2018 MOAPA Primary Care Update Conference

Susan T. Voss DNP, FNP-BC, DCNP, FAANPRiverside Dermatology

ATOPIC DERMATITIS & ITCH

DISCLOSURES

This speaker has no disclosures to declare

OBJECTIVES

Atopic Dermatitis

▪ Describe the pathophysiology of AD▪ Discuss the presentation and

diagnostic workup▪ Present treatment options

Itch/Pruritus

▪ Define itch/pruritus▪ Describe the pathophysiology of

itch▪ List/Describe the etiological

classifications of chronic pruritus▪ Present an algorithm for

assessment of itch▪ Discuss pharmacologic and

nonpharmacologic treatment options

ATOPIC DERMATITIS

▪Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disease of unknown origin▪Commonly referred to as eczema▪Usually starts in early infancy. ▪ In US impacts 10-12% of children

▪Affects a substantial number of adults. ▪ In US 0.9%

▪AD is commonly associated with elevated levels of immunoglobulin E (IgE).

ATOPIC DERMATITIS: PATHOPHYSIOLOGY

▪Atopic dermatitis arises because of a complex interaction of genetic and environmental factors. ▪These include defects in skin barrier function making the skin more susceptible to irritation by soap and other contact irritants, the weather, temperature and non-specific triggers.

ATOPIC DERMATITIS: PATHOPHYSIOLOGY

Two main hypotheses have been proposed regarding the development of inflammation that leads to AD. ▪The first suggests a primary immune dysfunction resulting in

IgE sensitization, allergic inflammation, and a secondary epithelial barrier disturbance. ▪The second proposes a primary defect in the epithelial barrier

leading to secondary immunologic dysregulation and resulting in inflammation.

ATOPIC DERMATITIS: PATHOPHYSIOLOGY

▪The fact that AD is the first disease to present in a series of allergic diseases—including food allergy, asthma, and allergic rhinitis, in order—has given rise to the “atopic march” theory, which suggests that AD is part of a progression that may lead to subsequent allergic disease at other epithelial barrier surfaces. 

ATOPIC DERMATITIS: STAGES▪ THREE STAGES▪ Infantile ▪ 2 months to 2 years of age

▪ Childhood ▪ 2 to 10 years

▪ Adolescent/Adult ▪ >10 years

In all stages, pruritus is the hallmark. Itching often precedes the appearance of lesions; hence the concept that AD is “the itch that rashes”

ATOPIC DERMATITIS CLASSES OF LESIONS▪Acute▪ Intensely pruritic erythematous papules and vesicles overlying

erythematous skin; frequently associated with extensive excoriations and erosions accompanied by serous exudates

▪ Subacute▪ Erythema, excoriation, and scaling

▪Chronic▪ Thickened plaques of skin, accentuated skin markings (lichenification),

fibrotic papules (prurigo nodularis); possible coexistence of all 3 types of lesions in chronic atopic dermatitis

AD DIAGNOSTIC CRITERIA: MAJOR

• Pruritus• Typical morphology and distribution• Flexural lichenification in adults• Facial and extensor involvement in infancy

• Chronic or chronically relapsing dermatitis• Personal or family history of atopic disease• Asthma, allergic rhinitis, atopic dermatitis

MUST HAVE THREE OF THE FOLLOWING

AD DIAGNOSTIC CRITERIA: MINOR

MUST ALSO HAVE AT LEAST THREE:

▪ Xerosis

▪ Ichthyosis/hyperlinear palms/keratosis pilaris

▪ IgE reactivity (immediate skin test reactivity, RAST test positive)

▪ Elevated serum IgE

▪ Early age of onset

▪ Tendency for cutaneous infections (especially Staphylococcus aureus and herpes simplex virus)

