fatigue in patients with MS result in increases in lower extremity spasticity. If correct, this would mean that physical therapists who perform gait-training activities in patients with MS would need to take the interaction between fatigue and spasticity into account as a factor that may impact outcomes and help determine an appropriate course of treatment.

A convenience sample of 16 ambulatory subjects with MS was recruited from New York City physical therapy practices that specialize in MS. Demographic and subject characteristics including MS type, years since diagnosis, age, gender, Expanded Disability Status Scale (EDSS) score, medications, and use of assistive devices were recorded and analyzed. The Fatigue Severity Scale (FSS), the MS Impact Scale–29 (MSIS–29), and the MS Severity Scale–88 (MSSS–88) were completed for baseline analysis.

Subjects were randomized into walking and resting groups. All subjects received spasticity testing using the Modified Ashworth Scale (MAS). Subjects in the walking group then underwent a six-minute walk to induce fatigue, while subjects in the resting group lay supine for six minutes to minimize fatigue. Immediately following either six-minute condition, MAS testing was repeated. This was performed on three separate trials during a five-day period, followed by a two-week detraining period. Subjects then crossed over to the opposite condition. Fatigue was measured using the Visual Analog Scale of Fatigue (VAS–F) before and after each six-minute condition.

Sixteen subjects (mean EDSS, 3.59) completed the study. Mean MAS scores decreased nonsignificantly following the six-minute walk from 1.054 to 0.827. MAS scores also decreased nonsignificantly in the nonfatigued condition from 0.841 to 0.839. Mean VAS–F scores increased 29.5 mm following the six-minute walk, indicating that MAS testing was performed in a fatigued condition.

NEW ORLEANS—Contrary to researchers’ hypothesis, fatigue did not result in worsening of spasticity in patients with multiple sclerosis (MS), resulting instead in a nonsignificant decrease. “Clinically, this suggests that the worsening of gait seen over time in persons with MS may be due to reasons other than spasticity,” reported Herbert Karpatkin, PT, DSc, NCS, MSCS, an Assistant Professor at Hunter College in New York, NY, and colleagues at the ACTRIMS 2016 Forum.

Herbert Karpatkin, PT, DSc, NCS, MSCS

Disturbance of gait is known to occur in approximately 80% of patients with MS. Fatigue and spasticity are among the most common and debilitating symptoms in this patient population and both have been known to worsen with physical performance. Anecdotal reports claim that spasticity is associated with worsening fatigue, but the literature provides little information regarding this relationship.

Dr. Karpatkin and colleagues sought to determine whether, as they hypothecized, increases in fatigue in patients with MS result in increases in lower extremity spasticity. If correct, this would mean that physical therapists who perform gait-training activities in patients with MS would need to take the interaction between fatigue and spasticity into account as a factor that may impact outcomes and help determine an appropriate course of treatment.

A convenience sample of 16 ambulatory subjects with MS was recruited from New York City physical therapy practices that specialize in MS. Demographic and subject characteristics including MS type, years since diagnosis, age, gender, Expanded Disability Status Scale (EDSS) score, medications, and use of assistive devices were recorded and analyzed. The Fatigue Severity Scale (FSS), the MS Impact Scale–29 (MSIS–29), and the MS Severity Scale–88 (MSSS–88) were completed for baseline analysis.

Subjects were randomized into walking and resting groups. All subjects received spasticity testing using the Modified Ashworth Scale (MAS). Subjects in the walking group then underwent a six-minute walk to induce fatigue, while subjects in the resting group lay supine for six minutes to minimize fatigue. Immediately following either six-minute condition, MAS testing was repeated. This was performed on three separate trials during a five-day period, followed by a two-week detraining period. Subjects then crossed over to the opposite condition. Fatigue was measured using the Visual Analog Scale of Fatigue (VAS–F) before and after each six-minute condition.

Sixteen subjects (mean EDSS, 3.59) completed the study. Mean MAS scores decreased nonsignificantly following the six-minute walk from 1.054 to 0.827. MAS scores also decreased nonsignificantly in the nonfatigued condition from 0.841 to 0.839. Mean VAS–F scores increased 29.5 mm following the six-minute walk, indicating that MAS testing was performed in a fatigued condition.

Editor’s note: “Everything We Say and Do” is an informational series developed by SHM’s Patient Experience Committee to provide readers with thoughtful and actionable communication tactics that have great potential to positively impact patients’ experience of care. Each article will focus on how the contributor applies one ormore of the “key communication” tactics in practice to maintain provider accountability for “Everything we say and do that affects our patients’ thoughts, feelings and well-being.”

What I Say and Do

I address patients by their preferred name and introduce myself with my full name.

Why I Do It

I have been surprised by how little discussion I have seen regarding how we address our patients. All the literature I have seen tells us that patients generally prefer first names, yet most doctors use last names. They also want us to introduce ourselves with our first and last name.

I have really found that using a first name personalizes the encounter a lot more than the formal Mr. or Mrs. Jones. Take, for example, “I am sorry you are still in pain, Mr. Jones,” versus, “I am sorry you are still in pain, Bill.”

Or for a family meeting regarding end of life: “What would Mrs. Jones want from us at this point in her life?” versus “What would Jenny want from us at this point in her life?”

