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Dermatologic Look-Alikes,
Module III
Lou Mancano MD, FAAFP
The Reading Hospital &
Medical Center
PAFP South Central Assembly
September 19, 2009
Objectives



Recognize characteristics that aid in
diagnosing similar-appearing skin lesions and
conditions
Use visual and other diagnostic modalities to
assist in differentiating skin conditions that may
look alike
Formulate treatment options for the presented
look-alike skin conditions
Disclosure Information
Louis D. Mancano, M.D.
I
have no relevant financial relationships to
disclose.
-AND –
I will discuss the following off-label and/or
investigational use in my presentation.
UVB
light therapy, topical immunomodulators, topical
tretinoin, topical calcipotriol, and oral
hydroxychloroquine are mentioned as off-label
treatments for some conditions presented
Practice Recommendation
Screening for Skin Cancer
The USPSTF concludes that the current
evidence is insufficient to assess the balance
of benefits and harms of using a whole-body
skin examination by a primary care clinician or
patient skin self-examination for the early
detection of cutaneous melanoma, basal cell
cancer, or squamous cell skin cancer in the
adult general population.
 This is an I statement.
http://www.ahrq.gov/clinic/uspstf09/skincancer/skincanrs.pdf

Flat Warts
Angiofibromas
Steroid Acne
Keratosis Pilaris
Flat Warts
Flat Warts (Verruca Plana)




Benign proliferations of keratinized epithelium
Caused by infection with types 3, 10, and 28 of
the human papillomavirus (HPV)
Autoinoculation also may occur
Incubation period ranges 1 - 6 months
Flat Warts (Verruca Plana)




Slightly elevated fleshcolored to
hyperpigmented papules
Smooth or slightly
hyperkeratotic
Size usually 1 - 5 mm
Numbers range from a
few to hundreds that
may become grouped or
confluent
Flat Warts (Verruca Plana)

May occur anywhere on the skin and mucous
membranes. Most common areas:
–
–
–
face (children)
hands
beard area and shins (adults)

Koebner phenomenon - irritation from shaving legs and
beard area probably accounts for this
Flat Warts

Treatment
–
–
–
Destructive methods - desiccation, freezing, and
lasers are 60 to 80% effective
Imiquimod - immune modifier approved for
treatment of genital warts, but reports indicate
successful tx of other warts.
Topical tretinoin (retinoic acid) has some success
Angiofibromas (Adenoma Sebaceum)
Angiofibromas (Adenoma Sebaceum)




Hamartomas composed of fibrous and vascular tissue
(do not represent sebaceous elements)
The most common skin lesions associated with
tuberous sclerosis (TS)
TS is an autosomal dominant disorder characterized by
hamartomas that may involve the skin, brain, heart,
kidneys, and other organs
Vogt’s classic triad of TS is seizure disorder, mental
retardation (<50%), and facial angiofibromas
Angiofibromas (Adenoma Sebaceum)

Typically appear as
freckles and progress
into erythematous, firm
papulonodular lesions in
adolescence or young
adulthood
Angiofibromas (Adenoma
Sebaceum)


Appear on the nose,
nasolabial folds, and
cheeks in a malar
distribution
Mature lesions
remain unchanged
and do not produce
pus or fluid
Tuberous Sclerosis

Other dermatologic
features include
hypomelanotic macules
or “ash leaf spots” on the
trunk, lower and upper
extremities, head, and
neck
Tuberous Sclerosis


Shagreen patches
(fibromas on the trunk)
Periungual fibromas
(flesh-colored lesions
along the nail folds)
Tuberous Sclerosis



National Tuberous Sclerosis Association
guidelines state facial angiofibromas are a
major diagnostic feature of suspected TS
Others are seizures and behavioral problems
(ADHD and autism)
Treatment of angiofibromas focuses on
cosmesis and use laser therapy, cryotherapy,
electrocautery, or dermabrasion
Steroid-Induced Acne
Steroid-Induced Acne




Topical, inhaled or systemic corticosteroids (as well as
lithium, some antiepileptics, and iodides) can promote
acne
Steroid acne is observed as monomorphous
papulopustules
On the trunk, extremities, and/or face
Usually resolves after discontinuation of the drug, but
may respond to the usual treatments of acne vulgaris.
Practice Recommendation
Treatment of Acne

14 Level A comparisons demonstrated the
efficacy over vehicle or placebo with aluminum
chlorhydroxide/sulphur, topical clindamycin,
topical erythromycin, benzoyl peroxide, topical
isotretinoin, tretinoin, oral tetracycline, and
norgestimate/ethinyl estradiol.

