Greetings,

As the Program Chair of CHEST Annual Meeting 2020, I’m excited to finally share the good news with all of you – our premiere educational event, CHEST 2020, will be taking place October 18-21! As you might have guessed, we’re migrating the meeting onto a virtual platform - not only will this change ensure your safety, it will enable so many more of you to attend. Colleagues who may have been excluded due to geographical restrictions in the past will now have the opportunity to experience all that we have to offer!

As always, we’ll be bringing you the latest, most relevant clinical topics in pulmonary, critical care, and sleep medicine. From COVID-19 to cultural diversity, we’ve carefully curated sessions to explore the issues that you want to learn about. Not to mention, our speakers are all experts in their field – at the forefront of the pandemic – and will bring a level of knowledge and insight to the meeting that is truly unparalleled. Afterall, that’s what our annual meeting is known for. Regardless of where or how it is taking place, it’s still “the very best of CHEST.”

Other highlights will include over 88 live sessions, including panel and case-based discussions, original investigation presentations with new, unpublished research, and CHEST Games.

Of course, we will have several networking opportunities where you will be able to connect with so many more of your colleagues because of the virtual nature of the meeting. While you may be sitting worlds apart, you’ll be socializing in an intimate online space.

While this isn’t exactly what we imagined for our meeting, it’s what we had to reimagine. Sometimes being pushed out of your comfort zone can lead to something extraordinary, and, in this instance, we think it did.

In closing, I’d like to acknowledge how challenging these past several months have been. For all the long hours, the time spent away from family, and the stress that continues to pile on – this is your chance to unplug and unwind.

We all need an event to look forward to right now, and at CHEST, we’ve worked hard to bring you one. I hope you’ll visit chestmeeting.chestnet.org to register for CHEST 2020.

Best,

Victor Test, MD, FCCP

Greetings,

As the Program Chair of CHEST Annual Meeting 2020, I’m excited to finally share the good news with all of you – our premiere educational event, CHEST 2020, will be taking place October 18-21! As you might have guessed, we’re migrating the meeting onto a virtual platform - not only will this change ensure your safety, it will enable so many more of you to attend. Colleagues who may have been excluded due to geographical restrictions in the past will now have the opportunity to experience all that we have to offer!

As always, we’ll be bringing you the latest, most relevant clinical topics in pulmonary, critical care, and sleep medicine. From COVID-19 to cultural diversity, we’ve carefully curated sessions to explore the issues that you want to learn about. Not to mention, our speakers are all experts in their field – at the forefront of the pandemic – and will bring a level of knowledge and insight to the meeting that is truly unparalleled. Afterall, that’s what our annual meeting is known for. Regardless of where or how it is taking place, it’s still “the very best of CHEST.”

Other highlights will include over 88 live sessions, including panel and case-based discussions, original investigation presentations with new, unpublished research, and CHEST Games.

Of course, we will have several networking opportunities where you will be able to connect with so many more of your colleagues because of the virtual nature of the meeting. While you may be sitting worlds apart, you’ll be socializing in an intimate online space.

While this isn’t exactly what we imagined for our meeting, it’s what we had to reimagine. Sometimes being pushed out of your comfort zone can lead to something extraordinary, and, in this instance, we think it did.

In closing, I’d like to acknowledge how challenging these past several months have been. For all the long hours, the time spent away from family, and the stress that continues to pile on – this is your chance to unplug and unwind.

We all need an event to look forward to right now, and at CHEST, we’ve worked hard to bring you one. I hope you’ll visit chestmeeting.chestnet.org to register for CHEST 2020.

Best,

Victor Test, MD, FCCP

Greetings,

As the Program Chair of CHEST Annual Meeting 2020, I’m excited to finally share the good news with all of you – our premiere educational event, CHEST 2020, will be taking place October 18-21! As you might have guessed, we’re migrating the meeting onto a virtual platform - not only will this change ensure your safety, it will enable so many more of you to attend. Colleagues who may have been excluded due to geographical restrictions in the past will now have the opportunity to experience all that we have to offer!

As always, we’ll be bringing you the latest, most relevant clinical topics in pulmonary, critical care, and sleep medicine. From COVID-19 to cultural diversity, we’ve carefully curated sessions to explore the issues that you want to learn about. Not to mention, our speakers are all experts in their field – at the forefront of the pandemic – and will bring a level of knowledge and insight to the meeting that is truly unparalleled. Afterall, that’s what our annual meeting is known for. Regardless of where or how it is taking place, it’s still “the very best of CHEST.”

Other highlights will include over 88 live sessions, including panel and case-based discussions, original investigation presentations with new, unpublished research, and CHEST Games.

Of course, we will have several networking opportunities where you will be able to connect with so many more of your colleagues because of the virtual nature of the meeting. While you may be sitting worlds apart, you’ll be socializing in an intimate online space.

While this isn’t exactly what we imagined for our meeting, it’s what we had to reimagine. Sometimes being pushed out of your comfort zone can lead to something extraordinary, and, in this instance, we think it did.

In closing, I’d like to acknowledge how challenging these past several months have been. For all the long hours, the time spent away from family, and the stress that continues to pile on – this is your chance to unplug and unwind.

We all need an event to look forward to right now, and at CHEST, we’ve worked hard to bring you one. I hope you’ll visit chestmeeting.chestnet.org to register for CHEST 2020.

Best,

Victor Test, MD, FCCP

As the NetWorks Challenge draws to a close, CHEST Foundation staff want to thank every member who donated to support this year’s drive for our COVID-19 Community Grants. When the fund was established in April, we started with a pool of $60,000 to award to patient support groups and small community organizations providing resources and interventions for those most vulnerable to develop severe complications from COVID-19 – American’s living with chronic lung disease. Within 2 months, we’d awarded all available funds to 25 organizations and had several others still seeking funding. The lion’s share of these groups were providing direct service to medically fragile and isolated patients – purchasing PPE, cleaning supplies, pulse oximeters, and even groceries to patients who otherwise wouldn’t have access to these critical supplies.

Because of YOUR support of the NetWorks Challenge, we are proud to share that we are providing an additional $43,850 in support of COVID-19 Community Grants. Because of you – we can continue to provide vital funding to support group members who lives’ you’ve changed forever.

“Receiving the CHEST Foundation grant for COVID-19 support was a real boost to all of our spirits. Our staff have been working tirelessly to care for our residents 24/7, and there have been some trying and exhausting moments. When we received the community-based grant, it reminded us that there are still people in our community cheering us on, and it’s an acknowledgment that our clients matter just as much to the community as they do to us, personally.” –– Katherine A. Brown, St. Coletta’s of Illinois

As the NetWorks Challenge draws to a close, CHEST Foundation staff want to thank every member who donated to support this year’s drive for our COVID-19 Community Grants. When the fund was established in April, we started with a pool of $60,000 to award to patient support groups and small community organizations providing resources and interventions for those most vulnerable to develop severe complications from COVID-19 – American’s living with chronic lung disease. Within 2 months, we’d awarded all available funds to 25 organizations and had several others still seeking funding. The lion’s share of these groups were providing direct service to medically fragile and isolated patients – purchasing PPE, cleaning supplies, pulse oximeters, and even groceries to patients who otherwise wouldn’t have access to these critical supplies.

Because of YOUR support of the NetWorks Challenge, we are proud to share that we are providing an additional $43,850 in support of COVID-19 Community Grants. Because of you – we can continue to provide vital funding to support group members who lives’ you’ve changed forever.

“Receiving the CHEST Foundation grant for COVID-19 support was a real boost to all of our spirits. Our staff have been working tirelessly to care for our residents 24/7, and there have been some trying and exhausting moments. When we received the community-based grant, it reminded us that there are still people in our community cheering us on, and it’s an acknowledgment that our clients matter just as much to the community as they do to us, personally.” –– Katherine A. Brown, St. Coletta’s of Illinois

As the NetWorks Challenge draws to a close, CHEST Foundation staff want to thank every member who donated to support this year’s drive for our COVID-19 Community Grants. When the fund was established in April, we started with a pool of $60,000 to award to patient support groups and small community organizations providing resources and interventions for those most vulnerable to develop severe complications from COVID-19 – American’s living with chronic lung disease. Within 2 months, we’d awarded all available funds to 25 organizations and had several others still seeking funding. The lion’s share of these groups were providing direct service to medically fragile and isolated patients – purchasing PPE, cleaning supplies, pulse oximeters, and even groceries to patients who otherwise wouldn’t have access to these critical supplies.

Because of YOUR support of the NetWorks Challenge, we are proud to share that we are providing an additional $43,850 in support of COVID-19 Community Grants. Because of you – we can continue to provide vital funding to support group members who lives’ you’ve changed forever.

“Receiving the CHEST Foundation grant for COVID-19 support was a real boost to all of our spirits. Our staff have been working tirelessly to care for our residents 24/7, and there have been some trying and exhausting moments. When we received the community-based grant, it reminded us that there are still people in our community cheering us on, and it’s an acknowledgment that our clients matter just as much to the community as they do to us, personally.” –– Katherine A. Brown, St. Coletta’s of Illinois

In rural counties, the absence of active labor and delivery (L&D) units is associated with a significant increase in perinatal mortality, according to a retrospective study using county-level data from the Alabama Department of Public Health.

stockce/Thinkstock

Although association does not establish causation, these data raise concern “for the current trend of diminishing L&D units that is occurring in many rural settings,” according to the authors of the study, led by John B. Waits, MD, of Cahaba Medical Care, Centreville, Ala., in Annals of Family Medicine.

When mortality per 1,000 live births was compared over a 15-year period (2003-2017) between 15 counties with and 21 counties without local L&D units, those with the units had lower overall infant mortality (9.23 vs. 7.89; P = .0011), perinatal mortality (8.89 vs. 10.82; P < .001), and neonatal mortality (4.74 vs. 5.67; P = .0034). The percentages of low-birth-weight babies born between 2003 and 2014 were 9.86% versus 10.61% (P < .001) for counties with and without L&D units, respectively.

The relative increased risks (RR) for these adverse outcomes in counties without L&D units were statistically significant and substantial, ranging from about 8% for a pregnancy resulting in a low-birth-weight infant to slightly more than 21% for perinatal mortality.

Over the study period, there were 165,525 live births in the 15 counties with L&D units and 72,177 births in the 21 counties with no such units. In counties without L&D units, the average proportion of White people was higher (73.47% vs. 60.86%), and that of African Americans was lower (22.76% vs. 36.23%). Median income ($40,759 vs. $35,604) and per capita income ($22,474 vs. $20,641) was slightly higher.

Of the 67 counties in Alabama, this study did not include those considered urbanized by the Alabama Office of Management and Budget even if classified rural by other statewide offices, such as the Alabama Rural Health Association. Any county with at least one L&D unit was considered to have a local unit. Three counties with L&D units that closed before the observation period was completed were excluded from the analysis.

The Alabama data appear to identify a major problem in need of an urgent solution, according to John S. Cullen, MD, a family physician in Valdez, Alaska, and chair of the American Academy of Family Physicians Board of Directors.

“Almost 20% of U.S. women of reproductive age live in rural communities,” he said in an interview. The data from this study provides compelling evidence “that the loss of rural maternity care in this country has contributed to the increase in newborn mortality in rural communities.”

There are many limitations for this study, according to the authors. They acknowledged that they could not control for many potentially important variables, such as travel time to hospitals for those in counties with L&D units when compared with those without. They also acknowledged the lack of data regarding availability of prenatal care in places with or without L&D units.

If lack of L&D services in rural areas is a source of adverse outcomes, data suggesting that the ongoing decline in L&D units are worrisome, according to the authors. Of studies they cited, one showed nearly a 10% loss in rural L&D services in a recent 10-year period.

The authors also noted that about half of the 3,143 counties in the United States do not have a practicing obstetrician, and that fewer than 7% of obstetricians-gynecologists practice in rural settings.

In many rural counties, including the county where the lead author practices, family practitioners provide 100% of local obstetric care, but access to these clinicians also appears to be declining, according to the paper. The ratio of primary care physicians to patients is already lower in non-metropolitan than metropolitan areas (39.8 vs. 53.3). The American Board of Family Medicine has reported that fewer than 10% of family physicians now provide maternity care, the authors wrote.

“If a causal relationship does exist [between lack of L&D units and adverse perinatal outcomes], then rural populations would definitively benefit from having local access to a L&D unit,” the authors stated.

The lead author, Dr. Waits, said in an interview that there are two obstacles to an increase in rural L&D units: malpractice premiums and reimbursement for indigent deliveries. The large malpractice premiums required to cover OB care are hurdles for caregivers, such as family physicians, as well as the hospitals where they practice.

Reforms from the legislative or regulatory perspective are needed to permit malpractice insurance to be issued at a reasonable cost, according to Dr. Waits. Such reforms are a “moral imperative” so that the malpractice issue is not allowed to “shipwreck infant and maternal mortality,” he said.

Of the many potential solutions, such as increased use of telemedicine, legislative initiatives to reduce the malpractice burden, or new support and incentives for family physicians to deliver OB care, each is burdened with obstacles to overcome, according to Dr. Waits. This does not mean these solutions should not be pursued alone or together, but he made it clear that the no solution is easy. In the meantime, Dr. Waits indicated a need to consider practical and immediate strategies to fix the problem.

“There should be incentives for rural emergency departments and ambulance systems to train in the [American Academy of Family Physicians’] Basic Life Support in Obstetrics (BLSO) certification courses each year. I am not aware of any specific evidence around this, but it is a known fact that, when L&Ds close, institutional memory of OB emergencies recede, and preparedness suffers,” he said.

Dr. Cullen agreed that if the closing of L&D units explains the higher rate of perinatal mortality in rural areas, both short-term and long-term solutions are needed.

“Every community must have a plan for obstetric and newborn emergencies. The decision to not offer maternity care means that rural providers will still provide maternity care but not be ready for emergencies,” he said, echoing a point made by Dr. Waits.

The study authors disclosed no conflicts. Dr. Cullen reported having no disclosures. 

SOURCE: Waits JB et al. Ann Fam Med. 2020;18:446-51.

