Download Dermatologic Therapeutics

Dermatologic Therapeutics
2015 Lecture Notes
Teresa O’Sullivan, PharmD, BCPS
Learning Goal
Attainment of a basic level of comfort with the choice of agent, vehicle/route, directions, and duration of therapy for common
skin diseases.
Learning objectives
At the end of this lecture, you should be able to:
 Select an appropriate agent for dermatology lesions you diagnose.
 Assess patient information to determine likelihood of a drug allergy label being correct.
General Information
Module 1 (online)
General Information
Fun facts about skin
 The single largest organ in the body (17% of body weight).
 The top layer of the skin is the epidermis. Keratinocytes originate in the bottom layer of epidermis and migrate upward,
dying near the top layer and forming a semi-permeable keratin layer that is sloughed off. Cycle (differentiation,
migration, death, sloughing) takes ~26 days (3-4 days with psoriasis).
 The dermal layer is the thickest part of the skin.
 Capillary network supplies nutrients for keratinocyte growth, generally regulates temperature, and introduces
topically applied drugs into the general circulation.
 Sweat glands, sebaceous glands, and hair follicles protect epidermis and facilitate temperature control.
 Nerves enable touch, itch, and pain sensations.
 Lymphocytes and macrophages combat entry of pathogens.
 The dermis is also a water storage organ.
 The subcutaneous layer serves as a fat storage area, providing cushioning and facilitating temperature control.
Choosing vehicles
Baths. Good for widespread eruptions: chicken pox, lichen planus, pityriasis rosea, viral or drug-induced itchy
maculopapular rashes, crusting eczemas. For itchiness: one packet of colloidal oatmeal (regular oatmeal will not work) or two
cups of cornstarch to a tub of lukewarm water q2-4hours prn. For dry skin: there is a large variety of bath oils with main
ingredient usually mineral oil. Generic fine; watch additives if sensitive skin. Main concern with all bath products: slippery
tub (hazard for falling), skin maceration (loss of protective keratin layer) with prolonged soaking.
Wet dressings. Good for acutely-inflamed, oozing lesions, erosions, and ulcers. These cause vasoconstriction by evaporative
cooling, promoting cleaning and drainage, and decreasing itching. 15-30minute soaks 3-6x/day. Saline or Burow’s solution
the standards. Burow’s solution is OTC with directions for use printed on package. Normal saline irrigation is legend drug so
patient will need prescription or can make at home by mixing 1/4 tsp table salt in 2/3 cup of water. Witch hazel is used for the
same purpose on hemorrhoids.
Solutions/gels. Drug dissolved is either a water or alcohol base. Best for very hairy areas, such as the scalp, since solutions
and gels are not oily and do not leave a residue.
Sprays. Only useful if mechanical contact with skin causes intolerable pain for the patient. Otherwise, sprays tend to be the
most expensive of the dosage forms.
Lotions. Suspensions of powder in a water or alcohol base. Good for slightly oozy lesions or widespread lesion areas (e.g.,
tinea versicolor). Generally not preferred for dry, flaky, calloused, or hairy areas.
Creams. Soft emulsion of drug in a water base. Medicated creams should be used sparingly; their soft texture means that
once rubbed in well they will “vanish.” Best for lesions that are not oozy. Emollient creams will be thicker and waxier than
medicated creams.
Ointments. Emulsion of drug in an oleaginous (oil) base. Best for dry, scaly, brittle, or thickened skin. Since these are stiffer
than creams, spreading is more controlled and thus about 5-10% less ointment is needed for any given area. Ointments also
block evaporation, increasing drug delivery (compared to cream or lotion) to the dermis. A paste is a very thick ointment so
the same rules apply.
Powders. Are drying and cooling, but the most important function is the ability of the particles to slip off each other,
decreasing friction in areas where rubbing occurs. Good for athlete’s foot, jock itch, diaper rash, pressure/friction sores.
DERM-1
Summary of vehicle choice
 Widespread itchy rash or dry skin  bath q4-6h
 Wet, oozy lesion or ulcer  wet dressing x 15-30 minutes q4-8h
 Red lesion that is not dry but has little to no oozing  cream
 Red, dry, excoriated lesion  ointment
 Itchy lesion in hairy area  gel or solution
 Itchy lesion in area where skin is rubbing against skin  powder
 Lesion too painful or itchy to touch  spray
Choosing amounts
 In general, BID dosing is fine for most topical agents (exceptions noted in text, as with baths and wet dressings above).
Therefore, you will need:
area size
amt for each application
amt to prescribe for 7 days
small lesion or collective lesion
1g cream or ointment
15g cream or ointment
group no more than 2” x 2”
2ml lotion/solution
30ml lotion/solution
many small lesions: collective size >
2g cream or ointment
30g cream or ointment
2” x 2”
3ml lotion/solution
60ml lotion/solution
area equal to one forearm
3g cream or ointment
45g cream or ointment
4ml lotion/solution
90ml lotion/solution
area equal to front or back of trunk
4g cream or ointment
60g cream or ointment
5ml lotion/solution
120ml lotion/solution
whole body
45g cream or ointment
21oz cream or ointment
60ml lotion/solution
750ml lotion/solution
Most creams and ointments come in 15g or 20g, 30g, and 60g tubes; many creams come in 45g tubes. Most lotions come in
30ml or 60ml bottles.
Tip: You may not know the available sizes of tubes for many products. Some pharmacists feel comfortable choosing the
closest available size, but some pharmacists do not and will interrupt you with a (unnecessary) phone call. Options to avoid
this:
 Note on the prescription the desired amount and then in parentheses write “(or closest larger available size)”
 Write “amount per pharmacy” if your interactions with the pharmacist likely to dispense the medication make you feel
comfortable that the pharmacist can determine a reasonable amount.
Application area and systemic absorption
Studies have examined mainly absorption of topical corticosteroids
 ≤1% absorption: soles, palms, tops of forearms
 2-15% absorption: scalp, face, legs, undersides of forearms
 >20% absorption: genitalia, axilla
Many other factors will affect rate and extent of systemic absorption including presence of inflammation or desquamation
(enhance absorption), use of occlusion (enhances absorption), type of vehicle (ointment enhances absorption versus cream),
and whether the drug is in salt or ionized form (e.g., ionized drug generally poorly absorbed)
It’s all in a name...
Reasons to use trade name:
 Easier to remember and (usually) to pronounce.
 The name most likely to be used by patients (and many health care professionals).
Reasons to use generic name:
 The name of the drug that will be on the prescription vial, any time a generic is dispensed.
 The generic name ending can often provide a clue to the class of the drug (e.g., “pril” for ACE inhibitors, “olol” for betablockers) so easier to identify a drug’s probable use and effects. Trade names do not provide such a clue and thus all
trade names need to be individually memorized.
 Every time trade name is used, it’s free advertising for the company.
DERM-2
Fact Sheet: Multiple-use Agents
Module 2 (online)
Protectants/keratotic agents
Used for dry skin (xerosis), otitis externa, diaper dermatitis prophylaxis, acne, corns
Mechanism: Various; many will slow fluid loss from skin, increasing hydration of area; keratolytics decrease skin thickness
Effect: Immediate relief for dry skin with emollients, improvement over days to weeks for acne and corns/calluses with
keratolytic agents; the keratolytic and cauterizing agents for warts will be covered in the antiviral section
Agents:
product
comments
Emollients for dry skin:
 Dry skin is often an inherited trait, particularly in
 Read ingredient list for product. Ingredient 1 will
atopic families; it typically worsens in winter,
always be water. Ingredient 2 should be mineral oil, a
when humidity is low
fat (e.g., cetyl alcohol), a wax (e.g., cetyl palmitate,
 Gloves are the most important investment for
lanolin), or oil (e.g., cocoa butter, shea butter). Ureaperson with dry skin, especially if that person
containing products more effective than non-urea
routinely washes dishes or uses cleansers
containing, but more expensive.
 Use lubricants daily; the best time to apply is
 Avoid product with glycerin as ingredient #2.
after showering—pat skin dry and apply
 Baby oil just out of shower helpful for dry extremities.
Emollients for diaper dermatitis prophylaxis:
 Zinc-oxide based products will discharge heavy
 Options: zinc oxide and non-zinc oxide products.
metal into wastewater or landfill so non-zinc
Apply after each diaper change. Use single application
oxide-based product friendlier for the
of hydrocortisone 1% cream if skin very inflamed.
environment.
Keratolytics for acne:
 For cystic-type acne only
 Tretinoin (Retin A), tazarotene (Tazorac), adapalene
 ADEs of topical retinoid products: local
(Differin); apply once daily at bedtime
irritation, price, potential for teratogenicity
 Isotretinoin (Accutane®) only for severe cases (consent  Isotretinoin available in 10mg, 20mg, 40mg
form + pregnancy test); 0.25mg/kg BID to start,
capsules. Bone loss, mucous membranes
increase to 0.5mg/kg at one month if patient not
irritation, hypertriglyceridemia are worries.
responding; treatment duration: 15-20 weeks; can do
 Suicide risk?? Causality not established.
second course of therapy after ≥ 2 months off therapy
Keratolytics for corns, calluses:
 Soak foot in warm water for 5 minutes before
 Salicyclic acid 40% in plaster cut to size of thickened
application.
area; put in place with waterproof tape; remove at 48
hours; max 5 applications in 2-week period .
Drying agents for otitis externa:
 Swimmer’s ear symptoms include itching,
 Swimmer’s ear: options include commercial OTC
watery discharge, mild pain, and muffled