Strength of Recommendation : Level A
http://www.ahrq.gov/clinic/epcsums/acnesum.htm
Practice Recommendation
Treatment of Acne

Level A conclusions demonstrating equivalence
include:
–
–
–
–
–
Benzoyl peroxide at various strengths was equally
efficacious in mild/moderate acne;
Adapalene and tretinoin were equally efficacious in
unspecified severity;
Motretinide and tretinoin were equally effective;
Adding vitamin A to oxytetracycline conferred no added
efficacy;
Cyproterone (an antiandrogen) was equally effective at two
different doses.
http://www.ahrq.gov/clinic/epcsums/acnesum.htm
Keratosis Pilaris
Keratosis Pilaris




Common benign condition with many small,
rough folliculocentric keratotic papules, often
described as chicken skin
Asymptomatic or pruritic
Characteristic areas are the face and extensor
surfaces of upper arms and thighs
Palpation reveals a fine, sandpaper-like texture
Keratosis Pilaris


Some papules may
be slightly
erythematous
Scratching away the
surface of some
bumps may reveal a
small, coiled hair
Keratosis Pilaris





Begins in childhood, becomes more exaggerated in
adolescence, and may improve with age.
Often accompanies dry skin conditions such as atopic
dermatitis, xerosis, and ichthyosis vulgaris
No clear etiology
30-50% of patients have a positive family history.
Seasonal variation
– dry skin in winter tends to worsen symptoms
– may improve in summer months
Keratosis Pilaris


The diagnosis of KP is
clinical and based on a
typical appearance in
areas such as the upper
arms.
No specific tests aid in
the diagnosis
Keratosis Pilaris Treatment




No single therapy is effective and complete clearing
may not be possible
Mainstay of treatment are measures to prevent
excessive skin dryness
Use mild cleansers (Dove, Cetaphil, others)
Lubrication with over-the-counter moisturizers
(Cetaphil, Purpose, Lubriderm, Eucerin, others)
Keratosis Pilaris Treatment


Additional options include:
– Lactic acid lotions (AmLactin, Lac-Hydrin 12%)
– Urea cream (Carmol 10, Carmol 20, Carmol 40, Urix
40, others)
– Salicylic acid (Salex lotion)
– Weekly or biweekly retinoic acid products such as
tretinoin (Retin-A), tazarotene (Tazorac), and
adapalene (Differin)
Irritated skin should be treated only with bland
moisturizers until the inflammation resolves
Keratosis Pilaris Treatment



For inflammed skin, use a 7- to 10-day course of
medium potency topical steroid cream (eg, Locoid,
Lipocream, triamcinolone 0.1%) daily to BID
May treat persistent hyperpigmentation with fading
creams such as hydroquinone 4% (Eldoquin, others),
kojic acid (SkinBright, Lumedia, others) and azelaic
acid 15-20% (Azelex, Finacea).
Topical immunomodulators such as pimecrolimus
(Elidel) or tacrolimus (Protopic) approved for atopic
dermatitis and eczema would be considered off label
for KP.
Erythrasma
Tinea Cruris
Candida Intertrigo
Tinea Cruris




Tinea corporis involving the
crural folds
Begins as an erythematous
patch on inner aspect of
thighs
Spreads centrifugally with
advancing scales and partial
central clearing
Slightly elevated, sharply
demarcated borders may
show tiny vesicles
Tinea Cruris

In North America the most common cause is
Trichophyton rubrum
–


less commonly Epidermophyton floccosum and T
mentagrophytes
When caused by T rubrum, the disease may
be more chronic and extensive
T mentagrophytes and E floccosum are usually
less extensive and may sometimes clear
spontaneously
Tinea Cruris


The source of the
infecting fungus is
usually the patient's own
tinea pedis.
More common in men, in
obesity, and with
physical activity that
results in perspiring
Diagnosis


KOH of scales scraped
from the lesion’s active
border will show
characteristic segmented
hyphae and arthrospores
Cultures on Sabouraud's
medium can also be
used to confirm the
diagnosis
Treatment





Daily application of talcum or other desiccant powders
Itching can be alleviated by over the counter
preparations (Sarna, Prax, others)
Wear loose-fitting cotton clothing
Topical antifungal treatment for 2 to 4 weeks required
for most cases
Lesions resistant to topical medications can be treated
with griseofulvin 250 mg PO TID for 14 days, or with
other systemic agents
Practice Recommendation – Topical
treatments for fungal infections of the skin of the
foot

Allylamines, azoles and undecenoic acid are
efficacious. Allylamines cure slightly more
infections than azoles but are much more
expensive. The most cost-effective strategy is
first to treat with azoles or undecenoic acid and
to use allylamines if that fails.

Strength of Recommendation: Level A
http://www.cochrane.org/reviews/en/ab001434.html
Antifungal Medications


Allylamines - terbenafine (Lamisil 1% cream, gel, lotion)
Azoles –
–
–
–
–
–
–
–


Fluconazole (Diflucan)
Itraconazole (Sporanox)
Ketoconazole (Nizoral 2% cream)
Clotrimazole (Mycelex, Lotrimin 1% cream, gel, solution others)
Voriconazole (Vfend)
Miconazole (Monistat-Derm 1% cream, gel, or powder)
Econazole (Spectazole 1% cream)
Tolnaftate (Tinactin 1% aerosol, liquid, powder, or solution,
Zeasorb, others)
Undecenoic acid (Desenex, Cruex, others)
Erythrasma
Erythrasma


A chronic bacterial
infection of
intertrigenous areas of
the groin; may include
toe webs, axillary and
submammary areas.
Caused by
Corynebacterium
minutissimum
Erythrasma


Typically a slightly pruritic reddish-brown
slightly scaly plaque with sharp borders.
More common in warm climates and among
overweight or diabetic patients
Diagnosis



Wood's lamp exam
causes the lesions to
glow a coral-red color
KOH is negative
Culture scrapings from
the lesion
Treatment


