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Diagnosing molluscum contagiosum can be tricky
The way James R. Treat, MD, sees it, if there ever were a truism in the field of dermatology, it’s that everyone hates molluscum contagiosum.
“It tortures all of us,” Dr. Treat, a pediatric dermatologist at Children’s Hospital of Philadelphia, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “It’s very distressing to parents, but often more distressing to parents than to kids.”
A viral disorder of the skin and mucous membranes characterized by discrete single or multiple, flesh-colored papules, “When you look at inflamed molluscum it can be very difficult to recognize because it looks like a more complicated infection,” said Dr. Treat, who is also associate professor of clinical pediatrics and dermatology, at the University of Pennsylvania, Philadelphia.
An epidemiologic review of 302 MC cases found that 80% of patients were aged younger than 8 years, 63% had more than 15 lesions, and 24% had concomitant atopic dermatitis (J Am Acad Dermatol. 2006; 2006;54[1]:47-54). “Children with atopic dermatitis often have their molluscum last longer,” he said. “The average time course for molluscum is 18 months, but it can certainly be longer than that. So if you say, ‘it’s probably going to go away in a few months,’ that’s probably not going to happen.”
The telltale MC lesion is glossy and contains a white core in the center that can be revealed by shining an otoscope sideways on the lesion. “Umbilication doesn’t always occur, but if the center part looks white, that will help with diagnosis,” Dr. Treat said. “If they’re inflamed and they’re red and you’re worried that there’s a bacterial infection, do a culture, pop the lesion open, and get some of the pus out. If you’re concerned, start them on antibiotics. It’s always worse to miss an infection than to overtreat molluscum. But once you’ve done it a few times and you realize that the cultures are coming back negative, then you’ll probably have your threshold a little higher.”
The most useful clinical sign of MC is the so-called “BOTE” (beginning of the end) sign, which is characterized by erythema and swelling of MC skin lesions. “When the parents come to us in pediatric dermatology, often it’s because their kids have had molluscum for a while,” he said. “It spreads and becomes inflamed and the parents ask, ‘Is it infected?’ The answer is, yes, it’s an infection, but it’s not infected with what you think it is [which is Staphylococcus or Streptococcus], it’s the virus being recognized by the body. When the virus is recognized by the body, it creates a huge inflammatory reaction. That’s usually the time at which the body has had enough of the virus, and it eradicates the rest of it. It means the inflammatory response is finding the molluscum and it’s going to take care of it.”
MC brings its own eczematous response, which can complicate efforts to confirm the diagnosis. Dr. Treat spoke of a young patient he recently saw who had an eczematous reaction on the inner parts of the arms and the upper flank – with no such clinical history. “It kind of came out of the blue,” he said. “You think about contact allergies and other types of dermatitis, but molluscum brings its own eczema. Often what the parents recognize is the eczematous eruption and not the little dots of molluscum. So if you see someone with a new eruption in typical molluscum areas – the flank and your thighs and the back of the legs – and they’ve never had eczema in the past, or they’ve only had mild eczema, think about eczema as a response to molluscum.”
MC can also result in a Gianotti-Crosti syndrome-like reactions (Arch Dermatol. 2012;148[11]:1257-64). “These are angry, inflamed red papules on the knees and on the elbows and on the buttocks and on the cheeks,” Dr. Treat said. “It typically spares the trunk, and they look like molluscum.”
He went on to note that MC can present as cysts, and that MC in the gluteal cleft is a mimicker of condyloma. MC can also cause conjunctivitis, which is increased in HIV patients and in those with atopic dermatitis. “These are patients who should probably see an ophthalmologist” to make no damage has occurred, Dr. Treat said.
He closed his remarks by noting that rarely, MC can be the presenting sign of an immunodeficiency. “The immune system dysregulation that shows up this way is called a DOCK8 mutation, which have eczema and widespread viral disease including warts and molluscum,” Dr. Treat said.
He reported having no financial disclosures.
The way James R. Treat, MD, sees it, if there ever were a truism in the field of dermatology, it’s that everyone hates molluscum contagiosum.
“It tortures all of us,” Dr. Treat, a pediatric dermatologist at Children’s Hospital of Philadelphia, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “It’s very distressing to parents, but often more distressing to parents than to kids.”
A viral disorder of the skin and mucous membranes characterized by discrete single or multiple, flesh-colored papules, “When you look at inflamed molluscum it can be very difficult to recognize because it looks like a more complicated infection,” said Dr. Treat, who is also associate professor of clinical pediatrics and dermatology, at the University of Pennsylvania, Philadelphia.
An epidemiologic review of 302 MC cases found that 80% of patients were aged younger than 8 years, 63% had more than 15 lesions, and 24% had concomitant atopic dermatitis (J Am Acad Dermatol. 2006; 2006;54[1]:47-54). “Children with atopic dermatitis often have their molluscum last longer,” he said. “The average time course for molluscum is 18 months, but it can certainly be longer than that. So if you say, ‘it’s probably going to go away in a few months,’ that’s probably not going to happen.”
The telltale MC lesion is glossy and contains a white core in the center that can be revealed by shining an otoscope sideways on the lesion. “Umbilication doesn’t always occur, but if the center part looks white, that will help with diagnosis,” Dr. Treat said. “If they’re inflamed and they’re red and you’re worried that there’s a bacterial infection, do a culture, pop the lesion open, and get some of the pus out. If you’re concerned, start them on antibiotics. It’s always worse to miss an infection than to overtreat molluscum. But once you’ve done it a few times and you realize that the cultures are coming back negative, then you’ll probably have your threshold a little higher.”
The most useful clinical sign of MC is the so-called “BOTE” (beginning of the end) sign, which is characterized by erythema and swelling of MC skin lesions. “When the parents come to us in pediatric dermatology, often it’s because their kids have had molluscum for a while,” he said. “It spreads and becomes inflamed and the parents ask, ‘Is it infected?’ The answer is, yes, it’s an infection, but it’s not infected with what you think it is [which is Staphylococcus or Streptococcus], it’s the virus being recognized by the body. When the virus is recognized by the body, it creates a huge inflammatory reaction. That’s usually the time at which the body has had enough of the virus, and it eradicates the rest of it. It means the inflammatory response is finding the molluscum and it’s going to take care of it.”
MC brings its own eczematous response, which can complicate efforts to confirm the diagnosis. Dr. Treat spoke of a young patient he recently saw who had an eczematous reaction on the inner parts of the arms and the upper flank – with no such clinical history. “It kind of came out of the blue,” he said. “You think about contact allergies and other types of dermatitis, but molluscum brings its own eczema. Often what the parents recognize is the eczematous eruption and not the little dots of molluscum. So if you see someone with a new eruption in typical molluscum areas – the flank and your thighs and the back of the legs – and they’ve never had eczema in the past, or they’ve only had mild eczema, think about eczema as a response to molluscum.”
MC can also result in a Gianotti-Crosti syndrome-like reactions (Arch Dermatol. 2012;148[11]:1257-64). “These are angry, inflamed red papules on the knees and on the elbows and on the buttocks and on the cheeks,” Dr. Treat said. “It typically spares the trunk, and they look like molluscum.”
He went on to note that MC can present as cysts, and that MC in the gluteal cleft is a mimicker of condyloma. MC can also cause conjunctivitis, which is increased in HIV patients and in those with atopic dermatitis. “These are patients who should probably see an ophthalmologist” to make no damage has occurred, Dr. Treat said.
He closed his remarks by noting that rarely, MC can be the presenting sign of an immunodeficiency. “The immune system dysregulation that shows up this way is called a DOCK8 mutation, which have eczema and widespread viral disease including warts and molluscum,” Dr. Treat said.
He reported having no financial disclosures.
The way James R. Treat, MD, sees it, if there ever were a truism in the field of dermatology, it’s that everyone hates molluscum contagiosum.
“It tortures all of us,” Dr. Treat, a pediatric dermatologist at Children’s Hospital of Philadelphia, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “It’s very distressing to parents, but often more distressing to parents than to kids.”
A viral disorder of the skin and mucous membranes characterized by discrete single or multiple, flesh-colored papules, “When you look at inflamed molluscum it can be very difficult to recognize because it looks like a more complicated infection,” said Dr. Treat, who is also associate professor of clinical pediatrics and dermatology, at the University of Pennsylvania, Philadelphia.
An epidemiologic review of 302 MC cases found that 80% of patients were aged younger than 8 years, 63% had more than 15 lesions, and 24% had concomitant atopic dermatitis (J Am Acad Dermatol. 2006; 2006;54[1]:47-54). “Children with atopic dermatitis often have their molluscum last longer,” he said. “The average time course for molluscum is 18 months, but it can certainly be longer than that. So if you say, ‘it’s probably going to go away in a few months,’ that’s probably not going to happen.”
The telltale MC lesion is glossy and contains a white core in the center that can be revealed by shining an otoscope sideways on the lesion. “Umbilication doesn’t always occur, but if the center part looks white, that will help with diagnosis,” Dr. Treat said. “If they’re inflamed and they’re red and you’re worried that there’s a bacterial infection, do a culture, pop the lesion open, and get some of the pus out. If you’re concerned, start them on antibiotics. It’s always worse to miss an infection than to overtreat molluscum. But once you’ve done it a few times and you realize that the cultures are coming back negative, then you’ll probably have your threshold a little higher.”
