After a year of gender-affirming hormone therapy, transgender youth showed significant improvement in body image dissatisfaction from baseline, based on data from 148 individuals.

“Understanding the impact of gender-affirming hormone therapy on the mental health of transgender youth is critical given the health disparities documented in this population,” wrote Laura E. Kuper, PhD, of Children’s Health Systems of Texas, Dallas, and colleagues.

In a study published in Pediatrics, the researchers reviewed data from 148 youth aged 9-18 years who underwent gender-affirming hormone therapy in a multidisciplinary program. The average age of the patients was 15 years; 25 were receiving puberty suppression hormones only, 93 were receiving just feminizing or masculinizing hormones, and 30 were receiving both treatments.

At baseline and at approximately 1 year follow-up, all patients completed the Body Image Scale, Quick Inventory of Depressive Symptoms, and Screen for Child Anxiety Related Emotional Disorders. In addition, clinicians collected information on patients’ suicidal ideation, suicide attempts, and nonsuicidal self-injury.

Overall, the average scores on the Body Image Scale on body dissatisfaction decreased from 70 to 52, and average scores on the Quick Inventory of Depressive Symptoms decreased from 9 to 7; both were statistically significant (P less than .001), as were changes from baseline on the anxiety subscale of the Screen for Child Anxiety Related Emotional Disorders, which decreased from 32 to 29 (P less than .01). No change occurred in the average overall clinician-reported depressive symptoms.

During the follow-up period, the rates of suicidal ideation, suicide attempts, and nonsuicidal self-injury were 38%, 5%, and 17%, respectively. Of patients who reported these experiences, the lifetime histories of suicidal ideation, suicide attempts, and nonsuicidal self-injury were 81%, 15%, and 52%, respectively.

The findings were limited by several factors including some missing data and the relatively small sample size, the researchers noted.

Nonetheless, the results suggest “that youth receiving gender-affirming hormone therapy experience meaningful short-term improvements in body dissatisfaction, and no participants discontinued feminizing or masculinizing hormone therapy.” These results support the use of such therapy, Dr. Kuper and associates wrote.

The study is important because of the need for evidence that hormones actually improve patient outcomes, said Shauna M. Lawlis, MD, of the University of Oklahoma Medical Center, Oklahoma City.

“Especially given the rash of legislation across the country aimed at blocking care for transgender youth, it is helpful to show that these treatments really do decrease patients’ anxiety and depressive symptoms,” she said in an interview. “In addition, previous research has been focused on those who have undergone puberty suppression followed by gender-affirming hormone therapy, but many patients are too far along in puberty for puberty suppression to be effective and providers often go straight to gender-affirming hormones in those cases.”

Dr. Lawlis said she was not at all surprised by the study findings. “In my own practice, I have seen patients improve greatly on gender-affirming hormones with overall improvement in anxiety and depression. As a patient’s outward appearance more closely matches their gender identity, they feel more comfortable in their own bodies and their interactions with the world around them, thus improving these symptoms.”

Dr. Lawlis added that the message for pediatricians who treat transgender youth is simple: Gender-affirming hormones improve patient outcomes. “They are essential for the mental health of this vulnerable population.”

She noted that long-term follow-up studies would be useful. “There is still a lot of concern about regret and detransitioning among health care providers and the general population – showing that patients maintain satisfaction in the long-term would be helpful.

“In addition, long-term studies about other health outcomes (cardiovascular disease, cancer risk, etc.) would also be helpful,” said Dr. Lawlis, who was asked to comment on this study, with which she had no involvement.

The study was supported in part by Children’s Health. The researchers had no financial conflicts to disclose. Dr. Lawlis had no relevant financial disclosures.

SOURCE: Kuper LE et al. Pediatrics. 2020 Mar 27. doi: 10.1542/peds.2019-3006.

After a year of gender-affirming hormone therapy, transgender youth showed significant improvement in body image dissatisfaction from baseline, based on data from 148 individuals.

“Understanding the impact of gender-affirming hormone therapy on the mental health of transgender youth is critical given the health disparities documented in this population,” wrote Laura E. Kuper, PhD, of Children’s Health Systems of Texas, Dallas, and colleagues.

In a study published in Pediatrics, the researchers reviewed data from 148 youth aged 9-18 years who underwent gender-affirming hormone therapy in a multidisciplinary program. The average age of the patients was 15 years; 25 were receiving puberty suppression hormones only, 93 were receiving just feminizing or masculinizing hormones, and 30 were receiving both treatments.

At baseline and at approximately 1 year follow-up, all patients completed the Body Image Scale, Quick Inventory of Depressive Symptoms, and Screen for Child Anxiety Related Emotional Disorders. In addition, clinicians collected information on patients’ suicidal ideation, suicide attempts, and nonsuicidal self-injury.

Overall, the average scores on the Body Image Scale on body dissatisfaction decreased from 70 to 52, and average scores on the Quick Inventory of Depressive Symptoms decreased from 9 to 7; both were statistically significant (P less than .001), as were changes from baseline on the anxiety subscale of the Screen for Child Anxiety Related Emotional Disorders, which decreased from 32 to 29 (P less than .01). No change occurred in the average overall clinician-reported depressive symptoms.

During the follow-up period, the rates of suicidal ideation, suicide attempts, and nonsuicidal self-injury were 38%, 5%, and 17%, respectively. Of patients who reported these experiences, the lifetime histories of suicidal ideation, suicide attempts, and nonsuicidal self-injury were 81%, 15%, and 52%, respectively.

The findings were limited by several factors including some missing data and the relatively small sample size, the researchers noted.

Nonetheless, the results suggest “that youth receiving gender-affirming hormone therapy experience meaningful short-term improvements in body dissatisfaction, and no participants discontinued feminizing or masculinizing hormone therapy.” These results support the use of such therapy, Dr. Kuper and associates wrote.

The study is important because of the need for evidence that hormones actually improve patient outcomes, said Shauna M. Lawlis, MD, of the University of Oklahoma Medical Center, Oklahoma City.

“Especially given the rash of legislation across the country aimed at blocking care for transgender youth, it is helpful to show that these treatments really do decrease patients’ anxiety and depressive symptoms,” she said in an interview. “In addition, previous research has been focused on those who have undergone puberty suppression followed by gender-affirming hormone therapy, but many patients are too far along in puberty for puberty suppression to be effective and providers often go straight to gender-affirming hormones in those cases.”

Dr. Lawlis said she was not at all surprised by the study findings. “In my own practice, I have seen patients improve greatly on gender-affirming hormones with overall improvement in anxiety and depression. As a patient’s outward appearance more closely matches their gender identity, they feel more comfortable in their own bodies and their interactions with the world around them, thus improving these symptoms.”

Dr. Lawlis added that the message for pediatricians who treat transgender youth is simple: Gender-affirming hormones improve patient outcomes. “They are essential for the mental health of this vulnerable population.”

She noted that long-term follow-up studies would be useful. “There is still a lot of concern about regret and detransitioning among health care providers and the general population – showing that patients maintain satisfaction in the long-term would be helpful.

“In addition, long-term studies about other health outcomes (cardiovascular disease, cancer risk, etc.) would also be helpful,” said Dr. Lawlis, who was asked to comment on this study, with which she had no involvement.

The study was supported in part by Children’s Health. The researchers had no financial conflicts to disclose. Dr. Lawlis had no relevant financial disclosures.

SOURCE: Kuper LE et al. Pediatrics. 2020 Mar 27. doi: 10.1542/peds.2019-3006.

After a year of gender-affirming hormone therapy, transgender youth showed significant improvement in body image dissatisfaction from baseline, based on data from 148 individuals.

“Understanding the impact of gender-affirming hormone therapy on the mental health of transgender youth is critical given the health disparities documented in this population,” wrote Laura E. Kuper, PhD, of Children’s Health Systems of Texas, Dallas, and colleagues.

In a study published in Pediatrics, the researchers reviewed data from 148 youth aged 9-18 years who underwent gender-affirming hormone therapy in a multidisciplinary program. The average age of the patients was 15 years; 25 were receiving puberty suppression hormones only, 93 were receiving just feminizing or masculinizing hormones, and 30 were receiving both treatments.

At baseline and at approximately 1 year follow-up, all patients completed the Body Image Scale, Quick Inventory of Depressive Symptoms, and Screen for Child Anxiety Related Emotional Disorders. In addition, clinicians collected information on patients’ suicidal ideation, suicide attempts, and nonsuicidal self-injury.

Overall, the average scores on the Body Image Scale on body dissatisfaction decreased from 70 to 52, and average scores on the Quick Inventory of Depressive Symptoms decreased from 9 to 7; both were statistically significant (P less than .001), as were changes from baseline on the anxiety subscale of the Screen for Child Anxiety Related Emotional Disorders, which decreased from 32 to 29 (P less than .01). No change occurred in the average overall clinician-reported depressive symptoms.

During the follow-up period, the rates of suicidal ideation, suicide attempts, and nonsuicidal self-injury were 38%, 5%, and 17%, respectively. Of patients who reported these experiences, the lifetime histories of suicidal ideation, suicide attempts, and nonsuicidal self-injury were 81%, 15%, and 52%, respectively.

The findings were limited by several factors including some missing data and the relatively small sample size, the researchers noted.

Nonetheless, the results suggest “that youth receiving gender-affirming hormone therapy experience meaningful short-term improvements in body dissatisfaction, and no participants discontinued feminizing or masculinizing hormone therapy.” These results support the use of such therapy, Dr. Kuper and associates wrote.

The study is important because of the need for evidence that hormones actually improve patient outcomes, said Shauna M. Lawlis, MD, of the University of Oklahoma Medical Center, Oklahoma City.

“Especially given the rash of legislation across the country aimed at blocking care for transgender youth, it is helpful to show that these treatments really do decrease patients’ anxiety and depressive symptoms,” she said in an interview. “In addition, previous research has been focused on those who have undergone puberty suppression followed by gender-affirming hormone therapy, but many patients are too far along in puberty for puberty suppression to be effective and providers often go straight to gender-affirming hormones in those cases.”

Dr. Lawlis said she was not at all surprised by the study findings. “In my own practice, I have seen patients improve greatly on gender-affirming hormones with overall improvement in anxiety and depression. As a patient’s outward appearance more closely matches their gender identity, they feel more comfortable in their own bodies and their interactions with the world around them, thus improving these symptoms.”

Dr. Lawlis added that the message for pediatricians who treat transgender youth is simple: Gender-affirming hormones improve patient outcomes. “They are essential for the mental health of this vulnerable population.”

She noted that long-term follow-up studies would be useful. “There is still a lot of concern about regret and detransitioning among health care providers and the general population – showing that patients maintain satisfaction in the long-term would be helpful.

“In addition, long-term studies about other health outcomes (cardiovascular disease, cancer risk, etc.) would also be helpful,” said Dr. Lawlis, who was asked to comment on this study, with which she had no involvement.

The study was supported in part by Children’s Health. The researchers had no financial conflicts to disclose. Dr. Lawlis had no relevant financial disclosures.

SOURCE: Kuper LE et al. Pediatrics. 2020 Mar 27. doi: 10.1542/peds.2019-3006.

During parturient transmission of gut bacteria from mothers to infants, the dominant maternal source of bacteria is rectal, according to investigators.

This challenges the hypothesis that exposure to the birth canal explains major differences in gut bacteria between infants born vaginally and those born via C-section, reported Moran Yassour, PhD, of Hebrew University in Jerusalem.

“It’s not how and if you entered the birth canal, but rather how you exited it,” Dr. Yassour said during a presentation at the annual Gut Microbiota for Health World Summit.

According to Dr. Yassour, a number of investigators have evaluated vertical transmission of gut bacteria from mothers to newborns, but most began collecting data a week or more after birth, potentially missing critical information.

“We wanted to generate large-scale, paired, longitudinal data, which means that we had [samples from] both mothers and children, and we wanted to start at birth,” Dr. Yassour said at the meeting, sponsored by the American Gastroenterological Association and the European Society for Neurogastroenterology and Motility.

