United States now over 1,000 measles cases this year

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Tue, 06/11/2019 - 09:58

 

Measles cases in the United States have topped 1,000 for the first time since 1992, according to the Centers for Disease Control and Prevention.

The 41 new cases reported for the week ending June 6 bring the total for the year to 1,022, the CDC reported June 10, and that is more than any year since 1992, when there were 2,237 cases.

Idaho and Virginia reported their first cases of 2019, which makes a total of 28 states with measles cases this year. The Idaho case was reported in Latah County and is the state’s first since 2001. In Virginia, health officials are investigating possible contacts with an infected individual at Dulles International Airport and two other locations on June 2 and 4.



Outbreaks in Georgia, Maryland, and Michigan have ended, while seven others continue in California (Butte, Los Angeles, and Sacramento Counties), New York (Rockland County and New York City), Pennsylvania, and Washington, the CDC said. New York City has the largest outbreak this year with 509 cases through June 3, most of them occurring in Brooklyn.

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Measles cases in the United States have topped 1,000 for the first time since 1992, according to the Centers for Disease Control and Prevention.

The 41 new cases reported for the week ending June 6 bring the total for the year to 1,022, the CDC reported June 10, and that is more than any year since 1992, when there were 2,237 cases.

Idaho and Virginia reported their first cases of 2019, which makes a total of 28 states with measles cases this year. The Idaho case was reported in Latah County and is the state’s first since 2001. In Virginia, health officials are investigating possible contacts with an infected individual at Dulles International Airport and two other locations on June 2 and 4.



Outbreaks in Georgia, Maryland, and Michigan have ended, while seven others continue in California (Butte, Los Angeles, and Sacramento Counties), New York (Rockland County and New York City), Pennsylvania, and Washington, the CDC said. New York City has the largest outbreak this year with 509 cases through June 3, most of them occurring in Brooklyn.

 

Measles cases in the United States have topped 1,000 for the first time since 1992, according to the Centers for Disease Control and Prevention.

The 41 new cases reported for the week ending June 6 bring the total for the year to 1,022, the CDC reported June 10, and that is more than any year since 1992, when there were 2,237 cases.

Idaho and Virginia reported their first cases of 2019, which makes a total of 28 states with measles cases this year. The Idaho case was reported in Latah County and is the state’s first since 2001. In Virginia, health officials are investigating possible contacts with an infected individual at Dulles International Airport and two other locations on June 2 and 4.



Outbreaks in Georgia, Maryland, and Michigan have ended, while seven others continue in California (Butte, Los Angeles, and Sacramento Counties), New York (Rockland County and New York City), Pennsylvania, and Washington, the CDC said. New York City has the largest outbreak this year with 509 cases through June 3, most of them occurring in Brooklyn.

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Discharge before noon: An appropriate metric for efficiency?

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Mon, 06/10/2019 - 14:18

 

I first heard the term “discharge before noon” (DCBN) as a third-year medical student starting my internal medicine rotation. The basic idea made sense: Get patients out of the hospital early so rooms can be cleaned more quickly and new patients wouldn’t have to wait so long in the ED.

Dr. Jennifer K. Chen

It quickly became apparent, however, that a lot of moving parts had to align perfectly for DCBN. Even if we prioritized rounding on dischargeable patients (starting 8-9 a.m. depending on the service/day), they still needed prescriptions filled, normal clothes to wear, and a way to get home, which wasn’t easy to coordinate while we were still trying to see all the other patients.

Fast forward through 5 years of residency/fellowship experience and DCBN seems even more unrealistic in hospitalized pediatric patients. As a simple example, discharge criteria for dehydration (one of the most common reasons for pediatric hospitalization) include demonstrating the ability to drink enough liquids to stay hydrated. Who’s going to force children to stay up all night sipping fluids (plus changing all those diapers or taking them to the bathroom)? If the child stays on intravenous fluids overnight, we have to monitor at least through breakfast, likely lunch, thus making DCBN nearly impossible.

In a January 2019 article in the Journal of Hospital Medicine, Hailey James, MHA, (@Haileyjms on Twitter) and her colleagues demonstrated an association between DCBN and decreased length of stay (LOS) for medical but not surgical pediatric discharges.1 This made them question if DCBN is an appropriate metric for discharge efficiency, as well as workflow differences between services. Many hospitals, however, still try to push DCBN as a goal (see Destino et al in the same January 2019 issue of JHM2), which could potentially lead to people trying to game the system.

How does your institution try to make discharge processes more efficient? Is it actually possible to do everything more quickly without sacrificing quality or trainee education? Whether your patients are kids, adults, or both, there are likely many issues in common where we could all learn from each other.

We discussed this topic in #JHMChat on April 15 on Twitter. New to Twitter or not familiar with #JHMChat? Since October 2015, JHM has reviewed and discussed dozens of articles spanning a wide variety of topics related to caring for hospitalized patients. All are welcome to join, including medical students, residents, nurses, practicing hospitalists, and more. It’s a great opportunity to virtually meet and learn from others while earning free CME.

To participate in future chats, type #JHMChat in the search box on the top right corner of your Twitter homepage, click on the “Latest” tab at the top left to see the most recent tweets, and join the conversation (don’t forget the hashtag)!
 

Dr. Chen is a pediatric hospital medicine fellow at Rady Children’s Hospital, University of California, San Diego. She is one of the cofounders/moderators of #PHMFellowJC, serves as a fellow district representative for the American Academy of Pediatrics, and is an active #tweetiatrician at @DrJenChen4kids. This article appeared originally in SHM's official blog The Hospital Leader. Read more recent posts here.

References

1. James HJ et al. The Association of Discharge Before Noon and Length of Stay in Hospitalized Pediatric Patients. J Hosp Med. 2019;14(1):28-32. doi: 10.12788/jhm.3111.

2. Destino L et al. Improving Patient Flow: Analysis of an Initiative to Improve Early Discharge. J Hosp Med. 2019;14(1):22-7. doi: 10.12788/jhm.3133.

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I first heard the term “discharge before noon” (DCBN) as a third-year medical student starting my internal medicine rotation. The basic idea made sense: Get patients out of the hospital early so rooms can be cleaned more quickly and new patients wouldn’t have to wait so long in the ED.

Dr. Jennifer K. Chen

It quickly became apparent, however, that a lot of moving parts had to align perfectly for DCBN. Even if we prioritized rounding on dischargeable patients (starting 8-9 a.m. depending on the service/day), they still needed prescriptions filled, normal clothes to wear, and a way to get home, which wasn’t easy to coordinate while we were still trying to see all the other patients.

Fast forward through 5 years of residency/fellowship experience and DCBN seems even more unrealistic in hospitalized pediatric patients. As a simple example, discharge criteria for dehydration (one of the most common reasons for pediatric hospitalization) include demonstrating the ability to drink enough liquids to stay hydrated. Who’s going to force children to stay up all night sipping fluids (plus changing all those diapers or taking them to the bathroom)? If the child stays on intravenous fluids overnight, we have to monitor at least through breakfast, likely lunch, thus making DCBN nearly impossible.

In a January 2019 article in the Journal of Hospital Medicine, Hailey James, MHA, (@Haileyjms on Twitter) and her colleagues demonstrated an association between DCBN and decreased length of stay (LOS) for medical but not surgical pediatric discharges.1 This made them question if DCBN is an appropriate metric for discharge efficiency, as well as workflow differences between services. Many hospitals, however, still try to push DCBN as a goal (see Destino et al in the same January 2019 issue of JHM2), which could potentially lead to people trying to game the system.

How does your institution try to make discharge processes more efficient? Is it actually possible to do everything more quickly without sacrificing quality or trainee education? Whether your patients are kids, adults, or both, there are likely many issues in common where we could all learn from each other.

We discussed this topic in #JHMChat on April 15 on Twitter. New to Twitter or not familiar with #JHMChat? Since October 2015, JHM has reviewed and discussed dozens of articles spanning a wide variety of topics related to caring for hospitalized patients. All are welcome to join, including medical students, residents, nurses, practicing hospitalists, and more. It’s a great opportunity to virtually meet and learn from others while earning free CME.

To participate in future chats, type #JHMChat in the search box on the top right corner of your Twitter homepage, click on the “Latest” tab at the top left to see the most recent tweets, and join the conversation (don’t forget the hashtag)!
 

Dr. Chen is a pediatric hospital medicine fellow at Rady Children’s Hospital, University of California, San Diego. She is one of the cofounders/moderators of #PHMFellowJC, serves as a fellow district representative for the American Academy of Pediatrics, and is an active #tweetiatrician at @DrJenChen4kids. This article appeared originally in SHM's official blog The Hospital Leader. Read more recent posts here.

References

1. James HJ et al. The Association of Discharge Before Noon and Length of Stay in Hospitalized Pediatric Patients. J Hosp Med. 2019;14(1):28-32. doi: 10.12788/jhm.3111.

2. Destino L et al. Improving Patient Flow: Analysis of an Initiative to Improve Early Discharge. J Hosp Med. 2019;14(1):22-7. doi: 10.12788/jhm.3133.

 

I first heard the term “discharge before noon” (DCBN) as a third-year medical student starting my internal medicine rotation. The basic idea made sense: Get patients out of the hospital early so rooms can be cleaned more quickly and new patients wouldn’t have to wait so long in the ED.

Dr. Jennifer K. Chen

It quickly became apparent, however, that a lot of moving parts had to align perfectly for DCBN. Even if we prioritized rounding on dischargeable patients (starting 8-9 a.m. depending on the service/day), they still needed prescriptions filled, normal clothes to wear, and a way to get home, which wasn’t easy to coordinate while we were still trying to see all the other patients.

Fast forward through 5 years of residency/fellowship experience and DCBN seems even more unrealistic in hospitalized pediatric patients. As a simple example, discharge criteria for dehydration (one of the most common reasons for pediatric hospitalization) include demonstrating the ability to drink enough liquids to stay hydrated. Who’s going to force children to stay up all night sipping fluids (plus changing all those diapers or taking them to the bathroom)? If the child stays on intravenous fluids overnight, we have to monitor at least through breakfast, likely lunch, thus making DCBN nearly impossible.

In a January 2019 article in the Journal of Hospital Medicine, Hailey James, MHA, (@Haileyjms on Twitter) and her colleagues demonstrated an association between DCBN and decreased length of stay (LOS) for medical but not surgical pediatric discharges.1 This made them question if DCBN is an appropriate metric for discharge efficiency, as well as workflow differences between services. Many hospitals, however, still try to push DCBN as a goal (see Destino et al in the same January 2019 issue of JHM2), which could potentially lead to people trying to game the system.

How does your institution try to make discharge processes more efficient? Is it actually possible to do everything more quickly without sacrificing quality or trainee education? Whether your patients are kids, adults, or both, there are likely many issues in common where we could all learn from each other.

We discussed this topic in #JHMChat on April 15 on Twitter. New to Twitter or not familiar with #JHMChat? Since October 2015, JHM has reviewed and discussed dozens of articles spanning a wide variety of topics related to caring for hospitalized patients. All are welcome to join, including medical students, residents, nurses, practicing hospitalists, and more. It’s a great opportunity to virtually meet and learn from others while earning free CME.

To participate in future chats, type #JHMChat in the search box on the top right corner of your Twitter homepage, click on the “Latest” tab at the top left to see the most recent tweets, and join the conversation (don’t forget the hashtag)!
 

Dr. Chen is a pediatric hospital medicine fellow at Rady Children’s Hospital, University of California, San Diego. She is one of the cofounders/moderators of #PHMFellowJC, serves as a fellow district representative for the American Academy of Pediatrics, and is an active #tweetiatrician at @DrJenChen4kids. This article appeared originally in SHM's official blog The Hospital Leader. Read more recent posts here.

References

1. James HJ et al. The Association of Discharge Before Noon and Length of Stay in Hospitalized Pediatric Patients. J Hosp Med. 2019;14(1):28-32. doi: 10.12788/jhm.3111.

2. Destino L et al. Improving Patient Flow: Analysis of an Initiative to Improve Early Discharge. J Hosp Med. 2019;14(1):22-7. doi: 10.12788/jhm.3133.

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4-year-old girl • genital discomfort and dysuria • clitoral hood swelling • Blood blister on the labia minora • Dx?

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4-year-old girl • genital discomfort and dysuria • clitoral hood swelling • Blood blister on the labia minora • Dx?

THE CASE

A 4-year-old girl presented to her pediatrician with genital discomfort and dysuria of 6 months’ duration. The patient’s mother said that 3 days earlier, she noticed a tear near the child’s clitoris and a scab on the labia minora that the mother attributed to minor trauma from scratching. The pediatrician was concerned about genital trauma from sexual abuse and referred the patient to the emergency department, where a report with child protective services (CPS) was filed. The mother reported that the patient and her 8-year-old sibling spent 3 to 4 hours a day with a babysitter, who was always supervised, and the parents had no concerns about possible sexual abuse.

Physical examination by our institution’s Child Protection Team revealed clitoral hood swelling with subepithelial hemorrhages, a blood blister on the right labia minora, a fissure and subepithelial hemorrhages on the posterior fourchette, and a thin depigmented figure-of-eight lesion around the vulva and anus.

THE DIAGNOSIS

Since the clinical findings were consistent with prepubertal lichen sclerosus (LS), the CPS case was closed and the patient was referred to Pediatric Gynecology. Treatment with high-potency topical steroids was initiated with clobetasol ointment 0.05% twice daily for 2 weeks, then once daily for 2 weeks. She was then switched to triamcinolone ointment 0.01% twice daily for 2 weeks, then once daily for 2 weeks. These treatments were enough to stop the LS flare and decrease the anogenital itching.

 

DISCUSSION

Lichen sclerosus is a chronic inflammatory skin disease that primarily presents in the anogenital region; however, extragenital lesions on the upper extremities, thighs, and breasts have been reported in 15% to 20% of patients.1 Lichen sclerosus most commonly affects females as a result of low estrogen and may occur during puberty or following menopause, but it also is seen in males.1,2 The estimated prevalence of LS in prepubertal girls is 1 in 900.3 The effects of increased estrogen exposure on LS during puberty are not entirely clear. Lichen sclerosus previously was thought to improve with puberty, since it is not as common in women of reproductive age; however, studies have shown persistent symptoms after menarche in some patients.4-6

The pathogenesis of LS is multifactorial, likely with an autoimmune component, as it often is associated with other autoimmune findings such as thyroiditis, alopecia, pernicious anemia, and vitiligo.2 Diagnosis of prepubertal LS usually is made based on a review of the patient’s history and clinical examination. Presenting symptoms may include pruritus, skin irritation, vulvar pain, dysuria, bleeding from excoriations, fissures, and constipation.1,3,7

On physical examination, LS can present on the anogenital skin as smooth white spots or wrinkled, blotchy, atrophic patches. The skin around the vaginal opening and anus is thin and often is described as resembling parchment or cigarette paper in a figure-of-eight pattern (FIGURE 1A). Vulvar and anal fissures and subepithelial hemorrhages with the appearance of blood blisters also can be found (FIGURE 1B).8 Affected areas are fragile and susceptible to minor trauma, which may result in bruising or bleeding (FIGURE 1C).