Gently scrubbing lesions with antibacterial
soap may help
Topical erythromycin 2% gel (Erygel, Emgel, TStat, others) to affected area twice daily or oral
erythromycin (Ery-TAB, PCE, others) 500 mg
PO Q. 12 hrs for 5 to 10 days
Candida Intertrigo
Candida Intertrigo



C. albicans is a commensal normal organism
of the GI tract, vagina, and oral cavity
Can become an opportunistic infection when
host defenses, physiology, or normal flora
become altered
C. albicans is the most frequent pathogen, but
other species include C. tropicalis, krusei, and
glabrata
Candida Intertrigo


Candida intertrigo is an inflammatory condition
of two closely opposed skin surfaces
Results from the overgrowth of Candida
species with/without bacteria in a favorable
environment and host
Risk Factors

Factors that may increase skin friction and
moisture that lead to infection include:
–
–
–
–
–
Obesity
Clothing or activities that rub/chafe skin
Occlusive clothing
Hyperhidrosis
Occupational exposure to moisture
Risk Factors


T-lymphocyte mediated immunity is the primary
defense mechanism against candidal infection
Factors that interfere with the immune response
include:
–
–
–
–
–
–
Diabetes mellitus
Glucocorticoids
Antibiotics
HIV
Radiation or Chemotherapy
Immunosuppressant medications
Diagnosis
KOH Prep
“Satellite” lesions
Treatment



Manage risk factors
Keep the infected area dry
Topical azoles and polyenes, including
clotrimazole, miconazole, and nystatin, are
effective
Linear Verrucous Epidermal nevus
Lichen striatus
Linear porokeratosis
Nevus Sebaceous
Blaschko’s lines

Blaschko lines are
thought to be
embryologic in origin.
They are believed to be
the result of the
segmental growth of
clones of cutaneous
cells or the mutationinduced mosaicism of
cutaneous cells.
Linear Verrucous Epidermal Nevus
Epidermal Nevi

Congenital hamartomas of ectodermal origin
classified by the main component:
–
–
–
–
–
Sebaceous
Apocrine
Eccrine
Follicular
Keratinocytic
Epidermal Nevi



Patches, plaques, or nodules
May be unilateral, bilateral or extensively
distributed
Usually asymptomatic with the exception of
inflammatory type of linear verrucous
epidermal nevus (LVEN).
Linear Verrucous Epidermal Nevus



Inflammatory LVEN is a linear, persistent,
pruritic plaque, usually first noted on a limb in
early childhood
Characterized by tiny, discrete, slightly warty
papules which tend to coalesce in a linear
formation
Unlike the other types of epidermal nevi, LVEN
demonstrates erythema and sometimes
pruritus
Linear Verrucous Epidermal Nevus

Lesions may be
observed at birth, but
most appear during
infancy and childhood
– half of patients have
lesions by age 6
months
– three quarters
develop lesions by
age 5 years
Epidermal Nevus Syndrome


An estimated 1/3 of individuals with epidermal
nevi have an epidermal nevus syndrome
(Solomon syndrome) involving neurocutaneous
ectodermal defects in the skin, brain, eyes,
and/or skeleton.
The clinical history may reflect symptoms
associated with underlying anomalies with
evidence of skeletal or neurologic alterations,
such as epilepsy or mental retardation.
Epidermal Nevus Syndrome


Skin lesions are less
obvious in infancy and
distribution pattern
usually follows the lines
of Blaschko.
Develop multiple, welldemarcated linear
plaques
Epidermal Nevus Syndrome




The last stage of nevus development occurs in late
adolescence or early adulthood
With age, lesions become darker, verrucous, and
hyperkeratotic
Cutaneous benign or malignant neoplasms noted in as
many as 20-30% of patients.
Failure to recognize the syndromic association can
result in a failure to diagnose a potentially serious
medical problem.
Workup



MRI to evaluate intracranial involvement and
may show cerebral atrophy, dilated ventricles,
hemimegalencephaly, etc.
EEGs are abnormal in approximately 90% of
patients with the epileptiform foci ipsilateral to
the major skin lesions.
If lesion is near the eye or an associated
cataract is present, consult an ophthalmologist
Treatment




Therapy is often challenging
Epidermal nevi are usually resistant to topical and
intralesional steroids, dithranol, topical retinoids, and
cryosurgery
Topical calcipotriol (Dovonex) may help but is not
approved for use in children younger than 12 years
If the size and the site are suitable, the nevus may be
excised if desired by the patient
Lichen Striatus
Lichen Striatus




Uncommon benign, self-limited linear
dermatosis of unknown origin
Clinically diagnosed on the basis of
appearance and characteristic developmental
pattern following the lines of Blaschko.
Is primarily a disease of children.
More than 50% of all cases occur in children
aged 5-15 years.
Lichen Striatus



Often appears as a sudden
asymptomatic linear eruption
of 1 to 3 mm pink, tan, or
skin-colored lichenoid
papules on an extremity
A continuous or interrupted,
linear band of smooth, scaly,
or flat topped papules
The band may range from a
few mm to 1-2 cm wide and
extends from a few
centimeters to the full length
an extremity
Lichen Striatus



The lesions are usually unilateral on a proximal
extremity
Less common on the trunk, head, neck, or
buttock
Nail involvement is uncommon (longitudinal
ridging, splitting, onycholysis, etc.), and
restricted to a single nail
Lichen Striatus



