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Patient-reported outcome measures complement clinician-reported outcomes in psoriasis

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Key clinical point: The disease severity assessment, guiding initiation of systemic therapy, differed when either patient- or clinician-reported outcomes were considered alone, highlighting the complementary value of both for appropriate treatment.

Major finding: Overall, 72.4% (95% confidence interval [CI], 67.3%-77.0%) of patients who qualified for systemic therapy initiation on account of Psoriasis Area Severity Index (PASI) scores or body surface area (BSA) of 10 or higher had a Dermatology Life Quality Index (DLQI) score of less than 10. Conversely, 10.4% (95% CI, 8.8%-12.1%) of patients with a DLQI score higher than 10 did not qualify for systemic therapy based on PASI scores or BSA.

Study details: Findings are from a cross-sectional, observational study including 1,733 patients with mild, moderate, or severe psoriasis who met the criteria for initiation of systemic therapy based on DLQI score, PASI score, or BSA.

Disclosures: No specific funding for the study was disclosed. Dr. Gelfand declared receiving consultation fees and research grants from various sources.

Source: Barbieri JS et al. JAMA Dermatol. 2021 Sep 8. doi: 10.1001/jamadermatol.2021.3341.

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Key clinical point: The disease severity assessment, guiding initiation of systemic therapy, differed when either patient- or clinician-reported outcomes were considered alone, highlighting the complementary value of both for appropriate treatment.

Major finding: Overall, 72.4% (95% confidence interval [CI], 67.3%-77.0%) of patients who qualified for systemic therapy initiation on account of Psoriasis Area Severity Index (PASI) scores or body surface area (BSA) of 10 or higher had a Dermatology Life Quality Index (DLQI) score of less than 10. Conversely, 10.4% (95% CI, 8.8%-12.1%) of patients with a DLQI score higher than 10 did not qualify for systemic therapy based on PASI scores or BSA.

Study details: Findings are from a cross-sectional, observational study including 1,733 patients with mild, moderate, or severe psoriasis who met the criteria for initiation of systemic therapy based on DLQI score, PASI score, or BSA.

Disclosures: No specific funding for the study was disclosed. Dr. Gelfand declared receiving consultation fees and research grants from various sources.

Source: Barbieri JS et al. JAMA Dermatol. 2021 Sep 8. doi: 10.1001/jamadermatol.2021.3341.

Key clinical point: The disease severity assessment, guiding initiation of systemic therapy, differed when either patient- or clinician-reported outcomes were considered alone, highlighting the complementary value of both for appropriate treatment.

Major finding: Overall, 72.4% (95% confidence interval [CI], 67.3%-77.0%) of patients who qualified for systemic therapy initiation on account of Psoriasis Area Severity Index (PASI) scores or body surface area (BSA) of 10 or higher had a Dermatology Life Quality Index (DLQI) score of less than 10. Conversely, 10.4% (95% CI, 8.8%-12.1%) of patients with a DLQI score higher than 10 did not qualify for systemic therapy based on PASI scores or BSA.

Study details: Findings are from a cross-sectional, observational study including 1,733 patients with mild, moderate, or severe psoriasis who met the criteria for initiation of systemic therapy based on DLQI score, PASI score, or BSA.

Disclosures: No specific funding for the study was disclosed. Dr. Gelfand declared receiving consultation fees and research grants from various sources.

Source: Barbieri JS et al. JAMA Dermatol. 2021 Sep 8. doi: 10.1001/jamadermatol.2021.3341.

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Risankizumab shows excellent long-term PASI response in psoriasis under real-world conditions

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Key clinical point: Risankizumab displayed superior long-term clinical efficacy against moderate-to-severe psoriasis, with no new safety signals in the 52-week update of a multicenter real-life study.

Major finding: Psoriasis Area and Severity Index (PASI) 75, PASI 90, and PASI 100 response rates at week 36 were 92.7%, 83.6%, and 65.5%, which were maintained through week 52 at 96.4%, 85.5%, and 60.0%, respectively. Unlike in phase 3 trials, more biologic-experienced patients reached PASI 100 at weeks 36 and 52 (71.8% and 69.2%, respectively) compared with biologic-naïve patients (50.0% and 37.5%, respectively).

Study details: Findings are from a real-life multicenter study including 57 adult patients with moderate-to-severe psoriasis who were receiving risankizumab therapy.

Disclosures: The study did not receive any funding. Some of the authors including the lead author declared receiving consultation/personal fees or research grants from various sources.

Source: Hansel K et al. J Eur Acad Dermatol Venereol. 2021 Sep 12. doi: 10.1111/jdv.17656.

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Key clinical point: Risankizumab displayed superior long-term clinical efficacy against moderate-to-severe psoriasis, with no new safety signals in the 52-week update of a multicenter real-life study.

Major finding: Psoriasis Area and Severity Index (PASI) 75, PASI 90, and PASI 100 response rates at week 36 were 92.7%, 83.6%, and 65.5%, which were maintained through week 52 at 96.4%, 85.5%, and 60.0%, respectively. Unlike in phase 3 trials, more biologic-experienced patients reached PASI 100 at weeks 36 and 52 (71.8% and 69.2%, respectively) compared with biologic-naïve patients (50.0% and 37.5%, respectively).

Study details: Findings are from a real-life multicenter study including 57 adult patients with moderate-to-severe psoriasis who were receiving risankizumab therapy.

Disclosures: The study did not receive any funding. Some of the authors including the lead author declared receiving consultation/personal fees or research grants from various sources.

Source: Hansel K et al. J Eur Acad Dermatol Venereol. 2021 Sep 12. doi: 10.1111/jdv.17656.

Key clinical point: Risankizumab displayed superior long-term clinical efficacy against moderate-to-severe psoriasis, with no new safety signals in the 52-week update of a multicenter real-life study.

Major finding: Psoriasis Area and Severity Index (PASI) 75, PASI 90, and PASI 100 response rates at week 36 were 92.7%, 83.6%, and 65.5%, which were maintained through week 52 at 96.4%, 85.5%, and 60.0%, respectively. Unlike in phase 3 trials, more biologic-experienced patients reached PASI 100 at weeks 36 and 52 (71.8% and 69.2%, respectively) compared with biologic-naïve patients (50.0% and 37.5%, respectively).

Study details: Findings are from a real-life multicenter study including 57 adult patients with moderate-to-severe psoriasis who were receiving risankizumab therapy.

Disclosures: The study did not receive any funding. Some of the authors including the lead author declared receiving consultation/personal fees or research grants from various sources.

Source: Hansel K et al. J Eur Acad Dermatol Venereol. 2021 Sep 12. doi: 10.1111/jdv.17656.

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Secukinumab hits mark against pediatric plaque psoriasis

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Key clinical point: Secukinumab demonstrated a high skin-clearing effect and favorable safety in pediatric patients with moderate-to-severe plaque psoriasis through week 24.

Major finding: At week 12, low dose (LD) and high dose (HD) groups showed a Psoriasis Area Severity Index (PASI) 75 response rate (RR) of 92.9%, whereas their Investigator's Global Assessment (IGA) 0/1 RRs were 78.5% and 83.4%, respectively. At week 24, the PASI 75 RR for LD and HD groups increased to 95.2% and IGA 0/1 RRs increased to 88.1% and 92.9%, respectively. Both groups displayed similar treatment-emergent adverse events.

Study details: These are 24-week findings of a 224-week, open-label, phase 3 study including 84 pediatric patients with moderate-to-severe plaque psoriasis randomly assigned to LD or HD secukinumab (75/75/150 or 75/150/300 mg for body weight (kg) less than 25/25 to less than 50/50 or more, respectively).

Disclosures: The study was sponsored by Novartis Pharma AG, Switzerland. R Mazur, P Forrer, and M Patekar declared being employees of Novartis Pharma AG. Some of the authors declared serving on advisory board, speaker, consultant, or principal/subinvestigator for various organizations including Novartis.

Source: Magnolo N et al. J Am Acad Dermatol. 2021 Sep 20. doi: 10.1016/j.jaad.2021.08.066.

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Key clinical point: Secukinumab demonstrated a high skin-clearing effect and favorable safety in pediatric patients with moderate-to-severe plaque psoriasis through week 24.

Major finding: At week 12, low dose (LD) and high dose (HD) groups showed a Psoriasis Area Severity Index (PASI) 75 response rate (RR) of 92.9%, whereas their Investigator's Global Assessment (IGA) 0/1 RRs were 78.5% and 83.4%, respectively. At week 24, the PASI 75 RR for LD and HD groups increased to 95.2% and IGA 0/1 RRs increased to 88.1% and 92.9%, respectively. Both groups displayed similar treatment-emergent adverse events.

Study details: These are 24-week findings of a 224-week, open-label, phase 3 study including 84 pediatric patients with moderate-to-severe plaque psoriasis randomly assigned to LD or HD secukinumab (75/75/150 or 75/150/300 mg for body weight (kg) less than 25/25 to less than 50/50 or more, respectively).

Disclosures: The study was sponsored by Novartis Pharma AG, Switzerland. R Mazur, P Forrer, and M Patekar declared being employees of Novartis Pharma AG. Some of the authors declared serving on advisory board, speaker, consultant, or principal/subinvestigator for various organizations including Novartis.

Source: Magnolo N et al. J Am Acad Dermatol. 2021 Sep 20. doi: 10.1016/j.jaad.2021.08.066.

Key clinical point: Secukinumab demonstrated a high skin-clearing effect and favorable safety in pediatric patients with moderate-to-severe plaque psoriasis through week 24.

Major finding: At week 12, low dose (LD) and high dose (HD) groups showed a Psoriasis Area Severity Index (PASI) 75 response rate (RR) of 92.9%, whereas their Investigator's Global Assessment (IGA) 0/1 RRs were 78.5% and 83.4%, respectively. At week 24, the PASI 75 RR for LD and HD groups increased to 95.2% and IGA 0/1 RRs increased to 88.1% and 92.9%, respectively. Both groups displayed similar treatment-emergent adverse events.

Study details: These are 24-week findings of a 224-week, open-label, phase 3 study including 84 pediatric patients with moderate-to-severe plaque psoriasis randomly assigned to LD or HD secukinumab (75/75/150 or 75/150/300 mg for body weight (kg) less than 25/25 to less than 50/50 or more, respectively).

Disclosures: The study was sponsored by Novartis Pharma AG, Switzerland. R Mazur, P Forrer, and M Patekar declared being employees of Novartis Pharma AG. Some of the authors declared serving on advisory board, speaker, consultant, or principal/subinvestigator for various organizations including Novartis.

Source: Magnolo N et al. J Am Acad Dermatol. 2021 Sep 20. doi: 10.1016/j.jaad.2021.08.066.

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Teen boy’s knee lesion has changed

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A biopsy of the lesion was performed which showed an increased number of eccrine glands and blood vessels within the dermis. Some areas showed an increase in adipocytes and smooth muscle bundles. The changes were consistent with eccrine angiomatous hamartoma (EAH).

On dermatoscopy the lesion showed multiple dilated red and violaceous lacunae and whitish-blue hue.

The boy was referred to vascular laser therapy for treatment of the lesion.

EAH is a rare benign vascular growth characterized by an increased number of mature eccrine glands and blood vessels in the dermis and subcutis. The lesions are mostly present on the extremities, but cases of diffuse congenital lesions and lesions on the face and trunk have also been described. The lesions can be seen at birth or during the first years of life in about half of the cases, and the others tend to occur later in puberty and rarely in adulthood.1

Clinically, EAH lesions present as red, yellow to brown papules and plaques. Different dermoscopic patterns have been described which include the popcorn pattern that presents as yellow, confluent nodules with popcornlike shapes over a background of erythema, and linear arborizing vessels. The spitzoid pattern are brown globules on a background of erythema and pseudoreticular pigmentation around the globules. The verrucous hemangiomalike pattern has a bluish-white hue, reddish-blue or bluish lacunae, as seen in our patient.2-4

Most of the lesions are asymptomatic, but in some patients, they can be associated with pain, hyperhidrosis, and sometimes bleeding. Hyperhidrosis has been reported early in the presentation or during puberty or pregnancy. Our patient had started on amphetamines when hyperhidrosis occurred. Hyperhidrosis is a knowns side effect of this type of medication and may have had a role in the increased sweating noted on the hamartoma.

EAH can clinically look like verrucous hemangiomas, angiokeratomas, and vascular malformations, and histopathology may be needed to differentiate between them. Eccrine nevi and EAH can be similar. Hyperhidrosis is an early and predominant component of eccrine nevi, compared with one-third of EAH.

The exact etiology of this lesion is not known. It is thought to be caused by an abnormal differentiation of the epithelium, adnexal structure, and the mesenchyme during organogenesis.3 No other associated conditions have been described with EAH.