I know that, for me personally, I feel treated more like an individual when someone uses my first name versus my last. This may seem like a small point, but I think it can truly improve communication and connectedness.

How I Do It

About four years ago, I began starting every encounter by addressing my patients by their first and last name. I then ask them what they would prefer to be called. Every patient has responded with either their first name or with a preferred nickname.

I always introduce myself as Dr. Rob Hoffman. About 90% of patients call me Dr. Hoffman, and the rest call me Rob. I used to be taken aback by being called Rob but eventually realized how egocentric that was. What should I care what my patient calls me? TH

Dr. Hoffman is a clinical associate professor and medical director for patient relations at the University of Wisconsin Hospital and Clinics and University of Wisconsin School of Medicine and Public Health in Madison.

Table 1.

Editor’s note: “Everything We Say and Do” is an informational series developed by SHM’s Patient Experience Committee to provide readers with thoughtful and actionable communication tactics that have great potential to positively impact patients’ experience of care. Each article will focus on how the contributor applies one ormore of the “key communication” tactics in practice to maintain provider accountability for “Everything we say and do that affects our patients’ thoughts, feelings and well-being.”

What I Say and Do

I address patients by their preferred name and introduce myself with my full name.

Why I Do It

I have been surprised by how little discussion I have seen regarding how we address our patients. All the literature I have seen tells us that patients generally prefer first names, yet most doctors use last names. They also want us to introduce ourselves with our first and last name.

I have really found that using a first name personalizes the encounter a lot more than the formal Mr. or Mrs. Jones. Take, for example, “I am sorry you are still in pain, Mr. Jones,” versus, “I am sorry you are still in pain, Bill.”

Or for a family meeting regarding end of life: “What would Mrs. Jones want from us at this point in her life?” versus “What would Jenny want from us at this point in her life?”

I know that, for me personally, I feel treated more like an individual when someone uses my first name versus my last. This may seem like a small point, but I think it can truly improve communication and connectedness.

How I Do It

About four years ago, I began starting every encounter by addressing my patients by their first and last name. I then ask them what they would prefer to be called. Every patient has responded with either their first name or with a preferred nickname.

I always introduce myself as Dr. Rob Hoffman. About 90% of patients call me Dr. Hoffman, and the rest call me Rob. I used to be taken aback by being called Rob but eventually realized how egocentric that was. What should I care what my patient calls me? TH

Dr. Hoffman is a clinical associate professor and medical director for patient relations at the University of Wisconsin Hospital and Clinics and University of Wisconsin School of Medicine and Public Health in Madison.

Table 1.

Editor’s note: “Everything We Say and Do” is an informational series developed by SHM’s Patient Experience Committee to provide readers with thoughtful and actionable communication tactics that have great potential to positively impact patients’ experience of care. Each article will focus on how the contributor applies one ormore of the “key communication” tactics in practice to maintain provider accountability for “Everything we say and do that affects our patients’ thoughts, feelings and well-being.”

What I Say and Do

I address patients by their preferred name and introduce myself with my full name.

Why I Do It

I have been surprised by how little discussion I have seen regarding how we address our patients. All the literature I have seen tells us that patients generally prefer first names, yet most doctors use last names. They also want us to introduce ourselves with our first and last name.

I have really found that using a first name personalizes the encounter a lot more than the formal Mr. or Mrs. Jones. Take, for example, “I am sorry you are still in pain, Mr. Jones,” versus, “I am sorry you are still in pain, Bill.”

Or for a family meeting regarding end of life: “What would Mrs. Jones want from us at this point in her life?” versus “What would Jenny want from us at this point in her life?”

I know that, for me personally, I feel treated more like an individual when someone uses my first name versus my last. This may seem like a small point, but I think it can truly improve communication and connectedness.

How I Do It

About four years ago, I began starting every encounter by addressing my patients by their first and last name. I then ask them what they would prefer to be called. Every patient has responded with either their first name or with a preferred nickname.

I always introduce myself as Dr. Rob Hoffman. About 90% of patients call me Dr. Hoffman, and the rest call me Rob. I used to be taken aback by being called Rob but eventually realized how egocentric that was. What should I care what my patient calls me? TH

Dr. Hoffman is a clinical associate professor and medical director for patient relations at the University of Wisconsin Hospital and Clinics and University of Wisconsin School of Medicine and Public Health in Madison.

Table 1.

NEW YORK (Reuters Health) - Only two strategies offer some effectiveness in preventing contrast-induced nephropathy (CIN), according to a systematic review and meta-analysis of 86 randomized, controlled trials.

Those are use of N-acetylcysteine (NAc) in patients receiving low-osmolar contrast media (LOCM), and statins plus NAc.

The reported incidence of CIN, defined as an increase in serum creatinine levels >25% or 44.2 mmol/L (0.5 mg/dL) within three days of IV administration of contrast media, ranges from 7% to 11% and adds an average $10,345 to a CIN-related hospital stay. There is no clear consensus about the most effective intervention to prevent or reduce CIN.

Dr. Rathan M. Subramaniam and colleagues from Johns Hopkins University in Baltimore compared five strategies for preventing CIN in their systematic review and meta-analysis: IV NAc plus saline versus IV saline alone; IV sodium bicarbonate versus IV saline; NAc plus IV saline versus IV sodium bicarbonate; statins with or without NAc versus IV saline; and ascorbic acid versus NAc or IV saline.