Clinical presentation of prepubertal lichen sclerosus

Over time, scarring can occur and may result in disruption of the anogenital architecture—specifically loss of the labia minora, narrowing of the introitus, and burying of the clitoris.1,2 These changes can be similar to the scarring seen in postmenopausal women with LS.

Continue to: The differential diagnosis...

 

 

The differential diagnosis for prepubertal LS includes vitiligo, lichen planus, lichen simplex chronicus, psoriasis, eczema, vulvovaginitis, contact dermatitis, and trauma.2,7 On average, it takes 1 to 2 years after onset of symptoms before a correct diagnosis of prepubertal LS is made, and trauma and/or sexual abuse often are first suspected.7,9 For clinicians who are unfamiliar with prepubertal LS, the clinical findings of anogenital bruising and bleeding understandably may be suggestive of abuse. It is important to note that diagnosis of LS does not preclude the possibility of sexual abuse; in some cases, LS can be triggered or exacerbated by anogenital trauma, known as the Koebner phenomenon.2

Treatment. After the diagnosis of prepubertal LS is established, the goals of treatment are to provide symptom relief and prevent scarring of the external genitalia. To our knowledge, there have been no randomized controlled trials for treatment of LS in prepubertal girls. In general, acute symptoms are treated with high-potency topical steroids, such as clobetasol propionate or betamethasone valerate, and treatment regimens are variable.7

LS has an unpredictable clinical course and there often are recurrences that require repeat courses of topical steroids.9 Since concurrent bacterial infection is common,10 genital cultures should be obtained prior to initiation of topical steroids if an infection is suspected.

Diagnosis of lichen sclerosus should not preclude screening for sexual abuse, as symptoms can be triggered or exacerbated by trauma to the area.

Topical calcineurin inhibitors have been used successfully, but proof of their effectiveness is limited to case reports in the literature.7 Surgical treatment of LS typically is reserved for complications associated with symptomatic adhesions that are refractory to medical management.7,11 Vulvar hygiene is paramount to symptom control, and topical emollients can be used to manage minor irritation.7,8 In our patient, clobetasol and triamcinolone ointments were enough to stop the LS flare and decrease the anogenital itching.

THE TAKEAWAY

Although LS has very characteristic skin findings, the diagnosis continues to be challenging for physicians who are unfamiliar with this condition. Failure to recognize prepubertal LS not only delays diagnosis and treatment but also may lead to repeated genital examinations and investigation by CPS for suspected sexual abuse. As with any genital complaint in a prepubertal girl, diagnosis of LS should not preclude appropriate screening for sexual abuse. Although providers should be vigilant about potential sexual abuse, familiarity with skin conditions that mimic genital trauma is essential.

CORRESPONDENCE
Monica Rosen, MD, L4000 Women’s Hospital, 1500 E Medical Center Drive, SPC 5276 Ann Arbor, MI 48109; [email protected]

References

1. Powell JJ, Wojnarowska F. Lichen sclerosus. Lancet. 1999;353:1777-1783.

2. Murphy R. Lichen sclerosus. Dermatol Clin. 2010;28:707-715.

3. Powell J, Wojnarowska F. Childhood vulvar lichen sclerosus: an increasingly common problem. J Am Acad Dermatol. 2001;44:803-806.

4. Powell J, Wojnarowska F. Childhood vulvar lichen sclerosus. The course after puberty. J Reprod Med. 2002;47:706-709.

5. Smith SD, Fischer G. Childhood onset vulvar lichen sclerosus does not resolve at puberty: a prospective case series. Pediatr Dermatol. 2009;26:725-729.

6. Focseneanu MA, Gupta M, Squires KC, et al. The course of lichen sclerosus diagnosed prior to puberty. J Pediatr Adolesc Gynecol. 2013;26:153-155.

7. Bercaw-Pratt JL, Boardman LA, Simms-Cendan JS. Clinical recommendation: pediatric lichen sclerosus. J Pediatr Adolesc Gynecol. 2014;27:111-116.

8. Jenny C, Kirby P, Fuquay D. Genital lichen sclerosus mistaken for child sexual abuse. Pediatrics. 1989;83:597-599.

9. Dendrinos ML, Quint EH. Lichen sclerosus in children and adolescents. Curr Opin Obstet Gynecol. 2013;25:370-374.

10. Lagerstedt M, Karvinen K, Joki-Erkkila M, et al. Childhood lichen sclerosus—a challenge for clinicians. Pediatr Dermatol. 2013;30:444-450.

11. Gurumurthy M, Morah N, Gioffre G, et al. The surgical management of complications of vulval lichen sclerosus. Eur J Obstet Gynecol Reprod Biol. 2012;162:79-82.

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The authors reported no potential conflict of interest relevant to this article.

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The authors reported no potential conflict of interest relevant to this article.

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The authors reported no potential conflict of interest relevant to this article.

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THE CASE

A 4-year-old girl presented to her pediatrician with genital discomfort and dysuria of 6 months’ duration. The patient’s mother said that 3 days earlier, she noticed a tear near the child’s clitoris and a scab on the labia minora that the mother attributed to minor trauma from scratching. The pediatrician was concerned about genital trauma from sexual abuse and referred the patient to the emergency department, where a report with child protective services (CPS) was filed. The mother reported that the patient and her 8-year-old sibling spent 3 to 4 hours a day with a babysitter, who was always supervised, and the parents had no concerns about possible sexual abuse.

Physical examination by our institution’s Child Protection Team revealed clitoral hood swelling with subepithelial hemorrhages, a blood blister on the right labia minora, a fissure and subepithelial hemorrhages on the posterior fourchette, and a thin depigmented figure-of-eight lesion around the vulva and anus.

THE DIAGNOSIS

Since the clinical findings were consistent with prepubertal lichen sclerosus (LS), the CPS case was closed and the patient was referred to Pediatric Gynecology. Treatment with high-potency topical steroids was initiated with clobetasol ointment 0.05% twice daily for 2 weeks, then once daily for 2 weeks. She was then switched to triamcinolone ointment 0.01% twice daily for 2 weeks, then once daily for 2 weeks. These treatments were enough to stop the LS flare and decrease the anogenital itching.

 

DISCUSSION

Lichen sclerosus is a chronic inflammatory skin disease that primarily presents in the anogenital region; however, extragenital lesions on the upper extremities, thighs, and breasts have been reported in 15% to 20% of patients.1 Lichen sclerosus most commonly affects females as a result of low estrogen and may occur during puberty or following menopause, but it also is seen in males.1,2 The estimated prevalence of LS in prepubertal girls is 1 in 900.3 The effects of increased estrogen exposure on LS during puberty are not entirely clear. Lichen sclerosus previously was thought to improve with puberty, since it is not as common in women of reproductive age; however, studies have shown persistent symptoms after menarche in some patients.4-6

The pathogenesis of LS is multifactorial, likely with an autoimmune component, as it often is associated with other autoimmune findings such as thyroiditis, alopecia, pernicious anemia, and vitiligo.2 Diagnosis of prepubertal LS usually is made based on a review of the patient’s history and clinical examination. Presenting symptoms may include pruritus, skin irritation, vulvar pain, dysuria, bleeding from excoriations, fissures, and constipation.1,3,7

On physical examination, LS can present on the anogenital skin as smooth white spots or wrinkled, blotchy, atrophic patches. The skin around the vaginal opening and anus is thin and often is described as resembling parchment or cigarette paper in a figure-of-eight pattern (FIGURE 1A). Vulvar and anal fissures and subepithelial hemorrhages with the appearance of blood blisters also can be found (FIGURE 1B).8 Affected areas are fragile and susceptible to minor trauma, which may result in bruising or bleeding (FIGURE 1C).

Clinical presentation of prepubertal lichen sclerosus

Over time, scarring can occur and may result in disruption of the anogenital architecture—specifically loss of the labia minora, narrowing of the introitus, and burying of the clitoris.1,2 These changes can be similar to the scarring seen in postmenopausal women with LS.

Continue to: The differential diagnosis...

 

 

The differential diagnosis for prepubertal LS includes vitiligo, lichen planus, lichen simplex chronicus, psoriasis, eczema, vulvovaginitis, contact dermatitis, and trauma.2,7 On average, it takes 1 to 2 years after onset of symptoms before a correct diagnosis of prepubertal LS is made, and trauma and/or sexual abuse often are first suspected.7,9 For clinicians who are unfamiliar with prepubertal LS, the clinical findings of anogenital bruising and bleeding understandably may be suggestive of abuse. It is important to note that diagnosis of LS does not preclude the possibility of sexual abuse; in some cases, LS can be triggered or exacerbated by anogenital trauma, known as the Koebner phenomenon.2

Treatment. After the diagnosis of prepubertal LS is established, the goals of treatment are to provide symptom relief and prevent scarring of the external genitalia. To our knowledge, there have been no randomized controlled trials for treatment of LS in prepubertal girls. In general, acute symptoms are treated with high-potency topical steroids, such as clobetasol propionate or betamethasone valerate, and treatment regimens are variable.7

LS has an unpredictable clinical course and there often are recurrences that require repeat courses of topical steroids.9 Since concurrent bacterial infection is common,10 genital cultures should be obtained prior to initiation of topical steroids if an infection is suspected.

Diagnosis of lichen sclerosus should not preclude screening for sexual abuse, as symptoms can be triggered or exacerbated by trauma to the area.

Topical calcineurin inhibitors have been used successfully, but proof of their effectiveness is limited to case reports in the literature.7 Surgical treatment of LS typically is reserved for complications associated with symptomatic adhesions that are refractory to medical management.7,11 Vulvar hygiene is paramount to symptom control, and topical emollients can be used to manage minor irritation.7,8 In our patient, clobetasol and triamcinolone ointments were enough to stop the LS flare and decrease the anogenital itching.

THE TAKEAWAY

Although LS has very characteristic skin findings, the diagnosis continues to be challenging for physicians who are unfamiliar with this condition. Failure to recognize prepubertal LS not only delays diagnosis and treatment but also may lead to repeated genital examinations and investigation by CPS for suspected sexual abuse. As with any genital complaint in a prepubertal girl, diagnosis of LS should not preclude appropriate screening for sexual abuse. Although providers should be vigilant about potential sexual abuse, familiarity with skin conditions that mimic genital trauma is essential.

CORRESPONDENCE
Monica Rosen, MD, L4000 Women’s Hospital, 1500 E Medical Center Drive, SPC 5276 Ann Arbor, MI 48109; [email protected]

THE CASE

A 4-year-old girl presented to her pediatrician with genital discomfort and dysuria of 6 months’ duration. The patient’s mother said that 3 days earlier, she noticed a tear near the child’s clitoris and a scab on the labia minora that the mother attributed to minor trauma from scratching. The pediatrician was concerned about genital trauma from sexual abuse and referred the patient to the emergency department, where a report with child protective services (CPS) was filed. The mother reported that the patient and her 8-year-old sibling spent 3 to 4 hours a day with a babysitter, who was always supervised, and the parents had no concerns about possible sexual abuse.

Physical examination by our institution’s Child Protection Team revealed clitoral hood swelling with subepithelial hemorrhages, a blood blister on the right labia minora, a fissure and subepithelial hemorrhages on the posterior fourchette, and a thin depigmented figure-of-eight lesion around the vulva and anus.

THE DIAGNOSIS

Since the clinical findings were consistent with prepubertal lichen sclerosus (LS), the CPS case was closed and the patient was referred to Pediatric Gynecology. Treatment with high-potency topical steroids was initiated with clobetasol ointment 0.05% twice daily for 2 weeks, then once daily for 2 weeks. She was then switched to triamcinolone ointment 0.01% twice daily for 2 weeks, then once daily for 2 weeks. These treatments were enough to stop the LS flare and decrease the anogenital itching.

 

DISCUSSION

Lichen sclerosus is a chronic inflammatory skin disease that primarily presents in the anogenital region; however, extragenital lesions on the upper extremities, thighs, and breasts have been reported in 15% to 20% of patients.1 Lichen sclerosus most commonly affects females as a result of low estrogen and may occur during puberty or following menopause, but it also is seen in males.1,2 The estimated prevalence of LS in prepubertal girls is 1 in 900.3 The effects of increased estrogen exposure on LS during puberty are not entirely clear. Lichen sclerosus previously was thought to improve with puberty, since it is not as common in women of reproductive age; however, studies have shown persistent symptoms after menarche in some patients.4-6

The pathogenesis of LS is multifactorial, likely with an autoimmune component, as it often is associated with other autoimmune findings such as thyroiditis, alopecia, pernicious anemia, and vitiligo.2 Diagnosis of prepubertal LS usually is made based on a review of the patient’s history and clinical examination. Presenting symptoms may include pruritus, skin irritation, vulvar pain, dysuria, bleeding from excoriations, fissures, and constipation.1,3,7

On physical examination, LS can present on the anogenital skin as smooth white spots or wrinkled, blotchy, atrophic patches. The skin around the vaginal opening and anus is thin and often is described as resembling parchment or cigarette paper in a figure-of-eight pattern (FIGURE 1A). Vulvar and anal fissures and subepithelial hemorrhages with the appearance of blood blisters also can be found (FIGURE 1B).8 Affected areas are fragile and susceptible to minor trauma, which may result in bruising or bleeding (FIGURE 1C).

Clinical presentation of prepubertal lichen sclerosus

Over time, scarring can occur and may result in disruption of the anogenital architecture—specifically loss of the labia minora, narrowing of the introitus, and burying of the clitoris.1,2 These changes can be similar to the scarring seen in postmenopausal women with LS.

Continue to: The differential diagnosis...

 

 

The differential diagnosis for prepubertal LS includes vitiligo, lichen planus, lichen simplex chronicus, psoriasis, eczema, vulvovaginitis, contact dermatitis, and trauma.2,7 On average, it takes 1 to 2 years after onset of symptoms before a correct diagnosis of prepubertal LS is made, and trauma and/or sexual abuse often are first suspected.7,9 For clinicians who are unfamiliar with prepubertal LS, the clinical findings of anogenital bruising and bleeding understandably may be suggestive of abuse. It is important to note that diagnosis of LS does not preclude the possibility of sexual abuse; in some cases, LS can be triggered or exacerbated by anogenital trauma, known as the Koebner phenomenon.2

Treatment. After the diagnosis of prepubertal LS is established, the goals of treatment are to provide symptom relief and prevent scarring of the external genitalia. To our knowledge, there have been no randomized controlled trials for treatment of LS in prepubertal girls. In general, acute symptoms are treated with high-potency topical steroids, such as clobetasol propionate or betamethasone valerate, and treatment regimens are variable.7

LS has an unpredictable clinical course and there often are recurrences that require repeat courses of topical steroids.9 Since concurrent bacterial infection is common,10 genital cultures should be obtained prior to initiation of topical steroids if an infection is suspected.

