Frank Morocco D.O. FAOCD
Case 1
51 y/o white male with
4 year history of silvery
scaling thickened
erythematous plaques
on his knees, elbows and
scalp. The patient has
25% BSA. Denies any
joint pain.
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A) Involves only the skin and should be
managed exclusively by a dermatologist
B) Is associated with multiple comorbidities
including diabetes, hyperlipidemia, and
arthritis
C) Statins have been shown to worsen psoriasis
D) Topical therapy should be continued as
monotherapy for multiple years before
switching to a different treatment modality
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Psoriasis is a hereditary, papulosquamous skin
disorder that affects 3 to5 million people in the
United States.
Affects men and women equally.
Psoriasis is a chronic and recurring disease that
is best characterized by well-demarcated
erythematous plaques
Most commonly plaques are seen on the
elbows, knees, and the scalp
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Psoriasis is an immune mediated
inflammatory skin disorder.
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TH1 driven with increase of IL-6, TNF-alpha and
Interferon
Unpredictable
Age of onset bimodal 23 y/o and 55 y/o
Aggravated by emotional stress
In addition to its cutaneous
manifestations, psoriasis has been
associated with arthritis
Psoriatic Arthritis
Psoriatic arthritis affects an
estimated 25% to 34% of patients
with psoriasis
Most commonly appears 10 years
after the onset of psoriasis
•Psoriatic Arthritis: 5 patterns
1.
Asymmetric DIP with
nail damage (16%)
2.
Arthritis mutilans
with osteolysis of
phalanges/metacarpal
s (5%)
3.
Symmetric
polyarthritis-like RA
with claw hands (15%)
4.
Oligoarthritis
with swelling
and
tenosynovitis of
one or a few
hand joints (70%)
5.
Ankylosing
spondylitis alone or
with peripheral
arthritis (5%)
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Psoriatic Arthritis (cont’d)
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X-rays resemble RA except:
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Erosion of terminal phalangeal tuft
Tapering or whittling of phalanges or metacarpals
Cupping of proximal phalanges
Bony ankylosis
Osteolysis of metatarsals
Prediliction for DIP and PIP
Sparing of MCP and MTP
Paravertebral ossification
Asymmetric sacroilitis; rarity of bamboo spine
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Quality of life
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A population-based survey looking at the
association between quality of life and extent of
disease.
60% of patients report psoriasis affects their
everyday life and 26% report a change or
discontinuation of daily activities.
This was higher than cancer and diabetes!!
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Economic
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The estimated total direct and indirect health care cost of
psoriasis in the United States is 11.25 billion dollars annually
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A two-year study by the National Psoriasis Foundation (NPF)
found that having psoriasis is associated with decreased
household incomes and reduced employment opportunities.
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Psoriasis patients have lower income and are less likely to work
full-time.
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Psoriasis was reported as the primary reason for
unemployment in 17% of patients with severe psoriasis.
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Psoriasis patients missed an average of 26 days of work each
year due to complications of psoriasis
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Psoriasis may predispose patients to increased
risk of atherosclerotic disease.
A chronic, proinflammatory state that fosters
the development of the metabolic syndrome.
40 % of psoriatic patients develop metabolic
syndrome
Chronic inflammation  to increased oxidative
modifications of lipoproteins, which are more
atherogenic than native lipoproteins
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Diabetes
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The studies suggest that psoriasis is associated with
a 59% increased prevalence of diabetes and a 27%
increased risk of developing diabetes among patients
with psoriasis
The altered immune pathways may also predispose
to impaired glucose tolerance and diabetes
Aggressive therapy ?
