Dermatology

A 61-year-old man is sent to dermatology by his primary care provider for evaluation of several facial lesions. Although they have been present for years, the patient says they have never caused any symptoms.

The patient’s work history includes extensive outdoor activity, as well as more than 20 years of driving a truck. He is now retired and spends most of his days fishing.

He has a history of at least two unspecified skin cancers but denies receiving facial radiation treatment. He has been a smoker since age 12 and admits to heavy drinking.

EXAMINATION
The patient’s face is uneven in appearance, with deep wrinkles and multiple areas of discoloration. His skin is type III.

Multiple open and closed comedones are seen around the left malar and brow areas, where the underlying skin has a whitish look to it. The comedones are not inflamed, and no pustules are observed. Some of the comedones extend into the infra-orbital area on the left side of his face. Almost no such changes are seen on the right side.

There is no increase in hair in the affected areas and no skin changes observed on his hands or arms, other than moderately severe sun damage.

What is the diagnosis?

DISCUSSION
In the 1930s, two French dermatologists, Favre and Racouchot, began to see several cases like this one. Following a review of available literature, they published their findings, calling the condition “nodular elastosis with cysts and comedones.” This quickly became known as Favre-Racouchot syndrome (FRS), the name it still bears today.

FRS is quite common, especially on the faces of white men older than 50. More men than woman are affected, and smoking almost certainly contributes to the problem.

The connection between FRS and sun exposure is well established: the basophilic degeneration of the dermis (solar elastosis) seen in FRS is identical to that seen from overexposure to the sun. Another clue to the cause is exemplified in cases involving truck drivers, since the side of the face nearest the window is usually affected more than the other side. In most countries, the left side of the face sustains the most damage; in countries with right-hand drive, the right side of the face is affected.

Significant focal nodular solar elastosis, along with open and closed comedones, notably worse on the more sun-exposed side, is unique to FRS. The lack of increase in facial hair in the affected area is significant, in that it effectively rules out the only other major item in the differential: porphyria cutanea tarda.

Treatment is problematic at best. Except in younger patients, sunscreens are largely a waste. The comedones can be manually extracted, but recurrence is certain. For the truly motivated patient, laser resurfacing and peels can help. To slow the progression of the disease, smoking cessation is necessary.

TAKE-HOME LEARNING POINTS

• Favre-Racouchot syndrome (FRS) is most commonly seen in older men with a history of excessive chronic sun exposure. Most are smokers.
• FRS primarily affects the malar and lateral brow areas with nodular elastosis, in which are embedded multiple cysts and comedones.
• In the United States, FRS is usually more pronounced on the left side of the face.
• Other signs of chronic sun damage (actinic weathering, also known as dermatoheliosis) are almost always seen over the entire face of FRS patients.

A 61-year-old man is sent to dermatology by his primary care provider for evaluation of several facial lesions. Although they have been present for years, the patient says they have never caused any symptoms.

The patient’s work history includes extensive outdoor activity, as well as more than 20 years of driving a truck. He is now retired and spends most of his days fishing.

He has a history of at least two unspecified skin cancers but denies receiving facial radiation treatment. He has been a smoker since age 12 and admits to heavy drinking.

EXAMINATION
The patient’s face is uneven in appearance, with deep wrinkles and multiple areas of discoloration. His skin is type III.

Multiple open and closed comedones are seen around the left malar and brow areas, where the underlying skin has a whitish look to it. The comedones are not inflamed, and no pustules are observed. Some of the comedones extend into the infra-orbital area on the left side of his face. Almost no such changes are seen on the right side.

There is no increase in hair in the affected areas and no skin changes observed on his hands or arms, other than moderately severe sun damage.

What is the diagnosis?

DISCUSSION
In the 1930s, two French dermatologists, Favre and Racouchot, began to see several cases like this one. Following a review of available literature, they published their findings, calling the condition “nodular elastosis with cysts and comedones.” This quickly became known as Favre-Racouchot syndrome (FRS), the name it still bears today.

FRS is quite common, especially on the faces of white men older than 50. More men than woman are affected, and smoking almost certainly contributes to the problem.

The connection between FRS and sun exposure is well established: the basophilic degeneration of the dermis (solar elastosis) seen in FRS is identical to that seen from overexposure to the sun. Another clue to the cause is exemplified in cases involving truck drivers, since the side of the face nearest the window is usually affected more than the other side. In most countries, the left side of the face sustains the most damage; in countries with right-hand drive, the right side of the face is affected.

Significant focal nodular solar elastosis, along with open and closed comedones, notably worse on the more sun-exposed side, is unique to FRS. The lack of increase in facial hair in the affected area is significant, in that it effectively rules out the only other major item in the differential: porphyria cutanea tarda.

Treatment is problematic at best. Except in younger patients, sunscreens are largely a waste. The comedones can be manually extracted, but recurrence is certain. For the truly motivated patient, laser resurfacing and peels can help. To slow the progression of the disease, smoking cessation is necessary.

TAKE-HOME LEARNING POINTS

• Favre-Racouchot syndrome (FRS) is most commonly seen in older men with a history of excessive chronic sun exposure. Most are smokers.
• FRS primarily affects the malar and lateral brow areas with nodular elastosis, in which are embedded multiple cysts and comedones.
• In the United States, FRS is usually more pronounced on the left side of the face.
• Other signs of chronic sun damage (actinic weathering, also known as dermatoheliosis) are almost always seen over the entire face of FRS patients.

A 61-year-old man is sent to dermatology by his primary care provider for evaluation of several facial lesions. Although they have been present for years, the patient says they have never caused any symptoms.

The patient’s work history includes extensive outdoor activity, as well as more than 20 years of driving a truck. He is now retired and spends most of his days fishing.

He has a history of at least two unspecified skin cancers but denies receiving facial radiation treatment. He has been a smoker since age 12 and admits to heavy drinking.

EXAMINATION
The patient’s face is uneven in appearance, with deep wrinkles and multiple areas of discoloration. His skin is type III.

Multiple open and closed comedones are seen around the left malar and brow areas, where the underlying skin has a whitish look to it. The comedones are not inflamed, and no pustules are observed. Some of the comedones extend into the infra-orbital area on the left side of his face. Almost no such changes are seen on the right side.

There is no increase in hair in the affected areas and no skin changes observed on his hands or arms, other than moderately severe sun damage.

What is the diagnosis?

DISCUSSION
In the 1930s, two French dermatologists, Favre and Racouchot, began to see several cases like this one. Following a review of available literature, they published their findings, calling the condition “nodular elastosis with cysts and comedones.” This quickly became known as Favre-Racouchot syndrome (FRS), the name it still bears today.

FRS is quite common, especially on the faces of white men older than 50. More men than woman are affected, and smoking almost certainly contributes to the problem.

The connection between FRS and sun exposure is well established: the basophilic degeneration of the dermis (solar elastosis) seen in FRS is identical to that seen from overexposure to the sun. Another clue to the cause is exemplified in cases involving truck drivers, since the side of the face nearest the window is usually affected more than the other side. In most countries, the left side of the face sustains the most damage; in countries with right-hand drive, the right side of the face is affected.

Significant focal nodular solar elastosis, along with open and closed comedones, notably worse on the more sun-exposed side, is unique to FRS. The lack of increase in facial hair in the affected area is significant, in that it effectively rules out the only other major item in the differential: porphyria cutanea tarda.

Treatment is problematic at best. Except in younger patients, sunscreens are largely a waste. The comedones can be manually extracted, but recurrence is certain. For the truly motivated patient, laser resurfacing and peels can help. To slow the progression of the disease, smoking cessation is necessary.

TAKE-HOME LEARNING POINTS

• Favre-Racouchot syndrome (FRS) is most commonly seen in older men with a history of excessive chronic sun exposure. Most are smokers.
• FRS primarily affects the malar and lateral brow areas with nodular elastosis, in which are embedded multiple cysts and comedones.
• In the United States, FRS is usually more pronounced on the left side of the face.
• Other signs of chronic sun damage (actinic weathering, also known as dermatoheliosis) are almost always seen over the entire face of FRS patients.

The FP recognized the lesion as a probable squamous cell carcinoma (SCC) due to its appearance and location on the lower lip. He was also aware that immunosuppressive medications increase a patient's risk for SCC.

The FP performed a shave biopsy of a portion of the lesion and the result confirmed SCC. (See the Watch & Learn video on “Shave biopsy.”)  A careful head and neck exam did not reveal palpable lymph nodes. Given the location of the lesion and the risk for metastases, the FP referred the patient for Mohs surgery and provided counseling about sun avoidance, the consistent use of a hat outdoors, and the use of sunscreens when exposed to the sun.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Squamous cell carcinoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:999-1007.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

The new third edition will be available in January 2019: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/.

You can also get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

The FP recognized the lesion as a probable squamous cell carcinoma (SCC) due to its appearance and location on the lower lip. He was also aware that immunosuppressive medications increase a patient's risk for SCC.

The FP performed a shave biopsy of a portion of the lesion and the result confirmed SCC. (See the Watch & Learn video on “Shave biopsy.”)  A careful head and neck exam did not reveal palpable lymph nodes. Given the location of the lesion and the risk for metastases, the FP referred the patient for Mohs surgery and provided counseling about sun avoidance, the consistent use of a hat outdoors, and the use of sunscreens when exposed to the sun.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Squamous cell carcinoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:999-1007.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

The new third edition will be available in January 2019: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/.

You can also get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

The FP recognized the lesion as a probable squamous cell carcinoma (SCC) due to its appearance and location on the lower lip. He was also aware that immunosuppressive medications increase a patient's risk for SCC.

The FP performed a shave biopsy of a portion of the lesion and the result confirmed SCC. (See the Watch & Learn video on “Shave biopsy.”)  A careful head and neck exam did not reveal palpable lymph nodes. Given the location of the lesion and the risk for metastases, the FP referred the patient for Mohs surgery and provided counseling about sun avoidance, the consistent use of a hat outdoors, and the use of sunscreens when exposed to the sun.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Squamous cell carcinoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:999-1007.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

The new third edition will be available in January 2019: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/.

You can also get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

Epidermal nevi are a subset of cutaneous hamartomas resulting from somatic mutations of epidermal cells, presenting as keratinocyte or epidermal appendage overgrowths. The most common type appear in a linear distribution and are termed linear epidermal nevi or linear verrucous epidermal nevi.

There are variations of epidermal nevi (EN) that can be composed of superficial epidermal keratinocytes, sebaceous glands, apocrine or eccrine glands, hair follicles, or smooth muscle. For example, many consider a nevus sebaceous to be a type of epidermal nevus as well. The incidence of EN is approximately 1 in 1,000 newborns. Postzygotic cell mutations result in a mosaic distribution that follows embryonic migration patterns, appearing in a Blaschkoid distribution.

EN present most frequently as unilateral linear or whorled hyperpigmented coalescing papules. The lesions can be present at birth or during childhood, and after appearing, grow with the patient. Typically the lesions become more raised and verrucous around puberty. The differential diagnosis of linear EN include lichen striatus, warts, and incontinentia pigmenti. Lichen striatus can be differentiated because it presents later in life and self-resolves. Verrucae are the most commonly mistaken diagnosis for EN; warts do not usually persist in the same pattern over time with proportionate growth and typically respond to locally destructive treatments such as liquid nitrogen, unlike EN. Incontinentia pigmenti presents as vesicles initially and shows a quick evolution, differentiating it from EN. Inflammatory linear verrucous epidermal nevus (ILVEN) is a variant of linear EN that has associated chronic and intermittent erythema, scale, and pruritus. Lichen nitidus often has a pruritic presentation; however, it is flat topped and skin colored, helping differentiate it from linear EN.

There has been recent research advancing gene associations for linear EN displaying many lesions associated with mosaic mutations in oncogenes. Multiple genes have been identified with EN including RAS, FGFR3, and PIK3CA¹. FGFR3 and PIK3CA mutations are associated with 50% of keratinocytic nevi. Of the RAS family, the HRAS pathway has been most closely associated with nevus sebaceous. While KRAS and NRAS genes have been associated with EN, it is to a lesser degree. However, there are multiple recent case reports demonstrating a potential association of G12D mosaicism of the KRAS gene in EN with rhabdomyosarcoma and bladder cancers².

The diagnosis of epidermal nevus syndrome should be considered when there is a nevus with associated developmental abnormality of the central nervous system, eyes, or musculoskeletal systems. The most common systemic symptoms include delays in developmental milestones, seizure disorders, coloboma, strabismus, muscle weakness, and hemihypertrophy. To date, there are six specific epidermal nevus syndromes identified: sebaceous nevus syndrome, nevus comedonicus syndrome, Becker nevus syndrome, phakomatosis pigmentokeratotica, Proteus syndrome, congenital hemidysplasia with ichthyosiform nevus and limb defects, and cutaneous-skeletal hypophosphatemia syndrome³. In addition to the syndromes described, there are reports of associations between keratinocytic nevi and ILVEN with hypophosphatemic rickets and precocious puberty.
 

Linear EN are rarely associated with malignant transformation to basal cell carcinoma or squamous cell carcinoma, depending on the cell type involved. Given the low risk of malignancy, the lesions do not need to be removed routinely. For small lesions, monitoring often is the preferred management. However, lesions with functional significance, or causing strangulation or deformity, can be treated with surgical excision, curettage, or laser destruction

Dr. Kaushik is with the division of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego, and Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. There are no conflicts of interest or financial disclosures for Dr. Kaushik or Dr. Eichenfield. Email them at [email protected].

References

1. Pediatr Dermatol. 2004 Jul-Aug;21(4):432-9.

2. J Med Genet. 2010 Dec;47(12):859-62.

3. Pediatr Dermatol. 2018 Jan;35(1):21-9.

Epidermal nevi are a subset of cutaneous hamartomas resulting from somatic mutations of epidermal cells, presenting as keratinocyte or epidermal appendage overgrowths. The most common type appear in a linear distribution and are termed linear epidermal nevi or linear verrucous epidermal nevi.