products (e.g., Auro-Dri) and compounded Burowshearing.
glycerin solution.
 Otitis externa infection symptoms include pain
 Itching with no redness or pain: try hydrocortisone
and visualization of a red and tender ear canal;
cream on a cotton tip applicator, but only in ear canal
need to cover Pseudomonas (11% of people are
entry.
colonized with this in outer ear canal) plus Staph
so need agent to cover both. Options are double
 If otitis externa infection: triple antibiotic + HC otic
or triple antibiotic (product will include HC 1%)
suspension 3-4 drops to fill ear canal, put in cotton to
or otic quinolone (ciprofloxacin, ofloxacin: $$$)
hold solution x 10 mins, then drain ear, TID x 5 days.
Antipruritics
Used for topical relief of itching
Mechanism: block histamine receptors in skin mast cells or block fast sodium channels in “itch” nerves.
Effect: onset 45 min – 1 hr after application with peak at 1-2 hours; re-emergence of itching at 4-8 hours after application.
Agents:
 Topical: combo product containing diphenhydramine 1-2%; prescription-only product is doxepin 5% cream (Zonalon)
which comes in a 30g tube.
 Oral: q4-6h: diphenhydramine 25mg po prn itching; q12h dosing: fexofenadine (Allegra) 60mg po; q24h dosing:
cetirizine (Zyrtec) 5-10mg, levocetirizine (Xyzal) 5mg, loratidine (Claritin) 10mg, desloratidine (Clarinex) 5mg
Side effects sedation, dry mouth, constipation with diphenhydramine; mild sedation with other oral agents
DERM-3
Topical pain relievers
Used for relief of skin pain and itching, muscular pain, neurogenic pain, hemorrhoids
Mechanism: slowing/blocking of nerve pain conduction (‘caines), depletion of substance P (capsicum), anti-inflammatory
effect (salicylates), counterirritant (menthol, camphor)
Effect: ‘caines will begin working within minutes, salicylates and counterirritants can take 1-2 hours before symptom relief
apparent, capsaicin may take several days to reach peak effect
Agents: topical: capsaicin, ‘caines, counterirritants (e.g., menthol); oral: NSAIDs, opiates
Antiinflammatory agents – topical corticosteroids
Used for all inflammatory and itchy eruptions, such as allergic contact dermatitis, atopic dermatitis (eczema), alopecia areata,
hypertropic scars and keloids, lichen planus, psoriasis flares, seborrheic dermatitis, and varicose eczema. If lesions worsen,
consider alternate diagnosis such as bacterial, fungal, or viral skin infection or sensitivity/allergy to corticosteroid agent.
Mechanism: block intracellular production of interleukins and other inflammatory mediators such as TNF, stabilize the
membranes of lysosomes within the cell and thus prevent the release of histamine, kinins, and proteoglycans.
Effect: Itching can begin to decrease within 2-4 hours (stabilization of lysosomal membranes) and the immune response
attenuation will be noticeable by around 6-8 hours after application. Full effect of decreased inflammation will not be seen
for 18-24 hours after therapy is begun. It will be 3-7 days before decreased excoriation/hyperkeratosis becomes apparent.
Agents. There are a lot of agents in a lot of strengths and a lot of vehicles—see appendix. In an effort to simplify this list, the
following recommendations are made:
product description
comments
low potency:
 use in all areas where skin is thinnest: face, groin, axillae
 hydrocortisone cream 0.5%,
 use in all lesions on any part of body for children (0.5% on face, groin,
1%, lotion 1%
axillae)
 use for acute discrete mild lesions, prophylaxis for chronic lesions
medium potency
 use for confluent, hyperkeratotic dermatitis lesions
 fluocinolone acetonide 0.01%  use for discrete lesions on elbows, knees, palms, soles
ointment, 0.025% cream, or
 once confluent lesions become discrete, or discrete lesions look benign,
 triamcinolone acetonide 0.1%
switch back to hydrocortisone 1%
cream, 0.025% ointment
 can use these with occlusive covering (plastic wrap) for very severe
dermatitis or for psoriatic lesions if higher potency corticosteroid is too
expensive for patient; occlusive dressing on 3-4 hours after application;
stop occlusion if itching increases
high potency
 good for psoriatic flares; allow several weeks between successive courses
 betamethasone diproprionate
of therapy to minimize tolerance development
0.05% cream, ointment, or
 use for max of 2 weeks before switching to lower potency agents
lotion
 monitor for signs of HPA axis suppression if large area being covered; if
these appear, need to taper agent
All of these products are available generically and are thus the least expensive options for prescribing. In general, avoid
combination steroid–antiinfective products. They are expensive and not usually necessary
Brand vs. generic. There is a lot of variability in activity of generic formulations.
Side effects of topical corticosteroids nearly non-existent with low-potency agents such as hydrocortisone). Adrenal axis
suppression, dermal atrophy and striae, and adrenal hyperglycemia can occur when agents are high potency (or moderate
potency applied to a thinned-skin area) and used for more than 2 weeks.
Antiinflammatory agents – topical calcineurin inhibitors
product description
comments
 topical tacrolimus (Protopic)
 inhibit Th1 and Th2 cytokine production
0.03% (kids) or 0.1% (adults)  very effective agents; not atrophic like corticosteroids
ointment BID
 expensive; use for people with non-responding atopic dermatitis or if
 pimecrolimus (Elidel) 1%
patients intolerant to steroids
BID
Side effects are burning/pruritis at application site which usually resolves within a week after starting. Some but not all
studies have shown an increased incidence of upper respiratory tract infections, folliculitis, or chicken pox, so patients should
be counseled to report any viral or dermal infections; minimize sunlight exposure as topically immunosuppressed patients at
theoretically higher risk of developing skin cancer.
DERM-4
Fact Sheet: Dermatitis and Similar Use Agents
Epidemiology
 Prevalence 10-20% children, 1-3% adults
 Prevalence higher in industrial areas, lower in agricultural areas
Etiology
 Often family history of atopy; 70-80% of patients have extrinsic IgE-mediated sensitization (usually childhood-onset);
20-30% have intrinsic non-IgE-mediated sensitization (usually adult-onset)
 Th1 and Th2 cell mutations cause dominance of Th2 functions and a shift from production of IgM to IgE Previously it
was thought that defects in immune response caused the characteristic inflammatory skin lesions.
 More recently, the focus has shifted to primary dysfunction of filaggrin and filaggrin-like substances, proteins produced
by keratinocytes that bind keratin, forming the fibrous matrix of the epidermis. Most individuals with eczema display
nonsense mutations in the gene coding for filaggrin and so produce an ineffective or less-effective stratum corneum. The
defect in the skin’s normal barrier function allows better allergen penetration, activating dendritic cells, and promoting
inflammation. So it appears that the characteristic inflammatory skin lesions of eczema are secondary to a defective skin
formation, rather than a defective immune response.
Features The family of diseases called dermatitis generally includes
 Eczema/atopic dermatitis: An inflammatory skin condition characterized by dry skin, erythematous papular (red and
raised) lesions in the acute form, and keratinization (thick or thin), lichenification and/or scales (chronic, non-acute form)
in the chronic form. Also called atopic dermatitis.
 Infant dermatitis/eczema: lesions usually papular and in clusters ranging in size from small to large, and is most often
seen on the face and crawling surfaces. By age of 2, lesions will begin to look more like adult lesions and will be
commonly seen in the trunk, extremities, and sub-facial areas.
 Contact dermatitis: papular erythematous lesions, initially; occur at point of contact with allergen.
 Nummular/discoid eczema: small disc-shaped eczema lesions usually occurring on the lower extremities; often occurs in
winter; herald lesion frequently near area of recent leg trauma; can be hard to get under control.
 Seborrheic dermatitis: mild seborrhea produces dandruff while moderate to severe lesions characterized by waxy
secretions; occurs primarily in the face (eyebrows, lashes, facial hair) and scalp, but also seen in hairy areas of the back,
chest, extremities, and groin. The lipophilic Malassezia genus of fungus may play a role. HIV+ patients seem to be more
susceptible to this kind of dermatitis.
+/ Perioral dermatitis: small papular lesions clustering about but not immediately adjacent to the mouth; sometimes
extending onto the area of the cheeks alongside the nose and below the eyes
 Varicose, asteatotic, or stasis dermatitis: lesions on one or both lower extremities occurring as a consequence of impaired
oxygen delivery. Usually due to arterial atherosclerosis or impaired venous drainage due to venous valve failure. Very
different in appearance from other kinds of dermatitis, with the exception of dry, roughened skin.
Triggers
 Food, aerogens (house dust mites, pollens, animal dander, mold); auto-allergens; Staph aureus ( #s in skin lesions;
cause or effect?); cold or dry weather (many forms of dermatitis worsen in winter)
 Chemicals will exacerbate dryness, excoriation, lichenification
 Use of corticosteroid creams on face associated with perioral dermatitis
Resources
 National Eczema Association: http://nationaleczema.org/
 American College of Allergy, Asthma, and Immunology: http://acaai.org/
Staging
 Mild disease: a few small lesions
 Moderate disease: multiple small clusters of lesions in several locations
 Severe exacerbation: extensive clusters of lesions in more than one body area
 Severe cases with suboptimal response to therapy, patient needs referral to dermatologist. Consider:
  for Staph infection overlaying eczematous lesions and treat with either topical mupirocin or systemic Staph
aureus agent like cephalexin or dicloxacillin;
 adding phototherapy (PUVA) helps some patients
DERM-5