The most useful clinical sign of MC is the so-called “BOTE” (beginning of the end) sign, which is characterized by erythema and swelling of MC skin lesions. “When the parents come to us in pediatric dermatology, often it’s because their kids have had molluscum for a while,” he said. “It spreads and becomes inflamed and the parents ask, ‘Is it infected?’ The answer is, yes, it’s an infection, but it’s not infected with what you think it is [which is Staphylococcus or Streptococcus], it’s the virus being recognized by the body. When the virus is recognized by the body, it creates a huge inflammatory reaction. That’s usually the time at which the body has had enough of the virus, and it eradicates the rest of it. It means the inflammatory response is finding the molluscum and it’s going to take care of it.”
MC brings its own eczematous response, which can complicate efforts to confirm the diagnosis. Dr. Treat spoke of a young patient he recently saw who had an eczematous reaction on the inner parts of the arms and the upper flank – with no such clinical history. “It kind of came out of the blue,” he said. “You think about contact allergies and other types of dermatitis, but molluscum brings its own eczema. Often what the parents recognize is the eczematous eruption and not the little dots of molluscum. So if you see someone with a new eruption in typical molluscum areas – the flank and your thighs and the back of the legs – and they’ve never had eczema in the past, or they’ve only had mild eczema, think about eczema as a response to molluscum.”
MC can also result in a Gianotti-Crosti syndrome-like reactions (Arch Dermatol. 2012;148[11]:1257-64). “These are angry, inflamed red papules on the knees and on the elbows and on the buttocks and on the cheeks,” Dr. Treat said. “It typically spares the trunk, and they look like molluscum.”
He went on to note that MC can present as cysts, and that MC in the gluteal cleft is a mimicker of condyloma. MC can also cause conjunctivitis, which is increased in HIV patients and in those with atopic dermatitis. “These are patients who should probably see an ophthalmologist” to make no damage has occurred, Dr. Treat said.
He closed his remarks by noting that rarely, MC can be the presenting sign of an immunodeficiency. “The immune system dysregulation that shows up this way is called a DOCK8 mutation, which have eczema and widespread viral disease including warts and molluscum,” Dr. Treat said.
He reported having no financial disclosures.
FROM PEDIATRIC DERMATOLOGY 2020
Sorting out the many mimickers of psoriasis
“It has an earlier age of onset, usually in infancy, and can occur with the atopic triad that presents with asthma and seasonal allergies as well,” Israel David “Izzy” Andrews, MD, said at the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “There is typically a very strong family history, as this is an autosomal dominant condition, and it’s far more common than psoriasis. The annual incidence is estimated to be 10%-15% of pediatric patients. It has classic areas of involvement depending on the age of the patient, and lesions are intensely pruritic at all times. There is induration and crust, but it’s important to distinguish crust from scale. Whereas crust is dried exudate, and scale is usually secondary to a hyperproliferation of the skin. Initially, treatments (especially topical) are similar and may also delay the formalized diagnosis of either of the two.”
Another psoriasis mimicker, pityriasis rosea, is thought to be secondary to human herpes virus 6 or 7 infection, said Dr. Andrews, of the department of dermatology at Phoenix Children’s Hospital. It typically appears in the teens and tweens and usually presents as a large herald patch or plaque on the trunk. As the herald patch resolves, smaller lesions will develop on the trunk following skin folds. “It’s rarely symptomatic and it’s very short lived, and clears within 6-12 weeks,” Dr. Andrews noted. “It can present with an inverse pattern involving the face, neck, and groin, but sparing the trunk. This variant, termed inverse pityriasis rosea, can be confused with inverse psoriasis, which has a similar distribution. However, the inverse pattern of pityriasis rosea will still resolve in a similar time frame to its more classic variant.”
Pityriasis lichenoides can also be mistaken for psoriasis. The acute form can present with erythematous, scaly papules and plaques, but lesions are often found in different phases of resolution or healing. “This benign lymphoproliferative skin disorder can be very difficult to distinguish from psoriasis and may require a biopsy to rule in or out,” Dr. Andrews said. “It can last months to years and there are few treatments that are effective. It is typically nonresponsive to topical steroids and other treatments that would be more effective for psoriasis, helping to distinguish the two. It is thought to exist in the spectrum with other lymphoproliferative diseases including cutaneous T-cell lymphoma [CTCL]. However, there are only a few cases in the literature that support a transformation from pityriasis lichenoides to CTCL.”
Seborrheic dermatitis is more common than atopic dermatitis and psoriasis, but it can be mistaken for psoriasis. It is caused by an inflammatory response secondary to overgrowth of Malassezia yeast and has a bimodal age distribution. “Seborrheic dermatitis affects babies, teens, and tweens, and can persist into adulthood,” he said. “Infants with cradle cap usually resolve with moisturization, gentle brushing, and occasional antifungal shampoos.” Petaloid seborrheic dermatitis can predominately involve the face with psoriatic-appearing induration, plaques, and varying degrees of scales. “In skin of color, this can be confused with discoid lupus, sarcoidosis, and psoriasis, occasionally requiring a biopsy to distinguish,” said Dr. Andrews, who is also an assistant professor of pediatrics at the Mayo Clinic College of Medicine and Science in Scottsdale, Ariz.
Another psoriasis mimicker, pityriasis amiantacea, is thought to be a more severe form of seborrheic dermatitis. It presents with concretions of scale around hair follicles that are highly adherent and are sometimes called sebopsoriasis. “It may be associated with cutaneous findings of psoriasis elsewhere, but may also be found with secondarily infected atopic dermatitis and tinea capitis; however, in my clinical experience, it is most often found in isolation,” he said. “There may be a seasonal association with exacerbation in warm temperatures, and treatment often consists of humectants like salicylic acid for loosening scale, topical steroids for inflammation, and gentle combing out of scale.”
Infections can also mimic psoriasis. For example, tinea infections are often misdiagnosed as eczema or psoriasis and treated with topical steroids. “This can lead to tinea incognito, making it harder to diagnose either condition without attention to detail,” Dr. Andrews said. “On the body, look for expanding lesions with more raised peripheral edges, and central flattening, giving a classic annular appearance. It’s also important to inquire about family history and contacts including pets, contact sports/mat sports (think yoga, gymnastics, martial arts), or other contacts with similar rashes.” Work-up typically includes a fungal culture and starting empiric oral antifungal medications. “It is important to be able to distinguish scalp psoriasis from tinea capitis to prevent the more inflammatory form of tinea capitis, kerion (a deeper more symptomatic, painful and purulent dermatitis), which can lead to permanent scarring alopecia,” he said.
Bacterial infections can also mimic psoriasis, specifically nonbullous impetigo and ecthyma, the more ulcerative form of impetigo. The most frequent associations are group A Streptococcus, methicillin-susceptible Staphylococcus aureus and methicillin-resistant S. aureus.
Dr. Andrews closed his presentation by noting that tumor necrosis factor–alpha inhibitor–induced psoriasiform drug eruptions can occur in psoriasis-naive patients or unmask a predilection for psoriasis in patients with Crohn’s disease, juvenile idiopathic arthritis, or other autoinflammatory or autoimmune conditions. “They may improve with continued treatment and resolve with switching treatments,” he said. “Early biopsy in psoriasiform drug eruptions can appear like atopic dermatitis on pathology. When suspecting psoriasis in a pediatric patient, it is important to consider the history and physical exam as well as family history and associated comorbidities. While a biopsy may aide in the work-up, diagnosis can be made clinically.”
Dr. Andrews reported having no financial disclosures.
“It has an earlier age of onset, usually in infancy, and can occur with the atopic triad that presents with asthma and seasonal allergies as well,” Israel David “Izzy” Andrews, MD, said at the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “There is typically a very strong family history, as this is an autosomal dominant condition, and it’s far more common than psoriasis. The annual incidence is estimated to be 10%-15% of pediatric patients. It has classic areas of involvement depending on the age of the patient, and lesions are intensely pruritic at all times. There is induration and crust, but it’s important to distinguish crust from scale. Whereas crust is dried exudate, and scale is usually secondary to a hyperproliferation of the skin. Initially, treatments (especially topical) are similar and may also delay the formalized diagnosis of either of the two.”
Another psoriasis mimicker, pityriasis rosea, is thought to be secondary to human herpes virus 6 or 7 infection, said Dr. Andrews, of the department of dermatology at Phoenix Children’s Hospital. It typically appears in the teens and tweens and usually presents as a large herald patch or plaque on the trunk. As the herald patch resolves, smaller lesions will develop on the trunk following skin folds. “It’s rarely symptomatic and it’s very short lived, and clears within 6-12 weeks,” Dr. Andrews noted. “It can present with an inverse pattern involving the face, neck, and groin, but sparing the trunk. This variant, termed inverse pityriasis rosea, can be confused with inverse psoriasis, which has a similar distribution. However, the inverse pattern of pityriasis rosea will still resolve in a similar time frame to its more classic variant.”
Pityriasis lichenoides can also be mistaken for psoriasis. The acute form can present with erythematous, scaly papules and plaques, but lesions are often found in different phases of resolution or healing. “This benign lymphoproliferative skin disorder can be very difficult to distinguish from psoriasis and may require a biopsy to rule in or out,” Dr. Andrews said. “It can last months to years and there are few treatments that are effective. It is typically nonresponsive to topical steroids and other treatments that would be more effective for psoriasis, helping to distinguish the two. It is thought to exist in the spectrum with other lymphoproliferative diseases including cutaneous T-cell lymphoma [CTCL]. However, there are only a few cases in the literature that support a transformation from pityriasis lichenoides to CTCL.”