Diagnosis of lichen sclerosus should not preclude screening for sexual abuse, as symptoms can be triggered or exacerbated by trauma to the area.

Topical calcineurin inhibitors have been used successfully, but proof of their effectiveness is limited to case reports in the literature.7 Surgical treatment of LS typically is reserved for complications associated with symptomatic adhesions that are refractory to medical management.7,11 Vulvar hygiene is paramount to symptom control, and topical emollients can be used to manage minor irritation.7,8 In our patient, clobetasol and triamcinolone ointments were enough to stop the LS flare and decrease the anogenital itching.

THE TAKEAWAY

Although LS has very characteristic skin findings, the diagnosis continues to be challenging for physicians who are unfamiliar with this condition. Failure to recognize prepubertal LS not only delays diagnosis and treatment but also may lead to repeated genital examinations and investigation by CPS for suspected sexual abuse. As with any genital complaint in a prepubertal girl, diagnosis of LS should not preclude appropriate screening for sexual abuse. Although providers should be vigilant about potential sexual abuse, familiarity with skin conditions that mimic genital trauma is essential.

CORRESPONDENCE
Monica Rosen, MD, L4000 Women’s Hospital, 1500 E Medical Center Drive, SPC 5276 Ann Arbor, MI 48109; [email protected]

References

1. Powell JJ, Wojnarowska F. Lichen sclerosus. Lancet. 1999;353:1777-1783.

2. Murphy R. Lichen sclerosus. Dermatol Clin. 2010;28:707-715.

3. Powell J, Wojnarowska F. Childhood vulvar lichen sclerosus: an increasingly common problem. J Am Acad Dermatol. 2001;44:803-806.

4. Powell J, Wojnarowska F. Childhood vulvar lichen sclerosus. The course after puberty. J Reprod Med. 2002;47:706-709.

5. Smith SD, Fischer G. Childhood onset vulvar lichen sclerosus does not resolve at puberty: a prospective case series. Pediatr Dermatol. 2009;26:725-729.

6. Focseneanu MA, Gupta M, Squires KC, et al. The course of lichen sclerosus diagnosed prior to puberty. J Pediatr Adolesc Gynecol. 2013;26:153-155.

7. Bercaw-Pratt JL, Boardman LA, Simms-Cendan JS. Clinical recommendation: pediatric lichen sclerosus. J Pediatr Adolesc Gynecol. 2014;27:111-116.

8. Jenny C, Kirby P, Fuquay D. Genital lichen sclerosus mistaken for child sexual abuse. Pediatrics. 1989;83:597-599.

9. Dendrinos ML, Quint EH. Lichen sclerosus in children and adolescents. Curr Opin Obstet Gynecol. 2013;25:370-374.

10. Lagerstedt M, Karvinen K, Joki-Erkkila M, et al. Childhood lichen sclerosus—a challenge for clinicians. Pediatr Dermatol. 2013;30:444-450.

11. Gurumurthy M, Morah N, Gioffre G, et al. The surgical management of complications of vulval lichen sclerosus. Eur J Obstet Gynecol Reprod Biol. 2012;162:79-82.

References

1. Powell JJ, Wojnarowska F. Lichen sclerosus. Lancet. 1999;353:1777-1783.

2. Murphy R. Lichen sclerosus. Dermatol Clin. 2010;28:707-715.

3. Powell J, Wojnarowska F. Childhood vulvar lichen sclerosus: an increasingly common problem. J Am Acad Dermatol. 2001;44:803-806.

4. Powell J, Wojnarowska F. Childhood vulvar lichen sclerosus. The course after puberty. J Reprod Med. 2002;47:706-709.

5. Smith SD, Fischer G. Childhood onset vulvar lichen sclerosus does not resolve at puberty: a prospective case series. Pediatr Dermatol. 2009;26:725-729.

6. Focseneanu MA, Gupta M, Squires KC, et al. The course of lichen sclerosus diagnosed prior to puberty. J Pediatr Adolesc Gynecol. 2013;26:153-155.

7. Bercaw-Pratt JL, Boardman LA, Simms-Cendan JS. Clinical recommendation: pediatric lichen sclerosus. J Pediatr Adolesc Gynecol. 2014;27:111-116.

8. Jenny C, Kirby P, Fuquay D. Genital lichen sclerosus mistaken for child sexual abuse. Pediatrics. 1989;83:597-599.

9. Dendrinos ML, Quint EH. Lichen sclerosus in children and adolescents. Curr Opin Obstet Gynecol. 2013;25:370-374.

10. Lagerstedt M, Karvinen K, Joki-Erkkila M, et al. Childhood lichen sclerosus—a challenge for clinicians. Pediatr Dermatol. 2013;30:444-450.

11. Gurumurthy M, Morah N, Gioffre G, et al. The surgical management of complications of vulval lichen sclerosus. Eur J Obstet Gynecol Reprod Biol. 2012;162:79-82.

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Varicella vaccine delivers doubled benefit to children

As memory of disease fades, vaccine questioning emerges
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Wed, 05/06/2020 - 12:21

 

Pediatric herpes zoster declined by 72% in the years following introduction of routine varicella vaccination, with the rates in vaccinated children 78% lower than those in unvaccinated children.

KatarzynaBialasiewicz/Thinkstock

The benefit became largely apparent after children received the second vaccination in the recommended series, and persisted throughout childhood, Sheila Weinmann, PhD, of Kaiser Permanente Northern California, Oakland, and colleagues said.*

The analysis included 6.37 million children in the Kaiser Permanente database, 50% of whom were vaccinated for all or some of the study period stretching from 2003 to 2014. Overall, the crude lab-confirmed herpes zoster (HZ) incidence rate was 74/100,000 person-years. When stratified by vaccine status, the crude rate of HZ among vaccinated children was 78% lower than among unvaccinated children (38 vs. 170 cases per 100,000 person years).

Herpes zoster was more common among girls than boys and up to six times more common in immunosuppressed children than in nonimmunosuppressed children.

The authors also found that unvaccinated children benefited from the high rate of vaccination around them. Although the HZ rate was always lower among vaccinated children, the rate among unvaccinated children fell sharply after 2007.

“The trend of decreasing HZ incidence among children who were unvaccinated is likely due to a lack of primary VZV [varicella-zoster virus] infection resulting from herd immunity in a highly vaccinated population,” Dr. Weinmann and her associates said.

There was some variability among age groups, especially among the youngest who were not fully vaccinated.

“In the group aged 1-2 years, the confirmation-adjusted HZ rate among children who were vaccinated was 70% higher than among those who were unvaccinated,” the authors said. In the “older groups, HZ rates were significantly higher in children who were unvaccinated than in those who were vaccinated,” the researchers noted.

The highest incidence was among vaccinated 1-year-olds, who had a 140% higher risk of HZ than did unvaccinated 1-year-olds. But this risk elevation disappeared by age 2 years. For everyone else, aged 2-17 years, the rate of HZ remained significantly lower in vaccinated children.

“Among the small number of children vaccinated at 11 months of age (for whom the vaccine is not recommended), the HZ incidence rate was significantly higher than in children vaccinated at 1 year of age and older. Similarly, children who contract wild-type varicella infection at younger than 1 year of age also have a higher risk of HZ (relative risk, 13.5). The immature adaptive T-cell response in children less than 1 year of age appears less able to contain VZV as a latent infection, compared with older children.

“Our findings for 11-month-olds who were vaccinated should be interpreted with caution because this population included only three cases of HZ and could have included children participating in a prelicensure study with a vaccine formulation different from Varivax,” Dr. Weinmann and her associates said.

Dr. Weinmann and her associates reported no relevant financial disclosures. The study was supported by the Centers for Disease Control and Prevention.

SOURCE: Weinmann S et al. Pediatrics. 2019 Jun 10. doi: 10.1542/peds.2018-2917.

* This article was updated 6/14/2019

Body

 

The finding of a 78% lower incidence of zoster in varicella-vaccinated children is nothing short of “remarkable,” Anne A Gershon, MD, wrote in an accompanying editorial.

But the benefit could be in jeopardy, as parents question the safety and effectiveness of all vaccines, she wrote.

“That the varicella vaccine prevents not only varicella but zoster as well is an exciting dual benefit from the varicella vaccine, further improving the health of children by immunization,” Dr. Gershon said. “Additional studies will be necessary to show the mechanism for the protection against zoster (viral, immunologic, or both), how long this benefit lasts, and whether additional doses of some form of VZV [varicella-zoster virus] vaccine will be more useful.”

But, she suggested, in a time when cases of clinical varicella are dwindling, so is public awareness of the vaccine’s benefit. Clinical varicella is worse for adults than it is for children.

“Efforts to immunize all children against chickenpox must continue to be made to protect our population from wild-type VZV. Fortunately, antiviral therapy is also available for individuals who are unvaccinated and develop varicella or zoster, but immunization is, as usual, preferable,” Dr. Gershon concluded.
 

Dr. Gershon, a pediatric infectious disease specialist, is a professor of pediatrics at Columbia University, New York. She wrote a commentary to accompany the article by Weinmann et al. (Pediatrics. 2019 Jun 10. doi: 10.1542/peds.2018-3561). Dr. Gershon had no relevant financial disclosures. The commentary was funded by the National Institutes of Health.

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The finding of a 78% lower incidence of zoster in varicella-vaccinated children is nothing short of “remarkable,” Anne A Gershon, MD, wrote in an accompanying editorial.

But the benefit could be in jeopardy, as parents question the safety and effectiveness of all vaccines, she wrote.

“That the varicella vaccine prevents not only varicella but zoster as well is an exciting dual benefit from the varicella vaccine, further improving the health of children by immunization,” Dr. Gershon said. “Additional studies will be necessary to show the mechanism for the protection against zoster (viral, immunologic, or both), how long this benefit lasts, and whether additional doses of some form of VZV [varicella-zoster virus] vaccine will be more useful.”

But, she suggested, in a time when cases of clinical varicella are dwindling, so is public awareness of the vaccine’s benefit. Clinical varicella is worse for adults than it is for children.

“Efforts to immunize all children against chickenpox must continue to be made to protect our population from wild-type VZV. Fortunately, antiviral therapy is also available for individuals who are unvaccinated and develop varicella or zoster, but immunization is, as usual, preferable,” Dr. Gershon concluded.
 

Dr. Gershon, a pediatric infectious disease specialist, is a professor of pediatrics at Columbia University, New York. She wrote a commentary to accompany the article by Weinmann et al. (Pediatrics. 2019 Jun 10. doi: 10.1542/peds.2018-3561). Dr. Gershon had no relevant financial disclosures. The commentary was funded by the National Institutes of Health.

Body

 

The finding of a 78% lower incidence of zoster in varicella-vaccinated children is nothing short of “remarkable,” Anne A Gershon, MD, wrote in an accompanying editorial.

But the benefit could be in jeopardy, as parents question the safety and effectiveness of all vaccines, she wrote.

“That the varicella vaccine prevents not only varicella but zoster as well is an exciting dual benefit from the varicella vaccine, further improving the health of children by immunization,” Dr. Gershon said. “Additional studies will be necessary to show the mechanism for the protection against zoster (viral, immunologic, or both), how long this benefit lasts, and whether additional doses of some form of VZV [varicella-zoster virus] vaccine will be more useful.”

But, she suggested, in a time when cases of clinical varicella are dwindling, so is public awareness of the vaccine’s benefit. Clinical varicella is worse for adults than it is for children.

“Efforts to immunize all children against chickenpox must continue to be made to protect our population from wild-type VZV. Fortunately, antiviral therapy is also available for individuals who are unvaccinated and develop varicella or zoster, but immunization is, as usual, preferable,” Dr. Gershon concluded.
 

Dr. Gershon, a pediatric infectious disease specialist, is a professor of pediatrics at Columbia University, New York. She wrote a commentary to accompany the article by Weinmann et al. (Pediatrics. 2019 Jun 10. doi: 10.1542/peds.2018-3561). Dr. Gershon had no relevant financial disclosures. The commentary was funded by the National Institutes of Health.

Title
As memory of disease fades, vaccine questioning emerges
As memory of disease fades, vaccine questioning emerges

 

Pediatric herpes zoster declined by 72% in the years following introduction of routine varicella vaccination, with the rates in vaccinated children 78% lower than those in unvaccinated children.

KatarzynaBialasiewicz/Thinkstock

The benefit became largely apparent after children received the second vaccination in the recommended series, and persisted throughout childhood, Sheila Weinmann, PhD, of Kaiser Permanente Northern California, Oakland, and colleagues said.*

The analysis included 6.37 million children in the Kaiser Permanente database, 50% of whom were vaccinated for all or some of the study period stretching from 2003 to 2014. Overall, the crude lab-confirmed herpes zoster (HZ) incidence rate was 74/100,000 person-years. When stratified by vaccine status, the crude rate of HZ among vaccinated children was 78% lower than among unvaccinated children (38 vs. 170 cases per 100,000 person years).

Herpes zoster was more common among girls than boys and up to six times more common in immunosuppressed children than in nonimmunosuppressed children.

The authors also found that unvaccinated children benefited from the high rate of vaccination around them. Although the HZ rate was always lower among vaccinated children, the rate among unvaccinated children fell sharply after 2007.

“The trend of decreasing HZ incidence among children who were unvaccinated is likely due to a lack of primary VZV [varicella-zoster virus] infection resulting from herd immunity in a highly vaccinated population,” Dr. Weinmann and her associates said.

There was some variability among age groups, especially among the youngest who were not fully vaccinated.

“In the group aged 1-2 years, the confirmation-adjusted HZ rate among children who were vaccinated was 70% higher than among those who were unvaccinated,” the authors said. In the “older groups, HZ rates were significantly higher in children who were unvaccinated than in those who were vaccinated,” the researchers noted.

The highest incidence was among vaccinated 1-year-olds, who had a 140% higher risk of HZ than did unvaccinated 1-year-olds. But this risk elevation disappeared by age 2 years. For everyone else, aged 2-17 years, the rate of HZ remained significantly lower in vaccinated children.

“Among the small number of children vaccinated at 11 months of age (for whom the vaccine is not recommended), the HZ incidence rate was significantly higher than in children vaccinated at 1 year of age and older. Similarly, children who contract wild-type varicella infection at younger than 1 year of age also have a higher risk of HZ (relative risk, 13.5). The immature adaptive T-cell response in children less than 1 year of age appears less able to contain VZV as a latent infection, compared with older children.

“Our findings for 11-month-olds who were vaccinated should be interpreted with caution because this population included only three cases of HZ and could have included children participating in a prelicensure study with a vaccine formulation different from Varivax,” Dr. Weinmann and her associates said.

Dr. Weinmann and her associates reported no relevant financial disclosures. The study was supported by the Centers for Disease Control and Prevention.