EAH are benign lesions that rarely require treatment. If the lesions are symptomatic or because of cosmetic reasons, they can be removed surgically. There are some reports of successful treatment with pulse dual-wavelength sequential 595- and 1064-nm lasers.5 Botulinum toxin has also been used in cases of symptomatic hyperhidrosis.
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She has no conflicts. Email her at [email protected].

References

1. Smith SD et al. Pediatr Dermatol. 2019 Nov;36(6):909-12.

2. Patterson AT et al. Am J Dermatopathol. 2016;38:413-7.

3. Garcıa-Garcıa SC et al. JAAD Case Rep. 2018;4(2):165-7.

4. Awatef Kelati et al. JAAD Case Rep. 2018;4(8)835-6.

5. Felgueiras J et al. Dermatol Surg. 2015 Mar;41(3):428-30.

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A biopsy of the lesion was performed which showed an increased number of eccrine glands and blood vessels within the dermis. Some areas showed an increase in adipocytes and smooth muscle bundles. The changes were consistent with eccrine angiomatous hamartoma (EAH).

On dermatoscopy the lesion showed multiple dilated red and violaceous lacunae and whitish-blue hue.

The boy was referred to vascular laser therapy for treatment of the lesion.

EAH is a rare benign vascular growth characterized by an increased number of mature eccrine glands and blood vessels in the dermis and subcutis. The lesions are mostly present on the extremities, but cases of diffuse congenital lesions and lesions on the face and trunk have also been described. The lesions can be seen at birth or during the first years of life in about half of the cases, and the others tend to occur later in puberty and rarely in adulthood.1

Clinically, EAH lesions present as red, yellow to brown papules and plaques. Different dermoscopic patterns have been described which include the popcorn pattern that presents as yellow, confluent nodules with popcornlike shapes over a background of erythema, and linear arborizing vessels. The spitzoid pattern are brown globules on a background of erythema and pseudoreticular pigmentation around the globules. The verrucous hemangiomalike pattern has a bluish-white hue, reddish-blue or bluish lacunae, as seen in our patient.2-4

Most of the lesions are asymptomatic, but in some patients, they can be associated with pain, hyperhidrosis, and sometimes bleeding. Hyperhidrosis has been reported early in the presentation or during puberty or pregnancy. Our patient had started on amphetamines when hyperhidrosis occurred. Hyperhidrosis is a knowns side effect of this type of medication and may have had a role in the increased sweating noted on the hamartoma.

EAH can clinically look like verrucous hemangiomas, angiokeratomas, and vascular malformations, and histopathology may be needed to differentiate between them. Eccrine nevi and EAH can be similar. Hyperhidrosis is an early and predominant component of eccrine nevi, compared with one-third of EAH.

The exact etiology of this lesion is not known. It is thought to be caused by an abnormal differentiation of the epithelium, adnexal structure, and the mesenchyme during organogenesis.3 No other associated conditions have been described with EAH.

EAH are benign lesions that rarely require treatment. If the lesions are symptomatic or because of cosmetic reasons, they can be removed surgically. There are some reports of successful treatment with pulse dual-wavelength sequential 595- and 1064-nm lasers.5 Botulinum toxin has also been used in cases of symptomatic hyperhidrosis.
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She has no conflicts. Email her at [email protected].

References

1. Smith SD et al. Pediatr Dermatol. 2019 Nov;36(6):909-12.

2. Patterson AT et al. Am J Dermatopathol. 2016;38:413-7.

3. Garcıa-Garcıa SC et al. JAAD Case Rep. 2018;4(2):165-7.

4. Awatef Kelati et al. JAAD Case Rep. 2018;4(8)835-6.

5. Felgueiras J et al. Dermatol Surg. 2015 Mar;41(3):428-30.

A biopsy of the lesion was performed which showed an increased number of eccrine glands and blood vessels within the dermis. Some areas showed an increase in adipocytes and smooth muscle bundles. The changes were consistent with eccrine angiomatous hamartoma (EAH).

On dermatoscopy the lesion showed multiple dilated red and violaceous lacunae and whitish-blue hue.

The boy was referred to vascular laser therapy for treatment of the lesion.

EAH is a rare benign vascular growth characterized by an increased number of mature eccrine glands and blood vessels in the dermis and subcutis. The lesions are mostly present on the extremities, but cases of diffuse congenital lesions and lesions on the face and trunk have also been described. The lesions can be seen at birth or during the first years of life in about half of the cases, and the others tend to occur later in puberty and rarely in adulthood.1

Clinically, EAH lesions present as red, yellow to brown papules and plaques. Different dermoscopic patterns have been described which include the popcorn pattern that presents as yellow, confluent nodules with popcornlike shapes over a background of erythema, and linear arborizing vessels. The spitzoid pattern are brown globules on a background of erythema and pseudoreticular pigmentation around the globules. The verrucous hemangiomalike pattern has a bluish-white hue, reddish-blue or bluish lacunae, as seen in our patient.2-4

Most of the lesions are asymptomatic, but in some patients, they can be associated with pain, hyperhidrosis, and sometimes bleeding. Hyperhidrosis has been reported early in the presentation or during puberty or pregnancy. Our patient had started on amphetamines when hyperhidrosis occurred. Hyperhidrosis is a knowns side effect of this type of medication and may have had a role in the increased sweating noted on the hamartoma.

EAH can clinically look like verrucous hemangiomas, angiokeratomas, and vascular malformations, and histopathology may be needed to differentiate between them. Eccrine nevi and EAH can be similar. Hyperhidrosis is an early and predominant component of eccrine nevi, compared with one-third of EAH.

The exact etiology of this lesion is not known. It is thought to be caused by an abnormal differentiation of the epithelium, adnexal structure, and the mesenchyme during organogenesis.3 No other associated conditions have been described with EAH.

EAH are benign lesions that rarely require treatment. If the lesions are symptomatic or because of cosmetic reasons, they can be removed surgically. There are some reports of successful treatment with pulse dual-wavelength sequential 595- and 1064-nm lasers.5 Botulinum toxin has also been used in cases of symptomatic hyperhidrosis.
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She has no conflicts. Email her at [email protected].

References

1. Smith SD et al. Pediatr Dermatol. 2019 Nov;36(6):909-12.

2. Patterson AT et al. Am J Dermatopathol. 2016;38:413-7.

3. Garcıa-Garcıa SC et al. JAAD Case Rep. 2018;4(2):165-7.

4. Awatef Kelati et al. JAAD Case Rep. 2018;4(8)835-6.

5. Felgueiras J et al. Dermatol Surg. 2015 Mar;41(3):428-30.

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A 14-year-old male was referred to our pediatric dermatology clinic for evaluation of a lesion on the left knee that appeared at 1 year of age. The lesion has been growing with him and was not symptomatic until 6 months prior to the consultation, when it started bleeding and feeling wet.  


He has a history of attention-deficit/hyperactivity disorder managed with dextroamphetamine-amphetamine. The changes noted on the knee lesion seem to occur at the same time that his ADHD medication was started.  
On physical exam he had a violaceous circular plaque on the left knee. 
On dermoscopy the lesion showed multiple dilated red and violaceous lacunae and whitish blue hue.

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Study finds plume generated during laser tattoo removal generally viewed as safe

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Results of a new analysis based on benchmarks from the National Institute for Occupational Safety and Health (NIOSH) suggest that the levels of metals and volatile organic compounds generated during laser tattoo removal procedures are generally safe.

Dr. Mathew M. Avram

While tattoo removal plume has not been previously studied, an analysis from 2016 found that laser hair removal plume contains toxic compounds, including carcinogens and environmental toxins, underscoring the importance of using smoke evacuators, good ventilation, and respiratory protection. “Ultrafine particles can become lodged in human alveoli in the lungs,” the study’s senior author, Mathew M. Avram, MD, JD, said during a virtual course on laser and aesthetic skin therapy. “This travels over distances, so it is potentially affecting people in your waiting room and others in areas within the clinic.”

For the study of laser tattoo removal plume, Yakir S. Levin, MD, PhD, a dermatologist at the Wellman Center for Photomedicine at Massachusetts General Hospital, Boston; Dr. Avram, director of laser, cosmetics, and dermatologic surgery at MGH; and coinvestigators from NIOSH, conducted air sampling to determine the gaseous, particulate, and microbiological content of laser tattoo removal plume. They performed the study in ex vivo pig skin and in humans undergoing routine laser tattoo removal, and measured ultrafine particulate concentrations, metals, volatile organic compounds, and airborne bacteria.

For the swine portion of the study, they found that levels of metals including aluminum, copper, manganese, phosphorus, potassium, titanium, and zirconium were all below occupational exposure limits. All organic compounds including acetone and benzene were also below occupational exposure limits. “This is different than what we found in the study of laser plume generated during hair removal,” Dr. Avram said. “In laser hair removal, these were all elevated to a concerning extent.”

For the human part of the study, particle concentrations for ultrafine particulates were higher in the dermatologist’s breathing zone and near the tattoo removal site than in the rest of the treatment room or outside of the room. Concentrations were 30 times lower for human skin than for pig skin. “We’re not sure why, but there were higher levels of ultrafine particulates right around the area we treated,” Dr. Avram said. “Still, they were all below exposure limits that would be concerning in terms of NIOSH. So, although they were elevated, they were still considered safe. That was the case for organic compounds as well.”

He pointed out that the study, which was supported by a grant from the American Society for Dermatologic Surgery (ASDS), did not include an analysis of viral particles generated during later tattoo removal “so there is a question about that,” and it is something worth studying, he said.

Dr. Avram, the current president of ASDS, noted that 17% of the estimated 40 million-plus Americans with tattoos have “tattoo regret,” and many turn to dermatologic surgeons for removal, which requires multiple treatments, and is painful and expensive.
 

Picosecond lasers

“One thing that’s changed in the past several years is the development of picosecond lasers, which produce extraordinarily high energy for an extraordinarily short period of time,” he said at the meeting, named “Laser & Aesthetic Skin Therapy: What’s the Truth?” and sponsored by Harvard Medical School, Massachusetts General Hospital, and the Wellman Center for Photomedicine. The desired endpoint is dermal whitening with cavitation and rupture. “You don’t want to see splatter with the epidermis flying off,” he said.

Several devices are commercially available with wavelengths of 532, 680, 755, 785, and 1064 nm, and pulse durations ranging from 300 to 750 picoseconds. Nd:Yag lasers target red and black ink, while alexandrite and ruby wavelengths target green and blue ink.

“After the treatment, we use simple Vaseline on top of the tattoo and a nonadherent Telfa dressing with paper tape over it,” Dr. Avram said. For patients with skin of color, he said, “occasionally I will add a steroid. Inflammation and redness can lead to hyperpigmentation. The steroid decreases some of that inflammation and therefore decreases the risk of hyperpigmentation.”

In his clinical experience, picosecond lasers are more effective at tattoo removal than Q-switched nanosecond lasers overall. With a picosecond laser, “you get some nonselective targeting of other pigments such as yellow to improve, even though you really don’t have the correct wavelength. I also think they are more effective for faded tattoos than the Q-switched nanosecond lasers, but they are significantly more expensive, so you need to think about that, and to what extent you are doing tattoo removal. In any event, it’s a multi-treatment process. You do it for multiple weeks between treatments and it takes time and patience. During the consultation, it is crucial to let patients know that.”

In 2012, R. Rox Anderson, MD, director of the Wellman Center for Photomedicine, and colleagues first described the R20 method for tattoo removal, which consists of four consecutive treatment passes with a Q-switched alexandrite laser separated by 20 minutes. “On the first treatment pass, there was an immediate whitening reaction “with little or no whitening on subsequent passes,” said Dr. Avram, who was not involved with the study. “Three months later, treatment with the R20 method was much more effective than conventional single-pass laser treatment. Light microscopy showed greater dispersion of the ink with the R20 method.” A follow-up study conducted at the Wellman Center did not completely support these findings, but a subsequent study led by Suzanne L. Kilmer, MD, was more supportive.



This concept has led to new treatment paradigms for tattoo removal, including the Food and Drug Administration–cleared perfluorodecalin patch, a transparent PFD-infused silicone patch that helps reduce scatter and improves efficacy. “It also allows for performing of repeat laser treatments at the same visit without waiting 20 minutes as you would with the R20 method,” Dr. Avram said. In a pilot study, 11 of the 17 patients showed more rapid clearance with the PFD patch than the control side versus one pass without the PFD patch. “It’s important to note that they used only one wavelength, and some of the tattoos weren’t appropriate for that wavelength, so 11 out of 17 is actually better than it might seem,” he said.