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Hyperlipidemia
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19 of 19 studies showed an association with
hyperlipidemia
Study subjects had higher levels of very low density
lipoproteins,total cholesterol and LDL,and lower
levels of cardioprotective high density lipoproteins
(HDL)
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63 pts
32 pts on Atorvastatin 20mg/day
31 pts on placebo
80% reached PASI 75 in 6 months
78% reach PASI 75 in 3 months with
ustekinumab
Also showed significant reduction of CRP and
TNF alpha after 3 weeks
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Topicals or localized tx (laser/pulsed light) for
limited plaques
Phototherapy
MTX
Cyclosporin
Biologics
Rotating therapies and combination therapies
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Corticosteroids: Class I for 2 weeks, then
weekend pulses
Occlusion for thick keratotic scale
– Low-mid strength intertriginous and face
– Can give ILK for refractory plaques and nail matrix
and lateral nailfold monthly
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Tazarotene: modulates keratinocyte
differentiation and hyperproliferation and
suppresses inflammation
Calcipotriene: keratinocyte differentiation
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Burning can cause Koebner’s phenomenon
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Artificial UVB broad or narrow band
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254, 280, 290 are ineffective
296, 300, 304, 313 give clearing
Narrow band = 311 and is more effective than broad band
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Psoriasis is associated with comorbid
conditions, including depression, arthritis,
diabetes, hypertension, metabolic syndrome,
and cardiovascular events
A systemic inflammatory processes may
underlie these disease processes.
Treatment must involve a multidisciplinary
approach between Dermatologists, PCP
cardiologists and rheumatologists
Case # 2
-Patient S.S. is a 16 month old boy
brought in to see you by his parents
for an itchy rash.
-“rashy skin” intermittently since
birth. -worst during the winter
months of the year.
-Mom reports that he scratches in
his sleep.
The parents tell you that S.S. was
hospitalized at age 6 months for
reactive airway disease for which
he required nebulizers.
-His mom has strong allergies to
pollens in the summer.
-Dad has asthma.
-S.S. uses Suave Berry Blast soap
and shampoo in the bathtub.
He takes one bath every other day.
They have tried Vaseline intensive
care lotion when his skin seems
dry.
The Itch that Rashes
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Eptheilial barrier disruption
50% of atopic dermatitis caused by Filaggrin
gene (FLG) disorder
FLG encodes profilaggrin which is the major
component of granular layer.
Filaggrin makes up the the major scaffolding
that forms the lipid cell envelope.
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Filaggrin is degraded and forms “natural
moisturizing factor”
Decreases pH which helps inhibit
Staphylococcus aureus growth
Activate enzymes in ceramide metabolism
Modulating the activity of serine proteases
Epidermal barrier repair is aimed at replacing
ceramides, inhibition of elevated protease
activity and decreasing skin pH
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In vitro studies have shown immunity still has
major effect.
IL-22 and IL-25 are involved in decreasing
filaggrin expression.
Decrease of active copies of fillagran by 5-10%
can increase severity of atopic dermatitis.
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Other Factors
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Delayed introduction of solid foods, early life
exposure to antibiotics, exposure to farm animals or
ingestion of fish oils have no effect on development
of AD
Breast-feeding has been shown to have no effect
 Physiologic and psychological benefits of breast feeding
makes it preferred feeding modality even in children
with risk of developing AD
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Children < 5 y/o with moderate to severe AD
should be considered for food allegies to milk,
egg, peanut wheat, and soy IF persistant atopic
dermatitis with optimal treatment or if there is a
history of immediate reaction after the ingestion
of a specific food
 Fifty
percent to 90% of presumed allergies are
not allergic in nature
 Solid foods should not be delayed beyond 4 to 6
months, because this may paradoxically increase
the incidence of food allergies
 Individuals without documented or proven
food allergies should not avoid potential
allergenic foods
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Proposed Mechanisms
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Negative effect of inflammatory cytokines on central
nervous system
Increased stress and sleep disturbances due to
pruritis.
Lack of impulse control and use of stimulatory
medication makes ADHD a risk factor for more
severe AD
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Dennie-Morgan fold: linear transverse fold just
below the lower eyelid
“Normal” skin is subclinically inflamed, dry,
scaly
Pityriasis alba:
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hypopigmentation with sclight scale on cheeks,
upper arms, trunk in young children. Responsive to
emollients and topical steroids
Keratosis pilaris:
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horny follicular lesions of outer aspects of upper
arms, legs, cheeks, and buttocks; refractory to
treatment
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Increased susceptibility of infection;
 Patients heavily colonized with Staph. Treatment of
lesional skin reduces colonization even w/o ABX
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Eczema herpeticum: generalized herpes simplex,
sudden vesicular, pustular, crusted or eroded
lesions. Become secondarily infected.
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Eczema vaccinatum: widespread vaccinia infxn
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Extensive flat wart or molluscum; poor tolerance to
Tx
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Infants and children:
Avoid hot baths, alkaline soaps, vigorous rubbing
and scrubbing.
