DISCLOSURES
2018 MOAPA Primary Care Update Conference ATOPIC This speaker has no disclosures to Susan T. Voss DNP, DERMATITIS declare FNP-BC, DCNP, FAANP & ITCH Riverside Dermatology
OBJECTIVES ATOPIC DERMATITIS
Atopic Dermatitis Itch/Pruritus ▪ Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disease of unknown origin ▪ Describe the pathophysiology of ▪ Define itch/pruritus ▪ Commonly referred to as eczema AD ▪ Describe the pathophysiology of ▪ Usually starts in early infancy. ▪ Discuss the presentation and itch ▪ In US impacts 10-12% of children diagnostic workup ▪ List/Describe the etiological ▪ Present treatment options classifications of chronic pruritus ▪ Affects a substantial number of adults. ▪ In US 0.9% ▪ Present an algorithm for assessment of itch ▪ AD is commonly associated with elevated levels of immunoglobulin ▪ Discuss pharmacologic and E (IgE). nonpharmacologic treatment options ATOPIC DERMATITIS: ATOPIC DERMATITIS: PATHOPHYSIOLOGY PATHOPHYSIOLOGY
▪Atopic dermatitis arises because of a complex Two main hypotheses have been proposed regarding the interaction of genetic and environmental development of inflammation that leads to AD. factors. ▪The first suggests a primary immune dysfunction resulting in IgE sensitization, allergic inflammation, and a secondary ▪These include defects in skin barrier function epithelial barrier disturbance. making the skin more susceptible to irritation ▪The second proposes a primary defect in the epithelial barrier by soap and other contact irritants, the leading to secondary immunologic dysregulation and resulting in inflammation. weather, temperature and non-specific triggers.
ATOPIC DERMATITIS: ATOPIC DERMATITIS: PATHOPHYSIOLOGY STAGES
▪The fact that AD is the first disease to present in a ▪ THREE STAGES series of allergic diseases—including food allergy, ▪ Infantile ▪ 2 months to 2 years of age asthma, and allergic rhinitis, in order—has given rise ▪ Childhood to the “atopic march” theory, which suggests that AD ▪ 2 to 10 years is part of a progression that may lead to subsequent ▪ Adolescent/Adult allergic disease at other epithelial barrier surfaces. ▪ >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 AD DIAGNOSTIC CRITERIA: CLASSES OF LESIONS MAJOR
▪ Acute ▪ Intensely pruritic erythematous papules and vesicles overlying erythematous skin; frequently associated with extensive excoriations and MUST HAVE THREE OF THE FOLLOWING erosions accompanied by serous exudates • Pruritus ▪ Subacute • Typical morphology and distribution ▪ Erythema, excoriation, and scaling • Flexural lichenification in adults ▪ Chronic • Facial and extensor involvement in infancy ▪ Thickened plaques of skin, accentuated skin markings (lichenification), • Chronic or chronically relapsing dermatitis fibrotic papules (prurigo nodularis); possible coexistence of all 3 types of • Personal or family history of atopic disease lesions in chronic atopic dermatitis • Asthma, allergic rhinitis, atopic dermatitis
MUST ALSO HAVE AT LEAST THREE: ▪ Xerosis ▪ Nipple eczema ▪ Ichthyosis/hyperlinear palms/keratosis pilaris ▪ Cheilitis ▪ IgE reactivity (immediate skin test reactivity, AD ▪ Recurrent conjunctivitis AD RAST test positive) DIAGNOSTIC ▪ Dennie–Morgan infraorbital fold DIAGNOSTIC ▪ Elevated serum IgE CRITERIA: ▪ Keratoconus CRITERIA: ▪ Early age of onset MINOR ▪ Anterior subcapsular cataracts ▪ Tendency for cutaneous infections MINOR Orbital darkening (especially Staphylococcus aureus and herpes CONTINUED ▪ simplex virus) ▪ Facial pallor/facial erythema ▪ Tendency to nonspecific hand/foot dermatitis ATOPIC DERMATITIS: PRESENTATION/HISTORY
▪ Pityriasis alba ▪ Itch when sweating ▪Essential historical features to diagnose: ▪ Intolerance to wool and lipid solvents AD ▪Pruritus DIAGNOSTIC ▪ Perifollicular accentuation CRITERIA: ▪ Food hypersensitivity ▪ Central and most debilitating symptom of AD, incessant ▪ Course influenced by environmental and/or MINOR emotional factors ▪Chronic or relapsing history of disease CONTINUED ▪ White dermatographism or delayed blanch to cholinergic agents ▪ Intermittent course with flares and remissions, often for unexplained reasons.