Dr. Yassour explained that newborns delivered vaginally often exhibit Bacteroides in their gut, whereas babies born via C-section do not exhibit these bacteria until 6-18 months of age; however, the vaginal microbiome typically lacks Bacteroides, making the birth canal an unlikely source. This disconnect served as the impetus for the present investigation, Dr. Yassour said.

The study, which is available as a preprint, involved 73 mothers and their infants. To determine the impact of birth canal exposure, the investigators compared gut bacteria of infants born vaginally with those born via pre-labor C-section (no exposure to the birth canal), and those born via post-labor C-section (exposure to the birth canal).

Initial results were surprising, Dr. Yassour said, as 54% of babies delivered via C-section had Bacteroides in their stool during the first week. But in the second week, 94% of the C-section group lacked Bacteroides, which aligns with characteristic findings and suggests failure of colonization, rather than complete lack of exposure.

Out of the 24 infants with persistent Bacteroides colonization, 22 (92%) were born vaginally, compared with 2 (8%) born via pre-labor C-section, and none born via post-labor C-section. This pattern was maintained in a multivariate analysis that accounted for antibiotic use and exposure to formula, both of which are more common among mothers that give birth via C-section.

The investigators also conducted a strain-level analysis of mothers and infants using metagenomic sequencing. Across all time points, 90% of matched maternal-infant strains were detected in babies delivered vaginally.

“[W]e found evidence for mother-to-child transmission of rectal rather than vaginal strains,” the investigators wrote. “These results challenge birth canal exposure as the dominant factor in infant gut microbiome establishment and implicate colonization efficiency rather than exposure as a dictating factor of the newborn gut microbiome composition.”

Dr. Yassour said that these findings may have an immediate effect on clinical practice.

“People have reported the practice of smearing babies that were born by C-section with vaginal fluids in the sense of trying to recapitulate the microbial signature that we find in kids born vaginally,” Dr. Yassour said. “But it’s probably not the vaginal fluid that we need to smear; it’s probably the proximity to the rectum and the bowel movements that happen during delivery ... and that is what’s causing this initial seeding from mother to child.”

Dr. Yassour disclosed no conflicts of interest.

SOURCE: Yassour M et al. GMFH 2020.

During parturient transmission of gut bacteria from mothers to infants, the dominant maternal source of bacteria is rectal, according to investigators.

This challenges the hypothesis that exposure to the birth canal explains major differences in gut bacteria between infants born vaginally and those born via C-section, reported Moran Yassour, PhD, of Hebrew University in Jerusalem.

“It’s not how and if you entered the birth canal, but rather how you exited it,” Dr. Yassour said during a presentation at the annual Gut Microbiota for Health World Summit.

According to Dr. Yassour, a number of investigators have evaluated vertical transmission of gut bacteria from mothers to newborns, but most began collecting data a week or more after birth, potentially missing critical information.

“We wanted to generate large-scale, paired, longitudinal data, which means that we had [samples from] both mothers and children, and we wanted to start at birth,” Dr. Yassour said at the meeting, sponsored by the American Gastroenterological Association and the European Society for Neurogastroenterology and Motility.

Dr. Yassour explained that newborns delivered vaginally often exhibit Bacteroides in their gut, whereas babies born via C-section do not exhibit these bacteria until 6-18 months of age; however, the vaginal microbiome typically lacks Bacteroides, making the birth canal an unlikely source. This disconnect served as the impetus for the present investigation, Dr. Yassour said.

The study, which is available as a preprint, involved 73 mothers and their infants. To determine the impact of birth canal exposure, the investigators compared gut bacteria of infants born vaginally with those born via pre-labor C-section (no exposure to the birth canal), and those born via post-labor C-section (exposure to the birth canal).

Initial results were surprising, Dr. Yassour said, as 54% of babies delivered via C-section had Bacteroides in their stool during the first week. But in the second week, 94% of the C-section group lacked Bacteroides, which aligns with characteristic findings and suggests failure of colonization, rather than complete lack of exposure.

Out of the 24 infants with persistent Bacteroides colonization, 22 (92%) were born vaginally, compared with 2 (8%) born via pre-labor C-section, and none born via post-labor C-section. This pattern was maintained in a multivariate analysis that accounted for antibiotic use and exposure to formula, both of which are more common among mothers that give birth via C-section.

The investigators also conducted a strain-level analysis of mothers and infants using metagenomic sequencing. Across all time points, 90% of matched maternal-infant strains were detected in babies delivered vaginally.

“[W]e found evidence for mother-to-child transmission of rectal rather than vaginal strains,” the investigators wrote. “These results challenge birth canal exposure as the dominant factor in infant gut microbiome establishment and implicate colonization efficiency rather than exposure as a dictating factor of the newborn gut microbiome composition.”

Dr. Yassour said that these findings may have an immediate effect on clinical practice.

“People have reported the practice of smearing babies that were born by C-section with vaginal fluids in the sense of trying to recapitulate the microbial signature that we find in kids born vaginally,” Dr. Yassour said. “But it’s probably not the vaginal fluid that we need to smear; it’s probably the proximity to the rectum and the bowel movements that happen during delivery ... and that is what’s causing this initial seeding from mother to child.”

Dr. Yassour disclosed no conflicts of interest.

SOURCE: Yassour M et al. GMFH 2020.

During parturient transmission of gut bacteria from mothers to infants, the dominant maternal source of bacteria is rectal, according to investigators.

This challenges the hypothesis that exposure to the birth canal explains major differences in gut bacteria between infants born vaginally and those born via C-section, reported Moran Yassour, PhD, of Hebrew University in Jerusalem.

“It’s not how and if you entered the birth canal, but rather how you exited it,” Dr. Yassour said during a presentation at the annual Gut Microbiota for Health World Summit.

According to Dr. Yassour, a number of investigators have evaluated vertical transmission of gut bacteria from mothers to newborns, but most began collecting data a week or more after birth, potentially missing critical information.

“We wanted to generate large-scale, paired, longitudinal data, which means that we had [samples from] both mothers and children, and we wanted to start at birth,” Dr. Yassour said at the meeting, sponsored by the American Gastroenterological Association and the European Society for Neurogastroenterology and Motility.

Dr. Yassour explained that newborns delivered vaginally often exhibit Bacteroides in their gut, whereas babies born via C-section do not exhibit these bacteria until 6-18 months of age; however, the vaginal microbiome typically lacks Bacteroides, making the birth canal an unlikely source. This disconnect served as the impetus for the present investigation, Dr. Yassour said.

The study, which is available as a preprint, involved 73 mothers and their infants. To determine the impact of birth canal exposure, the investigators compared gut bacteria of infants born vaginally with those born via pre-labor C-section (no exposure to the birth canal), and those born via post-labor C-section (exposure to the birth canal).

Initial results were surprising, Dr. Yassour said, as 54% of babies delivered via C-section had Bacteroides in their stool during the first week. But in the second week, 94% of the C-section group lacked Bacteroides, which aligns with characteristic findings and suggests failure of colonization, rather than complete lack of exposure.

Out of the 24 infants with persistent Bacteroides colonization, 22 (92%) were born vaginally, compared with 2 (8%) born via pre-labor C-section, and none born via post-labor C-section. This pattern was maintained in a multivariate analysis that accounted for antibiotic use and exposure to formula, both of which are more common among mothers that give birth via C-section.

The investigators also conducted a strain-level analysis of mothers and infants using metagenomic sequencing. Across all time points, 90% of matched maternal-infant strains were detected in babies delivered vaginally.

“[W]e found evidence for mother-to-child transmission of rectal rather than vaginal strains,” the investigators wrote. “These results challenge birth canal exposure as the dominant factor in infant gut microbiome establishment and implicate colonization efficiency rather than exposure as a dictating factor of the newborn gut microbiome composition.”

Dr. Yassour said that these findings may have an immediate effect on clinical practice.

“People have reported the practice of smearing babies that were born by C-section with vaginal fluids in the sense of trying to recapitulate the microbial signature that we find in kids born vaginally,” Dr. Yassour said. “But it’s probably not the vaginal fluid that we need to smear; it’s probably the proximity to the rectum and the bowel movements that happen during delivery ... and that is what’s causing this initial seeding from mother to child.”

Dr. Yassour disclosed no conflicts of interest.

SOURCE: Yassour M et al. GMFH 2020.

It’s already been a few years since I exited the Society of Hospital Medicine’s Board of Directors (2 years, or maybe 3 – I’ve already lost count), and sitting in my proverbial rocking chair in the Old Hospitalists’ Home, I heard, as many of you did, that Larry Wellikson, MD, MHM, the first and only CEO in the Society’s history, is stepping down soon.

With all the idle time that I find myself with these days, I have had the opportunity to ruminate on what Larry has brought to SHM in his 2 decades of leadership. And among the many answers, two stand out for me.

The first is Larry’s deep appreciation of the value of relationships that he has developed and nurtured, an attribute which he has imprinted on many of us who have worked with him over the years. Although Larry speaks of the camaraderie of the first years of SHM and the bonds that he, Bob Wachter, Win Whitcomb, and John Nelson established, he also has kept in touch with a vast network of hospitalists over the last 20-plus years.

Go to lunch with Larry, and be amazed at how much he knows about the goings-on of many of our colleagues. The fondness that Larry has for the people in his life is without parallel. These aren’t just professional colleagues who have impacted him in some way – for Larry, every one of these is a true lifetime friendship, and he continues to establish new ones every year. He makes each of his friends feel truly special to him.

The second is the critical value of and need for change and disruption. The specialty of hospital medicine was, from its beginning, disruptive, and from his career as a physician executive, Larry understood and has brought to SHM an understanding of the necessity of disruption to encourage growth and fresh thinking. If one steps back and looks at, for example, the composition of the Board over the years, or the Journal of Hospital Medicine’s editorial staff, or of our committees, one sees a pattern – a commitment to continuously bringing on young leaders who are still on the early and ascending part of their career paths.

Other organizations identify Board candidates at the peak of their careers, but at SHM, many of us were elected when we had just enough experience to contribute but then continued to grow in our careers after finishing our terms. I joined the Board in 2012 (I think) and while I would probably be a more seasoned and stately Board member if I joined at this point in my life, I would also have less new and novel to offer – and therefore be less effective for what the Society needs. While SHM respects its past leaders, it does not revere them. Our past is important, but our present and future are more important. Larry brought that mentality to SHM.

Ironically, the one position within SHM which has not, until this year, been subject to that same kind of transition is the CEO position itself. And this year, that domino will fall as well. While transitions are hard, change is good – and I am confident that our Society’s commitment to seeking out new, talented leaders, and making transitions at all levels – Board, committees, chapters, speakers – with the intent of bringing new perspectives and creativity, is firmly entrenched in our culture. And Larry can join me in the rocking chair as we relive our common SHM experiences together – and create new memories as well.

Congratulations Larry, and thank you.

Dr. Harte is a past president of SHM, and president of Cleveland Clinic Akron (Ohio) General and the Southern Region. He formerly served as president of Cleveland Clinic Hillcrest Hospital and Cleveland Clinic South Pointe Hospital.

It’s already been a few years since I exited the Society of Hospital Medicine’s Board of Directors (2 years, or maybe 3 – I’ve already lost count), and sitting in my proverbial rocking chair in the Old Hospitalists’ Home, I heard, as many of you did, that Larry Wellikson, MD, MHM, the first and only CEO in the Society’s history, is stepping down soon.

With all the idle time that I find myself with these days, I have had the opportunity to ruminate on what Larry has brought to SHM in his 2 decades of leadership. And among the many answers, two stand out for me.

The first is Larry’s deep appreciation of the value of relationships that he has developed and nurtured, an attribute which he has imprinted on many of us who have worked with him over the years. Although Larry speaks of the camaraderie of the first years of SHM and the bonds that he, Bob Wachter, Win Whitcomb, and John Nelson established, he also has kept in touch with a vast network of hospitalists over the last 20-plus years.