 Short, once-a-day, tepid baths followed by a barrier
cream using soak and smear; ointment bases are
preferred.
 Immediate change of wet or soiled diapers.
 Nighttime sedating antihistamines for itch
 Dietary restriction for a specific known antigen
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Adults
Avoid temperature extremes
 Hydrate dry skin especially in winter
 Avoid overbathing and hot water
 Avoid wool
 Biofeedback techniques for emotional stress
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Topical corticosteroids are the mainstay
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1-2.5% hydrocortisone in infants. Monitor growth in infants
and young children.
Mid-potency (TAC) in older children and adults except on the
face
1-2x a day is enough to saturate receptors; more provides only
emollient effect
Occlusion increases penetration and receptor saturation
Must be strong enough to control pruritus and remove
inflammation
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Regular emollients: petrolatum, hydrophilic creams with
ceremides
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Anti-Staph therapy for acute flares
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Topical calcineurin inhibitors
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Antihistamines for sedation: hydroxyzine,
diphenhydramine, or clopheniramine.
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The nonsedating antihistamines do not relieve pruritus
Short courses of anti-Staph ABX, topical mupirocin
for nasal carriage
Immunosuppressives and antiproliferatives
(Immuran, Cellcept, MTX) can be effective for
unresponsive dz
Phototherapy: PUVA, UVA, narrow-band UVB, or
Goeckerman with tar may be helpful
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Increased risk of S. Aureus infection and
colonization which leads to inflammation
◦ Decreased Human Beta-defensin-2 leads to
increased MSSA.
A recent study showed that diluted bleach baths
plus intranasal mupirocin led to significant
improvement in eczema severity scores.
◦ Typical recipe is ¼ cup of bleach for ½ tub of
water and ½ cup of bleach for tub full of water
◦ Mupirocin was administered 5 consecutive days a
month
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Wet dressing therapy was has been used in
past for severe AD.
Recent study from Mayo Clinic described their
institution’s wet dressing therapy for inpatient
hospitalizations.
45% had 75%-100% clearance
38% had 50%-75% clearance
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Traditional AD management dogma consisted
of application of anti-inflammatory medication
to areas of “active”disease.
Recent research shows a paradigm shift.
After twice daily active treatment of AD flare,
patients were given “proactive” twice weekly
treatment with topical tacrolimus and had
significant fewer AD flares
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An 18-year-old patient presents with a sore
throat and signs of streptococcal pharyngitis.
you start treatment with amoxicillinclavulanate, and results of a rapid strep test are
positive. The next day the patient calls
regarding a new rash that has erupted all over
his body. The palms and soles remain
uninvolved
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a. Drug rash
b. Pityriasis rosea
c. Streptococcal scalded skin syndrome
d. Mycoplasma pneumonia
e. Psoriasis
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Guttate psoriasis classically presents after infection
with streptococcus in children or young adults.
Guttate psoriasis presents with scaly, “droplike”
papules on the trunk and extremities.
It is often mistaken for a drug rash because
antibiotics may have been initiated for the
streptococcal infection.
Throat cultures for streptococcal pharyngitis
should be obtained.
Guttate psoriasis has a good prognosis and may
disappear spontaneously or may benefit from
phototherapy.
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A 28-year-old man presents with a rash and
pruritus that has been present for 3 weeks. He
has no history of skin or other health problems
and is not receiving any medications. He has
used no new products on the skin and has not
frequented wooded areas. On examination, he
has red papules and excoriations on the wrists,
groin, and axillae and nodular areas on his
scrotum
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A) Mineral oil preparation of a skin scraping
B). Tissue transglutaminase measurement
C). Skin biopsy
D). Lyme disease serology
E). Skin biopsy for tissue culture
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Scabies is caused by infestation of the epidermis with the
mite.
Infestation occurs as a result of direct skin-to-skin contact;
fomite transmission is uncommon.
Scabies causes epidemics in schools, nursing homes, and
hospitals.
Pruritus is the major complaint, prominently at night, and
there is often a history of itching or rash in family members
The rash is due to hypersensitivity reaction to the mite
protein.
It can take 4 to 6 weeks after initial mite exposure to develop
signs or symptoms of scabies infestation
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Clinical features include inflammatory,
excoriated papules in the web spaces of the
hands and feet, the axillae, groin, wrists, and
areolae, and submammary sites in women.
