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Pediatric Hospitalist Michael Beck, MD, FAAP, Measures Success By Others’ Success
Young boys sometimes see a firefighter or a police officer in the line of duty and decide that’s what they want to be when they get older. Michael Beck, MD, FAAP, saw his pediatrician that way.
“He was a very humanistic provider and found joy in serving children and their families,” Dr. Beck says. “I saw how a pediatrician could influence others and make the world a better place and still have fun serving a vulnerable patient population.”
His career in pediatric hospital medicine, though?
“It was largely pure luck,” Dr. Beck admits. “When I was seeking my first job, I was offered a position that was 50/50 internal medicine and pediatrics but purely a hospitalist position.”
Dr. Beck has risen through academic hospitalist ranks the past 15 years and now serves as the division chief of pediatric hospital medicine at Penn State Children’s Hospital at Milton S. Hershey (Pa.) Medical Center. He is one of eight new members of Team Hospitalist, The Hospitalist’s volunteer editorial advisory board.
Question: What was medical school and residency like for you? Was there a single moment you knew “I can do this”?
Answer: I always have been filled with self-doubt, which is a perpetual motivator for me. I guess I believed I could do hospital-based work when I started knowing the majority of what was going on with patients after hearing residents discuss cases and I knew what the labs, studies, and exam findings were going to be before I saw the patient.
Q: What do you like most about working as a hospitalist?
A: The acuity and pathology of cases. I get to see cases that some people only read about. It is very intellectual challenging, and I get to work with and learn from specialists every day.
Q: What do you dislike most?
A: Some of the cases are devastating to families. It is always important to remind yourself—and the team—that some of the diagnoses we help make affect families and the patient in very profound ways.
Q: Did you have a mentor during your training or early career? If so, who was the mentor, and what were the most important lessons you learned from him/her?
A: Dr. Barbara Ostrov. I learned what it really means to be a servant-leader. I witnessed her work ethic and saw that a leader of others should lead by example and be willing to work twice what is expected of others. She is always nonjudgmental and professional, yet forthright, when dealing with contentious situations. She trumpets the work of others, not her own, and sees others’ successes as her success. In the end, I believed she worked for me, not the other way around.
Q: Have you tried to mentor others? Why or why not?
A: Yes. As a division chief, I want others to succeed. The best quote I have read was by Richard Branson [CEO of Virgin]: “Train people so that they can leave, but treat them so they want to stay.”
Q: What’s the biggest change you’ve seen in HM in your career?
A: It has moved from a clinical service to a robust area of research and strong researchers.
Q: What’s the biggest change you would like to see in HM?
A: If hospital medicine is positioning itself to be a specialty with fellowship training, with access to knowledge different from PCPs, then I believe we should function like other specialty services with a different skill set. We should own our discharge process and follow-up plans. We should follow up with patients in a discharge clinic setting to review clinical course, health literacy issues, labs, and studies and even order follow-up studies based on incoming results.
Q: For group leaders, why is it important for you to continue seeing patients?
A: As a clinician leader, my charge is to foster teamwork and create a shared vision for improvement and change. This is not possible to do from an office space or conference room separate from where the work gets done.
Q: As a hospitalist, seeing most of your patients for the very first time, what aspect of patient care is most challenging?
A: Establishing trust and rapport in five to 10 minutes. Caring for a hospitalized patient, when they are surrounded by loved ones, is stressful and anxiety-provoking. Delivering information in a way that is honest and empathetic and timely without the benefit of having a personal historic connection with a patient is always challenging.
Q: What aspect of patient care is most rewarding?
A: Making a diagnosis in a patient that has eluded diagnosis for weeks or months.
Q: What aspect of teaching in the 21st century is most difficult? And what is most enjoyable?
A: Today’s learners have different expectations from mine [in terms] of what they want to get from a career in medicine. While I don’t always agree with them, it is the reality and puts me in a position to discuss and understand the rationale of a changing mindset. As a physician leader, it is important to understand this because it helps me create an environment that fosters successful recruitment and retention.
Q: You mention wanting to tackle the issue of physician burnout? Why is that something important to you?
A: I personally lived through it and felt the effects it had on the relationships I had with family, friends, medical students, residents, and patients. I know what it felt like to be angry, cynical, and distanced from those I cared about and from those whom I was charged with caring for. I never forgot how isolated [you] can feel in an academic center even when surrounded by hundreds. I vowed that if I ever found my way to a leadership position, I would begin by creating an environment that emphasized morale, honesty, integrity, and professionalism. If I succeeded in this, the other organizational missions of education, patient care, quality, and value would follow.
Since 2012, our division has monitored burnout, work-life balance, and, more recently, physician engagement. Although we take care of the sickest children in the region, our group supports each other, recognizing and respectful of the fact that we each have different comfort levels, skill sets, but we also have fun. Patients, nurses, social workers, care coordinators, and clerks see this. Like I teach the residents, you never get a second chance to make a first impression, but you also never get a second chance to make a last one, so make all interactions count. TH
Richard Quinn is a freelance writer in New Jersey.
Young boys sometimes see a firefighter or a police officer in the line of duty and decide that’s what they want to be when they get older. Michael Beck, MD, FAAP, saw his pediatrician that way.
“He was a very humanistic provider and found joy in serving children and their families,” Dr. Beck says. “I saw how a pediatrician could influence others and make the world a better place and still have fun serving a vulnerable patient population.”
His career in pediatric hospital medicine, though?
“It was largely pure luck,” Dr. Beck admits. “When I was seeking my first job, I was offered a position that was 50/50 internal medicine and pediatrics but purely a hospitalist position.”
Dr. Beck has risen through academic hospitalist ranks the past 15 years and now serves as the division chief of pediatric hospital medicine at Penn State Children’s Hospital at Milton S. Hershey (Pa.) Medical Center. He is one of eight new members of Team Hospitalist, The Hospitalist’s volunteer editorial advisory board.
Question: What was medical school and residency like for you? Was there a single moment you knew “I can do this”?
Answer: I always have been filled with self-doubt, which is a perpetual motivator for me. I guess I believed I could do hospital-based work when I started knowing the majority of what was going on with patients after hearing residents discuss cases and I knew what the labs, studies, and exam findings were going to be before I saw the patient.
Q: What do you like most about working as a hospitalist?
A: The acuity and pathology of cases. I get to see cases that some people only read about. It is very intellectual challenging, and I get to work with and learn from specialists every day.
Q: What do you dislike most?
A: Some of the cases are devastating to families. It is always important to remind yourself—and the team—that some of the diagnoses we help make affect families and the patient in very profound ways.
Q: Did you have a mentor during your training or early career? If so, who was the mentor, and what were the most important lessons you learned from him/her?
A: Dr. Barbara Ostrov. I learned what it really means to be a servant-leader. I witnessed her work ethic and saw that a leader of others should lead by example and be willing to work twice what is expected of others. She is always nonjudgmental and professional, yet forthright, when dealing with contentious situations. She trumpets the work of others, not her own, and sees others’ successes as her success. In the end, I believed she worked for me, not the other way around.
Q: Have you tried to mentor others? Why or why not?
A: Yes. As a division chief, I want others to succeed. The best quote I have read was by Richard Branson [CEO of Virgin]: “Train people so that they can leave, but treat them so they want to stay.”
Q: What’s the biggest change you’ve seen in HM in your career?
A: It has moved from a clinical service to a robust area of research and strong researchers.
Q: What’s the biggest change you would like to see in HM?
A: If hospital medicine is positioning itself to be a specialty with fellowship training, with access to knowledge different from PCPs, then I believe we should function like other specialty services with a different skill set. We should own our discharge process and follow-up plans. We should follow up with patients in a discharge clinic setting to review clinical course, health literacy issues, labs, and studies and even order follow-up studies based on incoming results.
Q: For group leaders, why is it important for you to continue seeing patients?
A: As a clinician leader, my charge is to foster teamwork and create a shared vision for improvement and change. This is not possible to do from an office space or conference room separate from where the work gets done.
Q: As a hospitalist, seeing most of your patients for the very first time, what aspect of patient care is most challenging?
A: Establishing trust and rapport in five to 10 minutes. Caring for a hospitalized patient, when they are surrounded by loved ones, is stressful and anxiety-provoking. Delivering information in a way that is honest and empathetic and timely without the benefit of having a personal historic connection with a patient is always challenging.
Q: What aspect of patient care is most rewarding?
A: Making a diagnosis in a patient that has eluded diagnosis for weeks or months.
Q: What aspect of teaching in the 21st century is most difficult? And what is most enjoyable?
A: Today’s learners have different expectations from mine [in terms] of what they want to get from a career in medicine. While I don’t always agree with them, it is the reality and puts me in a position to discuss and understand the rationale of a changing mindset. As a physician leader, it is important to understand this because it helps me create an environment that fosters successful recruitment and retention.
Q: You mention wanting to tackle the issue of physician burnout? Why is that something important to you?
A: I personally lived through it and felt the effects it had on the relationships I had with family, friends, medical students, residents, and patients. I know what it felt like to be angry, cynical, and distanced from those I cared about and from those whom I was charged with caring for. I never forgot how isolated [you] can feel in an academic center even when surrounded by hundreds. I vowed that if I ever found my way to a leadership position, I would begin by creating an environment that emphasized morale, honesty, integrity, and professionalism. If I succeeded in this, the other organizational missions of education, patient care, quality, and value would follow.
Since 2012, our division has monitored burnout, work-life balance, and, more recently, physician engagement. Although we take care of the sickest children in the region, our group supports each other, recognizing and respectful of the fact that we each have different comfort levels, skill sets, but we also have fun. Patients, nurses, social workers, care coordinators, and clerks see this. Like I teach the residents, you never get a second chance to make a first impression, but you also never get a second chance to make a last one, so make all interactions count. TH
Richard Quinn is a freelance writer in New Jersey.
Young boys sometimes see a firefighter or a police officer in the line of duty and decide that’s what they want to be when they get older. Michael Beck, MD, FAAP, saw his pediatrician that way.
“He was a very humanistic provider and found joy in serving children and their families,” Dr. Beck says. “I saw how a pediatrician could influence others and make the world a better place and still have fun serving a vulnerable patient population.”
His career in pediatric hospital medicine, though?
“It was largely pure luck,” Dr. Beck admits. “When I was seeking my first job, I was offered a position that was 50/50 internal medicine and pediatrics but purely a hospitalist position.”
Dr. Beck has risen through academic hospitalist ranks the past 15 years and now serves as the division chief of pediatric hospital medicine at Penn State Children’s Hospital at Milton S. Hershey (Pa.) Medical Center. He is one of eight new members of Team Hospitalist, The Hospitalist’s volunteer editorial advisory board.
Question: What was medical school and residency like for you? Was there a single moment you knew “I can do this”?
Answer: I always have been filled with self-doubt, which is a perpetual motivator for me. I guess I believed I could do hospital-based work when I started knowing the majority of what was going on with patients after hearing residents discuss cases and I knew what the labs, studies, and exam findings were going to be before I saw the patient.
Q: What do you like most about working as a hospitalist?
A: The acuity and pathology of cases. I get to see cases that some people only read about. It is very intellectual challenging, and I get to work with and learn from specialists every day.
Q: What do you dislike most?
A: Some of the cases are devastating to families. It is always important to remind yourself—and the team—that some of the diagnoses we help make affect families and the patient in very profound ways.
Q: Did you have a mentor during your training or early career? If so, who was the mentor, and what were the most important lessons you learned from him/her?
A: Dr. Barbara Ostrov. I learned what it really means to be a servant-leader. I witnessed her work ethic and saw that a leader of others should lead by example and be willing to work twice what is expected of others. She is always nonjudgmental and professional, yet forthright, when dealing with contentious situations. She trumpets the work of others, not her own, and sees others’ successes as her success. In the end, I believed she worked for me, not the other way around.
Q: Have you tried to mentor others? Why or why not?
A: Yes. As a division chief, I want others to succeed. The best quote I have read was by Richard Branson [CEO of Virgin]: “Train people so that they can leave, but treat them so they want to stay.”
Q: What’s the biggest change you’ve seen in HM in your career?
A: It has moved from a clinical service to a robust area of research and strong researchers.
Q: What’s the biggest change you would like to see in HM?
A: If hospital medicine is positioning itself to be a specialty with fellowship training, with access to knowledge different from PCPs, then I believe we should function like other specialty services with a different skill set. We should own our discharge process and follow-up plans. We should follow up with patients in a discharge clinic setting to review clinical course, health literacy issues, labs, and studies and even order follow-up studies based on incoming results.
Q: For group leaders, why is it important for you to continue seeing patients?
A: As a clinician leader, my charge is to foster teamwork and create a shared vision for improvement and change. This is not possible to do from an office space or conference room separate from where the work gets done.