systemic corticosteroids, interferon-, cyclosporin, mycophenoloate, methotrexate, or azathioprine can all help with
resistant cases, but have adverse effects needing careful monitoring
Treatments
 Avoidance of identified triggers, where possible.
 Antihistamines for acute pruritis; non-sedating during day (although less effective at relieving itch than
diphenhydramine), diphenhydramine at night when itching often worsens
 Emollients for all forms of eczema or dermatitis
condition
Infant dermatitis

Mild atopic dermatitis

Moderate atopic dermatitis

Severe atopic dermatitis

Refractory atopic dermatitis

Numular/discoid dermatitis

Contact dermatitis

Seborrheic dermatitis

Stasis dermatitis

Perioral dermatitis

therapy description
HC 0.5% or 1% applied once or once daily x a few days will often be enough to
get recession of lesion
HC 1% cream apply BID until lesion gone; use emollient on arms and legs after
every shower.
Fluocinolone acetonide 0.01% ointment applied BID prn to reduce size and
number of acute lesions until at mild stage or completely disappear. If this
therapy x 2 weeks has not brought lesions to mild stage, patient should consult
provider for re-evaluation. Emollient use daily or after each showering if done
every other day.
Betamethasone diproprionate 0.05% ointment applied BID to the area for a
maximum time of 2 weeks. At this time, patient should return for re-evaluation.
Severe atopic dermatitis that is unresponsive to 2 weeks of therapy with highpotency agent. Refer to dermatologist.
Fluocinolone acetonide 0.01% ointment applied BID. Emollient use daily. This
needs to be done until lesions are nearly or totally resolved, which may take
from 2-4 weeks.
HC 1% cream can be adequate, however may need 1 week of medium potency
steroid (fluocinolone actonide 0.01% ointment applied twice daily).
Treatments will not cure the disease and will only ameliorate symptoms.
Ketoconzole 2%, selenium sulfide 2.5%, ciclopirox 1%, and fluocinolone
acetonide 0.01% shampoos are effective for scalp seborrhea and probably useful
for treatment of hairy areas in the groin. Lesions on the face, trunk, and/or
extremities can be treated with a low-potency topical corticosteroid or topical
calcineurin inhibitor cream if mild disease and with moderate-potency
corticosteroid or antifungal such as miconazole 2% (OTC) or econazole 1%
(Rx) cream once or twice daily if moderate disease. Shaving (in men with facial
hair) may help control this condition.
Daily cleansing of the area with Cetaphil or similar mild cleanser. Daily to twice
daily application of relatively occlusive emollient. Apply fluocinolone or
triamcinolone cream or ointment once or twice daily to erythematous areas that
are itchy, vesicular, or mildly oozy. Apply wet dressings (saline or Burow’s
solution) to exudative lesions
Withhold application of any topical steroid for at least a few weeks as this may
exacerbate lesions.
DERM-6
Fact sheet: Psoriasis
Epidemiology
 prevalence 1-3%; Scandinavians have highest incidence; 1% incidence in North America
 most cases not severe and are treatable by primary care provider
Etiology
 genetic; 40% of patients have a family history of disorder in first degree relative; gene or group of genes have been
identified on the short arm of chromosome 6
 appears to involve Th1 lymphocyte cytokines: interferon-, TNF-, and IL-2
Features
 psoriasis is a papulosquamous (papules and scale formation) eruption characterized by discrete (bordered) lesions and
increased epidermal cell turnover  cells on the top layer of the skin still have intact nuclei and function (so no
protective keratin surface)
 plaque psoriasis: “classic” psoriasis; patients present with plaque-type lesions on scalp, extensor elbows and knees, and
back; often appears in young adulthood
 guttate psoriasis: abrupt appearance of multiple small psoriatic lesions, usually < 1cm in diameter; typically occurs in
child or young adult; are located primarily on the trunk; often associated with recent streptococcal infection
 pustular psoriasis: the most severe form (can be life-threatening): widespread erythema, scaling, sheets of superficial
pustules with erosions; associated with malaise, fever, diarrhea
 inverse psoriasis: presentation involving intertriginous areas; called “inverse” because in opposite areas of classic plaque
psoriasis; differential diagnosis of fungal or bacterial infection, atopic dermatitis (lack of pruritis can help delineate)
 nail psoriasis: nail involvement not usually isolated, but deserves mention because of troubling nature for patients; nails
have a few to multiple tiny pits scattered over the nail plate, can also develop a localized colour change—tan-brown like
new motor oil; severe nail involvement can resemble onychomycosis; psoriatic nails generally resistant to treatment
 psoriatic arthritis: seen in about 30% of psoriasis patients; arthritis can precede skin involvement in small fraction of
cases; different clinical patterns exist, some which resemble RA and others which resemble OA
 increasing evidence that psoriasis is a multisystem inflammatory disorder. In addition to arthritis, people with psoriasis
are at higher risk for obesity, metabolic syndrome, diabetes, cardiovascular disease, malignancies, and psychiatric
disorders.
Triggers
 HIV infection
 any other infection
 alcohol consumption
 several drugs: beta-blockers, lithium, antimalarial drugs, ACEIs, NSAIDs, terbinafine all have been documented to
worsen flares in some individuals
Treatment principles
 hydration and emollients beneficial to everyone; apply after bath; Eucerin, petrolatum, or any thick creams are most
effective.
 topical corticosteroids for flares:
 medium potency steroid BID for moderate lesions on extensor surface
 fluocinonide 0.05% BID on scalp lesions
 hydrocortisone 1% BID for intertriginous lesions
 for thick plaques on extensor surfaces, betamethasone 0.05% BID with added plastic wrap occlusion may be needed
acutely
 topical calcipotriene for maintenance once flare under control; anthralin or tazarotene or coal tar is second-line
 methotrexate for extensive involvement or if patient has psoriatic arthritis may also help with nail disease (give folic acid
1mg daily to prevent stomatits)
 phototherapy with UVB light can enhance drug therapy (psoralens + UVA light—PUVA—is second-line phototherapy)
 refer to dermatologist if these don’t work; severe pustular psoriasis: acitretin or etretinate, cyclosporine; etanercept
(Enbrel®) and infliximab (Remicade®) useful; alefacept (Amevive®)—some patients may have sustained clinical
response after cessation of therapy
Antipsoriatics
DERM-7
Used for chronic psoriatic lesions during and after topical steroid therapy has attenuated flare. Oral agents used for advanced
disease refractory to topical steroids.
Mechanism: most inhibit DNA synthesis or cell division in some way, in an effort to slow the rapidly-dividing and migrating
keratinocytes.
Effect: patients should notice an effect from these products within 1-2 days (since skin cell turnover is rapid, effect is seen
more rapidly than with other skin conditions)
product
description
calcipotriene (sometimes called calcipotriol) 0.005%
 vitamin D analog but less effect on bone compared
cream or ointment (Dovonex); apply thin layer and rub
to natural calcitriol; convenient, well-tolerated,
in gently BID for up to 8 weeks
expensive
 agent of choice for mild-moderate plaque psoriasis
once flare is controlled with steroid
coal tar 2-10%, available in a variety of creams, liquids,
 convenient, inexpensive, less irritating than steroids
lotions, ointments, soaps and gels (T-gel, Z-tar, Pentrax,
or anthralin
Ionil T, T-derm)
 messy, smelly, stains clothes so second-line agent
anthralin (called dithranol in Europe) 0.1%, 0.25%,
 good for scalp; apply to lesions BID. leave on for 20
0.5%, 1% ointment; 0.25%, 1% cream applied once
minutes, then remove; use daily until clearing
daily
achieved, then twice weekly
 irritant, staining, probably less effective than
calcipotriene, so second-line
tazarotene (Tazorac) 0.05%, 0.1% gel; apply qHS to
 clinical trials have examined up to 12 months of
psoriatic lesions
continuous use; second-line after calcipotriene in
non-reproductive individuals
 vitamin A analog, so usual warnings about
teratogenicity, skin irritation; expensive
methotrexate 2.5mg tablets; 10-20mg given as single
 the gold standard for patients with advanced joint
dose, once weekly
and skin disease; effective, prompt, relatively nontoxic
 liver biopsy at 2-4 months into therapy, once
efficacy established, then again when cumulative
dose reaches 1.5g and every 1g thereafter