There are variations of epidermal nevi (EN) that can be composed of superficial epidermal keratinocytes, sebaceous glands, apocrine or eccrine glands, hair follicles, or smooth muscle. For example, many consider a nevus sebaceous to be a type of epidermal nevus as well. The incidence of EN is approximately 1 in 1,000 newborns. Postzygotic cell mutations result in a mosaic distribution that follows embryonic migration patterns, appearing in a Blaschkoid distribution.

EN present most frequently as unilateral linear or whorled hyperpigmented coalescing papules. The lesions can be present at birth or during childhood, and after appearing, grow with the patient. Typically the lesions become more raised and verrucous around puberty. The differential diagnosis of linear EN include lichen striatus, warts, and incontinentia pigmenti. Lichen striatus can be differentiated because it presents later in life and self-resolves. Verrucae are the most commonly mistaken diagnosis for EN; warts do not usually persist in the same pattern over time with proportionate growth and typically respond to locally destructive treatments such as liquid nitrogen, unlike EN. Incontinentia pigmenti presents as vesicles initially and shows a quick evolution, differentiating it from EN. Inflammatory linear verrucous epidermal nevus (ILVEN) is a variant of linear EN that has associated chronic and intermittent erythema, scale, and pruritus. Lichen nitidus often has a pruritic presentation; however, it is flat topped and skin colored, helping differentiate it from linear EN.

There has been recent research advancing gene associations for linear EN displaying many lesions associated with mosaic mutations in oncogenes. Multiple genes have been identified with EN including RAS, FGFR3, and PIK3CA¹. FGFR3 and PIK3CA mutations are associated with 50% of keratinocytic nevi. Of the RAS family, the HRAS pathway has been most closely associated with nevus sebaceous. While KRAS and NRAS genes have been associated with EN, it is to a lesser degree. However, there are multiple recent case reports demonstrating a potential association of G12D mosaicism of the KRAS gene in EN with rhabdomyosarcoma and bladder cancers².

The diagnosis of epidermal nevus syndrome should be considered when there is a nevus with associated developmental abnormality of the central nervous system, eyes, or musculoskeletal systems. The most common systemic symptoms include delays in developmental milestones, seizure disorders, coloboma, strabismus, muscle weakness, and hemihypertrophy. To date, there are six specific epidermal nevus syndromes identified: sebaceous nevus syndrome, nevus comedonicus syndrome, Becker nevus syndrome, phakomatosis pigmentokeratotica, Proteus syndrome, congenital hemidysplasia with ichthyosiform nevus and limb defects, and cutaneous-skeletal hypophosphatemia syndrome³. In addition to the syndromes described, there are reports of associations between keratinocytic nevi and ILVEN with hypophosphatemic rickets and precocious puberty.
 

Linear EN are rarely associated with malignant transformation to basal cell carcinoma or squamous cell carcinoma, depending on the cell type involved. Given the low risk of malignancy, the lesions do not need to be removed routinely. For small lesions, monitoring often is the preferred management. However, lesions with functional significance, or causing strangulation or deformity, can be treated with surgical excision, curettage, or laser destruction

Dr. Kaushik is with the division of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego, and Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. There are no conflicts of interest or financial disclosures for Dr. Kaushik or Dr. Eichenfield. Email them at [email protected].

References

1. Pediatr Dermatol. 2004 Jul-Aug;21(4):432-9.

2. J Med Genet. 2010 Dec;47(12):859-62.

3. Pediatr Dermatol. 2018 Jan;35(1):21-9.

Epidermal nevi are a subset of cutaneous hamartomas resulting from somatic mutations of epidermal cells, presenting as keratinocyte or epidermal appendage overgrowths. The most common type appear in a linear distribution and are termed linear epidermal nevi or linear verrucous epidermal nevi.

There are variations of epidermal nevi (EN) that can be composed of superficial epidermal keratinocytes, sebaceous glands, apocrine or eccrine glands, hair follicles, or smooth muscle. For example, many consider a nevus sebaceous to be a type of epidermal nevus as well. The incidence of EN is approximately 1 in 1,000 newborns. Postzygotic cell mutations result in a mosaic distribution that follows embryonic migration patterns, appearing in a Blaschkoid distribution.

EN present most frequently as unilateral linear or whorled hyperpigmented coalescing papules. The lesions can be present at birth or during childhood, and after appearing, grow with the patient. Typically the lesions become more raised and verrucous around puberty. The differential diagnosis of linear EN include lichen striatus, warts, and incontinentia pigmenti. Lichen striatus can be differentiated because it presents later in life and self-resolves. Verrucae are the most commonly mistaken diagnosis for EN; warts do not usually persist in the same pattern over time with proportionate growth and typically respond to locally destructive treatments such as liquid nitrogen, unlike EN. Incontinentia pigmenti presents as vesicles initially and shows a quick evolution, differentiating it from EN. Inflammatory linear verrucous epidermal nevus (ILVEN) is a variant of linear EN that has associated chronic and intermittent erythema, scale, and pruritus. Lichen nitidus often has a pruritic presentation; however, it is flat topped and skin colored, helping differentiate it from linear EN.

There has been recent research advancing gene associations for linear EN displaying many lesions associated with mosaic mutations in oncogenes. Multiple genes have been identified with EN including RAS, FGFR3, and PIK3CA¹. FGFR3 and PIK3CA mutations are associated with 50% of keratinocytic nevi. Of the RAS family, the HRAS pathway has been most closely associated with nevus sebaceous. While KRAS and NRAS genes have been associated with EN, it is to a lesser degree. However, there are multiple recent case reports demonstrating a potential association of G12D mosaicism of the KRAS gene in EN with rhabdomyosarcoma and bladder cancers².

The diagnosis of epidermal nevus syndrome should be considered when there is a nevus with associated developmental abnormality of the central nervous system, eyes, or musculoskeletal systems. The most common systemic symptoms include delays in developmental milestones, seizure disorders, coloboma, strabismus, muscle weakness, and hemihypertrophy. To date, there are six specific epidermal nevus syndromes identified: sebaceous nevus syndrome, nevus comedonicus syndrome, Becker nevus syndrome, phakomatosis pigmentokeratotica, Proteus syndrome, congenital hemidysplasia with ichthyosiform nevus and limb defects, and cutaneous-skeletal hypophosphatemia syndrome³. In addition to the syndromes described, there are reports of associations between keratinocytic nevi and ILVEN with hypophosphatemic rickets and precocious puberty.
 

Linear EN are rarely associated with malignant transformation to basal cell carcinoma or squamous cell carcinoma, depending on the cell type involved. Given the low risk of malignancy, the lesions do not need to be removed routinely. For small lesions, monitoring often is the preferred management. However, lesions with functional significance, or causing strangulation or deformity, can be treated with surgical excision, curettage, or laser destruction

Dr. Kaushik is with the division of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego, and Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. There are no conflicts of interest or financial disclosures for Dr. Kaushik or Dr. Eichenfield. Email them at [email protected].

References

1. Pediatr Dermatol. 2004 Jul-Aug;21(4):432-9.

2. J Med Genet. 2010 Dec;47(12):859-62.

3. Pediatr Dermatol. 2018 Jan;35(1):21-9.

Myth: Psoriasis Is Only a Skin Problem

Psoriasis is predominantly regarded as a skin disease because of the outward clinical presentation of the condition. However, psoriasis is a disorder of the immune system and its damage may be more than skin deep.

Psoriasis commonly presents on the skin and nails, but a growing body of evidence has suggested that psoriasis is associated with systemic comorbidities. Up to 25% of psoriasis patients develop joint inflammation, and psoriatic arthritis (PsA) may precede skin involvement. There also is a risk for cardiovascular complications. Because of the emotional distress caused by psoriasis, patients may develop psychosocial disorders. Other conditions in patients with psoriasis include diabetes mellitus, high blood pressure, Crohn disease, and the metabolic syndrome.

Results from surveys conducted by the National Psoriasis Foundation from 2003 to 2011 found that the diagnosis of psoriasis preceded PsA in the majority of patients by a mean period of 14.6 years. Patients with moderate to severe psoriasis were more likely to develop PsA than patients with mild psoriasis. Furthermore, patients with severe psoriasis were more likely to develop diabetes mellitus and cardiovascular disease.

In a Cutis editorial, Dr. Jeffrey Weinberg emphasizes that the role of the dermatologist “is to identify and educate patients with psoriasis who are at risk of systemic complications and ensure appropriate follow-up for their treatment and overall health.” An infographic created by the American Academy of Dermatology illustrates areas of the body that may be impacted by psoriasis beyond the skin; for example, patients may develop eye problems, weight gain, or mood changes. Consider distributing this infographic to patients to show how psoriasis can affect more than their skin.

More Cutis content is available on psoriasis comorbidities:

• Do Psoriasis Patients Engage In Vigorous Physical Activity?
• The Role of Biologic Therapy for Psoriasis in Cardiovascular Risk Reduction
• VIDEO: Psoriasis and Internal Disease
• Uveitis and Psoriasis
• VIDEO: Update on Psoriasis Comorbidities

Myth: Psoriasis Is Only a Skin Problem

Psoriasis is predominantly regarded as a skin disease because of the outward clinical presentation of the condition. However, psoriasis is a disorder of the immune system and its damage may be more than skin deep.

Psoriasis commonly presents on the skin and nails, but a growing body of evidence has suggested that psoriasis is associated with systemic comorbidities. Up to 25% of psoriasis patients develop joint inflammation, and psoriatic arthritis (PsA) may precede skin involvement. There also is a risk for cardiovascular complications. Because of the emotional distress caused by psoriasis, patients may develop psychosocial disorders. Other conditions in patients with psoriasis include diabetes mellitus, high blood pressure, Crohn disease, and the metabolic syndrome.

Results from surveys conducted by the National Psoriasis Foundation from 2003 to 2011 found that the diagnosis of psoriasis preceded PsA in the majority of patients by a mean period of 14.6 years. Patients with moderate to severe psoriasis were more likely to develop PsA than patients with mild psoriasis. Furthermore, patients with severe psoriasis were more likely to develop diabetes mellitus and cardiovascular disease.

In a Cutis editorial, Dr. Jeffrey Weinberg emphasizes that the role of the dermatologist “is to identify and educate patients with psoriasis who are at risk of systemic complications and ensure appropriate follow-up for their treatment and overall health.” An infographic created by the American Academy of Dermatology illustrates areas of the body that may be impacted by psoriasis beyond the skin; for example, patients may develop eye problems, weight gain, or mood changes. Consider distributing this infographic to patients to show how psoriasis can affect more than their skin.

More Cutis content is available on psoriasis comorbidities:

• Do Psoriasis Patients Engage In Vigorous Physical Activity?
• The Role of Biologic Therapy for Psoriasis in Cardiovascular Risk Reduction
• VIDEO: Psoriasis and Internal Disease
• Uveitis and Psoriasis
• VIDEO: Update on Psoriasis Comorbidities

Myth: Psoriasis Is Only a Skin Problem

Psoriasis is predominantly regarded as a skin disease because of the outward clinical presentation of the condition. However, psoriasis is a disorder of the immune system and its damage may be more than skin deep.

Psoriasis commonly presents on the skin and nails, but a growing body of evidence has suggested that psoriasis is associated with systemic comorbidities. Up to 25% of psoriasis patients develop joint inflammation, and psoriatic arthritis (PsA) may precede skin involvement. There also is a risk for cardiovascular complications. Because of the emotional distress caused by psoriasis, patients may develop psychosocial disorders. Other conditions in patients with psoriasis include diabetes mellitus, high blood pressure, Crohn disease, and the metabolic syndrome.

Results from surveys conducted by the National Psoriasis Foundation from 2003 to 2011 found that the diagnosis of psoriasis preceded PsA in the majority of patients by a mean period of 14.6 years. Patients with moderate to severe psoriasis were more likely to develop PsA than patients with mild psoriasis. Furthermore, patients with severe psoriasis were more likely to develop diabetes mellitus and cardiovascular disease.

In a Cutis editorial, Dr. Jeffrey Weinberg emphasizes that the role of the dermatologist “is to identify and educate patients with psoriasis who are at risk of systemic complications and ensure appropriate follow-up for their treatment and overall health.” An infographic created by the American Academy of Dermatology illustrates areas of the body that may be impacted by psoriasis beyond the skin; for example, patients may develop eye problems, weight gain, or mood changes. Consider distributing this infographic to patients to show how psoriasis can affect more than their skin.

More Cutis content is available on psoriasis comorbidities:

• Do Psoriasis Patients Engage In Vigorous Physical Activity?
• The Role of Biologic Therapy for Psoriasis in Cardiovascular Risk Reduction
• VIDEO: Psoriasis and Internal Disease
• Uveitis and Psoriasis
• VIDEO: Update on Psoriasis Comorbidities

The American College of Rheumatology and the National Psoriasis Foundation have released a joint treatment guideline for psoriatic arthritis that, for the first time, includes a conditional recommendation to use tumor necrosis factor–inhibitor(TNFi) biologics over methotrexate and other oral small molecules as a first-line therapy in patients with active disease.

“The available low-quality evidence is inconclusive regarding the efficacy of OSMs [oral small molecules] in management of PsA, whereas there is moderate-quality evidence of the benefits of TNFi biologics, in particular regarding their impact on the prevention of disease progression and joint damage,” wrote the panel of authors, who were led by Jasvinder A. Singh, MD, of the University of Alabama at Birmingham. “In making their recommendation, the panel recognized the cost implications, but put considerations of quality of evidence for benefit over other considerations. This guideline provides recommendations for early and aggressive therapy in patients with newly diagnosed PsA.”

The 28-page guideline, published online Nov. 30 in the Journal of Psoriasis and Psoriatic Arthritis and also in Arthritis Care & Research and Arthritis & Rheumatology, is the first set of PsA-specific recommendations to be assembled using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology that the ACR has used for RA and other conditions. GRADE uses systematic reviews of the scientific literature available to evaluate and grade the quality of evidence in a particular domain. The evidence reviews are then used to create guideline recommendations for or against particular therapy options that range from strong to conditional, depending on the quality of evidence available.