▪ Tendency to nonspecific hand/foot dermatitis

AD DIAGNOSTIC CRITERIA: MINOR CONTINUED

▪ Nipple eczema

▪ Cheilitis

▪ Recurrent conjunctivitis

▪ Dennie–Morgan infraorbital fold

▪ Keratoconus

▪ Anterior subcapsular cataracts

▪ Orbital darkening

▪ Facial pallor/facial erythema

AD DIAGNOSTIC CRITERIA: MINOR CONTINUED

▪ Pityriasis alba

▪ Itch when sweating

▪ Intolerance to wool and lipid solvents

▪ Perifollicular accentuation

▪ Food hypersensitivity

▪ Course influenced by environmental and/or emotional factors

▪ White dermatographism or delayed blanch to cholinergic agents

ATOPIC DERMATITIS: PRESENTATION/HISTORY

▪Essential historical features to diagnose:

▪Pruritus

▪Central and most debilitating symptom of AD, incessant

▪Chronic or relapsing history of disease▪ Intermittent course with flares and remissions, often for unexplained

reasons.

ATOPIC DERMATITIS: PRESENTATION/HISTORY

▪Important historical features to supports the diagnosis:▪Early age of onset▪Atopy: Personal and/or family history▪Atopy refers to the genetic tendency to develop allergic diseases such

as allergic rhinitis, asthma, and atopic dermatitis. Atopy is typically associated with heightened immune responses to common allergens, especially inhaled allergens and food allergens.(AAAAI)

AD PRESENTATION INFANTILE▪ Infantile AD usually begins with erythema and scaling of the cheeks

AD PRESENTATION INFANTILE▪ Extend to the scalp, neck, forehead, wrists, and extensor extremities.

Exudative

AD PRESENTATION INFANTILE▪Can be more widely distributed in infants less than one year.

AD PRESENTATION CHILDHOOD▪Classic locations▪ antecubital and popliteal fossae, flexor wrists, eyelids, face, and around

the neck. ▪ Progresses from the extensor surfaces to flexor.

▪ Lesions are ▪ often lichenified, indurated plaques▪ African-American patients may have a lichenoid appearance and favor

the extensor surfaces. ▪ Intermingled with isolated, excoriated 2–4 mm papules that are

scattered more widely over the uncovered skin.▪ Severe AD with large BSA can lead to growth retardation

AD PRESENTATION CHILDHOOD▪Antecubital fossae

AD PRESENTATION CHILDHOOD▪ Popliteal Fossae

AD PRESENTATION CHILDHOOD▪Hand

AD PRESENTATION CHILDHOOD

▪ Eyelid

ADPRESENTATION CHILDHOOD▪Hyperlinear palms

AD PRESENTATION CHILDHOOD

AD PRESENTATION ADOLESCENT/ADULTADOLESCENTS▪ Eruption often involves:▪ classic antecubital and popliteal fossae▪ front and sides of the neck▪ forehead, and area around the eyes

AD PRESENTATION ADOLESCENT/ADULT

▪Neck

AD PRESENTATION ADOLESCENTS/ADULTSOLDER ADULTS ▪ Distribution is generally less characteristic▪ Localized dermatitis may be the predominant feature, especially hand,

nipple, or eyelid eczema.▪ The skin, in general, is dry and somewhat erythematous. Lichenification

and prurigo-like papules are common▪ Papular lesions tend to be dry, slightly elevated, and flat-topped.▪ Excoriated and often coalesce to form plaques. ▪ Staphylococcal colonization is nearly universal. ▪ In darker-skinned patients, the lesions are often dramatically

hyperpigmented, frequently with focal hypopigmented areas related to healed excoriations.

AD PRESENTATION ADOLESCENTS/ADULTS▪Nipple eczema

AD PRESENTATION ADOLESCENTS/ADULTS▪ Eyelid

AD PRESENTATION ADOLESCENT/ADULT▪ Secondary infection

ATOPIC DERMATITIS: ASSOCIATED FEATURES▪ Pityriasis alba

ATOPIC DERMATITIS: ASSOCIATED FEATURES

▪Dennie-Morgan fold

ATOPIC DERMATITIS: ASSOCIATED FEATURES

▪Cheilitis

ATOPIC DERMATITIS: ASSOCIATED FEATURES▪ Keratosis pilaris

ATOPIC DERMATITIS: DIAGNOSIS▪Diagnosis is often based on presentation and history of the rash