Ablative fractional resurfacing can play a role with tattoo removal, but Dr. Avram typically limits this option to recalcitrant tattoos. “Remember: You’re creating a zone of ablation with a cuff of coagulation, so you’re going to remove some of the tattoo just by creating those areas of clearance and vaporization,” he said. “You can do that in combination with the Q-switched or picosecond laser, which has better efficacy. The best way to do this is to start with the pigment laser – the picosecond or nanosecond laser – and then do the ablative fractional resurfacing afterward. You should never use IPL or laser hair removal lasers to remove tattoos, though. I see that occasionally. You’re going to burn your patients.”

Another approach is to use an Nd:Yag picosecond laser followed by microneedling. “What we’re trying to do here is get an egress of the tattoo pigments,” he explained. “We’re trying to mobilize the ink, get it out of the skin, and get it out of the macrophages to get improvement.”

In 2019, Soliton’s Rapid Acoustic Pulse (RAP) device was cleared by the FDA for tattoo removal. The device is indicated as an accessory to the 1064-nm Q-switched laser for black ink tattoo removal on the arms, legs, and torso in Fitzpatrick skin type I-III individuals. “It’s an application for 1 minute and that allows for additional laser passes,” Dr. Avram said. “You do the laser treatment, you do the acoustic shock wave device, and you do this as multiple passes. This is getting back to the R20 method, the idea that you are going to treat repeatedly. The rapid acoustic pulses result in dispersion and destruction of dermal vacuoles, which enables multiple laser passes in a single treatment session. If you can see the ink, you can ablate the ink.”

Dr. Avram disclosed that he has received consulting fees from Allergan, Merz, and Galderma. He is a member of the scientific advisory board for Allergan and Soliton, is an investigator for Endo, and holds stock options in La Jolla NanoMedical Inc.

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Results of a new analysis based on benchmarks from the National Institute for Occupational Safety and Health (NIOSH) suggest that the levels of metals and volatile organic compounds generated during laser tattoo removal procedures are generally safe.

Dr. Mathew M. Avram

While tattoo removal plume has not been previously studied, an analysis from 2016 found that laser hair removal plume contains toxic compounds, including carcinogens and environmental toxins, underscoring the importance of using smoke evacuators, good ventilation, and respiratory protection. “Ultrafine particles can become lodged in human alveoli in the lungs,” the study’s senior author, Mathew M. Avram, MD, JD, said during a virtual course on laser and aesthetic skin therapy. “This travels over distances, so it is potentially affecting people in your waiting room and others in areas within the clinic.”

For the study of laser tattoo removal plume, Yakir S. Levin, MD, PhD, a dermatologist at the Wellman Center for Photomedicine at Massachusetts General Hospital, Boston; Dr. Avram, director of laser, cosmetics, and dermatologic surgery at MGH; and coinvestigators from NIOSH, conducted air sampling to determine the gaseous, particulate, and microbiological content of laser tattoo removal plume. They performed the study in ex vivo pig skin and in humans undergoing routine laser tattoo removal, and measured ultrafine particulate concentrations, metals, volatile organic compounds, and airborne bacteria.

For the swine portion of the study, they found that levels of metals including aluminum, copper, manganese, phosphorus, potassium, titanium, and zirconium were all below occupational exposure limits. All organic compounds including acetone and benzene were also below occupational exposure limits. “This is different than what we found in the study of laser plume generated during hair removal,” Dr. Avram said. “In laser hair removal, these were all elevated to a concerning extent.”

For the human part of the study, particle concentrations for ultrafine particulates were higher in the dermatologist’s breathing zone and near the tattoo removal site than in the rest of the treatment room or outside of the room. Concentrations were 30 times lower for human skin than for pig skin. “We’re not sure why, but there were higher levels of ultrafine particulates right around the area we treated,” Dr. Avram said. “Still, they were all below exposure limits that would be concerning in terms of NIOSH. So, although they were elevated, they were still considered safe. That was the case for organic compounds as well.”

He pointed out that the study, which was supported by a grant from the American Society for Dermatologic Surgery (ASDS), did not include an analysis of viral particles generated during later tattoo removal “so there is a question about that,” and it is something worth studying, he said.

Dr. Avram, the current president of ASDS, noted that 17% of the estimated 40 million-plus Americans with tattoos have “tattoo regret,” and many turn to dermatologic surgeons for removal, which requires multiple treatments, and is painful and expensive.
 

Picosecond lasers

“One thing that’s changed in the past several years is the development of picosecond lasers, which produce extraordinarily high energy for an extraordinarily short period of time,” he said at the meeting, named “Laser & Aesthetic Skin Therapy: What’s the Truth?” and sponsored by Harvard Medical School, Massachusetts General Hospital, and the Wellman Center for Photomedicine. The desired endpoint is dermal whitening with cavitation and rupture. “You don’t want to see splatter with the epidermis flying off,” he said.

Several devices are commercially available with wavelengths of 532, 680, 755, 785, and 1064 nm, and pulse durations ranging from 300 to 750 picoseconds. Nd:Yag lasers target red and black ink, while alexandrite and ruby wavelengths target green and blue ink.

“After the treatment, we use simple Vaseline on top of the tattoo and a nonadherent Telfa dressing with paper tape over it,” Dr. Avram said. For patients with skin of color, he said, “occasionally I will add a steroid. Inflammation and redness can lead to hyperpigmentation. The steroid decreases some of that inflammation and therefore decreases the risk of hyperpigmentation.”

In his clinical experience, picosecond lasers are more effective at tattoo removal than Q-switched nanosecond lasers overall. With a picosecond laser, “you get some nonselective targeting of other pigments such as yellow to improve, even though you really don’t have the correct wavelength. I also think they are more effective for faded tattoos than the Q-switched nanosecond lasers, but they are significantly more expensive, so you need to think about that, and to what extent you are doing tattoo removal. In any event, it’s a multi-treatment process. You do it for multiple weeks between treatments and it takes time and patience. During the consultation, it is crucial to let patients know that.”

In 2012, R. Rox Anderson, MD, director of the Wellman Center for Photomedicine, and colleagues first described the R20 method for tattoo removal, which consists of four consecutive treatment passes with a Q-switched alexandrite laser separated by 20 minutes. “On the first treatment pass, there was an immediate whitening reaction “with little or no whitening on subsequent passes,” said Dr. Avram, who was not involved with the study. “Three months later, treatment with the R20 method was much more effective than conventional single-pass laser treatment. Light microscopy showed greater dispersion of the ink with the R20 method.” A follow-up study conducted at the Wellman Center did not completely support these findings, but a subsequent study led by Suzanne L. Kilmer, MD, was more supportive.



This concept has led to new treatment paradigms for tattoo removal, including the Food and Drug Administration–cleared perfluorodecalin patch, a transparent PFD-infused silicone patch that helps reduce scatter and improves efficacy. “It also allows for performing of repeat laser treatments at the same visit without waiting 20 minutes as you would with the R20 method,” Dr. Avram said. In a pilot study, 11 of the 17 patients showed more rapid clearance with the PFD patch than the control side versus one pass without the PFD patch. “It’s important to note that they used only one wavelength, and some of the tattoos weren’t appropriate for that wavelength, so 11 out of 17 is actually better than it might seem,” he said.

Ablative fractional resurfacing can play a role with tattoo removal, but Dr. Avram typically limits this option to recalcitrant tattoos. “Remember: You’re creating a zone of ablation with a cuff of coagulation, so you’re going to remove some of the tattoo just by creating those areas of clearance and vaporization,” he said. “You can do that in combination with the Q-switched or picosecond laser, which has better efficacy. The best way to do this is to start with the pigment laser – the picosecond or nanosecond laser – and then do the ablative fractional resurfacing afterward. You should never use IPL or laser hair removal lasers to remove tattoos, though. I see that occasionally. You’re going to burn your patients.”

Another approach is to use an Nd:Yag picosecond laser followed by microneedling. “What we’re trying to do here is get an egress of the tattoo pigments,” he explained. “We’re trying to mobilize the ink, get it out of the skin, and get it out of the macrophages to get improvement.”

In 2019, Soliton’s Rapid Acoustic Pulse (RAP) device was cleared by the FDA for tattoo removal. The device is indicated as an accessory to the 1064-nm Q-switched laser for black ink tattoo removal on the arms, legs, and torso in Fitzpatrick skin type I-III individuals. “It’s an application for 1 minute and that allows for additional laser passes,” Dr. Avram said. “You do the laser treatment, you do the acoustic shock wave device, and you do this as multiple passes. This is getting back to the R20 method, the idea that you are going to treat repeatedly. The rapid acoustic pulses result in dispersion and destruction of dermal vacuoles, which enables multiple laser passes in a single treatment session. If you can see the ink, you can ablate the ink.”

Dr. Avram disclosed that he has received consulting fees from Allergan, Merz, and Galderma. He is a member of the scientific advisory board for Allergan and Soliton, is an investigator for Endo, and holds stock options in La Jolla NanoMedical Inc.

Results of a new analysis based on benchmarks from the National Institute for Occupational Safety and Health (NIOSH) suggest that the levels of metals and volatile organic compounds generated during laser tattoo removal procedures are generally safe.

Dr. Mathew M. Avram

While tattoo removal plume has not been previously studied, an analysis from 2016 found that laser hair removal plume contains toxic compounds, including carcinogens and environmental toxins, underscoring the importance of using smoke evacuators, good ventilation, and respiratory protection. “Ultrafine particles can become lodged in human alveoli in the lungs,” the study’s senior author, Mathew M. Avram, MD, JD, said during a virtual course on laser and aesthetic skin therapy. “This travels over distances, so it is potentially affecting people in your waiting room and others in areas within the clinic.”

For the study of laser tattoo removal plume, Yakir S. Levin, MD, PhD, a dermatologist at the Wellman Center for Photomedicine at Massachusetts General Hospital, Boston; Dr. Avram, director of laser, cosmetics, and dermatologic surgery at MGH; and coinvestigators from NIOSH, conducted air sampling to determine the gaseous, particulate, and microbiological content of laser tattoo removal plume. They performed the study in ex vivo pig skin and in humans undergoing routine laser tattoo removal, and measured ultrafine particulate concentrations, metals, volatile organic compounds, and airborne bacteria.

For the swine portion of the study, they found that levels of metals including aluminum, copper, manganese, phosphorus, potassium, titanium, and zirconium were all below occupational exposure limits. All organic compounds including acetone and benzene were also below occupational exposure limits. “This is different than what we found in the study of laser plume generated during hair removal,” Dr. Avram said. “In laser hair removal, these were all elevated to a concerning extent.”

For the human part of the study, particle concentrations for ultrafine particulates were higher in the dermatologist’s breathing zone and near the tattoo removal site than in the rest of the treatment room or outside of the room. Concentrations were 30 times lower for human skin than for pig skin. “We’re not sure why, but there were higher levels of ultrafine particulates right around the area we treated,” Dr. Avram said. “Still, they were all below exposure limits that would be concerning in terms of NIOSH. So, although they were elevated, they were still considered safe. That was the case for organic compounds as well.”

He pointed out that the study, which was supported by a grant from the American Society for Dermatologic Surgery (ASDS), did not include an analysis of viral particles generated during later tattoo removal “so there is a question about that,” and it is something worth studying, he said.

Dr. Avram, the current president of ASDS, noted that 17% of the estimated 40 million-plus Americans with tattoos have “tattoo regret,” and many turn to dermatologic surgeons for removal, which requires multiple treatments, and is painful and expensive.
 

Picosecond lasers

“One thing that’s changed in the past several years is the development of picosecond lasers, which produce extraordinarily high energy for an extraordinarily short period of time,” he said at the meeting, named “Laser & Aesthetic Skin Therapy: What’s the Truth?” and sponsored by Harvard Medical School, Massachusetts General Hospital, and the Wellman Center for Photomedicine. The desired endpoint is dermal whitening with cavitation and rupture. “You don’t want to see splatter with the epidermis flying off,” he said.

Several devices are commercially available with wavelengths of 532, 680, 755, 785, and 1064 nm, and pulse durations ranging from 300 to 750 picoseconds. Nd:Yag lasers target red and black ink, while alexandrite and ruby wavelengths target green and blue ink.

“After the treatment, we use simple Vaseline on top of the tattoo and a nonadherent Telfa dressing with paper tape over it,” Dr. Avram said. For patients with skin of color, he said, “occasionally I will add a steroid. Inflammation and redness can lead to hyperpigmentation. The steroid decreases some of that inflammation and therefore decreases the risk of hyperpigmentation.”

In his clinical experience, picosecond lasers are more effective at tattoo removal than Q-switched nanosecond lasers overall. With a picosecond laser, “you get some nonselective targeting of other pigments such as yellow to improve, even though you really don’t have the correct wavelength. I also think they are more effective for faded tattoos than the Q-switched nanosecond lasers, but they are significantly more expensive, so you need to think about that, and to what extent you are doing tattoo removal. In any event, it’s a multi-treatment process. You do it for multiple weeks between treatments and it takes time and patience. During the consultation, it is crucial to let patients know that.”