In the NAc studies, all of which had low strength of evidence, NAc had a clinically important benefit in reducing CIN risk only when LOCM were used.

Low-dose NAc had a borderline clinically important effect on preventing CIN, whereas high-dose NAc had a statistically significant (but clinically unimportant) effect on reducing CIN risk (with low strength of evidence).

Similarly, statins when added to NAc showed a clinically important reduction in CIN risk, although with low strength of evidence.

IV sodium bicarbonate (versus IV saline), NAc (versus IV sodium bicarbonate), and ascorbic acid (versus other strategies) showed no statistically significant, clinically important benefit in reducing CIN risk, according to the report onine February 1 in Annals of Internal Medicine online.

"The studies span over two decades, and there may have been changes in the practice of CIN prevention, such as increased screening, variation in definition of acute kidney injury, and variation in hydration, over time," the researchers noted. "Such changes could contribute to differences in outcomes."

"This comprehensive review highlights the generally low strength of evidence on interventions for preventing CIN while indicating that the greatest reduction in CIN risk has been achieved with low-dose N-acetylcysteine in patients receiving LOCM or with statins plus N-acetylcysteine," they concluded.

In a related article, the group from Johns Hopkins University found no differences in CIN risk among the different types of LOCM. Iodixanol had a slightly lower risk of CIN than LOCM did, but the difference was not clinically important.

Dr. Guillaume Mahe from CHU de Rennes, Rennes, France recently reviewed remote ischemic preconditioning, another proposed method for preventing CIN (http://bit.ly/23EU40a). He told Reuters Health by email, "It seems of interest to use N-acetylcysteine, which is a low cost drug. Statins might be also a good option. This is another interesting effect of the statins, which is unknown by most physicians."

Even more important, Dr. Mahe said, is to "be sure that the patients need a computed tomography angiography with contrast media."

He expressed surprise that the authors did not assess the role of remote ischemic preconditioning in their review.

Dr. Subramaniam did not respond to a request for comments. The Agency for Healthcare Research and Quality funded both studies.

NEW YORK (Reuters Health) - Only two strategies offer some effectiveness in preventing contrast-induced nephropathy (CIN), according to a systematic review and meta-analysis of 86 randomized, controlled trials.

Those are use of N-acetylcysteine (NAc) in patients receiving low-osmolar contrast media (LOCM), and statins plus NAc.

The reported incidence of CIN, defined as an increase in serum creatinine levels >25% or 44.2 mmol/L (0.5 mg/dL) within three days of IV administration of contrast media, ranges from 7% to 11% and adds an average $10,345 to a CIN-related hospital stay. There is no clear consensus about the most effective intervention to prevent or reduce CIN.

Dr. Rathan M. Subramaniam and colleagues from Johns Hopkins University in Baltimore compared five strategies for preventing CIN in their systematic review and meta-analysis: IV NAc plus saline versus IV saline alone; IV sodium bicarbonate versus IV saline; NAc plus IV saline versus IV sodium bicarbonate; statins with or without NAc versus IV saline; and ascorbic acid versus NAc or IV saline.

In the NAc studies, all of which had low strength of evidence, NAc had a clinically important benefit in reducing CIN risk only when LOCM were used.

Low-dose NAc had a borderline clinically important effect on preventing CIN, whereas high-dose NAc had a statistically significant (but clinically unimportant) effect on reducing CIN risk (with low strength of evidence).

Similarly, statins when added to NAc showed a clinically important reduction in CIN risk, although with low strength of evidence.

IV sodium bicarbonate (versus IV saline), NAc (versus IV sodium bicarbonate), and ascorbic acid (versus other strategies) showed no statistically significant, clinically important benefit in reducing CIN risk, according to the report onine February 1 in Annals of Internal Medicine online.

"The studies span over two decades, and there may have been changes in the practice of CIN prevention, such as increased screening, variation in definition of acute kidney injury, and variation in hydration, over time," the researchers noted. "Such changes could contribute to differences in outcomes."

"This comprehensive review highlights the generally low strength of evidence on interventions for preventing CIN while indicating that the greatest reduction in CIN risk has been achieved with low-dose N-acetylcysteine in patients receiving LOCM or with statins plus N-acetylcysteine," they concluded.

In a related article, the group from Johns Hopkins University found no differences in CIN risk among the different types of LOCM. Iodixanol had a slightly lower risk of CIN than LOCM did, but the difference was not clinically important.

Dr. Guillaume Mahe from CHU de Rennes, Rennes, France recently reviewed remote ischemic preconditioning, another proposed method for preventing CIN (http://bit.ly/23EU40a). He told Reuters Health by email, "It seems of interest to use N-acetylcysteine, which is a low cost drug. Statins might be also a good option. This is another interesting effect of the statins, which is unknown by most physicians."

Even more important, Dr. Mahe said, is to "be sure that the patients need a computed tomography angiography with contrast media."

He expressed surprise that the authors did not assess the role of remote ischemic preconditioning in their review.

Dr. Subramaniam did not respond to a request for comments. The Agency for Healthcare Research and Quality funded both studies.

NEW YORK (Reuters Health) - Only two strategies offer some effectiveness in preventing contrast-induced nephropathy (CIN), according to a systematic review and meta-analysis of 86 randomized, controlled trials.