Based on the GRADE methodology and consensus building, the guideline authors crafted recommendations for eight different clinical scenarios, including the initial treatment of patients with active PsA who have not received either OSMs or other treatments; treatment of patients with active PsA despite treatment with an OSM; treatment of patients with active PsA despite treatment with a TNFi biologic either as monotherapy or in combination with methotrexate; treatment of patients with active PsA despite treatment with an interleukin (IL)-17 inhibitor or IL-12/23 inhibitor monotherapy; treatment of patients with active PsA including treat-to-target, active axial disease, enthesitis, or active inflammatory bowel disease; treatment of patients with active PsA and comorbidities, including concomitant diabetes and recurrent serious infections; vaccination in patients with active PsA; and treatment of patients with active PsA with nonpharmacologic interventions such as yoga and weight loss. Most of the treatment recommendations are conditional based on very low to moderate quality evidence. “Health care providers and patients must take into consideration all active disease domains, comorbidities, and the patient’s functional status in choosing the optimal therapy for an individual at a given point in time,” the authors emphasized.

Only five of the recommendations are listed as strong, including smoking cessation. Three of the strong recommendations concern adult patients with active PsA and concomitant active inflammatory bowel disease despite treatment with an OSM. They are “switch to a monoclonal antibody TNFi biologic over a TNFi biologic soluble receptor biologic,” “switch to a TNFi monoclonal antibody biologic over an IL-7i biologic,” and “switch to an IL-12/23i biologic over switching to an IL-17i biologic.”

The process of creating the guideline included input from a panel of nine adults who provided the authors with perspective on their values and preferences. “The concept of treat-to-target was challenging for patients,” the authors noted. “Although they saw value in improved outcomes, they also thought this strategy could increase costs to the patient (e.g., copayments, time traveling to more frequent appointments, etc.) and potentially increase adverse events. Therefore, a detailed conversation with the patient is needed to make decisions regarding treat-to-target.”

The authors concluded the guideline by calling for more comparative data to inform treatment selection in the future. “Several ongoing trials, including a trial to compare a TNFi biologic combination therapy with a TNFi biologic monotherapy and MTX monotherapy, will inform treatment decisions,” they wrote. “We anticipate future updates to the guideline when new evidence is available.”

Dr. Singh, who is also a staff rheumatologist at the Birmingham (Ala.) Veterans Affairs Medical Center, led development of the 2012 and 2015 ACR treatment guidelines for RA. He has received consulting fees from a variety of companies marketing rheumatologic drugs as well as research support from Takeda and Savient. The other guideline authors reported having numerous financial ties to industry.

[email protected]

SOURCE: Singh J et al. Arthritis Care Res. 2018 Nov 30. doi: 10.1002/acr.23789.

The American College of Rheumatology and the National Psoriasis Foundation have released a joint treatment guideline for psoriatic arthritis that, for the first time, includes a conditional recommendation to use tumor necrosis factor–inhibitor(TNFi) biologics over methotrexate and other oral small molecules as a first-line therapy in patients with active disease.

“The available low-quality evidence is inconclusive regarding the efficacy of OSMs [oral small molecules] in management of PsA, whereas there is moderate-quality evidence of the benefits of TNFi biologics, in particular regarding their impact on the prevention of disease progression and joint damage,” wrote the panel of authors, who were led by Jasvinder A. Singh, MD, of the University of Alabama at Birmingham. “In making their recommendation, the panel recognized the cost implications, but put considerations of quality of evidence for benefit over other considerations. This guideline provides recommendations for early and aggressive therapy in patients with newly diagnosed PsA.”

The 28-page guideline, published online Nov. 30 in the Journal of Psoriasis and Psoriatic Arthritis and also in Arthritis Care & Research and Arthritis & Rheumatology, is the first set of PsA-specific recommendations to be assembled using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology that the ACR has used for RA and other conditions. GRADE uses systematic reviews of the scientific literature available to evaluate and grade the quality of evidence in a particular domain. The evidence reviews are then used to create guideline recommendations for or against particular therapy options that range from strong to conditional, depending on the quality of evidence available.

Based on the GRADE methodology and consensus building, the guideline authors crafted recommendations for eight different clinical scenarios, including the initial treatment of patients with active PsA who have not received either OSMs or other treatments; treatment of patients with active PsA despite treatment with an OSM; treatment of patients with active PsA despite treatment with a TNFi biologic either as monotherapy or in combination with methotrexate; treatment of patients with active PsA despite treatment with an interleukin (IL)-17 inhibitor or IL-12/23 inhibitor monotherapy; treatment of patients with active PsA including treat-to-target, active axial disease, enthesitis, or active inflammatory bowel disease; treatment of patients with active PsA and comorbidities, including concomitant diabetes and recurrent serious infections; vaccination in patients with active PsA; and treatment of patients with active PsA with nonpharmacologic interventions such as yoga and weight loss. Most of the treatment recommendations are conditional based on very low to moderate quality evidence. “Health care providers and patients must take into consideration all active disease domains, comorbidities, and the patient’s functional status in choosing the optimal therapy for an individual at a given point in time,” the authors emphasized.

Only five of the recommendations are listed as strong, including smoking cessation. Three of the strong recommendations concern adult patients with active PsA and concomitant active inflammatory bowel disease despite treatment with an OSM. They are “switch to a monoclonal antibody TNFi biologic over a TNFi biologic soluble receptor biologic,” “switch to a TNFi monoclonal antibody biologic over an IL-7i biologic,” and “switch to an IL-12/23i biologic over switching to an IL-17i biologic.”

The process of creating the guideline included input from a panel of nine adults who provided the authors with perspective on their values and preferences. “The concept of treat-to-target was challenging for patients,” the authors noted. “Although they saw value in improved outcomes, they also thought this strategy could increase costs to the patient (e.g., copayments, time traveling to more frequent appointments, etc.) and potentially increase adverse events. Therefore, a detailed conversation with the patient is needed to make decisions regarding treat-to-target.”

The authors concluded the guideline by calling for more comparative data to inform treatment selection in the future. “Several ongoing trials, including a trial to compare a TNFi biologic combination therapy with a TNFi biologic monotherapy and MTX monotherapy, will inform treatment decisions,” they wrote. “We anticipate future updates to the guideline when new evidence is available.”

Dr. Singh, who is also a staff rheumatologist at the Birmingham (Ala.) Veterans Affairs Medical Center, led development of the 2012 and 2015 ACR treatment guidelines for RA. He has received consulting fees from a variety of companies marketing rheumatologic drugs as well as research support from Takeda and Savient. The other guideline authors reported having numerous financial ties to industry.

[email protected]

SOURCE: Singh J et al. Arthritis Care Res. 2018 Nov 30. doi: 10.1002/acr.23789.

The American College of Rheumatology and the National Psoriasis Foundation have released a joint treatment guideline for psoriatic arthritis that, for the first time, includes a conditional recommendation to use tumor necrosis factor–inhibitor(TNFi) biologics over methotrexate and other oral small molecules as a first-line therapy in patients with active disease.

“The available low-quality evidence is inconclusive regarding the efficacy of OSMs [oral small molecules] in management of PsA, whereas there is moderate-quality evidence of the benefits of TNFi biologics, in particular regarding their impact on the prevention of disease progression and joint damage,” wrote the panel of authors, who were led by Jasvinder A. Singh, MD, of the University of Alabama at Birmingham. “In making their recommendation, the panel recognized the cost implications, but put considerations of quality of evidence for benefit over other considerations. This guideline provides recommendations for early and aggressive therapy in patients with newly diagnosed PsA.”

The 28-page guideline, published online Nov. 30 in the Journal of Psoriasis and Psoriatic Arthritis and also in Arthritis Care & Research and Arthritis & Rheumatology, is the first set of PsA-specific recommendations to be assembled using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology that the ACR has used for RA and other conditions. GRADE uses systematic reviews of the scientific literature available to evaluate and grade the quality of evidence in a particular domain. The evidence reviews are then used to create guideline recommendations for or against particular therapy options that range from strong to conditional, depending on the quality of evidence available.

Based on the GRADE methodology and consensus building, the guideline authors crafted recommendations for eight different clinical scenarios, including the initial treatment of patients with active PsA who have not received either OSMs or other treatments; treatment of patients with active PsA despite treatment with an OSM; treatment of patients with active PsA despite treatment with a TNFi biologic either as monotherapy or in combination with methotrexate; treatment of patients with active PsA despite treatment with an interleukin (IL)-17 inhibitor or IL-12/23 inhibitor monotherapy; treatment of patients with active PsA including treat-to-target, active axial disease, enthesitis, or active inflammatory bowel disease; treatment of patients with active PsA and comorbidities, including concomitant diabetes and recurrent serious infections; vaccination in patients with active PsA; and treatment of patients with active PsA with nonpharmacologic interventions such as yoga and weight loss. Most of the treatment recommendations are conditional based on very low to moderate quality evidence. “Health care providers and patients must take into consideration all active disease domains, comorbidities, and the patient’s functional status in choosing the optimal therapy for an individual at a given point in time,” the authors emphasized.

Only five of the recommendations are listed as strong, including smoking cessation. Three of the strong recommendations concern adult patients with active PsA and concomitant active inflammatory bowel disease despite treatment with an OSM. They are “switch to a monoclonal antibody TNFi biologic over a TNFi biologic soluble receptor biologic,” “switch to a TNFi monoclonal antibody biologic over an IL-7i biologic,” and “switch to an IL-12/23i biologic over switching to an IL-17i biologic.”

The process of creating the guideline included input from a panel of nine adults who provided the authors with perspective on their values and preferences. “The concept of treat-to-target was challenging for patients,” the authors noted. “Although they saw value in improved outcomes, they also thought this strategy could increase costs to the patient (e.g., copayments, time traveling to more frequent appointments, etc.) and potentially increase adverse events. Therefore, a detailed conversation with the patient is needed to make decisions regarding treat-to-target.”

The authors concluded the guideline by calling for more comparative data to inform treatment selection in the future. “Several ongoing trials, including a trial to compare a TNFi biologic combination therapy with a TNFi biologic monotherapy and MTX monotherapy, will inform treatment decisions,” they wrote. “We anticipate future updates to the guideline when new evidence is available.”

Dr. Singh, who is also a staff rheumatologist at the Birmingham (Ala.) Veterans Affairs Medical Center, led development of the 2012 and 2015 ACR treatment guidelines for RA. He has received consulting fees from a variety of companies marketing rheumatologic drugs as well as research support from Takeda and Savient. The other guideline authors reported having numerous financial ties to industry.

[email protected]

SOURCE: Singh J et al. Arthritis Care Res. 2018 Nov 30. doi: 10.1002/acr.23789.

The FP recognized the severely sun damaged scalp as a major risk factor for skin cancers. He looked closely at the lesions and realized that the ulcerated areas were at particularly high risk for squamous cell carcinoma (SCC).

He performed broad shave biopsies with sufficient depth to obtain the needed diagnosis. (See the Watch & Learn video on “Shave biopsy.”) The pathology demonstrated that 2 of the 3 biopsy sites were positive for SCC (E and G were SCC, while F was read as actinic keratosis). Cutaneous SCC is a malignant tumor of keratinocytes. Most cutaneous SCCs arise from precursor lesions, often actinic keratoses. SCC usually spreads by local extension, but it is also capable of regional lymph node metastasis and distant metastasis.

Unsure of the margins of the tumors and aware that surgery of the scalp can be challenging, the FP referred the patient for Mohs surgery. The FP also provided counseling about sun avoidance, the consistent use of a hat outdoors, and the use of sunscreens when exposed to the sun.

The Mohs surgeon recommended field treatment with 5% fluorouracil cream twice daily for 4 weeks before surgery to minimize the amount of cutting that would be needed to clear the SCC from this diffusely sun-damaged scalp. After the 5% fluorouracil cream treatment, the surgeon waited 1 month to allow the scalp to heal before performing surgery.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Squamous cell carcinoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:999-1007.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

The new third edition will be available in January 2019: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/.

You can also get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

The FP recognized the severely sun damaged scalp as a major risk factor for skin cancers. He looked closely at the lesions and realized that the ulcerated areas were at particularly high risk for squamous cell carcinoma (SCC).

He performed broad shave biopsies with sufficient depth to obtain the needed diagnosis. (See the Watch & Learn video on “Shave biopsy.”) The pathology demonstrated that 2 of the 3 biopsy sites were positive for SCC (E and G were SCC, while F was read as actinic keratosis). Cutaneous SCC is a malignant tumor of keratinocytes. Most cutaneous SCCs arise from precursor lesions, often actinic keratoses. SCC usually spreads by local extension, but it is also capable of regional lymph node metastasis and distant metastasis.

Unsure of the margins of the tumors and aware that surgery of the scalp can be challenging, the FP referred the patient for Mohs surgery. The FP also provided counseling about sun avoidance, the consistent use of a hat outdoors, and the use of sunscreens when exposed to the sun.

The Mohs surgeon recommended field treatment with 5% fluorouracil cream twice daily for 4 weeks before surgery to minimize the amount of cutting that would be needed to clear the SCC from this diffusely sun-damaged scalp. After the 5% fluorouracil cream treatment, the surgeon waited 1 month to allow the scalp to heal before performing surgery.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Squamous cell carcinoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:999-1007.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

The new third edition will be available in January 2019: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/.

You can also get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

The FP recognized the severely sun damaged scalp as a major risk factor for skin cancers. He looked closely at the lesions and realized that the ulcerated areas were at particularly high risk for squamous cell carcinoma (SCC).

He performed broad shave biopsies with sufficient depth to obtain the needed diagnosis. (See the Watch & Learn video on “Shave biopsy.”) The pathology demonstrated that 2 of the 3 biopsy sites were positive for SCC (E and G were SCC, while F was read as actinic keratosis). Cutaneous SCC is a malignant tumor of keratinocytes. Most cutaneous SCCs arise from precursor lesions, often actinic keratoses. SCC usually spreads by local extension, but it is also capable of regional lymph node metastasis and distant metastasis.