Seborrheic dermatitis is more common than atopic dermatitis and psoriasis, but it can be mistaken for psoriasis. It is caused by an inflammatory response secondary to overgrowth of Malassezia yeast and has a bimodal age distribution. “Seborrheic dermatitis affects babies, teens, and tweens, and can persist into adulthood,” he said. “Infants with cradle cap usually resolve with moisturization, gentle brushing, and occasional antifungal shampoos.” Petaloid seborrheic dermatitis can predominately involve the face with psoriatic-appearing induration, plaques, and varying degrees of scales. “In skin of color, this can be confused with discoid lupus, sarcoidosis, and psoriasis, occasionally requiring a biopsy to distinguish,” said Dr. Andrews, who is also an assistant professor of pediatrics at the Mayo Clinic College of Medicine and Science in Scottsdale, Ariz.
Another psoriasis mimicker, pityriasis amiantacea, is thought to be a more severe form of seborrheic dermatitis. It presents with concretions of scale around hair follicles that are highly adherent and are sometimes called sebopsoriasis. “It may be associated with cutaneous findings of psoriasis elsewhere, but may also be found with secondarily infected atopic dermatitis and tinea capitis; however, in my clinical experience, it is most often found in isolation,” he said. “There may be a seasonal association with exacerbation in warm temperatures, and treatment often consists of humectants like salicylic acid for loosening scale, topical steroids for inflammation, and gentle combing out of scale.”
Infections can also mimic psoriasis. For example, tinea infections are often misdiagnosed as eczema or psoriasis and treated with topical steroids. “This can lead to tinea incognito, making it harder to diagnose either condition without attention to detail,” Dr. Andrews said. “On the body, look for expanding lesions with more raised peripheral edges, and central flattening, giving a classic annular appearance. It’s also important to inquire about family history and contacts including pets, contact sports/mat sports (think yoga, gymnastics, martial arts), or other contacts with similar rashes.” Work-up typically includes a fungal culture and starting empiric oral antifungal medications. “It is important to be able to distinguish scalp psoriasis from tinea capitis to prevent the more inflammatory form of tinea capitis, kerion (a deeper more symptomatic, painful and purulent dermatitis), which can lead to permanent scarring alopecia,” he said.
Bacterial infections can also mimic psoriasis, specifically nonbullous impetigo and ecthyma, the more ulcerative form of impetigo. The most frequent associations are group A Streptococcus, methicillin-susceptible Staphylococcus aureus and methicillin-resistant S. aureus.
Dr. Andrews closed his presentation by noting that tumor necrosis factor–alpha inhibitor–induced psoriasiform drug eruptions can occur in psoriasis-naive patients or unmask a predilection for psoriasis in patients with Crohn’s disease, juvenile idiopathic arthritis, or other autoinflammatory or autoimmune conditions. “They may improve with continued treatment and resolve with switching treatments,” he said. “Early biopsy in psoriasiform drug eruptions can appear like atopic dermatitis on pathology. When suspecting psoriasis in a pediatric patient, it is important to consider the history and physical exam as well as family history and associated comorbidities. While a biopsy may aide in the work-up, diagnosis can be made clinically.”
Dr. Andrews reported having no financial disclosures.
“It has an earlier age of onset, usually in infancy, and can occur with the atopic triad that presents with asthma and seasonal allergies as well,” Israel David “Izzy” Andrews, MD, said at the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “There is typically a very strong family history, as this is an autosomal dominant condition, and it’s far more common than psoriasis. The annual incidence is estimated to be 10%-15% of pediatric patients. It has classic areas of involvement depending on the age of the patient, and lesions are intensely pruritic at all times. There is induration and crust, but it’s important to distinguish crust from scale. Whereas crust is dried exudate, and scale is usually secondary to a hyperproliferation of the skin. Initially, treatments (especially topical) are similar and may also delay the formalized diagnosis of either of the two.”
Another psoriasis mimicker, pityriasis rosea, is thought to be secondary to human herpes virus 6 or 7 infection, said Dr. Andrews, of the department of dermatology at Phoenix Children’s Hospital. It typically appears in the teens and tweens and usually presents as a large herald patch or plaque on the trunk. As the herald patch resolves, smaller lesions will develop on the trunk following skin folds. “It’s rarely symptomatic and it’s very short lived, and clears within 6-12 weeks,” Dr. Andrews noted. “It can present with an inverse pattern involving the face, neck, and groin, but sparing the trunk. This variant, termed inverse pityriasis rosea, can be confused with inverse psoriasis, which has a similar distribution. However, the inverse pattern of pityriasis rosea will still resolve in a similar time frame to its more classic variant.”
Pityriasis lichenoides can also be mistaken for psoriasis. The acute form can present with erythematous, scaly papules and plaques, but lesions are often found in different phases of resolution or healing. “This benign lymphoproliferative skin disorder can be very difficult to distinguish from psoriasis and may require a biopsy to rule in or out,” Dr. Andrews said. “It can last months to years and there are few treatments that are effective. It is typically nonresponsive to topical steroids and other treatments that would be more effective for psoriasis, helping to distinguish the two. It is thought to exist in the spectrum with other lymphoproliferative diseases including cutaneous T-cell lymphoma [CTCL]. However, there are only a few cases in the literature that support a transformation from pityriasis lichenoides to CTCL.”
Seborrheic dermatitis is more common than atopic dermatitis and psoriasis, but it can be mistaken for psoriasis. It is caused by an inflammatory response secondary to overgrowth of Malassezia yeast and has a bimodal age distribution. “Seborrheic dermatitis affects babies, teens, and tweens, and can persist into adulthood,” he said. “Infants with cradle cap usually resolve with moisturization, gentle brushing, and occasional antifungal shampoos.” Petaloid seborrheic dermatitis can predominately involve the face with psoriatic-appearing induration, plaques, and varying degrees of scales. “In skin of color, this can be confused with discoid lupus, sarcoidosis, and psoriasis, occasionally requiring a biopsy to distinguish,” said Dr. Andrews, who is also an assistant professor of pediatrics at the Mayo Clinic College of Medicine and Science in Scottsdale, Ariz.
Another psoriasis mimicker, pityriasis amiantacea, is thought to be a more severe form of seborrheic dermatitis. It presents with concretions of scale around hair follicles that are highly adherent and are sometimes called sebopsoriasis. “It may be associated with cutaneous findings of psoriasis elsewhere, but may also be found with secondarily infected atopic dermatitis and tinea capitis; however, in my clinical experience, it is most often found in isolation,” he said. “There may be a seasonal association with exacerbation in warm temperatures, and treatment often consists of humectants like salicylic acid for loosening scale, topical steroids for inflammation, and gentle combing out of scale.”
Infections can also mimic psoriasis. For example, tinea infections are often misdiagnosed as eczema or psoriasis and treated with topical steroids. “This can lead to tinea incognito, making it harder to diagnose either condition without attention to detail,” Dr. Andrews said. “On the body, look for expanding lesions with more raised peripheral edges, and central flattening, giving a classic annular appearance. It’s also important to inquire about family history and contacts including pets, contact sports/mat sports (think yoga, gymnastics, martial arts), or other contacts with similar rashes.” Work-up typically includes a fungal culture and starting empiric oral antifungal medications. “It is important to be able to distinguish scalp psoriasis from tinea capitis to prevent the more inflammatory form of tinea capitis, kerion (a deeper more symptomatic, painful and purulent dermatitis), which can lead to permanent scarring alopecia,” he said.
Bacterial infections can also mimic psoriasis, specifically nonbullous impetigo and ecthyma, the more ulcerative form of impetigo. The most frequent associations are group A Streptococcus, methicillin-susceptible Staphylococcus aureus and methicillin-resistant S. aureus.
Dr. Andrews closed his presentation by noting that tumor necrosis factor–alpha inhibitor–induced psoriasiform drug eruptions can occur in psoriasis-naive patients or unmask a predilection for psoriasis in patients with Crohn’s disease, juvenile idiopathic arthritis, or other autoinflammatory or autoimmune conditions. “They may improve with continued treatment and resolve with switching treatments,” he said. “Early biopsy in psoriasiform drug eruptions can appear like atopic dermatitis on pathology. When suspecting psoriasis in a pediatric patient, it is important to consider the history and physical exam as well as family history and associated comorbidities. While a biopsy may aide in the work-up, diagnosis can be made clinically.”
Dr. Andrews reported having no financial disclosures.
FROM PEDIATRIC DERMATOLOGY 2020
Expert shares his approach to treating warts in children
In the clinical experience of Anthony J. Mancini, MD, one option for children and adolescents who present with common warts is to do nothing, since they may resolve on their own.
“Many effective treatments that we have are painful and poorly tolerated, especially in younger children,” Dr. Mancini, professor of pediatrics and dermatology at Northwestern University, Chicago, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “However, while they’re harmless and often self-limited, warts often form a social stigma, and parents often desire therapy.”
Even though warts may spontaneously resolve in up to 65% of patients at 2 years and 80% at 4 years, the goals of treatment are to eradicate them, minimize pain, avoid scarring, and help prevent recurrence.