Those are use of N-acetylcysteine (NAc) in patients receiving low-osmolar contrast media (LOCM), and statins plus NAc.

The reported incidence of CIN, defined as an increase in serum creatinine levels >25% or 44.2 mmol/L (0.5 mg/dL) within three days of IV administration of contrast media, ranges from 7% to 11% and adds an average $10,345 to a CIN-related hospital stay. There is no clear consensus about the most effective intervention to prevent or reduce CIN.

Dr. Rathan M. Subramaniam and colleagues from Johns Hopkins University in Baltimore compared five strategies for preventing CIN in their systematic review and meta-analysis: IV NAc plus saline versus IV saline alone; IV sodium bicarbonate versus IV saline; NAc plus IV saline versus IV sodium bicarbonate; statins with or without NAc versus IV saline; and ascorbic acid versus NAc or IV saline.

In the NAc studies, all of which had low strength of evidence, NAc had a clinically important benefit in reducing CIN risk only when LOCM were used.

Low-dose NAc had a borderline clinically important effect on preventing CIN, whereas high-dose NAc had a statistically significant (but clinically unimportant) effect on reducing CIN risk (with low strength of evidence).

Similarly, statins when added to NAc showed a clinically important reduction in CIN risk, although with low strength of evidence.

IV sodium bicarbonate (versus IV saline), NAc (versus IV sodium bicarbonate), and ascorbic acid (versus other strategies) showed no statistically significant, clinically important benefit in reducing CIN risk, according to the report onine February 1 in Annals of Internal Medicine online.

"The studies span over two decades, and there may have been changes in the practice of CIN prevention, such as increased screening, variation in definition of acute kidney injury, and variation in hydration, over time," the researchers noted. "Such changes could contribute to differences in outcomes."

"This comprehensive review highlights the generally low strength of evidence on interventions for preventing CIN while indicating that the greatest reduction in CIN risk has been achieved with low-dose N-acetylcysteine in patients receiving LOCM or with statins plus N-acetylcysteine," they concluded.

In a related article, the group from Johns Hopkins University found no differences in CIN risk among the different types of LOCM. Iodixanol had a slightly lower risk of CIN than LOCM did, but the difference was not clinically important.

Dr. Guillaume Mahe from CHU de Rennes, Rennes, France recently reviewed remote ischemic preconditioning, another proposed method for preventing CIN (http://bit.ly/23EU40a). He told Reuters Health by email, "It seems of interest to use N-acetylcysteine, which is a low cost drug. Statins might be also a good option. This is another interesting effect of the statins, which is unknown by most physicians."

Even more important, Dr. Mahe said, is to "be sure that the patients need a computed tomography angiography with contrast media."

He expressed surprise that the authors did not assess the role of remote ischemic preconditioning in their review.

Dr. Subramaniam did not respond to a request for comments. The Agency for Healthcare Research and Quality funded both studies.

Antihemophilic factor

The European Commission has approved a full-length recombinant factor VIII product for the treatment and prevention of bleeding in hemophilia A patients of all ages.

The product, Kovaltry (formerly BAY 81-8973), will be marketed for this indication in the 28 member countries of the European Union, as well as Iceland, Liechtenstein, and Norway.

The approval of Kovaltry is based on results from the LEOPOLD trials—3 multinational trials of patients with severe hemophilia A.

The trials were supported by Bayer HealthCare AG, the company developing Kovaltry.

LEOPOLD I

LEOPOLD I is an open-label, cross-over, phase 3 study of males, ages 12 to 65, with severe hemophilia A. Sixty-two patients were assigned to either 2- or 3-times-weekly dosing with Kovaltry, based on each patient’s phenotype, prior bleeding history, and other factors.

The median annualized bleeding rate (ABR) was 1.0 for all the patients who received Kovaltry prophylaxis, 1.0 for patients who received twice-weekly prophylaxis, and 2.0 for patients who received thrice-weekly prophylaxis.

LEOPOLD II

LEOPOLD II is a randomized, cross-over, open-label trial conducted in males ages 12 to 65. In this phase 3 study, 80 subjects were randomized to receive Kovaltry as a low-dose prophylaxis regimen (n=28) twice per week, high-dose prophylaxis (n=31) 3 times a week, or on-demand treatment (n=21).

The median ABR was significantly lower in patients who received either prophylactic regimen than those who received on-demand treatment—2.0 and 60.0, respectively (P<0.0001). The median ABR was 4.0 for patients who received twice-weekly prophylaxis and 2.0 for patients who received thrice-weekly prophylaxis.

LEOPOLD Kids

LEOPOLD Kids is an open-label, non-randomized, phase 3 study designed to evaluate Kovaltry in children age 12 and younger. The study is divided into 2 parts. Part A enrolled only previously treated children, and part B, which is ongoing, includes only untreated children.

For part A, 51 children received Kovaltry twice a week, 3 times a week, or every other day (according to investigator decision) for at least 50 exposure days. The median ABR within 48 hours of prophylactic injection was 0, and the median ABR independent of the time of injection was 1.9.

Safety results

For all 3 trials, 193 patients were evaluable for safety. Adverse reactions were defined as treatment-emergent adverse events with at least a reasonable suspected causal relationship to Kovaltry.