Q: As a hospitalist, seeing most of your patients for the very first time, what aspect of patient care is most challenging?
A: Establishing trust and rapport in five to 10 minutes. Caring for a hospitalized patient, when they are surrounded by loved ones, is stressful and anxiety-provoking. Delivering information in a way that is honest and empathetic and timely without the benefit of having a personal historic connection with a patient is always challenging.
Q: What aspect of patient care is most rewarding?
A: Making a diagnosis in a patient that has eluded diagnosis for weeks or months.
Q: What aspect of teaching in the 21st century is most difficult? And what is most enjoyable?
A: Today’s learners have different expectations from mine [in terms] of what they want to get from a career in medicine. While I don’t always agree with them, it is the reality and puts me in a position to discuss and understand the rationale of a changing mindset. As a physician leader, it is important to understand this because it helps me create an environment that fosters successful recruitment and retention.
Q: You mention wanting to tackle the issue of physician burnout? Why is that something important to you?
A: I personally lived through it and felt the effects it had on the relationships I had with family, friends, medical students, residents, and patients. I know what it felt like to be angry, cynical, and distanced from those I cared about and from those whom I was charged with caring for. I never forgot how isolated [you] can feel in an academic center even when surrounded by hundreds. I vowed that if I ever found my way to a leadership position, I would begin by creating an environment that emphasized morale, honesty, integrity, and professionalism. If I succeeded in this, the other organizational missions of education, patient care, quality, and value would follow.
Since 2012, our division has monitored burnout, work-life balance, and, more recently, physician engagement. Although we take care of the sickest children in the region, our group supports each other, recognizing and respectful of the fact that we each have different comfort levels, skill sets, but we also have fun. Patients, nurses, social workers, care coordinators, and clerks see this. Like I teach the residents, you never get a second chance to make a first impression, but you also never get a second chance to make a last one, so make all interactions count. TH
Richard Quinn is a freelance writer in New Jersey.
Plant sugars influence malaria transmission
feeding on Barleria lupilina.
Photo from Domonbabele
F. d. S. Hien et al.
A study published in PLOS Pathogens suggests the plant-based part of Anopheles mosquitoes’ diet affects malaria transmission by influencing the interaction between the mosquitoes and Plasmodium parasites.
Recent studies have shown that Anopheles female mosquitoes, which can transmit the malaria parasite P falciparum, locate and display preferences for natural sources of plant sugar.
These studies also suggested that environmental sugars influence the lifespan and blood-feeding rate of mosquitoes and, therefore, their malaria transmission potential.
Whether the type of plant sugar could also affect the malaria host-pathogen interactions was unclear.
To find out, Thierry Lefevre, PhD, of the Institut de Recherche en Sciences de la Santé in Bobo Dioulasso, Burkina Faso, and his colleagues examined the impact of plant diversity on mosquito susceptibility to malaria parasites.
The team studied the natural interactions between the P falciparum parasite, the Anopheles coluzzii mosquito (a major vector of P falciparum in Africa), and several natural plant-derived sugar sources growing in the vicinity of human dwellings in Burkina Faso.
The latter included 2 ornamental flowering plants (Barleria lupilina and Thevetia neriifolia) as well as mangoes and the grape-like fruit from the Lannea microcarpa tree.
The researchers raised groups of Anopheles mosquitos in cages and provided each of them with a different plant sugar source or with a 5% glucose solution.
Sugar-fed mosquitoes were then starved for 24 hours before being offered a parasite-containing blood meal. The blood was drawn from healthy Plasmodium-infected local human volunteers and diluted to a consistent concentration of parasites.
Blood-fed female mosquitoes were housed in a biosafety room and continued to be fed their assigned plant sugar source.
Seven or 14 days after the blood-meal, roughly 30 mosquitoes from each group were examined under the microscope for traits that influence malaria transmission.
The researchers found that different sugar sources had different effects on all traits examined, including the infection and survival rates of the mosquitoes and the survival rate of the parasites 7 days after the blood meal.
The plant sugar source also influenced the proportion of mosquitoes harboring sporozoites and the timing of sporozoite release.
To predict the relative contribution of the different plants to overall malaria transmission, the researchers used the various experimental results in an epidemiological model.
This suggested that plant sugar source can be a significant driver of malaria transmission dynamics.
Compared to the baseline scenario with the 5% glucose solution, both L microcarpa and B lupilina increased malaria transmission by an estimated 30% and 40%, respectively, mainly because of increased infection rates among mosquitoes exposed to parasites through their blood-meal.
In contrast, T neriifolia, with its negative effect on infection rate and decreased longevity, was predicted to decrease malaria transmission by 30% compared with sugar water.
The researchers said these findings suggest that planting anti-Plasmodium plant sugar sources could be a promising alternative strategy for controlling malaria. 
feeding on Barleria lupilina.
Photo from Domonbabele
F. d. S. Hien et al.
A study published in PLOS Pathogens suggests the plant-based part of Anopheles mosquitoes’ diet affects malaria transmission by influencing the interaction between the mosquitoes and Plasmodium parasites.
Recent studies have shown that Anopheles female mosquitoes, which can transmit the malaria parasite P falciparum, locate and display preferences for natural sources of plant sugar.
These studies also suggested that environmental sugars influence the lifespan and blood-feeding rate of mosquitoes and, therefore, their malaria transmission potential.
Whether the type of plant sugar could also affect the malaria host-pathogen interactions was unclear.
To find out, Thierry Lefevre, PhD, of the Institut de Recherche en Sciences de la Santé in Bobo Dioulasso, Burkina Faso, and his colleagues examined the impact of plant diversity on mosquito susceptibility to malaria parasites.
The team studied the natural interactions between the P falciparum parasite, the Anopheles coluzzii mosquito (a major vector of P falciparum in Africa), and several natural plant-derived sugar sources growing in the vicinity of human dwellings in Burkina Faso.
The latter included 2 ornamental flowering plants (Barleria lupilina and Thevetia neriifolia) as well as mangoes and the grape-like fruit from the Lannea microcarpa tree.
The researchers raised groups of Anopheles mosquitos in cages and provided each of them with a different plant sugar source or with a 5% glucose solution.
Sugar-fed mosquitoes were then starved for 24 hours before being offered a parasite-containing blood meal. The blood was drawn from healthy Plasmodium-infected local human volunteers and diluted to a consistent concentration of parasites.
Blood-fed female mosquitoes were housed in a biosafety room and continued to be fed their assigned plant sugar source.
Seven or 14 days after the blood-meal, roughly 30 mosquitoes from each group were examined under the microscope for traits that influence malaria transmission.
The researchers found that different sugar sources had different effects on all traits examined, including the infection and survival rates of the mosquitoes and the survival rate of the parasites 7 days after the blood meal.
The plant sugar source also influenced the proportion of mosquitoes harboring sporozoites and the timing of sporozoite release.
To predict the relative contribution of the different plants to overall malaria transmission, the researchers used the various experimental results in an epidemiological model.
This suggested that plant sugar source can be a significant driver of malaria transmission dynamics.
Compared to the baseline scenario with the 5% glucose solution, both L microcarpa and B lupilina increased malaria transmission by an estimated 30% and 40%, respectively, mainly because of increased infection rates among mosquitoes exposed to parasites through their blood-meal.
In contrast, T neriifolia, with its negative effect on infection rate and decreased longevity, was predicted to decrease malaria transmission by 30% compared with sugar water.
The researchers said these findings suggest that planting anti-Plasmodium plant sugar sources could be a promising alternative strategy for controlling malaria.
feeding on Barleria lupilina.
Photo from Domonbabele
F. d. S. Hien et al.
A study published in PLOS Pathogens suggests the plant-based part of Anopheles mosquitoes’ diet affects malaria transmission by influencing the interaction between the mosquitoes and Plasmodium parasites.
Recent studies have shown that Anopheles female mosquitoes, which can transmit the malaria parasite P falciparum, locate and display preferences for natural sources of plant sugar.
These studies also suggested that environmental sugars influence the lifespan and blood-feeding rate of mosquitoes and, therefore, their malaria transmission potential.
Whether the type of plant sugar could also affect the malaria host-pathogen interactions was unclear.
To find out, Thierry Lefevre, PhD, of the Institut de Recherche en Sciences de la Santé in Bobo Dioulasso, Burkina Faso, and his colleagues examined the impact of plant diversity on mosquito susceptibility to malaria parasites.
The team studied the natural interactions between the P falciparum parasite, the Anopheles coluzzii mosquito (a major vector of P falciparum in Africa), and several natural plant-derived sugar sources growing in the vicinity of human dwellings in Burkina Faso.
The latter included 2 ornamental flowering plants (Barleria lupilina and Thevetia neriifolia) as well as mangoes and the grape-like fruit from the Lannea microcarpa tree.
The researchers raised groups of Anopheles mosquitos in cages and provided each of them with a different plant sugar source or with a 5% glucose solution.
Sugar-fed mosquitoes were then starved for 24 hours before being offered a parasite-containing blood meal. The blood was drawn from healthy Plasmodium-infected local human volunteers and diluted to a consistent concentration of parasites.
Blood-fed female mosquitoes were housed in a biosafety room and continued to be fed their assigned plant sugar source.
Seven or 14 days after the blood-meal, roughly 30 mosquitoes from each group were examined under the microscope for traits that influence malaria transmission.
The researchers found that different sugar sources had different effects on all traits examined, including the infection and survival rates of the mosquitoes and the survival rate of the parasites 7 days after the blood meal.
The plant sugar source also influenced the proportion of mosquitoes harboring sporozoites and the timing of sporozoite release.
To predict the relative contribution of the different plants to overall malaria transmission, the researchers used the various experimental results in an epidemiological model.
This suggested that plant sugar source can be a significant driver of malaria transmission dynamics.
Compared to the baseline scenario with the 5% glucose solution, both L microcarpa and B lupilina increased malaria transmission by an estimated 30% and 40%, respectively, mainly because of increased infection rates among mosquitoes exposed to parasites through their blood-meal.
In contrast, T neriifolia, with its negative effect on infection rate and decreased longevity, was predicted to decrease malaria transmission by 30% compared with sugar water.
The researchers said these findings suggest that planting anti-Plasmodium plant sugar sources could be a promising alternative strategy for controlling malaria.
Drug interferes with testing for blood transfusion
Photo by Daniel Gay
Research has shown that daratumumab, a monoclonal antibody approved to treat multiple myeloma, interferes with routine compatibility testing for blood transfusion.
And this interference can cause delays in providing patients with compatible blood.
Investigators have discovered ways to eliminate or circumvent the interference, but implementing these methods in hospital blood banks may be challenging.
Michael F. Murphy, MD, of John Radcliffe Hospital in Oxford, UK, and his colleagues discussed this issue in a letter to NEJM.
In a phase 1/2 trial of daratumumab, investigators at different study sites observed that the drug consistently interfered with routine blood compatibility testing. This meant that daratumumab-treated patients sometimes experienced delays in receiving blood transfusions.
Investigation revealed that daratumumab in patient plasma directly binds to CD38 on reagent red blood cells used in the blood bank, which causes false-positive antibody screens.
Unfortunately, standard serological methods to eliminate panreactive antibodies did not affect daratumumab’s interference.
However, an investigator-initiated study revealed a dithiothreitol-based method that can eliminate the interference.1
Another method, involving an anti-daratumumab idiotype, also appears effective, though not readily available.2 And a third method is to issue phenotypically or genotypically matched red cell units.3,4
However, establishing these approaches as routine methods in hospital blood banks will be a major challenge, according to Dr Murphy and his colleagues.
The team also said this issue with daratumumab suggests there is a pressing need to investigate whether new drugs interfere with routine blood bank testing.
Investigations should be performed early during drug development. And if interference with compatibility tests is found, it should be brought to the attention of clinicians and blood banks with advice about how to overcome the interference.
Photo by Daniel Gay
Research has shown that daratumumab, a monoclonal antibody approved to treat multiple myeloma, interferes with routine compatibility testing for blood transfusion.
And this interference can cause delays in providing patients with compatible blood.
Investigators have discovered ways to eliminate or circumvent the interference, but implementing these methods in hospital blood banks may be challenging.
Michael F. Murphy, MD, of John Radcliffe Hospital in Oxford, UK, and his colleagues discussed this issue in a letter to NEJM.
In a phase 1/2 trial of daratumumab, investigators at different study sites observed that the drug consistently interfered with routine blood compatibility testing. This meant that daratumumab-treated patients sometimes experienced delays in receiving blood transfusions.
Investigation revealed that daratumumab in patient plasma directly binds to CD38 on reagent red blood cells used in the blood bank, which causes false-positive antibody screens.