In 2012, R. Rox Anderson, MD, director of the Wellman Center for Photomedicine, and colleagues first described the R20 method for tattoo removal, which consists of four consecutive treatment passes with a Q-switched alexandrite laser separated by 20 minutes. “On the first treatment pass, there was an immediate whitening reaction “with little or no whitening on subsequent passes,” said Dr. Avram, who was not involved with the study. “Three months later, treatment with the R20 method was much more effective than conventional single-pass laser treatment. Light microscopy showed greater dispersion of the ink with the R20 method.” A follow-up study conducted at the Wellman Center did not completely support these findings, but a subsequent study led by Suzanne L. Kilmer, MD, was more supportive.



This concept has led to new treatment paradigms for tattoo removal, including the Food and Drug Administration–cleared perfluorodecalin patch, a transparent PFD-infused silicone patch that helps reduce scatter and improves efficacy. “It also allows for performing of repeat laser treatments at the same visit without waiting 20 minutes as you would with the R20 method,” Dr. Avram said. In a pilot study, 11 of the 17 patients showed more rapid clearance with the PFD patch than the control side versus one pass without the PFD patch. “It’s important to note that they used only one wavelength, and some of the tattoos weren’t appropriate for that wavelength, so 11 out of 17 is actually better than it might seem,” he said.

Ablative fractional resurfacing can play a role with tattoo removal, but Dr. Avram typically limits this option to recalcitrant tattoos. “Remember: You’re creating a zone of ablation with a cuff of coagulation, so you’re going to remove some of the tattoo just by creating those areas of clearance and vaporization,” he said. “You can do that in combination with the Q-switched or picosecond laser, which has better efficacy. The best way to do this is to start with the pigment laser – the picosecond or nanosecond laser – and then do the ablative fractional resurfacing afterward. You should never use IPL or laser hair removal lasers to remove tattoos, though. I see that occasionally. You’re going to burn your patients.”

Another approach is to use an Nd:Yag picosecond laser followed by microneedling. “What we’re trying to do here is get an egress of the tattoo pigments,” he explained. “We’re trying to mobilize the ink, get it out of the skin, and get it out of the macrophages to get improvement.”

In 2019, Soliton’s Rapid Acoustic Pulse (RAP) device was cleared by the FDA for tattoo removal. The device is indicated as an accessory to the 1064-nm Q-switched laser for black ink tattoo removal on the arms, legs, and torso in Fitzpatrick skin type I-III individuals. “It’s an application for 1 minute and that allows for additional laser passes,” Dr. Avram said. “You do the laser treatment, you do the acoustic shock wave device, and you do this as multiple passes. This is getting back to the R20 method, the idea that you are going to treat repeatedly. The rapid acoustic pulses result in dispersion and destruction of dermal vacuoles, which enables multiple laser passes in a single treatment session. If you can see the ink, you can ablate the ink.”

Dr. Avram disclosed that he has received consulting fees from Allergan, Merz, and Galderma. He is a member of the scientific advisory board for Allergan and Soliton, is an investigator for Endo, and holds stock options in La Jolla NanoMedical Inc.

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FROM A LASER & AESTHETIC SKIN THERAPY COURSE

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Tender Annular Plaque on the Thigh

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The Diagnosis: Ecthyma Gangrenosum

Histopathology revealed basophilic bacterial rods around necrotic vessels with thrombosis and edema (Figure). Blood and tissue cultures grew Pseudomonas aeruginosa. Based on the histopathology and clinical presentation, a diagnosis of P aeruginosa–associated ecthyma gangrenosum (EG) was made. The patient’s symptoms resolved with intravenous cefepime, and he later was transitioned to oral levofloxacin for outpatient treatment.

Histopathology showed basophilic bacterial rods around necrotic vessels (arrows) with thrombosis and edema (H&E, original magnification ×200).

Ecthyma gangrenosum is an uncommon cutaneous manifestation of bacteremia that most commonly occurs secondary to P aeruginosa in immunocompromised patients, particularly patients with severe neutropenia in the setting of recent chemotherapy.1,2 Ecthyma gangrenosum can occur anywhere on the body, predominantly in moist areas such as the axillae and groin; the arms and legs, such as in our patient, as well as the trunk and face also may be involved.3 Other causes of EG skin lesions include methicillin-resistant Staphylococcus aureus, Citrobacter freundii, Escherichia coli, fungi such as Candida, and viruses such as herpes simplex virus.2,4-6 Common predisposing conditions associated with EG include neutropenia, leukemia, HIV, diabetes mellitus, extensive burn wounds, and a history of immunosuppressive medications. It also has been known to occur in otherwise healthy, immunocompetent individuals with no difference in clinical manifestation.2

The diagnosis is clinicopathologic, with initial evaluation including blood and wound cultures as well as a complete blood cell count once EG is suspected. An excisional or punch biopsy is performed for confirmation, showing many gram-negative, rod-shaped bacteria in cases of pseudomonal EG.7 Histopathology is characterized by bacterial perivascular invasion that then leads to secondary arteriole thrombosis, tissue edema, and separation of the epidermis.7,8 Resultant ischemic necrosis results in the classic macroscopic appearance of an erythematous macule that rapidly progresses into a central necrotic lesion surrounded by an erythematous or violaceous halo after undergoing a hemorrhagic bullous stage.1,9 A Wood lamp can be used to expedite the diagnosis, as Pseudomonas bacteria excretes a pigment (pyoverdine) that fluoresces yellowish green.10

Ecthyma gangrenosum can be classified as a primary skin lesion that may or may not be followed by bacteremia or as a lesion secondary to pseudomonal bacteremia.11 Bacteremia has been reported in half of cases, with hematogenous metastasis of the infection, likely in manifestations with multiple bilateral lesions.2 Our patient’s presentation of a single lesion revealed a positive blood culture result. Lesions also can develop by direct inoculation of the epidermis causing local destruction of the surrounding tissue. The nonbacteremic form of EG has been associated with a lower mortality rate of around 15% compared to patients with bacteremia ranging from 38% to 96%.12 The presence of neutropenia is the most important prognostic factor for mortality at the time of diagnosis.13

Prompt empiric therapy should be initiated after obtaining wound and blood cultures in those with infection until the causative organism and its susceptibility are identified. Pseudomonal infections account for 4% of all cases of hospital-acquired bacteremia and are the third leading cause of gram-negative bloodstream infection.7 Initial broad-spectrum antibiotics include antipseudomonal β-lactams (piperacillin-tazobactam), cephalosporins (cefepime), fluoroquinolones (levofloxacin), and carbapenems (imipenem).1,7 Medical therapy alone may be sufficient without requiring extensive surgical debridement to remove necrotic tissue in some patients. Surgical debridement usually is warranted for lesions larger than 10 cm in diameter.3 Our patient was treated with intravenous cefepime with resolution and was followed with outpatient oral levofloxacin as appropriate. A high index of suspicion should be maintained for relapsing pseudomonal EG infection among patients with AIDS, as the reported recurrence rate is 57%.14

Clinically, the differential diagnosis of EG presenting in immunocompromised patients or individuals with underlying malignancy includes pyoderma gangrenosum, papulonecrotic tuberculid, and leukemia cutis. An erythematous rash with central necrosis presenting in a patient with systemic symptoms is pathognomonic for erythema migrans and should be considered as a diagnostic possibility in areas endemic for Lyme disease in the United States, including the northeastern, mid-Atlantic, and north-central regions.15 A thorough history, physical examination, basic laboratory studies, and histopathology are critical to differentiate between these entities with similar macroscopic features. Pyoderma gangrenosum histologically manifests as a noninfectious, deep, suppurative folliculitis with leukocytoclastic vasculitis in 40% of cases.16 Although papulonecrotic tuberculid can present with dermal necrosis resulting from a hypersensitivity reaction to antigenic components of mycobacteria, there typically are granulomatous infiltrates present and a lack of observed organisms on histopathology.17 Although leukemia cutis infrequently occurs in patients diagnosed with leukemia, its salient features on pathology are nodular or diffuse infiltrates of leukemic cells in the dermis and subcutis with a high nuclear-to-cytoplasmic ratio, often with prominent nucleoli.18 Lyme disease can present in various ways; however, cutaneous involvement in the primary lesion is histologically characterized by a perivascular lymphohistiocytic infiltrate containing plasma cells at the periphery of the expanding annular lesion and eosinophils present at the center.19

References
  1. Abdou A, Hassam B. Ecthyma gangrenosum [in French]. Pan Afr Med J. 2018;30:95. doi:10.11604/pamj.2018.30.95.6244
  2. Vaiman M, Lazarovitch T, Heller L, et al. Ecthyma gangrenosum and ecthyma-like lesions: review article. Eur J Clin Microbiol Infect Dis. 2015;34:633-639. doi:10.1007/s10096-014-2277-6
  3. Vaiman M, Lasarovitch T, Heller L, et al. Ecthyma gangrenosum versus ecthyma-like lesions: should we separate these conditions? Acta Dermatovenerol Alp Pannonica Adriat. 2015;24:69-72. doi:10.15570 /actaapa.2015.18
  4. Reich HL, Williams Fadeyi D, Naik NS, et al. Nonpseudomonal ecthyma gangrenosum. J Am Acad Dermatol. 2004;50(5 suppl): S114-S117. doi:10.1016/j.jaad.2003.09.019
  5. Hawkley T, Chang D, Pollard W, et al. Ecthyma gangrenosum caused by Citrobacter freundii [published online July 27, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220996
  6. Santhaseelan RG, Muralidhar V. Non-pseudomonal ecthyma gangrenosum caused by methicillin-resistant Staphylococcus aureus (MRSA) in a chronic alcoholic patient [published online August 3, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220983m
  7. Bassetti M, Vena A, Croxatto A, et al. How to manage Pseudomonas aeruginosa infections [published online May 29, 2018]. Drugs Context. 2018;7:212527. doi:10.7573/dic.212527
  8. Llamas-Velasco M, Alegría V, Santos-Briz Á, et al. Occlusive nonvasculitic vasculopathy. Am J Dermatopathol. 2017;39:637-662. doi:10.1097/DAD.0000000000000766
  9. Sarkar S, Patra AK, Mondal M. Ecthyma gangrenosum in the periorbital region in a previously healthy immunocompetent woman without bacteremia. Indian Dermatol Online J. 2016;7:36-39. doi:10.4103/2229-5178.174326
  10. Ponka D, Baddar F. Wood lamp examination. Can Fam Physician. 2012;58:976.
  11. Van den Broek PJ, Van der Meer JWM, Kunst MW. The pathogenesis of ecthyma gangrenosum. J Infect. 1979;1:263-267. doi:10.1016 /S0163-4453(79)91329-X
  12. Downey DM, O’Bryan MC, Burdette SD, et al. Ecthyma gangrenosum in a patient with toxic epidermal necrolysis. J Burn Care Res. 2007;28:198-202. doi:10.1097/BCR.0B013E31802CA481
  13. Martínez-Longoria CA, Rosales-Solis GM, Ocampo-Garza J, et al. Ecthyma gangrenosum: a report of eight cases. An Bras Dermatol. 2017;92:698-700. doi:10.1590/abd1806-4841.20175580
  14. Khan MO, Montecalvo MA, Davis I, et al. Ecthyma gangrenosum in patients with acquired immunodeficiency syndrome. Cutis. 2000;66:121-123.
  15. Nadelman RB, Wormser GP. Lyme borreliosis. Lancet. 1998; 352:557-565.
  16. Su WP, Schroeter AL, Perry HO, et al. Histopathologic and immunopathologic study of pyoderma gangrenosum. J Cutan Pathol. 1986;13:323-330. doi:10.1111/j.1600-0560.1986.tb00466.x
  17. Tirumalae R, Yeliur IK, Antony M, et al. Papulonecrotic tuberculidclinicopathologic and molecular features of 12 Indian patients. Dermatol Pract Concept. 2014;4:17-22. doi:10.5826/dpc.0402a03
  18. Obiozor C, Ganguly S, Fraga GR. Leukemia cutis with lymphoglandular bodies: a clue to acute lymphoblastic leukemia cutis [published online August 15, 2015]. Dermatol Online J. 2015;21:13030/qt6m18g35f
  19. Vasudevan B, Chatterjee M. Lyme borreliosis and skin. Indian J Dermatol. 2013;58:167-174. doi:10.4103/0019-5154.110822
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From the Division of Dermatology, University of Kansas Medical Center, Kansas City.

The authors report no conflict of interest.

Correspondence: Spyros M. Siscos, MD, Division of Dermatology, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160 ([email protected]).

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From the Division of Dermatology, University of Kansas Medical Center, Kansas City.