etretinate (Tegison) 10mg, 20mg capsules; 1 mg/kg qd
 expensive, teratogenic, lots of systemic adverse
until response seen, then decrease to 0.5mg/kg/day
effects; reserve for severe cases unresponsive to
acitretin (Soriatane) 10mg, 25mg capsules; start at
methotrexate; terminate therapy when lesions
25mg/day, increase as needed
improved
 single daily dosing for both agents
alefacept (Amevive) 15mg (0.5mL) IM or IV once
 suppresses CD2+ T-lymphocytes
weekly
 both products will produce a ≥ 75% improvement in
efalizumab 1 or 2 mg/kg SC once weekly
about 20% of patients; relapse at therapy cessation
occurs in > 50% of patients
 ADRs: lymphopenia (get baseline WBC and have
patient report any infections), chills 6%, injection
site reaction 2%, pharyngitis
infliximab 5 mg/kg IV; repeat at 2 and 6 weeks
 block tumor-necrosis factor activity
etanercept 25 or 50mg SC twice weekly x 3 months
 black box warning for increased risk of severe skin
infections
cyclosporine ≥ 5 mg/kg/day
 Both moieties have about 70% incidence of clearing
PUVA
or almost clear for moderate - severe plaque
UV-B (narrow band)
psoriasis.
Side effects as noted above. Any topical product can cause stinging.
DERM-8
Fact Sheet: Bacterial Skin Infections
Suggested gram positive agents
Topical
 Bacitracin 500 units/gm; spectrum: Strep, MSSA
 Mupirocin (Bactroban®, generic) 2% cream and ointment; spectrum: Strep, MRSA
 Azelaic acid 20% cream, 15% gel; spectrum: Staph epi, propionibacterium
Oral
 Cephalexin (Keflex®, generic); spectrum: Strep, MSSA; adult dose 500mg po BID, TID, or QID depending on severity
of infection
 Trimethoprim/sulfamethoxazole (Bactrim DS®, generic); spectrum: MRSA; adult dose 160/800 po q12h
 Clindamycin (generic); spectrum: Strep, many anaerobes; adult dose 300mg po TID
 Amoxicillin (generic); spectrum: Strep, some respiratory gram negative organisms, some anaerobes; 500mg po BID or
TID
Parenteral
 Cefazolin; spectrum: Strep, MSSA; adult dose 1 g IV q8h
 Nafcillin; spectrum: Strep, MSSA; adult dose 500mg IV q4h
Suggested gram negative agents
Topical
 Neomycin-polymyxin; spectrum: most gram-negative organisms
Oral
 Ofloxacin (generic); spectrum: MSSA, most gram-negative pathogens; adult dose 400mg po q12h, ophthalmic solution
0.3%
Parenteral
 Gentamicin; spectrum: most gram-negative organisms; dose by weight (1 mg/kg IV q8h common starting dose)
Suggested broad spectrum agents
Topical
 Chlorhexidine gluconate (Hibiclens®, generic, Peridex®) 2%, 4% liquid scrub solution, 0.12% mouthwash); spectrum:
most gram positive organisms, including MRSA; many gram negative organisms, including Pseudomonas; facultative
anaerobes, including mouth flora; and some fungi
Oral
 Levofloxacin (Levaquin®, generic); Strep, MSSA, most gram negative pathogens; adult dose 500-750mg po daily
 Amoxicillin-clavulante (Augmentin®, generic); spectrum: Strep, MSSA, selected gram negative (including respiratory
pathogens), anaerobes; adult dose extended release 1 g/62.5mg po q12h
 Doxycycline; spectrum: spotty gram positive (Strep pneumo and some MRSA) and gram negative (respiratory
pathogens) coverage
Parenteral
 Levofloxacin (Levaquin®, generic); Strep, MSSA, most gram negative pathogens; adult dose 500mg or 750mg IV daily
 Piperacillin-tazobactam (Zosyn®, generic); Strep, MSSA, most gram negative pathogens; adult dose 3.375mg IV q6-8
hours
DERM-9
condition
For superficial dermal infections, dermal infection
prophylaxis:
 bacitracin ointment (OTC)
 polymixin/bacitracin/±neomycin ointment, cream;
called triple antibiotic, but read ingredient list—
some products have only bacitracin + polymixin
 mupirocin 2% cream, ointment (Bactroban®)
 gentamicin cream, ointment (Rx)
 silver sulfadiazine (Rx–Silvadene) 1/16 inch applied
qd-BID until eschar formation well underway; 20g
tube only for very small burn, 50g for burn < 2”x2”,
400g for larger burns, and 1kg tubs for big bad
burns.
For cellulitis, lymphadenitis:
 cellulitis (warm, tender, red area of the skin; Staph
or Strep is usually the cause) that is larger than a
fingerprint will need oral antibiotics (cephalexin
500mg po QID) and IV antibiotics if larger than a
handprint (will need consult here but want pip-tazo
or 2nd - 3rd gen ceph)
 lymphadenitis characterized by a red streak
extending up a limb from a site of skin trauma; may
be accompanied by fever, tachycardia, or headache;
Strep pyogenes is the most common cause if
symptoms appear within a day or two after a skin
wound, but other bacterial and nonbacterial
organisms can also cause
For acne, rosacea:
 erythromycin 2% gel, topical solution; clindamycin
1% gel, solution, lotion
 benzoyl peroxide 2.5%, 5%, and 10% available
generically in lotions, creams, gels, washes
 doxycycline 100mg po BID, erythromycin 500mg
po BID for acne
 metronidazole 0.75% gel (MetroGel)
 metronidazole 250mg po BID initially, can increase
to 500mg po BID if more control needed
 tea tree oil 5% applied daily found as effective as
benzoyl peroxide in one study
 azelaic acid (Azelex, Finevin) 20% cream BID
For bacterial conjunctivitis
 sodium sulfacetamide 10% solution will cover
Staph effectively
 gentamicin 0.3% solution or ofloxacin 0.3% will
cover gm (-) organisms and may effectively cover
gm (+) organisms
For bacterial vaginosis:
 metronidazole 500mg po BID x 7 days is cheapest;
don’t use during 1st trimester
Side effects as noted above.
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
comments
bacitracin spectrum: gm (+), so good for infection
prophylaxis of cuts, scrapes and for mildly infected
dermal insult; inexpensive
polymixin, neomycin add gm (-) activity, so triple
antibiotic cream is good for mild infection where
mixed flora is likely e.g., diabetic foot
mupirocin broad spectrum; hits MRSA so excellent
for catheter-related localized redness, erythema;
expensive; not related to other anti-MRSA agents so
unlikely to acquire resistance
gentamicin good for Strep, Staph, also gm (-)
spectrum; no advantage over triple antibiotic preps
one study found less scarring with triple antibiotic
ointment on dermabrasion wound healing
Can track effectiveness of cellulitis therapy by using
Sharpie to mark edges of inflammed (red) area at
start of therapy. If border recedes, antibiotic is
working. If not border extends will need to reevaluate therapy
Lymphadenitis often called “blood poisoning” by
lay individuals who can interpret it as a lifethreatening disease and then propose treatment with
home remedies. These remedies may appear to work
both because the body’s immune system responds to
the infection and warm compresses may enhance
migration of immune system responders to the area
(it’s all we had prior to antibiotics…)
many benzoyl peroxide products available OTC;
start use qOd for 1-2 weeks, then move to qd, then
BID in order to decrease initial irritation
oral agents for acne only if topical treatment failure
or nonadherence due to ADR; low-dose OCs (for
women) often effective
for rosacea, start with topical metronidazole daily or
BID – should see improvement within 3 weeks; go
to oral if no improvement by 8 weeks
www.rosacea.org is a good source of information
for your patients
doxycyline 40mg po qd only approved doxy product
for rosacea
85% bacterial conjunctivitis caused by Staph, which
is covered by sodium sulfacetamide
15% caused by gm (-) organism
metronidazole vag gel is expensive
clindamycin vag cream qHS x 7 days for 1 st
trimester
DERM-10
Fact Sheet: Acne and Rosacea
Focus skin condition: acne (a.k.a. acne vulgaris)
epidemiology
 85-100% of adolescents, 8% of 25-34-year-olds, 3% of 35-44 year-olds; affects more than 17 million Americans
 accounts for over 10% of all patient encounters with primary care providers; 4.8 million visits/year
 has psychosocial effects; scars can be permanent
etiology
 follicular hyperkeratination is earliest change; due to increased keratinocyte production and decreased desquamation
 androgens (e.g., dehydroepiandrosterone sulfate—DHEA-S) trigger increased sebum production; sebum overproduction
more likely due to hyperresponsiveness of sebaceous gland than androgen overproduction
 hyperkeratination meets excess sebum product; result: plug in hair follicle
 Propionibacterium acnes (anaerobic diphtheroid which is part of normal skin flora) thrives in this oxygen-poor, lipidrich environment (these organisms dine on triglycerides); hyperproliferation of P. acnes and localized irritation from free
fatty acids liberated from triglyceride hydrolysis causes localized inflammation
 inflammation attracts neutrophils which release chemokines, cytokines, lysosomal enzymes; these and keratin extrude
into surrounding dermis, forming a papule or nodule