In rural counties, the absence of active labor and delivery (L&D) units is associated with a significant increase in perinatal mortality, according to a retrospective study using county-level data from the Alabama Department of Public Health.

stockce/Thinkstock

Although association does not establish causation, these data raise concern “for the current trend of diminishing L&D units that is occurring in many rural settings,” according to the authors of the study, led by John B. Waits, MD, of Cahaba Medical Care, Centreville, Ala., in Annals of Family Medicine.

When mortality per 1,000 live births was compared over a 15-year period (2003-2017) between 15 counties with and 21 counties without local L&D units, those with the units had lower overall infant mortality (9.23 vs. 7.89; P = .0011), perinatal mortality (8.89 vs. 10.82; P < .001), and neonatal mortality (4.74 vs. 5.67; P = .0034). The percentages of low-birth-weight babies born between 2003 and 2014 were 9.86% versus 10.61% (P < .001) for counties with and without L&D units, respectively.

The relative increased risks (RR) for these adverse outcomes in counties without L&D units were statistically significant and substantial, ranging from about 8% for a pregnancy resulting in a low-birth-weight infant to slightly more than 21% for perinatal mortality.

Over the study period, there were 165,525 live births in the 15 counties with L&D units and 72,177 births in the 21 counties with no such units. In counties without L&D units, the average proportion of White people was higher (73.47% vs. 60.86%), and that of African Americans was lower (22.76% vs. 36.23%). Median income ($40,759 vs. $35,604) and per capita income ($22,474 vs. $20,641) was slightly higher.

Of the 67 counties in Alabama, this study did not include those considered urbanized by the Alabama Office of Management and Budget even if classified rural by other statewide offices, such as the Alabama Rural Health Association. Any county with at least one L&D unit was considered to have a local unit. Three counties with L&D units that closed before the observation period was completed were excluded from the analysis.

The Alabama data appear to identify a major problem in need of an urgent solution, according to John S. Cullen, MD, a family physician in Valdez, Alaska, and chair of the American Academy of Family Physicians Board of Directors.

“Almost 20% of U.S. women of reproductive age live in rural communities,” he said in an interview. The data from this study provides compelling evidence “that the loss of rural maternity care in this country has contributed to the increase in newborn mortality in rural communities.”

There are many limitations for this study, according to the authors. They acknowledged that they could not control for many potentially important variables, such as travel time to hospitals for those in counties with L&D units when compared with those without. They also acknowledged the lack of data regarding availability of prenatal care in places with or without L&D units.

If lack of L&D services in rural areas is a source of adverse outcomes, data suggesting that the ongoing decline in L&D units are worrisome, according to the authors. Of studies they cited, one showed nearly a 10% loss in rural L&D services in a recent 10-year period.

The authors also noted that about half of the 3,143 counties in the United States do not have a practicing obstetrician, and that fewer than 7% of obstetricians-gynecologists practice in rural settings.

In many rural counties, including the county where the lead author practices, family practitioners provide 100% of local obstetric care, but access to these clinicians also appears to be declining, according to the paper. The ratio of primary care physicians to patients is already lower in non-metropolitan than metropolitan areas (39.8 vs. 53.3). The American Board of Family Medicine has reported that fewer than 10% of family physicians now provide maternity care, the authors wrote.

“If a causal relationship does exist [between lack of L&D units and adverse perinatal outcomes], then rural populations would definitively benefit from having local access to a L&D unit,” the authors stated.

The lead author, Dr. Waits, said in an interview that there are two obstacles to an increase in rural L&D units: malpractice premiums and reimbursement for indigent deliveries. The large malpractice premiums required to cover OB care are hurdles for caregivers, such as family physicians, as well as the hospitals where they practice.

Reforms from the legislative or regulatory perspective are needed to permit malpractice insurance to be issued at a reasonable cost, according to Dr. Waits. Such reforms are a “moral imperative” so that the malpractice issue is not allowed to “shipwreck infant and maternal mortality,” he said.

Of the many potential solutions, such as increased use of telemedicine, legislative initiatives to reduce the malpractice burden, or new support and incentives for family physicians to deliver OB care, each is burdened with obstacles to overcome, according to Dr. Waits. This does not mean these solutions should not be pursued alone or together, but he made it clear that the no solution is easy. In the meantime, Dr. Waits indicated a need to consider practical and immediate strategies to fix the problem.

“There should be incentives for rural emergency departments and ambulance systems to train in the [American Academy of Family Physicians’] Basic Life Support in Obstetrics (BLSO) certification courses each year. I am not aware of any specific evidence around this, but it is a known fact that, when L&Ds close, institutional memory of OB emergencies recede, and preparedness suffers,” he said.

Dr. Cullen agreed that if the closing of L&D units explains the higher rate of perinatal mortality in rural areas, both short-term and long-term solutions are needed.

“Every community must have a plan for obstetric and newborn emergencies. The decision to not offer maternity care means that rural providers will still provide maternity care but not be ready for emergencies,” he said, echoing a point made by Dr. Waits.

The study authors disclosed no conflicts. Dr. Cullen reported having no disclosures. 

SOURCE: Waits JB et al. Ann Fam Med. 2020;18:446-51.

In rural counties, the absence of active labor and delivery (L&D) units is associated with a significant increase in perinatal mortality, according to a retrospective study using county-level data from the Alabama Department of Public Health.

stockce/Thinkstock

Although association does not establish causation, these data raise concern “for the current trend of diminishing L&D units that is occurring in many rural settings,” according to the authors of the study, led by John B. Waits, MD, of Cahaba Medical Care, Centreville, Ala., in Annals of Family Medicine.

When mortality per 1,000 live births was compared over a 15-year period (2003-2017) between 15 counties with and 21 counties without local L&D units, those with the units had lower overall infant mortality (9.23 vs. 7.89; P = .0011), perinatal mortality (8.89 vs. 10.82; P < .001), and neonatal mortality (4.74 vs. 5.67; P = .0034). The percentages of low-birth-weight babies born between 2003 and 2014 were 9.86% versus 10.61% (P < .001) for counties with and without L&D units, respectively.

The relative increased risks (RR) for these adverse outcomes in counties without L&D units were statistically significant and substantial, ranging from about 8% for a pregnancy resulting in a low-birth-weight infant to slightly more than 21% for perinatal mortality.

Over the study period, there were 165,525 live births in the 15 counties with L&D units and 72,177 births in the 21 counties with no such units. In counties without L&D units, the average proportion of White people was higher (73.47% vs. 60.86%), and that of African Americans was lower (22.76% vs. 36.23%). Median income ($40,759 vs. $35,604) and per capita income ($22,474 vs. $20,641) was slightly higher.

Of the 67 counties in Alabama, this study did not include those considered urbanized by the Alabama Office of Management and Budget even if classified rural by other statewide offices, such as the Alabama Rural Health Association. Any county with at least one L&D unit was considered to have a local unit. Three counties with L&D units that closed before the observation period was completed were excluded from the analysis.

The Alabama data appear to identify a major problem in need of an urgent solution, according to John S. Cullen, MD, a family physician in Valdez, Alaska, and chair of the American Academy of Family Physicians Board of Directors.

“Almost 20% of U.S. women of reproductive age live in rural communities,” he said in an interview. The data from this study provides compelling evidence “that the loss of rural maternity care in this country has contributed to the increase in newborn mortality in rural communities.”

There are many limitations for this study, according to the authors. They acknowledged that they could not control for many potentially important variables, such as travel time to hospitals for those in counties with L&D units when compared with those without. They also acknowledged the lack of data regarding availability of prenatal care in places with or without L&D units.

If lack of L&D services in rural areas is a source of adverse outcomes, data suggesting that the ongoing decline in L&D units are worrisome, according to the authors. Of studies they cited, one showed nearly a 10% loss in rural L&D services in a recent 10-year period.

The authors also noted that about half of the 3,143 counties in the United States do not have a practicing obstetrician, and that fewer than 7% of obstetricians-gynecologists practice in rural settings.

In many rural counties, including the county where the lead author practices, family practitioners provide 100% of local obstetric care, but access to these clinicians also appears to be declining, according to the paper. The ratio of primary care physicians to patients is already lower in non-metropolitan than metropolitan areas (39.8 vs. 53.3). The American Board of Family Medicine has reported that fewer than 10% of family physicians now provide maternity care, the authors wrote.

“If a causal relationship does exist [between lack of L&D units and adverse perinatal outcomes], then rural populations would definitively benefit from having local access to a L&D unit,” the authors stated.

The lead author, Dr. Waits, said in an interview that there are two obstacles to an increase in rural L&D units: malpractice premiums and reimbursement for indigent deliveries. The large malpractice premiums required to cover OB care are hurdles for caregivers, such as family physicians, as well as the hospitals where they practice.

Reforms from the legislative or regulatory perspective are needed to permit malpractice insurance to be issued at a reasonable cost, according to Dr. Waits. Such reforms are a “moral imperative” so that the malpractice issue is not allowed to “shipwreck infant and maternal mortality,” he said.

Of the many potential solutions, such as increased use of telemedicine, legislative initiatives to reduce the malpractice burden, or new support and incentives for family physicians to deliver OB care, each is burdened with obstacles to overcome, according to Dr. Waits. This does not mean these solutions should not be pursued alone or together, but he made it clear that the no solution is easy. In the meantime, Dr. Waits indicated a need to consider practical and immediate strategies to fix the problem.

“There should be incentives for rural emergency departments and ambulance systems to train in the [American Academy of Family Physicians’] Basic Life Support in Obstetrics (BLSO) certification courses each year. I am not aware of any specific evidence around this, but it is a known fact that, when L&Ds close, institutional memory of OB emergencies recede, and preparedness suffers,” he said.

Dr. Cullen agreed that if the closing of L&D units explains the higher rate of perinatal mortality in rural areas, both short-term and long-term solutions are needed.

“Every community must have a plan for obstetric and newborn emergencies. The decision to not offer maternity care means that rural providers will still provide maternity care but not be ready for emergencies,” he said, echoing a point made by Dr. Waits.

The study authors disclosed no conflicts. Dr. Cullen reported having no disclosures. 

SOURCE: Waits JB et al. Ann Fam Med. 2020;18:446-51.

For the first time, researchers detected active and prolonged infection of SARS-CoV-2 virus in the gastrointestinal (GI) tracts of people with confirmed COVID-19. Stool tests were positive among people with no GI symptoms, and in some cases up to 6 days after nasopharyngeal swabs yielded negative results.

The small pilot study suggests a quiescent but active infection in the gut. Stool testing revealed genomic evidence of active infection in 7 of the 15 participants tested in one of two hospitals in Hong Kong.

“We found active and prolonged SARS-CoV-2 infection in the stool of patients with COVID-19, even after recovery, suggesting that coronavirus could remain in the gut of asymptomatic carriers,” senior author Siew C. Ng, MBBS, PhD, told Medscape Medical News.

“Due to the potential threat of fecal-oral transmission, it is important to maintain long-term coronavirus and health surveillance,” said Ng, Associate Director of the Centre for Gut Microbiota Research at the Chinese University of Hong Kong (CUHK).

“Discharged patients and their caretakers should remain vigilant and observe strict personal and toileting hygiene,” she added.

The prospective, observational study was published online July 20 in Gut.
 

Ramping up COVID-19 testing

As a follow-up to these and other findings – including the testing of more than 2,000 stool samples in children and the needy arriving at Hong Kong airports starting March 29 – the same investigators are establishing a CUHK Coronavirus Testing Center.

As of Aug. 31, the detection rate in tested children was 0.28%. The Center plans to offer as many as 2,000 COVID-19 tests daily going forward to help identify asymptomatic carriers, the investigators announced in a Sept. 7 news release.

In contrast to nasopharyngeal sampling, stool specimens are “more convenient, safe and non-invasive to collect in the pediatric population,” professor Paul Chan, chairman of the Department of Microbiology, CU Medicine, said in the release. “This makes the stool test a better option for COVID-19 screening in babies, young children and those whose respiratory samples are difficult to collect.”

Even though previous researchers identified SARS-CoV-2 in the stool, the activity and infectivity of the virus in the gastrointestinal tract during and after COVID-19 respiratory positivity remained largely unknown.
 

Active infection detected in stool

This prospective study involved 15 people hospitalized with COVID-19 in March and April. Participants were a median 55 years old (range, 22-71 years) and all presented with respiratory symptoms. Only one patient had concurrent GI symptoms at admission. Median length of stay was 21 days.

Investigators collected fecal samples serially until discharge. They extracted viral DNA to test for transcriptional genetic evidence of active infection, which they detected in 7 of 15 patients. The patient with GI symptoms was not in this positive group.

The findings suggest a “quiescent but active GI infection,” the researchers note.

Three of the seven patients continued to test positive for active infection in their stool up to 6 days after respiratory clearance of SARS-CoV-2.
 

Microbiome matters

The investigators also extracted, amplified, and sequenced DNA from the stool samples. Their “metagenomic” profile revealed the type and amounts of bacterial strains in each patient’s gut microbiome.

Interestingly, bacterial strains differed between people with high SARS-CoV-2 infectivity versus participants with low to no evidence of active infection.

“Stool with high viral activity had higher abundance of pathogenic bacteria,” Ng said. In contrast, people with low or no infectivity had more beneficial bacterial strains, including bacteria that play critical roles in boosting host immunity.

Each patient’s microbiome composition changed during the course of the study. Whether the microbiome alters the course of COVID-19 or COVID-19 alters the composition of the microbiome requires further study, the authors note.

The U.S. Food and Drug Administration and officials in other countries have contacted the Hong Kong investigators for more details on their stool testing strategy, professor Francis K.L. Chan, dean of the faculty of medicine and director of the Centre for Gut Microbiota Research at CUHK, stated in the news release.

Further research into revealing the infectivity and pathogenesis of SARS-CoV-2 in the GI tract is warranted. The value of modulating the human gut microbiome in this patient population could be worthwhile to investigate as well, the researchers said.
 

Novel finding

“Some of it is not-so-new news and some is new,” David A. Johnson, MD, told Medscape Medical News when asked to comment on the study.

For example, previous researchers have detected SARS-CoV-2 virus in the stool. However, this study takes it a step further and shows that the virus present in stool can remain infectious on the basis of metagenomic signatures.