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The Diagnosis: Ecthyma Gangrenosum

Histopathology revealed basophilic bacterial rods around necrotic vessels with thrombosis and edema (Figure). Blood and tissue cultures grew Pseudomonas aeruginosa. Based on the histopathology and clinical presentation, a diagnosis of P aeruginosa–associated ecthyma gangrenosum (EG) was made. The patient’s symptoms resolved with intravenous cefepime, and he later was transitioned to oral levofloxacin for outpatient treatment.

Histopathology showed basophilic bacterial rods around necrotic vessels (arrows) with thrombosis and edema (H&E, original magnification ×200).

Ecthyma gangrenosum is an uncommon cutaneous manifestation of bacteremia that most commonly occurs secondary to P aeruginosa in immunocompromised patients, particularly patients with severe neutropenia in the setting of recent chemotherapy.1,2 Ecthyma gangrenosum can occur anywhere on the body, predominantly in moist areas such as the axillae and groin; the arms and legs, such as in our patient, as well as the trunk and face also may be involved.3 Other causes of EG skin lesions include methicillin-resistant Staphylococcus aureus, Citrobacter freundii, Escherichia coli, fungi such as Candida, and viruses such as herpes simplex virus.2,4-6 Common predisposing conditions associated with EG include neutropenia, leukemia, HIV, diabetes mellitus, extensive burn wounds, and a history of immunosuppressive medications. It also has been known to occur in otherwise healthy, immunocompetent individuals with no difference in clinical manifestation.2

The diagnosis is clinicopathologic, with initial evaluation including blood and wound cultures as well as a complete blood cell count once EG is suspected. An excisional or punch biopsy is performed for confirmation, showing many gram-negative, rod-shaped bacteria in cases of pseudomonal EG.7 Histopathology is characterized by bacterial perivascular invasion that then leads to secondary arteriole thrombosis, tissue edema, and separation of the epidermis.7,8 Resultant ischemic necrosis results in the classic macroscopic appearance of an erythematous macule that rapidly progresses into a central necrotic lesion surrounded by an erythematous or violaceous halo after undergoing a hemorrhagic bullous stage.1,9 A Wood lamp can be used to expedite the diagnosis, as Pseudomonas bacteria excretes a pigment (pyoverdine) that fluoresces yellowish green.10

Ecthyma gangrenosum can be classified as a primary skin lesion that may or may not be followed by bacteremia or as a lesion secondary to pseudomonal bacteremia.11 Bacteremia has been reported in half of cases, with hematogenous metastasis of the infection, likely in manifestations with multiple bilateral lesions.2 Our patient’s presentation of a single lesion revealed a positive blood culture result. Lesions also can develop by direct inoculation of the epidermis causing local destruction of the surrounding tissue. The nonbacteremic form of EG has been associated with a lower mortality rate of around 15% compared to patients with bacteremia ranging from 38% to 96%.12 The presence of neutropenia is the most important prognostic factor for mortality at the time of diagnosis.13

Prompt empiric therapy should be initiated after obtaining wound and blood cultures in those with infection until the causative organism and its susceptibility are identified. Pseudomonal infections account for 4% of all cases of hospital-acquired bacteremia and are the third leading cause of gram-negative bloodstream infection.7 Initial broad-spectrum antibiotics include antipseudomonal β-lactams (piperacillin-tazobactam), cephalosporins (cefepime), fluoroquinolones (levofloxacin), and carbapenems (imipenem).1,7 Medical therapy alone may be sufficient without requiring extensive surgical debridement to remove necrotic tissue in some patients. Surgical debridement usually is warranted for lesions larger than 10 cm in diameter.3 Our patient was treated with intravenous cefepime with resolution and was followed with outpatient oral levofloxacin as appropriate. A high index of suspicion should be maintained for relapsing pseudomonal EG infection among patients with AIDS, as the reported recurrence rate is 57%.14

Clinically, the differential diagnosis of EG presenting in immunocompromised patients or individuals with underlying malignancy includes pyoderma gangrenosum, papulonecrotic tuberculid, and leukemia cutis. An erythematous rash with central necrosis presenting in a patient with systemic symptoms is pathognomonic for erythema migrans and should be considered as a diagnostic possibility in areas endemic for Lyme disease in the United States, including the northeastern, mid-Atlantic, and north-central regions.15 A thorough history, physical examination, basic laboratory studies, and histopathology are critical to differentiate between these entities with similar macroscopic features. Pyoderma gangrenosum histologically manifests as a noninfectious, deep, suppurative folliculitis with leukocytoclastic vasculitis in 40% of cases.16 Although papulonecrotic tuberculid can present with dermal necrosis resulting from a hypersensitivity reaction to antigenic components of mycobacteria, there typically are granulomatous infiltrates present and a lack of observed organisms on histopathology.17 Although leukemia cutis infrequently occurs in patients diagnosed with leukemia, its salient features on pathology are nodular or diffuse infiltrates of leukemic cells in the dermis and subcutis with a high nuclear-to-cytoplasmic ratio, often with prominent nucleoli.18 Lyme disease can present in various ways; however, cutaneous involvement in the primary lesion is histologically characterized by a perivascular lymphohistiocytic infiltrate containing plasma cells at the periphery of the expanding annular lesion and eosinophils present at the center.19

The Diagnosis: Ecthyma Gangrenosum

Histopathology revealed basophilic bacterial rods around necrotic vessels with thrombosis and edema (Figure). Blood and tissue cultures grew Pseudomonas aeruginosa. Based on the histopathology and clinical presentation, a diagnosis of P aeruginosa–associated ecthyma gangrenosum (EG) was made. The patient’s symptoms resolved with intravenous cefepime, and he later was transitioned to oral levofloxacin for outpatient treatment.

Histopathology showed basophilic bacterial rods around necrotic vessels (arrows) with thrombosis and edema (H&E, original magnification ×200).

Ecthyma gangrenosum is an uncommon cutaneous manifestation of bacteremia that most commonly occurs secondary to P aeruginosa in immunocompromised patients, particularly patients with severe neutropenia in the setting of recent chemotherapy.1,2 Ecthyma gangrenosum can occur anywhere on the body, predominantly in moist areas such as the axillae and groin; the arms and legs, such as in our patient, as well as the trunk and face also may be involved.3 Other causes of EG skin lesions include methicillin-resistant Staphylococcus aureus, Citrobacter freundii, Escherichia coli, fungi such as Candida, and viruses such as herpes simplex virus.2,4-6 Common predisposing conditions associated with EG include neutropenia, leukemia, HIV, diabetes mellitus, extensive burn wounds, and a history of immunosuppressive medications. It also has been known to occur in otherwise healthy, immunocompetent individuals with no difference in clinical manifestation.2

The diagnosis is clinicopathologic, with initial evaluation including blood and wound cultures as well as a complete blood cell count once EG is suspected. An excisional or punch biopsy is performed for confirmation, showing many gram-negative, rod-shaped bacteria in cases of pseudomonal EG.7 Histopathology is characterized by bacterial perivascular invasion that then leads to secondary arteriole thrombosis, tissue edema, and separation of the epidermis.7,8 Resultant ischemic necrosis results in the classic macroscopic appearance of an erythematous macule that rapidly progresses into a central necrotic lesion surrounded by an erythematous or violaceous halo after undergoing a hemorrhagic bullous stage.1,9 A Wood lamp can be used to expedite the diagnosis, as Pseudomonas bacteria excretes a pigment (pyoverdine) that fluoresces yellowish green.10

Ecthyma gangrenosum can be classified as a primary skin lesion that may or may not be followed by bacteremia or as a lesion secondary to pseudomonal bacteremia.11 Bacteremia has been reported in half of cases, with hematogenous metastasis of the infection, likely in manifestations with multiple bilateral lesions.2 Our patient’s presentation of a single lesion revealed a positive blood culture result. Lesions also can develop by direct inoculation of the epidermis causing local destruction of the surrounding tissue. The nonbacteremic form of EG has been associated with a lower mortality rate of around 15% compared to patients with bacteremia ranging from 38% to 96%.12 The presence of neutropenia is the most important prognostic factor for mortality at the time of diagnosis.13

Prompt empiric therapy should be initiated after obtaining wound and blood cultures in those with infection until the causative organism and its susceptibility are identified. Pseudomonal infections account for 4% of all cases of hospital-acquired bacteremia and are the third leading cause of gram-negative bloodstream infection.7 Initial broad-spectrum antibiotics include antipseudomonal β-lactams (piperacillin-tazobactam), cephalosporins (cefepime), fluoroquinolones (levofloxacin), and carbapenems (imipenem).1,7 Medical therapy alone may be sufficient without requiring extensive surgical debridement to remove necrotic tissue in some patients. Surgical debridement usually is warranted for lesions larger than 10 cm in diameter.3 Our patient was treated with intravenous cefepime with resolution and was followed with outpatient oral levofloxacin as appropriate. A high index of suspicion should be maintained for relapsing pseudomonal EG infection among patients with AIDS, as the reported recurrence rate is 57%.14

Clinically, the differential diagnosis of EG presenting in immunocompromised patients or individuals with underlying malignancy includes pyoderma gangrenosum, papulonecrotic tuberculid, and leukemia cutis. An erythematous rash with central necrosis presenting in a patient with systemic symptoms is pathognomonic for erythema migrans and should be considered as a diagnostic possibility in areas endemic for Lyme disease in the United States, including the northeastern, mid-Atlantic, and north-central regions.15 A thorough history, physical examination, basic laboratory studies, and histopathology are critical to differentiate between these entities with similar macroscopic features. Pyoderma gangrenosum histologically manifests as a noninfectious, deep, suppurative folliculitis with leukocytoclastic vasculitis in 40% of cases.16 Although papulonecrotic tuberculid can present with dermal necrosis resulting from a hypersensitivity reaction to antigenic components of mycobacteria, there typically are granulomatous infiltrates present and a lack of observed organisms on histopathology.17 Although leukemia cutis infrequently occurs in patients diagnosed with leukemia, its salient features on pathology are nodular or diffuse infiltrates of leukemic cells in the dermis and subcutis with a high nuclear-to-cytoplasmic ratio, often with prominent nucleoli.18 Lyme disease can present in various ways; however, cutaneous involvement in the primary lesion is histologically characterized by a perivascular lymphohistiocytic infiltrate containing plasma cells at the periphery of the expanding annular lesion and eosinophils present at the center.19