SOURCE: Weinmann S et al. Pediatrics. 2019 Jun 10. doi: 10.1542/peds.2018-2917.

* This article was updated 6/14/2019

 

Pediatric herpes zoster declined by 72% in the years following introduction of routine varicella vaccination, with the rates in vaccinated children 78% lower than those in unvaccinated children.

KatarzynaBialasiewicz/Thinkstock

The benefit became largely apparent after children received the second vaccination in the recommended series, and persisted throughout childhood, Sheila Weinmann, PhD, of Kaiser Permanente Northern California, Oakland, and colleagues said.*

The analysis included 6.37 million children in the Kaiser Permanente database, 50% of whom were vaccinated for all or some of the study period stretching from 2003 to 2014. Overall, the crude lab-confirmed herpes zoster (HZ) incidence rate was 74/100,000 person-years. When stratified by vaccine status, the crude rate of HZ among vaccinated children was 78% lower than among unvaccinated children (38 vs. 170 cases per 100,000 person years).

Herpes zoster was more common among girls than boys and up to six times more common in immunosuppressed children than in nonimmunosuppressed children.

The authors also found that unvaccinated children benefited from the high rate of vaccination around them. Although the HZ rate was always lower among vaccinated children, the rate among unvaccinated children fell sharply after 2007.

“The trend of decreasing HZ incidence among children who were unvaccinated is likely due to a lack of primary VZV [varicella-zoster virus] infection resulting from herd immunity in a highly vaccinated population,” Dr. Weinmann and her associates said.

There was some variability among age groups, especially among the youngest who were not fully vaccinated.

“In the group aged 1-2 years, the confirmation-adjusted HZ rate among children who were vaccinated was 70% higher than among those who were unvaccinated,” the authors said. In the “older groups, HZ rates were significantly higher in children who were unvaccinated than in those who were vaccinated,” the researchers noted.

The highest incidence was among vaccinated 1-year-olds, who had a 140% higher risk of HZ than did unvaccinated 1-year-olds. But this risk elevation disappeared by age 2 years. For everyone else, aged 2-17 years, the rate of HZ remained significantly lower in vaccinated children.

“Among the small number of children vaccinated at 11 months of age (for whom the vaccine is not recommended), the HZ incidence rate was significantly higher than in children vaccinated at 1 year of age and older. Similarly, children who contract wild-type varicella infection at younger than 1 year of age also have a higher risk of HZ (relative risk, 13.5). The immature adaptive T-cell response in children less than 1 year of age appears less able to contain VZV as a latent infection, compared with older children.

“Our findings for 11-month-olds who were vaccinated should be interpreted with caution because this population included only three cases of HZ and could have included children participating in a prelicensure study with a vaccine formulation different from Varivax,” Dr. Weinmann and her associates said.

Dr. Weinmann and her associates reported no relevant financial disclosures. The study was supported by the Centers for Disease Control and Prevention.

SOURCE: Weinmann S et al. Pediatrics. 2019 Jun 10. doi: 10.1542/peds.2018-2917.

* This article was updated 6/14/2019

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Key clinical point: Varicella vaccine is preventing pediatric zoster among children aged 2-17 years.

Major finding: Varicella-vaccinated children have a 78% lower incidence of pediatric zoster than do unvaccinated children.

Study details: The population-based cohort study included more than 6.3 million children.

Disclosures: Dr. Weinmann and her associates reported no relevant financial disclosures. The study was supported by the Centers for Disease Control and Prevention.

Source: Weinmann S et al. Pediatrics. 2019. doi: 10.1542/peds.2018-2917.

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New help for peanut allergies

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Changed
Fri, 06/07/2019 - 12:00

Breakthrough therapy holds potential

 

When it comes to anaphylaxis episodes leading to pediatric intensive care–unit stays, peanuts are the most common culprit. Now the results of a recent clinical trial may lead to approval of the first oral medication to ameliorate reactions in children with severe peanut allergies.

copyright mates/Fotolia.com

After 6 months of treatment and 6 months of maintenance therapy, two-thirds of the 372 children who received this treatment could ingest the equivalent of two peanuts without allergic symptoms. Just 4% of the 124 children given a placebo powder were able to consume that amount of peanut without reacting. The treatment was not effective for the small number of adults in the study.

This trial of the drug, called AR101 and developed by Aimmune Therapeutics, was published in Nov. 2018 in the New England Journal of Medicine. The company has submitted a biologics license application to the U.S. Food and Drug Administration, and because the drug has been designated a breakthrough therapy, it will go through an accelerated approval process. It could be on the market by the end of 2019.
 

Reference

1. Rabin RC. New Peanut Allergy Drug Shows ‘Lifesaving’ Potential. New York Times. Nov. 18, 2018. https://www.nytimes.com/2018/11/18/well/live/new-peanut-allergy-drug-shows-lifesaving-potential.html. Accessed Nov. 26, 2018.

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Breakthrough therapy holds potential

Breakthrough therapy holds potential

 

When it comes to anaphylaxis episodes leading to pediatric intensive care–unit stays, peanuts are the most common culprit. Now the results of a recent clinical trial may lead to approval of the first oral medication to ameliorate reactions in children with severe peanut allergies.

copyright mates/Fotolia.com

After 6 months of treatment and 6 months of maintenance therapy, two-thirds of the 372 children who received this treatment could ingest the equivalent of two peanuts without allergic symptoms. Just 4% of the 124 children given a placebo powder were able to consume that amount of peanut without reacting. The treatment was not effective for the small number of adults in the study.

This trial of the drug, called AR101 and developed by Aimmune Therapeutics, was published in Nov. 2018 in the New England Journal of Medicine. The company has submitted a biologics license application to the U.S. Food and Drug Administration, and because the drug has been designated a breakthrough therapy, it will go through an accelerated approval process. It could be on the market by the end of 2019.
 

Reference

1. Rabin RC. New Peanut Allergy Drug Shows ‘Lifesaving’ Potential. New York Times. Nov. 18, 2018. https://www.nytimes.com/2018/11/18/well/live/new-peanut-allergy-drug-shows-lifesaving-potential.html. Accessed Nov. 26, 2018.

 

When it comes to anaphylaxis episodes leading to pediatric intensive care–unit stays, peanuts are the most common culprit. Now the results of a recent clinical trial may lead to approval of the first oral medication to ameliorate reactions in children with severe peanut allergies.

copyright mates/Fotolia.com

After 6 months of treatment and 6 months of maintenance therapy, two-thirds of the 372 children who received this treatment could ingest the equivalent of two peanuts without allergic symptoms. Just 4% of the 124 children given a placebo powder were able to consume that amount of peanut without reacting. The treatment was not effective for the small number of adults in the study.

This trial of the drug, called AR101 and developed by Aimmune Therapeutics, was published in Nov. 2018 in the New England Journal of Medicine. The company has submitted a biologics license application to the U.S. Food and Drug Administration, and because the drug has been designated a breakthrough therapy, it will go through an accelerated approval process. It could be on the market by the end of 2019.
 

Reference

1. Rabin RC. New Peanut Allergy Drug Shows ‘Lifesaving’ Potential. New York Times. Nov. 18, 2018. https://www.nytimes.com/2018/11/18/well/live/new-peanut-allergy-drug-shows-lifesaving-potential.html. Accessed Nov. 26, 2018.

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Diverse vaginal microbiome may signal risk for preterm birth

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Fri, 06/07/2019 - 08:02

 

Particular features of the vaginal microbiome were significantly associated with an increased risk of preterm birth in an analysis of approximately 12,000 samples, according to a study published in Nature Medicine.

CDC/Janice Carr

Preterm births, defined as less than 37 weeks’ gestation, remain the second most common cause of neonatal death worldwide, but few strategies exist to prevent and predict preterm birth (PTB) wrote Jennifer M. Fettweis, MD, of Virginia Commonwealth University, Richmond, and her colleagues. In the United States, women of African ancestry are at significantly greater risk for PTB.

A highly diverse vaginal microbiome is thought to be associated with an increased risk of inflammation, infection, and PTB, “however, many asymptomatic healthy women have diverse vaginal microbiota,” the researchers said.

To identify vaginal microbiota distinct to women who experienced PTB, the researchers analyzed data from the Multi-Omic Microbiome Study: Pregnancy Initiative (MOMS-PI), part of the National Institutes of Health–sponsored Integrative Human Microbiome Project. The MOMS-PI study included 12,039 samples of vaginal flora from 597 pregnancies; the analysis included 45 singleton pregnancies that met the criteria for spontaneous PTB (23-36 weeks, 6 days of gestation) and 90 case-matched full-term singleton pregnancies (greater than or equal to 39 weeks). Approximately 78% of the women were of African descent in both groups, and their average age was 26 years in both groups.

Overall, the diversity of the vaginal microbiome was greater among women who experienced PTB, compared with term birth (TB). Women who experienced PTB had less Lactobacillus crispatus, but more bacterial vaginosis–associated bacterium-1 (BVAB1), Prevotella cluster 2, and Sneathia amnii, compared with TB women.

Of note, vaginal cytokine data showed that proinflammatory cytokines, which may be associated with the induction of labor, may be prompted by inflammation in the vaginal microbiome, Dr. Fettweis and her associates said. “We observed that vaginal IP-10/CXCL10 levels were inversely correlated with BVAB1 in PTB, inversely correlated with L. crispatus in TB, and positively correlated with L. iners in TB, suggesting complex host-microbiome interactions in pregnancy,” they said.

“Further studies are needed to determine whether the signatures of PTB reported in the present study replicate in other cohorts of women of African ancestry, to examine whether the observed differences in vaginal microbiome composition between women of different ancestries has a direct causal link to the ethnic and racial disparities in PTB rates, and to establish whether population-specific microbial markers can be ultimately integrated into a generalizable spectrum of vaginal microbiome states linked to the risk for PTB,” Dr. Fettweis and her associates said.

In a companion study also published in Nature Medicine, Myrna G. Serrano, MD, also of Virginia Commonwealth University, and her colleagues as part of the MOMS-PI initially determined that vaginal microbiome profiles varied between 613 pregnant and 1,969 nonpregnant women in that “pregnant women had significantly higher prevalence of the four most common Lactobacillus vagitypes (L. crispatus, L. iners, L. gasseri, and L. jensenii) and a commensurately lower prevalence of vagitypes dominated by other taxa.” The primary driver of the differences was L. iners.

They then compared vaginal microbiome data from 300 pregnant and 300 nonpregnant case-matched women of African, Hispanic, or European ancestry, as well as 90 pregnant women (49 of African ancestry and 41 of European) ancestry.

In the subset of 300 pregnant and 300 nonpregnant women, the vaginal microbiome of the pregnant women overall became more dominated by Lactobacillus early in pregnancy. Further stratification by race showed that pregnant women of African and Hispanic ancestry had significantly higher levels of four types of Lactobacillus than their nonpregnant counterparts, but no significant difference was seen between pregnant and nonpregnant women of European ancestry.

“It appears that changes occurring during pregnancy may render the reproductive tracts of women of all racial backgrounds more hospitable to taxa of Lactobacillus and less favorable for Gardnerella vaginalis and other taxa associated with BV [bacterial vaginosis] and dysbiosis,” the researchers said.

“Interestingly, BVAB1, which has been associated with dysbiotic vaginal conditions and risk of PTB, and which is present as a major vagitype largely in women of African ancestry, is not noticeably decreased in prevalence in pregnancy,” Dr. Serrano and her associates said. “Thus, BVAB1, for reasons yet to be determined, is apparently resistant to factors sculpting the microbiome in pregnant women, possibly explaining in part the enhanced risk for PTB experienced by women of African ancestry.”

In a look at the 49 pregnant women of African ancestry and 41 of European ancestry, those of African ancestry had “significantly lower representation of the L. crispatus, L. gasseri and L. jensenii vagitypes, and higher representation of L. iners and BVAB1 vagitypes. Variability in women of African ancestry was driven by BVAB1 and L. iners, whereas variability in women of non-African ancestry was driven by L. crispatus and L. iners. Again, pregnancy had no significant effect on prevalence of the BVAB1 vagitype. Prevalence of Lactobacillus-dominated profiles in women of African ancestry was lower in the first than in later trimesters, whereas women of European ancestry had a higher prevalence of Lactobacillus vagitypes throughout pregnancy.”

The presence of vaginal microbiome profiles associated with adverse pregnancy outcomes highlights the need for further studies that take advantage of this information, Dr. Serrano and her associates said. “That the vaginal microbiomes known to confer higher risk of poor health and adverse outcomes of pregnancy are more highly associated with women of African and Hispanic ancestry, but that pregnancy tends to drive these microbiomes toward more favorable microbiota, suggests that an external intervention that favors this trend might be beneficial for these populations,” they concluded. “What remains is to verify the most favorable microbiome and the most effective strategy for intervention.”

Dr. Fettweis had no financial conflicts to disclose; two coauthors are full-time employees at Pacific Biosciences. Dr. Serrano and her coauthors had no relevant financial disclosures. Dr. Serrano’s study received grants from the National Institutes of Health and other sources, as well as support from the Common Fund, the National Center for Complementary and Integrative Health, the Office of Research on Women’s Health, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the National Institute of Allergy and Infectious Diseases.

SOURCES: Fettweis J et al. Nature Medicine 2019 May 29. doi: 10.1038/s41591-019-0450-2; Serrano M et al. Nature Medicine. 2019 May 29. doi: 10.1038/s41591-019-0465-8.

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Particular features of the vaginal microbiome were significantly associated with an increased risk of preterm birth in an analysis of approximately 12,000 samples, according to a study published in Nature Medicine.

CDC/Janice Carr

Preterm births, defined as less than 37 weeks’ gestation, remain the second most common cause of neonatal death worldwide, but few strategies exist to prevent and predict preterm birth (PTB) wrote Jennifer M. Fettweis, MD, of Virginia Commonwealth University, Richmond, and her colleagues. In the United States, women of African ancestry are at significantly greater risk for PTB.

A highly diverse vaginal microbiome is thought to be associated with an increased risk of inflammation, infection, and PTB, “however, many asymptomatic healthy women have diverse vaginal microbiota,” the researchers said.

To identify vaginal microbiota distinct to women who experienced PTB, the researchers analyzed data from the Multi-Omic Microbiome Study: Pregnancy Initiative (MOMS-PI), part of the National Institutes of Health–sponsored Integrative Human Microbiome Project. The MOMS-PI study included 12,039 samples of vaginal flora from 597 pregnancies; the analysis included 45 singleton pregnancies that met the criteria for spontaneous PTB (23-36 weeks, 6 days of gestation) and 90 case-matched full-term singleton pregnancies (greater than or equal to 39 weeks). Approximately 78% of the women were of African descent in both groups, and their average age was 26 years in both groups.