In darkly pigmented
individuals, eruptions
may appear as a
bandlike area of
hypopigmentation.
Papules usually reach
maximum involvement
within several days to
weeks.
May resolve with
postinflammatory hyperor hypopigmentation
Lichen Striatus – Management




Skin biopsy can be performed to confirm the
diagnosis
Because lesions spontaneously regress within
3 -12 months, no treatment is needed
Nail involvement resolves spontaneously
without deformity within 30 months
The patient and family should be reassured
Lichen Striatus – Management



Topical or intralesional corticosteroids do not
usually hasten resolution
Emollients and steroids may treat associated
dryness and pruritus, if present.
Topical tacrolimus 0.03%, 0.1% (Protopic) and
pimecrolimus 1% cream (Elidel) BID have been
successful in treating persistent, pruritic lesions
on the face and extremities.
Linear Porokeratosis
Porokeratosis



A clonal disorder of keratinization characterized by
atrophic patch(es) surrounded by a distinctive ridgelike
border called the cornoid lamella
Lesions are grouped, linearly arranged, usually
dermatomal, round papules and plaques with the
characteristic raised peripheral ridge and a central
furrow
Linear porokeratosis is one of five clinical variants
Linear Porokeratosis



Seen unilaterally on an extremity, the trunk,
and/or the head and neck area.
Multiple linear groups may be seen in one
patient, typically on the same side.
Several risk factors have been identified
including genetic inheritance, ultraviolet
radiation, and immunosuppression
Linear Porokeratosis


Most lesions are asymptomatic, but ulceration
has been described.
A 7.5% to 11% risk of malignant degeneration
to basal or squamous cell carcinoma has been
reported in all forms of porokeratosis
Porokeratosis - Management


Protection from the sun, use of emollients, and
watchful observation for signs of malignant
degeneration may be all that is needed for many
patients.
If lesions are widespread and medical treatment is
desired, several medications have potential benefit:
–
–
–
Topical 5-fluorouracil can induce remission
Topical vitamin D-3 analogues, calcipotriol and tacalcitol
Topical imiquimod 5% cream
Porokeratosis - Management


Oral retinoids (isotretinoin, etretinate, and
acitretin) may reduce the risk of carcinomatous
degeneration
Surgical treatment for porokeratosis lesions
that have undergone malignant transformation
Nevus Sebaceous
Nevus Sebaceous



Circumscribed hamartomas predominantly composed
of sebaceous glands.
Most are a solitary linear or oval, hairless velvety pink,
tan or orange-yellow plaque on the scalp, head or neck
at birth or in early childhood.
In adolescence, the lesion becomes verrucous and
nodular, round, oval, or linear in shape, varying in
length from about 1 cm to more than 10 cm.
Nevus Sebaceous


The medical importance
of a solitary nevus
sebaceous is an up to
15% risk of malignant
neoplastic change during
adolescence or adult life
The most common
malignant neoplasm
arising is basal cell
carcinoma
Nevus Sebaceous



Many authorities recommend complete full-thickness
surgical excision
The timing of excision remains a matter of debate.
Early removal is preferred to avoid social
consequences that a prominent lesion may invoke from
peers.
A 2007 study by Barkham et al concluded that
prophylactic excision of all sebaceus nevi is not
warranted and recommended only when benign or
malignant neoplasms are clinically suspected or for
cosmetic reasons.
Tinea Versicolor
Confluent and Reticulated
Papillomatosis of Gougerot &
Carteaud
Pityriasis rubra pilaris
Macular amyloidosis
Tinea Versicolor
Tinea Versicolor



Common, benign, superficial cutaneous yeast
infection localized to the stratum corneum
Characterized by hypopigmented or
hyperpigmented macules and patches varying
from almost white to reddish brown or fawn
colored.
Usually on the trunk, back, abdomen, and
proximal extremities; face, scalp, and genitalia
are less commonly involved
Tinea Versicolor


Caused by the dimorphic, lipophilic yeast,
Malassezia furfur, now the accepted name for
Pityrosporon orbiculare, Pityrosporon ovale,
and Malassezia ovalis.
M furfur is a normal human cutaneous flora
found in 18% of infants and 90-100% of adults.
Tinea Versicolor - Symptoms


Most common in
persons aged 15-24
years; rare before
puberty or after age 65
Common complaints:
–
–
–
Cosmetically abnormal
pigmentation
Involved skin fails to tan in
the summer
Occasional mild pruritus
Tinea Versicolor


Most cases occur in healthy immunocompetent
individuals.
Predisposing factors:
–
–
–
–
–

genetic predisposition
warm, humid environments
immunosuppression
malnutrition
Cushing disease
The reason M furfur causes TV in some while
remaining as normal flora in others is related to the
organism's nutritional requirements and host's immune
response.
Tinea Versicolor - Diagnosis



Is usually clinical
Gentle scraping causes
a fine scale
Diagnosis confirmed by
potassium hydroxide
(KOH) exam,
demonstrating
characteristic spores
with short mycelium
referred to as spaghetti
and meatballs or the
bacon and eggs sign
Tinea Versicolor - Management



The yeast is not considered contagious.
Does not leave a permanent scar and skin
color alterations resolve 1 - 2 months after
treatment
Many topical and oral treatment options are
effective
Tinea Versicolor - Management