Go to lunch with Larry, and be amazed at how much he knows about the goings-on of many of our colleagues. The fondness that Larry has for the people in his life is without parallel. These aren’t just professional colleagues who have impacted him in some way – for Larry, every one of these is a true lifetime friendship, and he continues to establish new ones every year. He makes each of his friends feel truly special to him.

The second is the critical value of and need for change and disruption. The specialty of hospital medicine was, from its beginning, disruptive, and from his career as a physician executive, Larry understood and has brought to SHM an understanding of the necessity of disruption to encourage growth and fresh thinking. If one steps back and looks at, for example, the composition of the Board over the years, or the Journal of Hospital Medicine’s editorial staff, or of our committees, one sees a pattern – a commitment to continuously bringing on young leaders who are still on the early and ascending part of their career paths.

Other organizations identify Board candidates at the peak of their careers, but at SHM, many of us were elected when we had just enough experience to contribute but then continued to grow in our careers after finishing our terms. I joined the Board in 2012 (I think) and while I would probably be a more seasoned and stately Board member if I joined at this point in my life, I would also have less new and novel to offer – and therefore be less effective for what the Society needs. While SHM respects its past leaders, it does not revere them. Our past is important, but our present and future are more important. Larry brought that mentality to SHM.

Ironically, the one position within SHM which has not, until this year, been subject to that same kind of transition is the CEO position itself. And this year, that domino will fall as well. While transitions are hard, change is good – and I am confident that our Society’s commitment to seeking out new, talented leaders, and making transitions at all levels – Board, committees, chapters, speakers – with the intent of bringing new perspectives and creativity, is firmly entrenched in our culture. And Larry can join me in the rocking chair as we relive our common SHM experiences together – and create new memories as well.

Congratulations Larry, and thank you.

Dr. Harte is a past president of SHM, and president of Cleveland Clinic Akron (Ohio) General and the Southern Region. He formerly served as president of Cleveland Clinic Hillcrest Hospital and Cleveland Clinic South Pointe Hospital.

It’s already been a few years since I exited the Society of Hospital Medicine’s Board of Directors (2 years, or maybe 3 – I’ve already lost count), and sitting in my proverbial rocking chair in the Old Hospitalists’ Home, I heard, as many of you did, that Larry Wellikson, MD, MHM, the first and only CEO in the Society’s history, is stepping down soon.

With all the idle time that I find myself with these days, I have had the opportunity to ruminate on what Larry has brought to SHM in his 2 decades of leadership. And among the many answers, two stand out for me.

The first is Larry’s deep appreciation of the value of relationships that he has developed and nurtured, an attribute which he has imprinted on many of us who have worked with him over the years. Although Larry speaks of the camaraderie of the first years of SHM and the bonds that he, Bob Wachter, Win Whitcomb, and John Nelson established, he also has kept in touch with a vast network of hospitalists over the last 20-plus years.

Go to lunch with Larry, and be amazed at how much he knows about the goings-on of many of our colleagues. The fondness that Larry has for the people in his life is without parallel. These aren’t just professional colleagues who have impacted him in some way – for Larry, every one of these is a true lifetime friendship, and he continues to establish new ones every year. He makes each of his friends feel truly special to him.

The second is the critical value of and need for change and disruption. The specialty of hospital medicine was, from its beginning, disruptive, and from his career as a physician executive, Larry understood and has brought to SHM an understanding of the necessity of disruption to encourage growth and fresh thinking. If one steps back and looks at, for example, the composition of the Board over the years, or the Journal of Hospital Medicine’s editorial staff, or of our committees, one sees a pattern – a commitment to continuously bringing on young leaders who are still on the early and ascending part of their career paths.

Other organizations identify Board candidates at the peak of their careers, but at SHM, many of us were elected when we had just enough experience to contribute but then continued to grow in our careers after finishing our terms. I joined the Board in 2012 (I think) and while I would probably be a more seasoned and stately Board member if I joined at this point in my life, I would also have less new and novel to offer – and therefore be less effective for what the Society needs. While SHM respects its past leaders, it does not revere them. Our past is important, but our present and future are more important. Larry brought that mentality to SHM.

Ironically, the one position within SHM which has not, until this year, been subject to that same kind of transition is the CEO position itself. And this year, that domino will fall as well. While transitions are hard, change is good – and I am confident that our Society’s commitment to seeking out new, talented leaders, and making transitions at all levels – Board, committees, chapters, speakers – with the intent of bringing new perspectives and creativity, is firmly entrenched in our culture. And Larry can join me in the rocking chair as we relive our common SHM experiences together – and create new memories as well.

Congratulations Larry, and thank you.

Dr. Harte is a past president of SHM, and president of Cleveland Clinic Akron (Ohio) General and the Southern Region. He formerly served as president of Cleveland Clinic Hillcrest Hospital and Cleveland Clinic South Pointe Hospital.

Differences in metabolism of levodopa between patients with Parkinson’s disease may be caused by variations in gut bacteria, according to investigators.

Specifically, patients with a higher abundance of Enterococcus faecalis may be converting levodopa into dopamine via decarboxylation before it can cross the blood-brain barrier, reported Emily P. Balskus, PhD, of Harvard University in Cambridge, Mass.

Although existing decarboxylase inhibitors, such as carbidopa, can reduce metabolism of levodopa by host enzymes, these drugs are unable to inhibit the enzymatic activity of E. faecalis in the gut, Dr. Balskus said at the annual Gut Microbiota for Health World Summit, sponsored by the American Gastroenterological Association and the European Society for Neurogastroenterology and Motility.

“[Carbidopa] is actually completely ineffective at inhibiting decarboxylation in human fecal suspension,” Dr. Balskus said, referring to research led by PhD student Vayu Maini Rekdal. “We think that this could indicate that patients who are taking carbidopa are not inhibiting any bacterial metabolism that they may have.”

While previous research showed that E. faecalis could decarboxylate levodopa, Dr. Balskus and colleagues linked this process with the tyrosine decarboxylase gene (TyrDC), and showed that the of abundance E. faecalis and TyrDC correlate with levodopa metabolism.

Unlike the human enzyme responsible for decarboxylation of levodopa, the E. faecalis enzyme preferentially binds with L-tyrosine. This could explain why existing decarboxylase inhibitors have little impact on decarboxylation in the gut, Dr. Balskus said.

She also noted that this unique characteristic may open doors to new therapeutics. In the lab, Dr. Balskus and colleagues tested a decarboxylase inhibitor that resembled L-tyrosine, (S)-alpha-fluoromethyltyrosine (AFMT). Indeed, AFMT completely inhibited of decarboxylation of levodopa in both E. faecalis cells and complex human microbiome samples.

“We think this is pretty exciting,” Dr. Balskus said.

Early animal studies support this enthusiasm, as germ-free mice colonized with E. faecalis maintain higher serum levels of levodopa with concurrent administration of AFMT.

“We think that this could indicate that a promising way to improve levodopa therapy for Parkinson’s patients would be to develop compounds that inhibit bacterial drug metabolism activity,” Dr. Balskus said.

Concluding her presentation, Dr. Balskus emphasized the importance of a biochemical approach to microbiome research. “Studying enzymes opens up new, exciting opportunities for microbiome manipulation. We can design or develop inhibitors of enzymes, use those inhibitors as tools to study the roles of individual metabolic activities, and potentially use them as therapeutics. We are very excited about the possibility of treating or preventing human disease not just by manipulating processes in our own cells, but by targeting activities in the microbiota.”

Dr. Balskus reported funding from HHMI, the Bill and Melinda Gates Foundation, the David and Lucile Packard Foundation, and Merck.

Differences in metabolism of levodopa between patients with Parkinson’s disease may be caused by variations in gut bacteria, according to investigators.

Specifically, patients with a higher abundance of Enterococcus faecalis may be converting levodopa into dopamine via decarboxylation before it can cross the blood-brain barrier, reported Emily P. Balskus, PhD, of Harvard University in Cambridge, Mass.

Although existing decarboxylase inhibitors, such as carbidopa, can reduce metabolism of levodopa by host enzymes, these drugs are unable to inhibit the enzymatic activity of E. faecalis in the gut, Dr. Balskus said at the annual Gut Microbiota for Health World Summit, sponsored by the American Gastroenterological Association and the European Society for Neurogastroenterology and Motility.

“[Carbidopa] is actually completely ineffective at inhibiting decarboxylation in human fecal suspension,” Dr. Balskus said, referring to research led by PhD student Vayu Maini Rekdal. “We think that this could indicate that patients who are taking carbidopa are not inhibiting any bacterial metabolism that they may have.”

While previous research showed that E. faecalis could decarboxylate levodopa, Dr. Balskus and colleagues linked this process with the tyrosine decarboxylase gene (TyrDC), and showed that the of abundance E. faecalis and TyrDC correlate with levodopa metabolism.

Unlike the human enzyme responsible for decarboxylation of levodopa, the E. faecalis enzyme preferentially binds with L-tyrosine. This could explain why existing decarboxylase inhibitors have little impact on decarboxylation in the gut, Dr. Balskus said.

She also noted that this unique characteristic may open doors to new therapeutics. In the lab, Dr. Balskus and colleagues tested a decarboxylase inhibitor that resembled L-tyrosine, (S)-alpha-fluoromethyltyrosine (AFMT). Indeed, AFMT completely inhibited of decarboxylation of levodopa in both E. faecalis cells and complex human microbiome samples.

“We think this is pretty exciting,” Dr. Balskus said.

Early animal studies support this enthusiasm, as germ-free mice colonized with E. faecalis maintain higher serum levels of levodopa with concurrent administration of AFMT.

“We think that this could indicate that a promising way to improve levodopa therapy for Parkinson’s patients would be to develop compounds that inhibit bacterial drug metabolism activity,” Dr. Balskus said.

Concluding her presentation, Dr. Balskus emphasized the importance of a biochemical approach to microbiome research. “Studying enzymes opens up new, exciting opportunities for microbiome manipulation. We can design or develop inhibitors of enzymes, use those inhibitors as tools to study the roles of individual metabolic activities, and potentially use them as therapeutics. We are very excited about the possibility of treating or preventing human disease not just by manipulating processes in our own cells, but by targeting activities in the microbiota.”

Dr. Balskus reported funding from HHMI, the Bill and Melinda Gates Foundation, the David and Lucile Packard Foundation, and Merck.

Differences in metabolism of levodopa between patients with Parkinson’s disease may be caused by variations in gut bacteria, according to investigators.

Specifically, patients with a higher abundance of Enterococcus faecalis may be converting levodopa into dopamine via decarboxylation before it can cross the blood-brain barrier, reported Emily P. Balskus, PhD, of Harvard University in Cambridge, Mass.

Although existing decarboxylase inhibitors, such as carbidopa, can reduce metabolism of levodopa by host enzymes, these drugs are unable to inhibit the enzymatic activity of E. faecalis in the gut, Dr. Balskus said at the annual Gut Microbiota for Health World Summit, sponsored by the American Gastroenterological Association and the European Society for Neurogastroenterology and Motility.

“[Carbidopa] is actually completely ineffective at inhibiting decarboxylation in human fecal suspension,” Dr. Balskus said, referring to research led by PhD student Vayu Maini Rekdal. “We think that this could indicate that patients who are taking carbidopa are not inhibiting any bacterial metabolism that they may have.”

While previous research showed that E. faecalis could decarboxylate levodopa, Dr. Balskus and colleagues linked this process with the tyrosine decarboxylase gene (TyrDC), and showed that the of abundance E. faecalis and TyrDC correlate with levodopa metabolism.

Unlike the human enzyme responsible for decarboxylation of levodopa, the E. faecalis enzyme preferentially binds with L-tyrosine. This could explain why existing decarboxylase inhibitors have little impact on decarboxylation in the gut, Dr. Balskus said.

She also noted that this unique characteristic may open doors to new therapeutics. In the lab, Dr. Balskus and colleagues tested a decarboxylase inhibitor that resembled L-tyrosine, (S)-alpha-fluoromethyltyrosine (AFMT). Indeed, AFMT completely inhibited of decarboxylation of levodopa in both E. faecalis cells and complex human microbiome samples.