▪ If necessary a skin biopsy can be performed▪ A punch biopsy for H&E▪ Findings are often nonspecific with spongiotic dermatitis

AD: GENERAL MANAGEMENT

▪ Education and support▪ Barrier repair▪Antimicrobial therapy▪ Environmental factors▪Antipruritics

AD: GENERAL MANAGEMENT EDUCATION AND SUPPORT

EDUCATION AND SUPPORT

▪ Patient and parent education is critical!!▪Action Plan or Stepwise Approach▪ Resources▪ National Eczema Association: www.nationaleczema.org▪ National Eczema Society: www.eczema.org

▪ Emotional Support▪ AD impacts the whole family▪ Sleep deprivation▪ Burnout with treatment which can be time consuming

AD: GENERAL MANAGEMENT BARRIER REPAIR▪ TO BATHE OR NOT TO BATHE

▪ Bathing with proper moisturization is key▪ Lightly towel dry and apply moisturizer within 3-5 minutes▪ Seals in moisture and allow water to be absorbed through the stratum

corneum.▪ Lukewarm water▪Avoid fragrance and dyes▪ If child wants to “play” in the water do that first▪ After applying soap rinse and get out as soon as possible.

▪Only apply soap to armpits, genitalia, and bottom of feet.

AD: GENERAL MANAGEMENT BARRIER REPAIR

MOISTURIZE / BARRIER REPAIR

▪At least twice a day, at least once after bath/shower▪Ointment and creams preferred over lotion▪ More humectants

▪ Petrolatum▪ Vaseline, Aquaphor▪ Moist wraps

▪Ceramide based ointments▪ Cerave, Cetaphil Restoraderm, Hylatopic Plus (Rx), Eucerin

AD: GENERAL MANAGEMENT ANTIMICROBIAL THERAPY▪ Treat infections with appropriate topical or systemic antibiotic▪ Key is to decrease chance for infection by reducing nasal

staphylococcal carriage pre-emptively and keeping the skin decolonized from Staphylococcus.▪ Mupirocin ointment three times a day to each nostril one week out of

each month.▪ Bleach water tepid baths twice weekly▪½ cup standard bleach to regular size tub (40 gallons)▪ Swimming in chlorine based pool

▪ Parents may also be colonized (80%)

AD: GENERAL MANAGEMENT ENVIRONMENTAL FACTORS▪Avoid external irritants▪ Stress ▪ Heat ▪ Sweating ▪Wool

▪Avoid contact allergens▪ Products with common allergens▪ Fragrance and dyes▪Wipes with methylisothiazolinone

▪ Test for allergens when appropriate

AD: GENERAL MANAGEMENT ANTIPRURITICS▪Oral antihistamines▪ Discuss more with itch discussion

▪ Topical▪ Ice or cool compresses▪ Moisturizers containing menthol, phenol, or pramocaine.

AD: TREATMENT TOPICAL CORTICOSTEROIDS▪ Lowest potency steroid▪ Fluocinolone acetonide topical oil, 0.01% ▪ Derma-Smoothe FS Body Oil▪Mineral oil and ultra-refined peanut oil based▪ Approved down to three months of age.

AD: TREATMENT TOPICAL CORTICOSTEROIDSMid potency steroid▪ Triamcinolone 0.1% ointment (cream) twice daily.High potency steroid▪ Betamethasone dipropionate augmented 0.05% ointment twice

daily.

▪Use under moist wraps increases absorption▪Use the right size hose for the right size fire▪Caution in areas of double absorptions▪ Striae and atrophy with chronic or overuse

AD: TREATMENT TOPICAL CALCINEURIN INHIBITORS

▪ Tacrolimus (Protopic)▪0.03% twice daily in children 2-15 yo▪0.1% twice daily in 16 years and up

▪ Pimecrolimus (Elidel)▪1% twice daily ages 2 and up

Black Box Warning:Increased risk for malignancies including skin and lymphoma.Warning applied to the whole class instead of just oral.REASSURE PARENTS!!!!

