Dermatology

A 9-day-old boy was brought to the emergency department by his mother. The infant had been doing well until his most recent diaper change when his mother noticed a rash around the umbilicus (FIGURE), genitalia, and anus.

The infant was born at term via spontaneous vaginal delivery. The pregnancy was uncomplicated; the infant’s mother was group B strep negative. Following a routine postpartum course, the infant underwent an elective circumcision before hospital discharge on his second day of life. There were no interval reports of irritability, poor feeding, fevers, vomiting, or changes in urine or stool output.

The mother denied any recent unusual exposures, sick contacts, or travel. However, upon further questioning, the mother noted that she herself had several small open wounds on the torso that she attributed to untreated methicillin-resistant Staphylococcus aureus (MRSA).

On physical examination, the infant was overall well-appearing and was breastfeeding vigorously without respiratory distress or cyanosis. He was afebrile with normal vital signs. The majority of the physical examination was normal; however, there was erythematous desquamation around the umbilical stump and genitalia with no vesicles noted. The umbilical stump had a small amount of purulent drainage and necrosis centrally. The infant had a 1-cm round, peeling lesion on the left temple (FIGURE) with a small amount of dried serosanguinous drainage and similar superficial peeling lesions at the left preauricular area and anterior chest. There was no underlying fluctuance and only minimal surrounding erythema.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Staphylococcal scalded skin syndrome

Based on the age of the patient, clinical presentation, and suspected maternal MRSA infection (with possible transmission to the infant), we diagnosed staphylococcal scalded skin syndrome (SSSS) in this patient. SSSS is rare, with annual incidence of 45 cases per million US infants under the age of 2.¹ Newborns with a generalized form of SSSS commonly present with fever, poor feeding, irritability, and lethargy. This is followed by a generalized erythematous rash that initially may appear on the head and neck and spread to the rest of the body. Large, fragile blisters subsequently appear. These blisters rupture on gentle pressure, which is known as a positive Nikolsky sign. Ultimately, large sheets of skin easily slough off, leaving raw, denuded skin.²

S aureus is not part of normal skin flora, yet it is found on the skin and mucous membranes of 19% to 55% of healthy adults and children.³S aureus can cause a wide range of infections ranging from abscesses to cellulitis; SSSS is caused by hematogenous spread of S aureus exfoliative toxin. Newborns and immunocompromised patients are particularly susceptible.

Staphylococcal scalded skin syndrome should be considered a pediatric emergency due to potential complications such as sepsis.

Neonatal patients with SSSS most commonly present at 3 to 16 days of age.² The lack of antitoxin antibody in neonates allows the toxin to reach the epidermis where it acts locally to produce the characteristic fragile skin lesions that often rupture prior to clinical presentation.^2,4 During progression of the disease, flaky skin desquamation will occur as the lesions heal.

A retrospective review of 39 cases of SSSS identified pneumonia as the most frequent complication, occurring in 74.4% of the cases.⁵ The mortality rate of SSSS is up to 5%, and is associated with sepsis, superinfection, electrolyte imbalances, and extensive skin involvement.^2,6

If SSSS is suspected, obtain cultures from the blood, urine, eyes, nose, throat, and skin lesions to identify the primary focus of infection.⁷ However, the retrospective review of 39 cases (noted above) found a positive rate of S aureus isolation of only 23.5%.⁵ Physicians will often have to make a diagnosis based on clinical presentation and empirically initiate broad-spectrum antibiotics while considering alternative diagnoses.

Continue to: A clinical diagnosis with a large differential

A clinical diagnosis with a large differential

While biopsy rarely is required, it may be helpful to distinguish SSSS from other entities in the differential diagnosis (TABLE^2,3,7-13).

Toxic epidermal necrolysis (TEN) is a rare and life-threatening desquamating disease nearly always caused by a reaction to medications, including antibiotics. TEN can occur at any age. Fever, diffuse erythema, and extensive epidermal involvement (>30% of skin) differentiate TEN from Stevens-Johnson syndrome (SJS), which affects less than 10% of the epidermis. It is worth mentioning that TEN and SJS are now considered to be a spectrum of one disease, and an overlap syndrome has been described with 10% to 30% of skin affected.⁸ Diagnosis is made clinically, although skin biopsy routinely is performed.^7,9

Congenital syphilis features a red or pink maculopapular rash followed by desquamation. Lesions are more common on the soles.¹⁰ Desquamation or ulcerative skin lesions should be examined for spirochetes.¹¹ A quantitative, nontreponemal test such as the rapid plasma reagin (RPR) or the Venereal Disease Research Laboratory (VDRL) will be positive in most infants if exposed through the placenta, but antibodies will disappear in uninfected infants by 6 months of age.⁸

Congenital cutaneous candidiasis presents with a generalized eruption of erythematous macules, papules, and/or pustules with widespread desquamating and/or erosive dermatitis. Premature neonates with extremely low birth weight are at higher risk.¹³ Diagnosis is confirmed on microscopy by the presence of Candida albicans spores in skin scrapings.¹³

Neonatal herpes simplex virus (HSV) symptoms typically appear between 1 and 3 weeks of life, with 60% to 70% of cases presenting with classic clustering vesicles on an erythematous base.¹⁴ Diagnosis is made with HSV viral culture or polymerase chain reaction (PCR).

Continue to: SSSS should be considered a pediatrics emergency

 

 

SSSS should be considered a pediatric emergency

SSSS should be considered a pediatric emergency due to potential complications. Core measures of SSSS treatment include immediate administration of intravenous (IV) antibiotics. US population studies suggest clindamycin and penicillinase-resistant penicillin as empiric therapy.¹⁵ However, local strains and resistance patterns, including the prevalence of MRSA, as well as age, comorbidities, and severity of illness should influence antibiotic selection.

IV nafcillin or oxacillin may be used with pediatric dosing of 150 mg/kg daily divided every 6 hours for methicillin-sensitive Staphylococcus aureus (MSSA). For suspected MRSA, IV vancomycin should be considered, with an infant dose of 40 to 60 mg/kg daily divided every 6 hours.¹⁶ Fluid, electrolyte, and nutritional management should be addressed immediately. Ongoing fluid losses due to exfoliated skin must be replaced, and skin care to desquamated areas also should be addressed urgently.

Our patient. Phone consultation with an infectious disease specialist at a local children’s hospital resulted in a recommendation to treat for sepsis empirically with IV vancomycin, cefotaxime, and acyclovir. Acyclovir was discontinued once the HSV PCR came back negative. The antibiotic coverage was narrowed to IV ampicillin 50 mg/kg every 8 hours when cerebrospinal fluid and blood cultures returned negative at 48 hours, wound culture sensitivity grew MSSA, and the patient’s clinical condition stabilized. Our patient received 10 days of IV antibiotics and was discharged on oral amoxicillin 50 mg/kg divided twice daily for a total of 14 days of treatment per recommendations by the infectious disease specialist. Our patient fully recovered without any residual skin findings after completion of the antibiotic course.

CORRESPONDENCE
Jennifer J. Walker, MD, MPH, Hawaii Island Family Health Center at Hilo Medical Center, 1190 Waianuenue Ave, Hilo, HI 96720; jjwalker@hhsc.org

A 9-day-old boy was brought to the emergency department by his mother. The infant had been doing well until his most recent diaper change when his mother noticed a rash around the umbilicus (FIGURE), genitalia, and anus.

The infant was born at term via spontaneous vaginal delivery. The pregnancy was uncomplicated; the infant’s mother was group B strep negative. Following a routine postpartum course, the infant underwent an elective circumcision before hospital discharge on his second day of life. There were no interval reports of irritability, poor feeding, fevers, vomiting, or changes in urine or stool output.

The mother denied any recent unusual exposures, sick contacts, or travel. However, upon further questioning, the mother noted that she herself had several small open wounds on the torso that she attributed to untreated methicillin-resistant Staphylococcus aureus (MRSA).

On physical examination, the infant was overall well-appearing and was breastfeeding vigorously without respiratory distress or cyanosis. He was afebrile with normal vital signs. The majority of the physical examination was normal; however, there was erythematous desquamation around the umbilical stump and genitalia with no vesicles noted. The umbilical stump had a small amount of purulent drainage and necrosis centrally. The infant had a 1-cm round, peeling lesion on the left temple (FIGURE) with a small amount of dried serosanguinous drainage and similar superficial peeling lesions at the left preauricular area and anterior chest. There was no underlying fluctuance and only minimal surrounding erythema.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Staphylococcal scalded skin syndrome

Based on the age of the patient, clinical presentation, and suspected maternal MRSA infection (with possible transmission to the infant), we diagnosed staphylococcal scalded skin syndrome (SSSS) in this patient. SSSS is rare, with annual incidence of 45 cases per million US infants under the age of 2.¹ Newborns with a generalized form of SSSS commonly present with fever, poor feeding, irritability, and lethargy. This is followed by a generalized erythematous rash that initially may appear on the head and neck and spread to the rest of the body. Large, fragile blisters subsequently appear. These blisters rupture on gentle pressure, which is known as a positive Nikolsky sign. Ultimately, large sheets of skin easily slough off, leaving raw, denuded skin.²

S aureus is not part of normal skin flora, yet it is found on the skin and mucous membranes of 19% to 55% of healthy adults and children.³S aureus can cause a wide range of infections ranging from abscesses to cellulitis; SSSS is caused by hematogenous spread of S aureus exfoliative toxin. Newborns and immunocompromised patients are particularly susceptible.

Staphylococcal scalded skin syndrome should be considered a pediatric emergency due to potential complications such as sepsis.

Neonatal patients with SSSS most commonly present at 3 to 16 days of age.² The lack of antitoxin antibody in neonates allows the toxin to reach the epidermis where it acts locally to produce the characteristic fragile skin lesions that often rupture prior to clinical presentation.^2,4 During progression of the disease, flaky skin desquamation will occur as the lesions heal.

A retrospective review of 39 cases of SSSS identified pneumonia as the most frequent complication, occurring in 74.4% of the cases.⁵ The mortality rate of SSSS is up to 5%, and is associated with sepsis, superinfection, electrolyte imbalances, and extensive skin involvement.^2,6

If SSSS is suspected, obtain cultures from the blood, urine, eyes, nose, throat, and skin lesions to identify the primary focus of infection.⁷ However, the retrospective review of 39 cases (noted above) found a positive rate of S aureus isolation of only 23.5%.⁵ Physicians will often have to make a diagnosis based on clinical presentation and empirically initiate broad-spectrum antibiotics while considering alternative diagnoses.

Continue to: A clinical diagnosis with a large differential

A clinical diagnosis with a large differential

While biopsy rarely is required, it may be helpful to distinguish SSSS from other entities in the differential diagnosis (TABLE^2,3,7-13).

Toxic epidermal necrolysis (TEN) is a rare and life-threatening desquamating disease nearly always caused by a reaction to medications, including antibiotics. TEN can occur at any age. Fever, diffuse erythema, and extensive epidermal involvement (>30% of skin) differentiate TEN from Stevens-Johnson syndrome (SJS), which affects less than 10% of the epidermis. It is worth mentioning that TEN and SJS are now considered to be a spectrum of one disease, and an overlap syndrome has been described with 10% to 30% of skin affected.⁸ Diagnosis is made clinically, although skin biopsy routinely is performed.^7,9

Congenital syphilis features a red or pink maculopapular rash followed by desquamation. Lesions are more common on the soles.¹⁰ Desquamation or ulcerative skin lesions should be examined for spirochetes.¹¹ A quantitative, nontreponemal test such as the rapid plasma reagin (RPR) or the Venereal Disease Research Laboratory (VDRL) will be positive in most infants if exposed through the placenta, but antibodies will disappear in uninfected infants by 6 months of age.⁸

Congenital cutaneous candidiasis presents with a generalized eruption of erythematous macules, papules, and/or pustules with widespread desquamating and/or erosive dermatitis. Premature neonates with extremely low birth weight are at higher risk.¹³ Diagnosis is confirmed on microscopy by the presence of Candida albicans spores in skin scrapings.¹³

Neonatal herpes simplex virus (HSV) symptoms typically appear between 1 and 3 weeks of life, with 60% to 70% of cases presenting with classic clustering vesicles on an erythematous base.¹⁴ Diagnosis is made with HSV viral culture or polymerase chain reaction (PCR).