References
  1. Abdou A, Hassam B. Ecthyma gangrenosum [in French]. Pan Afr Med J. 2018;30:95. doi:10.11604/pamj.2018.30.95.6244
  2. Vaiman M, Lazarovitch T, Heller L, et al. Ecthyma gangrenosum and ecthyma-like lesions: review article. Eur J Clin Microbiol Infect Dis. 2015;34:633-639. doi:10.1007/s10096-014-2277-6
  3. Vaiman M, Lasarovitch T, Heller L, et al. Ecthyma gangrenosum versus ecthyma-like lesions: should we separate these conditions? Acta Dermatovenerol Alp Pannonica Adriat. 2015;24:69-72. doi:10.15570 /actaapa.2015.18
  4. Reich HL, Williams Fadeyi D, Naik NS, et al. Nonpseudomonal ecthyma gangrenosum. J Am Acad Dermatol. 2004;50(5 suppl): S114-S117. doi:10.1016/j.jaad.2003.09.019
  5. Hawkley T, Chang D, Pollard W, et al. Ecthyma gangrenosum caused by Citrobacter freundii [published online July 27, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220996
  6. Santhaseelan RG, Muralidhar V. Non-pseudomonal ecthyma gangrenosum caused by methicillin-resistant Staphylococcus aureus (MRSA) in a chronic alcoholic patient [published online August 3, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220983m
  7. Bassetti M, Vena A, Croxatto A, et al. How to manage Pseudomonas aeruginosa infections [published online May 29, 2018]. Drugs Context. 2018;7:212527. doi:10.7573/dic.212527
  8. Llamas-Velasco M, Alegría V, Santos-Briz Á, et al. Occlusive nonvasculitic vasculopathy. Am J Dermatopathol. 2017;39:637-662. doi:10.1097/DAD.0000000000000766
  9. Sarkar S, Patra AK, Mondal M. Ecthyma gangrenosum in the periorbital region in a previously healthy immunocompetent woman without bacteremia. Indian Dermatol Online J. 2016;7:36-39. doi:10.4103/2229-5178.174326
  10. Ponka D, Baddar F. Wood lamp examination. Can Fam Physician. 2012;58:976.
  11. Van den Broek PJ, Van der Meer JWM, Kunst MW. The pathogenesis of ecthyma gangrenosum. J Infect. 1979;1:263-267. doi:10.1016 /S0163-4453(79)91329-X
  12. Downey DM, O’Bryan MC, Burdette SD, et al. Ecthyma gangrenosum in a patient with toxic epidermal necrolysis. J Burn Care Res. 2007;28:198-202. doi:10.1097/BCR.0B013E31802CA481
  13. Martínez-Longoria CA, Rosales-Solis GM, Ocampo-Garza J, et al. Ecthyma gangrenosum: a report of eight cases. An Bras Dermatol. 2017;92:698-700. doi:10.1590/abd1806-4841.20175580
  14. Khan MO, Montecalvo MA, Davis I, et al. Ecthyma gangrenosum in patients with acquired immunodeficiency syndrome. Cutis. 2000;66:121-123.
  15. Nadelman RB, Wormser GP. Lyme borreliosis. Lancet. 1998; 352:557-565.
  16. Su WP, Schroeter AL, Perry HO, et al. Histopathologic and immunopathologic study of pyoderma gangrenosum. J Cutan Pathol. 1986;13:323-330. doi:10.1111/j.1600-0560.1986.tb00466.x
  17. Tirumalae R, Yeliur IK, Antony M, et al. Papulonecrotic tuberculidclinicopathologic and molecular features of 12 Indian patients. Dermatol Pract Concept. 2014;4:17-22. doi:10.5826/dpc.0402a03
  18. Obiozor C, Ganguly S, Fraga GR. Leukemia cutis with lymphoglandular bodies: a clue to acute lymphoblastic leukemia cutis [published online August 15, 2015]. Dermatol Online J. 2015;21:13030/qt6m18g35f
  19. Vasudevan B, Chatterjee M. Lyme borreliosis and skin. Indian J Dermatol. 2013;58:167-174. doi:10.4103/0019-5154.110822
References
  1. Abdou A, Hassam B. Ecthyma gangrenosum [in French]. Pan Afr Med J. 2018;30:95. doi:10.11604/pamj.2018.30.95.6244
  2. Vaiman M, Lazarovitch T, Heller L, et al. Ecthyma gangrenosum and ecthyma-like lesions: review article. Eur J Clin Microbiol Infect Dis. 2015;34:633-639. doi:10.1007/s10096-014-2277-6
  3. Vaiman M, Lasarovitch T, Heller L, et al. Ecthyma gangrenosum versus ecthyma-like lesions: should we separate these conditions? Acta Dermatovenerol Alp Pannonica Adriat. 2015;24:69-72. doi:10.15570 /actaapa.2015.18
  4. Reich HL, Williams Fadeyi D, Naik NS, et al. Nonpseudomonal ecthyma gangrenosum. J Am Acad Dermatol. 2004;50(5 suppl): S114-S117. doi:10.1016/j.jaad.2003.09.019
  5. Hawkley T, Chang D, Pollard W, et al. Ecthyma gangrenosum caused by Citrobacter freundii [published online July 27, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220996
  6. Santhaseelan RG, Muralidhar V. Non-pseudomonal ecthyma gangrenosum caused by methicillin-resistant Staphylococcus aureus (MRSA) in a chronic alcoholic patient [published online August 3, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220983m
  7. Bassetti M, Vena A, Croxatto A, et al. How to manage Pseudomonas aeruginosa infections [published online May 29, 2018]. Drugs Context. 2018;7:212527. doi:10.7573/dic.212527
  8. Llamas-Velasco M, Alegría V, Santos-Briz Á, et al. Occlusive nonvasculitic vasculopathy. Am J Dermatopathol. 2017;39:637-662. doi:10.1097/DAD.0000000000000766
  9. Sarkar S, Patra AK, Mondal M. Ecthyma gangrenosum in the periorbital region in a previously healthy immunocompetent woman without bacteremia. Indian Dermatol Online J. 2016;7:36-39. doi:10.4103/2229-5178.174326
  10. Ponka D, Baddar F. Wood lamp examination. Can Fam Physician. 2012;58:976.
  11. Van den Broek PJ, Van der Meer JWM, Kunst MW. The pathogenesis of ecthyma gangrenosum. J Infect. 1979;1:263-267. doi:10.1016 /S0163-4453(79)91329-X
  12. Downey DM, O’Bryan MC, Burdette SD, et al. Ecthyma gangrenosum in a patient with toxic epidermal necrolysis. J Burn Care Res. 2007;28:198-202. doi:10.1097/BCR.0B013E31802CA481
  13. Martínez-Longoria CA, Rosales-Solis GM, Ocampo-Garza J, et al. Ecthyma gangrenosum: a report of eight cases. An Bras Dermatol. 2017;92:698-700. doi:10.1590/abd1806-4841.20175580
  14. Khan MO, Montecalvo MA, Davis I, et al. Ecthyma gangrenosum in patients with acquired immunodeficiency syndrome. Cutis. 2000;66:121-123.
  15. Nadelman RB, Wormser GP. Lyme borreliosis. Lancet. 1998; 352:557-565.
  16. Su WP, Schroeter AL, Perry HO, et al. Histopathologic and immunopathologic study of pyoderma gangrenosum. J Cutan Pathol. 1986;13:323-330. doi:10.1111/j.1600-0560.1986.tb00466.x
  17. Tirumalae R, Yeliur IK, Antony M, et al. Papulonecrotic tuberculidclinicopathologic and molecular features of 12 Indian patients. Dermatol Pract Concept. 2014;4:17-22. doi:10.5826/dpc.0402a03
  18. Obiozor C, Ganguly S, Fraga GR. Leukemia cutis with lymphoglandular bodies: a clue to acute lymphoblastic leukemia cutis [published online August 15, 2015]. Dermatol Online J. 2015;21:13030/qt6m18g35f
  19. Vasudevan B, Chatterjee M. Lyme borreliosis and skin. Indian J Dermatol. 2013;58:167-174. doi:10.4103/0019-5154.110822
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A 58-year-old man who was receiving gilteritinib therapy for relapsed acute myeloid leukemia presented to the emergency department with a painful, rapidly enlarging lesion on the right medial thigh of 2 days’ duration that was accompanied by fever (temperature, 39.2 °C) and body aches. Physical examination revealed a tender annular plaque with a dark violaceous halo overlying a larger area of erythema and induration. Laboratory evaluation revealed a white blood cell count of 600/μL (reference range, 4500–11,000/μL) and an absolute neutrophil count of 200/μL (reference range, 1800–7000/μL). A biopsy was performed.

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Timeless stories

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Let me tell you a story. In 5 billion years the sun will run out of hydrogen, the fuel it is currently burning to power my solar panels amongst other things. At that time, the sun will no longer be able to keep its core contracted and will expand into a fiery, red giant, engulfing earth and obliterating any sign that we ever existed. No buildings. No blog posts. No mausoleums. No stories. Nothing of us will remain.

Dr. Jeffrey Benabio

Well, here for a moment anyway, I’ve gotten you to think about something other than COVID. You’re welcome.

Fascinatingly, the image in your mind’s eye right now of a barren scorched landscape was put there by me. Simply by placing a few words together I have caused new thoughts in your head. You might even share this story with someone else – I would have actually changed your behavior through the power of language. This miraculous phenomenon seems to be unique to us humans; we are the only ones who can create whole worlds in another individual’s head just by making a few sounds. We in medicine have the privilege of experiencing this miracle every day.

Last week, a 97-year-old pale, frail, white man saw me for a basal cell carcinoma on his cheek. While performing a simple electrodesiccation and curettage, I asked if he remembers getting a lot of sunburns when he was young. He certainly remembered one. On a blustery sunny day, he fell asleep for hours on the deck of the USS West Virginia while in the Philippines. As a radio man, he was exhausted from days of conflict and he recalled how warm breezes lulled him asleep. He was so sunburned that for days he forgot how afraid he was of the Japanese.



After listening to his story, I had an image in my mind of palm trees swaying in the tropical winds while hundreds of hulking gray castles sat hidden in the vast surrounding oceans awaiting one of the greatest naval conflicts in history. I got to hear it from surely one of the last remaining people in existence to be able to tell that story. Listening to a patient’s tales is one of the benefits of being a physician. Not only do they help bond us with our patients, but also help lessen our burden of having to make diagnosis after diagnosis and write note after note for hours on end. Somehow performing yet another biopsy that day is made just a bit easier if I’m also learning about what it was like at the Battle of Leyte Gulf.

Encouraging patients to talk more can be risky. No physician, not even allergists, can afford to be waylaid by a retiree with nothing else to do today. But meaningful encounters can not only be a vaccine against burnout, they also lead to better patient adherence and satisfaction. Sometimes, there is simply not time. But often there is a little window during a procedure or when you’re reasonably caught up and don’t expect delays ahead. When patients say that a doctor really listened to me, it is often not their medical history, but their life story they mean. And like every story, they literally transform us, the listener. In a true physical sense, their stories live on in me, and now that I’ve shared this one in writing, also with you for perpetuity. That is at least for the next 5 billion years when it, too, will be swallowed by the sun, leaving only a crispy, smoking rock where we once existed.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

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Let me tell you a story. In 5 billion years the sun will run out of hydrogen, the fuel it is currently burning to power my solar panels amongst other things. At that time, the sun will no longer be able to keep its core contracted and will expand into a fiery, red giant, engulfing earth and obliterating any sign that we ever existed. No buildings. No blog posts. No mausoleums. No stories. Nothing of us will remain.

Dr. Jeffrey Benabio

Well, here for a moment anyway, I’ve gotten you to think about something other than COVID. You’re welcome.

Fascinatingly, the image in your mind’s eye right now of a barren scorched landscape was put there by me. Simply by placing a few words together I have caused new thoughts in your head. You might even share this story with someone else – I would have actually changed your behavior through the power of language. This miraculous phenomenon seems to be unique to us humans; we are the only ones who can create whole worlds in another individual’s head just by making a few sounds. We in medicine have the privilege of experiencing this miracle every day.

Last week, a 97-year-old pale, frail, white man saw me for a basal cell carcinoma on his cheek. While performing a simple electrodesiccation and curettage, I asked if he remembers getting a lot of sunburns when he was young. He certainly remembered one. On a blustery sunny day, he fell asleep for hours on the deck of the USS West Virginia while in the Philippines. As a radio man, he was exhausted from days of conflict and he recalled how warm breezes lulled him asleep. He was so sunburned that for days he forgot how afraid he was of the Japanese.



After listening to his story, I had an image in my mind of palm trees swaying in the tropical winds while hundreds of hulking gray castles sat hidden in the vast surrounding oceans awaiting one of the greatest naval conflicts in history. I got to hear it from surely one of the last remaining people in existence to be able to tell that story. Listening to a patient’s tales is one of the benefits of being a physician. Not only do they help bond us with our patients, but also help lessen our burden of having to make diagnosis after diagnosis and write note after note for hours on end. Somehow performing yet another biopsy that day is made just a bit easier if I’m also learning about what it was like at the Battle of Leyte Gulf.

Encouraging patients to talk more can be risky. No physician, not even allergists, can afford to be waylaid by a retiree with nothing else to do today. But meaningful encounters can not only be a vaccine against burnout, they also lead to better patient adherence and satisfaction. Sometimes, there is simply not time. But often there is a little window during a procedure or when you’re reasonably caught up and don’t expect delays ahead. When patients say that a doctor really listened to me, it is often not their medical history, but their life story they mean. And like every story, they literally transform us, the listener. In a true physical sense, their stories live on in me, and now that I’ve shared this one in writing, also with you for perpetuity. That is at least for the next 5 billion years when it, too, will be swallowed by the sun, leaving only a crispy, smoking rock where we once existed.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

Let me tell you a story. In 5 billion years the sun will run out of hydrogen, the fuel it is currently burning to power my solar panels amongst other things. At that time, the sun will no longer be able to keep its core contracted and will expand into a fiery, red giant, engulfing earth and obliterating any sign that we ever existed. No buildings. No blog posts. No mausoleums. No stories. Nothing of us will remain.

Dr. Jeffrey Benabio

Well, here for a moment anyway, I’ve gotten you to think about something other than COVID. You’re welcome.

Fascinatingly, the image in your mind’s eye right now of a barren scorched landscape was put there by me. Simply by placing a few words together I have caused new thoughts in your head. You might even share this story with someone else – I would have actually changed your behavior through the power of language. This miraculous phenomenon seems to be unique to us humans; we are the only ones who can create whole worlds in another individual’s head just by making a few sounds. We in medicine have the privilege of experiencing this miracle every day.

Last week, a 97-year-old pale, frail, white man saw me for a basal cell carcinoma on his cheek. While performing a simple electrodesiccation and curettage, I asked if he remembers getting a lot of sunburns when he was young. He certainly remembered one. On a blustery sunny day, he fell asleep for hours on the deck of the USS West Virginia while in the Philippines. As a radio man, he was exhausted from days of conflict and he recalled how warm breezes lulled him asleep. He was so sunburned that for days he forgot how afraid he was of the Japanese.