 the degree of follicular hyperkeratinization, sebum production, P. acnes growth, and inflammation will determine
whether the lesion evolves into a whitehead (closed comedome), blackhead (open comedome), inflamed papule, or
cyst/nodule
features:
 the following is one type of classification
 type 1: mainly comedones with occasional small inflamed papule or pustule; no scarring (mild)
 type 2: comedomes and more numerous papules and pustules (mainly facial); mild scarring (moderate 1)
 type 3: numerous comedomes, papules, and pustules; spread to back, chest, shoulders; occasional cyst or nodule;
moderate scarring (moderate 2)
 type 4: numerous large cysts on face, neck, upper trunk; severe scarring (severe)
triggers
 cosmetics and warm humid environments can exacerbate
 foods do not influence production of sebum; do not recommend diet modification
treatment
mild to moderate acne:
 benzoyl peroxide 2.5% (if available) BID (use 5% otherwise), increase to 5% if suboptimal effect; most people won’t
like the skin irritation (stinging, burning) from this product—apply 5% qOd x 1st two weeks, then qd, x 2 weeks, then
BID if too irritating
 next step: topical erythromycin or clindamycin;
 other options at this point are tea tree oil and azelaic acid (no published evidence on topical dapsone)
moderate to severe acne:
 oral antibiotics are often effective (doxycycline, erythromycin, TMP-SMX) and can be used concomitantly with benzoyl
peroxide
 oral contraceptives (OCs) are often quite effective in women desiring contraception (no, Tri-Levlen is probably not
significantly better for acne than any other OC, despite what the commercials imply)
 spironolactone 50mg or 100mg po daily; little evidence to support use for acne (Cochrane Database System Rev 2009
Apr 15;(2):CD000194)
 topical tretinoin is an option, although most people will notice skin irritation similar to that with benzoyl peroxide
 oral isotretinoin use should be reserved only for severe, cystic acne and needs two negative initial and then monthly
pregnancy tests in women, informed consent documentation, and birth control for female patients and partners of male
patients
resources
 http://www.rosacea.org/
DERM-11
Focus skin condition: rosacea (a.k.a acne rosacea)
epidemiology
 A chronic acneiform inflammatory facial skin disorder of middle-aged and older adults. It most commonly occurs in
patients between the ages of 30 an 60 years.
 Relatively common among individuals with fair skin and light hair and eye color. Also common among those who
experience frequent blushing or flushing. Many people experience flares starting in spring.
etiology
 The cause of the vascular dilation is unknown.
 One theory is that hair follicle mites Demodex folliculorum and Demodex brevis play a role in the condition. This idea is
supported by studies showing increased numbers of mites in the kin of patients with rosacea compared to unaffected
controls. It is also supported by a small study of 63 patients from Turkey who had papulopustular rosacea. Patients were
randomized to permethrin 5% cream, metronidazole 0.75% gel., or placebo, and were evaluated at days 15, 30, 45, and
60 of therapy. ITT analysis showed that permethrin was as effective as metronidazole for rosacea.
 Another postulation is that Helicobacter pylori plays a role, as a higher prevalence of infections has been reported in
rosacea patients. For the most part, current literature does not support this hypothesis.
 It seems likely that genetics plays a role (direct? indirect?) in this condition. In one National Rosacea Society survey,
33% of respondents reported Irish heritage and 27% were of English descent. Rosacea also seems to be associated with
Scandinavian, Scottish, Welsh and eastern European descent.
features:
 Hallmark: vascular dilation of the central face, including the nose, cheeks, and forehead.
 Rosacea subtypes:
 Erythematotelangiectatic rosacea. Characterized by noticeable persistent flushing, sometimes producing a burning or
stinging feeling. Can occur in response to triggers or without known stimuli. Patients with this subtype seem to have
lower threshold for topically-applied irritants, which can produce skin roughness and scaling.
 Papulopustular (“classic”) rosacea. Characterized by episodic or persistent small papules that may or may not have
pinpoint pustules, and (generally) sparing of periorbital skin. Telangiectases may be present. Skin not usually
sensitive to irritants. Edema around papules present in more severe form.
 Phymatous rosacea. Characterized by noticeable skin thickening, nodule development over most of the face.
Hyperplasia of the nose (rhinophyma; think W.C. Fields) seems to occur almost exclusively in males.
 Ocular rosacea. Characterized by blepharitis, conjunctivitis, and (less frequently) chalazions (meibomian gland
cysts). Can occur in conjunction with or separately from (often preceding) the other subtypes.
triggers
 hot or spicy foods (including hot beverages); alcohol ingestion (do not, however, assume that patients with rosacea drink
alcohol excessively)
 emotional reactions, heavy exercise, some skin care products
 heat, sunlight (UV light), wind
treatment
facial erythema
 Avoiding triggers reduces flare-ups; mild cleanser (Cetaphil, Dove) and broad-spectrum sunscreen use important.
 Brimonodine tartrate (Mirvaso) 0.33% gel applied once daily to affected facial areas; a topical vasoconstrictor
papules/pustules
 Initial therapy: topical antibiotics (metronidazole 1% cream, 0.75% cream, lotion, and gel; not yet available generically)
BID for papular/pustular stage; one study found qd dosing also effective. Azelaic acid 20% cream BID also useful for
treatment. Use for 4-6 weeks. Back-ups: sodium sulfacetamide 10% lotion; sulfur 5% cream or 10% lotion; clindamycin
1% solution, gel, or lotion; erythromycin 2% solution, all can be used BID and all are a little less effective than
metronidazole or azelaic acid.
 Next step if initial therapy not providing adequate effect: oral antibiotics (tetracycline 250 or 500mg po BID,
erythromycin 250mg BID, metronidazole 250mg BID, doxycycline 100mg po qd; TMP/SMX DS qd; taper oral abx
within 3 mos after skin clears) or topical tretinoin cream (0.025%, 0.05%, 0.1%) 2-3x/week initially and increasing to
qPM.
 dermatologist: surgical intervention; pulsed vascular laser therapy; isotretinoin (not as effective in rosacea)
DERM-12
Fact Sheet: Antifungal agents
Used for athlete’s foot, ringworm, jock itch, onychomycosis, fungal dermal rash, vaginal yeast infection, thrush
Mechanism: alteration of fungal cell membrane permeability; some agents also interfere with fungal mitochondrial activity
Effect: Symptom relief should start within 2-3 days after therapy begins, but clinical resolution may require 2-4 weeks of
therapy
Agents:
product
comments
For athlete’s foot, ringworm, jock itch, fungal dermal
 clotrimazole and miconazole also come in
rash:
prescription for those patients whose insurance
 clotrimazole or miconazole topical creams are
covers Rx but not OTC agents; if large area, use
available OTC (Lotrimin AF, Micatin); apply to
vaginal cream preparation - more spreadable plus
affected area BID; 15g, 30g tubes
larger tube (45g)
 tolnaftate (Tinactin) and undecylenic acid
 challenge: fungal infection versus diaper dermatitis
(Desenex) are also reasonable agents to recommend
(more common); fungal infections usually erosions;
(both OTC)
not sure? have mom apply 0.5% hydrocortisone at
bedtime – if diaper dermatitis then rash will
 if therapeutic failure: fluconazole 100mg po qd
attenuate overnight
 for tinea versicolor: selenium sulfide 2.5% shampoo
 tinea versicolor often not spotted until summer,
applied undiluted to all involved areas at bedtime
where it appears as hypopigmented, mildly scaly
and washed off in morning for 3-4 days; oral
spots on the chest, neck, and abdomen; most
imidazole for 7 days will also work
commonly diagnosed in young adults; often
recurrent
For vaginal yeast infection:
 a small amount of cream applied BID to vaginal
 miconazole or clotrimazole OTC vaginal cream for
vestibule will help decrease itching
patients who can pay – directions on package
 eating yogurt daily may also be effective for
 butaconazole (Femstat) or terconazole (Terazol 3)
prevention of recurrent vaginal yeast infections and
are Rx-only products and involve 3 days of vaginal
is worth a try in patients taking birth control pills or
administration; easiest prescription option is
qd doxycline for acne (both increase risk of vaginal
fluconazole 150mg po as single dose
yeast infection)
For thrush:
 nystatin and miconazole also available as troches
 nystatin suspension 5ml swish and swallow QID x