Furthermore, the virus can remain infectious in the gut even after a patient tests negative for COVID-19 through nasopharyngeal sampling – in this report up to 6 days later, said Johnson, professor of medicine, chief of gastroenterology, Eastern Virginia Medical School in Norfolk, Va.

The study carries important implications for people who currently test negative following active COVID-19 infection, he added. Centers for Disease Control and Prevention criteria clear a person as negative after two nasopharyngeal swabs at least 24 hours apart.

People in this category could believe they are no longer infectious and might return to a setting where they could infect others, Johnson said.

One potential means for spreading SARS-CoV-2 from the gut is from a toilet plume, as Johnson previously highlighted in a video report for Medscape Medical News.

The study authors disclosed no relevant financial relationships. Johnson serves as an adviser to WebMD/Medscape.
 

This article first appeared on Medscape.com.

For the first time, researchers detected active and prolonged infection of SARS-CoV-2 virus in the gastrointestinal (GI) tracts of people with confirmed COVID-19. Stool tests were positive among people with no GI symptoms, and in some cases up to 6 days after nasopharyngeal swabs yielded negative results.

The small pilot study suggests a quiescent but active infection in the gut. Stool testing revealed genomic evidence of active infection in 7 of the 15 participants tested in one of two hospitals in Hong Kong.

“We found active and prolonged SARS-CoV-2 infection in the stool of patients with COVID-19, even after recovery, suggesting that coronavirus could remain in the gut of asymptomatic carriers,” senior author Siew C. Ng, MBBS, PhD, told Medscape Medical News.

“Due to the potential threat of fecal-oral transmission, it is important to maintain long-term coronavirus and health surveillance,” said Ng, Associate Director of the Centre for Gut Microbiota Research at the Chinese University of Hong Kong (CUHK).

“Discharged patients and their caretakers should remain vigilant and observe strict personal and toileting hygiene,” she added.

The prospective, observational study was published online July 20 in Gut.
 

Ramping up COVID-19 testing

As a follow-up to these and other findings – including the testing of more than 2,000 stool samples in children and the needy arriving at Hong Kong airports starting March 29 – the same investigators are establishing a CUHK Coronavirus Testing Center.

As of Aug. 31, the detection rate in tested children was 0.28%. The Center plans to offer as many as 2,000 COVID-19 tests daily going forward to help identify asymptomatic carriers, the investigators announced in a Sept. 7 news release.

In contrast to nasopharyngeal sampling, stool specimens are “more convenient, safe and non-invasive to collect in the pediatric population,” professor Paul Chan, chairman of the Department of Microbiology, CU Medicine, said in the release. “This makes the stool test a better option for COVID-19 screening in babies, young children and those whose respiratory samples are difficult to collect.”

Even though previous researchers identified SARS-CoV-2 in the stool, the activity and infectivity of the virus in the gastrointestinal tract during and after COVID-19 respiratory positivity remained largely unknown.
 

Active infection detected in stool

This prospective study involved 15 people hospitalized with COVID-19 in March and April. Participants were a median 55 years old (range, 22-71 years) and all presented with respiratory symptoms. Only one patient had concurrent GI symptoms at admission. Median length of stay was 21 days.

Investigators collected fecal samples serially until discharge. They extracted viral DNA to test for transcriptional genetic evidence of active infection, which they detected in 7 of 15 patients. The patient with GI symptoms was not in this positive group.

The findings suggest a “quiescent but active GI infection,” the researchers note.

Three of the seven patients continued to test positive for active infection in their stool up to 6 days after respiratory clearance of SARS-CoV-2.
 

Microbiome matters

The investigators also extracted, amplified, and sequenced DNA from the stool samples. Their “metagenomic” profile revealed the type and amounts of bacterial strains in each patient’s gut microbiome.

Interestingly, bacterial strains differed between people with high SARS-CoV-2 infectivity versus participants with low to no evidence of active infection.

“Stool with high viral activity had higher abundance of pathogenic bacteria,” Ng said. In contrast, people with low or no infectivity had more beneficial bacterial strains, including bacteria that play critical roles in boosting host immunity.

Each patient’s microbiome composition changed during the course of the study. Whether the microbiome alters the course of COVID-19 or COVID-19 alters the composition of the microbiome requires further study, the authors note.

The U.S. Food and Drug Administration and officials in other countries have contacted the Hong Kong investigators for more details on their stool testing strategy, professor Francis K.L. Chan, dean of the faculty of medicine and director of the Centre for Gut Microbiota Research at CUHK, stated in the news release.

Further research into revealing the infectivity and pathogenesis of SARS-CoV-2 in the GI tract is warranted. The value of modulating the human gut microbiome in this patient population could be worthwhile to investigate as well, the researchers said.
 

Novel finding

“Some of it is not-so-new news and some is new,” David A. Johnson, MD, told Medscape Medical News when asked to comment on the study.

For example, previous researchers have detected SARS-CoV-2 virus in the stool. However, this study takes it a step further and shows that the virus present in stool can remain infectious on the basis of metagenomic signatures.

Furthermore, the virus can remain infectious in the gut even after a patient tests negative for COVID-19 through nasopharyngeal sampling – in this report up to 6 days later, said Johnson, professor of medicine, chief of gastroenterology, Eastern Virginia Medical School in Norfolk, Va.

The study carries important implications for people who currently test negative following active COVID-19 infection, he added. Centers for Disease Control and Prevention criteria clear a person as negative after two nasopharyngeal swabs at least 24 hours apart.

People in this category could believe they are no longer infectious and might return to a setting where they could infect others, Johnson said.

One potential means for spreading SARS-CoV-2 from the gut is from a toilet plume, as Johnson previously highlighted in a video report for Medscape Medical News.

The study authors disclosed no relevant financial relationships. Johnson serves as an adviser to WebMD/Medscape.
 

This article first appeared on Medscape.com.

For the first time, researchers detected active and prolonged infection of SARS-CoV-2 virus in the gastrointestinal (GI) tracts of people with confirmed COVID-19. Stool tests were positive among people with no GI symptoms, and in some cases up to 6 days after nasopharyngeal swabs yielded negative results.

The small pilot study suggests a quiescent but active infection in the gut. Stool testing revealed genomic evidence of active infection in 7 of the 15 participants tested in one of two hospitals in Hong Kong.

“We found active and prolonged SARS-CoV-2 infection in the stool of patients with COVID-19, even after recovery, suggesting that coronavirus could remain in the gut of asymptomatic carriers,” senior author Siew C. Ng, MBBS, PhD, told Medscape Medical News.

“Due to the potential threat of fecal-oral transmission, it is important to maintain long-term coronavirus and health surveillance,” said Ng, Associate Director of the Centre for Gut Microbiota Research at the Chinese University of Hong Kong (CUHK).

“Discharged patients and their caretakers should remain vigilant and observe strict personal and toileting hygiene,” she added.

The prospective, observational study was published online July 20 in Gut.
 

Ramping up COVID-19 testing

As a follow-up to these and other findings – including the testing of more than 2,000 stool samples in children and the needy arriving at Hong Kong airports starting March 29 – the same investigators are establishing a CUHK Coronavirus Testing Center.

As of Aug. 31, the detection rate in tested children was 0.28%. The Center plans to offer as many as 2,000 COVID-19 tests daily going forward to help identify asymptomatic carriers, the investigators announced in a Sept. 7 news release.

In contrast to nasopharyngeal sampling, stool specimens are “more convenient, safe and non-invasive to collect in the pediatric population,” professor Paul Chan, chairman of the Department of Microbiology, CU Medicine, said in the release. “This makes the stool test a better option for COVID-19 screening in babies, young children and those whose respiratory samples are difficult to collect.”

Even though previous researchers identified SARS-CoV-2 in the stool, the activity and infectivity of the virus in the gastrointestinal tract during and after COVID-19 respiratory positivity remained largely unknown.
 

Active infection detected in stool

This prospective study involved 15 people hospitalized with COVID-19 in March and April. Participants were a median 55 years old (range, 22-71 years) and all presented with respiratory symptoms. Only one patient had concurrent GI symptoms at admission. Median length of stay was 21 days.

Investigators collected fecal samples serially until discharge. They extracted viral DNA to test for transcriptional genetic evidence of active infection, which they detected in 7 of 15 patients. The patient with GI symptoms was not in this positive group.

The findings suggest a “quiescent but active GI infection,” the researchers note.

Three of the seven patients continued to test positive for active infection in their stool up to 6 days after respiratory clearance of SARS-CoV-2.
 

Microbiome matters

The investigators also extracted, amplified, and sequenced DNA from the stool samples. Their “metagenomic” profile revealed the type and amounts of bacterial strains in each patient’s gut microbiome.

Interestingly, bacterial strains differed between people with high SARS-CoV-2 infectivity versus participants with low to no evidence of active infection.

“Stool with high viral activity had higher abundance of pathogenic bacteria,” Ng said. In contrast, people with low or no infectivity had more beneficial bacterial strains, including bacteria that play critical roles in boosting host immunity.

Each patient’s microbiome composition changed during the course of the study. Whether the microbiome alters the course of COVID-19 or COVID-19 alters the composition of the microbiome requires further study, the authors note.

The U.S. Food and Drug Administration and officials in other countries have contacted the Hong Kong investigators for more details on their stool testing strategy, professor Francis K.L. Chan, dean of the faculty of medicine and director of the Centre for Gut Microbiota Research at CUHK, stated in the news release.

Further research into revealing the infectivity and pathogenesis of SARS-CoV-2 in the GI tract is warranted. The value of modulating the human gut microbiome in this patient population could be worthwhile to investigate as well, the researchers said.
 

Novel finding

“Some of it is not-so-new news and some is new,” David A. Johnson, MD, told Medscape Medical News when asked to comment on the study.

For example, previous researchers have detected SARS-CoV-2 virus in the stool. However, this study takes it a step further and shows that the virus present in stool can remain infectious on the basis of metagenomic signatures.

Furthermore, the virus can remain infectious in the gut even after a patient tests negative for COVID-19 through nasopharyngeal sampling – in this report up to 6 days later, said Johnson, professor of medicine, chief of gastroenterology, Eastern Virginia Medical School in Norfolk, Va.

The study carries important implications for people who currently test negative following active COVID-19 infection, he added. Centers for Disease Control and Prevention criteria clear a person as negative after two nasopharyngeal swabs at least 24 hours apart.

People in this category could believe they are no longer infectious and might return to a setting where they could infect others, Johnson said.

One potential means for spreading SARS-CoV-2 from the gut is from a toilet plume, as Johnson previously highlighted in a video report for Medscape Medical News.

The study authors disclosed no relevant financial relationships. Johnson serves as an adviser to WebMD/Medscape.
 

This article first appeared on Medscape.com.

The Diagnosis: Primary Cutaneous γδ T-cell Lymphoma

Primary cutaneous γδ T-cell lymphoma (PCGDTL) is a distinct entity that can be confused with other types of cutaneous T-cell lymphomas. Often rapidly fatal, PCGDTL has a broad clinical spectrum that may include indolent variants—subcutaneous, epidermotropic, and dermal.¹ Primary cutaneous γδ T-cell lymphoma represents less than 1% of all cutaneous T-cell lymphomas.² Diagnosis and treatment remain challenging. Patients typically present with nodular lesions that progress to ulceration and necrosis. Early lesions can be confused with erythema nodosum, mycosis fungoides, or infection on clinical examination; biopsy establishes the diagnosis. Typical findings include a cytotoxic phenotype, variable epidermotropism, dermal and subcutaneous involvement, and loss of CD4 and often CD8 expression. Testing for Epstein-Barr virus expression yields negative results. The neoplastic lymphocytes in dermal and subcutaneous PCGDTL typically are T-cell intracellular antigen-1 (TIA-1) and granzyme positive.¹

Immunohistochemistry failed to reveal CD8, CD56, granzyme, or T-cell intracellular antigen-1 staining of neoplastic cells in our patient but stained diffusely positive with CD3 and CD4. A CD20 stain decorated only a few dermal cells. The patient’s skin lesions continued to enlarge, and the massive lymphadenopathy made breathing difficult. Computed tomography revealed diffuse systemic involvement. An axillary lymph node biopsy revealed sinusoids with complete diffuse effacement of architecture as well as frequent mitotic figures and karyorrhectic debris (Figure 1A). Negative staining for T-cell receptor beta-F1 of the axillary lymph node biopsy and clonal rearrangement of the T-cell receptor gamma chain supported the diagnosis of PCGDTL. Nuclear staining for Epstein-Barr virus–encoded RNA was negative. Human T-cell leukemia virus type 1 antibodies and polymerase chain reaction also were negative. Flow cytometry demonstrated an atypical population of CD3⁺, CD4⁺, and CD7− γδ T lymphocytes, further supporting the diagnosis of lymphoma.

The median life expectancy for patients with dermal or subcutaneous PCGDTL is 10 to 15 months after diagnosis.³ The 5-year life expectancy for PCGDTL is approximately 11%.² Limited treatment options contribute to the poor outcome. Chemotherapy regimens such as CHOP (cyclophosphamide, doxorubicin, vincristine, prednisolone) and EPOCH (etoposide phosphate, prednisone, vincristine sulfate, cyclophosphamide, doxorubicin hydrochloride) have yielded inconsistent results. Stem cell transplant has been tried in progressive disease and also has yielded mixed results.² Brentuximab is indicated for individuals whose tumors express CD30.⁴ Associated hemophagic lymphohistiocytosis portends a poor prognosis.⁵

Despite treatment with etoposide, vincristine, doxorubicin, and high-dose oral steroids, our patient developed progressive difficulty breathing, stridor, kidney injury, and anemia. Our patient died less than 1 month after diagnosis—after only 1 round of chemotherapy—secondary to progressive disease and an uncontrollable gastrointestinal tract bleed. The leonine facies (Figure 1B) encountered in our patient can raise a differential diagnosis that includes infectious as well as neoplastic etiologies; however, most infectious etiologies associated with leonine facies manifest in a chronic fashion rather than with a sudden eruption, as noted in our patient.