The researchers said the frequency, type, and severity of adverse reactions in children were similar to those observed in adults and adolescents.

The adverse reactions included headache (7.3%), pyrexia (4.1%), pruritus (3.1%), injection site reactions (2.6%), insomnia (2.6%), rash (2.6%), abdominal pain (2.1%), dyspepsia (2.1%), abdominal discomfort (1.6%), lymphadenopathy (1%), dizziness (1%), allergic dermatitis (1%), heart palpitations (1%), sinus tachycardia (1%), chest discomfort (1%), hypersensitivity (0.5%), dysgeusia (0.5%), urticaria (0.5%), and flushing (0.5%).

None of the patients developed factor VIII inhibitors.

Antihemophilic factor

The European Commission has approved a full-length recombinant factor VIII product for the treatment and prevention of bleeding in hemophilia A patients of all ages.

The product, Kovaltry (formerly BAY 81-8973), will be marketed for this indication in the 28 member countries of the European Union, as well as Iceland, Liechtenstein, and Norway.

The approval of Kovaltry is based on results from the LEOPOLD trials—3 multinational trials of patients with severe hemophilia A.

The trials were supported by Bayer HealthCare AG, the company developing Kovaltry.

LEOPOLD I

LEOPOLD I is an open-label, cross-over, phase 3 study of males, ages 12 to 65, with severe hemophilia A. Sixty-two patients were assigned to either 2- or 3-times-weekly dosing with Kovaltry, based on each patient’s phenotype, prior bleeding history, and other factors.

The median annualized bleeding rate (ABR) was 1.0 for all the patients who received Kovaltry prophylaxis, 1.0 for patients who received twice-weekly prophylaxis, and 2.0 for patients who received thrice-weekly prophylaxis.

LEOPOLD II

LEOPOLD II is a randomized, cross-over, open-label trial conducted in males ages 12 to 65. In this phase 3 study, 80 subjects were randomized to receive Kovaltry as a low-dose prophylaxis regimen (n=28) twice per week, high-dose prophylaxis (n=31) 3 times a week, or on-demand treatment (n=21).

The median ABR was significantly lower in patients who received either prophylactic regimen than those who received on-demand treatment—2.0 and 60.0, respectively (P<0.0001). The median ABR was 4.0 for patients who received twice-weekly prophylaxis and 2.0 for patients who received thrice-weekly prophylaxis.

LEOPOLD Kids

LEOPOLD Kids is an open-label, non-randomized, phase 3 study designed to evaluate Kovaltry in children age 12 and younger. The study is divided into 2 parts. Part A enrolled only previously treated children, and part B, which is ongoing, includes only untreated children.

For part A, 51 children received Kovaltry twice a week, 3 times a week, or every other day (according to investigator decision) for at least 50 exposure days. The median ABR within 48 hours of prophylactic injection was 0, and the median ABR independent of the time of injection was 1.9.

Safety results

For all 3 trials, 193 patients were evaluable for safety. Adverse reactions were defined as treatment-emergent adverse events with at least a reasonable suspected causal relationship to Kovaltry.

The researchers said the frequency, type, and severity of adverse reactions in children were similar to those observed in adults and adolescents.

The adverse reactions included headache (7.3%), pyrexia (4.1%), pruritus (3.1%), injection site reactions (2.6%), insomnia (2.6%), rash (2.6%), abdominal pain (2.1%), dyspepsia (2.1%), abdominal discomfort (1.6%), lymphadenopathy (1%), dizziness (1%), allergic dermatitis (1%), heart palpitations (1%), sinus tachycardia (1%), chest discomfort (1%), hypersensitivity (0.5%), dysgeusia (0.5%), urticaria (0.5%), and flushing (0.5%).

None of the patients developed factor VIII inhibitors.

Antihemophilic factor

The European Commission has approved a full-length recombinant factor VIII product for the treatment and prevention of bleeding in hemophilia A patients of all ages.

The product, Kovaltry (formerly BAY 81-8973), will be marketed for this indication in the 28 member countries of the European Union, as well as Iceland, Liechtenstein, and Norway.

The approval of Kovaltry is based on results from the LEOPOLD trials—3 multinational trials of patients with severe hemophilia A.

The trials were supported by Bayer HealthCare AG, the company developing Kovaltry.

LEOPOLD I

LEOPOLD I is an open-label, cross-over, phase 3 study of males, ages 12 to 65, with severe hemophilia A. Sixty-two patients were assigned to either 2- or 3-times-weekly dosing with Kovaltry, based on each patient’s phenotype, prior bleeding history, and other factors.

The median annualized bleeding rate (ABR) was 1.0 for all the patients who received Kovaltry prophylaxis, 1.0 for patients who received twice-weekly prophylaxis, and 2.0 for patients who received thrice-weekly prophylaxis.

LEOPOLD II

LEOPOLD II is a randomized, cross-over, open-label trial conducted in males ages 12 to 65. In this phase 3 study, 80 subjects were randomized to receive Kovaltry as a low-dose prophylaxis regimen (n=28) twice per week, high-dose prophylaxis (n=31) 3 times a week, or on-demand treatment (n=21).

The median ABR was significantly lower in patients who received either prophylactic regimen than those who received on-demand treatment—2.0 and 60.0, respectively (P<0.0001). The median ABR was 4.0 for patients who received twice-weekly prophylaxis and 2.0 for patients who received thrice-weekly prophylaxis.