Facial or scalp involvement is uncommon,
except in children and elderly persons.
Nodules or thickened areas in the scrotum are
also a helpful clue
Scabies
The pathognomonic
finding is a burrow,
commonly located on the
hands.
Identification of mites,
eggs, or fecal material on
a scabies preparation is
diagnostic.
Treatment of classic
scabies includes the
topical
application of permethrin,
and/or oral ivermectin
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Permethrin is the gold standard therapy
Ivermectin is an effective oral alternative that is
especially useful in crusted scabies, patients
who are bedridden, and in institutional
outbreaks.
Treatment failures still occur, mostly secondary
to application error (ie, failure to treat the face
and scalp or close contacts, failure to reapply
medication) or failure to decontaminate
fomites.
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There has been a recent shift in standard of care
for scabies treatment.
Routine treatment of the scalp and face and retreating patients between day 4 and 7 based on
the scabies life cycle to ensure more efficient
mite eradication.
Practitioners should attempt to treat all close
contacts simultaneously with the source
patient.
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300 volunteers who lay nude in warm
beds recently vacated by scabetic hosts infected with
<20
mites, 4 (1.3%) became infested.
The number rose to 15% when hosts had >50 mites
May live on fomites 24-36 hrs in warm humid
environment
May live on fomites 19 DAYS in cool environment!!!
To eradicate mites, all fomites should be placed in a
dryer for 10 minutes on a high setting, furniture and
carpets vacuumed, and nonlaunderables isolated for a
minimum of 2 days
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An 18-year-old man originally presented to your
urgent care clinic 4 weeks ago with a small abscess on
his knee. He was otherwise healthy and taking no
medications. The abscess was incised and drained at
the clinic, and the culture and susceptibility studies
showed this lesion to be a methicillin-resistant
Staphylococcus aureus infection. He now presents with a
new abscess.
On physical examination, his temperature is 37°C,
blood pressure is 118/76 mm Hg, and heart rate is 80
beats/min. Skin examination shows a 2x2-cm
erythematous plaque on the forearm with a central
fluctuant area. There are areas of healing skin on the
knee.
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A). Education on wound care and personal
hygiene
B). Oral rifampin
C). Intravenous vancomycin
D). Oral clindamycin
E). Combination treatment with oral
trimethoprim-sulfamethoxazole and
minocycline
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This patient presents with the typical history and physical
findings of a skin and soft tissue infection (SSTI) with
community-associated methicillin-resistant S aureus (CAMRSA).
Infections caused by CA-MRSA usually present as a solitary
abscess, cellulitis, or soft tissue infection, often with central
necrosis.
Recurrence in an individual is common
This strain of MRSA has a distinct genetic resistance element
(SCCmec IV) and toxin (Panton-Valentine leukocidin toxin) and
develops in populations with close physical contact.
While resistant to beta-lactam antibiotics, CA-MRSA isolates
often remain sensitive to other antibiotics such as
clindamycin,trimethoprim-sulfamethoxazole, and minocycline
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The primary treatment for a small, simple cutaneous abscess
is incision and drainage of the abscess.
Management of recurrent MRSA infections should focus on
education about appropriate wound care and personal
hygiene.
Instruction should include keeping draining wounds
covered with clean, dry bandages, maintaining good
personal hygiene with regular bathing , cleaning of hands,
and avoiding reusing or sharing personal items.
Clinicians should consider attempting decolonization if a
patient experiences a recurrent SSTI despite optimal wound
care and hygiene measures.
Decolonization strategies may include nasal decolonization
with mupirocin twice a day for 5 to 10 days and body
decolonization with a skin antiseptic solution
(chlorhexidine) for 5 to 14 Days or dilute bleach baths.`
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Infantile hemangiomas are the most common
tumor of infancy and arise in 5% to 10% of
infants
Glucose 1 transporter (GLUT-1) has be shown
to be specific for infantile hemangiomas
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The expected proliferation phase of
hemangiomas is during the first year of life
with rapid growth until 6-9 months of age.
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A recent found most rapid growth between age 5.5 7.5 weeks
Best age for referral 4 weeks old
Hemangioma precursors were present at birth in
65% of patients
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Early white discoloration heralds impending
ulceration
Usually seen before 3months of age
In contrast to the whitish gray color of
involution seen several moths later
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One of the greatest breakthroughs in pediatric
dermatology has revolved around IH and
propranolol.