Unfortunately, standard serological methods to eliminate panreactive antibodies did not affect daratumumab’s interference.
However, an investigator-initiated study revealed a dithiothreitol-based method that can eliminate the interference.1
Another method, involving an anti-daratumumab idiotype, also appears effective, though not readily available.2 And a third method is to issue phenotypically or genotypically matched red cell units.3,4
However, establishing these approaches as routine methods in hospital blood banks will be a major challenge, according to Dr Murphy and his colleagues.
The team also said this issue with daratumumab suggests there is a pressing need to investigate whether new drugs interfere with routine blood bank testing.
Investigations should be performed early during drug development. And if interference with compatibility tests is found, it should be brought to the attention of clinicians and blood banks with advice about how to overcome the interference.
Photo by Daniel Gay
Research has shown that daratumumab, a monoclonal antibody approved to treat multiple myeloma, interferes with routine compatibility testing for blood transfusion.
And this interference can cause delays in providing patients with compatible blood.
Investigators have discovered ways to eliminate or circumvent the interference, but implementing these methods in hospital blood banks may be challenging.
Michael F. Murphy, MD, of John Radcliffe Hospital in Oxford, UK, and his colleagues discussed this issue in a letter to NEJM.
In a phase 1/2 trial of daratumumab, investigators at different study sites observed that the drug consistently interfered with routine blood compatibility testing. This meant that daratumumab-treated patients sometimes experienced delays in receiving blood transfusions.
Investigation revealed that daratumumab in patient plasma directly binds to CD38 on reagent red blood cells used in the blood bank, which causes false-positive antibody screens.
Unfortunately, standard serological methods to eliminate panreactive antibodies did not affect daratumumab’s interference.
However, an investigator-initiated study revealed a dithiothreitol-based method that can eliminate the interference.1
Another method, involving an anti-daratumumab idiotype, also appears effective, though not readily available.2 And a third method is to issue phenotypically or genotypically matched red cell units.3,4
However, establishing these approaches as routine methods in hospital blood banks will be a major challenge, according to Dr Murphy and his colleagues.
The team also said this issue with daratumumab suggests there is a pressing need to investigate whether new drugs interfere with routine blood bank testing.
Investigations should be performed early during drug development. And if interference with compatibility tests is found, it should be brought to the attention of clinicians and blood banks with advice about how to overcome the interference.
Team creates database of autophagy-related proteins
Image by Sarah Pfau
Scientists have identified previously undiscovered proteins related to autophagy and created a database containing them.
The team believes this database will enable the scientific community to find ways to activate autophagy inside human cells.
And it could aid the development of drugs to treat age-related conditions such as cancer.
The team described the creation of the database in the journal Autophagy.
The database is available here: https://ilir.warwick.ac.uk/.
“Our novel database resource will open a lot of new avenues in basic and translational science,” said Ioannis Nezis, PhD, of the University of Warwick in Coventry, UK.
“Identifying novel selective autophagy-related proteins will help for the development of novel pharmaceutical drug targets for a large variety of diseases like cancer, neurodegeneration, and other aging-related diseases, infections, diabetes, obesity, and Crohn’s disease.”
“Importantly, understanding the molecular mechanisms of selective autophagy will help researchers to find interventions to activate the autophagic pathway to prevent aging and promote healthy well-being during the life course.”
Image by Sarah Pfau
Scientists have identified previously undiscovered proteins related to autophagy and created a database containing them.
The team believes this database will enable the scientific community to find ways to activate autophagy inside human cells.
And it could aid the development of drugs to treat age-related conditions such as cancer.
The team described the creation of the database in the journal Autophagy.
The database is available here: https://ilir.warwick.ac.uk/.
“Our novel database resource will open a lot of new avenues in basic and translational science,” said Ioannis Nezis, PhD, of the University of Warwick in Coventry, UK.
“Identifying novel selective autophagy-related proteins will help for the development of novel pharmaceutical drug targets for a large variety of diseases like cancer, neurodegeneration, and other aging-related diseases, infections, diabetes, obesity, and Crohn’s disease.”
“Importantly, understanding the molecular mechanisms of selective autophagy will help researchers to find interventions to activate the autophagic pathway to prevent aging and promote healthy well-being during the life course.”
Image by Sarah Pfau
Scientists have identified previously undiscovered proteins related to autophagy and created a database containing them.
The team believes this database will enable the scientific community to find ways to activate autophagy inside human cells.
And it could aid the development of drugs to treat age-related conditions such as cancer.
The team described the creation of the database in the journal Autophagy.
The database is available here: https://ilir.warwick.ac.uk/.
“Our novel database resource will open a lot of new avenues in basic and translational science,” said Ioannis Nezis, PhD, of the University of Warwick in Coventry, UK.
“Identifying novel selective autophagy-related proteins will help for the development of novel pharmaceutical drug targets for a large variety of diseases like cancer, neurodegeneration, and other aging-related diseases, infections, diabetes, obesity, and Crohn’s disease.”
“Importantly, understanding the molecular mechanisms of selective autophagy will help researchers to find interventions to activate the autophagic pathway to prevent aging and promote healthy well-being during the life course.”
Checklist Captures New Predementia Diagnosis of Mild Behavioral Impairment
TORONTO – Researchers have described a behavioral syndrome that they say can be a forerunner of Alzheimer’s disease and other neurodegenerative diseases and released a tool for diagnosing it.
Mild behavioral impairment (MBI) defines a syndrome of new-onset neuropsychiatric symptoms that appear in nondemented people older than 50, and are sustained for at least 6 months. Symptoms can occur in any of five domains: apathy/drive/motivation; mood/affect/anxiety; impulse control/agitation/reward; social appropriateness; and thoughts/perception.
Zahinoor Ismail, MD, described the concept of MBI for the first time at the Alzheimer’s Association International Conference 2016, and unveiled the MBI Checklist (MBI-C), a two-page screen that identifies and scores these symptoms. The MBI-C is a project of the Alzheimer’s Association International Society to Advance Alzheimer’s Research and Treatment (ISTAART), and is still being validated, although is available for clinical use now, said Dr. Ismail of the University of Calgary (Alta.).
Changes in personality are often the earliest signs of an emerging neurocognitive disorder, appearing well before any problems with memory or cognition. The MBI-C will allow clinicians to identify and track these changes in patients.
“We can now describe this preclinical dementia phenotype and use this tool to diagnose it and to capture change over time,” Dr. Ismail said.
In addition to being clinically useful, he said the checklist will wield great power in research: It could target a population at the greatest risk for neurocognitive decline, at a time where any future disease-modifying drugs could be most beneficial.
“We all know that dementia is much more than memory or cognitive impairment alone. The neuropsychiatric symptoms of dementia are associated with functional impairment, caregiver burden, institutionalization, accelerated rates of progression, and a greater burden of plaques and tangles. There is a great need to identify people early on, people in whom we might be able to change the course of illness. These patients, who present with early neuropsychiatric symptoms, may be a population we can examine to see if that is possible.”
A large body of research has already linked new-onset neuropsychiatric symptoms with neurocognitive disease, particularly frontotemporal dementia, Dr. Ismail said. One of the most compelling studies comprised about 500 subjects enrolled in the ongoing Mayo Clinic Study of Aging, who were followed for 5 years (Am J Psychiatry. 2014;171[5];572-81). This study found that the emergence of neuropsychiatric symptoms in cognitively normal older adults was associated with significant increases in the risk of developing mild cognitive impairment. Agitation conferred the highest risk (hazard ratio, 3.06), followed by apathy (HR, 2.6), anxiety (HR, 1.87), irritability (HR, 1.84), and depression (HR, 1.63).
Dr. Ismail said new-onset neuropsychiatric symptoms are already quite common by the time patients enter care for memory concerns. At the meeting, he presented data on a group of about 300 patients with mild cognitive impairment who attended a memory clinic. A total of 82% endorsed at least one neuropsychiatric symptom. When sorted into the five MBI-C domains, 78% of patients expressed mood symptoms; 64% impulse control symptoms; 52% apathy symptoms; 28% social appropriateness symptoms; and 9% psychotic symptoms.
“Our study suggests that this concept of mild behavioral impairment may be a common and clinically relevant syndrome, particularly given that neuropsychiatric symptoms are associated with greater caregiver burden,” Dr. Ismail said.
Dr. Ismail did not address how the screen should be scored or interpreted. It is composed of five overall domains, each asking about the emergence of a new, persistent symptom. Patients rate the presences and severity of those symptoms on a 3-point scale. The researchers who developed it chose age 50 as the cutoff point because symptoms that emerge at that age can herald the onset of frontotemporal dementia in relatively young patients.
“This idea of symptoms persisting for at least 6 months is important,” Dr. Ismail said. “What we’re talking about is a sustained change from baseline personality. But these are still nondemented patients. Function is maintained. Independent activities of daily living are intact.”
The most comprehensive domain is impulse control, agitation, and reward. “This captures a lot of function with regard to agitation in dementia, new-onset substance abuse, irritability, new-onset road rage … things we might not otherwise capture.”
The social appropriateness domain examines symptoms like a loss of the ability to share appropriately, acting out sexually, and loss of social judgment. The psychosis domain inquires about feelings of aggrandizement, persecution, and suspicion, as well as auditory and visual hallucinations.
The mood domain asks about new-onset anxiety, panic, and depression. The motivation domain asks about the development of apathy or disinterest in family, friends, and activities.
Validation studies in large cohorts are ongoing, as well as studies that Dr. Ismail hopes will link these early behavioral changes to well-established Alzheimer’s biomarkers.
The MBI-C website is not yet complete, but the checklist is available for free by emailing [email protected].
Dr. Ismail had no financial disclosures.
TORONTO – Researchers have described a behavioral syndrome that they say can be a forerunner of Alzheimer’s disease and other neurodegenerative diseases and released a tool for diagnosing it.
Mild behavioral impairment (MBI) defines a syndrome of new-onset neuropsychiatric symptoms that appear in nondemented people older than 50, and are sustained for at least 6 months. Symptoms can occur in any of five domains: apathy/drive/motivation; mood/affect/anxiety; impulse control/agitation/reward; social appropriateness; and thoughts/perception.
Zahinoor Ismail, MD, described the concept of MBI for the first time at the Alzheimer’s Association International Conference 2016, and unveiled the MBI Checklist (MBI-C), a two-page screen that identifies and scores these symptoms. The MBI-C is a project of the Alzheimer’s Association International Society to Advance Alzheimer’s Research and Treatment (ISTAART), and is still being validated, although is available for clinical use now, said Dr. Ismail of the University of Calgary (Alta.).
Changes in personality are often the earliest signs of an emerging neurocognitive disorder, appearing well before any problems with memory or cognition. The MBI-C will allow clinicians to identify and track these changes in patients.
“We can now describe this preclinical dementia phenotype and use this tool to diagnose it and to capture change over time,” Dr. Ismail said.
In addition to being clinically useful, he said the checklist will wield great power in research: It could target a population at the greatest risk for neurocognitive decline, at a time where any future disease-modifying drugs could be most beneficial.
“We all know that dementia is much more than memory or cognitive impairment alone. The neuropsychiatric symptoms of dementia are associated with functional impairment, caregiver burden, institutionalization, accelerated rates of progression, and a greater burden of plaques and tangles. There is a great need to identify people early on, people in whom we might be able to change the course of illness. These patients, who present with early neuropsychiatric symptoms, may be a population we can examine to see if that is possible.”
A large body of research has already linked new-onset neuropsychiatric symptoms with neurocognitive disease, particularly frontotemporal dementia, Dr. Ismail said. One of the most compelling studies comprised about 500 subjects enrolled in the ongoing Mayo Clinic Study of Aging, who were followed for 5 years (Am J Psychiatry. 2014;171[5];572-81). This study found that the emergence of neuropsychiatric symptoms in cognitively normal older adults was associated with significant increases in the risk of developing mild cognitive impairment. Agitation conferred the highest risk (hazard ratio, 3.06), followed by apathy (HR, 2.6), anxiety (HR, 1.87), irritability (HR, 1.84), and depression (HR, 1.63).
Dr. Ismail said new-onset neuropsychiatric symptoms are already quite common by the time patients enter care for memory concerns. At the meeting, he presented data on a group of about 300 patients with mild cognitive impairment who attended a memory clinic. A total of 82% endorsed at least one neuropsychiatric symptom. When sorted into the five MBI-C domains, 78% of patients expressed mood symptoms; 64% impulse control symptoms; 52% apathy symptoms; 28% social appropriateness symptoms; and 9% psychotic symptoms.
“Our study suggests that this concept of mild behavioral impairment may be a common and clinically relevant syndrome, particularly given that neuropsychiatric symptoms are associated with greater caregiver burden,” Dr. Ismail said.