LEOPOLD Kids

LEOPOLD Kids is an open-label, non-randomized, phase 3 study designed to evaluate Kovaltry in children age 12 and younger. The study is divided into 2 parts. Part A enrolled only previously treated children, and part B, which is ongoing, includes only untreated children.

For part A, 51 children received Kovaltry twice a week, 3 times a week, or every other day (according to investigator decision) for at least 50 exposure days. The median ABR within 48 hours of prophylactic injection was 0, and the median ABR independent of the time of injection was 1.9.

Safety results

For all 3 trials, 193 patients were evaluable for safety. Adverse reactions were defined as treatment-emergent adverse events with at least a reasonable suspected causal relationship to Kovaltry.

The researchers said the frequency, type, and severity of adverse reactions in children were similar to those observed in adults and adolescents.

The adverse reactions included headache (7.3%), pyrexia (4.1%), pruritus (3.1%), injection site reactions (2.6%), insomnia (2.6%), rash (2.6%), abdominal pain (2.1%), dyspepsia (2.1%), abdominal discomfort (1.6%), lymphadenopathy (1%), dizziness (1%), allergic dermatitis (1%), heart palpitations (1%), sinus tachycardia (1%), chest discomfort (1%), hypersensitivity (0.5%), dysgeusia (0.5%), urticaria (0.5%), and flushing (0.5%).

None of the patients developed factor VIII inhibitors.

Prescription medications

Photo courtesy of the CDC

The European Commission has approved use of the antiplatelet agent ticagrelor (Brilique) at a 60 mg dose to treat patients beyond the first year after a heart attack who are at high risk of developing a further atherothrombotic event.

The treatment may be used as continuation therapy after an initial 1-year treatment with 90 mg ticagrelor plus aspirin or after a year of other dual antiplatelet therapy.

This approval is applicable to all 28 European Union (EU) member countries plus Iceland, Norway, and Liechtenstein.

Ticagrelor at a 90 mg dose is already approved in the EU for the prevention of atherothrombotic events in adults with acute coronary syndrome (ACS). In the management of ACS, the recommended maintenance dose of ticagrelor is 90 mg twice daily during the first year after an ACS event.

Now, after the first year, patients with a history of heart attack can continue to be treated with ticagrelor at 60 mg twice daily, which should be taken with a daily maintenance dose of aspirin at 75 mg to 150 mg.

Trial results

The latest EU approval of ticagrelor was based on results from the PEGASUS TIMI-54 study. This trial, which involved more than 21,000 patients, was presented at the American College of Cardiology Congress in March 2015 and simultaneously published in NEJM.

Investigators compared ticagrelor (at 60 mg or 90 mg) plus low-dose aspirin to placebo plus low-dose aspirin in patients who had experienced a heart attack 1 to 3 years prior to study enrollment.

The primary efficacy endpoint was a composite of cardiovascular death, myocardial infarction, or stroke.

The investigators found that patients in either ticagrelor arm were significantly less likely to achieve this endpoint than placebo-treated patients.

At 3 years, the proportion of patients meeting the primary endpoint was 7.85% in the 90 mg group, 7.77% in the 60 mg group, and 9.04% in the placebo group (P=0.008 for 90 mg vs placebo and P=0.004 for 60 mg vs placebo).

Patients receiving ticagrelor also had a significantly higher incidence of major bleeding and dyspnea. The rate of TIMI major bleeding was 2.60% in the 90 mg group, 2.30% in the 60 mg group, and 1.06% in the placebo group (P<0.001 for each ticagrelor dose vs placebo).

The rate of dyspnea was 18.93% in the 90 mg group, 15.84% in 60 mg group, and 6.38% in the placebo group (P<0.001 for both comparisons). The rate of dyspnea leading to treatment discontinuation was 6.5%, 4.55%, and 0.79%, respectively (P<0.001 for both comparisons).

Ticagrelor has been approved in more than 100 countries. The drug is under development by AstraZeneca.

Prescription medications

Photo courtesy of the CDC

The European Commission has approved use of the antiplatelet agent ticagrelor (Brilique) at a 60 mg dose to treat patients beyond the first year after a heart attack who are at high risk of developing a further atherothrombotic event.

The treatment may be used as continuation therapy after an initial 1-year treatment with 90 mg ticagrelor plus aspirin or after a year of other dual antiplatelet therapy.

This approval is applicable to all 28 European Union (EU) member countries plus Iceland, Norway, and Liechtenstein.

Ticagrelor at a 90 mg dose is already approved in the EU for the prevention of atherothrombotic events in adults with acute coronary syndrome (ACS). In the management of ACS, the recommended maintenance dose of ticagrelor is 90 mg twice daily during the first year after an ACS event.

Now, after the first year, patients with a history of heart attack can continue to be treated with ticagrelor at 60 mg twice daily, which should be taken with a daily maintenance dose of aspirin at 75 mg to 150 mg.

Trial results

The latest EU approval of ticagrelor was based on results from the PEGASUS TIMI-54 study. This trial, which involved more than 21,000 patients, was presented at the American College of Cardiology Congress in March 2015 and simultaneously published in NEJM.