which are to be dissolved in mouth; this dosage
14 days is gold standard
form is more expensive than the genericallyavailable nystatin suspension
 fluconazole 100mg po qd if topical nystatin doesn’t
work
 oral nystatin for baby + topical for mother is
standard for breastfeeding infant thrush
For onychomycosis:
 caution! triazoles (ketoconazole, fluconazole,
 terbinafine 250mg po qd x 12 weeks AOC, but
itraconazole) are CYP 3A4 enzyme inhibitors; your
expensive
pharmacist will assist you in scanning for 3A4
substrates in the patient's other meds; terbinafine is
 itraconazole 200mg po qd x 12 weeks (ketoconazole
a CYP 2D6 inhibitor, so look for concurrent opioid,
200mg po qd has also been used and may be
beta-blocker, antidysrhythmic, or TCA therapy
cheaper than itraconazole; griseofulvin
ultramicrosize 330mg po BID less expensive but not
as effective as newer agents
Side effects are rare with topical agents; oral agents most commonly cause tummy upset; can see hepatotoxicity with oral
agents, so get baseline LFTs if patient to be on > 1 month
DERM-13
Fact Sheet: Antiviral agents
Used for warts, cold sores, shingles, chicken pox, ocular viral infections
Mechanism: inhibits viral thymidine kinase (‘clovirs) or viral mitosis (podophyllum & co.)
Effect: onset of symptom relief should occur within 24-48 hours of initial administration
Agents:
product
comments
For warts:
 calluses can be mistaken for warts: keep this in
 cryotherapy in your office usual AOC
mind; a callus will have skin lines on the surface
whereas a wart will not
 OTC: salicylic acid lotions for plantar and common
warts, cryotherapy in a can: dimethyl ether, propane  cryotherapy with liquid nitrogen by you is the most
products include Dr. Scholl's Freeze Away®,
frequently-used treatment for warts; repeat visit for
Wartner®; use single application
cryotherapy reapplication often necessary; painful
 alternative home treatment: cut duct tape to the size
 “cryotherapy in a can” produces a reaction that
of the wart and place over the top; leave in place for
lowers temperature to around - 60°C (although one
6 days, remove, soak in water for 5-10 minutes,
study measured temp of only -20°C). For
debride with emery board; repeat process on day 7
comparison, cryotherapy with liquid nitrogen lowers
and continue until wart gone; most warts will
temperature to more than -100°C
resolve within 28 days with this therapy
 skin irritation and damage to healthy surrounding
 patient can use at home podofilox (Condylox®) for
tissue is the main ADR with any wart treatment
genital warts applied BID x 3 days, withhold 4 days,
(except duct tape)
then repeat cycle until wart tissue gone; female will
need help with administration
For chicken pox or shingles:
 for chicken pox, probably more effective for pre acyclovir 800mg po CID (5x/day) x 7-10 days for
school age child to be vaccinated prior to chicken
adults; 20mg/kg po QID for kids under 90 pounds
pox season (Jan-Mar)
For ocular viral infections:
 viral eye infections often diagnosed by exclusion
 trifluridine (Viroptic®) one drop on cornea of
i.e., antibacterial therapy doesn’t work
affected eye q2h WA; continue for 7 days beyond
 therapeutic alternative: vidarabine (Vira-A), thin
corneal ulcer re-epithelialization; max 21 days of
strip of ointment to conjunctival sac 5x/day; chronic
therapy.
blurry vision
For cold sores:
 wash hands after application to decrease interperson
 acyclovir or penciclovir ointment applied to
transmission
lesion(s) q2-3 hours while awake
 some patients swear by OTC products (e.g.,
Abreva®) ; they’re cheaper and it’s worth a try
Side effects mostly noted above; oral acyclovir can cause tummy upset
DERM-14
Fact Sheet: Antipediculocides
Used for scabies, head lice, pinworms
Mechanism: act on the critter’s nervous system to paralyze it, causing parasite suffocation
Effect: lice and scabies absorb pediculocide right away; killing takes hours to days. pinworm killing takes longer (slower
incubation)
Agents:
product
comments
For lice:
 eggs (nits) laid at hairline and take 10 days to hatch
 permethrin 1% (OTC - Nix) cream rinse (97-99%
(eggs > 1mm from scalp are non-viable), the infant
cure rate). Single application (left on the hair for 10
nymphs 7 days to mature, and adult lice live about
minutes) is pediculocidal and 60-70% ovacidal, due
30 days. Female lice will lay 6-7 eggs daily.
to residual persistence (up to 10 days after a single
 lice can move fairly quickly on dry hair, but
application). A follow-up application at 7-10 days is
movement slows when the hair is wet. Use only
often recommended anyway.
water to wet hair when doing lice checks. Start
 Spinosad 0.9% suspension an alternative to
behind ears and include nape of neck.
permethrin. More effective? More expensive. Rx
 conditioners coat hair and protect lice from
only
pediculocide penetration, so avoid use of
 Many cases of resistance are due to poor package
conditioners during lice infestations.
directions: review steps with your patients.
 diagnosis by combing is 4 times more reliable than
Pediculocide shampoo should always go on dry
diagnosis by observation. Wipe comb on white
hair.
tissue to better observe tan/brown lice.
 Combing is crucial! Mechanical removal of lice
 pediculocidal shampoo needs to go on dry hair.
eggs should always accompany pediculocide
Wait 10 minutes, then rinse. Begin combing
treatment; only method of treatment for kids < 2 and
immediately afterward. Wait 2-3 days after
eggs (pediculocide penetrates egg shell poorly); use
treatment before hair is next shampooed.
fine metal comb from pet store if hair too thick for
 lice products don’t penetrate nit shells well, so
plastic comb that comes with OTC product
pediculocide needs to have residual activity of
 vacuum rooms; soak combs and brushes x 1 hour in
several days for best effect; reapplication after 1
isopropyl alcohol; wash sheets, blankets,
week also best.
pillowcases, clothes in hot water. Tell your patients
 if lice are dead or moving slowly at 12-24 hours
not to be overzealous about this. Lice don’t live
after treatment, it is probably effective.
long off a host; within about 12 hours, lack of food
 if resistance suspected: combing crucial; one group
induces dehydration and non-viability, even if they
of researchers recommend leaving permethrin on for
are still able to move.
longer period of time (several hours) if resistance
 Malathion (Ovide – Rx) and lindane (Kwell®) less
seems to be occurring
effective and more toxic than permethrin
 No mayonnaise, please. Messy and ineffective.
For scabies:
 scabies mite rarely lives outside the human body for
 permethrin 5% cream (Rx – Elimite®, Acticin®
more than 30 minutes; it is transmitted by
both come in 60g tubes) has efficacy rate of 91%;
prolonged, still skin-to-skin contact – holding hands
apply from neck to toes and wash off after 8-14
is the most common way to become infested and
hours; < 2% of dose absorbed so toxicity not a
explains why mites are most often found on the
problem
hands and fingers
 backup: lindane (Rx – Kwell) has efficacy rate of
 the characteristic scabies rash is an allergic reaction
86%; same directions; crotamiton (Rx- Eurax) has
to the mite, its eggs, or its feces; rash appears 10-30
60% efficacy rate
days after infestation (time to build hypersensitivity
response)
 same laundry information as for lice; no evidence
scabies lives when off hosts
For pinworms:
 best to treat everyone in the household at the same
 pyrantel 50mg/ml oral suspension (OTC) is AOC;
time, since highly transmissable
single dose of 11 mg/kg (5 mg/lb); can repeat
 wash hands well after bathroom and before eating,
another dose in 2 weeks, if desired; efficacy 96%
otherwise no unusual cleansing procedures needed
DERM-15
Fact Sheet: Actinic Keratosis and Skin Cancer
epidemiology
 actinic keratosis (AK) has prevalence rates ranging from 11-26%, depending upon which study you examine; prevalence
rates are highest in Australia and New Zealand (sun exposure + heritage). About 1/1000 AK lesions develop into
squamous cell carcinoma, annually.
 estimates are that 550,000 new skin cancers diagnosed each year, currently; about 75% (>400,000) are basal cell
carcinoma (BCC), 20% (~100,000) squamous cell carcinoma (SCC) and 5% (25,000-55,000) are melanoma. Incidence is
increasing among older adults and decreasing in younger adults.
 risk factors: sun exposure is the strongest risk factor for AK and all skin cancers. Cumulative exposure is biggest
predictor, but exposure specifically in childhood or adolescence increases risk. Usual: fair skin, light hair and eye colour;
Scandanavian, Celt descent.
etiology and features:
etiology
features