One effective topical therapy he highlighted is WartPEEL cream, which is a proprietary, compounded formulation of 17% salicylic acid and 2% 5-fluorouracil. “It’s in a sustained release vehicle called Remedium, and is available from a compounding pharmacy, but not FDA approved,” said Dr. Mancini, who is also head of pediatric dermatology at Lurie Children’s Hospital of Chicago. “It’s applied nightly with plastic tape occlusion and rinsed off each morning.”
WartPEEL is available through NuCara Pharmacy at 877-268-2272. It is not covered by most insurance plans and it costs around $80. “It is very effective, tends to be totally painless, and has a much quicker response than over-the-counter salicylic acid-based treatments for warts,” he said.
Another treatment option is oral cimetidine, especially in patients who have multiple or recalcitrant warts. The recommended dosing is 30-40 mg/kg per day, divided into twice-daily dosing. “You have to give it for at least 8-12 weeks to determine whether it’s working or not,” Dr. Mancini said. “In the initial report, [investigators] described an 81% complete response rate, but subsequent randomized, controlled trials were not able to confirm that data against placebo or topical treatments. I will say, though, that cimetidine is well tolerated. It’s always worth a try but, if you do use it, always consider other medications the patient may be taking and potential drug-drug interactions.”
For flat warts, verrucous papules that commonly occur on the face, Dr. Mancini recommends off-label treatment with 5% 5-fluorouracil cream (Efudex), which is normally indicated for actinic keratoses in adults. “I have patients apply this for 3 nights per week and work their way up gradually to nightly application,” he said. “It’s really important that parents and patients understand the importance of sun protection when they’re using Efudex, and they need to know that some irritation is possible. Overall, this treatment seems to be very well tolerated.”
Other treatment options for common warts, in addition to over-the-counter products that contain salicylic acid, are home cryotherapy kits that contain a mixture of diethyl ether and propane. “These can be effective for small warts,” Dr. Mancini said. “But for larger, thicker lesions, they’re not going to quite as effective.”
Treatment options best reserved for dermatologists, he continued, include in-office liquid nitrogen cryotherapy, “if it’s tolerated,” he said. “I have a no-hold policy, so if we have to hold a child down who’s flailing and crying and screaming during treatment, we’re probably not going to use liquid nitrogen.” He also mentioned topical immunotherapy with agents like squaric acid dibutylester. “This is almost like putting poison ivy on your warts to get the immune system revved up,” he said. “It can be very effective.” Other treatment options include intralesional immune therapy, topical cidofovir, and even pulsed-dye laser.
Dr. Mancini disclosed that he is a consultant to and a member of the scientific advisory board for Verrica Pharmaceuticals.
In the clinical experience of Anthony J. Mancini, MD, one option for children and adolescents who present with common warts is to do nothing, since they may resolve on their own.
“Many effective treatments that we have are painful and poorly tolerated, especially in younger children,” Dr. Mancini, professor of pediatrics and dermatology at Northwestern University, Chicago, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “However, while they’re harmless and often self-limited, warts often form a social stigma, and parents often desire therapy.”
Even though warts may spontaneously resolve in up to 65% of patients at 2 years and 80% at 4 years, the goals of treatment are to eradicate them, minimize pain, avoid scarring, and help prevent recurrence.
One effective topical therapy he highlighted is WartPEEL cream, which is a proprietary, compounded formulation of 17% salicylic acid and 2% 5-fluorouracil. “It’s in a sustained release vehicle called Remedium, and is available from a compounding pharmacy, but not FDA approved,” said Dr. Mancini, who is also head of pediatric dermatology at Lurie Children’s Hospital of Chicago. “It’s applied nightly with plastic tape occlusion and rinsed off each morning.”
WartPEEL is available through NuCara Pharmacy at 877-268-2272. It is not covered by most insurance plans and it costs around $80. “It is very effective, tends to be totally painless, and has a much quicker response than over-the-counter salicylic acid-based treatments for warts,” he said.
Another treatment option is oral cimetidine, especially in patients who have multiple or recalcitrant warts. The recommended dosing is 30-40 mg/kg per day, divided into twice-daily dosing. “You have to give it for at least 8-12 weeks to determine whether it’s working or not,” Dr. Mancini said. “In the initial report, [investigators] described an 81% complete response rate, but subsequent randomized, controlled trials were not able to confirm that data against placebo or topical treatments. I will say, though, that cimetidine is well tolerated. It’s always worth a try but, if you do use it, always consider other medications the patient may be taking and potential drug-drug interactions.”
For flat warts, verrucous papules that commonly occur on the face, Dr. Mancini recommends off-label treatment with 5% 5-fluorouracil cream (Efudex), which is normally indicated for actinic keratoses in adults. “I have patients apply this for 3 nights per week and work their way up gradually to nightly application,” he said. “It’s really important that parents and patients understand the importance of sun protection when they’re using Efudex, and they need to know that some irritation is possible. Overall, this treatment seems to be very well tolerated.”
Other treatment options for common warts, in addition to over-the-counter products that contain salicylic acid, are home cryotherapy kits that contain a mixture of diethyl ether and propane. “These can be effective for small warts,” Dr. Mancini said. “But for larger, thicker lesions, they’re not going to quite as effective.”
Treatment options best reserved for dermatologists, he continued, include in-office liquid nitrogen cryotherapy, “if it’s tolerated,” he said. “I have a no-hold policy, so if we have to hold a child down who’s flailing and crying and screaming during treatment, we’re probably not going to use liquid nitrogen.” He also mentioned topical immunotherapy with agents like squaric acid dibutylester. “This is almost like putting poison ivy on your warts to get the immune system revved up,” he said. “It can be very effective.” Other treatment options include intralesional immune therapy, topical cidofovir, and even pulsed-dye laser.
Dr. Mancini disclosed that he is a consultant to and a member of the scientific advisory board for Verrica Pharmaceuticals.
In the clinical experience of Anthony J. Mancini, MD, one option for children and adolescents who present with common warts is to do nothing, since they may resolve on their own.
“Many effective treatments that we have are painful and poorly tolerated, especially in younger children,” Dr. Mancini, professor of pediatrics and dermatology at Northwestern University, Chicago, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “However, while they’re harmless and often self-limited, warts often form a social stigma, and parents often desire therapy.”
Even though warts may spontaneously resolve in up to 65% of patients at 2 years and 80% at 4 years, the goals of treatment are to eradicate them, minimize pain, avoid scarring, and help prevent recurrence.
One effective topical therapy he highlighted is WartPEEL cream, which is a proprietary, compounded formulation of 17% salicylic acid and 2% 5-fluorouracil. “It’s in a sustained release vehicle called Remedium, and is available from a compounding pharmacy, but not FDA approved,” said Dr. Mancini, who is also head of pediatric dermatology at Lurie Children’s Hospital of Chicago. “It’s applied nightly with plastic tape occlusion and rinsed off each morning.”
WartPEEL is available through NuCara Pharmacy at 877-268-2272. It is not covered by most insurance plans and it costs around $80. “It is very effective, tends to be totally painless, and has a much quicker response than over-the-counter salicylic acid-based treatments for warts,” he said.
Another treatment option is oral cimetidine, especially in patients who have multiple or recalcitrant warts. The recommended dosing is 30-40 mg/kg per day, divided into twice-daily dosing. “You have to give it for at least 8-12 weeks to determine whether it’s working or not,” Dr. Mancini said. “In the initial report, [investigators] described an 81% complete response rate, but subsequent randomized, controlled trials were not able to confirm that data against placebo or topical treatments. I will say, though, that cimetidine is well tolerated. It’s always worth a try but, if you do use it, always consider other medications the patient may be taking and potential drug-drug interactions.”
For flat warts, verrucous papules that commonly occur on the face, Dr. Mancini recommends off-label treatment with 5% 5-fluorouracil cream (Efudex), which is normally indicated for actinic keratoses in adults. “I have patients apply this for 3 nights per week and work their way up gradually to nightly application,” he said. “It’s really important that parents and patients understand the importance of sun protection when they’re using Efudex, and they need to know that some irritation is possible. Overall, this treatment seems to be very well tolerated.”
Other treatment options for common warts, in addition to over-the-counter products that contain salicylic acid, are home cryotherapy kits that contain a mixture of diethyl ether and propane. “These can be effective for small warts,” Dr. Mancini said. “But for larger, thicker lesions, they’re not going to quite as effective.”
Treatment options best reserved for dermatologists, he continued, include in-office liquid nitrogen cryotherapy, “if it’s tolerated,” he said. “I have a no-hold policy, so if we have to hold a child down who’s flailing and crying and screaming during treatment, we’re probably not going to use liquid nitrogen.” He also mentioned topical immunotherapy with agents like squaric acid dibutylester. “This is almost like putting poison ivy on your warts to get the immune system revved up,” he said. “It can be very effective.” Other treatment options include intralesional immune therapy, topical cidofovir, and even pulsed-dye laser.
Dr. Mancini disclosed that he is a consultant to and a member of the scientific advisory board for Verrica Pharmaceuticals.
FROM PEDIATRIC DERMATOLOGY 2020
Treat acne aggressively upfront, expert advises
First, determine the types of lesions they have. “Do they have comedones, papules/pustules, and nodules present?” she asked during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. Second, quantify the number of lesions that they have. Is it few? Several? Many? Third, determine the extent of their acne. “Is it limited to half the face, or is it generalized to the face, back, chest, and shoulders?” added Dr. Zaenglein, professor of dermatology and pediatrics at Penn State University, Hershey.