“We think this is pretty exciting,” Dr. Balskus said.

Early animal studies support this enthusiasm, as germ-free mice colonized with E. faecalis maintain higher serum levels of levodopa with concurrent administration of AFMT.

“We think that this could indicate that a promising way to improve levodopa therapy for Parkinson’s patients would be to develop compounds that inhibit bacterial drug metabolism activity,” Dr. Balskus said.

Concluding her presentation, Dr. Balskus emphasized the importance of a biochemical approach to microbiome research. “Studying enzymes opens up new, exciting opportunities for microbiome manipulation. We can design or develop inhibitors of enzymes, use those inhibitors as tools to study the roles of individual metabolic activities, and potentially use them as therapeutics. We are very excited about the possibility of treating or preventing human disease not just by manipulating processes in our own cells, but by targeting activities in the microbiota.”

Dr. Balskus reported funding from HHMI, the Bill and Melinda Gates Foundation, the David and Lucile Packard Foundation, and Merck.

Despite implementation of strict infection control and prevention procedures in a hospital in Wuhan, China, a minority of neonates born to mothers with COVID-19 tested positive with novel coronavirus 2019 shortly after birth, according to Lingkong Zeng, MD, of the department of neonatology at Wuhan Children’s Hospital, and associates.

CDC/ Dr. Fred Murphy; Sylvia Whitfield

Thirty-three neonates born to mothers with COVID-19 were included in the study, published as a research letter in JAMA Pediatrics. Of this group, three neonates (9%) were confirmed to be infected with the novel coronavirus 2019 at 2 and 4 days of life through nasopharyngeal and anal swabs.

Of the three infected neonates, two were born at 40 weeks’ gestation and the third was born at 31 weeks. The two full-term infants had mild symptoms such as lethargy and fever and were negative for the virus at 6 days of life. The preterm infant had somewhat worse symptoms, but the investigators acknowledged that “the most seriously ill neonate may have been symptomatic from prematurity, asphyxia, and sepsis, rather than [the novel coronavirus 2019] infection.” They added that outcomes for all three neonates were favorable, consistent with past research.

“Because strict infection control and prevention procedures were implemented during the delivery, it is likely that the sources of [novel coronavirus 2019] in the neonates’ upper respiratory tracts or anuses were maternal in origin,” Dr. Zeng and associates surmised.

While previous studies have shown no evidence of COVID-19 transmission between mothers and neonates, and all samples, including amniotic fluid, cord blood, and breast milk, were negative for the novel coronavirus 2019, “vertical maternal-fetal transmission cannot be ruled out in the current cohort. Therefore, it is crucial to screen pregnant women and implement strict infection control measures, quarantine of infected mothers, and close monitoring of neonates at risk of COVID-19,” the investigators concluded.

The study authors reported that they had no conflicts of interest.

[email protected]

SOURCE: Zeng L et al. JAMA Pediatrics. 2020 Mar 26. doi: 10.1001/jamapediatrics.2020.0878.

Despite implementation of strict infection control and prevention procedures in a hospital in Wuhan, China, a minority of neonates born to mothers with COVID-19 tested positive with novel coronavirus 2019 shortly after birth, according to Lingkong Zeng, MD, of the department of neonatology at Wuhan Children’s Hospital, and associates.

CDC/ Dr. Fred Murphy; Sylvia Whitfield

Thirty-three neonates born to mothers with COVID-19 were included in the study, published as a research letter in JAMA Pediatrics. Of this group, three neonates (9%) were confirmed to be infected with the novel coronavirus 2019 at 2 and 4 days of life through nasopharyngeal and anal swabs.

Of the three infected neonates, two were born at 40 weeks’ gestation and the third was born at 31 weeks. The two full-term infants had mild symptoms such as lethargy and fever and were negative for the virus at 6 days of life. The preterm infant had somewhat worse symptoms, but the investigators acknowledged that “the most seriously ill neonate may have been symptomatic from prematurity, asphyxia, and sepsis, rather than [the novel coronavirus 2019] infection.” They added that outcomes for all three neonates were favorable, consistent with past research.

“Because strict infection control and prevention procedures were implemented during the delivery, it is likely that the sources of [novel coronavirus 2019] in the neonates’ upper respiratory tracts or anuses were maternal in origin,” Dr. Zeng and associates surmised.

While previous studies have shown no evidence of COVID-19 transmission between mothers and neonates, and all samples, including amniotic fluid, cord blood, and breast milk, were negative for the novel coronavirus 2019, “vertical maternal-fetal transmission cannot be ruled out in the current cohort. Therefore, it is crucial to screen pregnant women and implement strict infection control measures, quarantine of infected mothers, and close monitoring of neonates at risk of COVID-19,” the investigators concluded.

The study authors reported that they had no conflicts of interest.

[email protected]

SOURCE: Zeng L et al. JAMA Pediatrics. 2020 Mar 26. doi: 10.1001/jamapediatrics.2020.0878.

Despite implementation of strict infection control and prevention procedures in a hospital in Wuhan, China, a minority of neonates born to mothers with COVID-19 tested positive with novel coronavirus 2019 shortly after birth, according to Lingkong Zeng, MD, of the department of neonatology at Wuhan Children’s Hospital, and associates.

CDC/ Dr. Fred Murphy; Sylvia Whitfield

Thirty-three neonates born to mothers with COVID-19 were included in the study, published as a research letter in JAMA Pediatrics. Of this group, three neonates (9%) were confirmed to be infected with the novel coronavirus 2019 at 2 and 4 days of life through nasopharyngeal and anal swabs.

Of the three infected neonates, two were born at 40 weeks’ gestation and the third was born at 31 weeks. The two full-term infants had mild symptoms such as lethargy and fever and were negative for the virus at 6 days of life. The preterm infant had somewhat worse symptoms, but the investigators acknowledged that “the most seriously ill neonate may have been symptomatic from prematurity, asphyxia, and sepsis, rather than [the novel coronavirus 2019] infection.” They added that outcomes for all three neonates were favorable, consistent with past research.

“Because strict infection control and prevention procedures were implemented during the delivery, it is likely that the sources of [novel coronavirus 2019] in the neonates’ upper respiratory tracts or anuses were maternal in origin,” Dr. Zeng and associates surmised.

While previous studies have shown no evidence of COVID-19 transmission between mothers and neonates, and all samples, including amniotic fluid, cord blood, and breast milk, were negative for the novel coronavirus 2019, “vertical maternal-fetal transmission cannot be ruled out in the current cohort. Therefore, it is crucial to screen pregnant women and implement strict infection control measures, quarantine of infected mothers, and close monitoring of neonates at risk of COVID-19,” the investigators concluded.

The study authors reported that they had no conflicts of interest.

[email protected]

SOURCE: Zeng L et al. JAMA Pediatrics. 2020 Mar 26. doi: 10.1001/jamapediatrics.2020.0878.

LAHAINA, HAWAII – Reassuring evidence of the safety of oral propranolol for treatment of complicated infantile hemangiomas in patients with PHACE syndrome comes from a recent multicenter study.

Bruce Jancin/MDedge News

Oral propranolol is now well-ensconced as first-line therapy for complicated infantile hemangiomas in otherwise healthy children. However, the beta-blocker’s use in PHACE (Posterior fossa malformations, Hemangiomas, Arterial anomalies, Cardiac defects, and Eye abnormalities) syndrome has been controversial, with concerns raised by some that it might raise the risk for arterial ischemic stroke. Not so, Moise L. Levy, MD, said at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

“I’m not suggesting you use propranolol with reckless abandon in this population, but this stroke concern is something that should be put to bed based on this study,” advised Dr. Levy, professor of dermatology and pediatrics at Dell Medical School in Austin, Tex., and physician-in-chief at Dell Children’s Medical Center.

PHACE syndrome is characterized by large, thick, plaque-like hemangiomas greater than 5 cm in size, most commonly on the face, although they can be located elsewhere.

“There was concern that if you found severely altered cerebrovascular arterial flow and you put a kid on a beta-blocker you might be causing some harm. But what I will tell you is that in this recently published paper this was not in fact an issue,” he said.

Dr. Levy was not an investigator in the multicenter retrospective study, which included 76 patients with PHACE syndrome treated for infantile hemangioma with oral propranolol at 0.3 mg/kg per dose or more at 11 academic tertiary care pediatric dermatology clinics. Treatment started at a median age of 56 days.

There were no strokes, TIAs, cardiovascular events, or other significant problems associated with treatment. Twenty-nine children experienced mild adverse events: minor gastrointestinal or respiratory symptoms, and sleep disturbances were threefold more frequent than reported with placebo in another study. The investigators noted that the safety experience in their PHACE syndrome population compared favorably with that in 726 infants without PHACE syndrome who received oral propranolol for hemangiomas, where the incidence of serious adverse events on treatment was 0.4% (JAMA Dermatol. 2019 Dec 11. doi: 10.1001/jamadermatol.2019.3839).

 

‘Hemangiomas – but we were taught that they go away’

Dr. Levy gave a shout-out to the American Academy of Pediatrics for publishing interdisciplinary expert consensus-based practice guidelines for the management of infantile hemangiomas, which he praised as “quite well done” (Pediatrics. 2019 Jan;143[1]. pii: e20183475. doi: 10.1542/peds.2018-3475).

Following release of the guidelines last year, he and other pediatric vascular anomalies experts saw an uptick in referrals from general pediatricians, which has since tapered off.

“It’s probably like for all of us: We read an article, it’s fresh on the mind, then you forget about the article and what you’ve read. So we need a little reinforcement from a learning perspective. This is a great article,” he said.

The guidelines debunk as myth the classic teaching that infantile hemangiomas go away. Explicit information is provided about the high-risk anatomic sites warranting consideration for early referral, including the periocular, lumbosacral, and perineal areas, the lip, and lower face.

“The major point is early identification of those lesions requiring evaluation and intervention. Hemangiomas generally speaking are at their ultimate size by 3-5 months of age. The bottom line is if you think something needs to be done, please send that patient, or act upon that patient, sooner rather than later. I can’t tell you how many cases of hemangiomas I’ve seen when the kid is 18 months of age, 3 years of age, 5 years, with a large area of redundant skin, scarring, or something of that sort, and it would have been really nice to have seen them earlier and acted upon them then,” the pediatric dermatologist said.

The guidelines recommend intervention or referral by 1 month of age, ideally. Guidance is provided about the use of oral propranolol as first-line therapy.

“Propranolol is something that has been a real game changer for us,” he noted. “Many people continue to be worried about side effects in using this, particularly in the young childhood population, but this paper shows pretty clearly that hypotension or bradycardia is not a real concern. I never hospitalize these patients for propranolol therapy except in high-risk populations: very preemie, any history of breathing problems. We check the blood pressure and heart rate at baseline, again at 7-10 days, and at every visit. We’ve never found any significant drop in blood pressure.”

Dr. Levy reported financial relationships with half a dozen pharmaceutical companies, none relevant to his presentation.

SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

LAHAINA, HAWAII – Reassuring evidence of the safety of oral propranolol for treatment of complicated infantile hemangiomas in patients with PHACE syndrome comes from a recent multicenter study.

Bruce Jancin/MDedge News

Oral propranolol is now well-ensconced as first-line therapy for complicated infantile hemangiomas in otherwise healthy children. However, the beta-blocker’s use in PHACE (Posterior fossa malformations, Hemangiomas, Arterial anomalies, Cardiac defects, and Eye abnormalities) syndrome has been controversial, with concerns raised by some that it might raise the risk for arterial ischemic stroke. Not so, Moise L. Levy, MD, said at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

“I’m not suggesting you use propranolol with reckless abandon in this population, but this stroke concern is something that should be put to bed based on this study,” advised Dr. Levy, professor of dermatology and pediatrics at Dell Medical School in Austin, Tex., and physician-in-chief at Dell Children’s Medical Center.