Unsure of the margins of the tumors and aware that surgery of the scalp can be challenging, the FP referred the patient for Mohs surgery. The FP also provided counseling about sun avoidance, the consistent use of a hat outdoors, and the use of sunscreens when exposed to the sun.

The Mohs surgeon recommended field treatment with 5% fluorouracil cream twice daily for 4 weeks before surgery to minimize the amount of cutting that would be needed to clear the SCC from this diffusely sun-damaged scalp. After the 5% fluorouracil cream treatment, the surgeon waited 1 month to allow the scalp to heal before performing surgery.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Squamous cell carcinoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:999-1007.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

The new third edition will be available in January 2019: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/.

You can also get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

Dermoscopy, the use of a handheld instrument to magnify the skin 10-fold while providing a light source, is a quick, useful, cost-effective tool for detecting melanoma in family medicine.^1-4 The device, which allows the physician to visualize structures below the stratum corneum that are not routinely discernible with the naked eye, can be attached to a smartphone so that photos can be taken and reviewed with the patient. The photo can also be reviewed after a biopsy result is obtained.

Its use among non-dermatologist US physicians appears to be relatively low, but rising. One small study of physicians working in family medicine, internal medicine, and plastic surgery found that only 15% had ever used a dermatoscope and 6% were currently using one.⁵

As a family physician, you can expand your diagnostic abilities in dermatology with the acquisition of a dermatoscope (FIGURE 1) and some time invested in learning to interpret visible patterns. With that in mind, this review focuses on the diagnosis of skin cancers and benign growths using dermoscopy. We begin with a brief look at the research on dermoscopy and how it is performed. From there, we’ll detail an algorithm to guide dermoscopic analysis. And to round things out, we provide guidance that will help you to get started. (See “Choosing a dermatoscope—and making the most of it,” and “To learn more about dermoscopy …”.)

Continue to: What the research says

Dermoscopy improves sensitivity for detecting melanoma over the naked eye alone; it also allows for the detection of melanoma at earlier stages, which improves prognosis.⁶

A meta-analysis of dermoscopy use in clinical settings showed that, following training, dermoscopy increases the average sensitivity of melanoma diagnosis from 71% to more than 90% without a significant decrease in specificity.⁷ In a study of 74 primary care physicians, there was an improvement in both clinical and dermoscopic diagnosis of melanoma among those who received training in dermoscopy, compared with a control group.⁸ Another study found that primary care physicians can reduce their baseline benign-to-melanoma ratio (the number of suspicious benign lesions biopsied to find 1 melanoma) from 9.5:1 with naked eye examination to 3.5:1 with dermoscopy.⁹

The exam begins by choosing 1 of 3 modes of dermoscopy

Dermatoscopes can have a polarized or nonpolarized light source. Some dermatoscopes combine both types of light (hybrid dermatoscopes; see “Choosing a dermatoscope—and making the most of it.”)

There are 3 modes of dermoscopy:

1. nonpolarized contact dermoscopy
2. polarized contact dermoscopy
3. polarized non-contact dermoscopy.

Dermatoscopes with nonpolarized light require direct skin contact and a liquid interface (eg, alcohol, gel, mineral oil) between the scope’s glass plate and the skin for the visualization of subsurface structures. In contrast, dermatoscopes with polarized light do not require direct skin contact or a liquid interface; however, contacting the skin and using a liquid interface will provide a sharper image.

Continue to: Two major algorithms guide dermoscopic analysis

The first of 2 major algorithms that can be used to guide dermoscopic analysis is a modified pattern analysis put forth by Kittler.¹⁰ This descriptive system based on geometric elements, patterns, colors, and clues guides the observer to a specific diagnosis without categorizing lesions as being either melanocytic or nonmelanocytic. Because this is not the preferred method of the authors, we will move on to Method 2.

The second method, a 2-step algorithm, is a qualitative system that guides the observer through differentiating melanocytic from nonmelanocytic lesions in order to differentiate nevi from melanoma (FIGURE 2). At the same time, it serves as an aid to correctly diagnose non-melanocytic lesions. The 2-step algorithm forms the foundation for the dermoscopic evaluation of skin lesions in this article.

Not all expert dermoscopists employ structured analytical systems or methods to reach a diagnosis. Because of their vast experience, many rely purely on pattern recognition. But algorithms can facilitate non-experts in dermoscopy in the differentiation of nevi from melanoma or, simply, in differentiating the benign from the malignant.

Although each algorithm has its unique criteria, all of them require training and practice and familiarity with the terms used to describe morphologic structures. The International Dermoscopy Society recently published a consensus paper designating some terms as preferred over others.¹¹

Continue to: Step 1...

Step 1 of the 2-step algorithm requires the observer to determine whether the lesion is melanocytic (ie, originates from melanocytes and, therefore, could be a melanoma) or nonmelanocytic in origin.

A melanocytic lesion usually will display at least 1 of the following structures:

• pigment network (FIGURE 3A) (This can include angulated lines.)
• negative network (FIGURE 3B) (hypopigmented lines connecting pigmented structures in a serpiginous fashion)
• streaks (FIGURE 3C)
• homogeneous blue pigmentation (FIGURE 3D)
• globules (aggregated or as a peripheral rim) (FIGURE 3E)
• pseudonetwork (facial skin) (FIGURE 3F)
• parallel pigment pattern (acral lesions) (FIGURE 3G).

Exceptions. Sometimes, nonmelanocytic lesions will present with pigment network. Dermatofibromas, for example, are one exception in which the pattern trumps the network. Two other exceptions are solar lentigo and supernumerary or accessory nipple.

If the lesion does not display any structure, it is considered structureless. In these cases, proceed to the second step to rule out a melanoma.

Doesn’t meet criteria for a melanocytic lesion?

If the lesion does not reveal any of the criteria for a melanocytic lesion, then look for structures seen in nonmelanocytic lesions: dermatofibromas; seborrheic keratosis; angiomas and angiokeratomas; sebaceous hyperplasia; clear-cell acanthomas; basal cell carcinomas (BCCs); and squamous cell carcinomas (SCCs).

Continue to: Benign nonmelanocytic lesions

Dermatofibromas are benign symmetric lesions that feel firm and may dimple upon application of lateral pressure. They are fibrotic scar-like lesions that present with 1 or more of the following dermoscopic features (FIGURE 4):

• peripheral pigment network, due to increased melanin in keratinocytes
• homogeneous brown pigmented areas
• central scar-like area
• shiny white lines
• vascular structures (ie, dotted, polymorphous vessels), usually seen within the scar-like area
• ring-like globules, usually seen in the zone between the scar-like depigmentation and the peripheral network. They correspond to widened hyperpigmented rete ridges.

Seborrheic keratosis (SK) is a benign skin growth that often has a stuck-on appearance (FIGURE 5). Features often include:

• multiple (>2) milia-like cysts
• comedo-like openings
• a network-like structure that corresponds to gyri and sulci and which in some cases can create a cerebriform pattern
• fingerprint-like structures
• moth-eaten borders
• jelly sign. This consists of semicircular u-shaped structures that have a smudged appearance and are aligned in the same direction. The appearance resembles jelly as it is spread on a piece of bread.
• hairpin (looped or twisted-looped) vessels surrounded by a white halo.

Other clues include a sharp demarcation and a negative wobble sign (which we’ll describe in a moment). The presence or absence of a wobble sign is determined by using a dermatoscope that touches the skin. Mild vertical pressure is applied to the lesion while moving the scope back and forth horizontally. If the lesion slides across the skin surface, the diagnosis of an epidermal keratinocytic tumor (ie, SK) is favored. If, on the other hand, the lesion wobbles (rolls back and forth), then the diagnosis of a neoplasm with a dermal component (ie, intradermal or compound nevus) is more likely.

Angiomas and angiokeratomas. Angiomas demonstrate lacunae that are often separated by septae (FIGURE 6). Lacunae can vary in size and color. They can be red, red-white, red-blue, maroon, blue, blue-black, or even black (when thrombosis is present).

Angiokeratomas (FIGURE 7) can reveal lacunae of varying colors including black, red, purple, and maroon. In addition, a blue-whitish veil, erythema, and hemorrhagic crusts can be present.

Continue to: Sebaceous hyperplasia...

Sebaceous hyperplasia is the overgrowth of sebaceous glands. It can mimic BCC on the face. Sebaceous hyperplasia presents with multiple vessels in a crown-like arrangement that do not cross the center of the lesion. The sebaceous glands resemble popcorn (FIGURE 8).

Clear-cell acanthoma is a benign erythematous epidermal tumor usually found on the leg with a string-of-pearls pattern. This pattern is vascular so the pearls are red in color (FIGURE 9).

Malignant nonmelanocytic lesions

BCC is the most common type of skin cancer. Features often include:

• spoke-wheel-like structures or concentric structures (FIGURE 10A)
• leaf-like areas (FIGURE 10B)
• arborizing vessels (FIGURE 10b and 10C)large blue-gray ovoid nest (FIGURE 10A)
• multiple blue-gray non-aggregated globules
• ulceration or multiple small erosions
• shiny white structures and strands (FIGURE 10C).

Additional dermoscopic clues include short, fine, superficial telangiectasias and multiple in-focus dots in a buck-shot scatter distribution.

Squamous cell carcinomas (SCCs) of the skin are keratinizing malignant tumors. Each SCC generally has some of the following features (FIGURE 11):

• dotted and/or glomerular vessels, commonly distributed focally at the periphery. They can also be diffuse or aligned linearly within the lesion.
• scale (yellow or white)
• rosettes (seen with polarized light)
• white circles or keratin pearls
• brown circles
• ulcerations
• brown dots or globules arranged in a linear configuration.

Continue to: Step 2...

Step 2: It’s melanocytic, but is it a nevus or a melanoma?

If, by following Step 1 of the algorithm, the lesion is determined to be of melanocytic origin, then one proceeds to Step 2 to decide whether the growth is a nevus, a suspicious lesion, or a melanoma. For this purpose, several additional algorithms are available.^12-17

Benign nevi tend to manifest with 1 of the following 10 patterns: (FIGURE 12)

1. diffuse reticular
2. patchy reticular
3. peripheral reticular with central hypopigmentation
4. peripheral reticular with central hyperpigmentation
5. homogeneous
6. peripheral globules/starburst. It has been suggested that lesions that show starburst morphology on dermoscopy require complete excision and follow-up since 13% of Spitzoid-looking symmetric lesions in patients older than 12 years were found to be melanoma in one study.¹⁸
7. peripheral reticular with central globules
8. globular
9. 2-component
10. symmetric multicomponent (this pattern should be interpreted with caution, and a biopsy is probably warranted for dermoscopic novices).

Melanomas tend to deviate from the benign patterns described earlier. Structures in melanomas are often distributed in an asymmetric fashion (which is the basis for diagnosis in many of the other algorithms), and most of them will reveal 1 or more of the melanoma-specific structures (FIGURE 13). The melanomas in FIGURES 14 A-H each show at least 2 melanoma-specific structures. On the face or sun-damaged skin, melanoma may present with grey color, a circle-in-circle pattern, and/or polygonal lines (FIGURE 15). Note that melanoma on the soles or palms may present with a parallel ridge pattern (FIGURE 16).

How to proceed after the evaluation of melanocytic lesions

After evaluating the lesion for benign patterns and melanoma-specific structures, there are 3 possible pathways:

1. The lesion adheres to one of the nevi patterns and does not display a melanoma-specific structure. You can reassure the patient that the lesion is benign.

2. The lesion:

A. Adheres to one nevus pattern, but also displays a melanoma-specific structure.

B. Does not adhere to any of the benign patterns and does not have any melanoma-specific structures.

This is considered a suspicious lesion, and the choices of action include performing a biopsy or short-term monitoring by comparing dermoscopic images over a 3-month interval. (Caveat: Never monitor raised lesions because nodular melanomas can grow quickly and develop a worsened prognosis in a short time. Instead you’ll want to biopsy the lesion that day or very soon thereafter.)

3. The lesion deviates from the benign patterns and has at least 1 melanoma-specific structure. Biopsy the lesion to rule out melanoma.

Continue to: A bonus...

Increasingly, dermoscopy is being used in the diagnosis of many other skin, nail, and hair problems. In fact, one great bonus to owning a dermatoscope is the accurate diagnosis of scabies. Dermoscopy can be helpful in detecting the scabies mite without having to scrape and use the microscope. Moreover, the sensitivity and specificity of a dermoscopic diagnosis is higher than for scraping and microscopy.¹⁹

What you’ll see

The anterior legs and mouth parts of the mite resemble a triangle (arrowhead, delta-wing jet) (FIGURE 17). Look for a burrow, and the mite can be seen at the end of the burrow as a faint circle with a leading darker triangle. The burrow itself has a distinctive pattern that has more morphology than an excoriation and has been described as the contrail of a jet plane. Using a dermatoscope attached to your smartphone allows you to magnify the image even further while maintaining a safe distance from the mite.

Dermoscopy, the use of a handheld instrument to magnify the skin 10-fold while providing a light source, is a quick, useful, cost-effective tool for detecting melanoma in family medicine.^1-4 The device, which allows the physician to visualize structures below the stratum corneum that are not routinely discernible with the naked eye, can be attached to a smartphone so that photos can be taken and reviewed with the patient. The photo can also be reviewed after a biopsy result is obtained.

Its use among non-dermatologist US physicians appears to be relatively low, but rising. One small study of physicians working in family medicine, internal medicine, and plastic surgery found that only 15% had ever used a dermatoscope and 6% were currently using one.⁵

As a family physician, you can expand your diagnostic abilities in dermatology with the acquisition of a dermatoscope (FIGURE 1) and some time invested in learning to interpret visible patterns. With that in mind, this review focuses on the diagnosis of skin cancers and benign growths using dermoscopy. We begin with a brief look at the research on dermoscopy and how it is performed. From there, we’ll detail an algorithm to guide dermoscopic analysis. And to round things out, we provide guidance that will help you to get started. (See “Choosing a dermatoscope—and making the most of it,” and “To learn more about dermoscopy …”.)