Investigators compared ticagrelor (at 60 mg or 90 mg) plus low-dose aspirin to placebo plus low-dose aspirin in patients who had experienced a heart attack 1 to 3 years prior to study enrollment.

The primary efficacy endpoint was a composite of cardiovascular death, myocardial infarction, or stroke.

The investigators found that patients in either ticagrelor arm were significantly less likely to achieve this endpoint than placebo-treated patients.

At 3 years, the proportion of patients meeting the primary endpoint was 7.85% in the 90 mg group, 7.77% in the 60 mg group, and 9.04% in the placebo group (P=0.008 for 90 mg vs placebo and P=0.004 for 60 mg vs placebo).

Patients receiving ticagrelor also had a significantly higher incidence of major bleeding and dyspnea. The rate of TIMI major bleeding was 2.60% in the 90 mg group, 2.30% in the 60 mg group, and 1.06% in the placebo group (P<0.001 for each ticagrelor dose vs placebo).

The rate of dyspnea was 18.93% in the 90 mg group, 15.84% in 60 mg group, and 6.38% in the placebo group (P<0.001 for both comparisons). The rate of dyspnea leading to treatment discontinuation was 6.5%, 4.55%, and 0.79%, respectively (P<0.001 for both comparisons).

Ticagrelor has been approved in more than 100 countries. The drug is under development by AstraZeneca.

Prescription medications

Photo courtesy of the CDC

The European Commission has approved use of the antiplatelet agent ticagrelor (Brilique) at a 60 mg dose to treat patients beyond the first year after a heart attack who are at high risk of developing a further atherothrombotic event.

The treatment may be used as continuation therapy after an initial 1-year treatment with 90 mg ticagrelor plus aspirin or after a year of other dual antiplatelet therapy.

This approval is applicable to all 28 European Union (EU) member countries plus Iceland, Norway, and Liechtenstein.

Ticagrelor at a 90 mg dose is already approved in the EU for the prevention of atherothrombotic events in adults with acute coronary syndrome (ACS). In the management of ACS, the recommended maintenance dose of ticagrelor is 90 mg twice daily during the first year after an ACS event.

Now, after the first year, patients with a history of heart attack can continue to be treated with ticagrelor at 60 mg twice daily, which should be taken with a daily maintenance dose of aspirin at 75 mg to 150 mg.

Trial results

The latest EU approval of ticagrelor was based on results from the PEGASUS TIMI-54 study. This trial, which involved more than 21,000 patients, was presented at the American College of Cardiology Congress in March 2015 and simultaneously published in NEJM.

Investigators compared ticagrelor (at 60 mg or 90 mg) plus low-dose aspirin to placebo plus low-dose aspirin in patients who had experienced a heart attack 1 to 3 years prior to study enrollment.

The primary efficacy endpoint was a composite of cardiovascular death, myocardial infarction, or stroke.

The investigators found that patients in either ticagrelor arm were significantly less likely to achieve this endpoint than placebo-treated patients.

At 3 years, the proportion of patients meeting the primary endpoint was 7.85% in the 90 mg group, 7.77% in the 60 mg group, and 9.04% in the placebo group (P=0.008 for 90 mg vs placebo and P=0.004 for 60 mg vs placebo).

Patients receiving ticagrelor also had a significantly higher incidence of major bleeding and dyspnea. The rate of TIMI major bleeding was 2.60% in the 90 mg group, 2.30% in the 60 mg group, and 1.06% in the placebo group (P<0.001 for each ticagrelor dose vs placebo).

The rate of dyspnea was 18.93% in the 90 mg group, 15.84% in 60 mg group, and 6.38% in the placebo group (P<0.001 for both comparisons). The rate of dyspnea leading to treatment discontinuation was 6.5%, 4.55%, and 0.79%, respectively (P<0.001 for both comparisons).

Ticagrelor has been approved in more than 100 countries. The drug is under development by AstraZeneca.

Andreas Strasser, PhD

Photo by Cameron Wells,

Walter and Eliza Hall

Institute of Medical Research

Research published in Cell Reports helps explain how the anticancer agent Nutlin3a fights lymphoma and other hematologic malignancies.

Nutlin3a is known to activate the tumor suppressor p53, but it hasn’t been clear exactly which p53 target genes are essential for the drug’s therapeutic activity.

The new research revealed that PUMA-mediated apoptosis—not p21-mediated cell-cycle arrest or senescence—is responsible for Nutlin3a’s therapeutic activity in lymphoid malignancies.

“By understanding how nutlins are killing cancer cells, we can begin to formulate their best possible use, including choosing the best partner drugs to combine the nutlins with,” said study author Andreas Strasser, PhD, of the Walter and Eliza Hall Institute of Medical Research in Parkville, Victoria, Australia.

With this study, Dr Strasser and his colleagues first found that Nutlin3a activates p53 target gene expression and causes cell-cycle arrest and apoptosis in non-transformed mouse lymphoid cells in vitro.

The team then showed that Nutlin3a-mediated killing of these cells requires PUMA but not p21. In vivo, loss of PUMA protected non-transformed mouse lymphoid cells against Nutlin3a-induced killing. Loss of p21 did not provide the same protection.

Next, the researchers found that malignant Eµ-Myc lymphoma cells were much more sensitive to Nutlin3a than were non-transformed lymphoid cells. In vitro experiments with Eµ-Myc lymphoma cells showed that Nutlin3a promotes p53 accumulation and downstream effector pathway activation.