AD TREATMENT

▪Crisaborale ointment 2% (Eucrisa)▪ PDE 4 inhibitor▪ Apply twice daily ages 2 years and older

▪ Phototherapy▪ Narrow band UVB three times weekly▪ Challenging for patients to make it that often

AD TREATMENT SYSTEMIC ▪ Systemic Treatments▪Oral steroids▪ Limit use to only acute exacerbations▪ Three weeks or less▪Osteoporosis

▪ Immunosuppresants ▪ Cyclosporine▪ Azathioprine▪Mycophenolate mofetil▪Methotrexate

AD TREATMENT

▪Dupilumab (Dupixent)▪ Interleukin 4/13 antagonist▪ 300 mg SC every 2 weeks

▪Don’t be afraid to refer to dermatology.

AD TREATMENT PLANS

* Advise patients if normal treatments not working think infection

GREEN LIGHTStable

Day to day management

Moisturizers

Avoiding irritants etc.

YELLOW LIGHTBeginning to flare

Add TCIs orCrisaborale

Low potency steroids if needed

RED LIGHTExacerbated

Higher potency steroids

Seek treatment for systemic options if not improving

CONCLUSION ATOPIC DERMATITIS▪Atopic dermatitis is a chronic itchy conditions with

exacerbations.▪Often is the beginning of the “atopic march”.▪ Impact of AD can be extreme and impact the entire family▪Management should be based on stage of lesions▪Patients and family need education and emotional support.▪Referral for severe cases is important

SHAMELESS PLUG

SHAMELESS PLUG DEFINITION OF ITCH

▪An unpleasant sensation of the skin leading to the desire to scratch

ITCH

Acute

•Less than six weeks in duration

Chronic

•Greater than six weeks in duration

PATHOPHYSIOLOGY OF ITCH

▪Complex and Multifactorial▪Skin does not contain dedicated receptors for itch.▪Itch transmitted through unmyelinated C fibers just as pain.▪Keratinocytes release a variety of mediators in response to the pruritic stimuli.▪Neurons may be located more superficially and are more sensitive to pruritogenic substances than pain receptors.

PATHOPHYSIOLOGY OF ITCH ACTIVATORS OF THE NEURONS

▪Histamines▪Cytokines▪ Leukotrienes▪Opioids▪ Kinins▪ Prostaglandins

▪Neuropeptide Substance P▪ Serotonin▪ Proteases ▪ mast cell tryptase

▪ Endothelin▪ Stimulates release nitric oxide

IMPACT OF ITCH

▪No matter the cause of the itch it can be disabling both physically and emotionally.▪Chronic itch as bad as chronic pain.▪Impacts not only the patient but the entire family.▪Loss of sleep and work time▪Stress to patient and family that treatment and diagnosis is a process.

DISEASES ASSOCIATED WITH PRURITUS: DERMATOLOGIC

• Atopic dermatitis, psoriasis, contact dermatitis, dry skin, drug reactions, scars, “invisible dermatoses”

Inflammatory dermatoses

• Mycotic, bacterial and viral infections and folliculitis, scabies, pediculosis, arthropod reactions, insect bites

Infectious dermatoses

DISEASES ASSOCIATED WITH PRURITUS: DERMATOLOGIC

• Bullous dermatoses, dermatitis herpetiformis, bullous pemphigoid, dermatomyositis

Autoimmune dermatoses

• Darier’s disease, Hailey-Hailey disease, ichthyoses, Sjögren-Larsson syndrome, epidermal bullosa pruriginosa

Genodermatoses

DISEASES ASSOCIATED WITH PRURITUS: DERMATOLOGIC

•Polymorphic eruption of pregnancy, pemphigoid gestationis, prurigo gestationis

Dermatoses of pregnancy

•Cutaneous T-cell-lymphoma, cutaneous B-cell lymphoma, leukemic infiltrates of the skin

Neoplasms

DISEASES ASSOCIATED WITH PRURITUS:SYSTEMIC DISEASE

• Chronic renal failure, liver diseases with or without cholestasis, hyperthyroid, hypothyroid, malabsorption, perimenopausal pruritus