Dr. Ismail did not address how the screen should be scored or interpreted. It is composed of five overall domains, each asking about the emergence of a new, persistent symptom. Patients rate the presences and severity of those symptoms on a 3-point scale. The researchers who developed it chose age 50 as the cutoff point because symptoms that emerge at that age can herald the onset of frontotemporal dementia in relatively young patients.
“This idea of symptoms persisting for at least 6 months is important,” Dr. Ismail said. “What we’re talking about is a sustained change from baseline personality. But these are still nondemented patients. Function is maintained. Independent activities of daily living are intact.”
The most comprehensive domain is impulse control, agitation, and reward. “This captures a lot of function with regard to agitation in dementia, new-onset substance abuse, irritability, new-onset road rage … things we might not otherwise capture.”
The social appropriateness domain examines symptoms like a loss of the ability to share appropriately, acting out sexually, and loss of social judgment. The psychosis domain inquires about feelings of aggrandizement, persecution, and suspicion, as well as auditory and visual hallucinations.
The mood domain asks about new-onset anxiety, panic, and depression. The motivation domain asks about the development of apathy or disinterest in family, friends, and activities.
Validation studies in large cohorts are ongoing, as well as studies that Dr. Ismail hopes will link these early behavioral changes to well-established Alzheimer’s biomarkers.
The MBI-C website is not yet complete, but the checklist is available for free by emailing [email protected].
Dr. Ismail had no financial disclosures.
TORONTO – Researchers have described a behavioral syndrome that they say can be a forerunner of Alzheimer’s disease and other neurodegenerative diseases and released a tool for diagnosing it.
Mild behavioral impairment (MBI) defines a syndrome of new-onset neuropsychiatric symptoms that appear in nondemented people older than 50, and are sustained for at least 6 months. Symptoms can occur in any of five domains: apathy/drive/motivation; mood/affect/anxiety; impulse control/agitation/reward; social appropriateness; and thoughts/perception.
Zahinoor Ismail, MD, described the concept of MBI for the first time at the Alzheimer’s Association International Conference 2016, and unveiled the MBI Checklist (MBI-C), a two-page screen that identifies and scores these symptoms. The MBI-C is a project of the Alzheimer’s Association International Society to Advance Alzheimer’s Research and Treatment (ISTAART), and is still being validated, although is available for clinical use now, said Dr. Ismail of the University of Calgary (Alta.).
Changes in personality are often the earliest signs of an emerging neurocognitive disorder, appearing well before any problems with memory or cognition. The MBI-C will allow clinicians to identify and track these changes in patients.
“We can now describe this preclinical dementia phenotype and use this tool to diagnose it and to capture change over time,” Dr. Ismail said.
In addition to being clinically useful, he said the checklist will wield great power in research: It could target a population at the greatest risk for neurocognitive decline, at a time where any future disease-modifying drugs could be most beneficial.
“We all know that dementia is much more than memory or cognitive impairment alone. The neuropsychiatric symptoms of dementia are associated with functional impairment, caregiver burden, institutionalization, accelerated rates of progression, and a greater burden of plaques and tangles. There is a great need to identify people early on, people in whom we might be able to change the course of illness. These patients, who present with early neuropsychiatric symptoms, may be a population we can examine to see if that is possible.”
A large body of research has already linked new-onset neuropsychiatric symptoms with neurocognitive disease, particularly frontotemporal dementia, Dr. Ismail said. One of the most compelling studies comprised about 500 subjects enrolled in the ongoing Mayo Clinic Study of Aging, who were followed for 5 years (Am J Psychiatry. 2014;171[5];572-81). This study found that the emergence of neuropsychiatric symptoms in cognitively normal older adults was associated with significant increases in the risk of developing mild cognitive impairment. Agitation conferred the highest risk (hazard ratio, 3.06), followed by apathy (HR, 2.6), anxiety (HR, 1.87), irritability (HR, 1.84), and depression (HR, 1.63).
Dr. Ismail said new-onset neuropsychiatric symptoms are already quite common by the time patients enter care for memory concerns. At the meeting, he presented data on a group of about 300 patients with mild cognitive impairment who attended a memory clinic. A total of 82% endorsed at least one neuropsychiatric symptom. When sorted into the five MBI-C domains, 78% of patients expressed mood symptoms; 64% impulse control symptoms; 52% apathy symptoms; 28% social appropriateness symptoms; and 9% psychotic symptoms.
“Our study suggests that this concept of mild behavioral impairment may be a common and clinically relevant syndrome, particularly given that neuropsychiatric symptoms are associated with greater caregiver burden,” Dr. Ismail said.
Dr. Ismail did not address how the screen should be scored or interpreted. It is composed of five overall domains, each asking about the emergence of a new, persistent symptom. Patients rate the presences and severity of those symptoms on a 3-point scale. The researchers who developed it chose age 50 as the cutoff point because symptoms that emerge at that age can herald the onset of frontotemporal dementia in relatively young patients.
“This idea of symptoms persisting for at least 6 months is important,” Dr. Ismail said. “What we’re talking about is a sustained change from baseline personality. But these are still nondemented patients. Function is maintained. Independent activities of daily living are intact.”
The most comprehensive domain is impulse control, agitation, and reward. “This captures a lot of function with regard to agitation in dementia, new-onset substance abuse, irritability, new-onset road rage … things we might not otherwise capture.”
The social appropriateness domain examines symptoms like a loss of the ability to share appropriately, acting out sexually, and loss of social judgment. The psychosis domain inquires about feelings of aggrandizement, persecution, and suspicion, as well as auditory and visual hallucinations.
The mood domain asks about new-onset anxiety, panic, and depression. The motivation domain asks about the development of apathy or disinterest in family, friends, and activities.
Validation studies in large cohorts are ongoing, as well as studies that Dr. Ismail hopes will link these early behavioral changes to well-established Alzheimer’s biomarkers.
The MBI-C website is not yet complete, but the checklist is available for free by emailing [email protected].
Dr. Ismail had no financial disclosures.
AT AAIC 2016
Checklist captures new predementia diagnosis of mild behavioral impairment
TORONTO – Researchers have described a behavioral syndrome that they say can be a forerunner of Alzheimer’s disease and other neurodegenerative diseases and released a tool for diagnosing it.
Mild behavioral impairment (MBI) defines a syndrome of new-onset neuropsychiatric symptoms that appear in nondemented people older than 50, and are sustained for at least 6 months. Symptoms can occur in any of five domains: apathy/drive/motivation; mood/affect/anxiety; impulse control/agitation/reward; social appropriateness; and thoughts/perception.
Zahinoor Ismail, MD, described the concept of MBI for the first time at the Alzheimer’s Association International Conference 2016, and unveiled the MBI Checklist (MBI-C), a two-page screen that identifies and scores these symptoms. The MBI-C is a project of the Alzheimer’s Association International Society to Advance Alzheimer’s Research and Treatment (ISTAART), and is still being validated, although is available for clinical use now, said Dr. Ismail of the University of Calgary (Alta.).
Changes in personality are often the earliest signs of an emerging neurocognitive disorder, appearing well before any problems with memory or cognition. The MBI-C will allow clinicians to identify and track these changes in patients.
“We can now describe this preclinical dementia phenotype and use this tool to diagnose it and to capture change over time,” Dr. Ismail said.
In addition to being clinically useful, he said the checklist will wield great power in research: It could target a population at the greatest risk for neurocognitive decline, at a time where any future disease-modifying drugs could be most beneficial.
“We all know that dementia is much more than memory or cognitive impairment alone. The neuropsychiatric symptoms of dementia are associated with functional impairment, caregiver burden, institutionalization, accelerated rates of progression, and a greater burden of plaques and tangles. There is a great need to identify people early on, people in whom we might be able to change the course of illness. These patients, who present with early neuropsychiatric symptoms, may be a population we can examine to see if that is possible.”
A large body of research has already linked new-onset neuropsychiatric symptoms with neurocognitive disease, particularly frontotemporal dementia, Dr. Ismail said. One of the most compelling studies comprised about 500 subjects enrolled in the ongoing Mayo Clinic Study of Aging, who were followed for 5 years (Am J Psychiatry. 2014;171[5];572-81). This study found that the emergence of neuropsychiatric symptoms in cognitively normal older adults was associated with significant increases in the risk of developing mild cognitive impairment. Agitation conferred the highest risk (hazard ratio, 3.06), followed by apathy (HR, 2.6), anxiety (HR, 1.87), irritability (HR, 1.84), and depression (HR, 1.63).
Dr. Ismail said new-onset neuropsychiatric symptoms are already quite common by the time patients enter care for memory concerns. At the meeting, he presented data on a group of about 300 patients with mild cognitive impairment who attended a memory clinic. A total of 82% endorsed at least one neuropsychiatric symptom. When sorted into the five MBI-C domains, 78% of patients expressed mood symptoms; 64% impulse control symptoms; 52% apathy symptoms; 28% social appropriateness symptoms; and 9% psychotic symptoms.
“Our study suggests that this concept of mild behavioral impairment may be a common and clinically relevant syndrome, particularly given that neuropsychiatric symptoms are associated with greater caregiver burden,” Dr. Ismail said.
Dr. Ismail did not address how the screen should be scored or interpreted. It is composed of five overall domains, each asking about the emergence of a new, persistent symptom. Patients rate the presences and severity of those symptoms on a 3-point scale. The researchers who developed it chose age 50 as the cutoff point because symptoms that emerge at that age can herald the onset of frontotemporal dementia in relatively young patients.
“This idea of symptoms persisting for at least 6 months is important,” Dr. Ismail said. “What we’re talking about is a sustained change from baseline personality. But these are still nondemented patients. Function is maintained. Independent activities of daily living are intact.”
The most comprehensive domain is impulse control, agitation, and reward. “This captures a lot of function with regard to agitation in dementia, new-onset substance abuse, irritability, new-onset road rage … things we might not otherwise capture.”
The social appropriateness domain examines symptoms like a loss of the ability to share appropriately, acting out sexually, and loss of social judgment. The psychosis domain inquires about feelings of aggrandizement, persecution, and suspicion, as well as auditory and visual hallucinations.
The mood domain asks about new-onset anxiety, panic, and depression. The motivation domain asks about the development of apathy or disinterest in family, friends, and activities.
Validation studies in large cohorts are ongoing, as well as studies that Dr. Ismail hopes will link these early behavioral changes to well-established Alzheimer’s biomarkers.
The MBI-C website is not yet complete, but the checklist is available for free by emailing [email protected].
Dr. Ismail had no financial disclosures.
On Twitter @alz_gal
TORONTO – Researchers have described a behavioral syndrome that they say can be a forerunner of Alzheimer’s disease and other neurodegenerative diseases and released a tool for diagnosing it.
Mild behavioral impairment (MBI) defines a syndrome of new-onset neuropsychiatric symptoms that appear in nondemented people older than 50, and are sustained for at least 6 months. Symptoms can occur in any of five domains: apathy/drive/motivation; mood/affect/anxiety; impulse control/agitation/reward; social appropriateness; and thoughts/perception.
Zahinoor Ismail, MD, described the concept of MBI for the first time at the Alzheimer’s Association International Conference 2016, and unveiled the MBI Checklist (MBI-C), a two-page screen that identifies and scores these symptoms. The MBI-C is a project of the Alzheimer’s Association International Society to Advance Alzheimer’s Research and Treatment (ISTAART), and is still being validated, although is available for clinical use now, said Dr. Ismail of the University of Calgary (Alta.).
Changes in personality are often the earliest signs of an emerging neurocognitive disorder, appearing well before any problems with memory or cognition. The MBI-C will allow clinicians to identify and track these changes in patients.
“We can now describe this preclinical dementia phenotype and use this tool to diagnose it and to capture change over time,” Dr. Ismail said.
In addition to being clinically useful, he said the checklist will wield great power in research: It could target a population at the greatest risk for neurocognitive decline, at a time where any future disease-modifying drugs could be most beneficial.
“We all know that dementia is much more than memory or cognitive impairment alone. The neuropsychiatric symptoms of dementia are associated with functional impairment, caregiver burden, institutionalization, accelerated rates of progression, and a greater burden of plaques and tangles. There is a great need to identify people early on, people in whom we might be able to change the course of illness. These patients, who present with early neuropsychiatric symptoms, may be a population we can examine to see if that is possible.”
A large body of research has already linked new-onset neuropsychiatric symptoms with neurocognitive disease, particularly frontotemporal dementia, Dr. Ismail said. One of the most compelling studies comprised about 500 subjects enrolled in the ongoing Mayo Clinic Study of Aging, who were followed for 5 years (Am J Psychiatry. 2014;171[5];572-81). This study found that the emergence of neuropsychiatric symptoms in cognitively normal older adults was associated with significant increases in the risk of developing mild cognitive impairment. Agitation conferred the highest risk (hazard ratio, 3.06), followed by apathy (HR, 2.6), anxiety (HR, 1.87), irritability (HR, 1.84), and depression (HR, 1.63).