As in previous experiments, PUMA (not p21) proved critical for Nutlin3a-induced killing of Eµ-Myc lymphoma cells in vitro. And loss of PUMA (but not p21) impaired the regression of Eµ-Myc lymphomas induced by Nutlin3a in vivo.

Finally, the researchers found that PUMA contributed to Nutlin3a-induced apoptosis in myeloid leukemia, multiple myeloma, and Burkitt lymphoma cell lines.

The team noted that, because PUMA, a pro-apoptotic BH3-only protein, is critical for the therapeutic impact of Nutlin3a, it may be possible to boost the drug’s efficacy by combining it with BH3 mimetic drugs such as navitoclax or venetoclax.

Andreas Strasser, PhD

Photo by Cameron Wells,

Walter and Eliza Hall

Institute of Medical Research

Research published in Cell Reports helps explain how the anticancer agent Nutlin3a fights lymphoma and other hematologic malignancies.

Nutlin3a is known to activate the tumor suppressor p53, but it hasn’t been clear exactly which p53 target genes are essential for the drug’s therapeutic activity.

The new research revealed that PUMA-mediated apoptosis—not p21-mediated cell-cycle arrest or senescence—is responsible for Nutlin3a’s therapeutic activity in lymphoid malignancies.

“By understanding how nutlins are killing cancer cells, we can begin to formulate their best possible use, including choosing the best partner drugs to combine the nutlins with,” said study author Andreas Strasser, PhD, of the Walter and Eliza Hall Institute of Medical Research in Parkville, Victoria, Australia.

With this study, Dr Strasser and his colleagues first found that Nutlin3a activates p53 target gene expression and causes cell-cycle arrest and apoptosis in non-transformed mouse lymphoid cells in vitro.

The team then showed that Nutlin3a-mediated killing of these cells requires PUMA but not p21. In vivo, loss of PUMA protected non-transformed mouse lymphoid cells against Nutlin3a-induced killing. Loss of p21 did not provide the same protection.

Next, the researchers found that malignant Eµ-Myc lymphoma cells were much more sensitive to Nutlin3a than were non-transformed lymphoid cells. In vitro experiments with Eµ-Myc lymphoma cells showed that Nutlin3a promotes p53 accumulation and downstream effector pathway activation.

As in previous experiments, PUMA (not p21) proved critical for Nutlin3a-induced killing of Eµ-Myc lymphoma cells in vitro. And loss of PUMA (but not p21) impaired the regression of Eµ-Myc lymphomas induced by Nutlin3a in vivo.

Finally, the researchers found that PUMA contributed to Nutlin3a-induced apoptosis in myeloid leukemia, multiple myeloma, and Burkitt lymphoma cell lines.

The team noted that, because PUMA, a pro-apoptotic BH3-only protein, is critical for the therapeutic impact of Nutlin3a, it may be possible to boost the drug’s efficacy by combining it with BH3 mimetic drugs such as navitoclax or venetoclax.

Andreas Strasser, PhD

Photo by Cameron Wells,

Walter and Eliza Hall

Institute of Medical Research

Research published in Cell Reports helps explain how the anticancer agent Nutlin3a fights lymphoma and other hematologic malignancies.

Nutlin3a is known to activate the tumor suppressor p53, but it hasn’t been clear exactly which p53 target genes are essential for the drug’s therapeutic activity.

The new research revealed that PUMA-mediated apoptosis—not p21-mediated cell-cycle arrest or senescence—is responsible for Nutlin3a’s therapeutic activity in lymphoid malignancies.

“By understanding how nutlins are killing cancer cells, we can begin to formulate their best possible use, including choosing the best partner drugs to combine the nutlins with,” said study author Andreas Strasser, PhD, of the Walter and Eliza Hall Institute of Medical Research in Parkville, Victoria, Australia.

With this study, Dr Strasser and his colleagues first found that Nutlin3a activates p53 target gene expression and causes cell-cycle arrest and apoptosis in non-transformed mouse lymphoid cells in vitro.

The team then showed that Nutlin3a-mediated killing of these cells requires PUMA but not p21. In vivo, loss of PUMA protected non-transformed mouse lymphoid cells against Nutlin3a-induced killing. Loss of p21 did not provide the same protection.

Next, the researchers found that malignant Eµ-Myc lymphoma cells were much more sensitive to Nutlin3a than were non-transformed lymphoid cells. In vitro experiments with Eµ-Myc lymphoma cells showed that Nutlin3a promotes p53 accumulation and downstream effector pathway activation.

As in previous experiments, PUMA (not p21) proved critical for Nutlin3a-induced killing of Eµ-Myc lymphoma cells in vitro. And loss of PUMA (but not p21) impaired the regression of Eµ-Myc lymphomas induced by Nutlin3a in vivo.

Finally, the researchers found that PUMA contributed to Nutlin3a-induced apoptosis in myeloid leukemia, multiple myeloma, and Burkitt lymphoma cell lines.

The team noted that, because PUMA, a pro-apoptotic BH3-only protein, is critical for the therapeutic impact of Nutlin3a, it may be possible to boost the drug’s efficacy by combining it with BH3 mimetic drugs such as navitoclax or venetoclax.