Fourth, identify postinflammatory changes such as erythema, hyperpigmentation, and scarring “because that’s going to influence your management,” she said. “Finally, you want to give a quick investigative global assessment of the acne severity where you quantify them as being clear, almost clear, mild, moderate, or severe. You want to do this with each patient at every visit so you can determine what their initial treatment’s going to be and what their management going forward is going to be.”
According to Dr. Zaenglein, the best acne treatments are based on the pathogenesis of the skin condition and trying to target as many pathogenic factors as possible. The four main pathogenic factors in acne include hyperkeratinization, increased sebum production, cutibacterium, and inflammation. “This is not a stepwise process; there’s an interplay between all of those factors,” she said. “All acne is inflammatory, but each of the treatments we have target specific factors. Retinoids target hyperkeratinization and inflammation, whereas the hormonal therapies will address decreased sebum production. Antimicrobial agents like benzoyl peroxide and antibiotics will work to decrease cutibacterium acnes. All of these are influenced by the exposome. This includes your genetics, external factors like pollution or changes in seasons that can affect your skin and the severity of your acne.” A state of hyperandrogenism, she added, “can definitely increase acne” and is seen in patients with polycystic ovary syndrome (PCOS).
For patients with mild acne, initial treatment should consist of a topical retinoid and, almost always, benzoyl peroxide, “unless it’s a pure comedonal form of acne,” Dr. Zaenglein said. She recommended using the combination of a topical retinoid and benzoyl peroxide, noting that while it used to be difficult to find benzoyl peroxide, “nowadays there are numerous manufacturers and different formulations of benzoyl peroxide. We also have over-the-counter adapalene now, which is great. So now we have a complete routine for patients with adapalene and benzoyl peroxide that you can combine together in a cost-effective way.”
If the initial regimen fails to improve the patient’s mild acne, a second-line treatment would be to change the retinoid and continue on the existing benzoyl peroxide formulation or to add dapsone gel if the patient is experiencing skin irritation. The four retinoids currently available include adapalene, tretinoin, tazarotene, and trifarotene. “These normalize keratinocyte differentiation, reduce keratinocyte proliferation, and decrease expression of inflammatory markers,” Dr. Zaenglein noted. “They also prevent scarring. Adapalene is considered to be the most tolerable, whereas tazarotene may have an edge on efficacy. There’s a lot of overlap; head-to-head studies may not always match them up exactly, but generally this is how it’s considered. Picking the right retinoid for your patient based on efficacy and tolerability is most important.”
The newest topical retinoid, trifarotene 50 mcg/g cream, is a fourth-generation retinoid which is retinoic acid receptor gamma selective. Pivotal trials were conducted in patients aged 9 years and older with moderate facial and truncal acne. With monotherapy there was a success rate of 36% at 12 weeks and 60% at 52 weeks based on the Investigator’s Global Assessment. Another newcomer, tazarotene 0.045% lotion, is a third-generation retinoid which is retinoic acid receptor alpha beta gamma selective. It’s approved for moderate to severe facial acne in patients 9 years and older.
To optimize tolerance to retinoids, Dr. Zaenglein asks patients about their typical skin care regimen. “I ask them what they’re washing their face with,” she said. “Are they using apricot scrubs or harsh cleansers? Make sure they’re applying it to the entire face and not spot-treating. You get less irritation when it’s applied to dry skin, so you can recommend that. Make sure that they use a bland unscented moisturizer in the morning and apply it over top of their retinoid. I always warn them that irritation usually peaks at about 2 weeks. If they can power through, the irritation will improve with continued use.”
To optimize adherence to retinoids, she asks patients how many nights per week that they apply it. If they are using it all seven nights, “they’re good at using it,” she said. “If they say three nights, then they need to work on getting it on more frequently.”
Topical dapsone gel (5% and 7.5%) is mainly used for patients with papular-pustular acne. “Its mechanism of action for acne is not known, but presumptively it’s anti-inflammatory,” Dr. Zaenglein said. “It doesn’t require G6PD [glucose-6-phosphate dehydrogenase] testing. It can cause some orange discoloration of your skin or fabrics if you use it with benzoyl peroxide, so you want to apply them at different times of the day. It’s well tolerated. I tend to use it in patients who have problems tolerating any topical retinoid or any benzoyl peroxide but have mild to moderate acne.”
For patients with moderate acne, consider combination therapy to target as many pathogenic factors as possible. “Use a topical retinoid plus benzoyl peroxide with or without a systemic antibiotic,” Dr. Zaenglein advised. “I may give them an oral antibiotic if their acne is not responsive to the routine. But you wouldn’t want to combine the systemic antibiotic with a topical antibiotic, like clindamycin with doxycycline, because you don’t need two antibiotics. Make sure that you treat aggressively up front. It can take up to 3 months to see improvement. I counsel my patients that we’ll rescue with the antibiotic and then we maintain, but we’re going to stop that antibiotic after 3 months.”
Systemic antibiotic options for acne include tetracyclines, doxycycline, minocycline, and sarecycline. “Tetracycline itself we don’t use too much because you have to take it on an empty stomach, and availability is sometimes an issue,” she said. “Primarily, we use doxycycline. You can take it with food, so that helps. The main side effects are gastrointestinal upset and photosensitivity. Alternately, you can use minocycline, which is also okay to take with food. It does have more potentially worrisome side effects, including pseudotumor cerebri, blue pigmentation, autoimmune hepatitis, and DRESS [drug reaction with eosinophilia and systemic symptoms].”
Sarecycline is the first narrow spectrum tetracycline for acne, with fewer vestibular and phototoxic side effects, compared with other tetracyclines. “It also has less effect on the GI flora,” Dr. Zaenglein said. “It’s a good alternative but it can be costly, so make sure to check the pricing for your patients.” She does not use other antibiotics such as TMP/SMX, penicillins, or cephalosporins for acne patients. “The reason is, the tetracyclines are not only antibacterial, but they’re anti-inflammatory,” she explained. “They also are lipophilic, so they will penetrate into the sebaceous unit where the heart of the acne is.”
For patients who don’t want to take an oral antibiotic, consider minocycline 4% foam, which was studied in moderate to severe acne in patients aged 9 years and older. The pooled results from the three studies showed a 47% mean improvement in inflammatory acne, compared with 37% among those in the vehicle arm. “You wouldn’t use this as monotherapy; you’d use this in combination with the topical retinoid and the benzoyl peroxide,” Dr. Zaenglein said.
Most primary care providers do not prescribe isotretinoin for patients with severe acne, but they can start patients on triple therapy with a topical retinoid, benzoyl peroxide, and a systemic antibiotic at its full dose. “The efficacy of triple therapy in patients you would typically deem as isotretinoin worthy is actually pretty good,” she said. “There have been several studies looking at this, and about 70%-80% of patients will respond to triple therapy, where they are no longer deemed isotretinoin candidates. They still may need to move on to isotretinoin, but they will be improved.”
Dr. Zaenglein disclosed that she is a consultant for Cassiopea, Novartis, and Pfizer. She has also received grants or research support from AbbVie, Incyte, and Pfizer.
First, determine the types of lesions they have. “Do they have comedones, papules/pustules, and nodules present?” she asked during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. Second, quantify the number of lesions that they have. Is it few? Several? Many? Third, determine the extent of their acne. “Is it limited to half the face, or is it generalized to the face, back, chest, and shoulders?” added Dr. Zaenglein, professor of dermatology and pediatrics at Penn State University, Hershey.
Fourth, identify postinflammatory changes such as erythema, hyperpigmentation, and scarring “because that’s going to influence your management,” she said. “Finally, you want to give a quick investigative global assessment of the acne severity where you quantify them as being clear, almost clear, mild, moderate, or severe. You want to do this with each patient at every visit so you can determine what their initial treatment’s going to be and what their management going forward is going to be.”
According to Dr. Zaenglein, the best acne treatments are based on the pathogenesis of the skin condition and trying to target as many pathogenic factors as possible. The four main pathogenic factors in acne include hyperkeratinization, increased sebum production, cutibacterium, and inflammation. “This is not a stepwise process; there’s an interplay between all of those factors,” she said. “All acne is inflammatory, but each of the treatments we have target specific factors. Retinoids target hyperkeratinization and inflammation, whereas the hormonal therapies will address decreased sebum production. Antimicrobial agents like benzoyl peroxide and antibiotics will work to decrease cutibacterium acnes. All of these are influenced by the exposome. This includes your genetics, external factors like pollution or changes in seasons that can affect your skin and the severity of your acne.” A state of hyperandrogenism, she added, “can definitely increase acne” and is seen in patients with polycystic ovary syndrome (PCOS).
For patients with mild acne, initial treatment should consist of a topical retinoid and, almost always, benzoyl peroxide, “unless it’s a pure comedonal form of acne,” Dr. Zaenglein said. She recommended using the combination of a topical retinoid and benzoyl peroxide, noting that while it used to be difficult to find benzoyl peroxide, “nowadays there are numerous manufacturers and different formulations of benzoyl peroxide. We also have over-the-counter adapalene now, which is great. So now we have a complete routine for patients with adapalene and benzoyl peroxide that you can combine together in a cost-effective way.”