Continue to: SSSS should be considered a pediatrics emergency

 

 

SSSS should be considered a pediatric emergency

SSSS should be considered a pediatric emergency due to potential complications. Core measures of SSSS treatment include immediate administration of intravenous (IV) antibiotics. US population studies suggest clindamycin and penicillinase-resistant penicillin as empiric therapy.¹⁵ However, local strains and resistance patterns, including the prevalence of MRSA, as well as age, comorbidities, and severity of illness should influence antibiotic selection.

IV nafcillin or oxacillin may be used with pediatric dosing of 150 mg/kg daily divided every 6 hours for methicillin-sensitive Staphylococcus aureus (MSSA). For suspected MRSA, IV vancomycin should be considered, with an infant dose of 40 to 60 mg/kg daily divided every 6 hours.¹⁶ Fluid, electrolyte, and nutritional management should be addressed immediately. Ongoing fluid losses due to exfoliated skin must be replaced, and skin care to desquamated areas also should be addressed urgently.

Our patient. Phone consultation with an infectious disease specialist at a local children’s hospital resulted in a recommendation to treat for sepsis empirically with IV vancomycin, cefotaxime, and acyclovir. Acyclovir was discontinued once the HSV PCR came back negative. The antibiotic coverage was narrowed to IV ampicillin 50 mg/kg every 8 hours when cerebrospinal fluid and blood cultures returned negative at 48 hours, wound culture sensitivity grew MSSA, and the patient’s clinical condition stabilized. Our patient received 10 days of IV antibiotics and was discharged on oral amoxicillin 50 mg/kg divided twice daily for a total of 14 days of treatment per recommendations by the infectious disease specialist. Our patient fully recovered without any residual skin findings after completion of the antibiotic course.

CORRESPONDENCE
Jennifer J. Walker, MD, MPH, Hawaii Island Family Health Center at Hilo Medical Center, 1190 Waianuenue Ave, Hilo, HI 96720; jjwalker@hhsc.org

A 9-day-old boy was brought to the emergency department by his mother. The infant had been doing well until his most recent diaper change when his mother noticed a rash around the umbilicus (FIGURE), genitalia, and anus.

The infant was born at term via spontaneous vaginal delivery. The pregnancy was uncomplicated; the infant’s mother was group B strep negative. Following a routine postpartum course, the infant underwent an elective circumcision before hospital discharge on his second day of life. There were no interval reports of irritability, poor feeding, fevers, vomiting, or changes in urine or stool output.

The mother denied any recent unusual exposures, sick contacts, or travel. However, upon further questioning, the mother noted that she herself had several small open wounds on the torso that she attributed to untreated methicillin-resistant Staphylococcus aureus (MRSA).

On physical examination, the infant was overall well-appearing and was breastfeeding vigorously without respiratory distress or cyanosis. He was afebrile with normal vital signs. The majority of the physical examination was normal; however, there was erythematous desquamation around the umbilical stump and genitalia with no vesicles noted. The umbilical stump had a small amount of purulent drainage and necrosis centrally. The infant had a 1-cm round, peeling lesion on the left temple (FIGURE) with a small amount of dried serosanguinous drainage and similar superficial peeling lesions at the left preauricular area and anterior chest. There was no underlying fluctuance and only minimal surrounding erythema.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Staphylococcal scalded skin syndrome

Based on the age of the patient, clinical presentation, and suspected maternal MRSA infection (with possible transmission to the infant), we diagnosed staphylococcal scalded skin syndrome (SSSS) in this patient. SSSS is rare, with annual incidence of 45 cases per million US infants under the age of 2.¹ Newborns with a generalized form of SSSS commonly present with fever, poor feeding, irritability, and lethargy. This is followed by a generalized erythematous rash that initially may appear on the head and neck and spread to the rest of the body. Large, fragile blisters subsequently appear. These blisters rupture on gentle pressure, which is known as a positive Nikolsky sign. Ultimately, large sheets of skin easily slough off, leaving raw, denuded skin.²

S aureus is not part of normal skin flora, yet it is found on the skin and mucous membranes of 19% to 55% of healthy adults and children.³S aureus can cause a wide range of infections ranging from abscesses to cellulitis; SSSS is caused by hematogenous spread of S aureus exfoliative toxin. Newborns and immunocompromised patients are particularly susceptible.

Staphylococcal scalded skin syndrome should be considered a pediatric emergency due to potential complications such as sepsis.

Neonatal patients with SSSS most commonly present at 3 to 16 days of age.² The lack of antitoxin antibody in neonates allows the toxin to reach the epidermis where it acts locally to produce the characteristic fragile skin lesions that often rupture prior to clinical presentation.^2,4 During progression of the disease, flaky skin desquamation will occur as the lesions heal.

A retrospective review of 39 cases of SSSS identified pneumonia as the most frequent complication, occurring in 74.4% of the cases.⁵ The mortality rate of SSSS is up to 5%, and is associated with sepsis, superinfection, electrolyte imbalances, and extensive skin involvement.^2,6

If SSSS is suspected, obtain cultures from the blood, urine, eyes, nose, throat, and skin lesions to identify the primary focus of infection.⁷ However, the retrospective review of 39 cases (noted above) found a positive rate of S aureus isolation of only 23.5%.⁵ Physicians will often have to make a diagnosis based on clinical presentation and empirically initiate broad-spectrum antibiotics while considering alternative diagnoses.

Continue to: A clinical diagnosis with a large differential

A clinical diagnosis with a large differential

While biopsy rarely is required, it may be helpful to distinguish SSSS from other entities in the differential diagnosis (TABLE^2,3,7-13).

Toxic epidermal necrolysis (TEN) is a rare and life-threatening desquamating disease nearly always caused by a reaction to medications, including antibiotics. TEN can occur at any age. Fever, diffuse erythema, and extensive epidermal involvement (>30% of skin) differentiate TEN from Stevens-Johnson syndrome (SJS), which affects less than 10% of the epidermis. It is worth mentioning that TEN and SJS are now considered to be a spectrum of one disease, and an overlap syndrome has been described with 10% to 30% of skin affected.⁸ Diagnosis is made clinically, although skin biopsy routinely is performed.^7,9

Congenital syphilis features a red or pink maculopapular rash followed by desquamation. Lesions are more common on the soles.¹⁰ Desquamation or ulcerative skin lesions should be examined for spirochetes.¹¹ A quantitative, nontreponemal test such as the rapid plasma reagin (RPR) or the Venereal Disease Research Laboratory (VDRL) will be positive in most infants if exposed through the placenta, but antibodies will disappear in uninfected infants by 6 months of age.⁸

Congenital cutaneous candidiasis presents with a generalized eruption of erythematous macules, papules, and/or pustules with widespread desquamating and/or erosive dermatitis. Premature neonates with extremely low birth weight are at higher risk.¹³ Diagnosis is confirmed on microscopy by the presence of Candida albicans spores in skin scrapings.¹³

Neonatal herpes simplex virus (HSV) symptoms typically appear between 1 and 3 weeks of life, with 60% to 70% of cases presenting with classic clustering vesicles on an erythematous base.¹⁴ Diagnosis is made with HSV viral culture or polymerase chain reaction (PCR).

Continue to: SSSS should be considered a pediatrics emergency

 

 

SSSS should be considered a pediatric emergency

SSSS should be considered a pediatric emergency due to potential complications. Core measures of SSSS treatment include immediate administration of intravenous (IV) antibiotics. US population studies suggest clindamycin and penicillinase-resistant penicillin as empiric therapy.¹⁵ However, local strains and resistance patterns, including the prevalence of MRSA, as well as age, comorbidities, and severity of illness should influence antibiotic selection.

IV nafcillin or oxacillin may be used with pediatric dosing of 150 mg/kg daily divided every 6 hours for methicillin-sensitive Staphylococcus aureus (MSSA). For suspected MRSA, IV vancomycin should be considered, with an infant dose of 40 to 60 mg/kg daily divided every 6 hours.¹⁶ Fluid, electrolyte, and nutritional management should be addressed immediately. Ongoing fluid losses due to exfoliated skin must be replaced, and skin care to desquamated areas also should be addressed urgently.

Our patient. Phone consultation with an infectious disease specialist at a local children’s hospital resulted in a recommendation to treat for sepsis empirically with IV vancomycin, cefotaxime, and acyclovir. Acyclovir was discontinued once the HSV PCR came back negative. The antibiotic coverage was narrowed to IV ampicillin 50 mg/kg every 8 hours when cerebrospinal fluid and blood cultures returned negative at 48 hours, wound culture sensitivity grew MSSA, and the patient’s clinical condition stabilized. Our patient received 10 days of IV antibiotics and was discharged on oral amoxicillin 50 mg/kg divided twice daily for a total of 14 days of treatment per recommendations by the infectious disease specialist. Our patient fully recovered without any residual skin findings after completion of the antibiotic course.

CORRESPONDENCE
Jennifer J. Walker, MD, MPH, Hawaii Island Family Health Center at Hilo Medical Center, 1190 Waianuenue Ave, Hilo, HI 96720; jjwalker@hhsc.org

Children with both atopic dermatitis (AD) and food allergy (FA) have structural and molecular differences in the top layers of their skin, according to a study of children with and without AD and FA.

The researchers included 62 children aged 4-17 years, who were divided into three groups: atopic dermatitis and food allergy (AD FA+, n = 21), atopic dermatitis and no food allergy (AD FA−, n = 19), and nonatopic controls (NA, n = 22).

“In this prospective clinical study with laboratory personnel blinded to minimize bias, we demonstrate that children with AD FA+ represent a unique endotype that can be distinguished from AD FA− or NA,” wrote Donald Y. M. Leung, MD, of National Jewish Health, Denver, and his coauthors. Their work was published online in Science Translational Medicine.

According to three different scoring systems, the two AD groups were measured to have similar skin disease severity. Dr. Leung and colleagues then used skin tape stripping to measure the first layer of skin tissue for transepidermal water loss (TEWL) and stratum corneum (SC) composition, along with other variables that would indicate a difference between AD FA+ and the other groups.

Upon analysis, children in the AD FA+ group were found to have “a constellation of SC attributes,” including increased TEWL and lower levels of filaggrin gene breakdown products (urocanic acid and pyroglutamic acid) at nonlesional layers. In addition, there was an increase of Staphylococcus aureus on the nonlesional skin of AD FA+, compared with NA.

The coauthors shared the study’s limitations, which included transcriptome analysis being successful for only a fraction of the patients and the lack of skin biopsies, which would be useful to confirm “the potential role of changes in the deeper layers of skin.” However, they also noted that using minimally invasive STS led to more patients providing samples, and thus less bias in collection. “Although future studies are needed to validate our findings,” Dr. Leung and his associates wrote, “our current data support the concept that primary and secondary prevention of AD and FA in this subset of AD should focus on improving skin barrier function.”

The study was funded by the National Institute of Health/The National Institute of Allergy and Infectious Diseases’ Atopic Dermatitis Research Network, with partial support from the Edelstein Family Chair for Pediatric Allergy at NIH and a NIH/National Center for Advancing Translational Sciences Colorado Clinical and Translational Science Awards grant. Three of the authors declared being inventors of a patent that covers methods of identifying AD with FA as a unique endotype. No other conflicts of interest were reported.

SOURCE: Leung DYM et al. Sci Transl Med. 2019 Feb 20. doi: 10.1126/scitranslmed.aav2685.

Children with both atopic dermatitis (AD) and food allergy (FA) have structural and molecular differences in the top layers of their skin, according to a study of children with and without AD and FA.

The researchers included 62 children aged 4-17 years, who were divided into three groups: atopic dermatitis and food allergy (AD FA+, n = 21), atopic dermatitis and no food allergy (AD FA−, n = 19), and nonatopic controls (NA, n = 22).