Leprosy is caused by Mycobacterium leprae, a grampositive bacillus. The condition manifests across a spectrum, with the poles being tuberculoid and lepromatous, and borderline variants in between.^6-8 Lepromatous leprosy arises in individuals who are unable to mount cellular immunity against M leprae secondary to anergy.⁶ Lepromatous leprosy often presents with numerous papules and nodules. Aside from cutaneous manifestations, lepromatous leprosy has a predilection for peripheral nerves and specifically Schwann cells. Histologically, biopsy reveals a flat epidermis and a cell-free subepidermal grenz zone. Within the dermis, there is a diffuse histiocytic infiltrate that typically is not centered around nerves (Figure 2).^6,7 Mycobacterium leprae can appear scattered throughout or clustered in globi. Mycobacterium leprae stains red with Ziehl-Neelsen or Wade-Fite stains.^6,7 Immunohistochemistry reveals a CD4⁺ helper T cell (TH2) predominance, supported by the increased expression of type 2 reaction cytokines such as IL-4, IL-5, IL-10, and IL-13.⁸

Diffuse large B-cell lymphoma (DLBCL) embodies 10% to 20% of all primary cutaneous lymphomas; it is more prevalent in older adults (age range, 70–82 years) and women. Clinically, DLBCL presents as either single or multiple rapidly progressing nodules or plaques, usually violaceous or blue-red in color.^9,10 The most common area of presentation is on the legs, though it also can surface at other sites.⁹ On histology, DLBCL has clearly malignant features including frequent mitotic figures, large immunoblasts, and involvement throughout the dermis as well as perivascularly (Figure 3). Spindle-shaped cells and anaplastic features can be present. Immunohistochemically, DLBCL stains strongly positive for CD20 and B-cell lymphoma 2 (Bcl-2) along with other pan–B-cell markers.^9-11 The aggressive leg type of DLBCL stains positively for multiple myeloma oncogene 1 (MUM-1).^9,11

Cutaneous metastatic adenocarcinoma from internal malignancies occurs in approximately 5% of cancer patients with metastatic spread.¹² Most of these cutaneous lesions develop in close proximity to the primary tumor such as on the trunk, head, or neck. All cutaneous metastases carry a poor prognosis. Clinical presentation can vary greatly, ranging from painless, firm, or elastic nodules to lesions that mimic inflammatory skin conditions such as erysipelas or scleroderma. The majority of these metastases develop as painless firm nodules that are flesh colored, pink, red-brown, or purple.^12,13 The histopathology of metastatic adenocarcinoma demonstrates an infiltrative nodular appearance, though there rarely are well-circumscribed nodules found.¹³ The lesion originates in the dermis or subcutaneous tissue. It is a glandulartype lesion that may reflect the tissue of the primary tumor (Figure 4).^12,14 Immunohistochemical stains likely will remain consistent with those of the primary tumor, which is not always the case.¹⁴

Merkel cell carcinoma (MCC) is an aggressive cutaneous malignancy of epithelial and neuroendocrine origin, first described as trabecular carcinoma due to the arrangement of tumor resembling cancellous bone.^15,16 Merkel cells are mechanoreceptors found near nerve terminals.¹⁷ Approximately 80% of MCCs are associated with Merkel cell polyomavirus, which is a small, double-stranded DNA virus with an icosahedral capsid.^17,18 Merkel cell polyomavirus–positive cases of MCC tend to have a better prognosis. In Merkel cell polyomavirus–negative MCC, there is an association with UV damage and increased chromosomal aberrations.¹⁸ Merkel cell carcinoma is known for its high rate of recurrence as well as local and distant metastasis. Nodal involvement is the most important prognostic indicator.¹⁵ Clinically, MCC is associated with the AEIOU mnemonic (asymptomatic, expanding rapidly, immunosuppression, older than 50 years, UV exposed/fair skin).^15-17 Lesions appear as red-blue papules on sun-exposed skin and usually are smaller than 2 cm by their greatest dimension. On histopathology, MCC demonstrates small, round, blue cells arranged in sheets or nests originating in the dermis and occasionally can infiltrate the subcutis and lymphovascular surroundings (Figure 5).^16-19 Cells have scant eosinophilic cytoplasm and may have fine granular chromatin. Numerous mitotic figures and apoptotic cells also are present. On immunohistochemistry, these cells will stain positive for cytokeratin AE1/AE3, anticytokeratin (CAM 5.2), CK20, and CD56. Due to their neuroendocrine derivation, they also are commonly synaptophysin, neuron-specific enolase, and chromogranin A positive. Notably, MCC will stain negative for leukocyte common antigen, CD20, CD3, CD34, and thyroid transcription factor 1 (TTF-1).^16,17

Primary cutaneous γδ T-cell lymphoma can be difficult to diagnose and requires urgent treatment. Clinicians and dermatopathologists need to work together to establish the diagnosis. There is a high mortality rate associated with PCGDTL, making prompt recognition and timely treatment critical. Acknowledgments—Thank you to our colleagues with the Penn State Health Hematology/Oncology Department (Hershey, Pennsylvania) for comanagement of this patient.

Acknowledgments
Thank you to our colleagues with the Penn State Health Hematology/Oncology Department (Hershey, Pennsylvania) for comanagement of this patient.

The Diagnosis: Primary Cutaneous γδ T-cell Lymphoma

Primary cutaneous γδ T-cell lymphoma (PCGDTL) is a distinct entity that can be confused with other types of cutaneous T-cell lymphomas. Often rapidly fatal, PCGDTL has a broad clinical spectrum that may include indolent variants—subcutaneous, epidermotropic, and dermal.¹ Primary cutaneous γδ T-cell lymphoma represents less than 1% of all cutaneous T-cell lymphomas.² Diagnosis and treatment remain challenging. Patients typically present with nodular lesions that progress to ulceration and necrosis. Early lesions can be confused with erythema nodosum, mycosis fungoides, or infection on clinical examination; biopsy establishes the diagnosis. Typical findings include a cytotoxic phenotype, variable epidermotropism, dermal and subcutaneous involvement, and loss of CD4 and often CD8 expression. Testing for Epstein-Barr virus expression yields negative results. The neoplastic lymphocytes in dermal and subcutaneous PCGDTL typically are T-cell intracellular antigen-1 (TIA-1) and granzyme positive.¹

Immunohistochemistry failed to reveal CD8, CD56, granzyme, or T-cell intracellular antigen-1 staining of neoplastic cells in our patient but stained diffusely positive with CD3 and CD4. A CD20 stain decorated only a few dermal cells. The patient’s skin lesions continued to enlarge, and the massive lymphadenopathy made breathing difficult. Computed tomography revealed diffuse systemic involvement. An axillary lymph node biopsy revealed sinusoids with complete diffuse effacement of architecture as well as frequent mitotic figures and karyorrhectic debris (Figure 1A). Negative staining for T-cell receptor beta-F1 of the axillary lymph node biopsy and clonal rearrangement of the T-cell receptor gamma chain supported the diagnosis of PCGDTL. Nuclear staining for Epstein-Barr virus–encoded RNA was negative. Human T-cell leukemia virus type 1 antibodies and polymerase chain reaction also were negative. Flow cytometry demonstrated an atypical population of CD3⁺, CD4⁺, and CD7− γδ T lymphocytes, further supporting the diagnosis of lymphoma.

The median life expectancy for patients with dermal or subcutaneous PCGDTL is 10 to 15 months after diagnosis.³ The 5-year life expectancy for PCGDTL is approximately 11%.² Limited treatment options contribute to the poor outcome. Chemotherapy regimens such as CHOP (cyclophosphamide, doxorubicin, vincristine, prednisolone) and EPOCH (etoposide phosphate, prednisone, vincristine sulfate, cyclophosphamide, doxorubicin hydrochloride) have yielded inconsistent results. Stem cell transplant has been tried in progressive disease and also has yielded mixed results.² Brentuximab is indicated for individuals whose tumors express CD30.⁴ Associated hemophagic lymphohistiocytosis portends a poor prognosis.⁵

Despite treatment with etoposide, vincristine, doxorubicin, and high-dose oral steroids, our patient developed progressive difficulty breathing, stridor, kidney injury, and anemia. Our patient died less than 1 month after diagnosis—after only 1 round of chemotherapy—secondary to progressive disease and an uncontrollable gastrointestinal tract bleed. The leonine facies (Figure 1B) encountered in our patient can raise a differential diagnosis that includes infectious as well as neoplastic etiologies; however, most infectious etiologies associated with leonine facies manifest in a chronic fashion rather than with a sudden eruption, as noted in our patient.

Leprosy is caused by Mycobacterium leprae, a grampositive bacillus. The condition manifests across a spectrum, with the poles being tuberculoid and lepromatous, and borderline variants in between.^6-8 Lepromatous leprosy arises in individuals who are unable to mount cellular immunity against M leprae secondary to anergy.⁶ Lepromatous leprosy often presents with numerous papules and nodules. Aside from cutaneous manifestations, lepromatous leprosy has a predilection for peripheral nerves and specifically Schwann cells. Histologically, biopsy reveals a flat epidermis and a cell-free subepidermal grenz zone. Within the dermis, there is a diffuse histiocytic infiltrate that typically is not centered around nerves (Figure 2).^6,7 Mycobacterium leprae can appear scattered throughout or clustered in globi. Mycobacterium leprae stains red with Ziehl-Neelsen or Wade-Fite stains.^6,7 Immunohistochemistry reveals a CD4⁺ helper T cell (TH2) predominance, supported by the increased expression of type 2 reaction cytokines such as IL-4, IL-5, IL-10, and IL-13.⁸

Diffuse large B-cell lymphoma (DLBCL) embodies 10% to 20% of all primary cutaneous lymphomas; it is more prevalent in older adults (age range, 70–82 years) and women. Clinically, DLBCL presents as either single or multiple rapidly progressing nodules or plaques, usually violaceous or blue-red in color.^9,10 The most common area of presentation is on the legs, though it also can surface at other sites.⁹ On histology, DLBCL has clearly malignant features including frequent mitotic figures, large immunoblasts, and involvement throughout the dermis as well as perivascularly (Figure 3). Spindle-shaped cells and anaplastic features can be present. Immunohistochemically, DLBCL stains strongly positive for CD20 and B-cell lymphoma 2 (Bcl-2) along with other pan–B-cell markers.^9-11 The aggressive leg type of DLBCL stains positively for multiple myeloma oncogene 1 (MUM-1).^9,11

Cutaneous metastatic adenocarcinoma from internal malignancies occurs in approximately 5% of cancer patients with metastatic spread.¹² Most of these cutaneous lesions develop in close proximity to the primary tumor such as on the trunk, head, or neck. All cutaneous metastases carry a poor prognosis. Clinical presentation can vary greatly, ranging from painless, firm, or elastic nodules to lesions that mimic inflammatory skin conditions such as erysipelas or scleroderma. The majority of these metastases develop as painless firm nodules that are flesh colored, pink, red-brown, or purple.^12,13 The histopathology of metastatic adenocarcinoma demonstrates an infiltrative nodular appearance, though there rarely are well-circumscribed nodules found.¹³ The lesion originates in the dermis or subcutaneous tissue. It is a glandulartype lesion that may reflect the tissue of the primary tumor (Figure 4).^12,14 Immunohistochemical stains likely will remain consistent with those of the primary tumor, which is not always the case.¹⁴

Merkel cell carcinoma (MCC) is an aggressive cutaneous malignancy of epithelial and neuroendocrine origin, first described as trabecular carcinoma due to the arrangement of tumor resembling cancellous bone.^15,16 Merkel cells are mechanoreceptors found near nerve terminals.¹⁷ Approximately 80% of MCCs are associated with Merkel cell polyomavirus, which is a small, double-stranded DNA virus with an icosahedral capsid.^17,18 Merkel cell polyomavirus–positive cases of MCC tend to have a better prognosis. In Merkel cell polyomavirus–negative MCC, there is an association with UV damage and increased chromosomal aberrations.¹⁸ Merkel cell carcinoma is known for its high rate of recurrence as well as local and distant metastasis. Nodal involvement is the most important prognostic indicator.¹⁵ Clinically, MCC is associated with the AEIOU mnemonic (asymptomatic, expanding rapidly, immunosuppression, older than 50 years, UV exposed/fair skin).^15-17 Lesions appear as red-blue papules on sun-exposed skin and usually are smaller than 2 cm by their greatest dimension. On histopathology, MCC demonstrates small, round, blue cells arranged in sheets or nests originating in the dermis and occasionally can infiltrate the subcutis and lymphovascular surroundings (Figure 5).^16-19 Cells have scant eosinophilic cytoplasm and may have fine granular chromatin. Numerous mitotic figures and apoptotic cells also are present. On immunohistochemistry, these cells will stain positive for cytokeratin AE1/AE3, anticytokeratin (CAM 5.2), CK20, and CD56. Due to their neuroendocrine derivation, they also are commonly synaptophysin, neuron-specific enolase, and chromogranin A positive. Notably, MCC will stain negative for leukocyte common antigen, CD20, CD3, CD34, and thyroid transcription factor 1 (TTF-1).^16,17

Primary cutaneous γδ T-cell lymphoma can be difficult to diagnose and requires urgent treatment. Clinicians and dermatopathologists need to work together to establish the diagnosis. There is a high mortality rate associated with PCGDTL, making prompt recognition and timely treatment critical. Acknowledgments—Thank you to our colleagues with the Penn State Health Hematology/Oncology Department (Hershey, Pennsylvania) for comanagement of this patient.

Acknowledgments
Thank you to our colleagues with the Penn State Health Hematology/Oncology Department (Hershey, Pennsylvania) for comanagement of this patient.