Topical agents include selenium sulfide, sodium
sulfacetamide, ciclopiroxolamine, azole and allylamine
antifungals.
–
–
–
Selenium sulfide lotion - liberally apply to affected areas daily
for 2 weeks, leave on for at least 10 minutes before rinsing. In
resistant cases, use overnight applications.
Apply topical azoles (ketoconazole, miconazole, etc.) or
allylamines (terbenafine) nightly for 2 weeks.
Weekly application of any of the topical agents for the following
few months may prevent recurrence.
Tinea Versicolor - Management







Oral therapy (ketoconazole, fluconazole, and itraconazole) is often
preferred by patients
Comparable results with ketoconazole 200 mg daily x 10 days or a
single 400-mg dose.
Fluconazole - a single 150 to 300 mg once weekly dose for 2 - 4
weeks.
Itraconazole - 200 mg/d for 7 days.
Oral therapy does not prevent the high rate of recurrence and is
not without risk
In the case of oral terbinafine, some subgroups of M furfur are not
clinically responsive
Prophylactic therapy may help reduce the high rate of recurrence.
Confluent and Reticulated Papillomatosis of
Gougerot and Carteaud
Confluent and Reticulated Papillomatosis
of Gougerot and Carteaud



Condition typically affecting young persons
Grayish blue, pink, or hypopigmented hyperkeratotic
papules, usually on the trunk, coalesce to form
confluent plaques centrally and a reticular pattern
peripherally.
Etiology is unclear and may represent an endocrine
disturbance, a disorder of keratinization, an abnormal
host reaction to Malassezia furfur or to Actinomyces
dietzia, a hereditary disorder, or a variant of
amyloidosis
Confluent and Reticulated Papillomatosis of
Gougerot and Carteaud


The eruption is chronic
with exacerbations and
remissions.
Differential diagnoses
include:
–
–
–
Tinea Versicolor
Pityriasis rubra pilaris
MacularAmyloidosis
Confluent and Reticulated Papillomatosis of
Gougerot and Carteaud


The most consistent
response is seen with
minocycline 50 to 100
mg daily, but frequently
recurs after
discontinuation of
therapy.
The lesions may regress
with weight reduction
Pityriasis rubra pilaris

A chronic
papulosquamous
disorder of unknown
etiology characterized by
reddish orange scaly
plaques, palmoplantar
keratoderma, and distal
keratotic follicular
papules.
Pityriasis rubra pilaris



May progress to erythroderma with distinct
areas of uninvolved skin, the so-called islands
of sparing
The familial form is autosomal dominant and
typically begins in early childhood
The acquired form has a bimodal age
distribution, with peaks in the first and fifth
decades of life
Pityriasis rubra pilaris

Plantar and palmar
keratoderma with an
orange hue on the
palms
Pityriasis rubra pilaris


Reddish-orange plaques
on the trunk
Follicular hyperkeratosis
seen on the dorsal
aspect of the proximal
phalanges.
Pityriasis rubra pilaris


No specific laboratory tests are available to
confirm the diagnosis of PRP
The diagnosis is usually made on clinical and
histologic findings
Pityriasis rubra pilaris - Treatment



Topical corticosteroids may provide comfort, but are
believed to have little long-term therapeutic effect
Emollients (petroleum jelly) reduce fissuring and
dryness, providing some patient comfort
Other potentially useful treatments include:
–
–
–
–
Vitamin D analogue calcipotriol
Topical retinoid tazarotene
Extracorporeal photochemotherapy if unresponsive to
standard treatments
Oral retinoid Acitretin (Soriatane) for 4-6 months
Macular Amyloidosis

MA is a pruritic eruption
of variable severity
consisting of small,
dusky-brown or grayish
pigmented macules
distributed symmetrically
over the upper back, and
sometimes the
extremities
Macular Amyloidosis


Pruritus may be a
primary trigger for the
deposition of amyloid
Amyloid deposits bind to
antikeratin antibodies
usually found within the
dermal papillae.
Macular Amyloidosis

Frequently, patients
seek medical attention
because of the
hyperpigmentation.
Macular Amyloidosis - Treatment


Antihistamines for relief of pruritus
Several therapies may help:
–
–
–
–
Topical dimethyl sulfoxide (DMSO), a chemical
solvent
Intralesional steroids
Ultraviolet B (UV-B) light for symptomatic relief.
Pulsed dye laser therapy may help pruritis and rash
Rosacea
Erysipelas
Polymorphous Light Eruption
Dermatomyositis
Erysipelas
Erysipelas




Acute group A beta-hemolytic streptococcal infection
involving the superficial dermal lymphatics
Characterized by local redness, heat, swelling, and a
characteristic raised, indurated border
Skin exam varies from transient hyperemia and slight
desquamation to intense inflammation with vesicles or
bullae, but there is no localized purulence
The eruption spreads by peripheral extension
Erysipelas
Associated lymphangitis and local
lymphadenopathy may occur.
 Legs and face are most frequently
affected
 Erysipelas on the face - a classic butterfly
distribution involving the cheeks and the
bridge of the nose

Erysipelas


Patients may be febrile and ill-appearing
Treat with anti-streptococcal antibiotics, such
as penicillins or cephalosporins
Rosacea
Rosacea


Acneiform disorder of middle-aged and older
adults with capillary dilation of central face
(nose, cheek, eyelids, and forehead)
Facial erythema and sebaceous gland growth
accompanied by papules, pustules, cysts, and
nodules (only look-alike in the group with these)
Rosacea