After listening to his story, I had an image in my mind of palm trees swaying in the tropical winds while hundreds of hulking gray castles sat hidden in the vast surrounding oceans awaiting one of the greatest naval conflicts in history. I got to hear it from surely one of the last remaining people in existence to be able to tell that story. Listening to a patient’s tales is one of the benefits of being a physician. Not only do they help bond us with our patients, but also help lessen our burden of having to make diagnosis after diagnosis and write note after note for hours on end. Somehow performing yet another biopsy that day is made just a bit easier if I’m also learning about what it was like at the Battle of Leyte Gulf.

Encouraging patients to talk more can be risky. No physician, not even allergists, can afford to be waylaid by a retiree with nothing else to do today. But meaningful encounters can not only be a vaccine against burnout, they also lead to better patient adherence and satisfaction. Sometimes, there is simply not time. But often there is a little window during a procedure or when you’re reasonably caught up and don’t expect delays ahead. When patients say that a doctor really listened to me, it is often not their medical history, but their life story they mean. And like every story, they literally transform us, the listener. In a true physical sense, their stories live on in me, and now that I’ve shared this one in writing, also with you for perpetuity. That is at least for the next 5 billion years when it, too, will be swallowed by the sun, leaving only a crispy, smoking rock where we once existed.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

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‘Multimorbidity’ more commonly seen in people with lupus

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People with systemic lupus erythematosus (SLE) have a threefold greater likelihood of having up to five or more comorbidities in comparison with people in the general population, according to the results of two separate U.S. population-based studies.

The higher rate of comorbidities seen included many of those commonly reported before, such as cardiovascular and renal disease, but also some that may be less frequently associated with SLE, notably chronic obstructive pulmonary disease (COPD) and cardiac arrhythmias.

“In the past, the characterization of SLE comorbidities has relied on individual comorbidity assessment,” Alí Duarte García, MD, said at the 14th International Congress on Systemic Lupus Erythematosus, held together will the 6th International Congress on Controversies in Rheumatology and Autoimmunity.

“However, a patient-centric approach where a patient as a whole is seen and how many comorbidities they accrue has not been performed.” added Duarte García, who is a rheumatologist at the Mayo Clinic in Rochester, Minn.


 

Multiple conditions “overrepresented” in SLE patients

Dr. Duarte García reported the findings of one of the studies, both of which used data from the Rochester Epidemiology Project, a record-linkage system that collates clinical and hospital data from individuals who live in 19 counties in southeast Minnesota and eight counties in western Wisconsin; these patients have agreed to share their medical records for research.

The study population included 479 individuals diagnosed with SLE according to joint 2019 European Alliance of Associations for Rheumatology and American College of Rheumatology criteria. These were matched by age, sex, race, and county to 479 individuals without SLE.

The mean age of the study population was 53 years, 82% were women, and 86% were White.

“We defined multimorbidity as those patients who have two or more comorbidities and substantial multimorbidity as those patients who have five or more comorbidities,” Dr. Duarte García explained.

A previously published list of 44 categories of comorbidities was used to classify the multimorbidity seen, and 27 of these were “overrepresented” in patients with SLE.

Patients with SLE averaged 5.3 comorbidities, whereas control study subjects had 2.9. Comparing SLE with non-SLE individuals, the odds ratio for having two or more comorbid conditions was 2.96, and for five or more comorbidities it was 3.06.

The highest odds ratio comparing SLE with non-SLE individuals was seen for pulmonary disorders (39.0).

Dr. Duarte García highlighted four comorbidities that occurred in SLE patients that were perhaps more unusual: congestive heart failure (OR, 13.3), valvular heart disease (OR, 4.2), cardiac arrhythmias (OR, 2.85), and COPD (OR, 2.7).

“Given the association of multimorbidity with poor outcomes, care delivery strategies to manage multimorbidity are needed in SLE,” Dr. Duarte García concluded.
 

Similar findings seen in cutaneous lupus

There is also an excess of comorbid conditions in people with cutaneous lupus erythematosus (CLE), Mehmet Hocaoglu, MD, said in reporting the findings of the second study.

Dr. Hocaoglu, an internal medicine resident at the University of Maryland Medical Center in Baltimore, and part of the same team of researchers as Dr. Duarte García, noted that in skin-related lupus the risk of multimorbidity was about doubled.

For this separate analysis, a total of 303 patients with cutaneous lupus had been matched to 303 controls from the general population. Odds ratios for having two or more or five or more comorbidities were a respective 2.27 and 1.65.

Among the comorbidities seen that were higher in those with cutaneous lupus than in the general population subjects were fibromyalgia, liver disease, hypertension, anemia, hypothyroidism, and COPD.

“Further research is definitely needed to identify if the driver of this multimorbidity in CLE patients is the disease itself or the treatments CLE patients are receiving or a multifactorial cause that is driving the disease association,” Dr. Hocaoglu said.
 

 

 

Comment and perspective

“Comorbidities that are not appropriate to the general population, compared to SLE,” seem to have been included in the overall SLE and the cutaneous lupus analyses, Raquel Faria, MD, suggested.

Dr. Faria, an internal medicine consultant at Unidade de Imunologia Clínica – Centro Hospitalar Universitário Porto (Portugal), chaired the poster discussion session in which the two studies had been presented.

She wondered if the researchers had analyzed the data while accounting for “the comorbidities that you knew are due to activity in lupus, like anemia?”

The number of patients with SLE who had pulmonary circulation disorders – 7.5% vs. 0.2% of the general population – also caught Dr. Faria’s attention.

That’s “a really huge number,” Dr. Faria pointed out, “I think it is pretty overrepresented.”

Dr. Duarte García acknowledged that they “took a very broad approach” in using a “very large comorbidity index.”

“What we were observing initially is precisely what you’re mentioning,” he responded to Dr. Faria.

“We were pulling patients who were having disease manifestation rather than a comorbidity,” Dr. Duarte-García said.

These are initial and very exploratory data, he stressed. “We have now moved on to modify the index.” Some of the changes that they have made were to incorporate the SLICC Damage Index Score and tighten up the list of ICD codes used.

No outside funding was received for either of the studies. Dr. Duarte García and Dr. Hocaoglu individually stated that they had no actual or potential conflicts of interest in relation to their presentations.

A version of this article first appeared on Medscape.com.

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People with systemic lupus erythematosus (SLE) have a threefold greater likelihood of having up to five or more comorbidities in comparison with people in the general population, according to the results of two separate U.S. population-based studies.

The higher rate of comorbidities seen included many of those commonly reported before, such as cardiovascular and renal disease, but also some that may be less frequently associated with SLE, notably chronic obstructive pulmonary disease (COPD) and cardiac arrhythmias.

“In the past, the characterization of SLE comorbidities has relied on individual comorbidity assessment,” Alí Duarte García, MD, said at the 14th International Congress on Systemic Lupus Erythematosus, held together will the 6th International Congress on Controversies in Rheumatology and Autoimmunity.

“However, a patient-centric approach where a patient as a whole is seen and how many comorbidities they accrue has not been performed.” added Duarte García, who is a rheumatologist at the Mayo Clinic in Rochester, Minn.


 

Multiple conditions “overrepresented” in SLE patients

Dr. Duarte García reported the findings of one of the studies, both of which used data from the Rochester Epidemiology Project, a record-linkage system that collates clinical and hospital data from individuals who live in 19 counties in southeast Minnesota and eight counties in western Wisconsin; these patients have agreed to share their medical records for research.

The study population included 479 individuals diagnosed with SLE according to joint 2019 European Alliance of Associations for Rheumatology and American College of Rheumatology criteria. These were matched by age, sex, race, and county to 479 individuals without SLE.

The mean age of the study population was 53 years, 82% were women, and 86% were White.

“We defined multimorbidity as those patients who have two or more comorbidities and substantial multimorbidity as those patients who have five or more comorbidities,” Dr. Duarte García explained.

A previously published list of 44 categories of comorbidities was used to classify the multimorbidity seen, and 27 of these were “overrepresented” in patients with SLE.

Patients with SLE averaged 5.3 comorbidities, whereas control study subjects had 2.9. Comparing SLE with non-SLE individuals, the odds ratio for having two or more comorbid conditions was 2.96, and for five or more comorbidities it was 3.06.

The highest odds ratio comparing SLE with non-SLE individuals was seen for pulmonary disorders (39.0).

Dr. Duarte García highlighted four comorbidities that occurred in SLE patients that were perhaps more unusual: congestive heart failure (OR, 13.3), valvular heart disease (OR, 4.2), cardiac arrhythmias (OR, 2.85), and COPD (OR, 2.7).

“Given the association of multimorbidity with poor outcomes, care delivery strategies to manage multimorbidity are needed in SLE,” Dr. Duarte García concluded.
 

Similar findings seen in cutaneous lupus

There is also an excess of comorbid conditions in people with cutaneous lupus erythematosus (CLE), Mehmet Hocaoglu, MD, said in reporting the findings of the second study.

Dr. Hocaoglu, an internal medicine resident at the University of Maryland Medical Center in Baltimore, and part of the same team of researchers as Dr. Duarte García, noted that in skin-related lupus the risk of multimorbidity was about doubled.

For this separate analysis, a total of 303 patients with cutaneous lupus had been matched to 303 controls from the general population. Odds ratios for having two or more or five or more comorbidities were a respective 2.27 and 1.65.

Among the comorbidities seen that were higher in those with cutaneous lupus than in the general population subjects were fibromyalgia, liver disease, hypertension, anemia, hypothyroidism, and COPD.

“Further research is definitely needed to identify if the driver of this multimorbidity in CLE patients is the disease itself or the treatments CLE patients are receiving or a multifactorial cause that is driving the disease association,” Dr. Hocaoglu said.
 

 

 

Comment and perspective

“Comorbidities that are not appropriate to the general population, compared to SLE,” seem to have been included in the overall SLE and the cutaneous lupus analyses, Raquel Faria, MD, suggested.

Dr. Faria, an internal medicine consultant at Unidade de Imunologia Clínica – Centro Hospitalar Universitário Porto (Portugal), chaired the poster discussion session in which the two studies had been presented.

She wondered if the researchers had analyzed the data while accounting for “the comorbidities that you knew are due to activity in lupus, like anemia?”

The number of patients with SLE who had pulmonary circulation disorders – 7.5% vs. 0.2% of the general population – also caught Dr. Faria’s attention.

That’s “a really huge number,” Dr. Faria pointed out, “I think it is pretty overrepresented.”

Dr. Duarte García acknowledged that they “took a very broad approach” in using a “very large comorbidity index.”

“What we were observing initially is precisely what you’re mentioning,” he responded to Dr. Faria.

“We were pulling patients who were having disease manifestation rather than a comorbidity,” Dr. Duarte-García said.

These are initial and very exploratory data, he stressed. “We have now moved on to modify the index.” Some of the changes that they have made were to incorporate the SLICC Damage Index Score and tighten up the list of ICD codes used.

No outside funding was received for either of the studies. Dr. Duarte García and Dr. Hocaoglu individually stated that they had no actual or potential conflicts of interest in relation to their presentations.

A version of this article first appeared on Medscape.com.

People with systemic lupus erythematosus (SLE) have a threefold greater likelihood of having up to five or more comorbidities in comparison with people in the general population, according to the results of two separate U.S. population-based studies.

The higher rate of comorbidities seen included many of those commonly reported before, such as cardiovascular and renal disease, but also some that may be less frequently associated with SLE, notably chronic obstructive pulmonary disease (COPD) and cardiac arrhythmias.

“In the past, the characterization of SLE comorbidities has relied on individual comorbidity assessment,” Alí Duarte García, MD, said at the 14th International Congress on Systemic Lupus Erythematosus, held together will the 6th International Congress on Controversies in Rheumatology and Autoimmunity.

“However, a patient-centric approach where a patient as a whole is seen and how many comorbidities they accrue has not been performed.” added Duarte García, who is a rheumatologist at the Mayo Clinic in Rochester, Minn.


 

Multiple conditions “overrepresented” in SLE patients

Dr. Duarte García reported the findings of one of the studies, both of which used data from the Rochester Epidemiology Project, a record-linkage system that collates clinical and hospital data from individuals who live in 19 counties in southeast Minnesota and eight counties in western Wisconsin; these patients have agreed to share their medical records for research.

The study population included 479 individuals diagnosed with SLE according to joint 2019 European Alliance of Associations for Rheumatology and American College of Rheumatology criteria. These were matched by age, sex, race, and county to 479 individuals without SLE.

The mean age of the study population was 53 years, 82% were women, and 86% were White.

“We defined multimorbidity as those patients who have two or more comorbidities and substantial multimorbidity as those patients who have five or more comorbidities,” Dr. Duarte García explained.

A previously published list of 44 categories of comorbidities was used to classify the multimorbidity seen, and 27 of these were “overrepresented” in patients with SLE.

Patients with SLE averaged 5.3 comorbidities, whereas control study subjects had 2.9. Comparing SLE with non-SLE individuals, the odds ratio for having two or more comorbid conditions was 2.96, and for five or more comorbidities it was 3.06.