If the initial regimen fails to improve the patient’s mild acne, a second-line treatment would be to change the retinoid and continue on the existing benzoyl peroxide formulation or to add dapsone gel if the patient is experiencing skin irritation. The four retinoids currently available include adapalene, tretinoin, tazarotene, and trifarotene. “These normalize keratinocyte differentiation, reduce keratinocyte proliferation, and decrease expression of inflammatory markers,” Dr. Zaenglein noted. “They also prevent scarring. Adapalene is considered to be the most tolerable, whereas tazarotene may have an edge on efficacy. There’s a lot of overlap; head-to-head studies may not always match them up exactly, but generally this is how it’s considered. Picking the right retinoid for your patient based on efficacy and tolerability is most important.”
The newest topical retinoid, trifarotene 50 mcg/g cream, is a fourth-generation retinoid which is retinoic acid receptor gamma selective. Pivotal trials were conducted in patients aged 9 years and older with moderate facial and truncal acne. With monotherapy there was a success rate of 36% at 12 weeks and 60% at 52 weeks based on the Investigator’s Global Assessment. Another newcomer, tazarotene 0.045% lotion, is a third-generation retinoid which is retinoic acid receptor alpha beta gamma selective. It’s approved for moderate to severe facial acne in patients 9 years and older.
To optimize tolerance to retinoids, Dr. Zaenglein asks patients about their typical skin care regimen. “I ask them what they’re washing their face with,” she said. “Are they using apricot scrubs or harsh cleansers? Make sure they’re applying it to the entire face and not spot-treating. You get less irritation when it’s applied to dry skin, so you can recommend that. Make sure that they use a bland unscented moisturizer in the morning and apply it over top of their retinoid. I always warn them that irritation usually peaks at about 2 weeks. If they can power through, the irritation will improve with continued use.”
To optimize adherence to retinoids, she asks patients how many nights per week that they apply it. If they are using it all seven nights, “they’re good at using it,” she said. “If they say three nights, then they need to work on getting it on more frequently.”
Topical dapsone gel (5% and 7.5%) is mainly used for patients with papular-pustular acne. “Its mechanism of action for acne is not known, but presumptively it’s anti-inflammatory,” Dr. Zaenglein said. “It doesn’t require G6PD [glucose-6-phosphate dehydrogenase] testing. It can cause some orange discoloration of your skin or fabrics if you use it with benzoyl peroxide, so you want to apply them at different times of the day. It’s well tolerated. I tend to use it in patients who have problems tolerating any topical retinoid or any benzoyl peroxide but have mild to moderate acne.”
For patients with moderate acne, consider combination therapy to target as many pathogenic factors as possible. “Use a topical retinoid plus benzoyl peroxide with or without a systemic antibiotic,” Dr. Zaenglein advised. “I may give them an oral antibiotic if their acne is not responsive to the routine. But you wouldn’t want to combine the systemic antibiotic with a topical antibiotic, like clindamycin with doxycycline, because you don’t need two antibiotics. Make sure that you treat aggressively up front. It can take up to 3 months to see improvement. I counsel my patients that we’ll rescue with the antibiotic and then we maintain, but we’re going to stop that antibiotic after 3 months.”
Systemic antibiotic options for acne include tetracyclines, doxycycline, minocycline, and sarecycline. “Tetracycline itself we don’t use too much because you have to take it on an empty stomach, and availability is sometimes an issue,” she said. “Primarily, we use doxycycline. You can take it with food, so that helps. The main side effects are gastrointestinal upset and photosensitivity. Alternately, you can use minocycline, which is also okay to take with food. It does have more potentially worrisome side effects, including pseudotumor cerebri, blue pigmentation, autoimmune hepatitis, and DRESS [drug reaction with eosinophilia and systemic symptoms].”
Sarecycline is the first narrow spectrum tetracycline for acne, with fewer vestibular and phototoxic side effects, compared with other tetracyclines. “It also has less effect on the GI flora,” Dr. Zaenglein said. “It’s a good alternative but it can be costly, so make sure to check the pricing for your patients.” She does not use other antibiotics such as TMP/SMX, penicillins, or cephalosporins for acne patients. “The reason is, the tetracyclines are not only antibacterial, but they’re anti-inflammatory,” she explained. “They also are lipophilic, so they will penetrate into the sebaceous unit where the heart of the acne is.”
For patients who don’t want to take an oral antibiotic, consider minocycline 4% foam, which was studied in moderate to severe acne in patients aged 9 years and older. The pooled results from the three studies showed a 47% mean improvement in inflammatory acne, compared with 37% among those in the vehicle arm. “You wouldn’t use this as monotherapy; you’d use this in combination with the topical retinoid and the benzoyl peroxide,” Dr. Zaenglein said.
Most primary care providers do not prescribe isotretinoin for patients with severe acne, but they can start patients on triple therapy with a topical retinoid, benzoyl peroxide, and a systemic antibiotic at its full dose. “The efficacy of triple therapy in patients you would typically deem as isotretinoin worthy is actually pretty good,” she said. “There have been several studies looking at this, and about 70%-80% of patients will respond to triple therapy, where they are no longer deemed isotretinoin candidates. They still may need to move on to isotretinoin, but they will be improved.”
Dr. Zaenglein disclosed that she is a consultant for Cassiopea, Novartis, and Pfizer. She has also received grants or research support from AbbVie, Incyte, and Pfizer.
First, determine the types of lesions they have. “Do they have comedones, papules/pustules, and nodules present?” she asked during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. Second, quantify the number of lesions that they have. Is it few? Several? Many? Third, determine the extent of their acne. “Is it limited to half the face, or is it generalized to the face, back, chest, and shoulders?” added Dr. Zaenglein, professor of dermatology and pediatrics at Penn State University, Hershey.
Fourth, identify postinflammatory changes such as erythema, hyperpigmentation, and scarring “because that’s going to influence your management,” she said. “Finally, you want to give a quick investigative global assessment of the acne severity where you quantify them as being clear, almost clear, mild, moderate, or severe. You want to do this with each patient at every visit so you can determine what their initial treatment’s going to be and what their management going forward is going to be.”
According to Dr. Zaenglein, the best acne treatments are based on the pathogenesis of the skin condition and trying to target as many pathogenic factors as possible. The four main pathogenic factors in acne include hyperkeratinization, increased sebum production, cutibacterium, and inflammation. “This is not a stepwise process; there’s an interplay between all of those factors,” she said. “All acne is inflammatory, but each of the treatments we have target specific factors. Retinoids target hyperkeratinization and inflammation, whereas the hormonal therapies will address decreased sebum production. Antimicrobial agents like benzoyl peroxide and antibiotics will work to decrease cutibacterium acnes. All of these are influenced by the exposome. This includes your genetics, external factors like pollution or changes in seasons that can affect your skin and the severity of your acne.” A state of hyperandrogenism, she added, “can definitely increase acne” and is seen in patients with polycystic ovary syndrome (PCOS).
For patients with mild acne, initial treatment should consist of a topical retinoid and, almost always, benzoyl peroxide, “unless it’s a pure comedonal form of acne,” Dr. Zaenglein said. She recommended using the combination of a topical retinoid and benzoyl peroxide, noting that while it used to be difficult to find benzoyl peroxide, “nowadays there are numerous manufacturers and different formulations of benzoyl peroxide. We also have over-the-counter adapalene now, which is great. So now we have a complete routine for patients with adapalene and benzoyl peroxide that you can combine together in a cost-effective way.”
If the initial regimen fails to improve the patient’s mild acne, a second-line treatment would be to change the retinoid and continue on the existing benzoyl peroxide formulation or to add dapsone gel if the patient is experiencing skin irritation. The four retinoids currently available include adapalene, tretinoin, tazarotene, and trifarotene. “These normalize keratinocyte differentiation, reduce keratinocyte proliferation, and decrease expression of inflammatory markers,” Dr. Zaenglein noted. “They also prevent scarring. Adapalene is considered to be the most tolerable, whereas tazarotene may have an edge on efficacy. There’s a lot of overlap; head-to-head studies may not always match them up exactly, but generally this is how it’s considered. Picking the right retinoid for your patient based on efficacy and tolerability is most important.”
The newest topical retinoid, trifarotene 50 mcg/g cream, is a fourth-generation retinoid which is retinoic acid receptor gamma selective. Pivotal trials were conducted in patients aged 9 years and older with moderate facial and truncal acne. With monotherapy there was a success rate of 36% at 12 weeks and 60% at 52 weeks based on the Investigator’s Global Assessment. Another newcomer, tazarotene 0.045% lotion, is a third-generation retinoid which is retinoic acid receptor alpha beta gamma selective. It’s approved for moderate to severe facial acne in patients 9 years and older.
To optimize tolerance to retinoids, Dr. Zaenglein asks patients about their typical skin care regimen. “I ask them what they’re washing their face with,” she said. “Are they using apricot scrubs or harsh cleansers? Make sure they’re applying it to the entire face and not spot-treating. You get less irritation when it’s applied to dry skin, so you can recommend that. Make sure that they use a bland unscented moisturizer in the morning and apply it over top of their retinoid. I always warn them that irritation usually peaks at about 2 weeks. If they can power through, the irritation will improve with continued use.”
To optimize adherence to retinoids, she asks patients how many nights per week that they apply it. If they are using it all seven nights, “they’re good at using it,” she said. “If they say three nights, then they need to work on getting it on more frequently.”