“In this prospective clinical study with laboratory personnel blinded to minimize bias, we demonstrate that children with AD FA+ represent a unique endotype that can be distinguished from AD FA− or NA,” wrote Donald Y. M. Leung, MD, of National Jewish Health, Denver, and his coauthors. Their work was published online in Science Translational Medicine.

According to three different scoring systems, the two AD groups were measured to have similar skin disease severity. Dr. Leung and colleagues then used skin tape stripping to measure the first layer of skin tissue for transepidermal water loss (TEWL) and stratum corneum (SC) composition, along with other variables that would indicate a difference between AD FA+ and the other groups.

Upon analysis, children in the AD FA+ group were found to have “a constellation of SC attributes,” including increased TEWL and lower levels of filaggrin gene breakdown products (urocanic acid and pyroglutamic acid) at nonlesional layers. In addition, there was an increase of Staphylococcus aureus on the nonlesional skin of AD FA+, compared with NA.

The coauthors shared the study’s limitations, which included transcriptome analysis being successful for only a fraction of the patients and the lack of skin biopsies, which would be useful to confirm “the potential role of changes in the deeper layers of skin.” However, they also noted that using minimally invasive STS led to more patients providing samples, and thus less bias in collection. “Although future studies are needed to validate our findings,” Dr. Leung and his associates wrote, “our current data support the concept that primary and secondary prevention of AD and FA in this subset of AD should focus on improving skin barrier function.”

The study was funded by the National Institute of Health/The National Institute of Allergy and Infectious Diseases’ Atopic Dermatitis Research Network, with partial support from the Edelstein Family Chair for Pediatric Allergy at NIH and a NIH/National Center for Advancing Translational Sciences Colorado Clinical and Translational Science Awards grant. Three of the authors declared being inventors of a patent that covers methods of identifying AD with FA as a unique endotype. No other conflicts of interest were reported.

SOURCE: Leung DYM et al. Sci Transl Med. 2019 Feb 20. doi: 10.1126/scitranslmed.aav2685.

Children with both atopic dermatitis (AD) and food allergy (FA) have structural and molecular differences in the top layers of their skin, according to a study of children with and without AD and FA.

The researchers included 62 children aged 4-17 years, who were divided into three groups: atopic dermatitis and food allergy (AD FA+, n = 21), atopic dermatitis and no food allergy (AD FA−, n = 19), and nonatopic controls (NA, n = 22).

“In this prospective clinical study with laboratory personnel blinded to minimize bias, we demonstrate that children with AD FA+ represent a unique endotype that can be distinguished from AD FA− or NA,” wrote Donald Y. M. Leung, MD, of National Jewish Health, Denver, and his coauthors. Their work was published online in Science Translational Medicine.

According to three different scoring systems, the two AD groups were measured to have similar skin disease severity. Dr. Leung and colleagues then used skin tape stripping to measure the first layer of skin tissue for transepidermal water loss (TEWL) and stratum corneum (SC) composition, along with other variables that would indicate a difference between AD FA+ and the other groups.

Upon analysis, children in the AD FA+ group were found to have “a constellation of SC attributes,” including increased TEWL and lower levels of filaggrin gene breakdown products (urocanic acid and pyroglutamic acid) at nonlesional layers. In addition, there was an increase of Staphylococcus aureus on the nonlesional skin of AD FA+, compared with NA.

The coauthors shared the study’s limitations, which included transcriptome analysis being successful for only a fraction of the patients and the lack of skin biopsies, which would be useful to confirm “the potential role of changes in the deeper layers of skin.” However, they also noted that using minimally invasive STS led to more patients providing samples, and thus less bias in collection. “Although future studies are needed to validate our findings,” Dr. Leung and his associates wrote, “our current data support the concept that primary and secondary prevention of AD and FA in this subset of AD should focus on improving skin barrier function.”

The study was funded by the National Institute of Health/The National Institute of Allergy and Infectious Diseases’ Atopic Dermatitis Research Network, with partial support from the Edelstein Family Chair for Pediatric Allergy at NIH and a NIH/National Center for Advancing Translational Sciences Colorado Clinical and Translational Science Awards grant. Three of the authors declared being inventors of a patent that covers methods of identifying AD with FA as a unique endotype. No other conflicts of interest were reported.

SOURCE: Leung DYM et al. Sci Transl Med. 2019 Feb 20. doi: 10.1126/scitranslmed.aav2685.

Study results showing an association between active atopic dermatitis (AD) and poor sleep quality were published in JAMA Pediatrics by a group of dermatologists at the University of California, San Francisco (JAMA Pediatr. 2019 Mar 4. doi: 10.1001/jamapediatrics.2019.0025). The data on the sleep quality and quantity of nearly 14,000 children were collected over span of 11 years. Of these children, slightly fewer than 5,000 met the researchers’ definition of atopic dermatitis.

deyangeorgiev/thinkstockphotos.com

Although the sleep duration of children with and without AD was not statistically different, the reports of poor sleep quality and sleep disturbances by children with AD were dramatically more frequent – a nearly 50% higher chance of having more sleep-quality disturbances. In addition, children with more severe active disease were even more likely to report poor sleep quality – almost 80%.

I suspect that you’re not surprised by these findings. You have probably heard numerous tales of poor sleep from families who have children with AD. It just makes sense that a child whose skin is dry and itchy will have trouble sleeping. I’m sure you have struggled to help parents be more diligent about applying moisturizing creams and lotions, and have been aggressive with steroid creams during flare-ups. You may have added sleep onset-promoting antihistamines when topical treatments haven’t been as effective as you had hoped.

Has your working assumption always been that if you can get the child’s skin settled down, the itching will improve and the child will have an easier time falling asleep? But have you ever considered flipping the equation over and tried to be more aggressive in managing the child’s sleep problems? Maybe if the child had healthier sleep habits and ended his day with a smaller sleep debt, he could more successfully resist the urge to scratch.

Like many other folks with psoriasis, I have noticed that my itching is worse when I am tired, and particularly worse in that evil interval between crawling into bed and falling asleep. As the grandparent of a child with AD, I have observed a similar phenomenon. While I am not going to claim that sleep deprivation causes psoriasis or AD, I think that we need to consider the association between poor sleep quality and itching as a feedback loop that must be interrupted. This means that in addition to recommending topicals and moisturizing strategies, we must learn more about our patients’ sleep habits and suggest appropriate sleep hygiene practices.

Many parents aren’t aware of the cruel paradox that an overtired child is more likely to have trouble falling asleep. Has the child been allowed to give up his nap prematurely? Is bedtime at an appropriate hour, and does it consist of a limited number of sleep-promoting rituals? Is the bedroom dark enough, cool enough, and free of electronic distractions?

Providing effective counseling on sleep hygiene is time consuming and requires that you have first convinced the parents that the child’s itching is being aggravated by his sleep deprivation and not just the other way around. Successful management may require a close working relationship between the child’s pediatrician and his dermatologist, with both physicians reinforcing each other’s message that atopic dermatitis isn’t just skin deep.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Is My Child Overtired?: The Sleep Solution for Raising Happier, Healthier Children.” Email him at pdnews@mdedge.com.

Study results showing an association between active atopic dermatitis (AD) and poor sleep quality were published in JAMA Pediatrics by a group of dermatologists at the University of California, San Francisco (JAMA Pediatr. 2019 Mar 4. doi: 10.1001/jamapediatrics.2019.0025). The data on the sleep quality and quantity of nearly 14,000 children were collected over span of 11 years. Of these children, slightly fewer than 5,000 met the researchers’ definition of atopic dermatitis.

deyangeorgiev/thinkstockphotos.com

Although the sleep duration of children with and without AD was not statistically different, the reports of poor sleep quality and sleep disturbances by children with AD were dramatically more frequent – a nearly 50% higher chance of having more sleep-quality disturbances. In addition, children with more severe active disease were even more likely to report poor sleep quality – almost 80%.

I suspect that you’re not surprised by these findings. You have probably heard numerous tales of poor sleep from families who have children with AD. It just makes sense that a child whose skin is dry and itchy will have trouble sleeping. I’m sure you have struggled to help parents be more diligent about applying moisturizing creams and lotions, and have been aggressive with steroid creams during flare-ups. You may have added sleep onset-promoting antihistamines when topical treatments haven’t been as effective as you had hoped.

Has your working assumption always been that if you can get the child’s skin settled down, the itching will improve and the child will have an easier time falling asleep? But have you ever considered flipping the equation over and tried to be more aggressive in managing the child’s sleep problems? Maybe if the child had healthier sleep habits and ended his day with a smaller sleep debt, he could more successfully resist the urge to scratch.

Like many other folks with psoriasis, I have noticed that my itching is worse when I am tired, and particularly worse in that evil interval between crawling into bed and falling asleep. As the grandparent of a child with AD, I have observed a similar phenomenon. While I am not going to claim that sleep deprivation causes psoriasis or AD, I think that we need to consider the association between poor sleep quality and itching as a feedback loop that must be interrupted. This means that in addition to recommending topicals and moisturizing strategies, we must learn more about our patients’ sleep habits and suggest appropriate sleep hygiene practices.

Many parents aren’t aware of the cruel paradox that an overtired child is more likely to have trouble falling asleep. Has the child been allowed to give up his nap prematurely? Is bedtime at an appropriate hour, and does it consist of a limited number of sleep-promoting rituals? Is the bedroom dark enough, cool enough, and free of electronic distractions?

Providing effective counseling on sleep hygiene is time consuming and requires that you have first convinced the parents that the child’s itching is being aggravated by his sleep deprivation and not just the other way around. Successful management may require a close working relationship between the child’s pediatrician and his dermatologist, with both physicians reinforcing each other’s message that atopic dermatitis isn’t just skin deep.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Is My Child Overtired?: The Sleep Solution for Raising Happier, Healthier Children.” Email him at pdnews@mdedge.com.

Study results showing an association between active atopic dermatitis (AD) and poor sleep quality were published in JAMA Pediatrics by a group of dermatologists at the University of California, San Francisco (JAMA Pediatr. 2019 Mar 4. doi: 10.1001/jamapediatrics.2019.0025). The data on the sleep quality and quantity of nearly 14,000 children were collected over span of 11 years. Of these children, slightly fewer than 5,000 met the researchers’ definition of atopic dermatitis.

deyangeorgiev/thinkstockphotos.com

Although the sleep duration of children with and without AD was not statistically different, the reports of poor sleep quality and sleep disturbances by children with AD were dramatically more frequent – a nearly 50% higher chance of having more sleep-quality disturbances. In addition, children with more severe active disease were even more likely to report poor sleep quality – almost 80%.

I suspect that you’re not surprised by these findings. You have probably heard numerous tales of poor sleep from families who have children with AD. It just makes sense that a child whose skin is dry and itchy will have trouble sleeping. I’m sure you have struggled to help parents be more diligent about applying moisturizing creams and lotions, and have been aggressive with steroid creams during flare-ups. You may have added sleep onset-promoting antihistamines when topical treatments haven’t been as effective as you had hoped.

Has your working assumption always been that if you can get the child’s skin settled down, the itching will improve and the child will have an easier time falling asleep? But have you ever considered flipping the equation over and tried to be more aggressive in managing the child’s sleep problems? Maybe if the child had healthier sleep habits and ended his day with a smaller sleep debt, he could more successfully resist the urge to scratch.

Like many other folks with psoriasis, I have noticed that my itching is worse when I am tired, and particularly worse in that evil interval between crawling into bed and falling asleep. As the grandparent of a child with AD, I have observed a similar phenomenon. While I am not going to claim that sleep deprivation causes psoriasis or AD, I think that we need to consider the association between poor sleep quality and itching as a feedback loop that must be interrupted. This means that in addition to recommending topicals and moisturizing strategies, we must learn more about our patients’ sleep habits and suggest appropriate sleep hygiene practices.