Dr. Ismail said new-onset neuropsychiatric symptoms are already quite common by the time patients enter care for memory concerns. At the meeting, he presented data on a group of about 300 patients with mild cognitive impairment who attended a memory clinic. A total of 82% endorsed at least one neuropsychiatric symptom. When sorted into the five MBI-C domains, 78% of patients expressed mood symptoms; 64% impulse control symptoms; 52% apathy symptoms; 28% social appropriateness symptoms; and 9% psychotic symptoms.
“Our study suggests that this concept of mild behavioral impairment may be a common and clinically relevant syndrome, particularly given that neuropsychiatric symptoms are associated with greater caregiver burden,” Dr. Ismail said.
Dr. Ismail did not address how the screen should be scored or interpreted. It is composed of five overall domains, each asking about the emergence of a new, persistent symptom. Patients rate the presences and severity of those symptoms on a 3-point scale. The researchers who developed it chose age 50 as the cutoff point because symptoms that emerge at that age can herald the onset of frontotemporal dementia in relatively young patients.
“This idea of symptoms persisting for at least 6 months is important,” Dr. Ismail said. “What we’re talking about is a sustained change from baseline personality. But these are still nondemented patients. Function is maintained. Independent activities of daily living are intact.”
The most comprehensive domain is impulse control, agitation, and reward. “This captures a lot of function with regard to agitation in dementia, new-onset substance abuse, irritability, new-onset road rage … things we might not otherwise capture.”
The social appropriateness domain examines symptoms like a loss of the ability to share appropriately, acting out sexually, and loss of social judgment. The psychosis domain inquires about feelings of aggrandizement, persecution, and suspicion, as well as auditory and visual hallucinations.
The mood domain asks about new-onset anxiety, panic, and depression. The motivation domain asks about the development of apathy or disinterest in family, friends, and activities.
Validation studies in large cohorts are ongoing, as well as studies that Dr. Ismail hopes will link these early behavioral changes to well-established Alzheimer’s biomarkers.
The MBI-C website is not yet complete, but the checklist is available for free by emailing [email protected].
Dr. Ismail had no financial disclosures.
On Twitter @alz_gal
TORONTO – Researchers have described a behavioral syndrome that they say can be a forerunner of Alzheimer’s disease and other neurodegenerative diseases and released a tool for diagnosing it.
Mild behavioral impairment (MBI) defines a syndrome of new-onset neuropsychiatric symptoms that appear in nondemented people older than 50, and are sustained for at least 6 months. Symptoms can occur in any of five domains: apathy/drive/motivation; mood/affect/anxiety; impulse control/agitation/reward; social appropriateness; and thoughts/perception.
Zahinoor Ismail, MD, described the concept of MBI for the first time at the Alzheimer’s Association International Conference 2016, and unveiled the MBI Checklist (MBI-C), a two-page screen that identifies and scores these symptoms. The MBI-C is a project of the Alzheimer’s Association International Society to Advance Alzheimer’s Research and Treatment (ISTAART), and is still being validated, although is available for clinical use now, said Dr. Ismail of the University of Calgary (Alta.).
Changes in personality are often the earliest signs of an emerging neurocognitive disorder, appearing well before any problems with memory or cognition. The MBI-C will allow clinicians to identify and track these changes in patients.
“We can now describe this preclinical dementia phenotype and use this tool to diagnose it and to capture change over time,” Dr. Ismail said.
In addition to being clinically useful, he said the checklist will wield great power in research: It could target a population at the greatest risk for neurocognitive decline, at a time where any future disease-modifying drugs could be most beneficial.
“We all know that dementia is much more than memory or cognitive impairment alone. The neuropsychiatric symptoms of dementia are associated with functional impairment, caregiver burden, institutionalization, accelerated rates of progression, and a greater burden of plaques and tangles. There is a great need to identify people early on, people in whom we might be able to change the course of illness. These patients, who present with early neuropsychiatric symptoms, may be a population we can examine to see if that is possible.”
A large body of research has already linked new-onset neuropsychiatric symptoms with neurocognitive disease, particularly frontotemporal dementia, Dr. Ismail said. One of the most compelling studies comprised about 500 subjects enrolled in the ongoing Mayo Clinic Study of Aging, who were followed for 5 years (Am J Psychiatry. 2014;171[5];572-81). This study found that the emergence of neuropsychiatric symptoms in cognitively normal older adults was associated with significant increases in the risk of developing mild cognitive impairment. Agitation conferred the highest risk (hazard ratio, 3.06), followed by apathy (HR, 2.6), anxiety (HR, 1.87), irritability (HR, 1.84), and depression (HR, 1.63).
Dr. Ismail said new-onset neuropsychiatric symptoms are already quite common by the time patients enter care for memory concerns. At the meeting, he presented data on a group of about 300 patients with mild cognitive impairment who attended a memory clinic. A total of 82% endorsed at least one neuropsychiatric symptom. When sorted into the five MBI-C domains, 78% of patients expressed mood symptoms; 64% impulse control symptoms; 52% apathy symptoms; 28% social appropriateness symptoms; and 9% psychotic symptoms.
“Our study suggests that this concept of mild behavioral impairment may be a common and clinically relevant syndrome, particularly given that neuropsychiatric symptoms are associated with greater caregiver burden,” Dr. Ismail said.
Dr. Ismail did not address how the screen should be scored or interpreted. It is composed of five overall domains, each asking about the emergence of a new, persistent symptom. Patients rate the presences and severity of those symptoms on a 3-point scale. The researchers who developed it chose age 50 as the cutoff point because symptoms that emerge at that age can herald the onset of frontotemporal dementia in relatively young patients.
“This idea of symptoms persisting for at least 6 months is important,” Dr. Ismail said. “What we’re talking about is a sustained change from baseline personality. But these are still nondemented patients. Function is maintained. Independent activities of daily living are intact.”
The most comprehensive domain is impulse control, agitation, and reward. “This captures a lot of function with regard to agitation in dementia, new-onset substance abuse, irritability, new-onset road rage … things we might not otherwise capture.”
The social appropriateness domain examines symptoms like a loss of the ability to share appropriately, acting out sexually, and loss of social judgment. The psychosis domain inquires about feelings of aggrandizement, persecution, and suspicion, as well as auditory and visual hallucinations.
The mood domain asks about new-onset anxiety, panic, and depression. The motivation domain asks about the development of apathy or disinterest in family, friends, and activities.
Validation studies in large cohorts are ongoing, as well as studies that Dr. Ismail hopes will link these early behavioral changes to well-established Alzheimer’s biomarkers.
The MBI-C website is not yet complete, but the checklist is available for free by emailing [email protected].
Dr. Ismail had no financial disclosures.
On Twitter @alz_gal
AT AAIC 2016
Common Allergic Dermatitis Culprits Are Hiding in Plain Sight
MINNEAPOLIS – When it comes to allergic contact dermatitis in children, the answer is sometimes hiding in plain sight. Cleansers, moisturizers, shampoos, detergents – all can contain ingredients that provoke significant reactions, yet many of these ingredients are not on the most common testing panels.
Erin Warshaw, MD, professor of dermatology at the University of Minnesota, reviewed common but often unsuspected causes of allergic dermatitis in the pediatric population at the annual meeting of the Society for Pediatric Dermatology.
Even some hypoallergenic and frequently recommended products can contain preservatives and other ingredients that provoke allergic reactions, according to Dr. Warshaw. A chief culprit is methylisothiazolinone (MI), a preservative that came into common use as formaldehyde has been gradually phased out.
“If there’s anything I could emphasize from this talk, it’s MI, MI, MI. This is the major epidemic of our time in the contact dermatitis world,” Dr. Warshaw said. Upcoming publications, she added, will place MI in the top five most common contact allergens. “MI is in everything, including things you would think would be hypoallergenic,” she said. She recommended looking at ingredient labels with a keen eye when making testing decisions.
Despite MI’s status as a frequent culprit, it’s not an allergen that appears on common test kits, Dr. Warshaw pointed out. For example, it’s absent from one of the most commonly used test kits, the Thin-Layer Rapid Use Epicutaneous Patch (T.R.U.E. test).
The T.R.U.E. test, said Dr. Warshaw, has reasonable sensitivity – it can detect 71% of relevant positive patch tests (RPPTs) in children. However, she added, a recent study showed that about 23% of children reacted to a supplemental allergen. “That’s significant. One quarter of these individuals only reacted to a preservative … or a sunscreen, or an acrylate. These aren’t on the T.R.U.E. test.”
Decyl glucoside is another frequent culprit that is not included in commercial patch test kits. “It’s really an important emerging allergen,” said Dr. Warshaw, noting that it commonly cross-reacts with coco and lauryl glucoside, frequently found in fragrance-free products. “It’s always humbling when we find the allergen in the product we’ve recommended to our patients.”
Other important allergens not on the T.R.U.E. test include propolis, tocopherol, oxybenzone, and many surfactants and botanicals.
In order to avoid a confounding reaction to aluminum, Dr. Warshaw recommends testing using plastic-backed test chambers, such as IQ chambers, rather than Finn chambers, which are aluminum backed.
When working with families to track down allergens in the pediatric population, Dr. Warshaw adjusts her approach from what she would use for adults.
“What do I do differently in kids? First of all, I set expectations for children and parents,” she said. Some of the most frequent parental questions deal with food allergies, so she allots time to explain the rationale for not testing for food allergens when allergic contact dermatitis is suspected.
For many patients, “I try and frame that there is probably baseline eczema, and our goal is to try to figure out if there is an allergy in addition to that that is contributing to the flares,” she said. She makes sure to convey that “all it takes is one exposure every 3 weeks; that will keep this reaction going.”
However, she’s judicious in interpreting equivocal results. “I feel a responsibility not to label children with an allergy” if results are unclear. Finally, providing enough time is key, said Dr. Warshaw, who allots an hour for reviewing final testing results.
The take-home points? It’s worthwhile to patch test children, since over half of children will have at least one RPPT. Also, contact dermatitis can be an overlay on preexisting allergic dermatitis, so patch testing can still be helpful for these children. Supplemental allergens are important in patch testing, “especially in children with a negative test to a screening series,” Dr. Warshaw said.
She recommended accessing the Contact Allergen Management Program (CAMP) database, found on the American Contact Dermatitis Society website. The list is a searchable database that generates a list of “safe” products that don’t contain a given allergen. This resource is available for society members, but a member’s access code can be shared among faculty members at academic institutions, she said. Patients can also be given unique codes that will give them access for life, so they can use the CAMP database on a computer or via a smartphone app.
Dr. Warshaw reported no relevant financial disclosures.
MINNEAPOLIS – When it comes to allergic contact dermatitis in children, the answer is sometimes hiding in plain sight. Cleansers, moisturizers, shampoos, detergents – all can contain ingredients that provoke significant reactions, yet many of these ingredients are not on the most common testing panels.
Erin Warshaw, MD, professor of dermatology at the University of Minnesota, reviewed common but often unsuspected causes of allergic dermatitis in the pediatric population at the annual meeting of the Society for Pediatric Dermatology.
Even some hypoallergenic and frequently recommended products can contain preservatives and other ingredients that provoke allergic reactions, according to Dr. Warshaw. A chief culprit is methylisothiazolinone (MI), a preservative that came into common use as formaldehyde has been gradually phased out.
“If there’s anything I could emphasize from this talk, it’s MI, MI, MI. This is the major epidemic of our time in the contact dermatitis world,” Dr. Warshaw said. Upcoming publications, she added, will place MI in the top five most common contact allergens. “MI is in everything, including things you would think would be hypoallergenic,” she said. She recommended looking at ingredient labels with a keen eye when making testing decisions.
Despite MI’s status as a frequent culprit, it’s not an allergen that appears on common test kits, Dr. Warshaw pointed out. For example, it’s absent from one of the most commonly used test kits, the Thin-Layer Rapid Use Epicutaneous Patch (T.R.U.E. test).
The T.R.U.E. test, said Dr. Warshaw, has reasonable sensitivity – it can detect 71% of relevant positive patch tests (RPPTs) in children. However, she added, a recent study showed that about 23% of children reacted to a supplemental allergen. “That’s significant. One quarter of these individuals only reacted to a preservative … or a sunscreen, or an acrylate. These aren’t on the T.R.U.E. test.”