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
“classic”
location
prognosis


AK
sun-induced;
develop only on
sun-exposed skin



small oval
nodule with
erythematous
border
sometimes will
scab
may appear as
fissure in lip or
like a cold sore,
except the sore
doesn’t heal
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backs of hands
face
lower lip
ear
scalp

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occasionally
metastasize
good prognosis if
detected early

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grayish-brown,
dicrete, raised,
scaly lesions
if scale removed,
small superficial
ulcer can develop
often
erythematous
edge around scaly
portion of lesion

all sun-exposed
areas
cosmetically
bothersome but
conversion to
SCC rare
SCC
sun-induced
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


BCC
sun-induced
can also be
arsenic and
radiation therapyinduced
small papule
which spreads
outwards, leaving
central ulcer
edges are raised
and pearlcoloured once
lesion ulcerates
these often bleed
and give patients
a persistent scab
that fails to heal
face, particularly
on nose and
below eyes










rarely metastasize
slow growing
good prognosis


melanoma
sun-influenced
(not sun-induced)
genetic
component
hormone
influenced?
solitary
pigmented
lesions
looks like a mole,
but often not
round
unlike mole, it
will spread
unlike mole, can
ulcerate or bleed
anywhere
females have
more commonly
on legs
males: more
commonly on
back
can metastasize
the deeper the
lesion, the poorer
the prognosis
treatment
 Non-chemo treatment. surgical excision is treatment of choice for BCC, SCC, early (not thick) melanoma (cure rate >
90%); radiation therapy for BCC, SCC if pt not candidate for surgical tx
 AK: 5-FU, masoprocol, imiquimod, diclofenac
 superficial BCC, SCC: excision and/or topical 5-FU and topical imiquimod
 metastatic disease will require systemic chemotherapy (outlined on next page) and lymph node dissection
DERM-16
Topical chemotherapy
Used for: actinic keratosis and treatment of skin cancer
Mechanism: as noted in chart below
Effect: resolution of lesions; avoid sun with all agents; don’t occlude lesions—cover with light gauze dressing only
Agents:
product
description
5-flurorouracil (5-FU; Efudex) applied qPM
 inhibits DNA synthesis
 1% cream, 1%, 2% solution for actinic
 little systemic absorption
keratosis
 stages: 1. early inflammation , erythema x several days 