Many parents aren’t aware of the cruel paradox that an overtired child is more likely to have trouble falling asleep. Has the child been allowed to give up his nap prematurely? Is bedtime at an appropriate hour, and does it consist of a limited number of sleep-promoting rituals? Is the bedroom dark enough, cool enough, and free of electronic distractions?

Providing effective counseling on sleep hygiene is time consuming and requires that you have first convinced the parents that the child’s itching is being aggravated by his sleep deprivation and not just the other way around. Successful management may require a close working relationship between the child’s pediatrician and his dermatologist, with both physicians reinforcing each other’s message that atopic dermatitis isn’t just skin deep.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Is My Child Overtired?: The Sleep Solution for Raising Happier, Healthier Children.” Email him at pdnews@mdedge.com.

There is no apparent association between proinflammatory foods and increased risk of incident psoriasis, psoriatic arthritis, or atopic dermatitis, reported Alanna C. Bridgman of Queen’s University, Kingston, Ont., and her associates.

©camij/thinkstockphotos.com

In a large, retrospective cohort study among women from the Nurses’ Health Study II (NHS-II), including 85,185 psoriasis participants and 63,443 atopic dermatitis participants, Ms. Bridgman and her associates sought to determine whether proinflammatory diet increased the risk of incident psoriasis, psoriatic arthritis, or atopic dermatitis. Clinicians administered food frequency questionnaires every 4 years beginning in 1991 among female nurses aged 25-42 years.

Food groups included in the evaluation were those most predictive of three plasma markers of inflammation: interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor–alpha R2 (TNF-R2). Proinflammatory foods included processed meat, red meat, organ meat, white fish, vegetables other than leafy green and dark yellow, refined grains, low- and high-energy drinks, and tomatoes. Anti-inflammatory foods included beer, wine, tea, coffee, dark yellow and green leafy vegetables, snacks such as popcorn and crackers, fruit juice, and pizza.

No association was found between proinflammatory diet and increased likelihood for incident psoriasis, psoriatic arthritis, or atopic dermatitis. Although proinflammatory dietary patterns were associated with psoriatic arthritis in the age-adjusted model, the hazard ratio was attenuated and found to be no longer statistically significant after adjustment for important confounders such as body mass index. In addition, no significant relationship between atopic dermatitis and proinflammatory diet was observed, they reported. The study was published in the Journal of the American Academy of Dermatology.

Ms. Bridgman and her associates measured dietary patterns using the Empirical Dietary Inflammatory Pattern (EDIP); dietary patterns measuring high on the EDIP scale were associated with higher levels of TNF-alpha, TNF-alpha R1, TNF-alpha R2, CRP, IL-6, and adiponectin. Psoriasis and psoriatic arthritis are Th1- and Th17-mediated diseases that exhibit higher serum levels of IL-6, CRP, and TNF-alpha, unlike atopic dermatitis, which is primarily a Th2-mediated condition featuring reduced involvement of the Th1/Th17 inflammatory cytokines.

Because a goal of the EDIP score was to “account for the overall effect of dietary patterns,” the researchers included in their analysis only those food groups that “explain the maximal variation in the three noted inflammatory biomarkers.”

All patients included in the study were questioned at baseline regarding their height and race/ethnicity. Weight, smoking status, and physical activity, and diagnoses of hypercholesterolemia, type 2 diabetes, cardiovascular disease, and asthma were monitored biennially.

Overall, patients with higher EDIP scores were found to have higher BMI, lower physical activity, and alcohol use, as well as increased rates of hypercholesterolemia and hypertension.

“Though we found no convincing evidence for an association with EDIP score for any of the investigated diseases, the results followed an internal pattern consistent with our hypotheses that higher EDIP scores would have more of an association with psoriatic disease than with atopic dermatitis,” the researchers wrote.

Citing recent evidence gathered in studies, such as the French NutriNet-Santé study, which demonstrated proinflammatory effects similar to those measured with the EDIP in cases where there was low adherence to the Mediterranean diet, the authors attributed their contradictory findings to “important methodological differences.” Unlike the NutriNet-Santé study, which classified psoriasis by severity, Ms. Bridgman and her colleagues examined the overall risk of incident psoriasis. “It is possible that a dietary index associated with more Th-2 inflammation would yield different results,” they noted.

The large sample size, prospectively collected dietary, and psoriatic disease data, as well as the ability to adjust for important confounding factors, were included among the strengths of the study.

That the participants were limited to U.S. women could be considered a limitation because the results may not be generalizable to other populations. The results also may not be relevant to child-onset disease because the patient population included only cases of adult-onset atopic dermatitis. Questionnaire-based diagnoses increase the likelihood of misclassification, so “dilution of the case pool with false-positive cases would bias our results towards the null,” they added.

Ultimately, the authors noted that proinflammatory diet may be associated with other health risks, but these do not warrant counseling patients concerning their possible impact in cases of psoriatic disease or atopic dermatitis.

The study was funded by Brown University department of dermatology and from Regeneron, Sanofi, the National Institutes of Health, and the National Cancer Institute. Two coauthors, one of whom has a patent pending for the nix-tix tick remover, disclosed ties with various companies.

SOURCE: Bridgman AC et al. J Am Acad Dermatol. 2019 Feb 21. pii: S0190-9622(19)30329-9.

There is no apparent association between proinflammatory foods and increased risk of incident psoriasis, psoriatic arthritis, or atopic dermatitis, reported Alanna C. Bridgman of Queen’s University, Kingston, Ont., and her associates.

©camij/thinkstockphotos.com

In a large, retrospective cohort study among women from the Nurses’ Health Study II (NHS-II), including 85,185 psoriasis participants and 63,443 atopic dermatitis participants, Ms. Bridgman and her associates sought to determine whether proinflammatory diet increased the risk of incident psoriasis, psoriatic arthritis, or atopic dermatitis. Clinicians administered food frequency questionnaires every 4 years beginning in 1991 among female nurses aged 25-42 years.

Food groups included in the evaluation were those most predictive of three plasma markers of inflammation: interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor–alpha R2 (TNF-R2). Proinflammatory foods included processed meat, red meat, organ meat, white fish, vegetables other than leafy green and dark yellow, refined grains, low- and high-energy drinks, and tomatoes. Anti-inflammatory foods included beer, wine, tea, coffee, dark yellow and green leafy vegetables, snacks such as popcorn and crackers, fruit juice, and pizza.

No association was found between proinflammatory diet and increased likelihood for incident psoriasis, psoriatic arthritis, or atopic dermatitis. Although proinflammatory dietary patterns were associated with psoriatic arthritis in the age-adjusted model, the hazard ratio was attenuated and found to be no longer statistically significant after adjustment for important confounders such as body mass index. In addition, no significant relationship between atopic dermatitis and proinflammatory diet was observed, they reported. The study was published in the Journal of the American Academy of Dermatology.

Ms. Bridgman and her associates measured dietary patterns using the Empirical Dietary Inflammatory Pattern (EDIP); dietary patterns measuring high on the EDIP scale were associated with higher levels of TNF-alpha, TNF-alpha R1, TNF-alpha R2, CRP, IL-6, and adiponectin. Psoriasis and psoriatic arthritis are Th1- and Th17-mediated diseases that exhibit higher serum levels of IL-6, CRP, and TNF-alpha, unlike atopic dermatitis, which is primarily a Th2-mediated condition featuring reduced involvement of the Th1/Th17 inflammatory cytokines.

Because a goal of the EDIP score was to “account for the overall effect of dietary patterns,” the researchers included in their analysis only those food groups that “explain the maximal variation in the three noted inflammatory biomarkers.”

All patients included in the study were questioned at baseline regarding their height and race/ethnicity. Weight, smoking status, and physical activity, and diagnoses of hypercholesterolemia, type 2 diabetes, cardiovascular disease, and asthma were monitored biennially.

Overall, patients with higher EDIP scores were found to have higher BMI, lower physical activity, and alcohol use, as well as increased rates of hypercholesterolemia and hypertension.

“Though we found no convincing evidence for an association with EDIP score for any of the investigated diseases, the results followed an internal pattern consistent with our hypotheses that higher EDIP scores would have more of an association with psoriatic disease than with atopic dermatitis,” the researchers wrote.

Citing recent evidence gathered in studies, such as the French NutriNet-Santé study, which demonstrated proinflammatory effects similar to those measured with the EDIP in cases where there was low adherence to the Mediterranean diet, the authors attributed their contradictory findings to “important methodological differences.” Unlike the NutriNet-Santé study, which classified psoriasis by severity, Ms. Bridgman and her colleagues examined the overall risk of incident psoriasis. “It is possible that a dietary index associated with more Th-2 inflammation would yield different results,” they noted.

The large sample size, prospectively collected dietary, and psoriatic disease data, as well as the ability to adjust for important confounding factors, were included among the strengths of the study.

That the participants were limited to U.S. women could be considered a limitation because the results may not be generalizable to other populations. The results also may not be relevant to child-onset disease because the patient population included only cases of adult-onset atopic dermatitis. Questionnaire-based diagnoses increase the likelihood of misclassification, so “dilution of the case pool with false-positive cases would bias our results towards the null,” they added.

Ultimately, the authors noted that proinflammatory diet may be associated with other health risks, but these do not warrant counseling patients concerning their possible impact in cases of psoriatic disease or atopic dermatitis.

The study was funded by Brown University department of dermatology and from Regeneron, Sanofi, the National Institutes of Health, and the National Cancer Institute. Two coauthors, one of whom has a patent pending for the nix-tix tick remover, disclosed ties with various companies.

SOURCE: Bridgman AC et al. J Am Acad Dermatol. 2019 Feb 21. pii: S0190-9622(19)30329-9.

There is no apparent association between proinflammatory foods and increased risk of incident psoriasis, psoriatic arthritis, or atopic dermatitis, reported Alanna C. Bridgman of Queen’s University, Kingston, Ont., and her associates.

©camij/thinkstockphotos.com

In a large, retrospective cohort study among women from the Nurses’ Health Study II (NHS-II), including 85,185 psoriasis participants and 63,443 atopic dermatitis participants, Ms. Bridgman and her associates sought to determine whether proinflammatory diet increased the risk of incident psoriasis, psoriatic arthritis, or atopic dermatitis. Clinicians administered food frequency questionnaires every 4 years beginning in 1991 among female nurses aged 25-42 years.

Food groups included in the evaluation were those most predictive of three plasma markers of inflammation: interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor–alpha R2 (TNF-R2). Proinflammatory foods included processed meat, red meat, organ meat, white fish, vegetables other than leafy green and dark yellow, refined grains, low- and high-energy drinks, and tomatoes. Anti-inflammatory foods included beer, wine, tea, coffee, dark yellow and green leafy vegetables, snacks such as popcorn and crackers, fruit juice, and pizza.

No association was found between proinflammatory diet and increased likelihood for incident psoriasis, psoriatic arthritis, or atopic dermatitis. Although proinflammatory dietary patterns were associated with psoriatic arthritis in the age-adjusted model, the hazard ratio was attenuated and found to be no longer statistically significant after adjustment for important confounders such as body mass index. In addition, no significant relationship between atopic dermatitis and proinflammatory diet was observed, they reported. The study was published in the Journal of the American Academy of Dermatology.

Ms. Bridgman and her associates measured dietary patterns using the Empirical Dietary Inflammatory Pattern (EDIP); dietary patterns measuring high on the EDIP scale were associated with higher levels of TNF-alpha, TNF-alpha R1, TNF-alpha R2, CRP, IL-6, and adiponectin. Psoriasis and psoriatic arthritis are Th1- and Th17-mediated diseases that exhibit higher serum levels of IL-6, CRP, and TNF-alpha, unlike atopic dermatitis, which is primarily a Th2-mediated condition featuring reduced involvement of the Th1/Th17 inflammatory cytokines.

Because a goal of the EDIP score was to “account for the overall effect of dietary patterns,” the researchers included in their analysis only those food groups that “explain the maximal variation in the three noted inflammatory biomarkers.”