PHACE syndrome is characterized by large, thick, plaque-like hemangiomas greater than 5 cm in size, most commonly on the face, although they can be located elsewhere.

“There was concern that if you found severely altered cerebrovascular arterial flow and you put a kid on a beta-blocker you might be causing some harm. But what I will tell you is that in this recently published paper this was not in fact an issue,” he said.

Dr. Levy was not an investigator in the multicenter retrospective study, which included 76 patients with PHACE syndrome treated for infantile hemangioma with oral propranolol at 0.3 mg/kg per dose or more at 11 academic tertiary care pediatric dermatology clinics. Treatment started at a median age of 56 days.

There were no strokes, TIAs, cardiovascular events, or other significant problems associated with treatment. Twenty-nine children experienced mild adverse events: minor gastrointestinal or respiratory symptoms, and sleep disturbances were threefold more frequent than reported with placebo in another study. The investigators noted that the safety experience in their PHACE syndrome population compared favorably with that in 726 infants without PHACE syndrome who received oral propranolol for hemangiomas, where the incidence of serious adverse events on treatment was 0.4% (JAMA Dermatol. 2019 Dec 11. doi: 10.1001/jamadermatol.2019.3839).

 

‘Hemangiomas – but we were taught that they go away’

Dr. Levy gave a shout-out to the American Academy of Pediatrics for publishing interdisciplinary expert consensus-based practice guidelines for the management of infantile hemangiomas, which he praised as “quite well done” (Pediatrics. 2019 Jan;143[1]. pii: e20183475. doi: 10.1542/peds.2018-3475).

Following release of the guidelines last year, he and other pediatric vascular anomalies experts saw an uptick in referrals from general pediatricians, which has since tapered off.

“It’s probably like for all of us: We read an article, it’s fresh on the mind, then you forget about the article and what you’ve read. So we need a little reinforcement from a learning perspective. This is a great article,” he said.

The guidelines debunk as myth the classic teaching that infantile hemangiomas go away. Explicit information is provided about the high-risk anatomic sites warranting consideration for early referral, including the periocular, lumbosacral, and perineal areas, the lip, and lower face.

“The major point is early identification of those lesions requiring evaluation and intervention. Hemangiomas generally speaking are at their ultimate size by 3-5 months of age. The bottom line is if you think something needs to be done, please send that patient, or act upon that patient, sooner rather than later. I can’t tell you how many cases of hemangiomas I’ve seen when the kid is 18 months of age, 3 years of age, 5 years, with a large area of redundant skin, scarring, or something of that sort, and it would have been really nice to have seen them earlier and acted upon them then,” the pediatric dermatologist said.

The guidelines recommend intervention or referral by 1 month of age, ideally. Guidance is provided about the use of oral propranolol as first-line therapy.

“Propranolol is something that has been a real game changer for us,” he noted. “Many people continue to be worried about side effects in using this, particularly in the young childhood population, but this paper shows pretty clearly that hypotension or bradycardia is not a real concern. I never hospitalize these patients for propranolol therapy except in high-risk populations: very preemie, any history of breathing problems. We check the blood pressure and heart rate at baseline, again at 7-10 days, and at every visit. We’ve never found any significant drop in blood pressure.”

Dr. Levy reported financial relationships with half a dozen pharmaceutical companies, none relevant to his presentation.

SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

LAHAINA, HAWAII – Reassuring evidence of the safety of oral propranolol for treatment of complicated infantile hemangiomas in patients with PHACE syndrome comes from a recent multicenter study.

Bruce Jancin/MDedge News

Oral propranolol is now well-ensconced as first-line therapy for complicated infantile hemangiomas in otherwise healthy children. However, the beta-blocker’s use in PHACE (Posterior fossa malformations, Hemangiomas, Arterial anomalies, Cardiac defects, and Eye abnormalities) syndrome has been controversial, with concerns raised by some that it might raise the risk for arterial ischemic stroke. Not so, Moise L. Levy, MD, said at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

“I’m not suggesting you use propranolol with reckless abandon in this population, but this stroke concern is something that should be put to bed based on this study,” advised Dr. Levy, professor of dermatology and pediatrics at Dell Medical School in Austin, Tex., and physician-in-chief at Dell Children’s Medical Center.

PHACE syndrome is characterized by large, thick, plaque-like hemangiomas greater than 5 cm in size, most commonly on the face, although they can be located elsewhere.

“There was concern that if you found severely altered cerebrovascular arterial flow and you put a kid on a beta-blocker you might be causing some harm. But what I will tell you is that in this recently published paper this was not in fact an issue,” he said.

Dr. Levy was not an investigator in the multicenter retrospective study, which included 76 patients with PHACE syndrome treated for infantile hemangioma with oral propranolol at 0.3 mg/kg per dose or more at 11 academic tertiary care pediatric dermatology clinics. Treatment started at a median age of 56 days.

There were no strokes, TIAs, cardiovascular events, or other significant problems associated with treatment. Twenty-nine children experienced mild adverse events: minor gastrointestinal or respiratory symptoms, and sleep disturbances were threefold more frequent than reported with placebo in another study. The investigators noted that the safety experience in their PHACE syndrome population compared favorably with that in 726 infants without PHACE syndrome who received oral propranolol for hemangiomas, where the incidence of serious adverse events on treatment was 0.4% (JAMA Dermatol. 2019 Dec 11. doi: 10.1001/jamadermatol.2019.3839).

 

‘Hemangiomas – but we were taught that they go away’

Dr. Levy gave a shout-out to the American Academy of Pediatrics for publishing interdisciplinary expert consensus-based practice guidelines for the management of infantile hemangiomas, which he praised as “quite well done” (Pediatrics. 2019 Jan;143[1]. pii: e20183475. doi: 10.1542/peds.2018-3475).

Following release of the guidelines last year, he and other pediatric vascular anomalies experts saw an uptick in referrals from general pediatricians, which has since tapered off.

“It’s probably like for all of us: We read an article, it’s fresh on the mind, then you forget about the article and what you’ve read. So we need a little reinforcement from a learning perspective. This is a great article,” he said.

The guidelines debunk as myth the classic teaching that infantile hemangiomas go away. Explicit information is provided about the high-risk anatomic sites warranting consideration for early referral, including the periocular, lumbosacral, and perineal areas, the lip, and lower face.

“The major point is early identification of those lesions requiring evaluation and intervention. Hemangiomas generally speaking are at their ultimate size by 3-5 months of age. The bottom line is if you think something needs to be done, please send that patient, or act upon that patient, sooner rather than later. I can’t tell you how many cases of hemangiomas I’ve seen when the kid is 18 months of age, 3 years of age, 5 years, with a large area of redundant skin, scarring, or something of that sort, and it would have been really nice to have seen them earlier and acted upon them then,” the pediatric dermatologist said.

The guidelines recommend intervention or referral by 1 month of age, ideally. Guidance is provided about the use of oral propranolol as first-line therapy.

“Propranolol is something that has been a real game changer for us,” he noted. “Many people continue to be worried about side effects in using this, particularly in the young childhood population, but this paper shows pretty clearly that hypotension or bradycardia is not a real concern. I never hospitalize these patients for propranolol therapy except in high-risk populations: very preemie, any history of breathing problems. We check the blood pressure and heart rate at baseline, again at 7-10 days, and at every visit. We’ve never found any significant drop in blood pressure.”

Dr. Levy reported financial relationships with half a dozen pharmaceutical companies, none relevant to his presentation.

SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On March 25, 2003, I was in Vancouver at my niece’s bat mitzvah when I saw a picture of my hospital in Toronto on the television news; a story about SARS patients in Toronto. Until then, SARS had been a distant event happening in mainland China and Hong Kong; it had been something that seemed very far away and theoretical. When I returned to Toronto, we had clusters of cases in several hospitals and healthcare workers were falling ill. I was the Physician in Chief at one of those hospitals and was responsible for the clinical care delivered by physicians in the Department of Medicine. So the burden of figuring out what we were going to do fell on me and the other members of the hospital leadership team.

As the outbreak evolved, we only knew a few things. It was a respiratory infection, likely viral, with a very high mortality rate, compared with most other viral respiratory infections. We learned the hard way that, while it was mostly transmitted by droplets, some patients were able to widely transmit it through the air, and therefore likely through ventilation systems. We knew that most infections were occurring in hospitals but there was also community spread at events like funerals. We had no test to confirm the presence of the virus and, indeed, only figured out it was a coronavirus well into the outbreak. Diagnoses were made using clinical criteria; this uncertainty was a major source of anxiety about potential community spread without direct links to known cases. We had no idea how long it was going to last, nor did we know how it would end. We were entering uncharted territory.

Decisions had to be made. Which patients needed isolation, and which did not? We made mistakes early on that caused hundreds of healthcare workers and people to be quarantined (complete isolation) for 10 days; this was a difficult situation for them, their families, and the people who had to replace them in the workplace.

Within a very short period we changed our way of life in hospitals. We screened everyone who entered with questionnaires and measured their temperatures. Once entering the hospital, we all wore N95 masks in public spaces and when in a room with another person—not just patients. We all got sore throats from wearing the masks 10 hours a day. All patients were placed in respiratory precautions, which meant that, any time we entered their rooms, we had to don all the personal protective equipment (PPE). Yet we didn’t run out of supplies. When a member of a provincial leadership team fell ill with SARS shortly after attending an in-person meeting of the committee, all the other members went into quarantine. As a result, we stopped having leadership team meetings in person, and mostly stayed in our own offices, communicating by phone and email.

The hospital took on a bizarre atmosphere: everyone in masks and little face-to-face contact. Yet outside the hospital, life went on mostly as normal. Some people wore masks on the street, but public events and businesses stayed open. Some healthcare workers were shunned in the community out of fear. But I went to another bat mitzvah and even a Stanley Cup playoff game at the height of the outbreak. Only healthcare workers were asked to stop meeting in large groups. The contrast for me was striking.

The Ontario Ministry of Health started a daily noon hour phone conference call; one physician and one administrator from every hospital in the province were on the call. I attended those for my hospital and, because I knew or taught many of the people on the line, was quickly asked to chair the calls. They were incredibly important and were a source of information exchange and emotional support for all of us. Before each call, I spoke with a person from Toronto Public Health who updated me on the number of cases and deaths. I needed to absorb that information before the calls to maintain my composure when she told the rest of the group. At times I could hear the fear in people’s voices as they described the clinical course of their patients.

Because I chaired the calls, I was asked to coordinate the study that documented the clinical outcomes of all the patients in the hopes that we could distinguish it from other common respiratory syndromes. With the help of my colleagues in the 11 hospitals that treated SARS patients, the ethics review boards, medical records personnel who copied the charts, Christopher Booth, MD, (a second- year resident at the time who headed the study), and a few medical students we were able to go from the idea to do the study to electronic publication in JAMA in 30 days.¹ It was JAMA’s first experience with rapid review, and the editors there were very helpful. Working on this study was very therapeutic; it allowed me to feel I was doing something that could help.

I was scared—both for my own health and the health of my family, but also terribly frightened for the health of the people who worked here. When I went home every night, I looked at the people on the street and wondered how many would still be there a few months later. And then it all ended. (Actually, it ended twice; we let up a bit too early because we so wanted it to be over.)

The COVID-19 pandemic has many similarities, but there are also significant differences. The most obvious is that because there is more community spread, life outside the hospital is much more severely disrupted. Countries have responded by sliding into more and more practices that try to limit person-to-person spread. First travel restrictions from other countries, then moral suasion to promote social distancing (which is really just physical distancing), then closing schools and nonessential businesses, and finally complete lock downs.

These events have spurred panic buying of some items (hand sanitizer, toilet paper, masks), and the fear of major disruptions of the supply chain for things like food. SARS was much more limited in its overall economic effect, though the WHO precautionary travel advisory against nonessential travel to Toronto, which lasted for only 1 week, resulted in a long-lasting reduction in tourism and a hit to the theatre business in our city.

