voss atopic dermatitis and itch atopic dermatitis and itch.pdf · 2018 moapa primary care update...
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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.