The Diagnosis: Primary Cutaneous γδ T-cell Lymphoma

Primary cutaneous γδ T-cell lymphoma (PCGDTL) is a distinct entity that can be confused with other types of cutaneous T-cell lymphomas. Often rapidly fatal, PCGDTL has a broad clinical spectrum that may include indolent variants—subcutaneous, epidermotropic, and dermal.¹ Primary cutaneous γδ T-cell lymphoma represents less than 1% of all cutaneous T-cell lymphomas.² Diagnosis and treatment remain challenging. Patients typically present with nodular lesions that progress to ulceration and necrosis. Early lesions can be confused with erythema nodosum, mycosis fungoides, or infection on clinical examination; biopsy establishes the diagnosis. Typical findings include a cytotoxic phenotype, variable epidermotropism, dermal and subcutaneous involvement, and loss of CD4 and often CD8 expression. Testing for Epstein-Barr virus expression yields negative results. The neoplastic lymphocytes in dermal and subcutaneous PCGDTL typically are T-cell intracellular antigen-1 (TIA-1) and granzyme positive.¹

Immunohistochemistry failed to reveal CD8, CD56, granzyme, or T-cell intracellular antigen-1 staining of neoplastic cells in our patient but stained diffusely positive with CD3 and CD4. A CD20 stain decorated only a few dermal cells. The patient’s skin lesions continued to enlarge, and the massive lymphadenopathy made breathing difficult. Computed tomography revealed diffuse systemic involvement. An axillary lymph node biopsy revealed sinusoids with complete diffuse effacement of architecture as well as frequent mitotic figures and karyorrhectic debris (Figure 1A). Negative staining for T-cell receptor beta-F1 of the axillary lymph node biopsy and clonal rearrangement of the T-cell receptor gamma chain supported the diagnosis of PCGDTL. Nuclear staining for Epstein-Barr virus–encoded RNA was negative. Human T-cell leukemia virus type 1 antibodies and polymerase chain reaction also were negative. Flow cytometry demonstrated an atypical population of CD3⁺, CD4⁺, and CD7− γδ T lymphocytes, further supporting the diagnosis of lymphoma.

The median life expectancy for patients with dermal or subcutaneous PCGDTL is 10 to 15 months after diagnosis.³ The 5-year life expectancy for PCGDTL is approximately 11%.² Limited treatment options contribute to the poor outcome. Chemotherapy regimens such as CHOP (cyclophosphamide, doxorubicin, vincristine, prednisolone) and EPOCH (etoposide phosphate, prednisone, vincristine sulfate, cyclophosphamide, doxorubicin hydrochloride) have yielded inconsistent results. Stem cell transplant has been tried in progressive disease and also has yielded mixed results.² Brentuximab is indicated for individuals whose tumors express CD30.⁴ Associated hemophagic lymphohistiocytosis portends a poor prognosis.⁵

Despite treatment with etoposide, vincristine, doxorubicin, and high-dose oral steroids, our patient developed progressive difficulty breathing, stridor, kidney injury, and anemia. Our patient died less than 1 month after diagnosis—after only 1 round of chemotherapy—secondary to progressive disease and an uncontrollable gastrointestinal tract bleed. The leonine facies (Figure 1B) encountered in our patient can raise a differential diagnosis that includes infectious as well as neoplastic etiologies; however, most infectious etiologies associated with leonine facies manifest in a chronic fashion rather than with a sudden eruption, as noted in our patient.

Leprosy is caused by Mycobacterium leprae, a grampositive bacillus. The condition manifests across a spectrum, with the poles being tuberculoid and lepromatous, and borderline variants in between.^6-8 Lepromatous leprosy arises in individuals who are unable to mount cellular immunity against M leprae secondary to anergy.⁶ Lepromatous leprosy often presents with numerous papules and nodules. Aside from cutaneous manifestations, lepromatous leprosy has a predilection for peripheral nerves and specifically Schwann cells. Histologically, biopsy reveals a flat epidermis and a cell-free subepidermal grenz zone. Within the dermis, there is a diffuse histiocytic infiltrate that typically is not centered around nerves (Figure 2).^6,7 Mycobacterium leprae can appear scattered throughout or clustered in globi. Mycobacterium leprae stains red with Ziehl-Neelsen or Wade-Fite stains.^6,7 Immunohistochemistry reveals a CD4⁺ helper T cell (TH2) predominance, supported by the increased expression of type 2 reaction cytokines such as IL-4, IL-5, IL-10, and IL-13.⁸

Diffuse large B-cell lymphoma (DLBCL) embodies 10% to 20% of all primary cutaneous lymphomas; it is more prevalent in older adults (age range, 70–82 years) and women. Clinically, DLBCL presents as either single or multiple rapidly progressing nodules or plaques, usually violaceous or blue-red in color.^9,10 The most common area of presentation is on the legs, though it also can surface at other sites.⁹ On histology, DLBCL has clearly malignant features including frequent mitotic figures, large immunoblasts, and involvement throughout the dermis as well as perivascularly (Figure 3). Spindle-shaped cells and anaplastic features can be present. Immunohistochemically, DLBCL stains strongly positive for CD20 and B-cell lymphoma 2 (Bcl-2) along with other pan–B-cell markers.^9-11 The aggressive leg type of DLBCL stains positively for multiple myeloma oncogene 1 (MUM-1).^9,11

Cutaneous metastatic adenocarcinoma from internal malignancies occurs in approximately 5% of cancer patients with metastatic spread.¹² Most of these cutaneous lesions develop in close proximity to the primary tumor such as on the trunk, head, or neck. All cutaneous metastases carry a poor prognosis. Clinical presentation can vary greatly, ranging from painless, firm, or elastic nodules to lesions that mimic inflammatory skin conditions such as erysipelas or scleroderma. The majority of these metastases develop as painless firm nodules that are flesh colored, pink, red-brown, or purple.^12,13 The histopathology of metastatic adenocarcinoma demonstrates an infiltrative nodular appearance, though there rarely are well-circumscribed nodules found.¹³ The lesion originates in the dermis or subcutaneous tissue. It is a glandulartype lesion that may reflect the tissue of the primary tumor (Figure 4).^12,14 Immunohistochemical stains likely will remain consistent with those of the primary tumor, which is not always the case.¹⁴

Merkel cell carcinoma (MCC) is an aggressive cutaneous malignancy of epithelial and neuroendocrine origin, first described as trabecular carcinoma due to the arrangement of tumor resembling cancellous bone.^15,16 Merkel cells are mechanoreceptors found near nerve terminals.¹⁷ Approximately 80% of MCCs are associated with Merkel cell polyomavirus, which is a small, double-stranded DNA virus with an icosahedral capsid.^17,18 Merkel cell polyomavirus–positive cases of MCC tend to have a better prognosis. In Merkel cell polyomavirus–negative MCC, there is an association with UV damage and increased chromosomal aberrations.¹⁸ Merkel cell carcinoma is known for its high rate of recurrence as well as local and distant metastasis. Nodal involvement is the most important prognostic indicator.¹⁵ Clinically, MCC is associated with the AEIOU mnemonic (asymptomatic, expanding rapidly, immunosuppression, older than 50 years, UV exposed/fair skin).^15-17 Lesions appear as red-blue papules on sun-exposed skin and usually are smaller than 2 cm by their greatest dimension. On histopathology, MCC demonstrates small, round, blue cells arranged in sheets or nests originating in the dermis and occasionally can infiltrate the subcutis and lymphovascular surroundings (Figure 5).^16-19 Cells have scant eosinophilic cytoplasm and may have fine granular chromatin. Numerous mitotic figures and apoptotic cells also are present. On immunohistochemistry, these cells will stain positive for cytokeratin AE1/AE3, anticytokeratin (CAM 5.2), CK20, and CD56. Due to their neuroendocrine derivation, they also are commonly synaptophysin, neuron-specific enolase, and chromogranin A positive. Notably, MCC will stain negative for leukocyte common antigen, CD20, CD3, CD34, and thyroid transcription factor 1 (TTF-1).^16,17

Primary cutaneous γδ T-cell lymphoma can be difficult to diagnose and requires urgent treatment. Clinicians and dermatopathologists need to work together to establish the diagnosis. There is a high mortality rate associated with PCGDTL, making prompt recognition and timely treatment critical. Acknowledgments—Thank you to our colleagues with the Penn State Health Hematology/Oncology Department (Hershey, Pennsylvania) for comanagement of this patient.

Acknowledgments
Thank you to our colleagues with the Penn State Health Hematology/Oncology Department (Hershey, Pennsylvania) for comanagement of this patient.

Bariatric surgery resolved nonalcoholic steatohepatitis (NASH) without worsening fibrosis in 84% of patients with evaluable biopsies, according to the findings of a prospective study.

The study included 180 severely or morbidly obese adults (body mass index >35 kg/m²) with NASH who underwent bariatric surgery at a center in France. Among 94 patients evaluated 5 years later, 68% had follow-up liver biopsies, of whom 84% (95% confidence interval, 73.1%-92.2%) met the primary endpoint of resolution of NASH without worsening of fibrosis. All histologic aspects of NASH had improved, median nonalcoholic fatty liver disease scores (NAS) fell from 5 (interquartile range, 4 to 5) to 1 (IQR, 0-2; P < .001), and 90% of patients achieved at least a 2-point NAS improvement. Hepatocellular ballooning also improved in 87.5% of patients. Baseline severity of NASH did not affect the chances of it resolving at 5 years. “The reduction of fibrosis [was] progressive, beginning during the first year and continuing through 5 years,” Guillaume Lassailly, MD, and associates wrote in Gastroenterology.

NASH is a priority for clinical research because of the substantial risk for subsequent cirrhosis, added Dr. Lassailly of CHU Lille (France). For NASH to resolve, most patients need to lose at least 7%-10% of their body weight, but “only 10% of patients reach this objective with lifestyle therapy at 1 year, and less than half maintain the weight loss 5 years later.” Despite ongoing drug development efforts, no medications have been approved for treating NASH. Although weight loss after bariatric surgery has been reported to resolve NASH in approximately 80% of patients at 1 year, longer-term data have been unavailable, and it has remained unclear whether bariatric surgery can slow or halt fibrosis progression.

All patients in this study had biopsy-confirmed NASH and at least a 5-year history of severe or morbid obesity as well as at least one comorbidity, such as diabetes mellitus or arterial hypertension. Patients were not heavy drinkers, and none had detectable markers of chronic liver disease.

Bariatric surgery produced a median 12-kg/m² drop in body mass index. At 5-year follow-up, 93% of patients meeting or exceeding this threshold who had biopsies performed showed resolution of NASH without worsening of fibrosis. Furthermore, 56% of patients (95% CI, 42.4%-69.3%) had no histologic evidence of fibrosis, including 45.5% of patients who had bridging fibrosis at baseline.

Participants in this study received intensive preoperative support, including evaluations by numerous specialists, a nutrition plan, and a 6- to 12-month therapeutic education program. Bariatric surgery techniques included Roux-en-Y gastric bypass, gastric banding, and sleeve gastrectomy. A subgroup analysis linked gastric bypass to a significantly higher probability of meeting the primary endpoint, compared with gastric banding. Refusal was the most common reason for not having a follow-up biopsy, the researchers said. “Patients without liver biopsy after bariatric surgery were not significantly different from those with a histological follow-up except for a lower BMI at 1 year. Baseline fibrosis did not influence the probability of undergoing histological reevaluation at 5 years.”

Two study participants died from surgical complications within 1 month after surgery, and one patient died from cardiac dysfunction 4 years later. No fatality was deemed liver related.

The study was funded by the French Ministry of Health, Conseil Régional Nord-Pas de Calais, National de la Recherche, and the European commission (FEDER). The researchers reported having no conflicts of interest.

SOURCE: Lassailly G et al. Gastroenterology. 2020 Jun 15. doi: 10.1053/j.gastro.2020.06.006.

Bariatric surgery resolved nonalcoholic steatohepatitis (NASH) without worsening fibrosis in 84% of patients with evaluable biopsies, according to the findings of a prospective study.

The study included 180 severely or morbidly obese adults (body mass index >35 kg/m²) with NASH who underwent bariatric surgery at a center in France. Among 94 patients evaluated 5 years later, 68% had follow-up liver biopsies, of whom 84% (95% confidence interval, 73.1%-92.2%) met the primary endpoint of resolution of NASH without worsening of fibrosis. All histologic aspects of NASH had improved, median nonalcoholic fatty liver disease scores (NAS) fell from 5 (interquartile range, 4 to 5) to 1 (IQR, 0-2; P < .001), and 90% of patients achieved at least a 2-point NAS improvement. Hepatocellular ballooning also improved in 87.5% of patients. Baseline severity of NASH did not affect the chances of it resolving at 5 years. “The reduction of fibrosis [was] progressive, beginning during the first year and continuing through 5 years,” Guillaume Lassailly, MD, and associates wrote in Gastroenterology.

NASH is a priority for clinical research because of the substantial risk for subsequent cirrhosis, added Dr. Lassailly of CHU Lille (France). For NASH to resolve, most patients need to lose at least 7%-10% of their body weight, but “only 10% of patients reach this objective with lifestyle therapy at 1 year, and less than half maintain the weight loss 5 years later.” Despite ongoing drug development efforts, no medications have been approved for treating NASH. Although weight loss after bariatric surgery has been reported to resolve NASH in approximately 80% of patients at 1 year, longer-term data have been unavailable, and it has remained unclear whether bariatric surgery can slow or halt fibrosis progression.

All patients in this study had biopsy-confirmed NASH and at least a 5-year history of severe or morbid obesity as well as at least one comorbidity, such as diabetes mellitus or arterial hypertension. Patients were not heavy drinkers, and none had detectable markers of chronic liver disease.

Bariatric surgery produced a median 12-kg/m² drop in body mass index. At 5-year follow-up, 93% of patients meeting or exceeding this threshold who had biopsies performed showed resolution of NASH without worsening of fibrosis. Furthermore, 56% of patients (95% CI, 42.4%-69.3%) had no histologic evidence of fibrosis, including 45.5% of patients who had bridging fibrosis at baseline.

Participants in this study received intensive preoperative support, including evaluations by numerous specialists, a nutrition plan, and a 6- to 12-month therapeutic education program. Bariatric surgery techniques included Roux-en-Y gastric bypass, gastric banding, and sleeve gastrectomy. A subgroup analysis linked gastric bypass to a significantly higher probability of meeting the primary endpoint, compared with gastric banding. Refusal was the most common reason for not having a follow-up biopsy, the researchers said. “Patients without liver biopsy after bariatric surgery were not significantly different from those with a histological follow-up except for a lower BMI at 1 year. Baseline fibrosis did not influence the probability of undergoing histological reevaluation at 5 years.”

Two study participants died from surgical complications within 1 month after surgery, and one patient died from cardiac dysfunction 4 years later. No fatality was deemed liver related.

The study was funded by the French Ministry of Health, Conseil Régional Nord-Pas de Calais, National de la Recherche, and the European commission (FEDER). The researchers reported having no conflicts of interest.