Decyl glucoside is another frequent culprit that is not included in commercial patch test kits. “It’s really an important emerging allergen,” said Dr. Warshaw, noting that it commonly cross-reacts with coco and lauryl glucoside, frequently found in fragrance-free products. “It’s always humbling when we find the allergen in the product we’ve recommended to our patients.”
Other important allergens not on the T.R.U.E. test include propolis, tocopherol, oxybenzone, and many surfactants and botanicals.
In order to avoid a confounding reaction to aluminum, Dr. Warshaw recommends testing using plastic-backed test chambers, such as IQ chambers, rather than Finn chambers, which are aluminum backed.
When working with families to track down allergens in the pediatric population, Dr. Warshaw adjusts her approach from what she would use for adults.
“What do I do differently in kids? First of all, I set expectations for children and parents,” she said. Some of the most frequent parental questions deal with food allergies, so she allots time to explain the rationale for not testing for food allergens when allergic contact dermatitis is suspected.
For many patients, “I try and frame that there is probably baseline eczema, and our goal is to try to figure out if there is an allergy in addition to that that is contributing to the flares,” she said. She makes sure to convey that “all it takes is one exposure every 3 weeks; that will keep this reaction going.”
However, she’s judicious in interpreting equivocal results. “I feel a responsibility not to label children with an allergy” if results are unclear. Finally, providing enough time is key, said Dr. Warshaw, who allots an hour for reviewing final testing results.
The take-home points? It’s worthwhile to patch test children, since over half of children will have at least one RPPT. Also, contact dermatitis can be an overlay on preexisting allergic dermatitis, so patch testing can still be helpful for these children. Supplemental allergens are important in patch testing, “especially in children with a negative test to a screening series,” Dr. Warshaw said.
She recommended accessing the Contact Allergen Management Program (CAMP) database, found on the American Contact Dermatitis Society website. The list is a searchable database that generates a list of “safe” products that don’t contain a given allergen. This resource is available for society members, but a member’s access code can be shared among faculty members at academic institutions, she said. Patients can also be given unique codes that will give them access for life, so they can use the CAMP database on a computer or via a smartphone app.
Dr. Warshaw reported no relevant financial disclosures.
MINNEAPOLIS – When it comes to allergic contact dermatitis in children, the answer is sometimes hiding in plain sight. Cleansers, moisturizers, shampoos, detergents – all can contain ingredients that provoke significant reactions, yet many of these ingredients are not on the most common testing panels.
Erin Warshaw, MD, professor of dermatology at the University of Minnesota, reviewed common but often unsuspected causes of allergic dermatitis in the pediatric population at the annual meeting of the Society for Pediatric Dermatology.
Even some hypoallergenic and frequently recommended products can contain preservatives and other ingredients that provoke allergic reactions, according to Dr. Warshaw. A chief culprit is methylisothiazolinone (MI), a preservative that came into common use as formaldehyde has been gradually phased out.
“If there’s anything I could emphasize from this talk, it’s MI, MI, MI. This is the major epidemic of our time in the contact dermatitis world,” Dr. Warshaw said. Upcoming publications, she added, will place MI in the top five most common contact allergens. “MI is in everything, including things you would think would be hypoallergenic,” she said. She recommended looking at ingredient labels with a keen eye when making testing decisions.
Despite MI’s status as a frequent culprit, it’s not an allergen that appears on common test kits, Dr. Warshaw pointed out. For example, it’s absent from one of the most commonly used test kits, the Thin-Layer Rapid Use Epicutaneous Patch (T.R.U.E. test).
The T.R.U.E. test, said Dr. Warshaw, has reasonable sensitivity – it can detect 71% of relevant positive patch tests (RPPTs) in children. However, she added, a recent study showed that about 23% of children reacted to a supplemental allergen. “That’s significant. One quarter of these individuals only reacted to a preservative … or a sunscreen, or an acrylate. These aren’t on the T.R.U.E. test.”
Decyl glucoside is another frequent culprit that is not included in commercial patch test kits. “It’s really an important emerging allergen,” said Dr. Warshaw, noting that it commonly cross-reacts with coco and lauryl glucoside, frequently found in fragrance-free products. “It’s always humbling when we find the allergen in the product we’ve recommended to our patients.”
Other important allergens not on the T.R.U.E. test include propolis, tocopherol, oxybenzone, and many surfactants and botanicals.
In order to avoid a confounding reaction to aluminum, Dr. Warshaw recommends testing using plastic-backed test chambers, such as IQ chambers, rather than Finn chambers, which are aluminum backed.
When working with families to track down allergens in the pediatric population, Dr. Warshaw adjusts her approach from what she would use for adults.
“What do I do differently in kids? First of all, I set expectations for children and parents,” she said. Some of the most frequent parental questions deal with food allergies, so she allots time to explain the rationale for not testing for food allergens when allergic contact dermatitis is suspected.
For many patients, “I try and frame that there is probably baseline eczema, and our goal is to try to figure out if there is an allergy in addition to that that is contributing to the flares,” she said. She makes sure to convey that “all it takes is one exposure every 3 weeks; that will keep this reaction going.”
However, she’s judicious in interpreting equivocal results. “I feel a responsibility not to label children with an allergy” if results are unclear. Finally, providing enough time is key, said Dr. Warshaw, who allots an hour for reviewing final testing results.
The take-home points? It’s worthwhile to patch test children, since over half of children will have at least one RPPT. Also, contact dermatitis can be an overlay on preexisting allergic dermatitis, so patch testing can still be helpful for these children. Supplemental allergens are important in patch testing, “especially in children with a negative test to a screening series,” Dr. Warshaw said.
She recommended accessing the Contact Allergen Management Program (CAMP) database, found on the American Contact Dermatitis Society website. The list is a searchable database that generates a list of “safe” products that don’t contain a given allergen. This resource is available for society members, but a member’s access code can be shared among faculty members at academic institutions, she said. Patients can also be given unique codes that will give them access for life, so they can use the CAMP database on a computer or via a smartphone app.
Dr. Warshaw reported no relevant financial disclosures.
EXPERT ANALYSIS FROM THE SPD ANNUAL MEETING
Common allergic dermatitis culprits are hiding in plain sight
MINNEAPOLIS – When it comes to allergic contact dermatitis in children, the answer is sometimes hiding in plain sight. Cleansers, moisturizers, shampoos, detergents – all can contain ingredients that provoke significant reactions, yet many of these ingredients are not on the most common testing panels.
Erin Warshaw, MD, professor of dermatology at the University of Minnesota, reviewed common but often unsuspected causes of allergic dermatitis in the pediatric population at the annual meeting of the Society for Pediatric Dermatology.
Even some hypoallergenic and frequently recommended products can contain preservatives and other ingredients that provoke allergic reactions, according to Dr. Warshaw. A chief culprit is methylisothiazolinone (MI), a preservative that came into common use as formaldehyde has been gradually phased out.
“If there’s anything I could emphasize from this talk, it’s MI, MI, MI. This is the major epidemic of our time in the contact dermatitis world,” Dr. Warshaw said. Upcoming publications, she added, will place MI in the top five most common contact allergens. “MI is in everything, including things you would think would be hypoallergenic,” she said. She recommended looking at ingredient labels with a keen eye when making testing decisions.
Despite MI’s status as a frequent culprit, it’s not an allergen that appears on common test kits, Dr. Warshaw pointed out. For example, it’s absent from one of the most commonly used test kits, the Thin-Layer Rapid Use Epicutaneous Patch (T.R.U.E. test).
The T.R.U.E. test, said Dr. Warshaw, has reasonable sensitivity – it can detect 71% of relevant positive patch tests (RPPTs) in children. However, she added, a recent study showed that about 23% of children reacted to a supplemental allergen. “That’s significant. One quarter of these individuals only reacted to a preservative … or a sunscreen, or an acrylate. These aren’t on the T.R.U.E. test.”
Decyl glucoside is another frequent culprit that is not included in commercial patch test kits. “It’s really an important emerging allergen,” said Dr. Warshaw, noting that it commonly cross-reacts with coco and lauryl glucoside, frequently found in fragrance-free products. “It’s always humbling when we find the allergen in the product we’ve recommended to our patients.”
Other important allergens not on the T.R.U.E. test include propolis, tocopherol, oxybenzone, and many surfactants and botanicals.
In order to avoid a confounding reaction to aluminum, Dr. Warshaw recommends testing using plastic-backed test chambers, such as IQ chambers, rather than Finn chambers, which are aluminum backed.
When working with families to track down allergens in the pediatric population, Dr. Warshaw adjusts her approach from what she would use for adults.
“What do I do differently in kids? First of all, I set expectations for children and parents,” she said. Some of the most frequent parental questions deal with food allergies, so she allots time to explain the rationale for not testing for food allergens when allergic contact dermatitis is suspected.
For many patients, “I try and frame that there is probably baseline eczema, and our goal is to try to figure out if there is an allergy in addition to that that is contributing to the flares,” she said. She makes sure to convey that “all it takes is one exposure every 3 weeks; that will keep this reaction going.”
However, she’s judicious in interpreting equivocal results. “I feel a responsibility not to label children with an allergy” if results are unclear. Finally, providing enough time is key, said Dr. Warshaw, who allots an hour for reviewing final testing results.
The take-home points? It’s worthwhile to patch test children, since over half of children will have at least one RPPT. Also, contact dermatitis can be an overlay on preexisting allergic dermatitis, so patch testing can still be helpful for these children. Supplemental allergens are important in patch testing, “especially in children with a negative test to a screening series,” Dr. Warshaw said.
She recommended accessing the Contact Allergen Management Program (CAMP) database, found on the American Contact Dermatitis Society website. The list is a searchable database that generates a list of “safe” products that don’t contain a given allergen. This resource is available for society members, but a member’s access code can be shared among faculty members at academic institutions, she said. Patients can also be given unique codes that will give them access for life, so they can use the CAMP database on a computer or via a smartphone app.
Dr. Warshaw reported no relevant financial disclosures.
On Twitter @karioakes
MINNEAPOLIS – When it comes to allergic contact dermatitis in children, the answer is sometimes hiding in plain sight. Cleansers, moisturizers, shampoos, detergents – all can contain ingredients that provoke significant reactions, yet many of these ingredients are not on the most common testing panels.
Erin Warshaw, MD, professor of dermatology at the University of Minnesota, reviewed common but often unsuspected causes of allergic dermatitis in the pediatric population at the annual meeting of the Society for Pediatric Dermatology.
Even some hypoallergenic and frequently recommended products can contain preservatives and other ingredients that provoke allergic reactions, according to Dr. Warshaw. A chief culprit is methylisothiazolinone (MI), a preservative that came into common use as formaldehyde has been gradually phased out.
“If there’s anything I could emphasize from this talk, it’s MI, MI, MI. This is the major epidemic of our time in the contact dermatitis world,” Dr. Warshaw said. Upcoming publications, she added, will place MI in the top five most common contact allergens. “MI is in everything, including things you would think would be hypoallergenic,” she said. She recommended looking at ingredient labels with a keen eye when making testing decisions.
Despite MI’s status as a frequent culprit, it’s not an allergen that appears on common test kits, Dr. Warshaw pointed out. For example, it’s absent from one of the most commonly used test kits, the Thin-Layer Rapid Use Epicutaneous Patch (T.R.U.E. test).
The T.R.U.E. test, said Dr. Warshaw, has reasonable sensitivity – it can detect 71% of relevant positive patch tests (RPPTs) in children. However, she added, a recent study showed that about 23% of children reacted to a supplemental allergen. “That’s significant. One quarter of these individuals only reacted to a preservative … or a sunscreen, or an acrylate. These aren’t on the T.R.U.E. test.”
Decyl glucoside is another frequent culprit that is not included in commercial patch test kits. “It’s really an important emerging allergen,” said Dr. Warshaw, noting that it commonly cross-reacts with coco and lauryl glucoside, frequently found in fragrance-free products. “It’s always humbling when we find the allergen in the product we’ve recommended to our patients.”
Other important allergens not on the T.R.U.E. test include propolis, tocopherol, oxybenzone, and many surfactants and botanicals.
In order to avoid a confounding reaction to aluminum, Dr. Warshaw recommends testing using plastic-backed test chambers, such as IQ chambers, rather than Finn chambers, which are aluminum backed.
When working with families to track down allergens in the pediatric population, Dr. Warshaw adjusts her approach from what she would use for adults.
“What do I do differently in kids? First of all, I set expectations for children and parents,” she said. Some of the most frequent parental questions deal with food allergies, so she allots time to explain the rationale for not testing for food allergens when allergic contact dermatitis is suspected.
For many patients, “I try and frame that there is probably baseline eczema, and our goal is to try to figure out if there is an allergy in addition to that that is contributing to the flares,” she said. She makes sure to convey that “all it takes is one exposure every 3 weeks; that will keep this reaction going.”