Overall, the diversity of the vaginal microbiome was greater among women who experienced PTB, compared with term birth (TB). Women who experienced PTB had less Lactobacillus crispatus, but more bacterial vaginosis–associated bacterium-1 (BVAB1), Prevotella cluster 2, and Sneathia amnii, compared with TB women.

Of note, vaginal cytokine data showed that proinflammatory cytokines, which may be associated with the induction of labor, may be prompted by inflammation in the vaginal microbiome, Dr. Fettweis and her associates said. “We observed that vaginal IP-10/CXCL10 levels were inversely correlated with BVAB1 in PTB, inversely correlated with L. crispatus in TB, and positively correlated with L. iners in TB, suggesting complex host-microbiome interactions in pregnancy,” they said.

“Further studies are needed to determine whether the signatures of PTB reported in the present study replicate in other cohorts of women of African ancestry, to examine whether the observed differences in vaginal microbiome composition between women of different ancestries has a direct causal link to the ethnic and racial disparities in PTB rates, and to establish whether population-specific microbial markers can be ultimately integrated into a generalizable spectrum of vaginal microbiome states linked to the risk for PTB,” Dr. Fettweis and her associates said.

In a companion study also published in Nature Medicine, Myrna G. Serrano, MD, also of Virginia Commonwealth University, and her colleagues as part of the MOMS-PI initially determined that vaginal microbiome profiles varied between 613 pregnant and 1,969 nonpregnant women in that “pregnant women had significantly higher prevalence of the four most common Lactobacillus vagitypes (L. crispatus, L. iners, L. gasseri, and L. jensenii) and a commensurately lower prevalence of vagitypes dominated by other taxa.” The primary driver of the differences was L. iners.

They then compared vaginal microbiome data from 300 pregnant and 300 nonpregnant case-matched women of African, Hispanic, or European ancestry, as well as 90 pregnant women (49 of African ancestry and 41 of European) ancestry.

In the subset of 300 pregnant and 300 nonpregnant women, the vaginal microbiome of the pregnant women overall became more dominated by Lactobacillus early in pregnancy. Further stratification by race showed that pregnant women of African and Hispanic ancestry had significantly higher levels of four types of Lactobacillus than their nonpregnant counterparts, but no significant difference was seen between pregnant and nonpregnant women of European ancestry.

“It appears that changes occurring during pregnancy may render the reproductive tracts of women of all racial backgrounds more hospitable to taxa of Lactobacillus and less favorable for Gardnerella vaginalis and other taxa associated with BV [bacterial vaginosis] and dysbiosis,” the researchers said.

“Interestingly, BVAB1, which has been associated with dysbiotic vaginal conditions and risk of PTB, and which is present as a major vagitype largely in women of African ancestry, is not noticeably decreased in prevalence in pregnancy,” Dr. Serrano and her associates said. “Thus, BVAB1, for reasons yet to be determined, is apparently resistant to factors sculpting the microbiome in pregnant women, possibly explaining in part the enhanced risk for PTB experienced by women of African ancestry.”

In a look at the 49 pregnant women of African ancestry and 41 of European ancestry, those of African ancestry had “significantly lower representation of the L. crispatus, L. gasseri and L. jensenii vagitypes, and higher representation of L. iners and BVAB1 vagitypes. Variability in women of African ancestry was driven by BVAB1 and L. iners, whereas variability in women of non-African ancestry was driven by L. crispatus and L. iners. Again, pregnancy had no significant effect on prevalence of the BVAB1 vagitype. Prevalence of Lactobacillus-dominated profiles in women of African ancestry was lower in the first than in later trimesters, whereas women of European ancestry had a higher prevalence of Lactobacillus vagitypes throughout pregnancy.”

The presence of vaginal microbiome profiles associated with adverse pregnancy outcomes highlights the need for further studies that take advantage of this information, Dr. Serrano and her associates said. “That the vaginal microbiomes known to confer higher risk of poor health and adverse outcomes of pregnancy are more highly associated with women of African and Hispanic ancestry, but that pregnancy tends to drive these microbiomes toward more favorable microbiota, suggests that an external intervention that favors this trend might be beneficial for these populations,” they concluded. “What remains is to verify the most favorable microbiome and the most effective strategy for intervention.”

Dr. Fettweis had no financial conflicts to disclose; two coauthors are full-time employees at Pacific Biosciences. Dr. Serrano and her coauthors had no relevant financial disclosures. Dr. Serrano’s study received grants from the National Institutes of Health and other sources, as well as support from the Common Fund, the National Center for Complementary and Integrative Health, the Office of Research on Women’s Health, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the National Institute of Allergy and Infectious Diseases.

SOURCES: Fettweis J et al. Nature Medicine 2019 May 29. doi: 10.1038/s41591-019-0450-2; Serrano M et al. Nature Medicine. 2019 May 29. doi: 10.1038/s41591-019-0465-8.

 

Particular features of the vaginal microbiome were significantly associated with an increased risk of preterm birth in an analysis of approximately 12,000 samples, according to a study published in Nature Medicine.

CDC/Janice Carr

Preterm births, defined as less than 37 weeks’ gestation, remain the second most common cause of neonatal death worldwide, but few strategies exist to prevent and predict preterm birth (PTB) wrote Jennifer M. Fettweis, MD, of Virginia Commonwealth University, Richmond, and her colleagues. In the United States, women of African ancestry are at significantly greater risk for PTB.

A highly diverse vaginal microbiome is thought to be associated with an increased risk of inflammation, infection, and PTB, “however, many asymptomatic healthy women have diverse vaginal microbiota,” the researchers said.

To identify vaginal microbiota distinct to women who experienced PTB, the researchers analyzed data from the Multi-Omic Microbiome Study: Pregnancy Initiative (MOMS-PI), part of the National Institutes of Health–sponsored Integrative Human Microbiome Project. The MOMS-PI study included 12,039 samples of vaginal flora from 597 pregnancies; the analysis included 45 singleton pregnancies that met the criteria for spontaneous PTB (23-36 weeks, 6 days of gestation) and 90 case-matched full-term singleton pregnancies (greater than or equal to 39 weeks). Approximately 78% of the women were of African descent in both groups, and their average age was 26 years in both groups.

Overall, the diversity of the vaginal microbiome was greater among women who experienced PTB, compared with term birth (TB). Women who experienced PTB had less Lactobacillus crispatus, but more bacterial vaginosis–associated bacterium-1 (BVAB1), Prevotella cluster 2, and Sneathia amnii, compared with TB women.

Of note, vaginal cytokine data showed that proinflammatory cytokines, which may be associated with the induction of labor, may be prompted by inflammation in the vaginal microbiome, Dr. Fettweis and her associates said. “We observed that vaginal IP-10/CXCL10 levels were inversely correlated with BVAB1 in PTB, inversely correlated with L. crispatus in TB, and positively correlated with L. iners in TB, suggesting complex host-microbiome interactions in pregnancy,” they said.

“Further studies are needed to determine whether the signatures of PTB reported in the present study replicate in other cohorts of women of African ancestry, to examine whether the observed differences in vaginal microbiome composition between women of different ancestries has a direct causal link to the ethnic and racial disparities in PTB rates, and to establish whether population-specific microbial markers can be ultimately integrated into a generalizable spectrum of vaginal microbiome states linked to the risk for PTB,” Dr. Fettweis and her associates said.

In a companion study also published in Nature Medicine, Myrna G. Serrano, MD, also of Virginia Commonwealth University, and her colleagues as part of the MOMS-PI initially determined that vaginal microbiome profiles varied between 613 pregnant and 1,969 nonpregnant women in that “pregnant women had significantly higher prevalence of the four most common Lactobacillus vagitypes (L. crispatus, L. iners, L. gasseri, and L. jensenii) and a commensurately lower prevalence of vagitypes dominated by other taxa.” The primary driver of the differences was L. iners.

They then compared vaginal microbiome data from 300 pregnant and 300 nonpregnant case-matched women of African, Hispanic, or European ancestry, as well as 90 pregnant women (49 of African ancestry and 41 of European) ancestry.

In the subset of 300 pregnant and 300 nonpregnant women, the vaginal microbiome of the pregnant women overall became more dominated by Lactobacillus early in pregnancy. Further stratification by race showed that pregnant women of African and Hispanic ancestry had significantly higher levels of four types of Lactobacillus than their nonpregnant counterparts, but no significant difference was seen between pregnant and nonpregnant women of European ancestry.

“It appears that changes occurring during pregnancy may render the reproductive tracts of women of all racial backgrounds more hospitable to taxa of Lactobacillus and less favorable for Gardnerella vaginalis and other taxa associated with BV [bacterial vaginosis] and dysbiosis,” the researchers said.

“Interestingly, BVAB1, which has been associated with dysbiotic vaginal conditions and risk of PTB, and which is present as a major vagitype largely in women of African ancestry, is not noticeably decreased in prevalence in pregnancy,” Dr. Serrano and her associates said. “Thus, BVAB1, for reasons yet to be determined, is apparently resistant to factors sculpting the microbiome in pregnant women, possibly explaining in part the enhanced risk for PTB experienced by women of African ancestry.”

In a look at the 49 pregnant women of African ancestry and 41 of European ancestry, those of African ancestry had “significantly lower representation of the L. crispatus, L. gasseri and L. jensenii vagitypes, and higher representation of L. iners and BVAB1 vagitypes. Variability in women of African ancestry was driven by BVAB1 and L. iners, whereas variability in women of non-African ancestry was driven by L. crispatus and L. iners. Again, pregnancy had no significant effect on prevalence of the BVAB1 vagitype. Prevalence of Lactobacillus-dominated profiles in women of African ancestry was lower in the first than in later trimesters, whereas women of European ancestry had a higher prevalence of Lactobacillus vagitypes throughout pregnancy.”

The presence of vaginal microbiome profiles associated with adverse pregnancy outcomes highlights the need for further studies that take advantage of this information, Dr. Serrano and her associates said. “That the vaginal microbiomes known to confer higher risk of poor health and adverse outcomes of pregnancy are more highly associated with women of African and Hispanic ancestry, but that pregnancy tends to drive these microbiomes toward more favorable microbiota, suggests that an external intervention that favors this trend might be beneficial for these populations,” they concluded. “What remains is to verify the most favorable microbiome and the most effective strategy for intervention.”

Dr. Fettweis had no financial conflicts to disclose; two coauthors are full-time employees at Pacific Biosciences. Dr. Serrano and her coauthors had no relevant financial disclosures. Dr. Serrano’s study received grants from the National Institutes of Health and other sources, as well as support from the Common Fund, the National Center for Complementary and Integrative Health, the Office of Research on Women’s Health, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the National Institute of Allergy and Infectious Diseases.

SOURCES: Fettweis J et al. Nature Medicine 2019 May 29. doi: 10.1038/s41591-019-0450-2; Serrano M et al. Nature Medicine. 2019 May 29. doi: 10.1038/s41591-019-0465-8.

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Pediatric MS often goes untreated in the year after diagnosis

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About 65% of patients with pediatric multiple sclerosis (MS) do not receive disease-modifying therapy (DMT) within 1 year of diagnosis, according to an analysis of insurance claims data. Females may be more likely than males to receive DMT during this time, said Chinmay Deshpande, PhD, at the annual meeting of the Consortium of Multiple Sclerosis Centers.

Pediatric onset of MS occurs in 3-5% of patients with the disease, and the median age of pediatric onset is 15 years. This population tends to have a high relapse rate and may develop disability at a younger age, said Dr. Deshpande, associate director of health economics and outcomes research at Novartis. “There have been very few studies done on this population, especially in the clinical trial setting. ... Physicians face considerable uncertainty in how to treat these patients.”
 

Observational data

To assess the proportion of patients with pediatric MS who receive DMT in the year after diagnosis, Dr. Deshpande and colleagues analyzed retrospective observational data from the Truven Health Marketscan Commercial and Encounters administrative claims databases. They studied patients who received an MS diagnosis between Jan. 1, 2010, and Dec. 31, 2016. In addition, they examined which DMTs were used as first-line therapies, whether prescribing patterns changed between 2010 and 2017, and time to treatment discontinuation or switch.

The databases included data from more than 182,000 patients with two or more claims of MS diagnosis. After including only patients age 17 years or younger at the index diagnosis date who had insurance during the 6 months prior to the index date and 12 months after the index date and who did not use DMT during the 6 months prior to the index date, 288 patients remained in the analysis. Patients had an average age of about 14 years.

The primary outcome was the proportion of patients who started DMT in the year after MS diagnosis. “The proportion of untreated patients within their first year of diagnosis was around 65%,” said Dr. Deshpande. On average, treated patients were slightly older than untreated patients (15.0 years vs. 13.3 years). Among treated patients, 75% were female, and 25% were male. Overall, however, 61% were female and 39% were male. The difference in treatment by gender was surprising and the reason for it is not understood, Dr. Deshpande said. One possibility is that the difference relates to earlier maturation in females, but that is only a hypothesis, he said.

Glatiramer acetate and interferon beta-1a were first-line DMTs for 48% and 30.6% of the treated patients, respectively. Dimethyl fumarate (7.1%), natalizumab (5.1%), fingolimod (4.1%), interferon beta-1b (4.1%), and peginterferon beta-1a (1%) also were used as first-line therapy.

Twenty percent of patients who received DMT switched to another medication during the follow-up period. The median time of switching was within 6 months of starting first-line therapy. Most patients who discontinued DMT – that is, they did not have any DMT for 60 days after stopping their first DMT – did so within 10 months of diagnosis.
 

Use of newer medications

Overall, the use of glatiramer acetate and interferons has decreased over time, and while the use of newer DMTs has increased, the trend is not consistent. “With the growing uptake of newer oral and infusible DMTs over the recent years, there is a need to increase treatment awareness in the pediatric MS population and to inform currently approved treatment options to the prescribers,” Dr. Deshpande and colleagues said.

The claims database is generalizable and nationally representative, but it does not include clinical or MRI data. “It’s hard to understand the reasoning why they discontinued or why they are switching,” Dr. Deshpande said. In addition, the sample size was relatively small, and the results should be interpreted accordingly, he said.

Novartis funded the study, and Dr. Deshpande and a coauthor are employees of Novartis. Other coauthors reported consulting fees from Novartis, as well as consulting fees and grant funding from other pharmaceutical companies.

SOURCE: Greenberg B et al. CMSC 2019, Abstract DXM02.


 

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About 65% of patients with pediatric multiple sclerosis (MS) do not receive disease-modifying therapy (DMT) within 1 year of diagnosis, according to an analysis of insurance claims data. Females may be more likely than males to receive DMT during this time, said Chinmay Deshpande, PhD, at the annual meeting of the Consortium of Multiple Sclerosis Centers.

Pediatric onset of MS occurs in 3-5% of patients with the disease, and the median age of pediatric onset is 15 years. This population tends to have a high relapse rate and may develop disability at a younger age, said Dr. Deshpande, associate director of health economics and outcomes research at Novartis. “There have been very few studies done on this population, especially in the clinical trial setting. ... Physicians face considerable uncertainty in how to treat these patients.”
 