All patients included in the study were questioned at baseline regarding their height and race/ethnicity. Weight, smoking status, and physical activity, and diagnoses of hypercholesterolemia, type 2 diabetes, cardiovascular disease, and asthma were monitored biennially.

Overall, patients with higher EDIP scores were found to have higher BMI, lower physical activity, and alcohol use, as well as increased rates of hypercholesterolemia and hypertension.

“Though we found no convincing evidence for an association with EDIP score for any of the investigated diseases, the results followed an internal pattern consistent with our hypotheses that higher EDIP scores would have more of an association with psoriatic disease than with atopic dermatitis,” the researchers wrote.

Citing recent evidence gathered in studies, such as the French NutriNet-Santé study, which demonstrated proinflammatory effects similar to those measured with the EDIP in cases where there was low adherence to the Mediterranean diet, the authors attributed their contradictory findings to “important methodological differences.” Unlike the NutriNet-Santé study, which classified psoriasis by severity, Ms. Bridgman and her colleagues examined the overall risk of incident psoriasis. “It is possible that a dietary index associated with more Th-2 inflammation would yield different results,” they noted.

The large sample size, prospectively collected dietary, and psoriatic disease data, as well as the ability to adjust for important confounding factors, were included among the strengths of the study.

That the participants were limited to U.S. women could be considered a limitation because the results may not be generalizable to other populations. The results also may not be relevant to child-onset disease because the patient population included only cases of adult-onset atopic dermatitis. Questionnaire-based diagnoses increase the likelihood of misclassification, so “dilution of the case pool with false-positive cases would bias our results towards the null,” they added.

Ultimately, the authors noted that proinflammatory diet may be associated with other health risks, but these do not warrant counseling patients concerning their possible impact in cases of psoriatic disease or atopic dermatitis.

The study was funded by Brown University department of dermatology and from Regeneron, Sanofi, the National Institutes of Health, and the National Cancer Institute. Two coauthors, one of whom has a patent pending for the nix-tix tick remover, disclosed ties with various companies.

SOURCE: Bridgman AC et al. J Am Acad Dermatol. 2019 Feb 21. pii: S0190-9622(19)30329-9.

ORLANDO – What’s new in infectious disease therapeutics for dermatologists? More topical choices, antiparasitics, and some “big guns” to target skin and skin structure infections, according to Justin Finch, MD. He ran through an array of updates at the Orlando Dermatology Aesthetic and Clinical Conference.

Kari Oakes/MDedge News

While naturally occurring smallpox was globally eradicated in 1980, small research stores are held in the United States and Russia, and effective antivirals are part of a strategy to combat bioweapons. Tecovirimat (TPOXX) is an antiviral that inhibits a major envelope protein that poxviruses need to produce extracellular virus. Approved by the Food and Drug Administration in mid-2018, it is currently the only antiviral for treating variola virus infection approved in the United States, noted Dr. Finch of the University of Connecticut, Farmington. He added that 2 million doses are currently held in the U.S. Strategic National Stockpile.

Another anti-infective agent that won’t be used by those practicing in the United States, but which promises to alleviate a significant source of suffering in the developing world, is moxidectin. The anthelmintic had previously been approved for veterinary uses, but in June 2018, the FDA approved moxidectin to treat onchocerciasis, also known as river blindness. The drug defeats the parasitic worm by binding to glutamate-gated chloride ion channels; it is licensed by the nonprofit Medicines Development for Global Health.

Another antiparasitic drug, benznidazole, was approved to treat children aged 2-12 years with Chagas disease in 2017, Dr. Finch said.

Also in 2017, a topical quinolone, ozenoxacin (Xepi) was approved to treat impetigo in adults and children aged at least 2 months. Formulated as a 1% cream, ozenoxacin is applied twice daily for 5 days. In clinical trials, ozenoxacin was shown to be noninferior to retapamulin, he said.

A new topical choice is important as mupirocin resistance climbs, Dr. Finch added. A recent Greek study showed that 20% (437) of 2,137 staph infections studied were mupirocin resistant. Of the 20%, all but one were skin and skin structure infections (SSSIs), with 88% of these being impetigo.

In the United States, mupirocin resistance has been seen in one in three outpatients in a Florida study and in 31% of patients in a New York City sample. Other studies have shown mupirocin resistance in Staphylococcus aureus isolates with resistance in the 10%-15% range among children with SSSIs, Dr. Finch said.

Two other new antibiotics to fight SSSIs can each be administered orally or intravenously. One, omadacycline (Nuzyra), is a novel tetracycline that maintains efficacy against bacteria that express tetracycline resistance through efflux and ribosomal protection. Approved in late 2018 for acute bacterial SSSIs, omadacycline treats not just methicillin-sensitive and methicillin-resistant S. aureus, but also Streptococcus species and gram-negative rods such as Enterobacter and Klebsiella pneumoniae, Dr. Finch noted.

Another new fluorinated quinolone, approved in 2017, delafloxacin (Baxdela) has broad spectrum activity against gram-negative and gram-positive bacteria.

Dr. Finch reported that he has no relevant conflicts of interest.

koakes@mdedge.com

ORLANDO – What’s new in infectious disease therapeutics for dermatologists? More topical choices, antiparasitics, and some “big guns” to target skin and skin structure infections, according to Justin Finch, MD. He ran through an array of updates at the Orlando Dermatology Aesthetic and Clinical Conference.

Kari Oakes/MDedge News

While naturally occurring smallpox was globally eradicated in 1980, small research stores are held in the United States and Russia, and effective antivirals are part of a strategy to combat bioweapons. Tecovirimat (TPOXX) is an antiviral that inhibits a major envelope protein that poxviruses need to produce extracellular virus. Approved by the Food and Drug Administration in mid-2018, it is currently the only antiviral for treating variola virus infection approved in the United States, noted Dr. Finch of the University of Connecticut, Farmington. He added that 2 million doses are currently held in the U.S. Strategic National Stockpile.

Another anti-infective agent that won’t be used by those practicing in the United States, but which promises to alleviate a significant source of suffering in the developing world, is moxidectin. The anthelmintic had previously been approved for veterinary uses, but in June 2018, the FDA approved moxidectin to treat onchocerciasis, also known as river blindness. The drug defeats the parasitic worm by binding to glutamate-gated chloride ion channels; it is licensed by the nonprofit Medicines Development for Global Health.

Another antiparasitic drug, benznidazole, was approved to treat children aged 2-12 years with Chagas disease in 2017, Dr. Finch said.

Also in 2017, a topical quinolone, ozenoxacin (Xepi) was approved to treat impetigo in adults and children aged at least 2 months. Formulated as a 1% cream, ozenoxacin is applied twice daily for 5 days. In clinical trials, ozenoxacin was shown to be noninferior to retapamulin, he said.

A new topical choice is important as mupirocin resistance climbs, Dr. Finch added. A recent Greek study showed that 20% (437) of 2,137 staph infections studied were mupirocin resistant. Of the 20%, all but one were skin and skin structure infections (SSSIs), with 88% of these being impetigo.

In the United States, mupirocin resistance has been seen in one in three outpatients in a Florida study and in 31% of patients in a New York City sample. Other studies have shown mupirocin resistance in Staphylococcus aureus isolates with resistance in the 10%-15% range among children with SSSIs, Dr. Finch said.

Two other new antibiotics to fight SSSIs can each be administered orally or intravenously. One, omadacycline (Nuzyra), is a novel tetracycline that maintains efficacy against bacteria that express tetracycline resistance through efflux and ribosomal protection. Approved in late 2018 for acute bacterial SSSIs, omadacycline treats not just methicillin-sensitive and methicillin-resistant S. aureus, but also Streptococcus species and gram-negative rods such as Enterobacter and Klebsiella pneumoniae, Dr. Finch noted.

Another new fluorinated quinolone, approved in 2017, delafloxacin (Baxdela) has broad spectrum activity against gram-negative and gram-positive bacteria.

Dr. Finch reported that he has no relevant conflicts of interest.

koakes@mdedge.com

ORLANDO – What’s new in infectious disease therapeutics for dermatologists? More topical choices, antiparasitics, and some “big guns” to target skin and skin structure infections, according to Justin Finch, MD. He ran through an array of updates at the Orlando Dermatology Aesthetic and Clinical Conference.

Kari Oakes/MDedge News

While naturally occurring smallpox was globally eradicated in 1980, small research stores are held in the United States and Russia, and effective antivirals are part of a strategy to combat bioweapons. Tecovirimat (TPOXX) is an antiviral that inhibits a major envelope protein that poxviruses need to produce extracellular virus. Approved by the Food and Drug Administration in mid-2018, it is currently the only antiviral for treating variola virus infection approved in the United States, noted Dr. Finch of the University of Connecticut, Farmington. He added that 2 million doses are currently held in the U.S. Strategic National Stockpile.

Another anti-infective agent that won’t be used by those practicing in the United States, but which promises to alleviate a significant source of suffering in the developing world, is moxidectin. The anthelmintic had previously been approved for veterinary uses, but in June 2018, the FDA approved moxidectin to treat onchocerciasis, also known as river blindness. The drug defeats the parasitic worm by binding to glutamate-gated chloride ion channels; it is licensed by the nonprofit Medicines Development for Global Health.

Another antiparasitic drug, benznidazole, was approved to treat children aged 2-12 years with Chagas disease in 2017, Dr. Finch said.

Also in 2017, a topical quinolone, ozenoxacin (Xepi) was approved to treat impetigo in adults and children aged at least 2 months. Formulated as a 1% cream, ozenoxacin is applied twice daily for 5 days. In clinical trials, ozenoxacin was shown to be noninferior to retapamulin, he said.

A new topical choice is important as mupirocin resistance climbs, Dr. Finch added. A recent Greek study showed that 20% (437) of 2,137 staph infections studied were mupirocin resistant. Of the 20%, all but one were skin and skin structure infections (SSSIs), with 88% of these being impetigo.

In the United States, mupirocin resistance has been seen in one in three outpatients in a Florida study and in 31% of patients in a New York City sample. Other studies have shown mupirocin resistance in Staphylococcus aureus isolates with resistance in the 10%-15% range among children with SSSIs, Dr. Finch said.

Two other new antibiotics to fight SSSIs can each be administered orally or intravenously. One, omadacycline (Nuzyra), is a novel tetracycline that maintains efficacy against bacteria that express tetracycline resistance through efflux and ribosomal protection. Approved in late 2018 for acute bacterial SSSIs, omadacycline treats not just methicillin-sensitive and methicillin-resistant S. aureus, but also Streptococcus species and gram-negative rods such as Enterobacter and Klebsiella pneumoniae, Dr. Finch noted.

Another new fluorinated quinolone, approved in 2017, delafloxacin (Baxdela) has broad spectrum activity against gram-negative and gram-positive bacteria.

Dr. Finch reported that he has no relevant conflicts of interest.

koakes@mdedge.com

For more than 2 years, this 36-year-old woman has had a slightly itchy rash that waxes and wanes on her posterior neck. She has consulted several primary care providers and received multiple diagnoses, the most consistent of which has been fungal infection. However, despite use of a variety of antifungal creams (nystatin, clotrimazole, and combination clotrimazole/betamethasone), a 1-month course of oral terbinafine, and OTC tolnaftate, no improvement has occurred.

The patient asserts that she is otherwise in good health, with no joint pain or fever and no history of recent health crises. Family history is free of dermatologic complaints except for psoriasis in her father.

EXAMINATION
A pink plaque with white, fairly adherent scale covers most of the patient’s posterior neck/upper midline back. When a 3-mm section of scaling is peeled away, 2 tiny dots of pinpoint bleeding are immediately noted.

The rest of her scalp is free of any such changes, as are her elbows and knees. But a similar rash is seen in the upper intergluteal area, and 3 of 10 fingernails are mildly pitted.

What’s the diagnosis?

DISCUSSION
Psoriasis vulgaris (common psoriasis) affects around 3% of the white population in this country. That incidence almost doubles in northern Europe and Scandinavia.