The highest odds ratio comparing SLE with non-SLE individuals was seen for pulmonary disorders (39.0).

Dr. Duarte García highlighted four comorbidities that occurred in SLE patients that were perhaps more unusual: congestive heart failure (OR, 13.3), valvular heart disease (OR, 4.2), cardiac arrhythmias (OR, 2.85), and COPD (OR, 2.7).

“Given the association of multimorbidity with poor outcomes, care delivery strategies to manage multimorbidity are needed in SLE,” Dr. Duarte García concluded.
 

Similar findings seen in cutaneous lupus

There is also an excess of comorbid conditions in people with cutaneous lupus erythematosus (CLE), Mehmet Hocaoglu, MD, said in reporting the findings of the second study.

Dr. Hocaoglu, an internal medicine resident at the University of Maryland Medical Center in Baltimore, and part of the same team of researchers as Dr. Duarte García, noted that in skin-related lupus the risk of multimorbidity was about doubled.

For this separate analysis, a total of 303 patients with cutaneous lupus had been matched to 303 controls from the general population. Odds ratios for having two or more or five or more comorbidities were a respective 2.27 and 1.65.

Among the comorbidities seen that were higher in those with cutaneous lupus than in the general population subjects were fibromyalgia, liver disease, hypertension, anemia, hypothyroidism, and COPD.

“Further research is definitely needed to identify if the driver of this multimorbidity in CLE patients is the disease itself or the treatments CLE patients are receiving or a multifactorial cause that is driving the disease association,” Dr. Hocaoglu said.
 

 

 

Comment and perspective

“Comorbidities that are not appropriate to the general population, compared to SLE,” seem to have been included in the overall SLE and the cutaneous lupus analyses, Raquel Faria, MD, suggested.

Dr. Faria, an internal medicine consultant at Unidade de Imunologia Clínica – Centro Hospitalar Universitário Porto (Portugal), chaired the poster discussion session in which the two studies had been presented.

She wondered if the researchers had analyzed the data while accounting for “the comorbidities that you knew are due to activity in lupus, like anemia?”

The number of patients with SLE who had pulmonary circulation disorders – 7.5% vs. 0.2% of the general population – also caught Dr. Faria’s attention.

That’s “a really huge number,” Dr. Faria pointed out, “I think it is pretty overrepresented.”

Dr. Duarte García acknowledged that they “took a very broad approach” in using a “very large comorbidity index.”

“What we were observing initially is precisely what you’re mentioning,” he responded to Dr. Faria.

“We were pulling patients who were having disease manifestation rather than a comorbidity,” Dr. Duarte-García said.

These are initial and very exploratory data, he stressed. “We have now moved on to modify the index.” Some of the changes that they have made were to incorporate the SLICC Damage Index Score and tighten up the list of ICD codes used.

No outside funding was received for either of the studies. Dr. Duarte García and Dr. Hocaoglu individually stated that they had no actual or potential conflicts of interest in relation to their presentations.

A version of this article first appeared on Medscape.com.

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Generalized Pustular Psoriasis: An Uncommon Diagnosis Carrying an Outsize Burden of Disease

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In this supplement to Dermatology News, Alan Menter, MD discusses best practices for the rare, severe, and chronic autoinflammatory disease known as Generalized Pustular Psoriasis (GPP). 

 

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In this supplement to Dermatology News, Alan Menter, MD discusses best practices for the rare, severe, and chronic autoinflammatory disease known as Generalized Pustular Psoriasis (GPP). 

 

Read More 

In this supplement to Dermatology News, Alan Menter, MD discusses best practices for the rare, severe, and chronic autoinflammatory disease known as Generalized Pustular Psoriasis (GPP). 

 

Read More 

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White House unveils plan to combat endocrine-disrupting PFAS pollution

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The federal government is stepping up actions to protect Americans from per- and polyfluoroalkyl substances that continue to threaten health through pollution in the air, water, and foods, according to a statement from the White House on Oct. 18.

tupungato/Thinkstock

The comprehensive plan includes efforts to prevent per- and polyfluoroalkyl substances (PFAS) from being released into the air, drinking and ground water, and the food supply chain, according to the statement. Other efforts will expand cleanup and remediation of the impact of PFAS already present in the environment.

PFAS are a category of endocrine-disrupting chemicals (EDCs) that have been used for decades in a range of consumer products including cookware, stain-resistant clothes, fast food wrappers, treatments for carpets and furniture, and firefighting foams. PFAS can be released into the air, and also into surface water, drinking water, and ground water, because of how they are disposed, according to a 2020 report from the Endocrine Society and the International Pollutants Elimination Network. The report suggested that creation of more plastic products will likely increase exposure to PFAS and other EDCs.



The Environmental Protection Agency will take the lead on the Biden administration’s PFAS reduction efforts. The agency announced a PFAS Roadmap, which outlines actions to control PFAS over the next 3 years. The Roadmap’s goals include keeping PFAS out of the environment, holding polluters accountable for their actions, investing in scientific research to learn more about the impact of PFAS on human health, and prioritizing protection for disadvantaged communities. The EPA described its approach to PFAS as three pronged (Research, Restrict, Remediate). Planned actions noted on the EPA website include publication of a national PFAS testing strategy, establishing an improved review process for new PFAS, reviewing existing PFAS, and enhancing reporting to track sources and quantities of PFAS.

White House statement noted that other agencies committed to controlling PFAS include the Department of Defense, which will conduct cleanups and assessments at DOD and National Guard locations; the Food and Drug Administration, which will to expand its food supply testing to estimate dietary exposure to PFAS; and the Department of Agriculture, which is investigating causes and impacts of PFAS in the food system, and supporting research on environmental contaminants including PFAS.

The Department of Homeland Security has conducted an inventory of PFAS use, notably the use of PFAS in firefighting foams, and established an Emerging Contaminants Working Group to remediate PFAS and other contaminants. In addition, the Department of Health & Human Services monitors the evolving science on human health and PFAS and anticipates a report by the Centers for Disease Control and Prevention on the health effects of PFAS exposure, with data from eight states.

The American Chemistry Council (ACC), a trade association for American chemistry companies, issued a statement in response to the EPA’s PFAS Strategic Roadmap in which they supported the value of science-based regulation, but emphasized that PFAS are distinct from one another, and should not be grouped together for regulation purposes.

“According to EPA, approximately 600 PFAS substances are manufactured or in use today, each with its own unique properties and uses, from cellphones to solar panels, for which alternatives are not always available,” according to the ACC statement. “EPA’s Roadmap reinforces the differences between these chemistries and that they should not all be grouped together.” The newly formed Interagency Policy Committee on PFAS will coordinate PFAS response efforts across agencies and “help develop new policy strategies to support research, remediation, and removal of PFAS in communities across the country,” according to the White House statement.

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The federal government is stepping up actions to protect Americans from per- and polyfluoroalkyl substances that continue to threaten health through pollution in the air, water, and foods, according to a statement from the White House on Oct. 18.

tupungato/Thinkstock

The comprehensive plan includes efforts to prevent per- and polyfluoroalkyl substances (PFAS) from being released into the air, drinking and ground water, and the food supply chain, according to the statement. Other efforts will expand cleanup and remediation of the impact of PFAS already present in the environment.

PFAS are a category of endocrine-disrupting chemicals (EDCs) that have been used for decades in a range of consumer products including cookware, stain-resistant clothes, fast food wrappers, treatments for carpets and furniture, and firefighting foams. PFAS can be released into the air, and also into surface water, drinking water, and ground water, because of how they are disposed, according to a 2020 report from the Endocrine Society and the International Pollutants Elimination Network. The report suggested that creation of more plastic products will likely increase exposure to PFAS and other EDCs.



The Environmental Protection Agency will take the lead on the Biden administration’s PFAS reduction efforts. The agency announced a PFAS Roadmap, which outlines actions to control PFAS over the next 3 years. The Roadmap’s goals include keeping PFAS out of the environment, holding polluters accountable for their actions, investing in scientific research to learn more about the impact of PFAS on human health, and prioritizing protection for disadvantaged communities. The EPA described its approach to PFAS as three pronged (Research, Restrict, Remediate). Planned actions noted on the EPA website include publication of a national PFAS testing strategy, establishing an improved review process for new PFAS, reviewing existing PFAS, and enhancing reporting to track sources and quantities of PFAS.

White House statement noted that other agencies committed to controlling PFAS include the Department of Defense, which will conduct cleanups and assessments at DOD and National Guard locations; the Food and Drug Administration, which will to expand its food supply testing to estimate dietary exposure to PFAS; and the Department of Agriculture, which is investigating causes and impacts of PFAS in the food system, and supporting research on environmental contaminants including PFAS.

The Department of Homeland Security has conducted an inventory of PFAS use, notably the use of PFAS in firefighting foams, and established an Emerging Contaminants Working Group to remediate PFAS and other contaminants. In addition, the Department of Health & Human Services monitors the evolving science on human health and PFAS and anticipates a report by the Centers for Disease Control and Prevention on the health effects of PFAS exposure, with data from eight states.

The American Chemistry Council (ACC), a trade association for American chemistry companies, issued a statement in response to the EPA’s PFAS Strategic Roadmap in which they supported the value of science-based regulation, but emphasized that PFAS are distinct from one another, and should not be grouped together for regulation purposes.

“According to EPA, approximately 600 PFAS substances are manufactured or in use today, each with its own unique properties and uses, from cellphones to solar panels, for which alternatives are not always available,” according to the ACC statement. “EPA’s Roadmap reinforces the differences between these chemistries and that they should not all be grouped together.” The newly formed Interagency Policy Committee on PFAS will coordinate PFAS response efforts across agencies and “help develop new policy strategies to support research, remediation, and removal of PFAS in communities across the country,” according to the White House statement.

 

The federal government is stepping up actions to protect Americans from per- and polyfluoroalkyl substances that continue to threaten health through pollution in the air, water, and foods, according to a statement from the White House on Oct. 18.

tupungato/Thinkstock

The comprehensive plan includes efforts to prevent per- and polyfluoroalkyl substances (PFAS) from being released into the air, drinking and ground water, and the food supply chain, according to the statement. Other efforts will expand cleanup and remediation of the impact of PFAS already present in the environment.

PFAS are a category of endocrine-disrupting chemicals (EDCs) that have been used for decades in a range of consumer products including cookware, stain-resistant clothes, fast food wrappers, treatments for carpets and furniture, and firefighting foams. PFAS can be released into the air, and also into surface water, drinking water, and ground water, because of how they are disposed, according to a 2020 report from the Endocrine Society and the International Pollutants Elimination Network. The report suggested that creation of more plastic products will likely increase exposure to PFAS and other EDCs.



The Environmental Protection Agency will take the lead on the Biden administration’s PFAS reduction efforts. The agency announced a PFAS Roadmap, which outlines actions to control PFAS over the next 3 years. The Roadmap’s goals include keeping PFAS out of the environment, holding polluters accountable for their actions, investing in scientific research to learn more about the impact of PFAS on human health, and prioritizing protection for disadvantaged communities. The EPA described its approach to PFAS as three pronged (Research, Restrict, Remediate). Planned actions noted on the EPA website include publication of a national PFAS testing strategy, establishing an improved review process for new PFAS, reviewing existing PFAS, and enhancing reporting to track sources and quantities of PFAS.

White House statement noted that other agencies committed to controlling PFAS include the Department of Defense, which will conduct cleanups and assessments at DOD and National Guard locations; the Food and Drug Administration, which will to expand its food supply testing to estimate dietary exposure to PFAS; and the Department of Agriculture, which is investigating causes and impacts of PFAS in the food system, and supporting research on environmental contaminants including PFAS.

The Department of Homeland Security has conducted an inventory of PFAS use, notably the use of PFAS in firefighting foams, and established an Emerging Contaminants Working Group to remediate PFAS and other contaminants. In addition, the Department of Health & Human Services monitors the evolving science on human health and PFAS and anticipates a report by the Centers for Disease Control and Prevention on the health effects of PFAS exposure, with data from eight states.

The American Chemistry Council (ACC), a trade association for American chemistry companies, issued a statement in response to the EPA’s PFAS Strategic Roadmap in which they supported the value of science-based regulation, but emphasized that PFAS are distinct from one another, and should not be grouped together for regulation purposes.

“According to EPA, approximately 600 PFAS substances are manufactured or in use today, each with its own unique properties and uses, from cellphones to solar panels, for which alternatives are not always available,” according to the ACC statement. “EPA’s Roadmap reinforces the differences between these chemistries and that they should not all be grouped together.” The newly formed Interagency Policy Committee on PFAS will coordinate PFAS response efforts across agencies and “help develop new policy strategies to support research, remediation, and removal of PFAS in communities across the country,” according to the White House statement.

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