Observational data

To assess the proportion of patients with pediatric MS who receive DMT in the year after diagnosis, Dr. Deshpande and colleagues analyzed retrospective observational data from the Truven Health Marketscan Commercial and Encounters administrative claims databases. They studied patients who received an MS diagnosis between Jan. 1, 2010, and Dec. 31, 2016. In addition, they examined which DMTs were used as first-line therapies, whether prescribing patterns changed between 2010 and 2017, and time to treatment discontinuation or switch.

The databases included data from more than 182,000 patients with two or more claims of MS diagnosis. After including only patients age 17 years or younger at the index diagnosis date who had insurance during the 6 months prior to the index date and 12 months after the index date and who did not use DMT during the 6 months prior to the index date, 288 patients remained in the analysis. Patients had an average age of about 14 years.

The primary outcome was the proportion of patients who started DMT in the year after MS diagnosis. “The proportion of untreated patients within their first year of diagnosis was around 65%,” said Dr. Deshpande. On average, treated patients were slightly older than untreated patients (15.0 years vs. 13.3 years). Among treated patients, 75% were female, and 25% were male. Overall, however, 61% were female and 39% were male. The difference in treatment by gender was surprising and the reason for it is not understood, Dr. Deshpande said. One possibility is that the difference relates to earlier maturation in females, but that is only a hypothesis, he said.

Glatiramer acetate and interferon beta-1a were first-line DMTs for 48% and 30.6% of the treated patients, respectively. Dimethyl fumarate (7.1%), natalizumab (5.1%), fingolimod (4.1%), interferon beta-1b (4.1%), and peginterferon beta-1a (1%) also were used as first-line therapy.

Twenty percent of patients who received DMT switched to another medication during the follow-up period. The median time of switching was within 6 months of starting first-line therapy. Most patients who discontinued DMT – that is, they did not have any DMT for 60 days after stopping their first DMT – did so within 10 months of diagnosis.
 

Use of newer medications

Overall, the use of glatiramer acetate and interferons has decreased over time, and while the use of newer DMTs has increased, the trend is not consistent. “With the growing uptake of newer oral and infusible DMTs over the recent years, there is a need to increase treatment awareness in the pediatric MS population and to inform currently approved treatment options to the prescribers,” Dr. Deshpande and colleagues said.

The claims database is generalizable and nationally representative, but it does not include clinical or MRI data. “It’s hard to understand the reasoning why they discontinued or why they are switching,” Dr. Deshpande said. In addition, the sample size was relatively small, and the results should be interpreted accordingly, he said.

Novartis funded the study, and Dr. Deshpande and a coauthor are employees of Novartis. Other coauthors reported consulting fees from Novartis, as well as consulting fees and grant funding from other pharmaceutical companies.

SOURCE: Greenberg B et al. CMSC 2019, Abstract DXM02.


 

 

About 65% of patients with pediatric multiple sclerosis (MS) do not receive disease-modifying therapy (DMT) within 1 year of diagnosis, according to an analysis of insurance claims data. Females may be more likely than males to receive DMT during this time, said Chinmay Deshpande, PhD, at the annual meeting of the Consortium of Multiple Sclerosis Centers.

Pediatric onset of MS occurs in 3-5% of patients with the disease, and the median age of pediatric onset is 15 years. This population tends to have a high relapse rate and may develop disability at a younger age, said Dr. Deshpande, associate director of health economics and outcomes research at Novartis. “There have been very few studies done on this population, especially in the clinical trial setting. ... Physicians face considerable uncertainty in how to treat these patients.”
 

Observational data

To assess the proportion of patients with pediatric MS who receive DMT in the year after diagnosis, Dr. Deshpande and colleagues analyzed retrospective observational data from the Truven Health Marketscan Commercial and Encounters administrative claims databases. They studied patients who received an MS diagnosis between Jan. 1, 2010, and Dec. 31, 2016. In addition, they examined which DMTs were used as first-line therapies, whether prescribing patterns changed between 2010 and 2017, and time to treatment discontinuation or switch.

The databases included data from more than 182,000 patients with two or more claims of MS diagnosis. After including only patients age 17 years or younger at the index diagnosis date who had insurance during the 6 months prior to the index date and 12 months after the index date and who did not use DMT during the 6 months prior to the index date, 288 patients remained in the analysis. Patients had an average age of about 14 years.

The primary outcome was the proportion of patients who started DMT in the year after MS diagnosis. “The proportion of untreated patients within their first year of diagnosis was around 65%,” said Dr. Deshpande. On average, treated patients were slightly older than untreated patients (15.0 years vs. 13.3 years). Among treated patients, 75% were female, and 25% were male. Overall, however, 61% were female and 39% were male. The difference in treatment by gender was surprising and the reason for it is not understood, Dr. Deshpande said. One possibility is that the difference relates to earlier maturation in females, but that is only a hypothesis, he said.

Glatiramer acetate and interferon beta-1a were first-line DMTs for 48% and 30.6% of the treated patients, respectively. Dimethyl fumarate (7.1%), natalizumab (5.1%), fingolimod (4.1%), interferon beta-1b (4.1%), and peginterferon beta-1a (1%) also were used as first-line therapy.

Twenty percent of patients who received DMT switched to another medication during the follow-up period. The median time of switching was within 6 months of starting first-line therapy. Most patients who discontinued DMT – that is, they did not have any DMT for 60 days after stopping their first DMT – did so within 10 months of diagnosis.
 

Use of newer medications

Overall, the use of glatiramer acetate and interferons has decreased over time, and while the use of newer DMTs has increased, the trend is not consistent. “With the growing uptake of newer oral and infusible DMTs over the recent years, there is a need to increase treatment awareness in the pediatric MS population and to inform currently approved treatment options to the prescribers,” Dr. Deshpande and colleagues said.

The claims database is generalizable and nationally representative, but it does not include clinical or MRI data. “It’s hard to understand the reasoning why they discontinued or why they are switching,” Dr. Deshpande said. In addition, the sample size was relatively small, and the results should be interpreted accordingly, he said.

Novartis funded the study, and Dr. Deshpande and a coauthor are employees of Novartis. Other coauthors reported consulting fees from Novartis, as well as consulting fees and grant funding from other pharmaceutical companies.

SOURCE: Greenberg B et al. CMSC 2019, Abstract DXM02.


 

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A warning song to keep our children safe

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Wed, 06/05/2019 - 12:04

Pay heed to “The House of the Rising Sun”

 

“There is a house in New Orleans. They call the Rising Sun. And it’s been the ruin of many a poor boy. And, God, I know I’m one.”

Dr. Jordan Messler

The 1960s rock band the Animals will tell you a tale to convince you to get vaccinated. Don’t believe me? Follow along.

The first hints of the song “House of the Rising Sun” rolled out of the hills of Appalachia.

Somewhere in the Golden Triangle, far away from New Orleans, where Virginia, Kentucky, and Tennessee rise in quiet desolation, a warning song about a tailor and a drunk emerged. Sometime around the Civil War, a hint of a tune began. Over the next century, it evolved, until it became cemented in rock culture 50 years ago by The Animals, existing as the version played most commonly today.

In the mid-19th century, medicine shows rambled through the South, stopping in places like Noetown or Daisy. The small towns would empty out for the day to see the entertainers, singers, and jugglers perform. Hundreds gathered in the hot summer day, the entertainment solely a pretext for the traveling doctors to sell their wares, the snake oil, and cure-alls, as well as various patent medicines.

These were isolated towns, with no deliveries, few visitors, and the railroad yet to arrive. Frequently, the only news from outside came from these caravans of entertainers and con men who swept into town. They were like Professor Marvel from The Wizard of Oz, or a current-day Dr. Oz, luring the crowd with false advertising, selling colored water, and then disappearing before you realized you were duped. Today, traveling doctors of the same ilk convince parents to not vaccinate their children, tell them to visit stem cell centers that claim false cures, and offer them a shiny object with one hand while taking their cash with the other.

Yet, there was a positive development in the wake of these patent medicine shows: the entertainment lingered. New songs traveled the same journeys as these medicine shows – new earworms that would then be warbled in the local bars, while doing chores around the barn, or simply during walks on the Appalachian trails.

In 1937, Alan Lomax arrived in Noetown, Ky., with a microphone and an acetate record and recorded the voice of 16-year-old Georgia Turner singing “House of the Rising Sun.” She didn’t know where she heard that song, but most likely picked it up at the medicine show.

One of those singers was Clarence Ashley, who would croon about the Rising Sun Blues. He sang with Doc Cloud and Doc Hauer, who offered tonics for whatever ailed you. Perhaps Georgia Turner heard the song in the early 1900s as well. Her 1937 version contains the lyrics most closely related to the Animals’ tune.

Lomax spent the 1940s gathering songs around the Appalachian South. He put these songs into a songbook and spread them throughout the country. He would also return to New York City and gather in a room with legendary folk singers. They would hear these new lyrics, new sounds, and make them their own.

In that room would be Lead Belly, Pete Seeger, Woody Guthrie, and Josh White, the fathers of folk music. The music Lomax pulled out of the mountains in small towns would become new again in the guitars and harmonicas of the Greenwich Village singers and musicians. Pete Seeger performed with the Weavers, named because they would weave songs from the past into new versions.

“House of the Rising Sun” was woven into the folk music landscape, evolving and growing. Josh White is credited with changing the song from a major key into the minor key we know today. Bob Dylan sang a version. And then in 1964, Eric Burdon and The Animals released their version, which became the standard. An arpeggio guitar opening, the rhythm sped up, a louder sound, and that minor key provides an emotional wallop for this warning song.

Numerous covers followed, including a beautiful version of “Amazing Grace”, sung to the tune of “House of the Rising Sun” by the Blind Boys of Alabama.

The song endures for its melody as well as for its lyrics. This was a warning song, a universal song, “not to do what I have done.” The small towns in Kentucky may have heard of the sinful ways of New Orleans and would spread the message with these songs to avoid the brothels, the drink, and the broken marriages that would reverberate with visits to the Crescent City.

“House of the Rising Sun” is one of the most covered songs, traveling wide and far, no longer with the need for a medicine show. It was a pivotal moment in rock ‘n roll, turning folk music into rock music. The Animals became huge because of this song, and their version became the standard on which all subsequent covers based their version. It made Bob Dylan’s older version seem quaint.

The song has been in my head for a while now. My wife is hoping writing about it will keep it from being played in our household any more. There are various reasons it has been resonating with me, including the following:

 

 

  • It traces the origins of folk music and the importance of people like Lomax and Guthrie to collect and save Americana.
  • The magic of musical evolution – a reminder of how art is built on the work of those who came before, each version with its unique personality.
  • The release of “House of the Rising Sun” was a seminal, transformative moment when folk became rock music.
  • The lasting power of warning songs.
  • The hucksters that enabled this song to be kept alive.

That last one has really stuck with me. The medicine shows are an important part of American history. For instance, Coca-Cola started as one of those patent medicines; it was one of the many concoctions of the Atlanta pharmacist John Stith Pemberton, sold to treat all that ails us. Dr. Pepper, too, was a medicine in a sugary bottle – another that often contained alcohol or cocaine. Society wants a cure-all, and the marketing and selling done during these medicine shows offered placebos.

The hucksters exist in various forms today, selling detoxifications, magic diet cures, psychic powers of healing, or convincing parents that their kids don’t need vaccines. We need a warning song that goes viral to keep our children safe. We are blessed to be in a world without smallpox, almost rid of polio, and we have the knowledge and opportunity to rid the world of other preventable illnesses. Measles was declared eliminated in the United States in 2000; now, outbreaks emerge in every news cycle.

The CDC admits they have not been targeting misinformation well. How can we spread the science, the truth, the message faster than the lies? Better marketing? The answer may be through stories and narratives and song, with the backing of good science. “House of the Rising Sun” is a warning song. Maybe we need more. We need that deep history, that long trail to remind us of the world before vaccines, when everyone knew someone, either in their own household or next door, who succumbed to one of the childhood illnesses.

Let the “House of the Rising Sun” play on. Create a new version, and let that message reverberate, too.

Tell your children; they need to be vaccinated.
 

Dr. Messler is a hospitalist at Morton Plant Hospitalist group in Clearwater, Fla. He previously chaired SHM’s Quality and Patient Safety Committee and has been active in several SHM mentoring programs, most recently with Project BOOST and Glycemic Control. This article appeared originally in SHM's official blog The Hospital Leader. Read more recent posts here.

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Pay heed to “The House of the Rising Sun”

Pay heed to “The House of the Rising Sun”

 

“There is a house in New Orleans. They call the Rising Sun. And it’s been the ruin of many a poor boy. And, God, I know I’m one.”

Dr. Jordan Messler

The 1960s rock band the Animals will tell you a tale to convince you to get vaccinated. Don’t believe me? Follow along.

The first hints of the song “House of the Rising Sun” rolled out of the hills of Appalachia.

Somewhere in the Golden Triangle, far away from New Orleans, where Virginia, Kentucky, and Tennessee rise in quiet desolation, a warning song about a tailor and a drunk emerged. Sometime around the Civil War, a hint of a tune began. Over the next century, it evolved, until it became cemented in rock culture 50 years ago by The Animals, existing as the version played most commonly today.

In the mid-19th century, medicine shows rambled through the South, stopping in places like Noetown or Daisy. The small towns would empty out for the day to see the entertainers, singers, and jugglers perform. Hundreds gathered in the hot summer day, the entertainment solely a pretext for the traveling doctors to sell their wares, the snake oil, and cure-alls, as well as various patent medicines.

These were isolated towns, with no deliveries, few visitors, and the railroad yet to arrive. Frequently, the only news from outside came from these caravans of entertainers and con men who swept into town. They were like Professor Marvel from The Wizard of Oz, or a current-day Dr. Oz, luring the crowd with false advertising, selling colored water, and then disappearing before you realized you were duped. Today, traveling doctors of the same ilk convince parents to not vaccinate their children, tell them to visit stem cell centers that claim false cures, and offer them a shiny object with one hand while taking their cash with the other.

Yet, there was a positive development in the wake of these patent medicine shows: the entertainment lingered. New songs traveled the same journeys as these medicine shows – new earworms that would then be warbled in the local bars, while doing chores around the barn, or simply during walks on the Appalachian trails.

In 1937, Alan Lomax arrived in Noetown, Ky., with a microphone and an acetate record and recorded the voice of 16-year-old Georgia Turner singing “House of the Rising Sun.” She didn’t know where she heard that song, but most likely picked it up at the medicine show.

One of those singers was Clarence Ashley, who would croon about the Rising Sun Blues. He sang with Doc Cloud and Doc Hauer, who offered tonics for whatever ailed you. Perhaps Georgia Turner heard the song in the early 1900s as well. Her 1937 version contains the lyrics most closely related to the Animals’ tune.