SOURCE: Lassailly G et al. Gastroenterology. 2020 Jun 15. doi: 10.1053/j.gastro.2020.06.006.

Bariatric surgery resolved nonalcoholic steatohepatitis (NASH) without worsening fibrosis in 84% of patients with evaluable biopsies, according to the findings of a prospective study.

The study included 180 severely or morbidly obese adults (body mass index >35 kg/m²) with NASH who underwent bariatric surgery at a center in France. Among 94 patients evaluated 5 years later, 68% had follow-up liver biopsies, of whom 84% (95% confidence interval, 73.1%-92.2%) met the primary endpoint of resolution of NASH without worsening of fibrosis. All histologic aspects of NASH had improved, median nonalcoholic fatty liver disease scores (NAS) fell from 5 (interquartile range, 4 to 5) to 1 (IQR, 0-2; P < .001), and 90% of patients achieved at least a 2-point NAS improvement. Hepatocellular ballooning also improved in 87.5% of patients. Baseline severity of NASH did not affect the chances of it resolving at 5 years. “The reduction of fibrosis [was] progressive, beginning during the first year and continuing through 5 years,” Guillaume Lassailly, MD, and associates wrote in Gastroenterology.

NASH is a priority for clinical research because of the substantial risk for subsequent cirrhosis, added Dr. Lassailly of CHU Lille (France). For NASH to resolve, most patients need to lose at least 7%-10% of their body weight, but “only 10% of patients reach this objective with lifestyle therapy at 1 year, and less than half maintain the weight loss 5 years later.” Despite ongoing drug development efforts, no medications have been approved for treating NASH. Although weight loss after bariatric surgery has been reported to resolve NASH in approximately 80% of patients at 1 year, longer-term data have been unavailable, and it has remained unclear whether bariatric surgery can slow or halt fibrosis progression.

All patients in this study had biopsy-confirmed NASH and at least a 5-year history of severe or morbid obesity as well as at least one comorbidity, such as diabetes mellitus or arterial hypertension. Patients were not heavy drinkers, and none had detectable markers of chronic liver disease.

Bariatric surgery produced a median 12-kg/m² drop in body mass index. At 5-year follow-up, 93% of patients meeting or exceeding this threshold who had biopsies performed showed resolution of NASH without worsening of fibrosis. Furthermore, 56% of patients (95% CI, 42.4%-69.3%) had no histologic evidence of fibrosis, including 45.5% of patients who had bridging fibrosis at baseline.

Participants in this study received intensive preoperative support, including evaluations by numerous specialists, a nutrition plan, and a 6- to 12-month therapeutic education program. Bariatric surgery techniques included Roux-en-Y gastric bypass, gastric banding, and sleeve gastrectomy. A subgroup analysis linked gastric bypass to a significantly higher probability of meeting the primary endpoint, compared with gastric banding. Refusal was the most common reason for not having a follow-up biopsy, the researchers said. “Patients without liver biopsy after bariatric surgery were not significantly different from those with a histological follow-up except for a lower BMI at 1 year. Baseline fibrosis did not influence the probability of undergoing histological reevaluation at 5 years.”

Two study participants died from surgical complications within 1 month after surgery, and one patient died from cardiac dysfunction 4 years later. No fatality was deemed liver related.

The study was funded by the French Ministry of Health, Conseil Régional Nord-Pas de Calais, National de la Recherche, and the European commission (FEDER). The researchers reported having no conflicts of interest.

SOURCE: Lassailly G et al. Gastroenterology. 2020 Jun 15. doi: 10.1053/j.gastro.2020.06.006.

A new model of gastric cancer screening suggests that, for Asian Americans, endoscopic screening alongside colonoscopy and follow-up surveillance of gastric preneoplasia is a cost-effective strategy. Incremental cost-effectiveness ratios (ICERs) were lowest for Chinese, Japanese, and Korean Americans. The model simulated results for asymptomatic 50-year-old subjects.

Gastric cancer risk is highest in Asian Pacific, Latin American, and Eastern European countries. Asia Pacific countries alone represent about half of all new cases. Helicobacter pylori–related gastritis is the strongest known risk factor for intestinal-type noncardia gastric adenocarcinoma (NCGA), which is the most common gastric cancer, and this chronic inflammation can lead to gastric intestinal metaplasia (GIM). Individuals with GIM have a 0.16% increased annual risk of NCGA, which makes them good candidates for endoscopic screening that could catch new cancers at an early stage.

In a previous study (Gastroenterology. 2018 May 17;155[3]:648-60), researchers at Vanderbilt University Medical Center in Durham, N.C., at Boston University School of Medicine, and at the University of Pennsylvania in Philadelphia showed that, in asymptomatic 50-year-old Asian Americans, Hispanic patients, and non-Hispanic Black patients, performing a single esophagogastroduodenoscopy (EGD) concomitantly with a colonoscopy, followed by screening EGDs if indicated (such as for a GIM diagnosis), is a cost-effective strategy. They found ongoing screening was not cost effective if the original results were normal.

In the new study published in Gastroenterology and Hepatology, the researchers followed up this finding with an attempt to tease out the cost-effectiveness of screening in different subgroups, as well as by sex. They built a Markov decision model focusing on the six most common Asian groups in the United States: Chinese, Filipino, Southeast Asian, Vietnamese, Korean, and Japanese Americans.

Model inputs were based on the published literature, and the outputs were compared with data from the Surveillance, Epidemiology, and End Results (SEER) data for disaggregated Asian Americans between 2001 and 2014 and separately with the California Cancer Registry (2011-2015). The model produced a good fit to the epidemiological data.

The model then compared cost-effectiveness of three hypothetical screening strategies in asymptomatic 50-year-old Asian Americans: one-time upper EGD with biopsies conducted at the time of colonoscopies for colorectal cancer screening, followed by EGDs every 3 years if GIM was detected (or other appropriate management of higher-grade pathology); EGD with biopsy at a colonoscopy for CRC screening followed by EGD biennially regardless of initial findings; and no endoscopy screening.

The one-time EGD strategy was the most cost-effective, regardless of sex, with an ICER of $75,959 per quality-adjusted life-year (QALY) in males and $74,329/QALY in females. The lowest ICER was found for Chinese Americans (males and females, $68,256/QALY), followed by Japanese Americans (males, $69,011/QALY; females, $73,748/QALY), and Korean Americans (males, $70,739/ QALY; females, $70,236/QALY). The highest ICERs were among Filipino American males and females, but the strategy was still cost-effective at the predetermined willingness-to-pay threshold of $100,000 ($83,732/QALY).

In all ethnic groups, the biennial screening strategy produced more harm than good and was costlier.

The authors believe that the strategy could be applied to other ethnic groups that come from countries with populations at higher relative risk of gastric cancer, such as Central and Latin American countries.

Asked to comment on the study, Mimi Tan, MD, an assistant professor of gastroenterology at Baylor College of Medicine in Houston, suggested that the estimates of precancerous lesions used in the Markov model were quite high because they were based on pathology databases. These sources tend to be biased toward symptomatic individuals since these are the patients typically referred for upper endoscopy biopsies. “Therefore, these probabilities may not represent true probability of these precancerous lesions among asymptomatic screening populations,” Dr. Tan said in an interview. She also questioned whether the study represented the true risk in female populations since the literature for women is sparse.

Dr. Tan suggested that a more cost-effective screening strategy might be one-time H. pylori immunoglobulin G testing in Asian Americans. The Houston Consensus Conference on Testing for H. pylori Infection already recommends testing for first-generation immigrants from high prevalence areas and Latino and African American racial or ethnic groups (Clin Gastroenterol Hepatol. 2018 Jul;16[7]:992-1002). “Future studies should compare cost-effectiveness of one-time upper endoscopy, which is more costly but able to detect premalignant lesions, to one-time H. pylori testing,” said Dr. Tan.

SOURCE: Shah SC et al. Clin Gastroenterol Hepatol. 2020 July 21. doi: 10.1016/j.cgh.2020.07.031.

A new model of gastric cancer screening suggests that, for Asian Americans, endoscopic screening alongside colonoscopy and follow-up surveillance of gastric preneoplasia is a cost-effective strategy. Incremental cost-effectiveness ratios (ICERs) were lowest for Chinese, Japanese, and Korean Americans. The model simulated results for asymptomatic 50-year-old subjects.

Gastric cancer risk is highest in Asian Pacific, Latin American, and Eastern European countries. Asia Pacific countries alone represent about half of all new cases. Helicobacter pylori–related gastritis is the strongest known risk factor for intestinal-type noncardia gastric adenocarcinoma (NCGA), which is the most common gastric cancer, and this chronic inflammation can lead to gastric intestinal metaplasia (GIM). Individuals with GIM have a 0.16% increased annual risk of NCGA, which makes them good candidates for endoscopic screening that could catch new cancers at an early stage.

In a previous study (Gastroenterology. 2018 May 17;155[3]:648-60), researchers at Vanderbilt University Medical Center in Durham, N.C., at Boston University School of Medicine, and at the University of Pennsylvania in Philadelphia showed that, in asymptomatic 50-year-old Asian Americans, Hispanic patients, and non-Hispanic Black patients, performing a single esophagogastroduodenoscopy (EGD) concomitantly with a colonoscopy, followed by screening EGDs if indicated (such as for a GIM diagnosis), is a cost-effective strategy. They found ongoing screening was not cost effective if the original results were normal.

In the new study published in Gastroenterology and Hepatology, the researchers followed up this finding with an attempt to tease out the cost-effectiveness of screening in different subgroups, as well as by sex. They built a Markov decision model focusing on the six most common Asian groups in the United States: Chinese, Filipino, Southeast Asian, Vietnamese, Korean, and Japanese Americans.

Model inputs were based on the published literature, and the outputs were compared with data from the Surveillance, Epidemiology, and End Results (SEER) data for disaggregated Asian Americans between 2001 and 2014 and separately with the California Cancer Registry (2011-2015). The model produced a good fit to the epidemiological data.

The model then compared cost-effectiveness of three hypothetical screening strategies in asymptomatic 50-year-old Asian Americans: one-time upper EGD with biopsies conducted at the time of colonoscopies for colorectal cancer screening, followed by EGDs every 3 years if GIM was detected (or other appropriate management of higher-grade pathology); EGD with biopsy at a colonoscopy for CRC screening followed by EGD biennially regardless of initial findings; and no endoscopy screening.

The one-time EGD strategy was the most cost-effective, regardless of sex, with an ICER of $75,959 per quality-adjusted life-year (QALY) in males and $74,329/QALY in females. The lowest ICER was found for Chinese Americans (males and females, $68,256/QALY), followed by Japanese Americans (males, $69,011/QALY; females, $73,748/QALY), and Korean Americans (males, $70,739/ QALY; females, $70,236/QALY). The highest ICERs were among Filipino American males and females, but the strategy was still cost-effective at the predetermined willingness-to-pay threshold of $100,000 ($83,732/QALY).

In all ethnic groups, the biennial screening strategy produced more harm than good and was costlier.

The authors believe that the strategy could be applied to other ethnic groups that come from countries with populations at higher relative risk of gastric cancer, such as Central and Latin American countries.

Asked to comment on the study, Mimi Tan, MD, an assistant professor of gastroenterology at Baylor College of Medicine in Houston, suggested that the estimates of precancerous lesions used in the Markov model were quite high because they were based on pathology databases. These sources tend to be biased toward symptomatic individuals since these are the patients typically referred for upper endoscopy biopsies. “Therefore, these probabilities may not represent true probability of these precancerous lesions among asymptomatic screening populations,” Dr. Tan said in an interview. She also questioned whether the study represented the true risk in female populations since the literature for women is sparse.

Dr. Tan suggested that a more cost-effective screening strategy might be one-time H. pylori immunoglobulin G testing in Asian Americans. The Houston Consensus Conference on Testing for H. pylori Infection already recommends testing for first-generation immigrants from high prevalence areas and Latino and African American racial or ethnic groups (Clin Gastroenterol Hepatol. 2018 Jul;16[7]:992-1002). “Future studies should compare cost-effectiveness of one-time upper endoscopy, which is more costly but able to detect premalignant lesions, to one-time H. pylori testing,” said Dr. Tan.

SOURCE: Shah SC et al. Clin Gastroenterol Hepatol. 2020 July 21. doi: 10.1016/j.cgh.2020.07.031.

A new model of gastric cancer screening suggests that, for Asian Americans, endoscopic screening alongside colonoscopy and follow-up surveillance of gastric preneoplasia is a cost-effective strategy. Incremental cost-effectiveness ratios (ICERs) were lowest for Chinese, Japanese, and Korean Americans. The model simulated results for asymptomatic 50-year-old subjects.

Gastric cancer risk is highest in Asian Pacific, Latin American, and Eastern European countries. Asia Pacific countries alone represent about half of all new cases. Helicobacter pylori–related gastritis is the strongest known risk factor for intestinal-type noncardia gastric adenocarcinoma (NCGA), which is the most common gastric cancer, and this chronic inflammation can lead to gastric intestinal metaplasia (GIM). Individuals with GIM have a 0.16% increased annual risk of NCGA, which makes them good candidates for endoscopic screening that could catch new cancers at an early stage.

In a previous study (Gastroenterology. 2018 May 17;155[3]:648-60), researchers at Vanderbilt University Medical Center in Durham, N.C., at Boston University School of Medicine, and at the University of Pennsylvania in Philadelphia showed that, in asymptomatic 50-year-old Asian Americans, Hispanic patients, and non-Hispanic Black patients, performing a single esophagogastroduodenoscopy (EGD) concomitantly with a colonoscopy, followed by screening EGDs if indicated (such as for a GIM diagnosis), is a cost-effective strategy. They found ongoing screening was not cost effective if the original results were normal.

In the new study published in Gastroenterology and Hepatology, the researchers followed up this finding with an attempt to tease out the cost-effectiveness of screening in different subgroups, as well as by sex. They built a Markov decision model focusing on the six most common Asian groups in the United States: Chinese, Filipino, Southeast Asian, Vietnamese, Korean, and Japanese Americans.

Model inputs were based on the published literature, and the outputs were compared with data from the Surveillance, Epidemiology, and End Results (SEER) data for disaggregated Asian Americans between 2001 and 2014 and separately with the California Cancer Registry (2011-2015). The model produced a good fit to the epidemiological data.