Ocular symptoms occur alone or with skin
symptoms
–
foreign body sensation, burning, telangiectasias, lid
margin irregularity, meibomian gland dysfunction,
blepharitis, keratitis, conjunctivitis, and episcleritis
Rosacea

Patients are susceptible to recurrent flushing
reactions provoked by hot or spicy foods,
alcohol, temperature extremes, and emotional
reactions
Rosacea

Rhinophyma or
metopophyma
(hyperplasia of the soft
tissues of the nose or
forehead) tends to occur
late in the course
Rosacea


Avoid topical
corticosteroids
Chronic topical facial
corticosteroid use
mimics or worsens the
condition
Rosacea - Treatment


Mild cleansers (eg, Cetaphil, Dove), avoid irritants,
use sunscreens
Topical benzoyl peroxide 2.5 to 10% daily - BID

Azelaic acid 20% cream (Azelex) or 15% gel
(Finacea) BID

Tretinoin cream (0.025, 0.05, 0.1%) or 0.04%
microgel two to three times per week HS
Rosacea - Treatment

Topical Antibiotics:
–
Metronidazole 1% cream daily or 0.75% cream, lotion, or
gel BID
–
–
Sodium sulfacetamide 10% / sulfur 5% lotion
Clindamycin 1% solution, gel, or lotion
–
Erythromycin 2% solution BID
Rosacea - Treatment

Oral antibiotics for nodular rosacea and
ocular symptoms
–
–
–
–
Tetracycline 250 to 500 mg PO BID
Doxycycline 50 to 100 mg once-twice a day or
40 mg daily (Oracea™)
Minocycline 50 to 100 mg by mouth once a day
Erythromycin 250 mg by mouth BID-QID
Rhinophyma laser treatments
Polymorphous Light Eruption
Polymorphous Light Eruption


The most common idiopathic photodermatosis
Is acquired and characterized by recurrent
delayed reactions to sunlight, ranging from
erythematous papules, papulovesicles, and
plaques to erythema multiforme-like lesions on
sunlight-exposed surfaces.
Polymorphous Light Eruptions
Polymorphous Light Eruptions


Within any one patient,
only one clinical form is
consistently manifested
Patients may state they
had the rash before and
it went away with time
Polymorphous Light Eruption




Affects 10% or more of the US population.
Affects all racial skin types, but more common
in fair-skinned individuals
Tends to manifest in the spring, or, rarely, in
winter following UV radiation exposure
reflected from snow.
Is a recurrent condition
Polymorphous Light Eruption








Etiology not fully known and is likely to be multifactorial
Sunlight (usually UV-A) is the primary etiologic factor.
At least 30 minutes of exposure required
Lesions erupt 30 min to 72 hours after sun exposure
Sudden onset on skin normally covered in winter
(upper chest, arms)
Autosensitization may lead to generalized involvement
Rash may be asymptomatic, pruritic, or painful
Eruption decreases in severity as the summer
progresses
Polymorphous Light Eruption



In African Americans, a variant of PMLE with
pinpoint papules (1-2 mm) can be observed on
sun-exposed areas, sparing the face and
flexural surfaces.
Cheilitis is uncommon in the U.S. but often
occurs in the tropics
Occasionally, patients experience systemic flulike symptoms
PMLE - Diagnosis


Lab tests are generally performed to rule out
other photodermatoses, such as erythropoietic
protoporphyria or lupus erythematosus.
Consider an Antinuclear antibody (ANA), antiRo (SS-A), and anti-La (SS-B) tests, as well as
urine, stool, and blood porphyrin levels
PMLE - Diagnosis



The diagnosis of PMLE is
usually based on the clinical
picture.
Normal ANA titers, normal
urine, stool, and blood
porphyrin levels support the
diagnosis.
A biopsy will show edema in
the upper part of the dermis
and tight, perivascular
lymphocytic infiltrates in the
upper and mid dermis.
PMLE - Prevention



Avoid sunlight, wear protective clothing, use
sunscreen
Many sunscreens with high sun protection
factor (SPF) values are not protective against
UV-A-induced PMLE.
Systemic vitamin C and vitamin E do not
prevent photoprovocation test reactions in
persons with PMLE.
PMLE - prevention



Topical 0.25% alpha-glucosylrutin (a natural, modified
flavonoid) and 1% tocopheryl acetate (vitamin E) with a
broad-spectrum sunscreen is more effective in
preventing PMLE than sunscreen alone
Prophylactic phototherapy at the beginning of spring
with PUVA or narrow-band UVB for several weeks may
prevent flare-ups throughout the summer
Oral prednisone may be useful in conjunction with
phototherapy
PMLE - treatment








When preventive measures fail, topical corticosteroids are useful
Antihistamines may help pruritus
Systemic steroids may suppress acute flares or extensive
generalized eruptions
Antimalarials (hydroxychloroquine 200 mg qd) are sometimes
helpful
Beta-carotene and canthaxanthin in a daily total dose of 100 mg
Nicotinamide 3 g/d orally for 2 weeks
Oral vitamin E supplementation (400 IU)
In severe cases, systemic immunosuppressants (azathioprine,
others) have been used
PMLE - Prognosis

Some patients experience a less severe
reaction with each consecutive year, but many
patients have reactions that may worsen with
time without appropriate preventive measures
and treatment
Dermatomyositis
Dermatomyositis