5% cream, 5% solution for superficial
2. inflammation increases in severity, burning, stingin,
basal cell carcinoma
vesiculation  3. disintegration with erosion, ulceration,
necrosis (DC 5-FU at this time), pain, crusting, beginning
of re-epithelialization  4. healing with residual erythema
x 1-2 weeks; length of stages 2 and 3 will depend upon
severity of lesions, but usually last several weeks
masoprocol 10% cream (Actinex), massage into
 derived from the creosote bush
area of actinic keratosis BID x 2-4 weeks
 a 5-lipoxygenase inhibitor, so  IL production; also
appears to inhibit DNA synthesis, possibly through free
radical production; inhibits keratinocyte growth
 may stain clothing; wash hands after application
 up to 70% reduction in lesion number
 no data comparing effectiveness to 5-FU
imiquimod 5% cream (Aldara), apply BID for
 an immunomodulator; MOA not precisely known
actinic keratosis and superficial basal cell
 approved for treating genital and perianal warts
carcinoma
diclofenac 3% gel (Solaraze)apply to lesion areas  diclofenac gel mechanism of action (MOA) is unknown
BID x 60-90 days
 little systemic absorption
Side effects: skin irritation (erythema, excoriation, erosion, contact dermatitis) and fungal infection most common ADRs
with these agents
Systemic chemotherapy
Used for: metastatic disease
Mechanism: cell cycle disruption
Agents:
cancer
product
SCC
 platin therapy ± bleomycin
 cetuximab
BCC


melanoma

platin therapy ± bleomycin
vismodegib first FDAapproved hedgehog inhibitor
surgical excision can be
curative if not metastatic
for metastatic disease:
 high-dose IL-2 or IFN
 ipilimumab 3 mg/kg IV q3
wks
 vemurafenib 960mg po BID
 dacarbazine 1000 mg/m2 q2-4
wks







comments
SCC metastatic disease is rare
case reports suggest that cetuximab has activity
against SCC metastatic disease
BCC metastatic disease is rare
tolerance of high-dose IL-2 is low
For malignant disease remissions are partial and shortlived, so the goal is to give the patient a few
additional months of life.
vemurafenib used in pts w/V600 BRAF mutation
temozolamide not FDA-approved but has been used
DERM-17
Fact Sheet: Drug Allergies
Drug eruptions
 allergic drug rashes are usually bright red, very itchy, confluent, and show up within a couple of days of starting the drug
 viral exanthems tend to be more pink or brownish, discrete, and the patient will often have a history of an upper
respiratory infection within a week preceding appearance of the rash
 amoxicillin non-allergic rashes show up later in therapy than allergic rashes (e.g., > day 3 of amoxicillin), are often not
very itchy and may or may not be raised; the rash will fade over around 3 days whether or not amoxicillin is continued;
the patient unlikely to experience rash upon amoxicillin readministration
 a maculopapular rash will not “turn into” an anaphylactic reaction if drug readministered
 a maculopapular rash that blisters and peels should be considered Stevens-Johnson syndrome and patient should be
labeled “allergic”
Important information to obtain from patient who claims allergy to drug (the most important information to get is in bold):
 name of drug
 reason patient was taking drug
 complete description of physical symptoms of reaction (DISCERN - Distribution, Itchiness, Shape, Colour, Elevation,
Running together (confluency), Number). Conduct physical assessment if ADR currently in progress.
 timing of reaction with regard to administration of drug
 "How many days into therapy were you when this reaction occurred?" “What was the length of time between
ingestion of the most recent dose of the drug and your detection of the reaction?”
 “How many times had you previously taken this drug?” (this is important - if the patient has received the suspected
drug 2-3 times in the past and nothing happened, you should be less than enthusiastic about labeling the patient as
allergic)
 amount of drug taken
 concomitant disease state(s) Be particularly interested in diagnosis of mononucleosis around the time of drug ingestion –
reaction between penicillin-type drug and Epstein-Barr virus causes a rash ≈80% of the time; has also been reported with
cephalexin)
 name of other drugs that patient took around the same time reaction occurred
 occurrence of same reaction when other medications in the same drug class administered
 any non-drug allergies that occur; family or personal history of asthma or other allergies
Cross-sensitivity of drugs
 between penicillins: reasonable cross-sensitivity; consider skin-testing with expired pen G, ampicillin, cefazolin, saline
control: skin tests have 70% sensitivity and 95% specificity; if positive skin test, avoid penicillins if skin test positive,
supervised challenge with low oral dose penicillin if skin test negative
 between cephalosporins: reasonable cross-reactivity amongst first-gen cephs, but third gen cephs have been used with
sequelae by pts with reported allergy to first-gen ceph
 between penicillins and cephalosporins: traditional number is 7-10% cross-reactivity. These numbers are based on two
poorly-done “studies” published in the ‘70s. Bottom line: there may be cross-sensitivity between the penicillin-related
drug and a cephalosporin with a similar side chain (think first-generation cephs), but cross-sensitivity approaches 0% if
the side chains of the ceph are different. This only a worry with anaphylactic reactions.
 sulfonamide antibiotics and other sulfonamides
(e.g., hydrochlorothiazide, glyburide, celecoxib): no
good evidence of cross-sensitivity
 n-4 amino group thought to be responsible for
maculopapular rashes
 in vitro evidence that 5-methyl-3-isoxazolyl
ring causes anaphylactic reaction
“All patients, regardless of allergy status, should be supervised when they take their first dose of any medication,
particularly an antibiotic.”
DERM-18
Corticosteroid Products
Product
Strength
Vehicle
Trade Name
0.05%
ointment
Diprolene
0.05%
0.05%
0.05%
ointment, cream, gel, lotion
ointment
ointment, cream
Temovate, generic
Florone, Maxiflor
Ultravate
0.1%
0.05%
0.1%
0.25%
0.05%
0.2%
0.05%
0.1%
0.5%
ointment
ointment, cream
ointment
ointment, cream
cream, ointment
cream
ointment, cream, gel, lotion
ointment, cream
ointment, cream
Cyclorcort
Diprosone
Valisone, generic
Topicort, generic
Psorcon, Florone, Maxiflor
Synalar, generic
Lidex, generic
Halog
Kenalog, Aristocort, generic
0.1%
0.05%
0.1%
0.1%
0.05%
0.025%
0.025,0.05%
0.05,0.005%
0.1%
0.2%
0.1%
0.025,0.1%
cream, gel, lotion
lotion
cream
cream
cream
ointment, cream
ointment, cream, lotion, tape
cream, ointment
ointment, cream, solution
ointment, cream
ointment, cream, lotion
ointment, cream, lotion
Cyclorcort
Diprosone
Valisone, generic
Cloderm
Topicort, generic
Synalar, generic
Cordran, generic
Cutivate
Locoid
Westcort, generic
Elocon
Kenalog, Aristocort, generic
0.05%
0.05%
0.1-0.4%
0.01%
0.5,1,2.5%
ointment, cream
cream
spray, cream
cream, solution, shampoo
ointment, cream, lotion
Aclovate
Tridesilon, generic
Decadron
Synalar, generic
generic; 0.5%, 1% OTC
very high potency—do not use
longer than 2 weeks
augmented betamethasone
diproprionate
clobetasol proprionate
diflorasone diacetate
halobetasone proprionate
high potency—switch to
medium potency when
exacerbation controlled
amcinonide
betamethasone diproprionate
betamethasone valerate
desoximetasone
diflorasone diacetate
fluocinolone acetonide
fluocinonide
halocinonide
triamcinlone acetonide
medium potency—for
moderate exacerbations
amcinonide
betamethasone diproprionate
betamethaseon valerate
clocortolone pivalate
desoximetasone
fluocinolone acetonide
fluradrenolide
fluticasone proprionate
hydrocortisone butyrate
hydrocortisone valerate
mometasone furoate
triamcinolone acetonide
low potency—for chronic use in
adults and children and on thin
skin
alclometasone diproprionate
desonide
desametasone (and NaP salt)
fluocinolone acetonide
hydrocortisone (plain and acetate)
DERM-19