Psoriasis is so common that you should expect to see it regularly; the important question is not “Will you see it?” but rather “Will you know it when you see it?” Sometimes the various clinical elements of psoriasis must be sought, and those dots connected, as this case demonstrates effectively.

For one thing, the nape of the neck is commonly affected, especially in women. It is pure speculation, but one imagines that the heat and sweat associated with longer hair might contribute to this predilection.

The pink color, whitish scale, and pinpoint bleeding (termed the Auspitz sign) all corroborate the diagnosis, as does the positive family history and nail pitting. The intergluteal involvement was the icing on the cake; this is seen in only 2 common conditions: psoriasis and seborrhea.

The lesson? Even though psoriasis is supposed to appear on elbows, knees, and other extensor surfaces, sometimes it breaks the rules. The posterior neck was the primary area of involvement in this case, but sometimes psoriasis is completely confined to the scalp or the palms. And, of course, there are different types of psoriasis, some of which bear scant resemblance to psoriasis vulgaris. That’s where biopsies and/or referrals prove to be useful.

It is true that this patient’s rash could have had a fungal origin. When in doubt, however, a punch or shave biopsy would most likely settle the matter, since the histologic picture is usually pathognomic.

TAKE-HOME LEARNING POINTS

• Psoriasis is often be easy to diagnose—but just as often, it takes a bit of detective work.
• This “investigation” consists of looking for and asking about findings that could corroborate the diagnosis.
• The morphology of the neck lesion, as well as the Auspitz sign, nail pitting, intergluteal involvement, and family history in this case all served quite well to establish the diagnosis of psoriasis.
• It is helpful to remember how utterly common psoriasis is, affecting around 10,000,000 Americans.

For more than 2 years, this 36-year-old woman has had a slightly itchy rash that waxes and wanes on her posterior neck. She has consulted several primary care providers and received multiple diagnoses, the most consistent of which has been fungal infection. However, despite use of a variety of antifungal creams (nystatin, clotrimazole, and combination clotrimazole/betamethasone), a 1-month course of oral terbinafine, and OTC tolnaftate, no improvement has occurred.

The patient asserts that she is otherwise in good health, with no joint pain or fever and no history of recent health crises. Family history is free of dermatologic complaints except for psoriasis in her father.

EXAMINATION
A pink plaque with white, fairly adherent scale covers most of the patient’s posterior neck/upper midline back. When a 3-mm section of scaling is peeled away, 2 tiny dots of pinpoint bleeding are immediately noted.

The rest of her scalp is free of any such changes, as are her elbows and knees. But a similar rash is seen in the upper intergluteal area, and 3 of 10 fingernails are mildly pitted.

What’s the diagnosis?

DISCUSSION
Psoriasis vulgaris (common psoriasis) affects around 3% of the white population in this country. That incidence almost doubles in northern Europe and Scandinavia.

Psoriasis is so common that you should expect to see it regularly; the important question is not “Will you see it?” but rather “Will you know it when you see it?” Sometimes the various clinical elements of psoriasis must be sought, and those dots connected, as this case demonstrates effectively.

For one thing, the nape of the neck is commonly affected, especially in women. It is pure speculation, but one imagines that the heat and sweat associated with longer hair might contribute to this predilection.

The pink color, whitish scale, and pinpoint bleeding (termed the Auspitz sign) all corroborate the diagnosis, as does the positive family history and nail pitting. The intergluteal involvement was the icing on the cake; this is seen in only 2 common conditions: psoriasis and seborrhea.

The lesson? Even though psoriasis is supposed to appear on elbows, knees, and other extensor surfaces, sometimes it breaks the rules. The posterior neck was the primary area of involvement in this case, but sometimes psoriasis is completely confined to the scalp or the palms. And, of course, there are different types of psoriasis, some of which bear scant resemblance to psoriasis vulgaris. That’s where biopsies and/or referrals prove to be useful.

It is true that this patient’s rash could have had a fungal origin. When in doubt, however, a punch or shave biopsy would most likely settle the matter, since the histologic picture is usually pathognomic.

TAKE-HOME LEARNING POINTS

• Psoriasis is often be easy to diagnose—but just as often, it takes a bit of detective work.
• This “investigation” consists of looking for and asking about findings that could corroborate the diagnosis.
• The morphology of the neck lesion, as well as the Auspitz sign, nail pitting, intergluteal involvement, and family history in this case all served quite well to establish the diagnosis of psoriasis.
• It is helpful to remember how utterly common psoriasis is, affecting around 10,000,000 Americans.

For more than 2 years, this 36-year-old woman has had a slightly itchy rash that waxes and wanes on her posterior neck. She has consulted several primary care providers and received multiple diagnoses, the most consistent of which has been fungal infection. However, despite use of a variety of antifungal creams (nystatin, clotrimazole, and combination clotrimazole/betamethasone), a 1-month course of oral terbinafine, and OTC tolnaftate, no improvement has occurred.

The patient asserts that she is otherwise in good health, with no joint pain or fever and no history of recent health crises. Family history is free of dermatologic complaints except for psoriasis in her father.

EXAMINATION
A pink plaque with white, fairly adherent scale covers most of the patient’s posterior neck/upper midline back. When a 3-mm section of scaling is peeled away, 2 tiny dots of pinpoint bleeding are immediately noted.

The rest of her scalp is free of any such changes, as are her elbows and knees. But a similar rash is seen in the upper intergluteal area, and 3 of 10 fingernails are mildly pitted.

What’s the diagnosis?

DISCUSSION
Psoriasis vulgaris (common psoriasis) affects around 3% of the white population in this country. That incidence almost doubles in northern Europe and Scandinavia.

Psoriasis is so common that you should expect to see it regularly; the important question is not “Will you see it?” but rather “Will you know it when you see it?” Sometimes the various clinical elements of psoriasis must be sought, and those dots connected, as this case demonstrates effectively.

For one thing, the nape of the neck is commonly affected, especially in women. It is pure speculation, but one imagines that the heat and sweat associated with longer hair might contribute to this predilection.

The pink color, whitish scale, and pinpoint bleeding (termed the Auspitz sign) all corroborate the diagnosis, as does the positive family history and nail pitting. The intergluteal involvement was the icing on the cake; this is seen in only 2 common conditions: psoriasis and seborrhea.

The lesson? Even though psoriasis is supposed to appear on elbows, knees, and other extensor surfaces, sometimes it breaks the rules. The posterior neck was the primary area of involvement in this case, but sometimes psoriasis is completely confined to the scalp or the palms. And, of course, there are different types of psoriasis, some of which bear scant resemblance to psoriasis vulgaris. That’s where biopsies and/or referrals prove to be useful.

It is true that this patient’s rash could have had a fungal origin. When in doubt, however, a punch or shave biopsy would most likely settle the matter, since the histologic picture is usually pathognomic.

TAKE-HOME LEARNING POINTS

• Psoriasis is often be easy to diagnose—but just as often, it takes a bit of detective work.
• This “investigation” consists of looking for and asking about findings that could corroborate the diagnosis.
• The morphology of the neck lesion, as well as the Auspitz sign, nail pitting, intergluteal involvement, and family history in this case all served quite well to establish the diagnosis of psoriasis.
• It is helpful to remember how utterly common psoriasis is, affecting around 10,000,000 Americans.

A 38-year-old man is admitted to the hospital with a painful, swollen left leg. This was not the first instance of this kind for him. He had been admitted for the same problem 3 months earlier. During the earlier admission, he was diagnosed with cellulitis and treated with intravenous cefazolin for 4 days, then discharged on cephalexin with resolution of his swelling and pain. Today, his blood pressure is 120/70, pulse is 90, temperature is 38.2°C, his left leg is edematous from the mid-calf to the ankle, and he has erythema and warmth over the calf. His white blood cell count is 13,000, and a diagnosis of cellulitis is made. Which of the following treatments is most likely to shorten his hospital stay?

Concheiro and colleagues did a retrospective study of 122 cases of cellulitis and found tinea pedis in 33% of the cases.⁶ Muller et al. studied the importance of toe web microorganisms and erysipelas and found that the presence of interdigital tinea pedis was correlated with recurrent infection.⁷ Treatment of tinea pedis is an easily modifiable risk factor in patients with recurrent cellulitis.

Pearls: Consider adding a short course of steroids in patients with more severe erysipelas/cellulitis, as it can decrease hospital stay and IV antibiotics.

Look for tinea pedis and treat if present in patients who have erysipelas/cellulitis.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Arch Intern Med. 2008 May 26;168(10):1034-46.

2. Scand J Infect Dis 1997;29(4):377-82.

3. Scand J Infect Dis. 1998;30(2):206-7.

4. Isr Med Assoc J. 2018 Mar;20(3):137-40.

5. J Dtsch Dermatol Ges. 2004 Feb;2(2):89-95.

6. Actas Dermosifiliogr. 2009 Dec;100(10):888-94.

7. J Dtsch Dermatol Ges. 2014 Aug;12(8):691-5.

A 38-year-old man is admitted to the hospital with a painful, swollen left leg. This was not the first instance of this kind for him. He had been admitted for the same problem 3 months earlier. During the earlier admission, he was diagnosed with cellulitis and treated with intravenous cefazolin for 4 days, then discharged on cephalexin with resolution of his swelling and pain. Today, his blood pressure is 120/70, pulse is 90, temperature is 38.2°C, his left leg is edematous from the mid-calf to the ankle, and he has erythema and warmth over the calf. His white blood cell count is 13,000, and a diagnosis of cellulitis is made. Which of the following treatments is most likely to shorten his hospital stay?

Concheiro and colleagues did a retrospective study of 122 cases of cellulitis and found tinea pedis in 33% of the cases.⁶ Muller et al. studied the importance of toe web microorganisms and erysipelas and found that the presence of interdigital tinea pedis was correlated with recurrent infection.⁷ Treatment of tinea pedis is an easily modifiable risk factor in patients with recurrent cellulitis.

Pearls: Consider adding a short course of steroids in patients with more severe erysipelas/cellulitis, as it can decrease hospital stay and IV antibiotics.

Look for tinea pedis and treat if present in patients who have erysipelas/cellulitis.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Arch Intern Med. 2008 May 26;168(10):1034-46.

2. Scand J Infect Dis 1997;29(4):377-82.

3. Scand J Infect Dis. 1998;30(2):206-7.

4. Isr Med Assoc J. 2018 Mar;20(3):137-40.

5. J Dtsch Dermatol Ges. 2004 Feb;2(2):89-95.

6. Actas Dermosifiliogr. 2009 Dec;100(10):888-94.

7. J Dtsch Dermatol Ges. 2014 Aug;12(8):691-5.

A 38-year-old man is admitted to the hospital with a painful, swollen left leg. This was not the first instance of this kind for him. He had been admitted for the same problem 3 months earlier. During the earlier admission, he was diagnosed with cellulitis and treated with intravenous cefazolin for 4 days, then discharged on cephalexin with resolution of his swelling and pain. Today, his blood pressure is 120/70, pulse is 90, temperature is 38.2°C, his left leg is edematous from the mid-calf to the ankle, and he has erythema and warmth over the calf. His white blood cell count is 13,000, and a diagnosis of cellulitis is made. Which of the following treatments is most likely to shorten his hospital stay?

Concheiro and colleagues did a retrospective study of 122 cases of cellulitis and found tinea pedis in 33% of the cases.⁶ Muller et al. studied the importance of toe web microorganisms and erysipelas and found that the presence of interdigital tinea pedis was correlated with recurrent infection.⁷ Treatment of tinea pedis is an easily modifiable risk factor in patients with recurrent cellulitis.

Pearls: Consider adding a short course of steroids in patients with more severe erysipelas/cellulitis, as it can decrease hospital stay and IV antibiotics.

Look for tinea pedis and treat if present in patients who have erysipelas/cellulitis.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Arch Intern Med. 2008 May 26;168(10):1034-46.