An idiopathic inflammatory myopathy with
characteristic cutaneous findings.
Diagnostic criteria include:
–
–
–
–
–
progressive proximal symmetrical weakness
elevated levels of muscle enzymes
an abnormal finding on electromyography
an abnormal finding on muscle biopsy
characteristic cutaneous manifestations
Dermatomyositis


Muscle disease affects the esophagus, lungs
and, less commonly, the heart and may occur
concurrently, or may precede or follow the skin
disease by weeks to years.
An association between dermatomyositis and
malignancy has been recognized
Dermatomyositis


In as many as 40% of patients, the skin
disease may be the sole manifestation at the
onset.
Patients often notice an intense pruritic
eruption on exposed surfaces
Dermatomyositis

The characteristic, and possibly pathognomonic, cutaneous
features include the heliotrope rash…
Dermatomyositis

Gottron’s papules slightly elevated,
violaceous papules and
plaques with a scale
found over bony
prominences, particularly
the MCP, PIP, and DIP
joints and sometimes the
elbows, knees, and/or
feet.
Dermatomyositis - Other cutaneous
features


Malar erythema in a
photosensitive
distribution
Poikiloderma (variegated
telangiectasias,
erythema and
hypopigmentation) on
extensor surfaces of the
arm, the V of the neck or
the upper part of the
back (Shawl sign).
Dermatomyositis

Scalp involvement is
relatively common and
manifests as an
erythematous to
violaceous, psoriasiform
dermatitis or diffuse hair
loss (non-scarring
alopecia)
Dermatomyositis


Calcinosis cutis
manifests as firm, yellow
or flesh-colored nodules,
often over bony
prominences.
Calcinosis is unusual in
adults, but it may occur
in as many as 40% of
children or adolescents
with dermatomyositis
Dermatomyositis - Diagnosis




In addition to the criteria previously mentioned:
Skin biopsy reveals an interface dermatitis that is
difficult to differentiate from lupus erythematosus.
Except in the amyopathic variant, most common
enzyme elevations are to CPK, aldolase, AST and LDH
Muscle biopsy, either open or needle biopsy, may be
necessary to diagnose dermatomyositis
Dermatomyositis – Evaluation



An age-appropriate evaluation for a possible
malignancy should be performed at the time of
diagnosis and then annually for the first 3 years
Female patients should be carefully screened
for ovarian cancer
After 3 years, patients should be evaluated for
malignancy at intervals similar to other persons
of the same age and sex
Dermatomyositis - Treatment




Skin disease is treated with sun avoidance,
sunscreens, topical corticosteroids, antimalarial
agents, methotrexate, IVIG, and biological agents
Muscle treatment involves corticosteroids with or
without an immunosuppressive agent (methotrexate,
hydroxychloroquine) or rituximab
Prognosis depends on the severity of the myopathy,
the presence of malignancy, and/or the presence of
cardiopulmonary involvement.
Residual weakness is common, even in patients who
recover
Pityriasis Alba
Morphea
Lichen Sclerosis
Vitiligo
Pityriasis Alba
Pityriasis Alba



Atopy and postinflammatory changes are the
leading current theories as to its origin
Is relatively common occurring in up to 5% of
children
Is often an incidental finding on clinical exam
and generally a self-limited asymptomatic
condition that may resolve without intervention
Pityriasis Alba



Pityriasis alba lesions often
occur on the face, particularly
the cheek
Lesions may begin as
erythematous or pruritic and
evolve into scaly,
hypopigmented macules
Patients may say lesions are
more prominent in the
summer, secondary to the
surrounding
hyperpigmentation associated
with sun exposure.
Pityriasis Alba




Ill-defined hypopigmented,
patchy dermatitis with fine
scales
May also involve the neck,
shoulders, trunk and
extremities
Few or numerous (up to 20 or
more) hypopigmented
macules range from 1 - 4 cm
These lesions have less welldefined borders than lesions
seen in vitiligo, and they do
not coalesce as seen in tinea
versicolor.
Pityriasis Alba - Differential
Diagnosis









Differential diagnosis is extensive and includes:
Atopic Dermatitis
Contact Dermatitis
Tinea
Vitiligo
Scleroderma
Lichen Sclerosis
Mycosis fungoides – appearances vary considerably
Leprosy - This must be considered in arid regions, including areas
with armadillo exposure in the southern United States
Pityriasis Alba - Diagnosis


Is clinical
Wood's light examination may help differentiate from
vitiligo.
–


Vitiligo will glow more brightly and have edges with sharper
demarcation.
Potassium hydroxide stain of a skin scraping will be
negative
A biopsy would be required for atypical lesions as
noted in the differential
Pityriasis Alba - Treatment


Because the disease usually is self-limited and
asymptomatic, medical therapy is often
unnecessary.
PA has no medical consequences, and the
side effects of medications may outweigh the
cosmetic benefit of intervention.
Pityriasis Alba - Treatment





The most commonly used remedies have limited efficacy:
Emollients - used to reduce scaling
Topical steroids may help with initial erythema and pruritus and
may accelerate repigmentation of existing lesions.
– Use should be limited, with frequent breaks to avoid long-term
skin atrophy and depigmentation
Topical Pimecrolimus 1% - an option for a 3-month period
Psoralen plus ultraviolet light A photochemotherapy (PUVA) may
help with repigmentation in extensive cases, although the
recurrence rate is high
Morphea
Morphea