Topical dapsone gel (5% and 7.5%) is mainly used for patients with papular-pustular acne. “Its mechanism of action for acne is not known, but presumptively it’s anti-inflammatory,” Dr. Zaenglein said. “It doesn’t require G6PD [glucose-6-phosphate dehydrogenase] testing. It can cause some orange discoloration of your skin or fabrics if you use it with benzoyl peroxide, so you want to apply them at different times of the day. It’s well tolerated. I tend to use it in patients who have problems tolerating any topical retinoid or any benzoyl peroxide but have mild to moderate acne.”
For patients with moderate acne, consider combination therapy to target as many pathogenic factors as possible. “Use a topical retinoid plus benzoyl peroxide with or without a systemic antibiotic,” Dr. Zaenglein advised. “I may give them an oral antibiotic if their acne is not responsive to the routine. But you wouldn’t want to combine the systemic antibiotic with a topical antibiotic, like clindamycin with doxycycline, because you don’t need two antibiotics. Make sure that you treat aggressively up front. It can take up to 3 months to see improvement. I counsel my patients that we’ll rescue with the antibiotic and then we maintain, but we’re going to stop that antibiotic after 3 months.”
Systemic antibiotic options for acne include tetracyclines, doxycycline, minocycline, and sarecycline. “Tetracycline itself we don’t use too much because you have to take it on an empty stomach, and availability is sometimes an issue,” she said. “Primarily, we use doxycycline. You can take it with food, so that helps. The main side effects are gastrointestinal upset and photosensitivity. Alternately, you can use minocycline, which is also okay to take with food. It does have more potentially worrisome side effects, including pseudotumor cerebri, blue pigmentation, autoimmune hepatitis, and DRESS [drug reaction with eosinophilia and systemic symptoms].”
Sarecycline is the first narrow spectrum tetracycline for acne, with fewer vestibular and phototoxic side effects, compared with other tetracyclines. “It also has less effect on the GI flora,” Dr. Zaenglein said. “It’s a good alternative but it can be costly, so make sure to check the pricing for your patients.” She does not use other antibiotics such as TMP/SMX, penicillins, or cephalosporins for acne patients. “The reason is, the tetracyclines are not only antibacterial, but they’re anti-inflammatory,” she explained. “They also are lipophilic, so they will penetrate into the sebaceous unit where the heart of the acne is.”
For patients who don’t want to take an oral antibiotic, consider minocycline 4% foam, which was studied in moderate to severe acne in patients aged 9 years and older. The pooled results from the three studies showed a 47% mean improvement in inflammatory acne, compared with 37% among those in the vehicle arm. “You wouldn’t use this as monotherapy; you’d use this in combination with the topical retinoid and the benzoyl peroxide,” Dr. Zaenglein said.
Most primary care providers do not prescribe isotretinoin for patients with severe acne, but they can start patients on triple therapy with a topical retinoid, benzoyl peroxide, and a systemic antibiotic at its full dose. “The efficacy of triple therapy in patients you would typically deem as isotretinoin worthy is actually pretty good,” she said. “There have been several studies looking at this, and about 70%-80% of patients will respond to triple therapy, where they are no longer deemed isotretinoin candidates. They still may need to move on to isotretinoin, but they will be improved.”
Dr. Zaenglein disclosed that she is a consultant for Cassiopea, Novartis, and Pfizer. She has also received grants or research support from AbbVie, Incyte, and Pfizer.
FROM PEDIATRIC DERMATOLOGY 2020
Phase 3 COVID-19 vaccine trials launching in July, expert says
The race to develop a SARS-CoV-2 vaccine is unlike any other global research and development effort in modern medicine.
According to Paul A. Offit, MD, there are now 120 Investigational New Drug applications to the Food and Drug Administration for these vaccines, and researchers at more than 70 companies across the globe are interested in making a vaccine. The Biomedical Advanced Research and Development Authority (BARDA) has awarded $2.5 billion to five different pharmaceutical companies to make a vaccine.
“The good news is that the new coronavirus is relatively stable,” Dr. Offit, director of the Vaccine Education Center at the Children’s Hospital of Philadelphia, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “Although it is a single-stranded RNA virus, it does mutate to some extent, but it doesn’t look like it’s going to mutate away from the vaccine. So, this is not going to be like influenza virus, where you must give a vaccine every year. I think we can make a vaccine that will last for several years. And we know the protein we’re interested in. We’re interested in antibodies directed against the spike glycoprotein, which is abundantly present on the surface of the virus. We know that if we make an antibody response to that protein, we can therefore prevent infection.”
Some research groups are interested in developing a whole, killed virus like those used in the inactivated polio vaccine, and vaccines for hepatitis A virus and rabies, said Dr. Offit, who is a member of Accelerating COVID-19 Technical Innovations And Vaccines, a public-private partnership formed by the National Institutes of Health. Other groups are interested in making a live-attenuated vaccine like those for measles, mumps, and rubella. “Some are interested in using a vectored vaccine, where you take a virus that is relatively weak and doesn’t cause disease in people, like vesicular stomatitis virus, and then clone into that the gene that codes for this coronavirus spike protein, which is the way that we made the Ebola virus vaccine,” Dr. Offit said. “Those approaches have all been used before, with success.”
Novel approaches are also being employed to make this vaccine, including using a replication-defective adenovirus. “That means that the virus can’t reproduce itself, but it can make proteins,” he explained. “There are some proteins that are made, but most aren’t. Therefore, the virus can’t reproduce itself. We’ll see whether or not that [approach] works, but it’s never been used before.”
Another approach is to inject messenger RNA that codes for the coronavirus spike protein, where that genetic material is translated into the spike protein. The other platform being evaluated is a DNA vaccine, in which “you give DNA which is coded for that spike protein, which is transcribed to messenger RNA and then is translated to other proteins.”
Typical vaccine development involves animal models to prove the concept, dose-ranging studies in humans, and progressively larger safety and immunogenicity studies in hundreds of thousands of people. Next come phase 3 studies, “where the proof is in the pudding,” he said. “These are large, prospective placebo-controlled trials to prove that the vaccine is safe. This is the only way whether you can prove or not a vaccine is effective.”
“Some companies may branch out on their own and do smaller studies than that,” he said. “We’ll see how this plays out. Keep your eyes open for that, because you really want to make sure you have a fairly large phase 3 trial. That’s the best way to show whether something works and whether it’s safe.”
The tried and true vaccines that emerge from the effort will not be FDA-licensed products. Rather, they will be approved products under the Emergency Use Authorization program. “Ever since the 1950s, every vaccine that has been used in the U.S. has been under the auspices of FDA licensure,” said Dr. Offit, who is also professor of pediatrics and the Maurice R. Hilleman professor of vaccinology at the University of Pennsylvania, Philadelphia. “That’s not going to be true here. The FDA is involved every step of the way but here they have a somewhat lighter touch.”
A few candidate vaccines are being mass-produced at risk, “meaning they’re being produced not knowing whether these vaccines are safe and effective yet or not,” he said. “But when they’re shown in a phase 3 trial to be safe and effective, you will have already produced it, and then it’s much easier to roll it out to the general public the minute you’ve shown that it works. This is what we did for the polio vaccine back in the 1950s. We mass-produced that vaccine at risk.”
Dr. Offit emphasized the importance of managing expectations once a COVID-19 vaccine gets approved for use. “Regarding safety, these vaccines will be tested in tens of thousands of people, not tens of millions of people, so although you can disprove a relatively uncommon side effect preapproval, you’re not going to disprove a rare side effect preapproval. You’re only going to know that post approval. I think we need to make people aware of that and to let them know that through groups like the Vaccine Safety Datalink, we’re going to be monitoring these vaccines once they’re approved.”
Regarding efficacy, he continued, “we’re not going know about the rates of immunity initially; we’re only going to know about that after the vaccine [has been administered]. My guess is the protection is going to be short lived and incomplete. By short lived, I mean that protection would last for years but not decades. By incomplete, I mean that protection will be against moderate to severe disease, which is fine. You don’t need protection against all of the disease; it’s hard to do that with respiratory viruses. That means you can keep people out of the hospital, and you can keep them from dying. That’s the main goal.”
Dr. Offit closed his remarks by noting that much is at stake in this effort to develop a vaccine so quickly and that it “could go one of two ways. We could find that the vaccine is a lifesaver, and [that] we can finally end this awful pandemic. Or, if we cut corners and don’t prove that the vaccines are safe and effective as we should before they’re released, we could shake what is a fragile vaccine confidence in this country. Hopefully, it doesn’t play out that way.”
The race to develop a SARS-CoV-2 vaccine is unlike any other global research and development effort in modern medicine.
According to Paul A. Offit, MD, there are now 120 Investigational New Drug applications to the Food and Drug Administration for these vaccines, and researchers at more than 70 companies across the globe are interested in making a vaccine. The Biomedical Advanced Research and Development Authority (BARDA) has awarded $2.5 billion to five different pharmaceutical companies to make a vaccine.
“The good news is that the new coronavirus is relatively stable,” Dr. Offit, director of the Vaccine Education Center at the Children’s Hospital of Philadelphia, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “Although it is a single-stranded RNA virus, it does mutate to some extent, but it doesn’t look like it’s going to mutate away from the vaccine. So, this is not going to be like influenza virus, where you must give a vaccine every year. I think we can make a vaccine that will last for several years. And we know the protein we’re interested in. We’re interested in antibodies directed against the spike glycoprotein, which is abundantly present on the surface of the virus. We know that if we make an antibody response to that protein, we can therefore prevent infection.”