However, she’s judicious in interpreting equivocal results. “I feel a responsibility not to label children with an allergy” if results are unclear. Finally, providing enough time is key, said Dr. Warshaw, who allots an hour for reviewing final testing results.
The take-home points? It’s worthwhile to patch test children, since over half of children will have at least one RPPT. Also, contact dermatitis can be an overlay on preexisting allergic dermatitis, so patch testing can still be helpful for these children. Supplemental allergens are important in patch testing, “especially in children with a negative test to a screening series,” Dr. Warshaw said.
She recommended accessing the Contact Allergen Management Program (CAMP) database, found on the American Contact Dermatitis Society website. The list is a searchable database that generates a list of “safe” products that don’t contain a given allergen. This resource is available for society members, but a member’s access code can be shared among faculty members at academic institutions, she said. Patients can also be given unique codes that will give them access for life, so they can use the CAMP database on a computer or via a smartphone app.
Dr. Warshaw reported no relevant financial disclosures.
On Twitter @karioakes
MINNEAPOLIS – When it comes to allergic contact dermatitis in children, the answer is sometimes hiding in plain sight. Cleansers, moisturizers, shampoos, detergents – all can contain ingredients that provoke significant reactions, yet many of these ingredients are not on the most common testing panels.
Erin Warshaw, MD, professor of dermatology at the University of Minnesota, reviewed common but often unsuspected causes of allergic dermatitis in the pediatric population at the annual meeting of the Society for Pediatric Dermatology.
Even some hypoallergenic and frequently recommended products can contain preservatives and other ingredients that provoke allergic reactions, according to Dr. Warshaw. A chief culprit is methylisothiazolinone (MI), a preservative that came into common use as formaldehyde has been gradually phased out.
“If there’s anything I could emphasize from this talk, it’s MI, MI, MI. This is the major epidemic of our time in the contact dermatitis world,” Dr. Warshaw said. Upcoming publications, she added, will place MI in the top five most common contact allergens. “MI is in everything, including things you would think would be hypoallergenic,” she said. She recommended looking at ingredient labels with a keen eye when making testing decisions.
Despite MI’s status as a frequent culprit, it’s not an allergen that appears on common test kits, Dr. Warshaw pointed out. For example, it’s absent from one of the most commonly used test kits, the Thin-Layer Rapid Use Epicutaneous Patch (T.R.U.E. test).
The T.R.U.E. test, said Dr. Warshaw, has reasonable sensitivity – it can detect 71% of relevant positive patch tests (RPPTs) in children. However, she added, a recent study showed that about 23% of children reacted to a supplemental allergen. “That’s significant. One quarter of these individuals only reacted to a preservative … or a sunscreen, or an acrylate. These aren’t on the T.R.U.E. test.”
Decyl glucoside is another frequent culprit that is not included in commercial patch test kits. “It’s really an important emerging allergen,” said Dr. Warshaw, noting that it commonly cross-reacts with coco and lauryl glucoside, frequently found in fragrance-free products. “It’s always humbling when we find the allergen in the product we’ve recommended to our patients.”
Other important allergens not on the T.R.U.E. test include propolis, tocopherol, oxybenzone, and many surfactants and botanicals.
In order to avoid a confounding reaction to aluminum, Dr. Warshaw recommends testing using plastic-backed test chambers, such as IQ chambers, rather than Finn chambers, which are aluminum backed.
When working with families to track down allergens in the pediatric population, Dr. Warshaw adjusts her approach from what she would use for adults.
“What do I do differently in kids? First of all, I set expectations for children and parents,” she said. Some of the most frequent parental questions deal with food allergies, so she allots time to explain the rationale for not testing for food allergens when allergic contact dermatitis is suspected.
For many patients, “I try and frame that there is probably baseline eczema, and our goal is to try to figure out if there is an allergy in addition to that that is contributing to the flares,” she said. She makes sure to convey that “all it takes is one exposure every 3 weeks; that will keep this reaction going.”
However, she’s judicious in interpreting equivocal results. “I feel a responsibility not to label children with an allergy” if results are unclear. Finally, providing enough time is key, said Dr. Warshaw, who allots an hour for reviewing final testing results.
The take-home points? It’s worthwhile to patch test children, since over half of children will have at least one RPPT. Also, contact dermatitis can be an overlay on preexisting allergic dermatitis, so patch testing can still be helpful for these children. Supplemental allergens are important in patch testing, “especially in children with a negative test to a screening series,” Dr. Warshaw said.
She recommended accessing the Contact Allergen Management Program (CAMP) database, found on the American Contact Dermatitis Society website. The list is a searchable database that generates a list of “safe” products that don’t contain a given allergen. This resource is available for society members, but a member’s access code can be shared among faculty members at academic institutions, she said. Patients can also be given unique codes that will give them access for life, so they can use the CAMP database on a computer or via a smartphone app.
Dr. Warshaw reported no relevant financial disclosures.
On Twitter @karioakes
EXPERT ANALYSIS FROM THE SPD ANNUAL MEETING
New EULAR gout guidelines garner praise, criticism
The European League Against Rheumatism’s updated recommendations on gout generally resemble those from the American College of Rheumatology, but with several important caveats, two prominent U.S. rheumatologists said in interviews.
First came the praise. “Both ACR and EULAR are sending a consistent message that gout needs more attention and improvement in the quality of care that’s being provided,” said John FitzGerald, MD, PhD, who coauthored the 2012 ACR guidelines and is a professor of medicine and rheumatology at the University of California, Los Angeles.
EULAR also strengthened its advice to start urate-lowering therapy (ULT) early (Ann Rheum Dis. 2016 Jul 25. doi: 10.1136/annrheumdis-2016-209707). This choice reflects “the opinion of many gout experts, that delaying treatment only allows for further accumulation of monosodium urate deposition around the body, which promotes inflammation and tissue destruction and makes it harder to achieve clinical and biologic remission,” said N. Lawrence Edwards, MD, who also helped write the ACR guidelines and is a vice chairman of the department of medicine at the University of Florida, Gainesville.
Finally, EULAR again emphasized treating to a target serum urate level of less than 6.0 mg/dL. “That is definitely consistent with the current recommendations from ACR, and with the way most rheumatologists think,” Dr. FitzGerald said. “The recommendations for future research are also very good and should be commended.”
But several other points depart from the ACR guidance and have prompted critiques.
Allopurinol
Perhaps most strikingly, EULAR now recommends adjusting maximum allopurinol dose based on creatinine clearance if patients have renal impairment. “This modification is very surprising, since [it has] never been shown to affect the incidence of severe allopurinol hypersensitivity reactions,” Dr. Edwards said. “Instead, these antiquated treatment schedules have only added to the epidemic of underdosing of allopurinol by both general practitioners and rheumatologists alike.”
Indeed, requiring clinicians to consider creatinine clearance when using allopurinol in many of their gout patients might push them toward other drugs and their accompanying side effects, “without first trying a slow, safe titration” of allopurinol, Dr. FitzGerald said.
Instead, both he and Dr. Edwards recommended following the gradual allopurinol dose escalation detailed in the 2012 ACR recommendations. “The biggest risk of adverse effects with allopurinol is during the initial treatment period, whereas there is little data about maximum dose,” Dr. FitzGerald emphasized. “I think the starting dose should be 50 mg every day, or even 50 mg every other day – the latter if patients have stage 4 chronic kidney disease.”
Serum urate
EULAR also advises against letting serum urate fall below 3.0 mg/dL “in the long term” – that is, over several years. This guidance stems from reports that hyperuricemia could help prevent neurodegenerative diseases, Dr. Edwards said. But studies have never clearly linked serum urate to neurologic processes, nor have they shown that low serum urate triggers or worsens disease, he added. “The harm of this EULAR recommendation comes from the chilling effect it might have on getting internists and general practitioners to more fully engage in urate lowering in subjects with gout. They could view a therapeutic serum urate window of 3.0 mg/dL to 6.0 mg/dL as too narrow and requiring too much oversight – leading once again to undertreatment.”
Comorbidities
ACR already had recommended ULT for gout patients with chronic kidney disease or urate renoliths, but EULAR expanded this list to include not only renal impairment, but also hypertension, ischemic heart disease, and heart failure, Dr. FitzGerald pointed out. “The recommendation for hypertension was based on a systematic literature review, but hypertension is so prevalent that this additional recommendation really expands the number of patients that would be treated with ULT,” he added. “If it is a patient’s first attack of gout, I think a lot of primary care providers would be uncomfortable starting patients on ULT.”
EULAR and ACR have always diverged in their recommendations about who should receive ULT, and widening these criteria further without direct supporting evidence from a clinical trial will provoke concerns, according to Dr. FitzGerald. “The EULAR authors lay out the logic for it, but without direct evidence it will be controversial, and the risk-benefit ratio of treating this expanded list of patients is unclear.”
Febuxostat
Dr. FitzGerald also recommended starting the xanthine oxidase inhibitor febuxostat (Uloric) at 40 mg, rather than 80 mg as recommended by EULAR. “This is based on a similar logic, that starting lower and titrating up has less risks than starting at a higher dose.”
Dr. Pascal Richette, first author of the updated EULAR recommendations, disclosed fees from Ipsen Pharma/Menarini, AstraZeneca, and Savient. Dr. FitzGerald and Dr. Edwards were coauthors of the 2012 ACR guidelines on gout, part 1 and part 2.
The European League Against Rheumatism’s updated recommendations on gout generally resemble those from the American College of Rheumatology, but with several important caveats, two prominent U.S. rheumatologists said in interviews.
First came the praise. “Both ACR and EULAR are sending a consistent message that gout needs more attention and improvement in the quality of care that’s being provided,” said John FitzGerald, MD, PhD, who coauthored the 2012 ACR guidelines and is a professor of medicine and rheumatology at the University of California, Los Angeles.
EULAR also strengthened its advice to start urate-lowering therapy (ULT) early (Ann Rheum Dis. 2016 Jul 25. doi: 10.1136/annrheumdis-2016-209707). This choice reflects “the opinion of many gout experts, that delaying treatment only allows for further accumulation of monosodium urate deposition around the body, which promotes inflammation and tissue destruction and makes it harder to achieve clinical and biologic remission,” said N. Lawrence Edwards, MD, who also helped write the ACR guidelines and is a vice chairman of the department of medicine at the University of Florida, Gainesville.
Finally, EULAR again emphasized treating to a target serum urate level of less than 6.0 mg/dL. “That is definitely consistent with the current recommendations from ACR, and with the way most rheumatologists think,” Dr. FitzGerald said. “The recommendations for future research are also very good and should be commended.”
But several other points depart from the ACR guidance and have prompted critiques.
Allopurinol
Perhaps most strikingly, EULAR now recommends adjusting maximum allopurinol dose based on creatinine clearance if patients have renal impairment. “This modification is very surprising, since [it has] never been shown to affect the incidence of severe allopurinol hypersensitivity reactions,” Dr. Edwards said. “Instead, these antiquated treatment schedules have only added to the epidemic of underdosing of allopurinol by both general practitioners and rheumatologists alike.”
Indeed, requiring clinicians to consider creatinine clearance when using allopurinol in many of their gout patients might push them toward other drugs and their accompanying side effects, “without first trying a slow, safe titration” of allopurinol, Dr. FitzGerald said.
Instead, both he and Dr. Edwards recommended following the gradual allopurinol dose escalation detailed in the 2012 ACR recommendations. “The biggest risk of adverse effects with allopurinol is during the initial treatment period, whereas there is little data about maximum dose,” Dr. FitzGerald emphasized. “I think the starting dose should be 50 mg every day, or even 50 mg every other day – the latter if patients have stage 4 chronic kidney disease.”
Serum urate
EULAR also advises against letting serum urate fall below 3.0 mg/dL “in the long term” – that is, over several years. This guidance stems from reports that hyperuricemia could help prevent neurodegenerative diseases, Dr. Edwards said. But studies have never clearly linked serum urate to neurologic processes, nor have they shown that low serum urate triggers or worsens disease, he added. “The harm of this EULAR recommendation comes from the chilling effect it might have on getting internists and general practitioners to more fully engage in urate lowering in subjects with gout. They could view a therapeutic serum urate window of 3.0 mg/dL to 6.0 mg/dL as too narrow and requiring too much oversight – leading once again to undertreatment.”
Comorbidities
ACR already had recommended ULT for gout patients with chronic kidney disease or urate renoliths, but EULAR expanded this list to include not only renal impairment, but also hypertension, ischemic heart disease, and heart failure, Dr. FitzGerald pointed out. “The recommendation for hypertension was based on a systematic literature review, but hypertension is so prevalent that this additional recommendation really expands the number of patients that would be treated with ULT,” he added. “If it is a patient’s first attack of gout, I think a lot of primary care providers would be uncomfortable starting patients on ULT.”