Continue to: What the research says

Dermoscopy improves sensitivity for detecting melanoma over the naked eye alone; it also allows for the detection of melanoma at earlier stages, which improves prognosis.⁶

A meta-analysis of dermoscopy use in clinical settings showed that, following training, dermoscopy increases the average sensitivity of melanoma diagnosis from 71% to more than 90% without a significant decrease in specificity.⁷ In a study of 74 primary care physicians, there was an improvement in both clinical and dermoscopic diagnosis of melanoma among those who received training in dermoscopy, compared with a control group.⁸ Another study found that primary care physicians can reduce their baseline benign-to-melanoma ratio (the number of suspicious benign lesions biopsied to find 1 melanoma) from 9.5:1 with naked eye examination to 3.5:1 with dermoscopy.⁹

The exam begins by choosing 1 of 3 modes of dermoscopy

Dermatoscopes can have a polarized or nonpolarized light source. Some dermatoscopes combine both types of light (hybrid dermatoscopes; see “Choosing a dermatoscope—and making the most of it.”)

There are 3 modes of dermoscopy:

1. nonpolarized contact dermoscopy
2. polarized contact dermoscopy
3. polarized non-contact dermoscopy.

Dermatoscopes with nonpolarized light require direct skin contact and a liquid interface (eg, alcohol, gel, mineral oil) between the scope’s glass plate and the skin for the visualization of subsurface structures. In contrast, dermatoscopes with polarized light do not require direct skin contact or a liquid interface; however, contacting the skin and using a liquid interface will provide a sharper image.

Continue to: Two major algorithms guide dermoscopic analysis

The first of 2 major algorithms that can be used to guide dermoscopic analysis is a modified pattern analysis put forth by Kittler.¹⁰ This descriptive system based on geometric elements, patterns, colors, and clues guides the observer to a specific diagnosis without categorizing lesions as being either melanocytic or nonmelanocytic. Because this is not the preferred method of the authors, we will move on to Method 2.

The second method, a 2-step algorithm, is a qualitative system that guides the observer through differentiating melanocytic from nonmelanocytic lesions in order to differentiate nevi from melanoma (FIGURE 2). At the same time, it serves as an aid to correctly diagnose non-melanocytic lesions. The 2-step algorithm forms the foundation for the dermoscopic evaluation of skin lesions in this article.

Not all expert dermoscopists employ structured analytical systems or methods to reach a diagnosis. Because of their vast experience, many rely purely on pattern recognition. But algorithms can facilitate non-experts in dermoscopy in the differentiation of nevi from melanoma or, simply, in differentiating the benign from the malignant.

Although each algorithm has its unique criteria, all of them require training and practice and familiarity with the terms used to describe morphologic structures. The International Dermoscopy Society recently published a consensus paper designating some terms as preferred over others.¹¹

Continue to: Step 1...

Step 1 of the 2-step algorithm requires the observer to determine whether the lesion is melanocytic (ie, originates from melanocytes and, therefore, could be a melanoma) or nonmelanocytic in origin.

A melanocytic lesion usually will display at least 1 of the following structures:

• pigment network (FIGURE 3A) (This can include angulated lines.)
• negative network (FIGURE 3B) (hypopigmented lines connecting pigmented structures in a serpiginous fashion)
• streaks (FIGURE 3C)
• homogeneous blue pigmentation (FIGURE 3D)
• globules (aggregated or as a peripheral rim) (FIGURE 3E)
• pseudonetwork (facial skin) (FIGURE 3F)
• parallel pigment pattern (acral lesions) (FIGURE 3G).

Exceptions. Sometimes, nonmelanocytic lesions will present with pigment network. Dermatofibromas, for example, are one exception in which the pattern trumps the network. Two other exceptions are solar lentigo and supernumerary or accessory nipple.

If the lesion does not display any structure, it is considered structureless. In these cases, proceed to the second step to rule out a melanoma.

Doesn’t meet criteria for a melanocytic lesion?

If the lesion does not reveal any of the criteria for a melanocytic lesion, then look for structures seen in nonmelanocytic lesions: dermatofibromas; seborrheic keratosis; angiomas and angiokeratomas; sebaceous hyperplasia; clear-cell acanthomas; basal cell carcinomas (BCCs); and squamous cell carcinomas (SCCs).

Continue to: Benign nonmelanocytic lesions

Dermatofibromas are benign symmetric lesions that feel firm and may dimple upon application of lateral pressure. They are fibrotic scar-like lesions that present with 1 or more of the following dermoscopic features (FIGURE 4):

• peripheral pigment network, due to increased melanin in keratinocytes
• homogeneous brown pigmented areas
• central scar-like area
• shiny white lines
• vascular structures (ie, dotted, polymorphous vessels), usually seen within the scar-like area
• ring-like globules, usually seen in the zone between the scar-like depigmentation and the peripheral network. They correspond to widened hyperpigmented rete ridges.

Seborrheic keratosis (SK) is a benign skin growth that often has a stuck-on appearance (FIGURE 5). Features often include:

• multiple (>2) milia-like cysts
• comedo-like openings
• a network-like structure that corresponds to gyri and sulci and which in some cases can create a cerebriform pattern
• fingerprint-like structures
• moth-eaten borders
• jelly sign. This consists of semicircular u-shaped structures that have a smudged appearance and are aligned in the same direction. The appearance resembles jelly as it is spread on a piece of bread.
• hairpin (looped or twisted-looped) vessels surrounded by a white halo.

Other clues include a sharp demarcation and a negative wobble sign (which we’ll describe in a moment). The presence or absence of a wobble sign is determined by using a dermatoscope that touches the skin. Mild vertical pressure is applied to the lesion while moving the scope back and forth horizontally. If the lesion slides across the skin surface, the diagnosis of an epidermal keratinocytic tumor (ie, SK) is favored. If, on the other hand, the lesion wobbles (rolls back and forth), then the diagnosis of a neoplasm with a dermal component (ie, intradermal or compound nevus) is more likely.

Angiomas and angiokeratomas. Angiomas demonstrate lacunae that are often separated by septae (FIGURE 6). Lacunae can vary in size and color. They can be red, red-white, red-blue, maroon, blue, blue-black, or even black (when thrombosis is present).

Angiokeratomas (FIGURE 7) can reveal lacunae of varying colors including black, red, purple, and maroon. In addition, a blue-whitish veil, erythema, and hemorrhagic crusts can be present.

Continue to: Sebaceous hyperplasia...

Sebaceous hyperplasia is the overgrowth of sebaceous glands. It can mimic BCC on the face. Sebaceous hyperplasia presents with multiple vessels in a crown-like arrangement that do not cross the center of the lesion. The sebaceous glands resemble popcorn (FIGURE 8).

Clear-cell acanthoma is a benign erythematous epidermal tumor usually found on the leg with a string-of-pearls pattern. This pattern is vascular so the pearls are red in color (FIGURE 9).

Malignant nonmelanocytic lesions

BCC is the most common type of skin cancer. Features often include:

• spoke-wheel-like structures or concentric structures (FIGURE 10A)
• leaf-like areas (FIGURE 10B)
• arborizing vessels (FIGURE 10b and 10C)large blue-gray ovoid nest (FIGURE 10A)
• multiple blue-gray non-aggregated globules
• ulceration or multiple small erosions
• shiny white structures and strands (FIGURE 10C).

Additional dermoscopic clues include short, fine, superficial telangiectasias and multiple in-focus dots in a buck-shot scatter distribution.

Squamous cell carcinomas (SCCs) of the skin are keratinizing malignant tumors. Each SCC generally has some of the following features (FIGURE 11):

• dotted and/or glomerular vessels, commonly distributed focally at the periphery. They can also be diffuse or aligned linearly within the lesion.
• scale (yellow or white)
• rosettes (seen with polarized light)
• white circles or keratin pearls
• brown circles
• ulcerations
• brown dots or globules arranged in a linear configuration.

Continue to: Step 2...

Step 2: It’s melanocytic, but is it a nevus or a melanoma?

If, by following Step 1 of the algorithm, the lesion is determined to be of melanocytic origin, then one proceeds to Step 2 to decide whether the growth is a nevus, a suspicious lesion, or a melanoma. For this purpose, several additional algorithms are available.^12-17

Benign nevi tend to manifest with 1 of the following 10 patterns: (FIGURE 12)

1. diffuse reticular
2. patchy reticular
3. peripheral reticular with central hypopigmentation
4. peripheral reticular with central hyperpigmentation
5. homogeneous
6. peripheral globules/starburst. It has been suggested that lesions that show starburst morphology on dermoscopy require complete excision and follow-up since 13% of Spitzoid-looking symmetric lesions in patients older than 12 years were found to be melanoma in one study.¹⁸
7. peripheral reticular with central globules
8. globular
9. 2-component
10. symmetric multicomponent (this pattern should be interpreted with caution, and a biopsy is probably warranted for dermoscopic novices).

Melanomas tend to deviate from the benign patterns described earlier. Structures in melanomas are often distributed in an asymmetric fashion (which is the basis for diagnosis in many of the other algorithms), and most of them will reveal 1 or more of the melanoma-specific structures (FIGURE 13). The melanomas in FIGURES 14 A-H each show at least 2 melanoma-specific structures. On the face or sun-damaged skin, melanoma may present with grey color, a circle-in-circle pattern, and/or polygonal lines (FIGURE 15). Note that melanoma on the soles or palms may present with a parallel ridge pattern (FIGURE 16).

How to proceed after the evaluation of melanocytic lesions

After evaluating the lesion for benign patterns and melanoma-specific structures, there are 3 possible pathways:

1. The lesion adheres to one of the nevi patterns and does not display a melanoma-specific structure. You can reassure the patient that the lesion is benign.

2. The lesion:

A. Adheres to one nevus pattern, but also displays a melanoma-specific structure.

B. Does not adhere to any of the benign patterns and does not have any melanoma-specific structures.

This is considered a suspicious lesion, and the choices of action include performing a biopsy or short-term monitoring by comparing dermoscopic images over a 3-month interval. (Caveat: Never monitor raised lesions because nodular melanomas can grow quickly and develop a worsened prognosis in a short time. Instead you’ll want to biopsy the lesion that day or very soon thereafter.)

3. The lesion deviates from the benign patterns and has at least 1 melanoma-specific structure. Biopsy the lesion to rule out melanoma.

Continue to: A bonus...

Increasingly, dermoscopy is being used in the diagnosis of many other skin, nail, and hair problems. In fact, one great bonus to owning a dermatoscope is the accurate diagnosis of scabies. Dermoscopy can be helpful in detecting the scabies mite without having to scrape and use the microscope. Moreover, the sensitivity and specificity of a dermoscopic diagnosis is higher than for scraping and microscopy.¹⁹

What you’ll see

The anterior legs and mouth parts of the mite resemble a triangle (arrowhead, delta-wing jet) (FIGURE 17). Look for a burrow, and the mite can be seen at the end of the burrow as a faint circle with a leading darker triangle. The burrow itself has a distinctive pattern that has more morphology than an excoriation and has been described as the contrail of a jet plane. Using a dermatoscope attached to your smartphone allows you to magnify the image even further while maintaining a safe distance from the mite.

Dermoscopy, the use of a handheld instrument to magnify the skin 10-fold while providing a light source, is a quick, useful, cost-effective tool for detecting melanoma in family medicine.^1-4 The device, which allows the physician to visualize structures below the stratum corneum that are not routinely discernible with the naked eye, can be attached to a smartphone so that photos can be taken and reviewed with the patient. The photo can also be reviewed after a biopsy result is obtained.

Its use among non-dermatologist US physicians appears to be relatively low, but rising. One small study of physicians working in family medicine, internal medicine, and plastic surgery found that only 15% had ever used a dermatoscope and 6% were currently using one.⁵

As a family physician, you can expand your diagnostic abilities in dermatology with the acquisition of a dermatoscope (FIGURE 1) and some time invested in learning to interpret visible patterns. With that in mind, this review focuses on the diagnosis of skin cancers and benign growths using dermoscopy. We begin with a brief look at the research on dermoscopy and how it is performed. From there, we’ll detail an algorithm to guide dermoscopic analysis. And to round things out, we provide guidance that will help you to get started. (See “Choosing a dermatoscope—and making the most of it,” and “To learn more about dermoscopy …”.)

Continue to: What the research says

Dermoscopy improves sensitivity for detecting melanoma over the naked eye alone; it also allows for the detection of melanoma at earlier stages, which improves prognosis.⁶

A meta-analysis of dermoscopy use in clinical settings showed that, following training, dermoscopy increases the average sensitivity of melanoma diagnosis from 71% to more than 90% without a significant decrease in specificity.⁷ In a study of 74 primary care physicians, there was an improvement in both clinical and dermoscopic diagnosis of melanoma among those who received training in dermoscopy, compared with a control group.⁸ Another study found that primary care physicians can reduce their baseline benign-to-melanoma ratio (the number of suspicious benign lesions biopsied to find 1 melanoma) from 9.5:1 with naked eye examination to 3.5:1 with dermoscopy.⁹

The exam begins by choosing 1 of 3 modes of dermoscopy

Dermatoscopes can have a polarized or nonpolarized light source. Some dermatoscopes combine both types of light (hybrid dermatoscopes; see “Choosing a dermatoscope—and making the most of it.”)

There are 3 modes of dermoscopy:

1. nonpolarized contact dermoscopy
2. polarized contact dermoscopy
3. polarized non-contact dermoscopy.

Dermatoscopes with nonpolarized light require direct skin contact and a liquid interface (eg, alcohol, gel, mineral oil) between the scope’s glass plate and the skin for the visualization of subsurface structures. In contrast, dermatoscopes with polarized light do not require direct skin contact or a liquid interface; however, contacting the skin and using a liquid interface will provide a sharper image.