Mechanism of action is unknown
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Vasocostriction
Blocking proangiogenic signals
Apoptosis of endothelial cells
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2008- The discovery was made after 2 children
with cardiac issues were treated with oral beta
blockers with great effectiveness
2009- 32 children treated with oral propranolol
all had good response
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2011 – 40 pts given 2 mg/kg per day divided 3
times daily for 6 months.
Baseline electrocardiogram, echocardiogram,
and laboratory evaluations were performed.
Monitoring of heart rate, blood pressure, and
blood glucose was performed at each visit.
No significant hypoglycemia, hypotension, or
bradycardia occurred.
Growth stopped at 4 weeks
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2011- Propranolol vs corticosteroids
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multicenter retrospective analysis
139 patients
82% achieved clearance of 75% or more on
propranolol compared to 29% who were receiving
oral corticosteroids
This study helped show superior efficacy with fewer
side effects.
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Infantile Hemangiomas that ulcerate are prone to
considerable morbidity with pain, infection, and scarring
Challenging to treat
When compared to traditional modalities for treatment
(PDL, wound care, oral antibiotics and oral corticosteroids)
propranolol was found to shorten time to healing after the
onset of ulceration
Average time to heal from onset of ulceration with
propranolol 8.7 weeks compared to 22.4 weeks with wound
care
 Head and neck hemangiomas 4.3 weeks to heal and 14.5
days to achieve pain control
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Propranolol is now considered standard of care
for severe IH but it is being used more in less
aggressive IH.
Most patients are started on a low dose and
titrated up to 2 mg/kg/day in divided doses
Rare side effects include hypoglycemia,
hypotension, and exacerbation of asthma
More common side effects are cold extremities
and night terrors
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Other systemic beta blocker are being examined.
Atenolol is a hydrophilic beta-1 antagonist that may
decrease pulmonary side effects and sleep
disturbances.
Nadolol has been compared to propranolol in a
small case study which showed superior efficacy
decreased side effects and easier dosing schedules
due to a longer half life.
Topical beta-blocker in the form of timolol has been
tried with success for superficial small
hemangiomas not requiring systemic treatment
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Tinea capitis occurs mainly in children,
although it may be seen at all ages.
Boys have tinea capitis more frequently than
girls
Tinea Capitis is more prominent in African
Americans
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Tinea capitis must be differentiated clinically from
chronic staphylococcal folliculitis, psoriasis,
seborrheic dermatitis, various inflammatory
follicular conditions.
The distinctive clinical features of tinea capitis are
broken-off stumps of hairs, often in rounded
patches in which there are crusts or pustules and
few hairs.
The broken-off hairs are loose and when examined
are found to be surrounded by, or to contain, the
fungus.
Diffuse seborrheic scaling with hair loss is a
common presentation of T. tonsurans infections.
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In seborrheic dermatitis the involved areas are
covered by fine, dry, or greasy scales. Hair may be
lost, but the hairs are not broken.
Atopic dermatitis is rarely associated with
localized scalp involvement, and clinical
examination frequently reveals more typical
generalized findings.
In psoriasis, well-demarcated, sometimes diffuse,
areas of erythema and white or silver scaling are
noted.
Lichen simplex chronicus is frequently localized to
the inferior margin of the occipital scalp.
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Numerous clinical trials exist that demonstrate the
effectiveness of itraconazole, terbinafine, and fluconazole.
Despite these studies, griseofulvin remains the most
commonly used antifungal agent in children.
A meta-analysis of published studies shows mean efficacy
for griseofulvin treatment of about 68% for Trichophyton spp
For the ultramicronized form, doses start at 10 mg/kg/day.
The tablets can be crushed and given with ice cream.
Grifulvin V oral suspension is less readily absorbed. The
dose is 20 mg/kg/day.
Treatment should continue for 2–4 months, or for at least 2
weeks after negative laboratory examinations are obtained.
Doses much higher than those reflected in drug labeling are
commonly needed.
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For Trichophyton infections, terbinafine is commonly
effective in doses of 3–6 mg/kg/day for 1–4 weeks.