EULAR and ACR have always diverged in their recommendations about who should receive ULT, and widening these criteria further without direct supporting evidence from a clinical trial will provoke concerns, according to Dr. FitzGerald. “The EULAR authors lay out the logic for it, but without direct evidence it will be controversial, and the risk-benefit ratio of treating this expanded list of patients is unclear.”
Febuxostat
Dr. FitzGerald also recommended starting the xanthine oxidase inhibitor febuxostat (Uloric) at 40 mg, rather than 80 mg as recommended by EULAR. “This is based on a similar logic, that starting lower and titrating up has less risks than starting at a higher dose.”
Dr. Pascal Richette, first author of the updated EULAR recommendations, disclosed fees from Ipsen Pharma/Menarini, AstraZeneca, and Savient. Dr. FitzGerald and Dr. Edwards were coauthors of the 2012 ACR guidelines on gout, part 1 and part 2.
The European League Against Rheumatism’s updated recommendations on gout generally resemble those from the American College of Rheumatology, but with several important caveats, two prominent U.S. rheumatologists said in interviews.
First came the praise. “Both ACR and EULAR are sending a consistent message that gout needs more attention and improvement in the quality of care that’s being provided,” said John FitzGerald, MD, PhD, who coauthored the 2012 ACR guidelines and is a professor of medicine and rheumatology at the University of California, Los Angeles.
EULAR also strengthened its advice to start urate-lowering therapy (ULT) early (Ann Rheum Dis. 2016 Jul 25. doi: 10.1136/annrheumdis-2016-209707). This choice reflects “the opinion of many gout experts, that delaying treatment only allows for further accumulation of monosodium urate deposition around the body, which promotes inflammation and tissue destruction and makes it harder to achieve clinical and biologic remission,” said N. Lawrence Edwards, MD, who also helped write the ACR guidelines and is a vice chairman of the department of medicine at the University of Florida, Gainesville.
Finally, EULAR again emphasized treating to a target serum urate level of less than 6.0 mg/dL. “That is definitely consistent with the current recommendations from ACR, and with the way most rheumatologists think,” Dr. FitzGerald said. “The recommendations for future research are also very good and should be commended.”
But several other points depart from the ACR guidance and have prompted critiques.
Allopurinol
Perhaps most strikingly, EULAR now recommends adjusting maximum allopurinol dose based on creatinine clearance if patients have renal impairment. “This modification is very surprising, since [it has] never been shown to affect the incidence of severe allopurinol hypersensitivity reactions,” Dr. Edwards said. “Instead, these antiquated treatment schedules have only added to the epidemic of underdosing of allopurinol by both general practitioners and rheumatologists alike.”
Indeed, requiring clinicians to consider creatinine clearance when using allopurinol in many of their gout patients might push them toward other drugs and their accompanying side effects, “without first trying a slow, safe titration” of allopurinol, Dr. FitzGerald said.
Instead, both he and Dr. Edwards recommended following the gradual allopurinol dose escalation detailed in the 2012 ACR recommendations. “The biggest risk of adverse effects with allopurinol is during the initial treatment period, whereas there is little data about maximum dose,” Dr. FitzGerald emphasized. “I think the starting dose should be 50 mg every day, or even 50 mg every other day – the latter if patients have stage 4 chronic kidney disease.”
Serum urate
EULAR also advises against letting serum urate fall below 3.0 mg/dL “in the long term” – that is, over several years. This guidance stems from reports that hyperuricemia could help prevent neurodegenerative diseases, Dr. Edwards said. But studies have never clearly linked serum urate to neurologic processes, nor have they shown that low serum urate triggers or worsens disease, he added. “The harm of this EULAR recommendation comes from the chilling effect it might have on getting internists and general practitioners to more fully engage in urate lowering in subjects with gout. They could view a therapeutic serum urate window of 3.0 mg/dL to 6.0 mg/dL as too narrow and requiring too much oversight – leading once again to undertreatment.”
Comorbidities
ACR already had recommended ULT for gout patients with chronic kidney disease or urate renoliths, but EULAR expanded this list to include not only renal impairment, but also hypertension, ischemic heart disease, and heart failure, Dr. FitzGerald pointed out. “The recommendation for hypertension was based on a systematic literature review, but hypertension is so prevalent that this additional recommendation really expands the number of patients that would be treated with ULT,” he added. “If it is a patient’s first attack of gout, I think a lot of primary care providers would be uncomfortable starting patients on ULT.”
EULAR and ACR have always diverged in their recommendations about who should receive ULT, and widening these criteria further without direct supporting evidence from a clinical trial will provoke concerns, according to Dr. FitzGerald. “The EULAR authors lay out the logic for it, but without direct evidence it will be controversial, and the risk-benefit ratio of treating this expanded list of patients is unclear.”
Febuxostat
Dr. FitzGerald also recommended starting the xanthine oxidase inhibitor febuxostat (Uloric) at 40 mg, rather than 80 mg as recommended by EULAR. “This is based on a similar logic, that starting lower and titrating up has less risks than starting at a higher dose.”
Dr. Pascal Richette, first author of the updated EULAR recommendations, disclosed fees from Ipsen Pharma/Menarini, AstraZeneca, and Savient. Dr. FitzGerald and Dr. Edwards were coauthors of the 2012 ACR guidelines on gout, part 1 and part 2.
FROM ANNALS OF THE RHEUMATIC DISEASES
PHM16: Pediatric Hospital Medicine Leaders Kick Off 2016 Conference
Speaker: Lisa Zaoutis, MD, Pediatric Residency Program Director at the Children’s Hospital of Philadelphia.
Amid the skyscrapers of the Windy City, Pediatric Hospital Medicine (PHM) 2016 swept into town, bringing with it the denizens of pediatric hospitalist programs across the country. Some 1,150 attendees, comprised of hospitalists, PHM program leaders, and advanced care practitioners, gathered to educate and inspire one another in the the care of hospitalized children.
Dr. Lisa Zaoutis, director of the pediatric residency program at Children’s Hospital of Philadelphia, kicked off the conference with the opening plenary. Initially titled “North Star and Space,” she quickly changed the title to, “Changing Our Minds.” Touching on the disconnect between positive experiences that bring physicians into PHM and negative experiences that often drive behavior, she started with the beginning, the evolution of our brains.
“We are wired toward the negative,” stated Dr. Zaoutis. “We are Teflon for positive experiences and Velcro for negative experiences.” In addition, negative experiences are more likely to be stored in our memories. “It’s easy to park negative experiences.”
Delving deeper into neuroanatomy, Dr. Zaoutis spoke of “amygdala hijack,” where chronic stress inherent to the professional lives of pediatric hospitalists lead to anxiety responses that are faster, more robust, and triggered more easily.
But all is not lost, asserted Dr. Zaoutis, as our brains are more plastic than previously known. The “neural Darwinism,” of our brains, as Dr. Zaoutis states, leads to epigenetic intracellular changes, more sensitive synapses, improved blood flow, and even new cells as a result of experience dependent neuroplasticity. For example, stated Dr. Zaoutis, London taxi drivers have thicker white matter in their hippocampus as a result of the effect of learning London city streets, and mindfulness meditators have thicker gray matter in regions that control attention and self-insight.
Key Takeaways:
The lesson for pediatric hospitalists, stated Dr. Zaoutis, is that you can shape your brain for greater joy. “Consciously choose activities,” said Dr. Zaoutis, that counter our evolutionary negativity bias. How is this done?
1. Have a positive experience (you can create one or retrieve a prior one);
2. Enrich it and install it by dwelling on it for at least 15-30 seconds; and
3. Absorb it into your body, which my require somatisizing it – Dr. Zaoutis presses her hand into her chest to aid in this.
Further, spread this to your group by the old medical training technique of “see one, do one, teach one.” See if you can start your signout with the best thing that happened to you in the week. Most importantly, start with observing yourself.
Speaker: Lisa Zaoutis, MD, Pediatric Residency Program Director at the Children’s Hospital of Philadelphia.
Amid the skyscrapers of the Windy City, Pediatric Hospital Medicine (PHM) 2016 swept into town, bringing with it the denizens of pediatric hospitalist programs across the country. Some 1,150 attendees, comprised of hospitalists, PHM program leaders, and advanced care practitioners, gathered to educate and inspire one another in the the care of hospitalized children.
Dr. Lisa Zaoutis, director of the pediatric residency program at Children’s Hospital of Philadelphia, kicked off the conference with the opening plenary. Initially titled “North Star and Space,” she quickly changed the title to, “Changing Our Minds.” Touching on the disconnect between positive experiences that bring physicians into PHM and negative experiences that often drive behavior, she started with the beginning, the evolution of our brains.
“We are wired toward the negative,” stated Dr. Zaoutis. “We are Teflon for positive experiences and Velcro for negative experiences.” In addition, negative experiences are more likely to be stored in our memories. “It’s easy to park negative experiences.”
Delving deeper into neuroanatomy, Dr. Zaoutis spoke of “amygdala hijack,” where chronic stress inherent to the professional lives of pediatric hospitalists lead to anxiety responses that are faster, more robust, and triggered more easily.
But all is not lost, asserted Dr. Zaoutis, as our brains are more plastic than previously known. The “neural Darwinism,” of our brains, as Dr. Zaoutis states, leads to epigenetic intracellular changes, more sensitive synapses, improved blood flow, and even new cells as a result of experience dependent neuroplasticity. For example, stated Dr. Zaoutis, London taxi drivers have thicker white matter in their hippocampus as a result of the effect of learning London city streets, and mindfulness meditators have thicker gray matter in regions that control attention and self-insight.
Key Takeaways:
The lesson for pediatric hospitalists, stated Dr. Zaoutis, is that you can shape your brain for greater joy. “Consciously choose activities,” said Dr. Zaoutis, that counter our evolutionary negativity bias. How is this done?
1. Have a positive experience (you can create one or retrieve a prior one);
2. Enrich it and install it by dwelling on it for at least 15-30 seconds; and
3. Absorb it into your body, which my require somatisizing it – Dr. Zaoutis presses her hand into her chest to aid in this.
Further, spread this to your group by the old medical training technique of “see one, do one, teach one.” See if you can start your signout with the best thing that happened to you in the week. Most importantly, start with observing yourself.
Speaker: Lisa Zaoutis, MD, Pediatric Residency Program Director at the Children’s Hospital of Philadelphia.
Amid the skyscrapers of the Windy City, Pediatric Hospital Medicine (PHM) 2016 swept into town, bringing with it the denizens of pediatric hospitalist programs across the country. Some 1,150 attendees, comprised of hospitalists, PHM program leaders, and advanced care practitioners, gathered to educate and inspire one another in the the care of hospitalized children.
Dr. Lisa Zaoutis, director of the pediatric residency program at Children’s Hospital of Philadelphia, kicked off the conference with the opening plenary. Initially titled “North Star and Space,” she quickly changed the title to, “Changing Our Minds.” Touching on the disconnect between positive experiences that bring physicians into PHM and negative experiences that often drive behavior, she started with the beginning, the evolution of our brains.
“We are wired toward the negative,” stated Dr. Zaoutis. “We are Teflon for positive experiences and Velcro for negative experiences.” In addition, negative experiences are more likely to be stored in our memories. “It’s easy to park negative experiences.”
Delving deeper into neuroanatomy, Dr. Zaoutis spoke of “amygdala hijack,” where chronic stress inherent to the professional lives of pediatric hospitalists lead to anxiety responses that are faster, more robust, and triggered more easily.
But all is not lost, asserted Dr. Zaoutis, as our brains are more plastic than previously known. The “neural Darwinism,” of our brains, as Dr. Zaoutis states, leads to epigenetic intracellular changes, more sensitive synapses, improved blood flow, and even new cells as a result of experience dependent neuroplasticity. For example, stated Dr. Zaoutis, London taxi drivers have thicker white matter in their hippocampus as a result of the effect of learning London city streets, and mindfulness meditators have thicker gray matter in regions that control attention and self-insight.
Key Takeaways:
The lesson for pediatric hospitalists, stated Dr. Zaoutis, is that you can shape your brain for greater joy. “Consciously choose activities,” said Dr. Zaoutis, that counter our evolutionary negativity bias. How is this done?
1. Have a positive experience (you can create one or retrieve a prior one);
2. Enrich it and install it by dwelling on it for at least 15-30 seconds; and
3. Absorb it into your body, which my require somatisizing it – Dr. Zaoutis presses her hand into her chest to aid in this.
Further, spread this to your group by the old medical training technique of “see one, do one, teach one.” See if you can start your signout with the best thing that happened to you in the week. Most importantly, start with observing yourself.