2. Scand J Infect Dis 1997;29(4):377-82.

3. Scand J Infect Dis. 1998;30(2):206-7.

4. Isr Med Assoc J. 2018 Mar;20(3):137-40.

5. J Dtsch Dermatol Ges. 2004 Feb;2(2):89-95.

6. Actas Dermosifiliogr. 2009 Dec;100(10):888-94.

7. J Dtsch Dermatol Ges. 2014 Aug;12(8):691-5.

The presence of the large red to purple, well-demarcated patches with a lateral predilection led the FP to diagnose a port-wine-stain.^1,2

Port-wine-stains are a type of capillary malformation that fall under the over-arching category of “simple vascular malformations.”³ Occurring in approximately 3/1000 live births, port-wine-stains have no gender predilection and can occur anywhere on the body, however, 80% of cases are associated with the head and neck.^1,4 Lesions tend to be present at birth and grow in proportion with the child.^1-4 While port-wine-stains may lighten during the infant’s first year of life, they tend to darken and become more nodular with time.^1,3-5 Darkening of lesions is thought to be due to a lack of neural input to the capillaries, leading to poor vascular tone and dilation.⁵

Port-wine-stains are often isolated and benign, but their presence may indicate an underlying syndrome. Two of the more common syndromes associated with port-wine-stains include Sturge-Webber syndrome and Klippel-Trenaunay syndrome.^1,4

Sturge-Webber syndrome is characterized by a port-wine-stain in the distribution of the first trigeminal division (V1), with possible involvement of the second or third trigeminal divisions (V2 and V3).^1,4 Central nervous system abnormalities are also characteristic of Sturge-Webber Syndrome and can include cerebral atrophy, leptomeningeal angiomatosis, and cortical calcifications that can cause seizures, mental retardation, and hemiparesis.^1,2,4

Ophthalmologic complications of Sturge-Webber syndrome can include glaucoma, and are seen in 10% to 30% of patients with a port-wine-stain in the periocular region and in 30% to 70% of patients with leptomeningeal involvement.² A larger facial distribution of a port-wine-stain correlates to a stronger association with Sturge-Webber syndrome.²

Klippel-Trenaunay syndrome is characterized by port-wine-stains on the lower extremities with limb hypertrophy and length discrepancy, varicose veins, lymphedema, and phleboliths.^1,4 Diagnosis is typically clinical and based on physical exam findings. However, an elevated d-dimer, magnetic resonance imaging (MRI), or ultrasound may aid in confirmation. The MRI or ultrasound may reveal tissue hypertrophy and the associated vascular malformations.⁶

The differential diagnosis for a port-wine stain includes nevus simplex, another type of capillary malformation. Nevus simplex is the most common capillary malformation, occurring in up to 82% of newborns.² Depending on the location, nevus simplex is also referred to as a “stork bite” (lesion on nape of neck) or “angel’s kiss” (lesion on forehead).² Nevus simplex is distinguished from a  port-wine-stain by a more central location, indistinct borders, and a pale pink to red coloring.^2,3 Nevus simplex lesions tend to fade as the child grows, while port-wine-stains tend to darken.^2,3

Port-wine-stains also can be confused with infantile or congenital hemangiomas, which were considered in this case.  Congenital hemangiomas are present at birth, while infantile hemangiomas appear within the first few weeks of life.^1,2 Superficial hemangiomas can be red and macular, and often have well-defined borders, which makes distinction from port-wine-stains difficult at times.¹ Hemangiomas will typically go through proliferations and involution stages making them dynamic lesions, whereas port-wine-stains grow in proportion to the child.^1,2

Pulsed-dye laser (PDL) treatments are the gold standard for treatment of port-wine-stains.^1,4 PDL selectively targets the vascular chromophore, which minimizes the appearance of the vascular stain but can’t completely eradicate it.^1,4 Treatment is generally initiated after 6 months of life.¹ In this case, the patient was referred to Dermatology for a discussion of the benefits of PDL therapy.

The presence of the large red to purple, well-demarcated patches with a lateral predilection led the FP to diagnose a port-wine-stain.^1,2

Port-wine-stains are a type of capillary malformation that fall under the over-arching category of “simple vascular malformations.”³ Occurring in approximately 3/1000 live births, port-wine-stains have no gender predilection and can occur anywhere on the body, however, 80% of cases are associated with the head and neck.^1,4 Lesions tend to be present at birth and grow in proportion with the child.^1-4 While port-wine-stains may lighten during the infant’s first year of life, they tend to darken and become more nodular with time.^1,3-5 Darkening of lesions is thought to be due to a lack of neural input to the capillaries, leading to poor vascular tone and dilation.⁵

Port-wine-stains are often isolated and benign, but their presence may indicate an underlying syndrome. Two of the more common syndromes associated with port-wine-stains include Sturge-Webber syndrome and Klippel-Trenaunay syndrome.^1,4

Sturge-Webber syndrome is characterized by a port-wine-stain in the distribution of the first trigeminal division (V1), with possible involvement of the second or third trigeminal divisions (V2 and V3).^1,4 Central nervous system abnormalities are also characteristic of Sturge-Webber Syndrome and can include cerebral atrophy, leptomeningeal angiomatosis, and cortical calcifications that can cause seizures, mental retardation, and hemiparesis.^1,2,4

Ophthalmologic complications of Sturge-Webber syndrome can include glaucoma, and are seen in 10% to 30% of patients with a port-wine-stain in the periocular region and in 30% to 70% of patients with leptomeningeal involvement.² A larger facial distribution of a port-wine-stain correlates to a stronger association with Sturge-Webber syndrome.²

Klippel-Trenaunay syndrome is characterized by port-wine-stains on the lower extremities with limb hypertrophy and length discrepancy, varicose veins, lymphedema, and phleboliths.^1,4 Diagnosis is typically clinical and based on physical exam findings. However, an elevated d-dimer, magnetic resonance imaging (MRI), or ultrasound may aid in confirmation. The MRI or ultrasound may reveal tissue hypertrophy and the associated vascular malformations.⁶

The differential diagnosis for a port-wine stain includes nevus simplex, another type of capillary malformation. Nevus simplex is the most common capillary malformation, occurring in up to 82% of newborns.² Depending on the location, nevus simplex is also referred to as a “stork bite” (lesion on nape of neck) or “angel’s kiss” (lesion on forehead).² Nevus simplex is distinguished from a  port-wine-stain by a more central location, indistinct borders, and a pale pink to red coloring.^2,3 Nevus simplex lesions tend to fade as the child grows, while port-wine-stains tend to darken.^2,3

Port-wine-stains also can be confused with infantile or congenital hemangiomas, which were considered in this case.  Congenital hemangiomas are present at birth, while infantile hemangiomas appear within the first few weeks of life.^1,2 Superficial hemangiomas can be red and macular, and often have well-defined borders, which makes distinction from port-wine-stains difficult at times.¹ Hemangiomas will typically go through proliferations and involution stages making them dynamic lesions, whereas port-wine-stains grow in proportion to the child.^1,2

Pulsed-dye laser (PDL) treatments are the gold standard for treatment of port-wine-stains.^1,4 PDL selectively targets the vascular chromophore, which minimizes the appearance of the vascular stain but can’t completely eradicate it.^1,4 Treatment is generally initiated after 6 months of life.¹ In this case, the patient was referred to Dermatology for a discussion of the benefits of PDL therapy.

The presence of the large red to purple, well-demarcated patches with a lateral predilection led the FP to diagnose a port-wine-stain.^1,2

Port-wine-stains are a type of capillary malformation that fall under the over-arching category of “simple vascular malformations.”³ Occurring in approximately 3/1000 live births, port-wine-stains have no gender predilection and can occur anywhere on the body, however, 80% of cases are associated with the head and neck.^1,4 Lesions tend to be present at birth and grow in proportion with the child.^1-4 While port-wine-stains may lighten during the infant’s first year of life, they tend to darken and become more nodular with time.^1,3-5 Darkening of lesions is thought to be due to a lack of neural input to the capillaries, leading to poor vascular tone and dilation.⁵

Port-wine-stains are often isolated and benign, but their presence may indicate an underlying syndrome. Two of the more common syndromes associated with port-wine-stains include Sturge-Webber syndrome and Klippel-Trenaunay syndrome.^1,4

Sturge-Webber syndrome is characterized by a port-wine-stain in the distribution of the first trigeminal division (V1), with possible involvement of the second or third trigeminal divisions (V2 and V3).^1,4 Central nervous system abnormalities are also characteristic of Sturge-Webber Syndrome and can include cerebral atrophy, leptomeningeal angiomatosis, and cortical calcifications that can cause seizures, mental retardation, and hemiparesis.^1,2,4

Ophthalmologic complications of Sturge-Webber syndrome can include glaucoma, and are seen in 10% to 30% of patients with a port-wine-stain in the periocular region and in 30% to 70% of patients with leptomeningeal involvement.² A larger facial distribution of a port-wine-stain correlates to a stronger association with Sturge-Webber syndrome.²

Klippel-Trenaunay syndrome is characterized by port-wine-stains on the lower extremities with limb hypertrophy and length discrepancy, varicose veins, lymphedema, and phleboliths.^1,4 Diagnosis is typically clinical and based on physical exam findings. However, an elevated d-dimer, magnetic resonance imaging (MRI), or ultrasound may aid in confirmation. The MRI or ultrasound may reveal tissue hypertrophy and the associated vascular malformations.⁶

The differential diagnosis for a port-wine stain includes nevus simplex, another type of capillary malformation. Nevus simplex is the most common capillary malformation, occurring in up to 82% of newborns.² Depending on the location, nevus simplex is also referred to as a “stork bite” (lesion on nape of neck) or “angel’s kiss” (lesion on forehead).² Nevus simplex is distinguished from a  port-wine-stain by a more central location, indistinct borders, and a pale pink to red coloring.^2,3 Nevus simplex lesions tend to fade as the child grows, while port-wine-stains tend to darken.^2,3

Port-wine-stains also can be confused with infantile or congenital hemangiomas, which were considered in this case.  Congenital hemangiomas are present at birth, while infantile hemangiomas appear within the first few weeks of life.^1,2 Superficial hemangiomas can be red and macular, and often have well-defined borders, which makes distinction from port-wine-stains difficult at times.¹ Hemangiomas will typically go through proliferations and involution stages making them dynamic lesions, whereas port-wine-stains grow in proportion to the child.^1,2

Pulsed-dye laser (PDL) treatments are the gold standard for treatment of port-wine-stains.^1,4 PDL selectively targets the vascular chromophore, which minimizes the appearance of the vascular stain but can’t completely eradicate it.^1,4 Treatment is generally initiated after 6 months of life.¹ In this case, the patient was referred to Dermatology for a discussion of the benefits of PDL therapy.

All individuals with psoriasis or psoriatic arthritis aged over 50 years should receive the recombinant herpes zoster vaccine, according to a systematic review and consensus recommendations from the National Psoriasis Foundation.

Joloei/Thinkstock

Emily Baumrin, MD, of Brigham and Women’s Hospital, Boston, and her coauthors reviewed 41 studies of herpes zoster in people with psoriasis or psoriatic arthritis according to treatment modality. Their report is in the Journal of the American Academy of Dermatology.

Overall, psoriasis was associated with an increased rate of herpes zoster when compared with the general population: 13.3 cases per 1,000 patient-years for psoriasis and 15.9 for psoriatic arthritis, compared with 8.5 in healthy controls after adjustment for age, sex, and systemic medications. Most of this increased incidence was seen in patients with more severe disease: Those with mild disease who were not receiving systemic therapy had a risk similar to that of healthy controls.

However, one study suggested much of the increased risk of herpes zoster in psoriasis was accounted for by immunosuppressive therapy; when those patients were excluded, there was an 8% increase in risk.


The authors found that people whose psoriasis was treated with tofacitinib (Xeljanz) had a two- to threefold increased risk of herpes zoster, compared with those treated with tumor necrosis factor (TNF) inhibitors or conventional synthetic disease-modifying antirheumatic drugs (DMARDs).