Some research groups are interested in developing a whole, killed virus like those used in the inactivated polio vaccine, and vaccines for hepatitis A virus and rabies, said Dr. Offit, who is a member of Accelerating COVID-19 Technical Innovations And Vaccines, a public-private partnership formed by the National Institutes of Health. Other groups are interested in making a live-attenuated vaccine like those for measles, mumps, and rubella. “Some are interested in using a vectored vaccine, where you take a virus that is relatively weak and doesn’t cause disease in people, like vesicular stomatitis virus, and then clone into that the gene that codes for this coronavirus spike protein, which is the way that we made the Ebola virus vaccine,” Dr. Offit said. “Those approaches have all been used before, with success.”
Novel approaches are also being employed to make this vaccine, including using a replication-defective adenovirus. “That means that the virus can’t reproduce itself, but it can make proteins,” he explained. “There are some proteins that are made, but most aren’t. Therefore, the virus can’t reproduce itself. We’ll see whether or not that [approach] works, but it’s never been used before.”
Another approach is to inject messenger RNA that codes for the coronavirus spike protein, where that genetic material is translated into the spike protein. The other platform being evaluated is a DNA vaccine, in which “you give DNA which is coded for that spike protein, which is transcribed to messenger RNA and then is translated to other proteins.”
Typical vaccine development involves animal models to prove the concept, dose-ranging studies in humans, and progressively larger safety and immunogenicity studies in hundreds of thousands of people. Next come phase 3 studies, “where the proof is in the pudding,” he said. “These are large, prospective placebo-controlled trials to prove that the vaccine is safe. This is the only way whether you can prove or not a vaccine is effective.”
“Some companies may branch out on their own and do smaller studies than that,” he said. “We’ll see how this plays out. Keep your eyes open for that, because you really want to make sure you have a fairly large phase 3 trial. That’s the best way to show whether something works and whether it’s safe.”
The tried and true vaccines that emerge from the effort will not be FDA-licensed products. Rather, they will be approved products under the Emergency Use Authorization program. “Ever since the 1950s, every vaccine that has been used in the U.S. has been under the auspices of FDA licensure,” said Dr. Offit, who is also professor of pediatrics and the Maurice R. Hilleman professor of vaccinology at the University of Pennsylvania, Philadelphia. “That’s not going to be true here. The FDA is involved every step of the way but here they have a somewhat lighter touch.”
A few candidate vaccines are being mass-produced at risk, “meaning they’re being produced not knowing whether these vaccines are safe and effective yet or not,” he said. “But when they’re shown in a phase 3 trial to be safe and effective, you will have already produced it, and then it’s much easier to roll it out to the general public the minute you’ve shown that it works. This is what we did for the polio vaccine back in the 1950s. We mass-produced that vaccine at risk.”
Dr. Offit emphasized the importance of managing expectations once a COVID-19 vaccine gets approved for use. “Regarding safety, these vaccines will be tested in tens of thousands of people, not tens of millions of people, so although you can disprove a relatively uncommon side effect preapproval, you’re not going to disprove a rare side effect preapproval. You’re only going to know that post approval. I think we need to make people aware of that and to let them know that through groups like the Vaccine Safety Datalink, we’re going to be monitoring these vaccines once they’re approved.”
Regarding efficacy, he continued, “we’re not going know about the rates of immunity initially; we’re only going to know about that after the vaccine [has been administered]. My guess is the protection is going to be short lived and incomplete. By short lived, I mean that protection would last for years but not decades. By incomplete, I mean that protection will be against moderate to severe disease, which is fine. You don’t need protection against all of the disease; it’s hard to do that with respiratory viruses. That means you can keep people out of the hospital, and you can keep them from dying. That’s the main goal.”
Dr. Offit closed his remarks by noting that much is at stake in this effort to develop a vaccine so quickly and that it “could go one of two ways. We could find that the vaccine is a lifesaver, and [that] we can finally end this awful pandemic. Or, if we cut corners and don’t prove that the vaccines are safe and effective as we should before they’re released, we could shake what is a fragile vaccine confidence in this country. Hopefully, it doesn’t play out that way.”
The race to develop a SARS-CoV-2 vaccine is unlike any other global research and development effort in modern medicine.
According to Paul A. Offit, MD, there are now 120 Investigational New Drug applications to the Food and Drug Administration for these vaccines, and researchers at more than 70 companies across the globe are interested in making a vaccine. The Biomedical Advanced Research and Development Authority (BARDA) has awarded $2.5 billion to five different pharmaceutical companies to make a vaccine.
“The good news is that the new coronavirus is relatively stable,” Dr. Offit, director of the Vaccine Education Center at the Children’s Hospital of Philadelphia, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “Although it is a single-stranded RNA virus, it does mutate to some extent, but it doesn’t look like it’s going to mutate away from the vaccine. So, this is not going to be like influenza virus, where you must give a vaccine every year. I think we can make a vaccine that will last for several years. And we know the protein we’re interested in. We’re interested in antibodies directed against the spike glycoprotein, which is abundantly present on the surface of the virus. We know that if we make an antibody response to that protein, we can therefore prevent infection.”
Some research groups are interested in developing a whole, killed virus like those used in the inactivated polio vaccine, and vaccines for hepatitis A virus and rabies, said Dr. Offit, who is a member of Accelerating COVID-19 Technical Innovations And Vaccines, a public-private partnership formed by the National Institutes of Health. Other groups are interested in making a live-attenuated vaccine like those for measles, mumps, and rubella. “Some are interested in using a vectored vaccine, where you take a virus that is relatively weak and doesn’t cause disease in people, like vesicular stomatitis virus, and then clone into that the gene that codes for this coronavirus spike protein, which is the way that we made the Ebola virus vaccine,” Dr. Offit said. “Those approaches have all been used before, with success.”
Novel approaches are also being employed to make this vaccine, including using a replication-defective adenovirus. “That means that the virus can’t reproduce itself, but it can make proteins,” he explained. “There are some proteins that are made, but most aren’t. Therefore, the virus can’t reproduce itself. We’ll see whether or not that [approach] works, but it’s never been used before.”
Another approach is to inject messenger RNA that codes for the coronavirus spike protein, where that genetic material is translated into the spike protein. The other platform being evaluated is a DNA vaccine, in which “you give DNA which is coded for that spike protein, which is transcribed to messenger RNA and then is translated to other proteins.”
Typical vaccine development involves animal models to prove the concept, dose-ranging studies in humans, and progressively larger safety and immunogenicity studies in hundreds of thousands of people. Next come phase 3 studies, “where the proof is in the pudding,” he said. “These are large, prospective placebo-controlled trials to prove that the vaccine is safe. This is the only way whether you can prove or not a vaccine is effective.”
“Some companies may branch out on their own and do smaller studies than that,” he said. “We’ll see how this plays out. Keep your eyes open for that, because you really want to make sure you have a fairly large phase 3 trial. That’s the best way to show whether something works and whether it’s safe.”
The tried and true vaccines that emerge from the effort will not be FDA-licensed products. Rather, they will be approved products under the Emergency Use Authorization program. “Ever since the 1950s, every vaccine that has been used in the U.S. has been under the auspices of FDA licensure,” said Dr. Offit, who is also professor of pediatrics and the Maurice R. Hilleman professor of vaccinology at the University of Pennsylvania, Philadelphia. “That’s not going to be true here. The FDA is involved every step of the way but here they have a somewhat lighter touch.”
A few candidate vaccines are being mass-produced at risk, “meaning they’re being produced not knowing whether these vaccines are safe and effective yet or not,” he said. “But when they’re shown in a phase 3 trial to be safe and effective, you will have already produced it, and then it’s much easier to roll it out to the general public the minute you’ve shown that it works. This is what we did for the polio vaccine back in the 1950s. We mass-produced that vaccine at risk.”
Dr. Offit emphasized the importance of managing expectations once a COVID-19 vaccine gets approved for use. “Regarding safety, these vaccines will be tested in tens of thousands of people, not tens of millions of people, so although you can disprove a relatively uncommon side effect preapproval, you’re not going to disprove a rare side effect preapproval. You’re only going to know that post approval. I think we need to make people aware of that and to let them know that through groups like the Vaccine Safety Datalink, we’re going to be monitoring these vaccines once they’re approved.”
Regarding efficacy, he continued, “we’re not going know about the rates of immunity initially; we’re only going to know about that after the vaccine [has been administered]. My guess is the protection is going to be short lived and incomplete. By short lived, I mean that protection would last for years but not decades. By incomplete, I mean that protection will be against moderate to severe disease, which is fine. You don’t need protection against all of the disease; it’s hard to do that with respiratory viruses. That means you can keep people out of the hospital, and you can keep them from dying. That’s the main goal.”
Dr. Offit closed his remarks by noting that much is at stake in this effort to develop a vaccine so quickly and that it “could go one of two ways. We could find that the vaccine is a lifesaver, and [that] we can finally end this awful pandemic. Or, if we cut corners and don’t prove that the vaccines are safe and effective as we should before they’re released, we could shake what is a fragile vaccine confidence in this country. Hopefully, it doesn’t play out that way.”
FROM PEDIATRIC DERMATOLOGY 2020