The model then compared cost-effectiveness of three hypothetical screening strategies in asymptomatic 50-year-old Asian Americans: one-time upper EGD with biopsies conducted at the time of colonoscopies for colorectal cancer screening, followed by EGDs every 3 years if GIM was detected (or other appropriate management of higher-grade pathology); EGD with biopsy at a colonoscopy for CRC screening followed by EGD biennially regardless of initial findings; and no endoscopy screening.

The one-time EGD strategy was the most cost-effective, regardless of sex, with an ICER of $75,959 per quality-adjusted life-year (QALY) in males and $74,329/QALY in females. The lowest ICER was found for Chinese Americans (males and females, $68,256/QALY), followed by Japanese Americans (males, $69,011/QALY; females, $73,748/QALY), and Korean Americans (males, $70,739/ QALY; females, $70,236/QALY). The highest ICERs were among Filipino American males and females, but the strategy was still cost-effective at the predetermined willingness-to-pay threshold of $100,000 ($83,732/QALY).

In all ethnic groups, the biennial screening strategy produced more harm than good and was costlier.

The authors believe that the strategy could be applied to other ethnic groups that come from countries with populations at higher relative risk of gastric cancer, such as Central and Latin American countries.

Asked to comment on the study, Mimi Tan, MD, an assistant professor of gastroenterology at Baylor College of Medicine in Houston, suggested that the estimates of precancerous lesions used in the Markov model were quite high because they were based on pathology databases. These sources tend to be biased toward symptomatic individuals since these are the patients typically referred for upper endoscopy biopsies. “Therefore, these probabilities may not represent true probability of these precancerous lesions among asymptomatic screening populations,” Dr. Tan said in an interview. She also questioned whether the study represented the true risk in female populations since the literature for women is sparse.

Dr. Tan suggested that a more cost-effective screening strategy might be one-time H. pylori immunoglobulin G testing in Asian Americans. The Houston Consensus Conference on Testing for H. pylori Infection already recommends testing for first-generation immigrants from high prevalence areas and Latino and African American racial or ethnic groups (Clin Gastroenterol Hepatol. 2018 Jul;16[7]:992-1002). “Future studies should compare cost-effectiveness of one-time upper endoscopy, which is more costly but able to detect premalignant lesions, to one-time H. pylori testing,” said Dr. Tan.

SOURCE: Shah SC et al. Clin Gastroenterol Hepatol. 2020 July 21. doi: 10.1016/j.cgh.2020.07.031.

The rising incidence of colorectal cancer in adults younger than 50 years heightens the need to evaluate the colon and rectum of any patient, regardless of age, who presents with symptoms such as rectal bleeding, weight loss, abdominal pain, iron-deficiency anemia, or changes in bowel habits, according to a new American Gastroenterological Association clinical practice update.

In addition to receiving cancer staging or being referred to an oncologist, newly diagnosed patients should be counseled about both germline genetic testing and fertility preservation, wrote Lisa A. Boardman, MD, of Mayo Clinic in Rochester, Minn., with associates in Clinical Gastroenterology and Hepatology. “Clinicians should present the role of fertility preservation prior to [administering] cancer-directed therapy, including surgery, pelvic radiation, or chemotherapy.”

It remains unclear why the incidence of young adult–onset colorectal cancer is rising, but the trend is not limited to the United States. Implicated risk factors include inflammatory bowel disease, prior irradiation, harboring a pathogenic germline mutation for a known hereditary cancer syndrome, and having a first- or second-degree relative with colorectal cancer. Indeed, the odds of developing young adult–onset disease are nearly 4 times higher if a parent has colorectal cancer and nearly 12 times higher if a sibling is affected.

For newly diagnosed young adults, it is important to collect a family cancer history but vital, regardless of history, to discuss targeted or multiplex germline mutation testing. Detecting hereditary colorectal cancer syndromes is crucial because their nature informs surgical options for treatment. “Roughly one in five young adult–onset colorectal cancers will be caused by a germline mutation, and among those with a detectable hereditary condition, half of those patients with young adult–onset colorectal cancer will have Lynch syndrome,” the experts noted. For these patients (who have mutations involving MSH2, EPCAM, MLH1, MSH6, and PMS2), ileorectostomy (IRA) for colorectal cancer should be considered.

For patients with the classic subtype of familial adenomatous polyposis, ileal pouch anal anastomosis is recommended after the polyp burden can no longer be managed endoscopically, although initial IRA with subsequent conversion to IPAA is an option for women of child-bearing age, according to the clinical practice update. Patients with the attenuated subtype of familial adenomatous polyposis should consider IRA or colectomy if colorectal cancer develops or if the polyp burden exceeds endoscopic control. In contrast, colectomy is the only type of surgery recommended for patients with serrated polyposis syndrome requiring surgical treatment.

Finally, clinicians should offer only screening for hereditary cancer syndromes if young adults cancer have been diagnosed with a hereditary colorectal cancer syndrome. “For patients with sporadic young adult–onset colorectal cancer, extracolonic screening and colorectal cancer surveillance intervals are the same as for patients with older adult–onset colorectal cancer,” the experts wrote. For young patients without an apparent underlying genetic syndrome, molecular studies may eventually help tailor treatment options, “but at this point, more extensive surgery or more aggressive chemotherapy cannot be recommended. As cancer treatments evolve to use patient tumor specific therapeutics, our management of patients with young adult–onset colorectal cancer will improve.”

Dr. Boardman and associates reported having no relevant conflicts of interest.

SOURCE: Boardman LA et al. Clin Gastroenterol Hepatol. 2020 Jun 7. doi: 10.1016/j.cgh.2020.05.058.
 

The rising incidence of colorectal cancer in adults younger than 50 years heightens the need to evaluate the colon and rectum of any patient, regardless of age, who presents with symptoms such as rectal bleeding, weight loss, abdominal pain, iron-deficiency anemia, or changes in bowel habits, according to a new American Gastroenterological Association clinical practice update.

In addition to receiving cancer staging or being referred to an oncologist, newly diagnosed patients should be counseled about both germline genetic testing and fertility preservation, wrote Lisa A. Boardman, MD, of Mayo Clinic in Rochester, Minn., with associates in Clinical Gastroenterology and Hepatology. “Clinicians should present the role of fertility preservation prior to [administering] cancer-directed therapy, including surgery, pelvic radiation, or chemotherapy.”

It remains unclear why the incidence of young adult–onset colorectal cancer is rising, but the trend is not limited to the United States. Implicated risk factors include inflammatory bowel disease, prior irradiation, harboring a pathogenic germline mutation for a known hereditary cancer syndrome, and having a first- or second-degree relative with colorectal cancer. Indeed, the odds of developing young adult–onset disease are nearly 4 times higher if a parent has colorectal cancer and nearly 12 times higher if a sibling is affected.

For newly diagnosed young adults, it is important to collect a family cancer history but vital, regardless of history, to discuss targeted or multiplex germline mutation testing. Detecting hereditary colorectal cancer syndromes is crucial because their nature informs surgical options for treatment. “Roughly one in five young adult–onset colorectal cancers will be caused by a germline mutation, and among those with a detectable hereditary condition, half of those patients with young adult–onset colorectal cancer will have Lynch syndrome,” the experts noted. For these patients (who have mutations involving MSH2, EPCAM, MLH1, MSH6, and PMS2), ileorectostomy (IRA) for colorectal cancer should be considered.

For patients with the classic subtype of familial adenomatous polyposis, ileal pouch anal anastomosis is recommended after the polyp burden can no longer be managed endoscopically, although initial IRA with subsequent conversion to IPAA is an option for women of child-bearing age, according to the clinical practice update. Patients with the attenuated subtype of familial adenomatous polyposis should consider IRA or colectomy if colorectal cancer develops or if the polyp burden exceeds endoscopic control. In contrast, colectomy is the only type of surgery recommended for patients with serrated polyposis syndrome requiring surgical treatment.

Finally, clinicians should offer only screening for hereditary cancer syndromes if young adults cancer have been diagnosed with a hereditary colorectal cancer syndrome. “For patients with sporadic young adult–onset colorectal cancer, extracolonic screening and colorectal cancer surveillance intervals are the same as for patients with older adult–onset colorectal cancer,” the experts wrote. For young patients without an apparent underlying genetic syndrome, molecular studies may eventually help tailor treatment options, “but at this point, more extensive surgery or more aggressive chemotherapy cannot be recommended. As cancer treatments evolve to use patient tumor specific therapeutics, our management of patients with young adult–onset colorectal cancer will improve.”

Dr. Boardman and associates reported having no relevant conflicts of interest.

SOURCE: Boardman LA et al. Clin Gastroenterol Hepatol. 2020 Jun 7. doi: 10.1016/j.cgh.2020.05.058.
 

The rising incidence of colorectal cancer in adults younger than 50 years heightens the need to evaluate the colon and rectum of any patient, regardless of age, who presents with symptoms such as rectal bleeding, weight loss, abdominal pain, iron-deficiency anemia, or changes in bowel habits, according to a new American Gastroenterological Association clinical practice update.

In addition to receiving cancer staging or being referred to an oncologist, newly diagnosed patients should be counseled about both germline genetic testing and fertility preservation, wrote Lisa A. Boardman, MD, of Mayo Clinic in Rochester, Minn., with associates in Clinical Gastroenterology and Hepatology. “Clinicians should present the role of fertility preservation prior to [administering] cancer-directed therapy, including surgery, pelvic radiation, or chemotherapy.”

It remains unclear why the incidence of young adult–onset colorectal cancer is rising, but the trend is not limited to the United States. Implicated risk factors include inflammatory bowel disease, prior irradiation, harboring a pathogenic germline mutation for a known hereditary cancer syndrome, and having a first- or second-degree relative with colorectal cancer. Indeed, the odds of developing young adult–onset disease are nearly 4 times higher if a parent has colorectal cancer and nearly 12 times higher if a sibling is affected.

For newly diagnosed young adults, it is important to collect a family cancer history but vital, regardless of history, to discuss targeted or multiplex germline mutation testing. Detecting hereditary colorectal cancer syndromes is crucial because their nature informs surgical options for treatment. “Roughly one in five young adult–onset colorectal cancers will be caused by a germline mutation, and among those with a detectable hereditary condition, half of those patients with young adult–onset colorectal cancer will have Lynch syndrome,” the experts noted. For these patients (who have mutations involving MSH2, EPCAM, MLH1, MSH6, and PMS2), ileorectostomy (IRA) for colorectal cancer should be considered.

For patients with the classic subtype of familial adenomatous polyposis, ileal pouch anal anastomosis is recommended after the polyp burden can no longer be managed endoscopically, although initial IRA with subsequent conversion to IPAA is an option for women of child-bearing age, according to the clinical practice update. Patients with the attenuated subtype of familial adenomatous polyposis should consider IRA or colectomy if colorectal cancer develops or if the polyp burden exceeds endoscopic control. In contrast, colectomy is the only type of surgery recommended for patients with serrated polyposis syndrome requiring surgical treatment.

Finally, clinicians should offer only screening for hereditary cancer syndromes if young adults cancer have been diagnosed with a hereditary colorectal cancer syndrome. “For patients with sporadic young adult–onset colorectal cancer, extracolonic screening and colorectal cancer surveillance intervals are the same as for patients with older adult–onset colorectal cancer,” the experts wrote. For young patients without an apparent underlying genetic syndrome, molecular studies may eventually help tailor treatment options, “but at this point, more extensive surgery or more aggressive chemotherapy cannot be recommended. As cancer treatments evolve to use patient tumor specific therapeutics, our management of patients with young adult–onset colorectal cancer will improve.”

Dr. Boardman and associates reported having no relevant conflicts of interest.

SOURCE: Boardman LA et al. Clin Gastroenterol Hepatol. 2020 Jun 7. doi: 10.1016/j.cgh.2020.05.058.
 

I have been studying, writing about, and treating posttraumatic stress disorder for many years. Over this time, I have seen PTSD expand to more and more areas of life, including my own view of a “subthreshold” version, which occurs in vulnerable people who experience a job loss, divorce, financial setbacks, or any number of painful life events.

As I noted in my recent book, “Find Freedom Fast,” for some people, PTSD can be triggered in the wake of events that are not life-threatening yet catastrophic for them and not tied to manmade or natural disasters, torture, assault, or war zone experiences.

The expansion of PTSD has led to the disorder being recognized in ICU patients during and after recovery (Crit Care Med. 2015 May;43[5]:1121-9), as well as in people diagnosed with cancer (Lancet Psychiatry. 2017 Apr;4[4]:330-8) and other illnesses that may cause emotional trauma – where one feels that one’s life is threatened. In some instances, the person’s life might indeed be in danger, not unlike what can happen in disasters, wars, torture, and even in some encounters with law enforcement.

This leads me to yet another circumstance that in some, may be tied to PTSD – and that is racial, religious, ethnic, and gender-related bigotry. In these cases, individuals feel threatened just for who they are in a society. Being on the receiving end of a circumstance that threatens a person’s very existence would seem to me to place a person as a potential survivor of PTSD, as well as any number of disorders, including anxiety, depression, or even paranoia.

Yes, discrimination and prejudice have been with us for a long time, and what concerns me is the psychological effect it has on children as well as adults. Friends of Irish descent remind me of hearing stories from parents and grandparents about employment signs reading, “Irish need not apply.” Certainly, those of Italian ancestry will easily recall the prejudice focused against them. And members of the Jewish community also can easily remember the bigotry and exclusion they have been subject to in certain neighborhoods and organizations, in addition to the horrors of the Holocaust during World War II, and the anti-Semitic chants in Charlottesville, Va., from just 3 years ago – with gun-carrying militants doing the chanting.

Obviously, in certain circles, we still have private clubs, plus neighborhoods and residential buildings that exclude people for a variety of reasons.

Coming from a medical family, years ago I heard stories that, if you were Roman Catholic, it would be hard to get into certain medical schools – which might explain the establishment of Catholic medical schools that often were open to people of other faiths. Then we had medical school discrimination toward Jewish students, which was followed by the establishment of medical schools focused on admitting more Jewish students. The African American community also responded to discrimination by establishing medical schools, such as the school at Howard University in Washington.