Lomax spent the 1940s gathering songs around the Appalachian South. He put these songs into a songbook and spread them throughout the country. He would also return to New York City and gather in a room with legendary folk singers. They would hear these new lyrics, new sounds, and make them their own.

In that room would be Lead Belly, Pete Seeger, Woody Guthrie, and Josh White, the fathers of folk music. The music Lomax pulled out of the mountains in small towns would become new again in the guitars and harmonicas of the Greenwich Village singers and musicians. Pete Seeger performed with the Weavers, named because they would weave songs from the past into new versions.

“House of the Rising Sun” was woven into the folk music landscape, evolving and growing. Josh White is credited with changing the song from a major key into the minor key we know today. Bob Dylan sang a version. And then in 1964, Eric Burdon and The Animals released their version, which became the standard. An arpeggio guitar opening, the rhythm sped up, a louder sound, and that minor key provides an emotional wallop for this warning song.

Numerous covers followed, including a beautiful version of “Amazing Grace”, sung to the tune of “House of the Rising Sun” by the Blind Boys of Alabama.

The song endures for its melody as well as for its lyrics. This was a warning song, a universal song, “not to do what I have done.” The small towns in Kentucky may have heard of the sinful ways of New Orleans and would spread the message with these songs to avoid the brothels, the drink, and the broken marriages that would reverberate with visits to the Crescent City.

“House of the Rising Sun” is one of the most covered songs, traveling wide and far, no longer with the need for a medicine show. It was a pivotal moment in rock ‘n roll, turning folk music into rock music. The Animals became huge because of this song, and their version became the standard on which all subsequent covers based their version. It made Bob Dylan’s older version seem quaint.

The song has been in my head for a while now. My wife is hoping writing about it will keep it from being played in our household any more. There are various reasons it has been resonating with me, including the following:

 

 

  • It traces the origins of folk music and the importance of people like Lomax and Guthrie to collect and save Americana.
  • The magic of musical evolution – a reminder of how art is built on the work of those who came before, each version with its unique personality.
  • The release of “House of the Rising Sun” was a seminal, transformative moment when folk became rock music.
  • The lasting power of warning songs.
  • The hucksters that enabled this song to be kept alive.

That last one has really stuck with me. The medicine shows are an important part of American history. For instance, Coca-Cola started as one of those patent medicines; it was one of the many concoctions of the Atlanta pharmacist John Stith Pemberton, sold to treat all that ails us. Dr. Pepper, too, was a medicine in a sugary bottle – another that often contained alcohol or cocaine. Society wants a cure-all, and the marketing and selling done during these medicine shows offered placebos.

The hucksters exist in various forms today, selling detoxifications, magic diet cures, psychic powers of healing, or convincing parents that their kids don’t need vaccines. We need a warning song that goes viral to keep our children safe. We are blessed to be in a world without smallpox, almost rid of polio, and we have the knowledge and opportunity to rid the world of other preventable illnesses. Measles was declared eliminated in the United States in 2000; now, outbreaks emerge in every news cycle.

The CDC admits they have not been targeting misinformation well. How can we spread the science, the truth, the message faster than the lies? Better marketing? The answer may be through stories and narratives and song, with the backing of good science. “House of the Rising Sun” is a warning song. Maybe we need more. We need that deep history, that long trail to remind us of the world before vaccines, when everyone knew someone, either in their own household or next door, who succumbed to one of the childhood illnesses.

Let the “House of the Rising Sun” play on. Create a new version, and let that message reverberate, too.

Tell your children; they need to be vaccinated.
 

Dr. Messler is a hospitalist at Morton Plant Hospitalist group in Clearwater, Fla. He previously chaired SHM’s Quality and Patient Safety Committee and has been active in several SHM mentoring programs, most recently with Project BOOST and Glycemic Control. This article appeared originally in SHM's official blog The Hospital Leader. Read more recent posts here.

 

“There is a house in New Orleans. They call the Rising Sun. And it’s been the ruin of many a poor boy. And, God, I know I’m one.”

Dr. Jordan Messler

The 1960s rock band the Animals will tell you a tale to convince you to get vaccinated. Don’t believe me? Follow along.

The first hints of the song “House of the Rising Sun” rolled out of the hills of Appalachia.

Somewhere in the Golden Triangle, far away from New Orleans, where Virginia, Kentucky, and Tennessee rise in quiet desolation, a warning song about a tailor and a drunk emerged. Sometime around the Civil War, a hint of a tune began. Over the next century, it evolved, until it became cemented in rock culture 50 years ago by The Animals, existing as the version played most commonly today.

In the mid-19th century, medicine shows rambled through the South, stopping in places like Noetown or Daisy. The small towns would empty out for the day to see the entertainers, singers, and jugglers perform. Hundreds gathered in the hot summer day, the entertainment solely a pretext for the traveling doctors to sell their wares, the snake oil, and cure-alls, as well as various patent medicines.

These were isolated towns, with no deliveries, few visitors, and the railroad yet to arrive. Frequently, the only news from outside came from these caravans of entertainers and con men who swept into town. They were like Professor Marvel from The Wizard of Oz, or a current-day Dr. Oz, luring the crowd with false advertising, selling colored water, and then disappearing before you realized you were duped. Today, traveling doctors of the same ilk convince parents to not vaccinate their children, tell them to visit stem cell centers that claim false cures, and offer them a shiny object with one hand while taking their cash with the other.

Yet, there was a positive development in the wake of these patent medicine shows: the entertainment lingered. New songs traveled the same journeys as these medicine shows – new earworms that would then be warbled in the local bars, while doing chores around the barn, or simply during walks on the Appalachian trails.

In 1937, Alan Lomax arrived in Noetown, Ky., with a microphone and an acetate record and recorded the voice of 16-year-old Georgia Turner singing “House of the Rising Sun.” She didn’t know where she heard that song, but most likely picked it up at the medicine show.

One of those singers was Clarence Ashley, who would croon about the Rising Sun Blues. He sang with Doc Cloud and Doc Hauer, who offered tonics for whatever ailed you. Perhaps Georgia Turner heard the song in the early 1900s as well. Her 1937 version contains the lyrics most closely related to the Animals’ tune.

Lomax spent the 1940s gathering songs around the Appalachian South. He put these songs into a songbook and spread them throughout the country. He would also return to New York City and gather in a room with legendary folk singers. They would hear these new lyrics, new sounds, and make them their own.

In that room would be Lead Belly, Pete Seeger, Woody Guthrie, and Josh White, the fathers of folk music. The music Lomax pulled out of the mountains in small towns would become new again in the guitars and harmonicas of the Greenwich Village singers and musicians. Pete Seeger performed with the Weavers, named because they would weave songs from the past into new versions.

“House of the Rising Sun” was woven into the folk music landscape, evolving and growing. Josh White is credited with changing the song from a major key into the minor key we know today. Bob Dylan sang a version. And then in 1964, Eric Burdon and The Animals released their version, which became the standard. An arpeggio guitar opening, the rhythm sped up, a louder sound, and that minor key provides an emotional wallop for this warning song.

Numerous covers followed, including a beautiful version of “Amazing Grace”, sung to the tune of “House of the Rising Sun” by the Blind Boys of Alabama.

The song endures for its melody as well as for its lyrics. This was a warning song, a universal song, “not to do what I have done.” The small towns in Kentucky may have heard of the sinful ways of New Orleans and would spread the message with these songs to avoid the brothels, the drink, and the broken marriages that would reverberate with visits to the Crescent City.

“House of the Rising Sun” is one of the most covered songs, traveling wide and far, no longer with the need for a medicine show. It was a pivotal moment in rock ‘n roll, turning folk music into rock music. The Animals became huge because of this song, and their version became the standard on which all subsequent covers based their version. It made Bob Dylan’s older version seem quaint.

The song has been in my head for a while now. My wife is hoping writing about it will keep it from being played in our household any more. There are various reasons it has been resonating with me, including the following:

 

 

  • It traces the origins of folk music and the importance of people like Lomax and Guthrie to collect and save Americana.
  • The magic of musical evolution – a reminder of how art is built on the work of those who came before, each version with its unique personality.
  • The release of “House of the Rising Sun” was a seminal, transformative moment when folk became rock music.
  • The lasting power of warning songs.
  • The hucksters that enabled this song to be kept alive.

That last one has really stuck with me. The medicine shows are an important part of American history. For instance, Coca-Cola started as one of those patent medicines; it was one of the many concoctions of the Atlanta pharmacist John Stith Pemberton, sold to treat all that ails us. Dr. Pepper, too, was a medicine in a sugary bottle – another that often contained alcohol or cocaine. Society wants a cure-all, and the marketing and selling done during these medicine shows offered placebos.

The hucksters exist in various forms today, selling detoxifications, magic diet cures, psychic powers of healing, or convincing parents that their kids don’t need vaccines. We need a warning song that goes viral to keep our children safe. We are blessed to be in a world without smallpox, almost rid of polio, and we have the knowledge and opportunity to rid the world of other preventable illnesses. Measles was declared eliminated in the United States in 2000; now, outbreaks emerge in every news cycle.

The CDC admits they have not been targeting misinformation well. How can we spread the science, the truth, the message faster than the lies? Better marketing? The answer may be through stories and narratives and song, with the backing of good science. “House of the Rising Sun” is a warning song. Maybe we need more. We need that deep history, that long trail to remind us of the world before vaccines, when everyone knew someone, either in their own household or next door, who succumbed to one of the childhood illnesses.

Let the “House of the Rising Sun” play on. Create a new version, and let that message reverberate, too.

Tell your children; they need to be vaccinated.
 

Dr. Messler is a hospitalist at Morton Plant Hospitalist group in Clearwater, Fla. He previously chaired SHM’s Quality and Patient Safety Committee and has been active in several SHM mentoring programs, most recently with Project BOOST and Glycemic Control. This article appeared originally in SHM's official blog The Hospital Leader. Read more recent posts here.

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The urge to move

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Tue, 06/04/2019 - 12:52

When you have a few spare minutes on your lunch break, walk by the grade school playground in your neighborhood. Even at a quick glance you will notice that almost all the children are in motion – running, chasing, or being chased. Don’t linger too long or make repeat visits because unfortunately your presence may raise suspicions about your motives. But, even on your brief visit, you will also notice that there are a few children who are sitting down either chatting with a classmate or playing by themselves. If despite my caution you returned several days in a row, you would have noticed that the sedentary outliers tend to be the same children.

©Jupiterimages/Thinkstock.com

Some of the children playing alone simply may be shy loners or socially inept. But I’ve always suspected that there are some people who come in the world genetically predisposed to being sedentary. You can try to make the environment more enticing and stimulating, but the children predestined to be inactive will choose to sit and watch. Not surprisingly, most of those less active children are predestined to be overweight and obese.

At least as young children we seem to be driven to be active, and it is the few outliers who are sedentary. A recent investigation from the department of health and kinesiology at Texas A&M University at College Station is beginning to shed some light on when in our evolutionary history the urge to be active was incorporated into our genome (PLOS ONE. 2019 Apr 29. doi: 10.1371/journal.pone.0216155). The researchers found that snippets of DNA already known to be associated with levels of activity emerged in our ancestors before we were Homo sapiens about 500,000 years ago. This finding surprised the investigators who had suspected that this incorporation of a gene sequence driving activity was more likely to have occurred ten thousand years ago when subsistence farming and its physical demands first appeared.

The authors now postulate that the drive to be active coincided as pre–Homo sapiens grew larger and moved from a treed landscape into the open savanna (“To Move Is to Thrive. It’s in Our Genes” by Gretchen Reynolds. The New York Times, May 15, 2019). As J. Timothy Lightfoot, the senior investigator, observed, “If you were lazy then, you did not survive.”

So if the drive to be active is so deeply buried in our genome why have we slipped so easily into a species in which being sedentary is the norm? Our observation of a playground in contact motion is probably evidence that those snippets of DNA still are buried in our genome. However, it is abundantly clear that in North America one doesn’t need to be active to survive, at least in the sense of being reproductively fit. It only takes a few us who must be physically active to grow and build things that we in the sedentary majority can buy or trade for.

There are some of us who have inherited some DNA snippets that drive us to be active post early childhood. My father walked two or three times a day until a few months before his death at 92, and not because someone told him it do it for his health. Like him, I just feel better if I have spent a couple of hours being active every day.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff

The challenge for us as pediatricians is to help families create environments that foster continued activity by discouraging sedentary entertainments and modeling active lifestyles. For example, simple things like choosing a spot at the periphery of the parking lot instead of close to the store. Choosing stairs instead of the elevator. Of course, anything you will be doing is artificial because the truth is we don’t need to be active to survive even though the urge to move is deeply rooted in our genes.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

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When you have a few spare minutes on your lunch break, walk by the grade school playground in your neighborhood. Even at a quick glance you will notice that almost all the children are in motion – running, chasing, or being chased. Don’t linger too long or make repeat visits because unfortunately your presence may raise suspicions about your motives. But, even on your brief visit, you will also notice that there are a few children who are sitting down either chatting with a classmate or playing by themselves. If despite my caution you returned several days in a row, you would have noticed that the sedentary outliers tend to be the same children.

©Jupiterimages/Thinkstock.com

Some of the children playing alone simply may be shy loners or socially inept. But I’ve always suspected that there are some people who come in the world genetically predisposed to being sedentary. You can try to make the environment more enticing and stimulating, but the children predestined to be inactive will choose to sit and watch. Not surprisingly, most of those less active children are predestined to be overweight and obese.

At least as young children we seem to be driven to be active, and it is the few outliers who are sedentary. A recent investigation from the department of health and kinesiology at Texas A&M University at College Station is beginning to shed some light on when in our evolutionary history the urge to be active was incorporated into our genome (PLOS ONE. 2019 Apr 29. doi: 10.1371/journal.pone.0216155). The researchers found that snippets of DNA already known to be associated with levels of activity emerged in our ancestors before we were Homo sapiens about 500,000 years ago. This finding surprised the investigators who had suspected that this incorporation of a gene sequence driving activity was more likely to have occurred ten thousand years ago when subsistence farming and its physical demands first appeared.

The authors now postulate that the drive to be active coincided as pre–Homo sapiens grew larger and moved from a treed landscape into the open savanna (“To Move Is to Thrive. It’s in Our Genes” by Gretchen Reynolds. The New York Times, May 15, 2019). As J. Timothy Lightfoot, the senior investigator, observed, “If you were lazy then, you did not survive.”

So if the drive to be active is so deeply buried in our genome why have we slipped so easily into a species in which being sedentary is the norm? Our observation of a playground in contact motion is probably evidence that those snippets of DNA still are buried in our genome. However, it is abundantly clear that in North America one doesn’t need to be active to survive, at least in the sense of being reproductively fit. It only takes a few us who must be physically active to grow and build things that we in the sedentary majority can buy or trade for.