Corticosteroids – either alone or in combination with DMARDs – were also associated with significant increases in the risk of herpes zoster. Patients treated with TNF inhibitor monotherapy had a risk of herpes zoster similar to that of those treated with conventional synthetic DMARDs or no synthetic therapy.

On the question of immunization, the authors pointed to guidelines recommending use of the live attenuated zoster vaccine (Zostavax) in immunocompetent patients or those on low-dose immunosuppression, although they noted that the vaccine is currently contraindicated for patients on biologic DMARDs.

They also examined the evidence for the use of the recently-released non-live recombinant herpes zoster vaccine (Shingrix) in immunocompromised patients, which found no evidence of vaccine-related serious adverse events in individuals with HIV and low CD4 cell counts and in autologous hematopoietic stem cell transplant recipients.

Given this, they recommended that the recombinant vaccine be administered to all patients aged over 50 years with psoriasis or psoriatic arthritis, and to those aged under 50 years who were being treated with tofacitinib, systemic corticosteroids, or combination systemic therapy.

There were insufficient data to draw conclusions about the impact of treatment with the interleukin-12/23 blocker ustekinumab (Stelara) on herpes zoster risk, but the authors noted that there was a trend toward an increased risk. They found no increase in the risk of herpes zoster with interleukin-17 inhibitors (ixekizumab [Taltz], secukinumab [Cosentyx], and brodalumab [Siliq]) and interleukin-23 (p19 subunit) inhibitors (guselkumab [Tremfya], tildrakizumab [Ilumya], and risankizumab) but noted an absence of long-term safety data for these drugs.

Four authors declared advisory, consultancy, or speaker positions with the pharmaceutical sector.

SOURCE: Baumrin E et al. J Am Acad Dermatol. 2019 March 15. doi: 10.1016/j.jaad.2019.03.017.

All individuals with psoriasis or psoriatic arthritis aged over 50 years should receive the recombinant herpes zoster vaccine, according to a systematic review and consensus recommendations from the National Psoriasis Foundation.

Joloei/Thinkstock

Emily Baumrin, MD, of Brigham and Women’s Hospital, Boston, and her coauthors reviewed 41 studies of herpes zoster in people with psoriasis or psoriatic arthritis according to treatment modality. Their report is in the Journal of the American Academy of Dermatology.

Overall, psoriasis was associated with an increased rate of herpes zoster when compared with the general population: 13.3 cases per 1,000 patient-years for psoriasis and 15.9 for psoriatic arthritis, compared with 8.5 in healthy controls after adjustment for age, sex, and systemic medications. Most of this increased incidence was seen in patients with more severe disease: Those with mild disease who were not receiving systemic therapy had a risk similar to that of healthy controls.

However, one study suggested much of the increased risk of herpes zoster in psoriasis was accounted for by immunosuppressive therapy; when those patients were excluded, there was an 8% increase in risk.


The authors found that people whose psoriasis was treated with tofacitinib (Xeljanz) had a two- to threefold increased risk of herpes zoster, compared with those treated with tumor necrosis factor (TNF) inhibitors or conventional synthetic disease-modifying antirheumatic drugs (DMARDs).

Corticosteroids – either alone or in combination with DMARDs – were also associated with significant increases in the risk of herpes zoster. Patients treated with TNF inhibitor monotherapy had a risk of herpes zoster similar to that of those treated with conventional synthetic DMARDs or no synthetic therapy.

On the question of immunization, the authors pointed to guidelines recommending use of the live attenuated zoster vaccine (Zostavax) in immunocompetent patients or those on low-dose immunosuppression, although they noted that the vaccine is currently contraindicated for patients on biologic DMARDs.

They also examined the evidence for the use of the recently-released non-live recombinant herpes zoster vaccine (Shingrix) in immunocompromised patients, which found no evidence of vaccine-related serious adverse events in individuals with HIV and low CD4 cell counts and in autologous hematopoietic stem cell transplant recipients.

Given this, they recommended that the recombinant vaccine be administered to all patients aged over 50 years with psoriasis or psoriatic arthritis, and to those aged under 50 years who were being treated with tofacitinib, systemic corticosteroids, or combination systemic therapy.

There were insufficient data to draw conclusions about the impact of treatment with the interleukin-12/23 blocker ustekinumab (Stelara) on herpes zoster risk, but the authors noted that there was a trend toward an increased risk. They found no increase in the risk of herpes zoster with interleukin-17 inhibitors (ixekizumab [Taltz], secukinumab [Cosentyx], and brodalumab [Siliq]) and interleukin-23 (p19 subunit) inhibitors (guselkumab [Tremfya], tildrakizumab [Ilumya], and risankizumab) but noted an absence of long-term safety data for these drugs.

Four authors declared advisory, consultancy, or speaker positions with the pharmaceutical sector.

SOURCE: Baumrin E et al. J Am Acad Dermatol. 2019 March 15. doi: 10.1016/j.jaad.2019.03.017.

All individuals with psoriasis or psoriatic arthritis aged over 50 years should receive the recombinant herpes zoster vaccine, according to a systematic review and consensus recommendations from the National Psoriasis Foundation.

Joloei/Thinkstock

Emily Baumrin, MD, of Brigham and Women’s Hospital, Boston, and her coauthors reviewed 41 studies of herpes zoster in people with psoriasis or psoriatic arthritis according to treatment modality. Their report is in the Journal of the American Academy of Dermatology.

Overall, psoriasis was associated with an increased rate of herpes zoster when compared with the general population: 13.3 cases per 1,000 patient-years for psoriasis and 15.9 for psoriatic arthritis, compared with 8.5 in healthy controls after adjustment for age, sex, and systemic medications. Most of this increased incidence was seen in patients with more severe disease: Those with mild disease who were not receiving systemic therapy had a risk similar to that of healthy controls.

However, one study suggested much of the increased risk of herpes zoster in psoriasis was accounted for by immunosuppressive therapy; when those patients were excluded, there was an 8% increase in risk.


The authors found that people whose psoriasis was treated with tofacitinib (Xeljanz) had a two- to threefold increased risk of herpes zoster, compared with those treated with tumor necrosis factor (TNF) inhibitors or conventional synthetic disease-modifying antirheumatic drugs (DMARDs).

Corticosteroids – either alone or in combination with DMARDs – were also associated with significant increases in the risk of herpes zoster. Patients treated with TNF inhibitor monotherapy had a risk of herpes zoster similar to that of those treated with conventional synthetic DMARDs or no synthetic therapy.

On the question of immunization, the authors pointed to guidelines recommending use of the live attenuated zoster vaccine (Zostavax) in immunocompetent patients or those on low-dose immunosuppression, although they noted that the vaccine is currently contraindicated for patients on biologic DMARDs.

They also examined the evidence for the use of the recently-released non-live recombinant herpes zoster vaccine (Shingrix) in immunocompromised patients, which found no evidence of vaccine-related serious adverse events in individuals with HIV and low CD4 cell counts and in autologous hematopoietic stem cell transplant recipients.

Given this, they recommended that the recombinant vaccine be administered to all patients aged over 50 years with psoriasis or psoriatic arthritis, and to those aged under 50 years who were being treated with tofacitinib, systemic corticosteroids, or combination systemic therapy.

There were insufficient data to draw conclusions about the impact of treatment with the interleukin-12/23 blocker ustekinumab (Stelara) on herpes zoster risk, but the authors noted that there was a trend toward an increased risk. They found no increase in the risk of herpes zoster with interleukin-17 inhibitors (ixekizumab [Taltz], secukinumab [Cosentyx], and brodalumab [Siliq]) and interleukin-23 (p19 subunit) inhibitors (guselkumab [Tremfya], tildrakizumab [Ilumya], and risankizumab) but noted an absence of long-term safety data for these drugs.

Four authors declared advisory, consultancy, or speaker positions with the pharmaceutical sector.

SOURCE: Baumrin E et al. J Am Acad Dermatol. 2019 March 15. doi: 10.1016/j.jaad.2019.03.017.

WAIKOLOA, HAWAII – It’s easy to misdiagnose scabies in infants because it doesn’t present with the usual signs and symptoms in this age group.

“It’s really important to think of scabies in any widespread rash that a baby presents with,” said Andrea Zaenglein, MD, professor of dermatology and pediatric dermatology at Penn State University, Hershey. It’s often missed in the ED because it’s not recognized.

While lesions might be limited to the webbing of the hands in older patients, infants generally have a widespread rash with many different lesion types involving the armpits, trunk, and even the scalp. “In older kids, we always think of itch as our primary criteria, but for infants with scabies, that’s not always the case. The younger the kid, the less able they’re to manifest the itch in a way that we recognize,” she said in an interview at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

Standard treatment for infants with scabies is permethrin cream, which, Dr. Zaenglein advises, should be applied from head to toe. “And make sure to treat all family members, even if they’re not demonstrating any symptoms. It’s really important, because that baby had to get scabies from somebody,” she said. Although permethrin isn’t approved for use under 2 months old, she said she has no problem with it in younger, otherwise healthy infants, but cases below 2 months are uncommon. Even if infants are exposed at birth, it takes several weeks for scabies to manifest.

Topical corticosteroids are useful as well to speed healing and help with itch. Ivermectin is held in reserve for older patients, especially in institutional settings where many people have to be treated at a time, or when permethrin cream is not effective.

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

aotto@mdedge.com

WAIKOLOA, HAWAII – It’s easy to misdiagnose scabies in infants because it doesn’t present with the usual signs and symptoms in this age group.

“It’s really important to think of scabies in any widespread rash that a baby presents with,” said Andrea Zaenglein, MD, professor of dermatology and pediatric dermatology at Penn State University, Hershey. It’s often missed in the ED because it’s not recognized.

While lesions might be limited to the webbing of the hands in older patients, infants generally have a widespread rash with many different lesion types involving the armpits, trunk, and even the scalp. “In older kids, we always think of itch as our primary criteria, but for infants with scabies, that’s not always the case. The younger the kid, the less able they’re to manifest the itch in a way that we recognize,” she said in an interview at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

Standard treatment for infants with scabies is permethrin cream, which, Dr. Zaenglein advises, should be applied from head to toe. “And make sure to treat all family members, even if they’re not demonstrating any symptoms. It’s really important, because that baby had to get scabies from somebody,” she said. Although permethrin isn’t approved for use under 2 months old, she said she has no problem with it in younger, otherwise healthy infants, but cases below 2 months are uncommon. Even if infants are exposed at birth, it takes several weeks for scabies to manifest.

Topical corticosteroids are useful as well to speed healing and help with itch. Ivermectin is held in reserve for older patients, especially in institutional settings where many people have to be treated at a time, or when permethrin cream is not effective.

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

aotto@mdedge.com

WAIKOLOA, HAWAII – It’s easy to misdiagnose scabies in infants because it doesn’t present with the usual signs and symptoms in this age group.

“It’s really important to think of scabies in any widespread rash that a baby presents with,” said Andrea Zaenglein, MD, professor of dermatology and pediatric dermatology at Penn State University, Hershey. It’s often missed in the ED because it’s not recognized.

While lesions might be limited to the webbing of the hands in older patients, infants generally have a widespread rash with many different lesion types involving the armpits, trunk, and even the scalp. “In older kids, we always think of itch as our primary criteria, but for infants with scabies, that’s not always the case. The younger the kid, the less able they’re to manifest the itch in a way that we recognize,” she said in an interview at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

Standard treatment for infants with scabies is permethrin cream, which, Dr. Zaenglein advises, should be applied from head to toe. “And make sure to treat all family members, even if they’re not demonstrating any symptoms. It’s really important, because that baby had to get scabies from somebody,” she said. Although permethrin isn’t approved for use under 2 months old, she said she has no problem with it in younger, otherwise healthy infants, but cases below 2 months are uncommon. Even if infants are exposed at birth, it takes several weeks for scabies to manifest.

Topical corticosteroids are useful as well to speed healing and help with itch. Ivermectin is held in reserve for older patients, especially in institutional settings where many people have to be treated at a time, or when permethrin cream is not effective.

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

aotto@mdedge.com