Furthermore, we cannot forget the discrimination that women faced in institutions of higher learning. My father had two women in his medical school class, I was told. In my era, I would say at least 30% were women, and today, in the United States, medical school classes are more equally balanced with men and women. Some schools have more women than men.

The question I ask, is: How did all those women feel for so many years knowing that, for reasons beyond their control, they were prevented from achieving their chosen goals? Some might have felt badly, and others might have internalized the rejection. Others might have developed PTSD based on feelings of rejection.

However, the question here mainly is: Can PTSD result when exclusion and prejudice induce fear and terror in those on the receiving end – especially innocent children? Children separated from their parents at the U.S.-Mexico border and those who witness their parents being shot immediately come to mind. This trauma can last well beyond childhood.

What we know today about structural racism should give the mental health community pause and make us realize the extent to which the African American community has been traumatized. Perhaps we should not be surprised by a study that found that the prevalence of PTSD among African Americans is 9.1%, compared with 6.8% for Whites (J Anxiety Dis. 2009 Jun;23[5]:573-90). Speaking with Black colleagues, friends, and patients, reading books such “The Warmth of Other Suns,” and watching films such as “Green Book,” give us a sense of how dangerous it was for Black families to travel in certain parts of the country in the recent past. I recall as a child hearing that, in Miami Beach, people of color could not stay overnight. (Even as a child I was surprised – having never heard anything like that. After all, I went to school with people of many religions and backgrounds. My parents thought those practices were terrible, and were appalled when they learned that some hotels were closed to Jews and others closed to Catholics.)
 

DSM-5, ICD-10 fall short

The DSM-5 describes trauma using a more or less one-dimensional set of guidelines as the focus. Those guidelines include exposure to direct violence, manmade or natural disasters, war, or torture, as well as exposure to a disaster or a life-threatening situation affecting a loved one. The ICD-10 is less restrictive about trauma but still has some limitations.

While considering potential PTSD, I try to use a less rigid diagnostic multidimensional approach, where I assess individual differences and experiences that play a role in those experiences as well as the patient’s vulnerability to the causation of PTSD – which also has to include any exposure to trauma (Curr Opin Psychol. 2017 Apr;14:29-34) before age 11 or 12. The data suggest that such early exposure leaves people more vulnerable to PTSD as adults (Soc Sci Med. 2018 Feb;199:230-40).

In my view, if individuals are frightened because of who they are – be it tied to their religion, race, sexual identity, or ethnicity – and what harm may come to them, and if they live in fear and avoidance of these potential traumatic situations that affect their mental stability and the way they live their lives, they might fit the PTSD model.

If we clinicians focus on what’s currently being brought vividly into the public eye today regarding the African American community, we would see that some of the ongoing fears of racism – whether tied to residential or workplace discrimination, unfair treatment by figures of authority, harassment, health inequities, or microaggressions – may give rise to PTSD. I know we can do better. We should broaden our definition and awareness of this very serious disorder – and be prepared to treat it.
 

Dr. London has been a practicing psychiatrist for 4 decades and a newspaper columnist for almost as long. He has a private practice in New York and is author of “Find Freedom Fast: Short-Term Therapy That Works” (New York: Kettlehole Publishing, 2019). Dr. London has no conflicts of interest.

I have been studying, writing about, and treating posttraumatic stress disorder for many years. Over this time, I have seen PTSD expand to more and more areas of life, including my own view of a “subthreshold” version, which occurs in vulnerable people who experience a job loss, divorce, financial setbacks, or any number of painful life events.

As I noted in my recent book, “Find Freedom Fast,” for some people, PTSD can be triggered in the wake of events that are not life-threatening yet catastrophic for them and not tied to manmade or natural disasters, torture, assault, or war zone experiences.

The expansion of PTSD has led to the disorder being recognized in ICU patients during and after recovery (Crit Care Med. 2015 May;43[5]:1121-9), as well as in people diagnosed with cancer (Lancet Psychiatry. 2017 Apr;4[4]:330-8) and other illnesses that may cause emotional trauma – where one feels that one’s life is threatened. In some instances, the person’s life might indeed be in danger, not unlike what can happen in disasters, wars, torture, and even in some encounters with law enforcement.

This leads me to yet another circumstance that in some, may be tied to PTSD – and that is racial, religious, ethnic, and gender-related bigotry. In these cases, individuals feel threatened just for who they are in a society. Being on the receiving end of a circumstance that threatens a person’s very existence would seem to me to place a person as a potential survivor of PTSD, as well as any number of disorders, including anxiety, depression, or even paranoia.

Yes, discrimination and prejudice have been with us for a long time, and what concerns me is the psychological effect it has on children as well as adults. Friends of Irish descent remind me of hearing stories from parents and grandparents about employment signs reading, “Irish need not apply.” Certainly, those of Italian ancestry will easily recall the prejudice focused against them. And members of the Jewish community also can easily remember the bigotry and exclusion they have been subject to in certain neighborhoods and organizations, in addition to the horrors of the Holocaust during World War II, and the anti-Semitic chants in Charlottesville, Va., from just 3 years ago – with gun-carrying militants doing the chanting.

Obviously, in certain circles, we still have private clubs, plus neighborhoods and residential buildings that exclude people for a variety of reasons.

Coming from a medical family, years ago I heard stories that, if you were Roman Catholic, it would be hard to get into certain medical schools – which might explain the establishment of Catholic medical schools that often were open to people of other faiths. Then we had medical school discrimination toward Jewish students, which was followed by the establishment of medical schools focused on admitting more Jewish students. The African American community also responded to discrimination by establishing medical schools, such as the school at Howard University in Washington.

Furthermore, we cannot forget the discrimination that women faced in institutions of higher learning. My father had two women in his medical school class, I was told. In my era, I would say at least 30% were women, and today, in the United States, medical school classes are more equally balanced with men and women. Some schools have more women than men.

The question I ask, is: How did all those women feel for so many years knowing that, for reasons beyond their control, they were prevented from achieving their chosen goals? Some might have felt badly, and others might have internalized the rejection. Others might have developed PTSD based on feelings of rejection.

However, the question here mainly is: Can PTSD result when exclusion and prejudice induce fear and terror in those on the receiving end – especially innocent children? Children separated from their parents at the U.S.-Mexico border and those who witness their parents being shot immediately come to mind. This trauma can last well beyond childhood.

What we know today about structural racism should give the mental health community pause and make us realize the extent to which the African American community has been traumatized. Perhaps we should not be surprised by a study that found that the prevalence of PTSD among African Americans is 9.1%, compared with 6.8% for Whites (J Anxiety Dis. 2009 Jun;23[5]:573-90). Speaking with Black colleagues, friends, and patients, reading books such “The Warmth of Other Suns,” and watching films such as “Green Book,” give us a sense of how dangerous it was for Black families to travel in certain parts of the country in the recent past. I recall as a child hearing that, in Miami Beach, people of color could not stay overnight. (Even as a child I was surprised – having never heard anything like that. After all, I went to school with people of many religions and backgrounds. My parents thought those practices were terrible, and were appalled when they learned that some hotels were closed to Jews and others closed to Catholics.)
 

DSM-5, ICD-10 fall short

The DSM-5 describes trauma using a more or less one-dimensional set of guidelines as the focus. Those guidelines include exposure to direct violence, manmade or natural disasters, war, or torture, as well as exposure to a disaster or a life-threatening situation affecting a loved one. The ICD-10 is less restrictive about trauma but still has some limitations.

While considering potential PTSD, I try to use a less rigid diagnostic multidimensional approach, where I assess individual differences and experiences that play a role in those experiences as well as the patient’s vulnerability to the causation of PTSD – which also has to include any exposure to trauma (Curr Opin Psychol. 2017 Apr;14:29-34) before age 11 or 12. The data suggest that such early exposure leaves people more vulnerable to PTSD as adults (Soc Sci Med. 2018 Feb;199:230-40).

In my view, if individuals are frightened because of who they are – be it tied to their religion, race, sexual identity, or ethnicity – and what harm may come to them, and if they live in fear and avoidance of these potential traumatic situations that affect their mental stability and the way they live their lives, they might fit the PTSD model.

If we clinicians focus on what’s currently being brought vividly into the public eye today regarding the African American community, we would see that some of the ongoing fears of racism – whether tied to residential or workplace discrimination, unfair treatment by figures of authority, harassment, health inequities, or microaggressions – may give rise to PTSD. I know we can do better. We should broaden our definition and awareness of this very serious disorder – and be prepared to treat it.
 

Dr. London has been a practicing psychiatrist for 4 decades and a newspaper columnist for almost as long. He has a private practice in New York and is author of “Find Freedom Fast: Short-Term Therapy That Works” (New York: Kettlehole Publishing, 2019). Dr. London has no conflicts of interest.

I have been studying, writing about, and treating posttraumatic stress disorder for many years. Over this time, I have seen PTSD expand to more and more areas of life, including my own view of a “subthreshold” version, which occurs in vulnerable people who experience a job loss, divorce, financial setbacks, or any number of painful life events.

As I noted in my recent book, “Find Freedom Fast,” for some people, PTSD can be triggered in the wake of events that are not life-threatening yet catastrophic for them and not tied to manmade or natural disasters, torture, assault, or war zone experiences.

The expansion of PTSD has led to the disorder being recognized in ICU patients during and after recovery (Crit Care Med. 2015 May;43[5]:1121-9), as well as in people diagnosed with cancer (Lancet Psychiatry. 2017 Apr;4[4]:330-8) and other illnesses that may cause emotional trauma – where one feels that one’s life is threatened. In some instances, the person’s life might indeed be in danger, not unlike what can happen in disasters, wars, torture, and even in some encounters with law enforcement.

This leads me to yet another circumstance that in some, may be tied to PTSD – and that is racial, religious, ethnic, and gender-related bigotry. In these cases, individuals feel threatened just for who they are in a society. Being on the receiving end of a circumstance that threatens a person’s very existence would seem to me to place a person as a potential survivor of PTSD, as well as any number of disorders, including anxiety, depression, or even paranoia.

Yes, discrimination and prejudice have been with us for a long time, and what concerns me is the psychological effect it has on children as well as adults. Friends of Irish descent remind me of hearing stories from parents and grandparents about employment signs reading, “Irish need not apply.” Certainly, those of Italian ancestry will easily recall the prejudice focused against them. And members of the Jewish community also can easily remember the bigotry and exclusion they have been subject to in certain neighborhoods and organizations, in addition to the horrors of the Holocaust during World War II, and the anti-Semitic chants in Charlottesville, Va., from just 3 years ago – with gun-carrying militants doing the chanting.

Obviously, in certain circles, we still have private clubs, plus neighborhoods and residential buildings that exclude people for a variety of reasons.

Coming from a medical family, years ago I heard stories that, if you were Roman Catholic, it would be hard to get into certain medical schools – which might explain the establishment of Catholic medical schools that often were open to people of other faiths. Then we had medical school discrimination toward Jewish students, which was followed by the establishment of medical schools focused on admitting more Jewish students. The African American community also responded to discrimination by establishing medical schools, such as the school at Howard University in Washington.

Furthermore, we cannot forget the discrimination that women faced in institutions of higher learning. My father had two women in his medical school class, I was told. In my era, I would say at least 30% were women, and today, in the United States, medical school classes are more equally balanced with men and women. Some schools have more women than men.

The question I ask, is: How did all those women feel for so many years knowing that, for reasons beyond their control, they were prevented from achieving their chosen goals? Some might have felt badly, and others might have internalized the rejection. Others might have developed PTSD based on feelings of rejection.

However, the question here mainly is: Can PTSD result when exclusion and prejudice induce fear and terror in those on the receiving end – especially innocent children? Children separated from their parents at the U.S.-Mexico border and those who witness their parents being shot immediately come to mind. This trauma can last well beyond childhood.

What we know today about structural racism should give the mental health community pause and make us realize the extent to which the African American community has been traumatized. Perhaps we should not be surprised by a study that found that the prevalence of PTSD among African Americans is 9.1%, compared with 6.8% for Whites (J Anxiety Dis. 2009 Jun;23[5]:573-90). Speaking with Black colleagues, friends, and patients, reading books such “The Warmth of Other Suns,” and watching films such as “Green Book,” give us a sense of how dangerous it was for Black families to travel in certain parts of the country in the recent past. I recall as a child hearing that, in Miami Beach, people of color could not stay overnight. (Even as a child I was surprised – having never heard anything like that. After all, I went to school with people of many religions and backgrounds. My parents thought those practices were terrible, and were appalled when they learned that some hotels were closed to Jews and others closed to Catholics.)
 

DSM-5, ICD-10 fall short

The DSM-5 describes trauma using a more or less one-dimensional set of guidelines as the focus. Those guidelines include exposure to direct violence, manmade or natural disasters, war, or torture, as well as exposure to a disaster or a life-threatening situation affecting a loved one. The ICD-10 is less restrictive about trauma but still has some limitations.

While considering potential PTSD, I try to use a less rigid diagnostic multidimensional approach, where I assess individual differences and experiences that play a role in those experiences as well as the patient’s vulnerability to the causation of PTSD – which also has to include any exposure to trauma (Curr Opin Psychol. 2017 Apr;14:29-34) before age 11 or 12. The data suggest that such early exposure leaves people more vulnerable to PTSD as adults (Soc Sci Med. 2018 Feb;199:230-40).

In my view, if individuals are frightened because of who they are – be it tied to their religion, race, sexual identity, or ethnicity – and what harm may come to them, and if they live in fear and avoidance of these potential traumatic situations that affect their mental stability and the way they live their lives, they might fit the PTSD model.

If we clinicians focus on what’s currently being brought vividly into the public eye today regarding the African American community, we would see that some of the ongoing fears of racism – whether tied to residential or workplace discrimination, unfair treatment by figures of authority, harassment, health inequities, or microaggressions – may give rise to PTSD. I know we can do better. We should broaden our definition and awareness of this very serious disorder – and be prepared to treat it.
 

Dr. London has been a practicing psychiatrist for 4 decades and a newspaper columnist for almost as long. He has a private practice in New York and is author of “Find Freedom Fast: Short-Term Therapy That Works” (New York: Kettlehole Publishing, 2019). Dr. London has no conflicts of interest.