Alternate dosing schedules for terbinafine include one
250 mg tablet for patients over 40 kg, 125 mg (half of a
250 mg tablet) for those 20–40 kg, and 62.5 mg (onequarter of a 250 mg tablet) for those under 20 kg.
Selenium sulfide shampoo or ketoconazole shampoo
left on the scalp for 5 min three times a week can be
used as adjunctive therapy to oral antifungal agents to
reduce the shedding of fungal spores.
Combs, brushes, and hats should be cleaned carefully
and natural bristle brushes
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Mild inflammatory exanthem: salmoncolored oval/circinate papules/macules
with collarette scale
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Hanging curtain sign: scales fold across lines of
stretched skin
Long axis parallels lines of cleavage
Herald patch
Age 15-40 in spring and autumn
May have mild pruritus
Spontaneous resolution after 3-8 weeks
Inverse and papular variants
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Etiology: may be associated with HHV-6 and 7
reactivation
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A similar eruption may occur as reaction to drugs
Histology: mild acanthosis, focal parakeratosis,
erythrocyte extravasion, spongiosis, mild dermal
perivascular infiltrate
DDX: seb derm, tinea corporis, macular syphilid,
drug eruption, viral exanthem, PSO
Treatment: most require none
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UVB may expedite the involution
Corticosteroid lotions or creams, oral antihistamines,
erythromycin
emollients
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15-year-old male
Non-inflammatory &
inflammatory papules
Face only
 Open/closed comedones
 Papules
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Diagnosis ?
Treatment Plan?
Noninflammatory
Acne
Mild
Inflammatory
Acne
Topical
Therapies
Retinoids
Antibiotics
Salacylic Acid
BPO
+/- Washes
Adjunctive
Therapies
OCPs, chemical peels,
anti-androgens
Moderate-Severe
Inflammatory
Acne
Oral
antibiotics
Severe or
Scarring
Adjunctive
Therapies
Isotretinoin
Tetracyclines
Failure of
oral
antibiotics
Pregnant
Azelaic Acid (Cat
B)
Clindamycin
Lotion (Cat B)
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Early, appropriate treatment is best to
minimize potential for acne scars
Approach should be multi-therapy, not
monotherapy
Combination of a topical retinoid and
antimicrobial agent remains the preferred
approach for almost all patients with acne
.
Thiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group J Am
Acad Dermatol 2009;60:S1-50.
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
Topical retinoids should be first-line agents in
acne maintenance therapy
Avoid contributing to antibiotic resistance
.
Thiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group J Am
Acad Dermatol 2009;60:S1-50.
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Mechanism of action1
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Bactericidal for P. acnes
Inhibits triglyceride hydrolysis
Decreases inflammation of acne lesions
Advantages
No resistance demonstrated to date1
When used in combination with a topical antibiotic can
help to prevent resistance2
– Activity is enhanced when combined with other topicals
(i.e. clindamycin)1,2
–
–
•
Formulations
–
–
OTC & prescription
Washes, gels, lotion, solution
1. Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
2. Thiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne
Group. J Am
Acad Dermatol 2009;60:S1-50.
•
•
•
Most important class of drugs used to treat
acne
Topical form of vitamin A
Mechanism of Action1
–
–
•
Normalize follicular keratinization
Act on the microcomedone
Proper instruction on application is essential to
compliance
–
–
Gradual application with small amount of drug
“Training for a marathon”
1. Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
•
“Least Irritating” (most tolerable)
–
–
•
Adapalene gel (Differin® 0.1%, 0.3%)
May be appropriate starting point for ethnic and/or
sensitive skin
“Moderately Irritating”
–
Tretinoin (cream, gel)
•
•
•
•
•
Tretinoin 0.01%, 0.05%, 0.025%
Retin-A Micro® 0.1%, 0.04%
Atralin™ Gel 0.05%
Renova® 0.02%, 0.05%
“Most Irritating” (least tolerable)
–
Tazarotene (Tazorac®/Avage® 0.05%, 0.01%)
Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
•
Erythromycin
–
–
–
•
Clindamycin phosphate 1%
–
–
–
–
•
Akne-mycin® 2% gel, Erygel ® 2% gel,
Resistance of some P. acnes strains
Usage fallen out of favor
Generic, Cleocin T® (lotion, gel, solution), Evoclin® foam
Antibiotic-associated colitis very unlikely
Work best in combination with BPO
Good choice for pregnant women (Pregnancy Category B)
Azelaic acid
–
–
–
Finacea™
Bacteristatic/bactericidal against P. acnes
Good choice for pregnant women (Pregnancy Category B)
Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
•
Clindamycin/Benzoyl peroxide
–
–
–
•
Erythromycin/Benzoyl peroxide
–
•
Erythromycin 3%/benzoyl peroxide 5% (Benzamycin®)
Retinoid/Benzoyl peroxide
–
•
Clindamycin phosphate 1%/benzoyl peroxide 5% (Benzaclin®Gel)
Clindamycin phosphate 1%/benzoyl peroxide 5% (Duac®Gel)
Clindamycin phosphate 1.2% /benzoyl peroxide 2.5% (Acanya™
Gel)
Adapalene 0.1%/benzoyl peroxide 2.5% (Epiduo™ Gel)
Retinoid/Clindamycin
–
Tretinoin 0.025%/Clindamycin phosphate 1.2% (Ziana® Gel)
Thiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group. J Am
Acad Dermatol 2009;60:S1-50.