Endocrine and metabolic

• HIV infection, helminthiasis, parasitosisInfectious

DISEASES ASSOCIATED WITH PRURITUS:SYSTEMIC DISEASE

• Iron deficiency, polycythemia vera, Hodgkin disease, Non-Hodgkin lymphoma, plasmocytoma

Hematologic and Lymphoproliferative

• Solid tumors of the cervix, prostate, or colon, carcinoid syndromeVisceral

• Pruritus gravidarum with and without cholestasisPregnancy

DISEASES ASSOCIATED WITH PRURITUS: SYSTEMIC DISEASE : DRUG ASSOCIATED

Common Drugs▪Opioids▪ACE Inhibitors▪Amiodarone▪Hydrochlorothiazide▪Estrogens▪Statins▪Hydroxyethyl starch▪Allopurinol

DISEASES ASSOCIATED WITH PRURITUS NEUROLOGIC AND PSYCHIATRIC

• Multiple sclerosis, neoplasms, abscesses, cerebral or spinal infarcts, brachioradial pruritus, nostalgia parastethica, postherpetic neuralgia, vulvodynia, small fiber neuropathy

Neuropathic

• Psychiatric/psychosomatic diseases, depression, anxiety disorders, obsessive-compulsive disorders, schizophrenia, tactile hallucinosis, fatigue

Somatoform

Pruritus

HH&P, ROS

+ ROS

Primary Skin

Lesion

Distinguish Primary & Secondary Lesions

WorkupAs

Indicated

Generalized Pruritus with undetermined

origin

Localized:•Consider biopsy•Consider dermatologic conditionGeneralized:•Consider dermatologic cause•Drug eruption•Atopic Dermatitis•Scabies•Lichen Planus•Etc

Yes No

PRURITUS

CONSIDERATION FROM HISTORY TO DETERMINE CAUSE OF ITCH▪ Itch With or Without Skin Lesions?▪ Primary or secondary itch lesion? Distribution? Morphology?▪Alloknesis? (itch produced by innocuous mech stim)▪Dermatographism: White? Red? Urticarial?▪Quality and quantity (on a scale from 0 to 10) of the itch?▪ Impact on the quality of life?▪Allergies (subtype?)▪Medications?

CONSIDERATION FROM HISTORY TO DETERMINE CAUSE OF ITCH

▪Age : Xerosis? Neuropathy? Neurodegeneration? Metabolic? Cancer? Infection? Immunosuppression?▪Trigger factors: Temp changes? Water? Chemicals? Haptens? Medication?▪Signs for systemic cause: anemia, cholestasis, jaundice, wt. loss, signs for neoplasia or paraneoplastic syndrome, nerve compression, neurological symptoms, signs of psychiatric disease▪One or more causes likely? ▪ Adapted from: Steinhoff, M., Cevikbas, F., Ikoma, A., & G, B. T. (2011). Pruritus: Management algorithms

and experimental therpaies. Seminars in Cutaneous Medicine and Surgery, 30

Pruritus

HH&P, ROS

+ ROS

Primary Skin

Lesion

Distinguish Primary & Secondary Lesions

WorkupAs

Indicated

Generalized Pruritus with undetermined

origin

Localized:•Consider biopsy•Consider dermatologic conditionGeneralized:•Consider dermatologic cause•Drug eruption•Atopic Dermatitis•Scabies•Lichen Planus•Etc

Yes No

PRURITUSGeneralized pruritus with undetermined origin

Skin CareTopical: coolants, anesthetics, corticosteroids, calcineurin inhibitors, and doxepinOral: antihistaminesContinue good skin

care. Taper antihistamines.Followup 2-4 wks

Improved

SystemicRenal DiseaseCholestasisHematologic DiseaseEndocrine DisorderLymphoreticular MalignancySolid Organ TumorPolycythemia VeraAquagenic ItchPruritus of senescence

PsychogenicDelusions of ParasitosisSubstance AbuseOCDDepressionFibromyalgiaAnorexia Nervosa