The internet and social media have made it easier to disseminate valuable information and instructions, while at the same time easier to spread false information. But we had a lot of false information during SARS, too. One of the biggest differences for the United States (which was almost unaffected by SARS) is that the current extreme political divide creates two separate tracks of information and beliefs. A united message is very important.

Finally, the shortage of PPE in some jurisdictions, which was not an issue in Toronto during SARS, has severely heightened the fear for healthcare workers. In 2003, we also had lots of discussion about the tension between our professional duty and the safety of healthcare workers and their families (many of us separated ourselves from our families in our own homes while working clinically). To my recollection, two nurses and one physician died of SARS in Toronto. But when hospitals actually run out of PPE—something that is happening with COVID-19—those discussions take on a much more ominous tone.

In my opinion, SARS was a dry run for us in Toronto and the other places in the world that it affected (Taiwan, Hong Kong, Singapore); one that helped us prepare in advance and will help us cope with COVID-19. But what did I personally learn from my SARS experience?

First, I learned that accurate information in these kinds of situations is hard to come by. We heard lots of rumors from people all over the world. But when I found that it was very difficult for me to figure out exactly what was going on in my own hospital (eg, who was in contact with people who fell ill or went into quarantine, how patients were faring), I realized that figuring out what was happening half way around the world from news reports was near impossible. I learned to wait for official announcements.

Second, I learned that talking to my colleagues was both therapeutic—providing emotional support and an outlet for feelings—and anxiety provoking when we overreacted to rumors.

Third, I learned that, like others, I was susceptible to exhibiting obsessive behaviors in an attempt to establish control over uncertainty. Constantly washing my hands, checking my temperature, and seeking reassuring facts from others only worked to calm me for a few minutes. And then I felt the need to do it again. This time I find myself checking my twitter account constantly; half afraid I will see something frightening, half looking for good news from people I trust. I now recognize this behavior and it helps me contain it.

Fourth, I learned that events that occurred remotely had much less effect on everyone than those that occurred close by. Having two people I knew get SARS, and then learning they recovered was perhaps the most meaningful event for me during the entire episode.

Finally, I learned that in the end I and the people I care about survived—nothing bad happened to us. The world did not end after SARS. It took me about a year, including some time with a terrific psychiatrist, to realize I was safe after all. And that realization is what I am most hanging on to today.

Acknowledgments

Sanjay Saint (University of Michigan), Christopher Booth (Queens University), and Sagar Rohailla (University of Toronto) provided comments on an earlier draft. None were compensated for doing so.

On March 25, 2003, I was in Vancouver at my niece’s bat mitzvah when I saw a picture of my hospital in Toronto on the television news; a story about SARS patients in Toronto. Until then, SARS had been a distant event happening in mainland China and Hong Kong; it had been something that seemed very far away and theoretical. When I returned to Toronto, we had clusters of cases in several hospitals and healthcare workers were falling ill. I was the Physician in Chief at one of those hospitals and was responsible for the clinical care delivered by physicians in the Department of Medicine. So the burden of figuring out what we were going to do fell on me and the other members of the hospital leadership team.

As the outbreak evolved, we only knew a few things. It was a respiratory infection, likely viral, with a very high mortality rate, compared with most other viral respiratory infections. We learned the hard way that, while it was mostly transmitted by droplets, some patients were able to widely transmit it through the air, and therefore likely through ventilation systems. We knew that most infections were occurring in hospitals but there was also community spread at events like funerals. We had no test to confirm the presence of the virus and, indeed, only figured out it was a coronavirus well into the outbreak. Diagnoses were made using clinical criteria; this uncertainty was a major source of anxiety about potential community spread without direct links to known cases. We had no idea how long it was going to last, nor did we know how it would end. We were entering uncharted territory.

Decisions had to be made. Which patients needed isolation, and which did not? We made mistakes early on that caused hundreds of healthcare workers and people to be quarantined (complete isolation) for 10 days; this was a difficult situation for them, their families, and the people who had to replace them in the workplace.

Within a very short period we changed our way of life in hospitals. We screened everyone who entered with questionnaires and measured their temperatures. Once entering the hospital, we all wore N95 masks in public spaces and when in a room with another person—not just patients. We all got sore throats from wearing the masks 10 hours a day. All patients were placed in respiratory precautions, which meant that, any time we entered their rooms, we had to don all the personal protective equipment (PPE). Yet we didn’t run out of supplies. When a member of a provincial leadership team fell ill with SARS shortly after attending an in-person meeting of the committee, all the other members went into quarantine. As a result, we stopped having leadership team meetings in person, and mostly stayed in our own offices, communicating by phone and email.

The hospital took on a bizarre atmosphere: everyone in masks and little face-to-face contact. Yet outside the hospital, life went on mostly as normal. Some people wore masks on the street, but public events and businesses stayed open. Some healthcare workers were shunned in the community out of fear. But I went to another bat mitzvah and even a Stanley Cup playoff game at the height of the outbreak. Only healthcare workers were asked to stop meeting in large groups. The contrast for me was striking.

The Ontario Ministry of Health started a daily noon hour phone conference call; one physician and one administrator from every hospital in the province were on the call. I attended those for my hospital and, because I knew or taught many of the people on the line, was quickly asked to chair the calls. They were incredibly important and were a source of information exchange and emotional support for all of us. Before each call, I spoke with a person from Toronto Public Health who updated me on the number of cases and deaths. I needed to absorb that information before the calls to maintain my composure when she told the rest of the group. At times I could hear the fear in people’s voices as they described the clinical course of their patients.

Because I chaired the calls, I was asked to coordinate the study that documented the clinical outcomes of all the patients in the hopes that we could distinguish it from other common respiratory syndromes. With the help of my colleagues in the 11 hospitals that treated SARS patients, the ethics review boards, medical records personnel who copied the charts, Christopher Booth, MD, (a second- year resident at the time who headed the study), and a few medical students we were able to go from the idea to do the study to electronic publication in JAMA in 30 days.¹ It was JAMA’s first experience with rapid review, and the editors there were very helpful. Working on this study was very therapeutic; it allowed me to feel I was doing something that could help.

I was scared—both for my own health and the health of my family, but also terribly frightened for the health of the people who worked here. When I went home every night, I looked at the people on the street and wondered how many would still be there a few months later. And then it all ended. (Actually, it ended twice; we let up a bit too early because we so wanted it to be over.)

The COVID-19 pandemic has many similarities, but there are also significant differences. The most obvious is that because there is more community spread, life outside the hospital is much more severely disrupted. Countries have responded by sliding into more and more practices that try to limit person-to-person spread. First travel restrictions from other countries, then moral suasion to promote social distancing (which is really just physical distancing), then closing schools and nonessential businesses, and finally complete lock downs.

These events have spurred panic buying of some items (hand sanitizer, toilet paper, masks), and the fear of major disruptions of the supply chain for things like food. SARS was much more limited in its overall economic effect, though the WHO precautionary travel advisory against nonessential travel to Toronto, which lasted for only 1 week, resulted in a long-lasting reduction in tourism and a hit to the theatre business in our city.

The internet and social media have made it easier to disseminate valuable information and instructions, while at the same time easier to spread false information. But we had a lot of false information during SARS, too. One of the biggest differences for the United States (which was almost unaffected by SARS) is that the current extreme political divide creates two separate tracks of information and beliefs. A united message is very important.

Finally, the shortage of PPE in some jurisdictions, which was not an issue in Toronto during SARS, has severely heightened the fear for healthcare workers. In 2003, we also had lots of discussion about the tension between our professional duty and the safety of healthcare workers and their families (many of us separated ourselves from our families in our own homes while working clinically). To my recollection, two nurses and one physician died of SARS in Toronto. But when hospitals actually run out of PPE—something that is happening with COVID-19—those discussions take on a much more ominous tone.

In my opinion, SARS was a dry run for us in Toronto and the other places in the world that it affected (Taiwan, Hong Kong, Singapore); one that helped us prepare in advance and will help us cope with COVID-19. But what did I personally learn from my SARS experience?

First, I learned that accurate information in these kinds of situations is hard to come by. We heard lots of rumors from people all over the world. But when I found that it was very difficult for me to figure out exactly what was going on in my own hospital (eg, who was in contact with people who fell ill or went into quarantine, how patients were faring), I realized that figuring out what was happening half way around the world from news reports was near impossible. I learned to wait for official announcements.

Second, I learned that talking to my colleagues was both therapeutic—providing emotional support and an outlet for feelings—and anxiety provoking when we overreacted to rumors.

Third, I learned that, like others, I was susceptible to exhibiting obsessive behaviors in an attempt to establish control over uncertainty. Constantly washing my hands, checking my temperature, and seeking reassuring facts from others only worked to calm me for a few minutes. And then I felt the need to do it again. This time I find myself checking my twitter account constantly; half afraid I will see something frightening, half looking for good news from people I trust. I now recognize this behavior and it helps me contain it.

Fourth, I learned that events that occurred remotely had much less effect on everyone than those that occurred close by. Having two people I knew get SARS, and then learning they recovered was perhaps the most meaningful event for me during the entire episode.

Finally, I learned that in the end I and the people I care about survived—nothing bad happened to us. The world did not end after SARS. It took me about a year, including some time with a terrific psychiatrist, to realize I was safe after all. And that realization is what I am most hanging on to today.

Acknowledgments

Sanjay Saint (University of Michigan), Christopher Booth (Queens University), and Sagar Rohailla (University of Toronto) provided comments on an earlier draft. None were compensated for doing so.

On March 25, 2003, I was in Vancouver at my niece’s bat mitzvah when I saw a picture of my hospital in Toronto on the television news; a story about SARS patients in Toronto. Until then, SARS had been a distant event happening in mainland China and Hong Kong; it had been something that seemed very far away and theoretical. When I returned to Toronto, we had clusters of cases in several hospitals and healthcare workers were falling ill. I was the Physician in Chief at one of those hospitals and was responsible for the clinical care delivered by physicians in the Department of Medicine. So the burden of figuring out what we were going to do fell on me and the other members of the hospital leadership team.

As the outbreak evolved, we only knew a few things. It was a respiratory infection, likely viral, with a very high mortality rate, compared with most other viral respiratory infections. We learned the hard way that, while it was mostly transmitted by droplets, some patients were able to widely transmit it through the air, and therefore likely through ventilation systems. We knew that most infections were occurring in hospitals but there was also community spread at events like funerals. We had no test to confirm the presence of the virus and, indeed, only figured out it was a coronavirus well into the outbreak. Diagnoses were made using clinical criteria; this uncertainty was a major source of anxiety about potential community spread without direct links to known cases. We had no idea how long it was going to last, nor did we know how it would end. We were entering uncharted territory.

Decisions had to be made. Which patients needed isolation, and which did not? We made mistakes early on that caused hundreds of healthcare workers and people to be quarantined (complete isolation) for 10 days; this was a difficult situation for them, their families, and the people who had to replace them in the workplace.

Within a very short period we changed our way of life in hospitals. We screened everyone who entered with questionnaires and measured their temperatures. Once entering the hospital, we all wore N95 masks in public spaces and when in a room with another person—not just patients. We all got sore throats from wearing the masks 10 hours a day. All patients were placed in respiratory precautions, which meant that, any time we entered their rooms, we had to don all the personal protective equipment (PPE). Yet we didn’t run out of supplies. When a member of a provincial leadership team fell ill with SARS shortly after attending an in-person meeting of the committee, all the other members went into quarantine. As a result, we stopped having leadership team meetings in person, and mostly stayed in our own offices, communicating by phone and email.

The hospital took on a bizarre atmosphere: everyone in masks and little face-to-face contact. Yet outside the hospital, life went on mostly as normal. Some people wore masks on the street, but public events and businesses stayed open. Some healthcare workers were shunned in the community out of fear. But I went to another bat mitzvah and even a Stanley Cup playoff game at the height of the outbreak. Only healthcare workers were asked to stop meeting in large groups. The contrast for me was striking.