Continue to: Two major algorithms guide dermoscopic analysis

The first of 2 major algorithms that can be used to guide dermoscopic analysis is a modified pattern analysis put forth by Kittler.¹⁰ This descriptive system based on geometric elements, patterns, colors, and clues guides the observer to a specific diagnosis without categorizing lesions as being either melanocytic or nonmelanocytic. Because this is not the preferred method of the authors, we will move on to Method 2.

The second method, a 2-step algorithm, is a qualitative system that guides the observer through differentiating melanocytic from nonmelanocytic lesions in order to differentiate nevi from melanoma (FIGURE 2). At the same time, it serves as an aid to correctly diagnose non-melanocytic lesions. The 2-step algorithm forms the foundation for the dermoscopic evaluation of skin lesions in this article.

Not all expert dermoscopists employ structured analytical systems or methods to reach a diagnosis. Because of their vast experience, many rely purely on pattern recognition. But algorithms can facilitate non-experts in dermoscopy in the differentiation of nevi from melanoma or, simply, in differentiating the benign from the malignant.

Although each algorithm has its unique criteria, all of them require training and practice and familiarity with the terms used to describe morphologic structures. The International Dermoscopy Society recently published a consensus paper designating some terms as preferred over others.¹¹

Continue to: Step 1...

Step 1 of the 2-step algorithm requires the observer to determine whether the lesion is melanocytic (ie, originates from melanocytes and, therefore, could be a melanoma) or nonmelanocytic in origin.

A melanocytic lesion usually will display at least 1 of the following structures:

• pigment network (FIGURE 3A) (This can include angulated lines.)
• negative network (FIGURE 3B) (hypopigmented lines connecting pigmented structures in a serpiginous fashion)
• streaks (FIGURE 3C)
• homogeneous blue pigmentation (FIGURE 3D)
• globules (aggregated or as a peripheral rim) (FIGURE 3E)
• pseudonetwork (facial skin) (FIGURE 3F)
• parallel pigment pattern (acral lesions) (FIGURE 3G).

Exceptions. Sometimes, nonmelanocytic lesions will present with pigment network. Dermatofibromas, for example, are one exception in which the pattern trumps the network. Two other exceptions are solar lentigo and supernumerary or accessory nipple.

If the lesion does not display any structure, it is considered structureless. In these cases, proceed to the second step to rule out a melanoma.

Doesn’t meet criteria for a melanocytic lesion?

If the lesion does not reveal any of the criteria for a melanocytic lesion, then look for structures seen in nonmelanocytic lesions: dermatofibromas; seborrheic keratosis; angiomas and angiokeratomas; sebaceous hyperplasia; clear-cell acanthomas; basal cell carcinomas (BCCs); and squamous cell carcinomas (SCCs).

Continue to: Benign nonmelanocytic lesions

Dermatofibromas are benign symmetric lesions that feel firm and may dimple upon application of lateral pressure. They are fibrotic scar-like lesions that present with 1 or more of the following dermoscopic features (FIGURE 4):

• peripheral pigment network, due to increased melanin in keratinocytes
• homogeneous brown pigmented areas
• central scar-like area
• shiny white lines
• vascular structures (ie, dotted, polymorphous vessels), usually seen within the scar-like area
• ring-like globules, usually seen in the zone between the scar-like depigmentation and the peripheral network. They correspond to widened hyperpigmented rete ridges.

Seborrheic keratosis (SK) is a benign skin growth that often has a stuck-on appearance (FIGURE 5). Features often include:

• multiple (>2) milia-like cysts
• comedo-like openings
• a network-like structure that corresponds to gyri and sulci and which in some cases can create a cerebriform pattern
• fingerprint-like structures
• moth-eaten borders
• jelly sign. This consists of semicircular u-shaped structures that have a smudged appearance and are aligned in the same direction. The appearance resembles jelly as it is spread on a piece of bread.
• hairpin (looped or twisted-looped) vessels surrounded by a white halo.

Other clues include a sharp demarcation and a negative wobble sign (which we’ll describe in a moment). The presence or absence of a wobble sign is determined by using a dermatoscope that touches the skin. Mild vertical pressure is applied to the lesion while moving the scope back and forth horizontally. If the lesion slides across the skin surface, the diagnosis of an epidermal keratinocytic tumor (ie, SK) is favored. If, on the other hand, the lesion wobbles (rolls back and forth), then the diagnosis of a neoplasm with a dermal component (ie, intradermal or compound nevus) is more likely.

Angiomas and angiokeratomas. Angiomas demonstrate lacunae that are often separated by septae (FIGURE 6). Lacunae can vary in size and color. They can be red, red-white, red-blue, maroon, blue, blue-black, or even black (when thrombosis is present).

Angiokeratomas (FIGURE 7) can reveal lacunae of varying colors including black, red, purple, and maroon. In addition, a blue-whitish veil, erythema, and hemorrhagic crusts can be present.

Continue to: Sebaceous hyperplasia...

Sebaceous hyperplasia is the overgrowth of sebaceous glands. It can mimic BCC on the face. Sebaceous hyperplasia presents with multiple vessels in a crown-like arrangement that do not cross the center of the lesion. The sebaceous glands resemble popcorn (FIGURE 8).

Clear-cell acanthoma is a benign erythematous epidermal tumor usually found on the leg with a string-of-pearls pattern. This pattern is vascular so the pearls are red in color (FIGURE 9).

Malignant nonmelanocytic lesions

BCC is the most common type of skin cancer. Features often include:

• spoke-wheel-like structures or concentric structures (FIGURE 10A)
• leaf-like areas (FIGURE 10B)
• arborizing vessels (FIGURE 10b and 10C)large blue-gray ovoid nest (FIGURE 10A)
• multiple blue-gray non-aggregated globules
• ulceration or multiple small erosions
• shiny white structures and strands (FIGURE 10C).

Additional dermoscopic clues include short, fine, superficial telangiectasias and multiple in-focus dots in a buck-shot scatter distribution.

Squamous cell carcinomas (SCCs) of the skin are keratinizing malignant tumors. Each SCC generally has some of the following features (FIGURE 11):

• dotted and/or glomerular vessels, commonly distributed focally at the periphery. They can also be diffuse or aligned linearly within the lesion.
• scale (yellow or white)
• rosettes (seen with polarized light)
• white circles or keratin pearls
• brown circles
• ulcerations
• brown dots or globules arranged in a linear configuration.

Continue to: Step 2...

Step 2: It’s melanocytic, but is it a nevus or a melanoma?

If, by following Step 1 of the algorithm, the lesion is determined to be of melanocytic origin, then one proceeds to Step 2 to decide whether the growth is a nevus, a suspicious lesion, or a melanoma. For this purpose, several additional algorithms are available.^12-17

Benign nevi tend to manifest with 1 of the following 10 patterns: (FIGURE 12)

1. diffuse reticular
2. patchy reticular
3. peripheral reticular with central hypopigmentation
4. peripheral reticular with central hyperpigmentation
5. homogeneous
6. peripheral globules/starburst. It has been suggested that lesions that show starburst morphology on dermoscopy require complete excision and follow-up since 13% of Spitzoid-looking symmetric lesions in patients older than 12 years were found to be melanoma in one study.¹⁸
7. peripheral reticular with central globules
8. globular
9. 2-component
10. symmetric multicomponent (this pattern should be interpreted with caution, and a biopsy is probably warranted for dermoscopic novices).

Melanomas tend to deviate from the benign patterns described earlier. Structures in melanomas are often distributed in an asymmetric fashion (which is the basis for diagnosis in many of the other algorithms), and most of them will reveal 1 or more of the melanoma-specific structures (FIGURE 13). The melanomas in FIGURES 14 A-H each show at least 2 melanoma-specific structures. On the face or sun-damaged skin, melanoma may present with grey color, a circle-in-circle pattern, and/or polygonal lines (FIGURE 15). Note that melanoma on the soles or palms may present with a parallel ridge pattern (FIGURE 16).

How to proceed after the evaluation of melanocytic lesions

After evaluating the lesion for benign patterns and melanoma-specific structures, there are 3 possible pathways:

1. The lesion adheres to one of the nevi patterns and does not display a melanoma-specific structure. You can reassure the patient that the lesion is benign.

2. The lesion:

A. Adheres to one nevus pattern, but also displays a melanoma-specific structure.

B. Does not adhere to any of the benign patterns and does not have any melanoma-specific structures.

This is considered a suspicious lesion, and the choices of action include performing a biopsy or short-term monitoring by comparing dermoscopic images over a 3-month interval. (Caveat: Never monitor raised lesions because nodular melanomas can grow quickly and develop a worsened prognosis in a short time. Instead you’ll want to biopsy the lesion that day or very soon thereafter.)

3. The lesion deviates from the benign patterns and has at least 1 melanoma-specific structure. Biopsy the lesion to rule out melanoma.

Continue to: A bonus...

Increasingly, dermoscopy is being used in the diagnosis of many other skin, nail, and hair problems. In fact, one great bonus to owning a dermatoscope is the accurate diagnosis of scabies. Dermoscopy can be helpful in detecting the scabies mite without having to scrape and use the microscope. Moreover, the sensitivity and specificity of a dermoscopic diagnosis is higher than for scraping and microscopy.¹⁹

What you’ll see

The anterior legs and mouth parts of the mite resemble a triangle (arrowhead, delta-wing jet) (FIGURE 17). Look for a burrow, and the mite can be seen at the end of the burrow as a faint circle with a leading darker triangle. The burrow itself has a distinctive pattern that has more morphology than an excoriation and has been described as the contrail of a jet plane. Using a dermatoscope attached to your smartphone allows you to magnify the image even further while maintaining a safe distance from the mite.

Vitamin D levels measured in maternal sera during gestation and in umbilical cord blood were not predictive of the prevalence of eczema, food allergy, asthma and allergic rhinitis in children at ages 2 years and 5 years, according to study results published in the journal Allergy.

copyright istock/Thinkstock

Áine Hennessy, PhD, from the School of Food and Nutritional Sciences at the University College Cork (Ireland), and her colleagues performed a prospective cohort study of 1,537 women in the Cork BASELINE Birth Cohort Study who underwent measurement of serum 25-hydroxyvitamin D (25[OH]D) from maternal sera followed by measurement of 25(OH)D in umbilical cord blood (1,050 cases). They then measured the prevalence of eczema, food allergy, allergic rhinitis, and asthma in infants at aged 2 and 5 years.

The researchers found at 2 years old, 5% of infants had persistent eczema, 4% of infants had a food allergy and 8% of infants had aeroallergen sensitization. At age 5 years, 15% of infants had asthma, while 5% had allergic rhinitis. Mothers whose children went on to have atopy did not differ in their 25(OH)D levels at 15 weeks’ gestation (mean 58.4 nmol/L vs. 58.5 nmol/L) or in the levels in umbilical cord blood (mean 35.2 nmol/L and 35.4 nmol/L).

Of the women in the cohort, 74% ranged in age from 25 to 34 years; 49% reported a personal history of allergy and 37% reported a paternal allergy. The mean birth weight of the infants was 3,458 g; infants were breastfed for mean 11.9 weeks, 73% of infants were breastfeeding by the time they left the hospital and 45% of infants were breastfeeding by age 2 months.

Limitations of the study included that parental atopy status was self-reported and that the researchers noted they did not examine genetic variants of immunoglobulin E synthesis or vitamin D receptor polymorphisms.

“To fully characterize relationships between intrauterine vitamin D exposure and allergic disease, analysis of well‐constructed, large‐scale prospective cohorts of maternal‐infant dyads, which take due consideration of an individual’s inherited risk, early‐life exposures and environmental confounders, is still needed,” Dr. Hennessy and her colleagues wrote.

The study was funded by grants from the European Commission, Ireland Health Research Board, National Children’s Research Centre, Food Standards Agency and Science Foundation Ireland. The authors report no relevant conflicts of interest.

SOURCE: Hennessy A et al. Allergy. 2018 Aug 7. doi: 10.1111/all.13590.

Vitamin D levels measured in maternal sera during gestation and in umbilical cord blood were not predictive of the prevalence of eczema, food allergy, asthma and allergic rhinitis in children at ages 2 years and 5 years, according to study results published in the journal Allergy.

copyright istock/Thinkstock

Áine Hennessy, PhD, from the School of Food and Nutritional Sciences at the University College Cork (Ireland), and her colleagues performed a prospective cohort study of 1,537 women in the Cork BASELINE Birth Cohort Study who underwent measurement of serum 25-hydroxyvitamin D (25[OH]D) from maternal sera followed by measurement of 25(OH)D in umbilical cord blood (1,050 cases). They then measured the prevalence of eczema, food allergy, allergic rhinitis, and asthma in infants at aged 2 and 5 years.

The researchers found at 2 years old, 5% of infants had persistent eczema, 4% of infants had a food allergy and 8% of infants had aeroallergen sensitization. At age 5 years, 15% of infants had asthma, while 5% had allergic rhinitis. Mothers whose children went on to have atopy did not differ in their 25(OH)D levels at 15 weeks’ gestation (mean 58.4 nmol/L vs. 58.5 nmol/L) or in the levels in umbilical cord blood (mean 35.2 nmol/L and 35.4 nmol/L).

Of the women in the cohort, 74% ranged in age from 25 to 34 years; 49% reported a personal history of allergy and 37% reported a paternal allergy. The mean birth weight of the infants was 3,458 g; infants were breastfed for mean 11.9 weeks, 73% of infants were breastfeeding by the time they left the hospital and 45% of infants were breastfeeding by age 2 months.

Limitations of the study included that parental atopy status was self-reported and that the researchers noted they did not examine genetic variants of immunoglobulin E synthesis or vitamin D receptor polymorphisms.