There are some of us who have inherited some DNA snippets that drive us to be active post early childhood. My father walked two or three times a day until a few months before his death at 92, and not because someone told him it do it for his health. Like him, I just feel better if I have spent a couple of hours being active every day.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff

The challenge for us as pediatricians is to help families create environments that foster continued activity by discouraging sedentary entertainments and modeling active lifestyles. For example, simple things like choosing a spot at the periphery of the parking lot instead of close to the store. Choosing stairs instead of the elevator. Of course, anything you will be doing is artificial because the truth is we don’t need to be active to survive even though the urge to move is deeply rooted in our genes.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

When you have a few spare minutes on your lunch break, walk by the grade school playground in your neighborhood. Even at a quick glance you will notice that almost all the children are in motion – running, chasing, or being chased. Don’t linger too long or make repeat visits because unfortunately your presence may raise suspicions about your motives. But, even on your brief visit, you will also notice that there are a few children who are sitting down either chatting with a classmate or playing by themselves. If despite my caution you returned several days in a row, you would have noticed that the sedentary outliers tend to be the same children.

©Jupiterimages/Thinkstock.com

Some of the children playing alone simply may be shy loners or socially inept. But I’ve always suspected that there are some people who come in the world genetically predisposed to being sedentary. You can try to make the environment more enticing and stimulating, but the children predestined to be inactive will choose to sit and watch. Not surprisingly, most of those less active children are predestined to be overweight and obese.

At least as young children we seem to be driven to be active, and it is the few outliers who are sedentary. A recent investigation from the department of health and kinesiology at Texas A&M University at College Station is beginning to shed some light on when in our evolutionary history the urge to be active was incorporated into our genome (PLOS ONE. 2019 Apr 29. doi: 10.1371/journal.pone.0216155). The researchers found that snippets of DNA already known to be associated with levels of activity emerged in our ancestors before we were Homo sapiens about 500,000 years ago. This finding surprised the investigators who had suspected that this incorporation of a gene sequence driving activity was more likely to have occurred ten thousand years ago when subsistence farming and its physical demands first appeared.

The authors now postulate that the drive to be active coincided as pre–Homo sapiens grew larger and moved from a treed landscape into the open savanna (“To Move Is to Thrive. It’s in Our Genes” by Gretchen Reynolds. The New York Times, May 15, 2019). As J. Timothy Lightfoot, the senior investigator, observed, “If you were lazy then, you did not survive.”

So if the drive to be active is so deeply buried in our genome why have we slipped so easily into a species in which being sedentary is the norm? Our observation of a playground in contact motion is probably evidence that those snippets of DNA still are buried in our genome. However, it is abundantly clear that in North America one doesn’t need to be active to survive, at least in the sense of being reproductively fit. It only takes a few us who must be physically active to grow and build things that we in the sedentary majority can buy or trade for.

There are some of us who have inherited some DNA snippets that drive us to be active post early childhood. My father walked two or three times a day until a few months before his death at 92, and not because someone told him it do it for his health. Like him, I just feel better if I have spent a couple of hours being active every day.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff

The challenge for us as pediatricians is to help families create environments that foster continued activity by discouraging sedentary entertainments and modeling active lifestyles. For example, simple things like choosing a spot at the periphery of the parking lot instead of close to the store. Choosing stairs instead of the elevator. Of course, anything you will be doing is artificial because the truth is we don’t need to be active to survive even though the urge to move is deeply rooted in our genes.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

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Pediatricians report low knowledge, comfort discussing e-cigarettes

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Tue, 06/04/2019 - 11:45

Pediatricians appear less comfortable discussing e-cigarettes and their harms with adolescents and parents than they do discussing dangers of tobacco products, according to a recent study.

LiudmylaSupynska/Thinkstock

“Providers are aware of the increased prevalence, harms [of e-cigs] and [the] positive impact of counseling teens about e-cigs,” said Allison Heinly, MD, of Hasbro Children’s Hospital in Providence, R.I., and her colleagues. But, “providers are less likely to ask, advise, or assist parents [and teens] regarding e-cig use, compared to tobacco, and are less comfortable doing so.” The researchers presented their findings at the Pediatric Academic Societies annual meeting.

A variety of concerns exist regarding ingredients in e-cigarettes, Dr. Heinly noted, including nicotine, volatile organic compounds, carcinogenic chemicals, flavorings, and ultra-fine particles.

Dr. Heinly and her associates aimed to assess pediatricians’ knowledge, attitudes, and behaviors toward both teens’ and parents’ use of e-cigarettes, as well as the barrier pediatricians perceived when it came to screening and counseling those who use e-cigarettes.

Among 69 providers at a large Northeastern urban academic primary care clinic who received surveys, 62 responded, primarily residents (84%). The respondents included 44 pediatric residents, eight triple-board residents, and 10 attending physicians.

The researchers collapsed “most of the time”/“always” and “some of the time”/“never” responses into two categories.

Most of the respondents (82%) knew e-cigarettes are the most common tobacco product that youth use, and nearly all (97%) believed e-cigarettes were addictive and harmful to users’ health. In addition, most (79%) believed using e-cigarettes could be a pathway toward students beginning to use other drugs.

Even though respondents believed counseling teens about use of tobacco or e-cigarettes can reduce the likelihood that they will start using them, providers were much less likely to discuss e-cigarettes than tobacco with teens.

Nearly all the doctors (97%) reported asking teens about their use of tobacco, but only about half (52%) asked about e-cigarette use (P less than .001). And only about one in five doctors (21%) reported counseling teens about using e-cigarettes, compared with 47% of those who advised teens regarding tobacco use (P = .002).

Over a third of responding physicians (37%) reported helping adolescent patients quit using tobacco, but just 7% reported doing so with e-cigarettes (P less than .001).

Doctors overwhelmingly reported feeling comfortable talking about tobacco with teens (98%), but fewer felt comfortable discussing e-cigarettes (77%; P less than .001). Respondents similarly were less comfortable discussing e-cigarettes (55%) than tobacco (87%) with parents (P less than .001).

Very few pediatricians asked parents about their use of e-cigarettes (5%) or advised them about e-cigarettes’ harms (7%), and even fewer reported helping parents quit using them (2%). By contrast, more than half of pediatricians (60%) asked parents about smoking or advised them about tobacco use harms (52%), and nearly one-third (31%) reported helping parents quit smoking (P less than .001 for all comparisons).

The biggest barrier to discussing e-cigarettes with families was, as with discussing tobacco, not having enough time. But about twice as many respondents cited insufficient knowledge as a barrier for e-cigarettes as for tobacco (P = .003). A small percentage of respondents (less than 20%) also reported feeling unsure about the harm of e-cigarettes (P = .001).

Lack of training was a significant barrier to physicians’ discussion of e-cigarettes as well. Many more physicians reported receiving training in medical school on tobacco and traditional cigarettes (78%) than on e-cigarettes (13%), possibly because of how recently e-cigarettes have become widely available (P less than .001).

More physicians reported receiving training related to e-cigarettes during residency (36%), but it still fell well short of how many reported other tobacco and smoking training during residency (61%; P = .001).

The findings “emphasize the importance of increasing training about e-cig counseling,” Dr. Heinly and her associates concluded.

The researchers noted no external funding or disclosures.

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Pediatricians appear less comfortable discussing e-cigarettes and their harms with adolescents and parents than they do discussing dangers of tobacco products, according to a recent study.

LiudmylaSupynska/Thinkstock

“Providers are aware of the increased prevalence, harms [of e-cigs] and [the] positive impact of counseling teens about e-cigs,” said Allison Heinly, MD, of Hasbro Children’s Hospital in Providence, R.I., and her colleagues. But, “providers are less likely to ask, advise, or assist parents [and teens] regarding e-cig use, compared to tobacco, and are less comfortable doing so.” The researchers presented their findings at the Pediatric Academic Societies annual meeting.

A variety of concerns exist regarding ingredients in e-cigarettes, Dr. Heinly noted, including nicotine, volatile organic compounds, carcinogenic chemicals, flavorings, and ultra-fine particles.

Dr. Heinly and her associates aimed to assess pediatricians’ knowledge, attitudes, and behaviors toward both teens’ and parents’ use of e-cigarettes, as well as the barrier pediatricians perceived when it came to screening and counseling those who use e-cigarettes.

Among 69 providers at a large Northeastern urban academic primary care clinic who received surveys, 62 responded, primarily residents (84%). The respondents included 44 pediatric residents, eight triple-board residents, and 10 attending physicians.

The researchers collapsed “most of the time”/“always” and “some of the time”/“never” responses into two categories.

Most of the respondents (82%) knew e-cigarettes are the most common tobacco product that youth use, and nearly all (97%) believed e-cigarettes were addictive and harmful to users’ health. In addition, most (79%) believed using e-cigarettes could be a pathway toward students beginning to use other drugs.

Even though respondents believed counseling teens about use of tobacco or e-cigarettes can reduce the likelihood that they will start using them, providers were much less likely to discuss e-cigarettes than tobacco with teens.

Nearly all the doctors (97%) reported asking teens about their use of tobacco, but only about half (52%) asked about e-cigarette use (P less than .001). And only about one in five doctors (21%) reported counseling teens about using e-cigarettes, compared with 47% of those who advised teens regarding tobacco use (P = .002).

Over a third of responding physicians (37%) reported helping adolescent patients quit using tobacco, but just 7% reported doing so with e-cigarettes (P less than .001).

Doctors overwhelmingly reported feeling comfortable talking about tobacco with teens (98%), but fewer felt comfortable discussing e-cigarettes (77%; P less than .001). Respondents similarly were less comfortable discussing e-cigarettes (55%) than tobacco (87%) with parents (P less than .001).

Very few pediatricians asked parents about their use of e-cigarettes (5%) or advised them about e-cigarettes’ harms (7%), and even fewer reported helping parents quit using them (2%). By contrast, more than half of pediatricians (60%) asked parents about smoking or advised them about tobacco use harms (52%), and nearly one-third (31%) reported helping parents quit smoking (P less than .001 for all comparisons).

The biggest barrier to discussing e-cigarettes with families was, as with discussing tobacco, not having enough time. But about twice as many respondents cited insufficient knowledge as a barrier for e-cigarettes as for tobacco (P = .003). A small percentage of respondents (less than 20%) also reported feeling unsure about the harm of e-cigarettes (P = .001).

Lack of training was a significant barrier to physicians’ discussion of e-cigarettes as well. Many more physicians reported receiving training in medical school on tobacco and traditional cigarettes (78%) than on e-cigarettes (13%), possibly because of how recently e-cigarettes have become widely available (P less than .001).

More physicians reported receiving training related to e-cigarettes during residency (36%), but it still fell well short of how many reported other tobacco and smoking training during residency (61%; P = .001).

The findings “emphasize the importance of increasing training about e-cig counseling,” Dr. Heinly and her associates concluded.

The researchers noted no external funding or disclosures.

Pediatricians appear less comfortable discussing e-cigarettes and their harms with adolescents and parents than they do discussing dangers of tobacco products, according to a recent study.

LiudmylaSupynska/Thinkstock

“Providers are aware of the increased prevalence, harms [of e-cigs] and [the] positive impact of counseling teens about e-cigs,” said Allison Heinly, MD, of Hasbro Children’s Hospital in Providence, R.I., and her colleagues. But, “providers are less likely to ask, advise, or assist parents [and teens] regarding e-cig use, compared to tobacco, and are less comfortable doing so.” The researchers presented their findings at the Pediatric Academic Societies annual meeting.

A variety of concerns exist regarding ingredients in e-cigarettes, Dr. Heinly noted, including nicotine, volatile organic compounds, carcinogenic chemicals, flavorings, and ultra-fine particles.

Dr. Heinly and her associates aimed to assess pediatricians’ knowledge, attitudes, and behaviors toward both teens’ and parents’ use of e-cigarettes, as well as the barrier pediatricians perceived when it came to screening and counseling those who use e-cigarettes.

Among 69 providers at a large Northeastern urban academic primary care clinic who received surveys, 62 responded, primarily residents (84%). The respondents included 44 pediatric residents, eight triple-board residents, and 10 attending physicians.

The researchers collapsed “most of the time”/“always” and “some of the time”/“never” responses into two categories.

Most of the respondents (82%) knew e-cigarettes are the most common tobacco product that youth use, and nearly all (97%) believed e-cigarettes were addictive and harmful to users’ health. In addition, most (79%) believed using e-cigarettes could be a pathway toward students beginning to use other drugs.

Even though respondents believed counseling teens about use of tobacco or e-cigarettes can reduce the likelihood that they will start using them, providers were much less likely to discuss e-cigarettes than tobacco with teens.

Nearly all the doctors (97%) reported asking teens about their use of tobacco, but only about half (52%) asked about e-cigarette use (P less than .001). And only about one in five doctors (21%) reported counseling teens about using e-cigarettes, compared with 47% of those who advised teens regarding tobacco use (P = .002).

Over a third of responding physicians (37%) reported helping adolescent patients quit using tobacco, but just 7% reported doing so with e-cigarettes (P less than .001).

Doctors overwhelmingly reported feeling comfortable talking about tobacco with teens (98%), but fewer felt comfortable discussing e-cigarettes (77%; P less than .001). Respondents similarly were less comfortable discussing e-cigarettes (55%) than tobacco (87%) with parents (P less than .001).

Very few pediatricians asked parents about their use of e-cigarettes (5%) or advised them about e-cigarettes’ harms (7%), and even fewer reported helping parents quit using them (2%). By contrast, more than half of pediatricians (60%) asked parents about smoking or advised them about tobacco use harms (52%), and nearly one-third (31%) reported helping parents quit smoking (P less than .001 for all comparisons).

The biggest barrier to discussing e-cigarettes with families was, as with discussing tobacco, not having enough time. But about twice as many respondents cited insufficient knowledge as a barrier for e-cigarettes as for tobacco (P = .003). A small percentage of respondents (less than 20%) also reported feeling unsure about the harm of e-cigarettes (P = .001).

Lack of training was a significant barrier to physicians’ discussion of e-cigarettes as well. Many more physicians reported receiving training in medical school on tobacco and traditional cigarettes (78%) than on e-cigarettes (13%), possibly because of how recently e-cigarettes have become widely available (P less than .001).

More physicians reported receiving training related to e-cigarettes during residency (36%), but it still fell well short of how many reported other tobacco and smoking training during residency (61%; P = .001).

The findings “emphasize the importance of increasing training about e-cig counseling,” Dr. Heinly and her associates concluded.

The researchers noted no external funding or disclosures.

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Key clinical point: Physicians report less training and less comfort when discussing e-cigarettes with teens and parents than when discussing tobacco products.

Major finding: 7% of physicians reported helping adolescent patients quit using e-cigarettes, compared with 37% helping with quitting tobacco use (P less than .001).

Study details: The findings are based on a cross-sectional survey of 62 pediatric residents and attendings at a large urban academic primary care clinic in the Northeast.

Disclosures: The researchers noted no external funding or disclosures.

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