The Ontario Ministry of Health started a daily noon hour phone conference call; one physician and one administrator from every hospital in the province were on the call. I attended those for my hospital and, because I knew or taught many of the people on the line, was quickly asked to chair the calls. They were incredibly important and were a source of information exchange and emotional support for all of us. Before each call, I spoke with a person from Toronto Public Health who updated me on the number of cases and deaths. I needed to absorb that information before the calls to maintain my composure when she told the rest of the group. At times I could hear the fear in people’s voices as they described the clinical course of their patients.

Because I chaired the calls, I was asked to coordinate the study that documented the clinical outcomes of all the patients in the hopes that we could distinguish it from other common respiratory syndromes. With the help of my colleagues in the 11 hospitals that treated SARS patients, the ethics review boards, medical records personnel who copied the charts, Christopher Booth, MD, (a second- year resident at the time who headed the study), and a few medical students we were able to go from the idea to do the study to electronic publication in JAMA in 30 days.¹ It was JAMA’s first experience with rapid review, and the editors there were very helpful. Working on this study was very therapeutic; it allowed me to feel I was doing something that could help.

I was scared—both for my own health and the health of my family, but also terribly frightened for the health of the people who worked here. When I went home every night, I looked at the people on the street and wondered how many would still be there a few months later. And then it all ended. (Actually, it ended twice; we let up a bit too early because we so wanted it to be over.)

The COVID-19 pandemic has many similarities, but there are also significant differences. The most obvious is that because there is more community spread, life outside the hospital is much more severely disrupted. Countries have responded by sliding into more and more practices that try to limit person-to-person spread. First travel restrictions from other countries, then moral suasion to promote social distancing (which is really just physical distancing), then closing schools and nonessential businesses, and finally complete lock downs.

These events have spurred panic buying of some items (hand sanitizer, toilet paper, masks), and the fear of major disruptions of the supply chain for things like food. SARS was much more limited in its overall economic effect, though the WHO precautionary travel advisory against nonessential travel to Toronto, which lasted for only 1 week, resulted in a long-lasting reduction in tourism and a hit to the theatre business in our city.

The internet and social media have made it easier to disseminate valuable information and instructions, while at the same time easier to spread false information. But we had a lot of false information during SARS, too. One of the biggest differences for the United States (which was almost unaffected by SARS) is that the current extreme political divide creates two separate tracks of information and beliefs. A united message is very important.

Finally, the shortage of PPE in some jurisdictions, which was not an issue in Toronto during SARS, has severely heightened the fear for healthcare workers. In 2003, we also had lots of discussion about the tension between our professional duty and the safety of healthcare workers and their families (many of us separated ourselves from our families in our own homes while working clinically). To my recollection, two nurses and one physician died of SARS in Toronto. But when hospitals actually run out of PPE—something that is happening with COVID-19—those discussions take on a much more ominous tone.

In my opinion, SARS was a dry run for us in Toronto and the other places in the world that it affected (Taiwan, Hong Kong, Singapore); one that helped us prepare in advance and will help us cope with COVID-19. But what did I personally learn from my SARS experience?

First, I learned that accurate information in these kinds of situations is hard to come by. We heard lots of rumors from people all over the world. But when I found that it was very difficult for me to figure out exactly what was going on in my own hospital (eg, who was in contact with people who fell ill or went into quarantine, how patients were faring), I realized that figuring out what was happening half way around the world from news reports was near impossible. I learned to wait for official announcements.

Second, I learned that talking to my colleagues was both therapeutic—providing emotional support and an outlet for feelings—and anxiety provoking when we overreacted to rumors.

Third, I learned that, like others, I was susceptible to exhibiting obsessive behaviors in an attempt to establish control over uncertainty. Constantly washing my hands, checking my temperature, and seeking reassuring facts from others only worked to calm me for a few minutes. And then I felt the need to do it again. This time I find myself checking my twitter account constantly; half afraid I will see something frightening, half looking for good news from people I trust. I now recognize this behavior and it helps me contain it.

Fourth, I learned that events that occurred remotely had much less effect on everyone than those that occurred close by. Having two people I knew get SARS, and then learning they recovered was perhaps the most meaningful event for me during the entire episode.

Finally, I learned that in the end I and the people I care about survived—nothing bad happened to us. The world did not end after SARS. It took me about a year, including some time with a terrific psychiatrist, to realize I was safe after all. And that realization is what I am most hanging on to today.

Acknowledgments

Sanjay Saint (University of Michigan), Christopher Booth (Queens University), and Sagar Rohailla (University of Toronto) provided comments on an earlier draft. None were compensated for doing so.

LAHAINA, HAWAII – The rash commonly called perioral dermatitis is more appropriately termed periorificial dermatitis, according to Jessica Sprague, MD, a pediatric dermatologist at the University of California, San Diego, and Rady Children’s Hospital.

Bruce Jancin/MDedge News

Years ago, some of her senior colleagues at the children’s hospital carried out a retrospective study of 79 patients, aged 6 months to 18 years, who were treated for what’s typically called perioral dermatitis. Of note, only 40% of patients had isolated perioral involvement, while 30% of the patients had no perioral lesions at all. Perinasal lesions were present in 43%, and 25% had periocular involvement, she noted at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

The peak incidence of periorificial dermatitis in this series was under age 5 years. At presentation, the rash had been present for an average of 8 months. Seventy-two percent of patients had a history of exposure to corticosteroids, most often in the form of topical steroids, but in some cases inhaled or systemic steroids.

“Obviously you want to discontinue the topical steroid. Sometimes you need to taper them off, or you can switch to a topical calcineurin inhibitor [TCI] because they tend to flare a lot when you stop their topical steroid, although there are cases of TCIs precipitating periorificial dermatitis, so keep that in mind,” Dr. Sprague said.

If a patient is on inhaled steroids by mask for asthma, switching to a tube can sometimes limit the exposure, she continued.

Dr. Jessica Sprague, University of California, San Diego; Rady Children's

[email protected]

LAHAINA, HAWAII – The rash commonly called perioral dermatitis is more appropriately termed periorificial dermatitis, according to Jessica Sprague, MD, a pediatric dermatologist at the University of California, San Diego, and Rady Children’s Hospital.

Bruce Jancin/MDedge News

Years ago, some of her senior colleagues at the children’s hospital carried out a retrospective study of 79 patients, aged 6 months to 18 years, who were treated for what’s typically called perioral dermatitis. Of note, only 40% of patients had isolated perioral involvement, while 30% of the patients had no perioral lesions at all. Perinasal lesions were present in 43%, and 25% had periocular involvement, she noted at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

The peak incidence of periorificial dermatitis in this series was under age 5 years. At presentation, the rash had been present for an average of 8 months. Seventy-two percent of patients had a history of exposure to corticosteroids, most often in the form of topical steroids, but in some cases inhaled or systemic steroids.

“Obviously you want to discontinue the topical steroid. Sometimes you need to taper them off, or you can switch to a topical calcineurin inhibitor [TCI] because they tend to flare a lot when you stop their topical steroid, although there are cases of TCIs precipitating periorificial dermatitis, so keep that in mind,” Dr. Sprague said.

If a patient is on inhaled steroids by mask for asthma, switching to a tube can sometimes limit the exposure, she continued.

Dr. Jessica Sprague, University of California, San Diego; Rady Children's

[email protected]

LAHAINA, HAWAII – The rash commonly called perioral dermatitis is more appropriately termed periorificial dermatitis, according to Jessica Sprague, MD, a pediatric dermatologist at the University of California, San Diego, and Rady Children’s Hospital.

Bruce Jancin/MDedge News

Years ago, some of her senior colleagues at the children’s hospital carried out a retrospective study of 79 patients, aged 6 months to 18 years, who were treated for what’s typically called perioral dermatitis. Of note, only 40% of patients had isolated perioral involvement, while 30% of the patients had no perioral lesions at all. Perinasal lesions were present in 43%, and 25% had periocular involvement, she noted at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

The peak incidence of periorificial dermatitis in this series was under age 5 years. At presentation, the rash had been present for an average of 8 months. Seventy-two percent of patients had a history of exposure to corticosteroids, most often in the form of topical steroids, but in some cases inhaled or systemic steroids.

“Obviously you want to discontinue the topical steroid. Sometimes you need to taper them off, or you can switch to a topical calcineurin inhibitor [TCI] because they tend to flare a lot when you stop their topical steroid, although there are cases of TCIs precipitating periorificial dermatitis, so keep that in mind,” Dr. Sprague said.

If a patient is on inhaled steroids by mask for asthma, switching to a tube can sometimes limit the exposure, she continued.

Dr. Jessica Sprague, University of California, San Diego; Rady Children's

[email protected]

MAUI, HAWAII – Viewing seronegative rheumatoid arthritis as something akin to RA-lite would be a big mistake, John J. Cush, MD, asserted at the 2020 Rheumatology Winter Clinical Symposium.

Bruce Jancin/MDedge News

“It’s not a benign subtype of RA. And then again, it may not be RA,” Dr. Cush observed,

“Seronegative RA means that either you need to get serious about what is probably badass disease or you need to reevaluate whether this really is RA and your need for DMARDs [disease-modifying antirheumatic drugs] in an ongoing fashion,” the rheumatologist said. “Always reconsider whether they need less therapy or maybe no therapy at all. Maybe they had inflammation at one point and now they’re left with degenerative and mechanical changes that don’t require a DMARD or biologic.”

He highlighted a Finnish 10-year, prospective, observational study that sheds light on the subject. The study demonstrated that seronegative RA is seldom what it at first seems. The Finnish rheumatologists followed 435 consecutive patients initially diagnosed as having seronegative early RA. The structured follow-up entailed four or five interdisciplinary clinic visits within the first 2 years after diagnosis and again at 5 and 10 years.

By the 10-year mark only 4 of the 435 initially seronegative RA patients had been reclassified as having seropositive RA, while another 9 were reclassified as having erosive RA based upon the development of pathognomonic joint lesions. That’s a paltry 3% reclassification rate to classic RA.

Nearly two-thirds of patients were ultimately reclassified within 10 years as they evolved into diagnoses other than their original seronegative RA. The most common included nonerosive polymyalgia rheumatica in 16% of participants, psoriatic arthritis in 11%, osteoarthritis in 10%, spondyloarthritis in 8.7%, gout in 2.3%, and pseudogout in 3.9%.

“I think that’s sobering for you if you’re taking care of these patients, that maybe you need to rethink the diagnosis at every visit or at periodic intervals, especially if you’re going to change therapy,” advised Dr. Cush, who is professor of medicine and rheumatology at Baylor University Medical Center, Dallas, and director of clinical rheumatology at the Baylor Research Institute.

The Finnish rheumatologists observed that their findings have important implications both for clinical practice and for research, since RA clinical trials typically include a substantial proportion of seronegative patients.

“If seronegative patients are treated according to the treatment guidelines for progressive RA, a substantial proportion of patients is exposed to unnecessary long-term medication,” the investigators wrote, adding that their “results suggest that it may not be reasonable to study seronegative arthritis patients as a homogeneous entity in RA studies.”

The best recent data suggests about 15% of RA patients are seronegative, Dr. Cush said.

Delay in diagnosis is common in seronegative RA, as highlighted in a recent population-based study by Mayo Clinic rheumatologists. They reported that the median time from first joint swelling to diagnosis of seronegative RA using the 2010 American College of Rheumatology/European League Against Rheumatism criteria was 187 days, compared with a mere 11 days for seropositive RA. The median time to DMARD initiation was longer, too. Half of seropositive RA patients achieved remission within 5 years, as did 28% of seronegative patients, prompting the investigators to conclude “the window of opportunity for intervention may be more frequently missed in this group.”
 

Choosing the best treatment

Several medications appear to have greater efficacy in seropositive than seronegative RA patients. For example, a meta-analysis of four randomized trials including a collective 2,177 RA patients assigned 2:1 to rituximab (Rituxan) or placebo concluded that 75% of seropositive RA patients had a EULAR moderate or good response at week 24 on the biologic, compared with 44% of seronegative patients.