“To fully characterize relationships between intrauterine vitamin D exposure and allergic disease, analysis of well‐constructed, large‐scale prospective cohorts of maternal‐infant dyads, which take due consideration of an individual’s inherited risk, early‐life exposures and environmental confounders, is still needed,” Dr. Hennessy and her colleagues wrote.

The study was funded by grants from the European Commission, Ireland Health Research Board, National Children’s Research Centre, Food Standards Agency and Science Foundation Ireland. The authors report no relevant conflicts of interest.

SOURCE: Hennessy A et al. Allergy. 2018 Aug 7. doi: 10.1111/all.13590.

Vitamin D levels measured in maternal sera during gestation and in umbilical cord blood were not predictive of the prevalence of eczema, food allergy, asthma and allergic rhinitis in children at ages 2 years and 5 years, according to study results published in the journal Allergy.

copyright istock/Thinkstock

Áine Hennessy, PhD, from the School of Food and Nutritional Sciences at the University College Cork (Ireland), and her colleagues performed a prospective cohort study of 1,537 women in the Cork BASELINE Birth Cohort Study who underwent measurement of serum 25-hydroxyvitamin D (25[OH]D) from maternal sera followed by measurement of 25(OH)D in umbilical cord blood (1,050 cases). They then measured the prevalence of eczema, food allergy, allergic rhinitis, and asthma in infants at aged 2 and 5 years.

The researchers found at 2 years old, 5% of infants had persistent eczema, 4% of infants had a food allergy and 8% of infants had aeroallergen sensitization. At age 5 years, 15% of infants had asthma, while 5% had allergic rhinitis. Mothers whose children went on to have atopy did not differ in their 25(OH)D levels at 15 weeks’ gestation (mean 58.4 nmol/L vs. 58.5 nmol/L) or in the levels in umbilical cord blood (mean 35.2 nmol/L and 35.4 nmol/L).

Of the women in the cohort, 74% ranged in age from 25 to 34 years; 49% reported a personal history of allergy and 37% reported a paternal allergy. The mean birth weight of the infants was 3,458 g; infants were breastfed for mean 11.9 weeks, 73% of infants were breastfeeding by the time they left the hospital and 45% of infants were breastfeeding by age 2 months.

Limitations of the study included that parental atopy status was self-reported and that the researchers noted they did not examine genetic variants of immunoglobulin E synthesis or vitamin D receptor polymorphisms.

“To fully characterize relationships between intrauterine vitamin D exposure and allergic disease, analysis of well‐constructed, large‐scale prospective cohorts of maternal‐infant dyads, which take due consideration of an individual’s inherited risk, early‐life exposures and environmental confounders, is still needed,” Dr. Hennessy and her colleagues wrote.

The study was funded by grants from the European Commission, Ireland Health Research Board, National Children’s Research Centre, Food Standards Agency and Science Foundation Ireland. The authors report no relevant conflicts of interest.

SOURCE: Hennessy A et al. Allergy. 2018 Aug 7. doi: 10.1111/all.13590.

A 22-year-old Caucasian man with a history of atopic dermatitis (AD) was referred to our dermatology clinic for evaluation of a diffuse facial rash that had been present for the previous 7 days. The rash initially presented as erythema on the right malar cheek that rapidly spread to the entire face. Initially diagnosed as impetigo, empiric treatment with sulfamethoxazole/trimethoprim (800 mg/160 mg PO BID for 7 days), dicloxacillin (500 mg PO BID for 6 days), cephalexin (500 mg TID for 5 days), and mupirocin (2% topical cream applied TID for 6 days) failed to improve the patient’s symptoms. He reported mild pain associated with facial movements.

The patient had a history of similar (but more limited) rashes, which he described as “recurrent impetigo,” that began during his career as a high school and collegiate wrestler. These rashes were different from the rashes he described as his history of AD, which consisted of pruritic and erythematous skin in his antecubital and popliteal fossae. He denied any history of herpes simplex virus (HSV) infection.

A physical examination revealed numerous monomorphic, 1- to 3-mm, punched-out erosions and ulcers with overlying yellow-brown crust encompassing the patient’s entire face and portions of his anterior neck. Several clustered vesicles on erythematous bases also were noted (FIGUREs 1A and 1B). We used a Dermablade to unroof some of the vesicles and sent the scrapings to the lab for Tzanck, direct fluorescent antibody assay (DFA), and HSV polymerase chain reaction (PCR) testing.

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

Diagnosis: Eczema herpeticum secondary to herpes gladiatorum

The patient’s laboratory results came back and the Tzanck preparation was positive for multinucleated giant cells, and both the DFA and HSV PCR were positive for HSV infection. This, paired with the widely disseminated rash observed on examination and the patient’s history of AD, was consistent with a diagnosis of eczema herpeticum (EH).

Rather than primary impetigo, the patient’s self-described history of recurrent rashes was felt to represent a history of HSV outbreaks. Given his denial of prior oral or genital HSV infection, as well as the coincident onset of these outbreaks during his career as a competitive wrestler, the most likely primary infection source was direct contact with another HSV-infected wrestler.

Herpes gladiatorum refers to a primary cutaneous HSV infection contracted by an athlete through direct skin-to-skin contact with another athlete.¹ It is common in contact sports, such as rugby and wrestling, and particularly common at organized wrestling camps, where mass outbreaks are a frequent occurrence.² Herpes gladiatorum is so common at these camps that many recommend prophylactic valacyclovir treatment for all participants to mitigate the risk of contracting HSV. In a 2016 review, Anderson et al concluded that prophylactic valacyclovir treatment at a 28-day high school wrestling camp effectively reduced outbreak incidence by 89.5%.²

Prophylactic valacyclovir treatment at a 28-day high school wrestling camp reduced outbreak incidence of herpes gladiatorum by 89.5%.

The lesions of herpes gladiatorum are classically limited in distribution and reflective of the areas of direct contact with infected skin, most commonly the face, neck, and arms. Our patient’s history of more limited outbreaks on his face was consistent with this typical presentation. His current outbreak, however, had become much more widely disseminated, which led to the diagnosis of EH secondary to herpes gladiatorum.

Eczema herpeticum: Pathogenesis and diagnosis

Also known as Kaposi’s varicelliform eruption, EH is a rapid, widespread cutaneous dissemination of HSV infection in areas of dermatitis or skin barrier disruption, most commonly caused by HSV-1 infection.³ It is classically associated with AD, but also can occur in patients with impaired epidermal barrier function due to other conditions, such as burns, pemphigus vulgaris, mycosis fungoides, and Darier disease.⁴ It occurs in <3% of patients with AD and is more commonly observed in infants and children with AD than adults.⁵

Continue to: Clinically, the most common manifestations are discrete..

Clinically, the most common manifestations are discrete, monomorphic, 2- to 3-mm, punched-out erosions with hemorrhagic crusts; intact vesicles are less commonly observed.⁴ Involved skin is typically painful and may be pruritic. Clinical diagnosis should be confirmed by laboratory evaluation, typically Tzanck preparation, DFA, and/or HSV PCR.

Complications and the importance of rapid treatment

The most common complication of EH is bacterial superinfection (impetigo), usually by Staphylococcus aureus or group A streptococci. Signs of bacterial superinfection include weeping lesions, pustules, honey-colored/golden crusting, worsening of existing dermatitis, and failure to respond to antiviral treatment. Topical mupirocin 2% cream is generally effective for controlling limited infection. However, systemic antibiotics (cephalosporins or penicillinase-resistant penicillins) may be necessary to control widespread disease.⁴ Clinical improvement should be observed within a single course of an appropriate antibiotic.

In contrast to impetigo, less common but more serious complications of EH can be life threatening. Systemic dissemination of disease is of particular importance in vulnerable populations such as pediatric and immunocompromised patients. Meningoencephalitis, secondary bacteremia, and herpes keratitis can all develop secondary to EH and incur significant morbidity and mortality.¹

Fever, malaise, lymphadenopathy, or eye pain should prompt immediate consideration of inpatient evaluation and treatment for these potentially deadly or debilitating complications. All patients with EH distributed near the eyes should be referred to ophthalmology to rule out ocular involvement.

A diagnosis of eczema herpeticum requires immediate treatment with oral or intravenous antiviral medication.

Immediately treat with antivirals

Due to the potential complications discussed above, a diagnosis of EH necessitates immediate treatment with oral or intravenous antiviral medication. Acyclovir, valacyclovir, or famciclovir may be used, with typical treatment courses ranging from 10 to 14 days or until all mucocutaneous lesions are healed.⁴ Although typically reserved for patients with recurrent genital herpes resulting in 6 or more outbreaks annually, chronic suppressive therapy also may be considered for patients with EH who suffer from frequent or severe recurrent outbreaks.

Continue to: Our patient

Our patient. Given his otherwise excellent health and the absence of symptoms of potentially serious complications, our patient was treated as an outpatient with a 10-day course of valacyclovir 1000 mg PO BID. He was additionally prescribed a 7-day course of cephalexin 500 mg PO TID for coverage of bacterial superinfection. He responded well to treatment.

Ten days after his initial presentation to our clinic, his erosions and vesicles had completely cleared, and the associated erythema had significantly improved (FIGURE 2). Given the severity of his presentation and his history of 2 to 3 outbreaks annually, he opted to continue prophylactic valacyclovir (500 mg/d) for long-term suppression.

CORRESPONDENCE
Jonathan Madden, MD, 221 3rd Street West, JBSA-Randolph, TX 78150, [email protected]

A 22-year-old Caucasian man with a history of atopic dermatitis (AD) was referred to our dermatology clinic for evaluation of a diffuse facial rash that had been present for the previous 7 days. The rash initially presented as erythema on the right malar cheek that rapidly spread to the entire face. Initially diagnosed as impetigo, empiric treatment with sulfamethoxazole/trimethoprim (800 mg/160 mg PO BID for 7 days), dicloxacillin (500 mg PO BID for 6 days), cephalexin (500 mg TID for 5 days), and mupirocin (2% topical cream applied TID for 6 days) failed to improve the patient’s symptoms. He reported mild pain associated with facial movements.

The patient had a history of similar (but more limited) rashes, which he described as “recurrent impetigo,” that began during his career as a high school and collegiate wrestler. These rashes were different from the rashes he described as his history of AD, which consisted of pruritic and erythematous skin in his antecubital and popliteal fossae. He denied any history of herpes simplex virus (HSV) infection.

A physical examination revealed numerous monomorphic, 1- to 3-mm, punched-out erosions and ulcers with overlying yellow-brown crust encompassing the patient’s entire face and portions of his anterior neck. Several clustered vesicles on erythematous bases also were noted (FIGUREs 1A and 1B). We used a Dermablade to unroof some of the vesicles and sent the scrapings to the lab for Tzanck, direct fluorescent antibody assay (DFA), and HSV polymerase chain reaction (PCR) testing.

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

Diagnosis: Eczema herpeticum secondary to herpes gladiatorum

The patient’s laboratory results came back and the Tzanck preparation was positive for multinucleated giant cells, and both the DFA and HSV PCR were positive for HSV infection. This, paired with the widely disseminated rash observed on examination and the patient’s history of AD, was consistent with a diagnosis of eczema herpeticum (EH).

Rather than primary impetigo, the patient’s self-described history of recurrent rashes was felt to represent a history of HSV outbreaks. Given his denial of prior oral or genital HSV infection, as well as the coincident onset of these outbreaks during his career as a competitive wrestler, the most likely primary infection source was direct contact with another HSV-infected wrestler.

Herpes gladiatorum refers to a primary cutaneous HSV infection contracted by an athlete through direct skin-to-skin contact with another athlete.¹ It is common in contact sports, such as rugby and wrestling, and particularly common at organized wrestling camps, where mass outbreaks are a frequent occurrence.² Herpes gladiatorum is so common at these camps that many recommend prophylactic valacyclovir treatment for all participants to mitigate the risk of contracting HSV. In a 2016 review, Anderson et al concluded that prophylactic valacyclovir treatment at a 28-day high school wrestling camp effectively reduced outbreak incidence by 89.5%.²

Prophylactic valacyclovir treatment at a 28-day high school wrestling camp reduced outbreak incidence of herpes gladiatorum by 89.5%.

The lesions of herpes gladiatorum are classically limited in distribution and reflective of the areas of direct contact with infected skin, most commonly the face, neck, and arms. Our patient’s history of more limited outbreaks on his face was consistent with this typical presentation. His current outbreak, however, had become much more widely disseminated, which led to the diagnosis of EH secondary to herpes gladiatorum.

Eczema herpeticum: Pathogenesis and diagnosis

Also known as Kaposi’s varicelliform eruption, EH is a rapid, widespread cutaneous dissemination of HSV infection in areas of dermatitis or skin barrier disruption, most commonly caused by HSV-1 infection.³ It is classically associated with AD, but also can occur in patients with impaired epidermal barrier function due to other conditions, such as burns, pemphigus vulgaris, mycosis fungoides, and Darier disease.⁴ It occurs in <3% of patients with AD and is more commonly observed in infants and children with AD than adults.⁵

Continue to: Clinically, the most common manifestations are discrete..

Clinically, the most common manifestations are discrete, monomorphic, 2- to 3-mm, punched-out erosions with hemorrhagic crusts; intact vesicles are less commonly observed.⁴ Involved skin is typically painful and may be pruritic. Clinical diagnosis should be confirmed by laboratory evaluation, typically Tzanck preparation, DFA, and/or HSV PCR.

Complications and the importance of rapid treatment

The most common complication of EH is bacterial superinfection (impetigo), usually by Staphylococcus aureus or group A streptococci. Signs of bacterial superinfection include weeping lesions, pustules, honey-colored/golden crusting, worsening of existing dermatitis, and failure to respond to antiviral treatment. Topical mupirocin 2% cream is generally effective for controlling limited infection. However, systemic antibiotics (cephalosporins or penicillinase-resistant penicillins) may be necessary to control widespread disease.⁴ Clinical improvement should be observed within a single course of an appropriate antibiotic.