NeurogenicBrachioradialNotalgia parestheticaPHNPost CVAMultiple Sclerosis

No Improvement: Consider underlying cause

Initial Workup•Detailed drug history•Complete Blood Count•Creatinine and BUN•Liver function tests•TSH, free T4•Erythrocyte sedimentation rate•HIV Screening•Chest radiography•Fecal occult•Age appropriate cancer screenings•Other test based on ROS

Periodic re-evaluation (every 4-6 wks, change of season)•H&P, ROSConsider additional diagnostics:•Hepatitis B&C, Stool for O&P, Ferritin, Imaging (CT chest & abdomen)Consider 2nd and 3rd line therapies

Diagnostic Indications of a Systemic Disease•Complete evaluation to confirm underlying disease or illness•Treatment of underlying condition

AbnormalFindings

Normal Findings

TREATMENT FOR PRURITUS WITHOUT RASH: FIRST LINE TOPICAL THERAPIES▪Good Skin Care▪ Emollients- petrolatum, ceramide-based creams▪ Topical anti-inflammatory▪ Corticosteroids, calcineurin inhibitors

▪Cooling agents▪ Menthol, camphor, ice

▪ Topical anesthetics▪ Capsaicin, pramoxine, lidocaine/prilocaine

▪ Predominantly nerve modulation▪ Doxepin

TREATMENT FOR PRURITUS SYSTEMIC: ANTIHISTAMINES (AH)

▪Low dose▪Nonsedating AH daily▪Cetirizine, levocetirizine, fexofenadine, loratidine, desloratidine

▪High dose▪Nonsedating AH, BID to QID, or combination with sedating AH at bedtime▪Hydroxyzine, diphenhydramine, cyproheptadine

TREATMENT FOR PRURITUS OTHER SYSTEMIC AGENTS

▪First Level▪Systemic Glucocorticoids▪Gabapentin▪Pregabalin▪Selective serotonin reuptake inhibitors (SSRI)▪Especially for paraneoplastic, polycythemia vera, or depression

▪Naltrexone▪Especially for renal or liver dysfunction

TREATMENT FOR PRURITUS: OTHER SYSTEMIC AGENTS

▪ Second Level▪ SSRI▪ Mirtazapine▪ Tricyclic and tetracyclic antidepressants▪ Phototherapy: Narrow Band UVB

▪ Third Level▪ Naltrexone*▪ Lidocaine 5% patch

▪ Fourth Level▪ IVIG▪ Extracorporal Photophoresis

CONCLUSION: ITCH

▪Itch can be acute or chronic▪The pathophysiology is complex and multifactorial▪Impact of itch can be extreme and impact the entire family▪There are numerous etiologies for itch▪Diagnosing and treating itch is a process

THANK YOU!! CASE # 1, “C.O.”

▪ 76 year old Caucasian female. ▪ Presents with diffuse itching and mildly

erythematous papular rash on her trunk. Worse underneath the bra area and waist band.▪ Scratching during appointment. Scratching

makes it feel better, briefly.▪Onset two weeks prior. Progressively

getting worse.

CASE # 1, “C.O.”▪Denies anything new over the last two months, medications or products.▪No obvious aggravating factors.▪No relieving factors.▪Keeps her awake at night.▪MISERABLE

CASE # 1, “C.O.”

Treated for allergic contact dermatitis.▪Medications▪Levocetirizine 5 mg in am▪Fexofenadine 180 mg in the afternoon.▪Hydroxyzine 10 mg, i, ii, or iii at HS▪Triamcinolone 0.1 % ointment BID to affected areas, leaving small area untreated for possible biopsy.

CASE # 1, “C.O.”

▪Other measures▪Elimination of all dyes and fragrances▪Laundry detergent, fabric softener, cleansers, moisturizers, shampoo, etc.

▪Topical emollient twice daily ▪Ceramide based, dye and fragrance free.▪Avoid hot showers, scratching, etc.

CASE # 1, “C.O.”

Two Week Followup▪Mild improvement. ▪Rash slightly improved, itch still present. ▪Husband present now.▪“Something has got to be done!”▪Triamcinolone changed to clobetasol▪Punch biopsy performed.