“Would you not use rituximab in someone who’s seronegative? No, I actually would use it. I may not rush to use it as much, maybe give it earlier in someone who’s seropositive, but I’ve used rituximab in seronegative patients who’ve done just fine,” according to Dr. Cush.

The published experience with abatacept (Orencia) is mixed, most of it coming from European observational datasets. On balance though, 80% of the articles addressing the issue have concluded that response rates to the biologic are better in seropositive RA, he continued.

Australian investigators who pooled data from five phase 3 randomized clinical trials of tofacitinib (Xeljanz) in RA concluded that double-positive patients – that is, those who were seropositive for both rheumatoid factor and anti–citrullinated protein antibody (ACPA) – were roughly twice as likely to achieve ACR20 and ACR50 responses to the oral Janus kinase inhibitor at either 5 or 10 mg twice daily than patients who were double negative.

“Double positivity is very important in prognosis and severity, compared to single positivity,” the rheumatologist observed. “I think you should worry most about the patients who have the highest titers of rheumatoid factor and ACPA.”

Asked about the merits of supplemental laboratory testing for serum 14-3-3 eta, a proposed novel biomarker in RA, as well as for anti–carbamylated protein antibodies (anti-CarP), Dr. Cush replied that it’s unclear that the additional testing is really worthwhile.

“Ordering more tests doesn’t make us smarter,” he commented. “Quite simply, with rheumatoid factor and ACPA, adding one on top of the other, you just gain maybe 10% more certainty in the diagnosis. Adding anti-CarP antibodies or serum 14-3-3 eta doesn’t add more than a few percentage points, but now you’ve quadrupled the cost of testing.”

Dr. Cush reported receiving research funding from and/or serving as a consultant to numerous pharmaceutical companies.

[email protected]

MAUI, HAWAII – Viewing seronegative rheumatoid arthritis as something akin to RA-lite would be a big mistake, John J. Cush, MD, asserted at the 2020 Rheumatology Winter Clinical Symposium.

Bruce Jancin/MDedge News

“It’s not a benign subtype of RA. And then again, it may not be RA,” Dr. Cush observed,

“Seronegative RA means that either you need to get serious about what is probably badass disease or you need to reevaluate whether this really is RA and your need for DMARDs [disease-modifying antirheumatic drugs] in an ongoing fashion,” the rheumatologist said. “Always reconsider whether they need less therapy or maybe no therapy at all. Maybe they had inflammation at one point and now they’re left with degenerative and mechanical changes that don’t require a DMARD or biologic.”

He highlighted a Finnish 10-year, prospective, observational study that sheds light on the subject. The study demonstrated that seronegative RA is seldom what it at first seems. The Finnish rheumatologists followed 435 consecutive patients initially diagnosed as having seronegative early RA. The structured follow-up entailed four or five interdisciplinary clinic visits within the first 2 years after diagnosis and again at 5 and 10 years.

By the 10-year mark only 4 of the 435 initially seronegative RA patients had been reclassified as having seropositive RA, while another 9 were reclassified as having erosive RA based upon the development of pathognomonic joint lesions. That’s a paltry 3% reclassification rate to classic RA.

Nearly two-thirds of patients were ultimately reclassified within 10 years as they evolved into diagnoses other than their original seronegative RA. The most common included nonerosive polymyalgia rheumatica in 16% of participants, psoriatic arthritis in 11%, osteoarthritis in 10%, spondyloarthritis in 8.7%, gout in 2.3%, and pseudogout in 3.9%.

“I think that’s sobering for you if you’re taking care of these patients, that maybe you need to rethink the diagnosis at every visit or at periodic intervals, especially if you’re going to change therapy,” advised Dr. Cush, who is professor of medicine and rheumatology at Baylor University Medical Center, Dallas, and director of clinical rheumatology at the Baylor Research Institute.

The Finnish rheumatologists observed that their findings have important implications both for clinical practice and for research, since RA clinical trials typically include a substantial proportion of seronegative patients.

“If seronegative patients are treated according to the treatment guidelines for progressive RA, a substantial proportion of patients is exposed to unnecessary long-term medication,” the investigators wrote, adding that their “results suggest that it may not be reasonable to study seronegative arthritis patients as a homogeneous entity in RA studies.”

The best recent data suggests about 15% of RA patients are seronegative, Dr. Cush said.

Delay in diagnosis is common in seronegative RA, as highlighted in a recent population-based study by Mayo Clinic rheumatologists. They reported that the median time from first joint swelling to diagnosis of seronegative RA using the 2010 American College of Rheumatology/European League Against Rheumatism criteria was 187 days, compared with a mere 11 days for seropositive RA. The median time to DMARD initiation was longer, too. Half of seropositive RA patients achieved remission within 5 years, as did 28% of seronegative patients, prompting the investigators to conclude “the window of opportunity for intervention may be more frequently missed in this group.”
 

Choosing the best treatment

Several medications appear to have greater efficacy in seropositive than seronegative RA patients. For example, a meta-analysis of four randomized trials including a collective 2,177 RA patients assigned 2:1 to rituximab (Rituxan) or placebo concluded that 75% of seropositive RA patients had a EULAR moderate or good response at week 24 on the biologic, compared with 44% of seronegative patients.

“Would you not use rituximab in someone who’s seronegative? No, I actually would use it. I may not rush to use it as much, maybe give it earlier in someone who’s seropositive, but I’ve used rituximab in seronegative patients who’ve done just fine,” according to Dr. Cush.

The published experience with abatacept (Orencia) is mixed, most of it coming from European observational datasets. On balance though, 80% of the articles addressing the issue have concluded that response rates to the biologic are better in seropositive RA, he continued.

Australian investigators who pooled data from five phase 3 randomized clinical trials of tofacitinib (Xeljanz) in RA concluded that double-positive patients – that is, those who were seropositive for both rheumatoid factor and anti–citrullinated protein antibody (ACPA) – were roughly twice as likely to achieve ACR20 and ACR50 responses to the oral Janus kinase inhibitor at either 5 or 10 mg twice daily than patients who were double negative.

“Double positivity is very important in prognosis and severity, compared to single positivity,” the rheumatologist observed. “I think you should worry most about the patients who have the highest titers of rheumatoid factor and ACPA.”

Asked about the merits of supplemental laboratory testing for serum 14-3-3 eta, a proposed novel biomarker in RA, as well as for anti–carbamylated protein antibodies (anti-CarP), Dr. Cush replied that it’s unclear that the additional testing is really worthwhile.

“Ordering more tests doesn’t make us smarter,” he commented. “Quite simply, with rheumatoid factor and ACPA, adding one on top of the other, you just gain maybe 10% more certainty in the diagnosis. Adding anti-CarP antibodies or serum 14-3-3 eta doesn’t add more than a few percentage points, but now you’ve quadrupled the cost of testing.”

Dr. Cush reported receiving research funding from and/or serving as a consultant to numerous pharmaceutical companies.

[email protected]

MAUI, HAWAII – Viewing seronegative rheumatoid arthritis as something akin to RA-lite would be a big mistake, John J. Cush, MD, asserted at the 2020 Rheumatology Winter Clinical Symposium.

Bruce Jancin/MDedge News

“It’s not a benign subtype of RA. And then again, it may not be RA,” Dr. Cush observed,

“Seronegative RA means that either you need to get serious about what is probably badass disease or you need to reevaluate whether this really is RA and your need for DMARDs [disease-modifying antirheumatic drugs] in an ongoing fashion,” the rheumatologist said. “Always reconsider whether they need less therapy or maybe no therapy at all. Maybe they had inflammation at one point and now they’re left with degenerative and mechanical changes that don’t require a DMARD or biologic.”

He highlighted a Finnish 10-year, prospective, observational study that sheds light on the subject. The study demonstrated that seronegative RA is seldom what it at first seems. The Finnish rheumatologists followed 435 consecutive patients initially diagnosed as having seronegative early RA. The structured follow-up entailed four or five interdisciplinary clinic visits within the first 2 years after diagnosis and again at 5 and 10 years.

By the 10-year mark only 4 of the 435 initially seronegative RA patients had been reclassified as having seropositive RA, while another 9 were reclassified as having erosive RA based upon the development of pathognomonic joint lesions. That’s a paltry 3% reclassification rate to classic RA.

Nearly two-thirds of patients were ultimately reclassified within 10 years as they evolved into diagnoses other than their original seronegative RA. The most common included nonerosive polymyalgia rheumatica in 16% of participants, psoriatic arthritis in 11%, osteoarthritis in 10%, spondyloarthritis in 8.7%, gout in 2.3%, and pseudogout in 3.9%.

“I think that’s sobering for you if you’re taking care of these patients, that maybe you need to rethink the diagnosis at every visit or at periodic intervals, especially if you’re going to change therapy,” advised Dr. Cush, who is professor of medicine and rheumatology at Baylor University Medical Center, Dallas, and director of clinical rheumatology at the Baylor Research Institute.

The Finnish rheumatologists observed that their findings have important implications both for clinical practice and for research, since RA clinical trials typically include a substantial proportion of seronegative patients.

“If seronegative patients are treated according to the treatment guidelines for progressive RA, a substantial proportion of patients is exposed to unnecessary long-term medication,” the investigators wrote, adding that their “results suggest that it may not be reasonable to study seronegative arthritis patients as a homogeneous entity in RA studies.”

The best recent data suggests about 15% of RA patients are seronegative, Dr. Cush said.

Delay in diagnosis is common in seronegative RA, as highlighted in a recent population-based study by Mayo Clinic rheumatologists. They reported that the median time from first joint swelling to diagnosis of seronegative RA using the 2010 American College of Rheumatology/European League Against Rheumatism criteria was 187 days, compared with a mere 11 days for seropositive RA. The median time to DMARD initiation was longer, too. Half of seropositive RA patients achieved remission within 5 years, as did 28% of seronegative patients, prompting the investigators to conclude “the window of opportunity for intervention may be more frequently missed in this group.”
 

Choosing the best treatment

Several medications appear to have greater efficacy in seropositive than seronegative RA patients. For example, a meta-analysis of four randomized trials including a collective 2,177 RA patients assigned 2:1 to rituximab (Rituxan) or placebo concluded that 75% of seropositive RA patients had a EULAR moderate or good response at week 24 on the biologic, compared with 44% of seronegative patients.

“Would you not use rituximab in someone who’s seronegative? No, I actually would use it. I may not rush to use it as much, maybe give it earlier in someone who’s seropositive, but I’ve used rituximab in seronegative patients who’ve done just fine,” according to Dr. Cush.

The published experience with abatacept (Orencia) is mixed, most of it coming from European observational datasets. On balance though, 80% of the articles addressing the issue have concluded that response rates to the biologic are better in seropositive RA, he continued.

Australian investigators who pooled data from five phase 3 randomized clinical trials of tofacitinib (Xeljanz) in RA concluded that double-positive patients – that is, those who were seropositive for both rheumatoid factor and anti–citrullinated protein antibody (ACPA) – were roughly twice as likely to achieve ACR20 and ACR50 responses to the oral Janus kinase inhibitor at either 5 or 10 mg twice daily than patients who were double negative.

“Double positivity is very important in prognosis and severity, compared to single positivity,” the rheumatologist observed. “I think you should worry most about the patients who have the highest titers of rheumatoid factor and ACPA.”

Asked about the merits of supplemental laboratory testing for serum 14-3-3 eta, a proposed novel biomarker in RA, as well as for anti–carbamylated protein antibodies (anti-CarP), Dr. Cush replied that it’s unclear that the additional testing is really worthwhile.

“Ordering more tests doesn’t make us smarter,” he commented. “Quite simply, with rheumatoid factor and ACPA, adding one on top of the other, you just gain maybe 10% more certainty in the diagnosis. Adding anti-CarP antibodies or serum 14-3-3 eta doesn’t add more than a few percentage points, but now you’ve quadrupled the cost of testing.”

Dr. Cush reported receiving research funding from and/or serving as a consultant to numerous pharmaceutical companies.

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