Morphea, also called localized scleroderma, is
a disorder characterized by excessive collagen
deposition leading to thickening of the dermis,
subcutaneous tissues, or both.
Morphea is classified into plaque, generalized,
linear, and deep subtypes
Morphea

Unlike systemic
sclerosis, morphea lacks
features such as
sclerodactyly, Raynaud’s
phenomenon, and
internal organ
involvement
Morphea



Begins as small red or purple
patches that develop firm,
white or ivory centers.
In active phases of the
disease, a violaceous border
(lilac ring) may surround the
indurated region
The affected skin becomes
tight and less flexible
Morphea



Plaque-type morphea
gradually develops a waxy,
ivory color.
The clinical appearance may
overlap with extragenital
lichen sclerosus.
Hyperpigmentation often
ensues as lesions evolve and
eventually involute over 3 to 5
years
Morphea


The plaque-type typically has a benign, selflimited course.
Survival rates are no different from those of the
general population.
Morphea

Linear and deep lesions in adults can be
associated with arthritis, arthralgias, myalgias,
carpal tunnel syndrome, and other peripheral
neuropathies localized to an affected extremity
Morphea – Linear subtype



Up to half of all morphea
cases occur in pediatric
patients, where linear
morphea predominates
Linear and deep morphea can
cause considerable morbidity,
especially when they interfere
with growth
Joint contractures, limb-length
discrepancy, and prominent
facial atrophy result in
substantial disability and
deformity in a quarter to half
of these patients.
Morphea - Treatment


Treatment of active lesions with superpotent
topical or intralesional corticosteroids may help
reduce inflammation and prevent progression
Topical calcipotriene may also be beneficial
Lichen Sclerosis
Lichen Sclerosis




Lichen sclerosus (LS) is a chronic inflammatory
dermatosis that results in white plaques with
epidermal atrophy.
The cause is unknown
Has both genital and extragenital presentations
Inflammation and altered fibroblast function in
the papillary dermis leads to fibrosis of the
upper dermis
Lichen Sclerosis
Lichen Sclerosis



Usually begins as white,
polygonal papules that
coalesce into plaques
Extragenital lesions may
occur anywhere on the body
Koebner’s phenomenon is
described, with the resultant
lesions in old surgical scars,
burn scars, and areas subject
to repeated trauma.
Lichen Sclerosis




May be asymptomatic or it may itch
The male-to-female ratio is 1:6, with female
genital cases making up the bulk of reports.
Punch biopsy in the most mature area of the
lesion usually is diagnostic
Lichen sclerosus has no associated increased
mortality unless the patient develops a
malignancy in the area.
Lichen Sclerosis (LS) - Treatment






Asymptomatic extragenital LS usually requires no treatment
Genital LS may respond to potent topical corticosteroids although
the clinical appearance does not always reverse.
Control of pruritus rather than resolution of the lesion is a more
realistic goal
Clobetasol, a Class I superpotent topical steroids, has shown
benefit in most published studies
Pulse dosing (2 consecutive d/wk) may be used long-term, even in
genital cases.
The calcineurin inhibitors (tacrolimus, pimecrolimus) help some
patients
Vitiligo
Vitiligo



An acquired pigmentary
disorder characterized by
circumscribed depigmented
macules and patches.
Progressive until some or all
melanocytes in the affected
area are destroyed.
Macules are milk-white, welldemarcated, and surrounded
by normal skin.
Vitiligo


The autoimmune theory proposes alteration in humoral
and cellular immunity in the destruction of
melanocytes.
Associated with other autoimmune conditions:
–
–
–
–
–
–
–
Thyroid disorders - Hashimoto thyroiditis and Graves disease
Addison disease
Diabetes mellitus
Alopecia areata
Pernicious anemia
Inflammatory bowel disease
Psoriasis
Vitiligo



Vitiligo lesions may be
localized or generalized
Lesions are not readily
apparent in lightly
pigmented individuals
Are easily
distinguishable with a
Wood lamp examination
Vitiligo


Affects 0.5-2% of the
world population, and
average age of onset is
20 years.
Initial lesions occur most
frequently on the hands,
forearms, feet, face, and
neck
Vitiligo - Treatment







No single therapy for vitiligo produces predictably good results
Systemic phototherapy induces cosmetically satisfactory
repigmentation in up to 70% of patients with early or localized
disease
Narrow-band UV-B phototherapy is widely used 2-3 times weekly,
but never on consecutive days.
Has become the first choice of therapy for adults and children
Psoralen with UV-A light (PUVA) photochemotherapy has often
been the most practical choice for treatment in patients with skin
types IV-VI who have widespread vitiligo.
Excimer laser therapy
Topical tacrolimus ointment (0.03% or 0.1%) is an effective
alternative
Conclusion



Depending on individual characteristics, any
dermatologic condition can vary in appearance
Serious and benign conditions can look
identical
When in doubt, biopsy lesions to establish a
diagnosis
References





http://tray.dermatology.uiowa.edu
http://emedicine.medscape.com
http://www.ncbi.nlm.nih.gov/pubmed/
http://dermatlas.med.jhmi.edu/
Drago F, Vecchio F, Rebora A. Use of highdose acyclovir in pityriasis rosea. J Am Acad
Dermatol. Jan 2006;54(1):82-5.
Thank you