CASE # 1, “C.O.”

▪Pathology Results▪ Acute Spongiotic Dermatitis▪ Most probably allergic contact dermatitis.

▪Patch Test Allergies▪ Nickel, Paraben mix, Mercapto mix, thimerosol, Gold sodium thiosulfate,

disperse blue

▪Discussed avoidance▪Labs all WNL▪To use pimecrolimus cream BID prn

CASE # 1, “C.O.”▪ Follow up in 3 months and was still doing well.▪ 6 months later presents with itching of entire upper body for one

week duration, miserable again.▪ Started Narrow band UVB three times weekly.▪ Improved for 6 months▪ Biopsy for H&E and DIF▪ Superficial perivascular dermatitis▪ Positive Direct Immunofluorescense consistent with bullous pemphigoid

CASE # 1, “C.O.”

▪Treatment▪Prednisone Taper▪Doxycycline 100mg bid▪Niacinamide 500mg tid▪Mycophenolate mofetil (CellCept) 500mg daily, increased to BID. (Max 1 gram bid)

▪Patient has had lab monitoring and has been doing quite well.

CASE #2 “J.C.”

▪35 yo female▪Presents with rash and itch in popliteal area bilateral and lower legs.▪Duration 5 to 10 years▪Biopsy performed: possible psoriasis▪Histology proven psoriasiform dermatitis with eosinophils: most likely contact dermatitis▪Features of lichen simplex chronicus

CASE #2 “J.C.”

▪T.R.U.E Test Patch Testing▪Disperse Blue▪Immunocap ▪Region 8 (Central Midwest, MO, IL, IA)▪Multiple moderate to highly allergic ▪Food▪None▪IgE elevated

CASE #2 “J.C.”

▪ Started ▪ cetirizine 10 mg twice daily ▪ hydroxyzine 10mg, i,ii, or iii at HS

▪ Referred to Allergist▪Did not follow up UNTIL 2 ½ years later.▪ Still itching and legs lichenified from scratching

▪Had not seen the allergist.▪Discussed proper skin care, restart the antihistamines and topical

steroids, reinforced need for allergist.▪ Follow up pending

CASE #3 “D.B.”

▪ 84 yo female▪ Rash on and off for ten years.▪ Located on trunk, arms, legs, feet▪ Erythematous inflammatory papules with excoriations

▪ Prior treatment camphor/menthol/triamcinolone/aqua/lact compounded lotion with temporary relief.▪Dial soap▪No new drugs or products

CASE #3 “D.B.”

▪ Elimination of dyes and fragrance▪ Proper skin care▪OTC anti-itch lotions and cleansers▪ Levocetirizine 5mg in am▪ Fexofenadine 180 mg in afternoon▪Hydroxyzine 10, i,ii, or ii @ HS▪ T.R.U.E. Test in 2 weeks when skin calmed, too flared today▪CBC and CMP all WNL

CASE #3 “D.B.”

▪ T.R.U.E Test all negative▪ Rash resolved▪ Itch improved for now▪Did well for 6 months then itch returned without the rash.▪ TSH, free T4, ANA all WNL▪Narrow band UVB three times weekly▪ Patient was improving slowly but sadly suffered a CVA, required long

term care. Husband reports since CVA no itch.

REFERENCES

▪ Reich, A., Stander, S., & Szepietowski, J. C. (2009). Drug-induced pruritus: A review. Acta Dermato Venereologica, 89, 236-244. doi: 10.2340/00015555-0650▪ Stander, S., Weisshaar, E., Mettang, T., Szepietowski, J. C., Carstens, E.,

Ikoma, A., et al. (2007). Clinical classification of itch: A position paper of the International Forum for the Study of Itch. Acta Dermato-Vernereologica, 87, 291-294. ▪ Steinhoff, M., Cevikbas, F., Ikoma, A., & G, B. T. (2011). Pruritus:

Management algorithms and experimental therpaies. Seminars in Cutaneous Medicine and Surgery, 30, 127-137.