•
•
17-year-old-female
Inflammatory acne
Regular menstrual
cycles (-flares)
– Face, chest, back
involved
– Pustules, papules
– Open & closed
comedones
–
•
Treatment plan?
Noninflammatory
Acne
Mild
Inflammatory
Acne
Topical
Therapies
Retinoids
Antibiotics
Salacylic Acid
BPO
+/- Washes
Adjunctive
Therapies
OCPs, chemical peels,
anti-androgens
Moderate-Severe
Inflammatory
Acne
Oral
antibiotics
Severe or
Scarring
Adjunctive
Therapies
Isotretinoin
Tetracyclines
Failure of
oral
antibiotics
Pregnant
Azelaic Acid (Cat
B)
Clindamycin
Lotion (Cat B)

Therapeutic role in acne



Reduction of P. acnes
Anti-inflammatory activity
Dosing



Start high then taper down after control is achieved
Use PRN during flares
Do not use as monotherapy
Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
•
Antibiotic Choice
–
Tetracylcine Class (minocycline, doxycycline,
tetracycline)
• Solodyn® (minocycline HCl), Minocin ® (minocycline)
• Doryx® (doxycycline hyclate), Adoxa® (doxycycline
monohydrate)
Erythromycin (Ery-tab®)
– Trimethoprim/sulfamethoxazole
– Amoxicillin
–
•
Anti-inflammatory antibiotics/no antimicrobial
activity
Doxycycline 20 mg (Periostat®)
– Doxycycline 40 mg (Oracea®)
–
Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
•
•
•
•
Combine a topical retinoid plus an
antimicrobial
Limit the use of antibiotics to short periods and
discontinue when there is no further
improvement or the improvement is only slight
Co-prescribe a BPO-containing product or use
as washout
Oral and topical antibiotics should not be used
as monotherapy
Thiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group. J Am
Acad Dermatol 2009;60:S1-50.
•
•
19-year-old female
moderate to severe inflammatory
acne
–
Regular menstrual
cycles (+ flares)
–
–
–
–
–
•
Face involved scarring
Chest, back spared
Nodular lesions along
jawline
Comedones
Scarring
Treatment plan?
Noninflammatory
Acne
Mild
Inflammatory
Acne
Topical
Therapies
Retinoids
Antibiotics
Salacylic Acid
BPO
+/- Washes
Adjunctive
Therapies
OCPs, chemical peels,
anti-androgens
Moderate-Severe
Inflammatory
Acne
Oral
antibiotics
Severe or
Scarring
Adjunctive
Therapies
Isotretinoin
Tetracyclines
Failure of
oral
antibiotics
Pregnant
Azelaic Acid (Cat
B)
Clindamycin
Lotion (Cat B)



Approved for the treatment of severe
recalcitrant nodular acne in 1982
Member of the Vitamin A family
Effects on acne




Normalizes the keratinization process
Reduces sebocytes and secretions
Reduces inflammation
Reduction in numbers of P. acnes
Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.

Pre-medication counseling
Side Effects
 Contraception
 Compliance/duration of treatment
 Laboratory monitoring
 iPledge registration


Dosing 1-2 mg/kg/day

Goal 120-150 mg/kg over course of treatment
Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.



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