In contrast to impetigo, less common but more serious complications of EH can be life threatening. Systemic dissemination of disease is of particular importance in vulnerable populations such as pediatric and immunocompromised patients. Meningoencephalitis, secondary bacteremia, and herpes keratitis can all develop secondary to EH and incur significant morbidity and mortality.¹

Fever, malaise, lymphadenopathy, or eye pain should prompt immediate consideration of inpatient evaluation and treatment for these potentially deadly or debilitating complications. All patients with EH distributed near the eyes should be referred to ophthalmology to rule out ocular involvement.

A diagnosis of eczema herpeticum requires immediate treatment with oral or intravenous antiviral medication.

Immediately treat with antivirals

Due to the potential complications discussed above, a diagnosis of EH necessitates immediate treatment with oral or intravenous antiviral medication. Acyclovir, valacyclovir, or famciclovir may be used, with typical treatment courses ranging from 10 to 14 days or until all mucocutaneous lesions are healed.⁴ Although typically reserved for patients with recurrent genital herpes resulting in 6 or more outbreaks annually, chronic suppressive therapy also may be considered for patients with EH who suffer from frequent or severe recurrent outbreaks.

Continue to: Our patient

Our patient. Given his otherwise excellent health and the absence of symptoms of potentially serious complications, our patient was treated as an outpatient with a 10-day course of valacyclovir 1000 mg PO BID. He was additionally prescribed a 7-day course of cephalexin 500 mg PO TID for coverage of bacterial superinfection. He responded well to treatment.

Ten days after his initial presentation to our clinic, his erosions and vesicles had completely cleared, and the associated erythema had significantly improved (FIGURE 2). Given the severity of his presentation and his history of 2 to 3 outbreaks annually, he opted to continue prophylactic valacyclovir (500 mg/d) for long-term suppression.

CORRESPONDENCE
Jonathan Madden, MD, 221 3rd Street West, JBSA-Randolph, TX 78150, [email protected]

A 22-year-old Caucasian man with a history of atopic dermatitis (AD) was referred to our dermatology clinic for evaluation of a diffuse facial rash that had been present for the previous 7 days. The rash initially presented as erythema on the right malar cheek that rapidly spread to the entire face. Initially diagnosed as impetigo, empiric treatment with sulfamethoxazole/trimethoprim (800 mg/160 mg PO BID for 7 days), dicloxacillin (500 mg PO BID for 6 days), cephalexin (500 mg TID for 5 days), and mupirocin (2% topical cream applied TID for 6 days) failed to improve the patient’s symptoms. He reported mild pain associated with facial movements.

The patient had a history of similar (but more limited) rashes, which he described as “recurrent impetigo,” that began during his career as a high school and collegiate wrestler. These rashes were different from the rashes he described as his history of AD, which consisted of pruritic and erythematous skin in his antecubital and popliteal fossae. He denied any history of herpes simplex virus (HSV) infection.

A physical examination revealed numerous monomorphic, 1- to 3-mm, punched-out erosions and ulcers with overlying yellow-brown crust encompassing the patient’s entire face and portions of his anterior neck. Several clustered vesicles on erythematous bases also were noted (FIGUREs 1A and 1B). We used a Dermablade to unroof some of the vesicles and sent the scrapings to the lab for Tzanck, direct fluorescent antibody assay (DFA), and HSV polymerase chain reaction (PCR) testing.

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

Diagnosis: Eczema herpeticum secondary to herpes gladiatorum

The patient’s laboratory results came back and the Tzanck preparation was positive for multinucleated giant cells, and both the DFA and HSV PCR were positive for HSV infection. This, paired with the widely disseminated rash observed on examination and the patient’s history of AD, was consistent with a diagnosis of eczema herpeticum (EH).

Rather than primary impetigo, the patient’s self-described history of recurrent rashes was felt to represent a history of HSV outbreaks. Given his denial of prior oral or genital HSV infection, as well as the coincident onset of these outbreaks during his career as a competitive wrestler, the most likely primary infection source was direct contact with another HSV-infected wrestler.

Herpes gladiatorum refers to a primary cutaneous HSV infection contracted by an athlete through direct skin-to-skin contact with another athlete.¹ It is common in contact sports, such as rugby and wrestling, and particularly common at organized wrestling camps, where mass outbreaks are a frequent occurrence.² Herpes gladiatorum is so common at these camps that many recommend prophylactic valacyclovir treatment for all participants to mitigate the risk of contracting HSV. In a 2016 review, Anderson et al concluded that prophylactic valacyclovir treatment at a 28-day high school wrestling camp effectively reduced outbreak incidence by 89.5%.²

Prophylactic valacyclovir treatment at a 28-day high school wrestling camp reduced outbreak incidence of herpes gladiatorum by 89.5%.

The lesions of herpes gladiatorum are classically limited in distribution and reflective of the areas of direct contact with infected skin, most commonly the face, neck, and arms. Our patient’s history of more limited outbreaks on his face was consistent with this typical presentation. His current outbreak, however, had become much more widely disseminated, which led to the diagnosis of EH secondary to herpes gladiatorum.

Eczema herpeticum: Pathogenesis and diagnosis

Also known as Kaposi’s varicelliform eruption, EH is a rapid, widespread cutaneous dissemination of HSV infection in areas of dermatitis or skin barrier disruption, most commonly caused by HSV-1 infection.³ It is classically associated with AD, but also can occur in patients with impaired epidermal barrier function due to other conditions, such as burns, pemphigus vulgaris, mycosis fungoides, and Darier disease.⁴ It occurs in <3% of patients with AD and is more commonly observed in infants and children with AD than adults.⁵

Continue to: Clinically, the most common manifestations are discrete..

Clinically, the most common manifestations are discrete, monomorphic, 2- to 3-mm, punched-out erosions with hemorrhagic crusts; intact vesicles are less commonly observed.⁴ Involved skin is typically painful and may be pruritic. Clinical diagnosis should be confirmed by laboratory evaluation, typically Tzanck preparation, DFA, and/or HSV PCR.

Complications and the importance of rapid treatment

The most common complication of EH is bacterial superinfection (impetigo), usually by Staphylococcus aureus or group A streptococci. Signs of bacterial superinfection include weeping lesions, pustules, honey-colored/golden crusting, worsening of existing dermatitis, and failure to respond to antiviral treatment. Topical mupirocin 2% cream is generally effective for controlling limited infection. However, systemic antibiotics (cephalosporins or penicillinase-resistant penicillins) may be necessary to control widespread disease.⁴ Clinical improvement should be observed within a single course of an appropriate antibiotic.

In contrast to impetigo, less common but more serious complications of EH can be life threatening. Systemic dissemination of disease is of particular importance in vulnerable populations such as pediatric and immunocompromised patients. Meningoencephalitis, secondary bacteremia, and herpes keratitis can all develop secondary to EH and incur significant morbidity and mortality.¹

Fever, malaise, lymphadenopathy, or eye pain should prompt immediate consideration of inpatient evaluation and treatment for these potentially deadly or debilitating complications. All patients with EH distributed near the eyes should be referred to ophthalmology to rule out ocular involvement.

A diagnosis of eczema herpeticum requires immediate treatment with oral or intravenous antiviral medication.

Immediately treat with antivirals

Due to the potential complications discussed above, a diagnosis of EH necessitates immediate treatment with oral or intravenous antiviral medication. Acyclovir, valacyclovir, or famciclovir may be used, with typical treatment courses ranging from 10 to 14 days or until all mucocutaneous lesions are healed.⁴ Although typically reserved for patients with recurrent genital herpes resulting in 6 or more outbreaks annually, chronic suppressive therapy also may be considered for patients with EH who suffer from frequent or severe recurrent outbreaks.

Continue to: Our patient

Our patient. Given his otherwise excellent health and the absence of symptoms of potentially serious complications, our patient was treated as an outpatient with a 10-day course of valacyclovir 1000 mg PO BID. He was additionally prescribed a 7-day course of cephalexin 500 mg PO TID for coverage of bacterial superinfection. He responded well to treatment.

Ten days after his initial presentation to our clinic, his erosions and vesicles had completely cleared, and the associated erythema had significantly improved (FIGURE 2). Given the severity of his presentation and his history of 2 to 3 outbreaks annually, he opted to continue prophylactic valacyclovir (500 mg/d) for long-term suppression.

CORRESPONDENCE
Jonathan Madden, MD, 221 3rd Street West, JBSA-Randolph, TX 78150, [email protected]

Tanning use disorder is an addiction, and should be added to the DSM-5, Raghav Tripathi and his associates maintained in a letter to the editor of the Journal of the European Academy of Dermatology and Venereology.

Ibrakovic/iStock/Getty Images Plus

“Strong evidence suggests that tanning use disorder should be included in the DSM-5,” they wrote, noting that individuals who show signs of tanning use disorder have problems quitting, and also are more likely to smoke cigarettes, drink alcohol excessively, and engage in other high-risk behaviors.

In the letter, Mr. Tripathi, a medical student at Case Western Reserve University, Cleveland, and his associates also noted that frequent tanners have been found to prefer tanning beds that used UV radiation (UVR) over beds that did not, even though they were blinded to which ones did and did not. Reports of pain relief and improved mood following UVR exposure, withdrawal symptoms upon discontinuation of UVR, and the successful use of opioid antagonists to reduce UVR dependence “underscore the importance of viewing tanning as a use disorder.”

The same “brain circuitry and neurotransmitters involved in the reward pathways of other use disorders” are associated with the addictive characteristics of UVR, they wrote.

In one study, people who were compulsive tanners were found to have an increase in “cerebral blood flow in the mesostriatal reward pathway when exposed to UVR.” In another study, opioid antagonism using naltrexone was found to reduce “UVR preference in frequent tanners.”

Understanding the biologic connections is crucial to advocating for formalization of the condition as a recognized disorder in the DSM-5; classification would not only increase awareness of the condition but also standardize approaches to diagnosis and treatment that are key to improving patient care, the authors wrote. Moreover, inclusion of the disorder in the DSM-5 could help to pave the way for inclusion in the ICD-10, which would have broader implications for limiting the overall harmful effects that tanning poses.

The authors had no relevant financial disclosures to report.

SOURCE: Tripathi R et al. J Eur Acad Dermatol Venereol. 2018 Oct 13. doi: 10.1111/jdv.15286.

Tanning use disorder is an addiction, and should be added to the DSM-5, Raghav Tripathi and his associates maintained in a letter to the editor of the Journal of the European Academy of Dermatology and Venereology.

Ibrakovic/iStock/Getty Images Plus

“Strong evidence suggests that tanning use disorder should be included in the DSM-5,” they wrote, noting that individuals who show signs of tanning use disorder have problems quitting, and also are more likely to smoke cigarettes, drink alcohol excessively, and engage in other high-risk behaviors.

In the letter, Mr. Tripathi, a medical student at Case Western Reserve University, Cleveland, and his associates also noted that frequent tanners have been found to prefer tanning beds that used UV radiation (UVR) over beds that did not, even though they were blinded to which ones did and did not. Reports of pain relief and improved mood following UVR exposure, withdrawal symptoms upon discontinuation of UVR, and the successful use of opioid antagonists to reduce UVR dependence “underscore the importance of viewing tanning as a use disorder.”

The same “brain circuitry and neurotransmitters involved in the reward pathways of other use disorders” are associated with the addictive characteristics of UVR, they wrote.

In one study, people who were compulsive tanners were found to have an increase in “cerebral blood flow in the mesostriatal reward pathway when exposed to UVR.” In another study, opioid antagonism using naltrexone was found to reduce “UVR preference in frequent tanners.”

Understanding the biologic connections is crucial to advocating for formalization of the condition as a recognized disorder in the DSM-5; classification would not only increase awareness of the condition but also standardize approaches to diagnosis and treatment that are key to improving patient care, the authors wrote. Moreover, inclusion of the disorder in the DSM-5 could help to pave the way for inclusion in the ICD-10, which would have broader implications for limiting the overall harmful effects that tanning poses.

The authors had no relevant financial disclosures to report.

SOURCE: Tripathi R et al. J Eur Acad Dermatol Venereol. 2018 Oct 13. doi: 10.1111/jdv.15286.

Tanning use disorder is an addiction, and should be added to the DSM-5, Raghav Tripathi and his associates maintained in a letter to the editor of the Journal of the European Academy of Dermatology and Venereology.

Ibrakovic/iStock/Getty Images Plus

“Strong evidence suggests that tanning use disorder should be included in the DSM-5,” they wrote, noting that individuals who show signs of tanning use disorder have problems quitting, and also are more likely to smoke cigarettes, drink alcohol excessively, and engage in other high-risk behaviors.

In the letter, Mr. Tripathi, a medical student at Case Western Reserve University, Cleveland, and his associates also noted that frequent tanners have been found to prefer tanning beds that used UV radiation (UVR) over beds that did not, even though they were blinded to which ones did and did not. Reports of pain relief and improved mood following UVR exposure, withdrawal symptoms upon discontinuation of UVR, and the successful use of opioid antagonists to reduce UVR dependence “underscore the importance of viewing tanning as a use disorder.”

The same “brain circuitry and neurotransmitters involved in the reward pathways of other use disorders” are associated with the addictive characteristics of UVR, they wrote.

In one study, people who were compulsive tanners were found to have an increase in “cerebral blood flow in the mesostriatal reward pathway when exposed to UVR.” In another study, opioid antagonism using naltrexone was found to reduce “UVR preference in frequent tanners.”

Understanding the biologic connections is crucial to advocating for formalization of the condition as a recognized disorder in the DSM-5; classification would not only increase awareness of the condition but also standardize approaches to diagnosis and treatment that are key to improving patient care, the authors wrote. Moreover, inclusion of the disorder in the DSM-5 could help to pave the way for inclusion in the ICD-10, which would have broader implications for limiting the overall harmful effects that tanning poses.

The authors had no relevant financial disclosures to report.

SOURCE: Tripathi R et al. J Eur Acad Dermatol Venereol. 2018 Oct 13. doi: 10.1111/jdv.15286.