ATOPIC DERMATITIS: AD PRESENTATION PRESENTATION/HISTORY INFANTILE
▪Important historical features to supports the ▪ Infantile AD usually begins with erythema and scaling of the cheeks 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 AD PRESENTATION INFANTILE INFANTILE
▪ Extend to the scalp, neck, forehead, wrists, and extensor extremities. ▪ Can be more widely distributed in infants less than one year. Exudative
AD PRESENTATION AD PRESENTATION CHILDHOOD CHILDHOOD
▪ Classic locations ▪ Antecubital fossae ▪ 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 AD PRESENTATION CHILDHOOD CHILDHOOD
▪ Popliteal Fossae ▪Hand
AD ADPRESENTATION PRESENTATION CHILDHOOD CHILDHOOD
▪ Eyelid ▪ Hyperlinear palms AD PRESENTATION AD PRESENTATION CHILDHOOD ADOLESCENT/ADULT
ADOLESCENTS ▪ Eruption often involves: ▪ classic antecubital and popliteal fossae ▪ front and sides of the neck ▪ forehead, and area around the eyes
AD PRESENTATION AD PRESENTATION ADOLESCENT/ADULT ADOLESCENTS/ADULTS
▪ Neck OLDER 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 AD PRESENTATION ADOLESCENTS/ADULTS ADOLESCENTS/ADULTS
▪ Nipple eczema ▪ Eyelid
AD PRESENTATION ATOPIC DERMATITIS: ADOLESCENT/ADULT ASSOCIATED FEATURES
▪ Secondary infection ▪ Pityriasis alba ATOPIC ATOPIC DERMATITIS: DERMATITIS: ASSOCIATED ASSOCIATED FEATURES FEATURES
▪ Dennie-Morgan fold ▪ Cheilitis
ATOPIC DERMATITIS: ATOPIC DERMATITIS: ASSOCIATED FEATURES DIAGNOSIS
▪ Keratosis pilaris ▪ 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 AD: GENERAL MANAGEMENT EDUCATION AND SUPPORT
▪ Education and support EDUCATION AND SUPPORT ▪ Barrier repair ▪ Patient and parent education is critical!! ▪ Antimicrobial therapy ▪ Action Plan or Stepwise Approach ▪ Environmental factors ▪ Resources ▪ National Eczema Association: www.nationaleczema.org ▪ Antipruritics ▪ 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 AD: GENERAL MANAGEMENT BARRIER REPAIR BARRIER REPAIR
▪ TO BATHE OR NOT TO BATHE MOISTURIZE / BARRIER REPAIR ▪ Bathing with proper moisturization is key ▪ At least twice a day, at least once after bath/shower ▪ Lightly towel dry and apply moisturizer within 3-5 minutes ▪ Ointment and creams preferred over lotion Seals in moisture and allow water to be absorbed through the stratum ▪ ▪ More humectants corneum. ▪ ▪ Lukewarm water Petrolatum ▪ Vaseline, Aquaphor ▪ Avoid fragrance and dyes ▪ Moist wraps ▪ If child wants to “play” in the water do that first ▪ Ceramide based ointments ▪ After applying soap rinse and get out as soon as possible. ▪ Cerave, Cetaphil Restoraderm, Hylatopic Plus (Rx), Eucerin ▪ Only apply soap to armpits, genitalia, and bottom of feet. AD: GENERAL MANAGEMENT AD: GENERAL MANAGEMENT ANTIMICROBIAL THERAPY ENVIRONMENTAL FACTORS
▪ Treat infections with appropriate topical or systemic antibiotic ▪ Avoid external irritants Stress ▪ Key is to decrease chance for infection by reducing nasal ▪ staphylococcal carriage pre-emptively and keeping the skin ▪ Heat decolonized from Staphylococcus. ▪ Sweating ▪ Mupirocin ointment three times a day to each nostril one week out of ▪ Wool each month. ▪ Avoid contact allergens ▪ Bleach water tepid baths twice weekly ▪ Products with common allergens ▪ ½ cup standard bleach to regular size tub (40 gallons) ▪ Fragrance and dyes ▪ Swimming in chlorine based pool ▪ Wipes with methylisothiazolinone ▪ Parents may also be colonized (80%) ▪ Test for allergens when appropriate
AD: GENERAL MANAGEMENT AD: TREATMENT ANTIPRURITICS TOPICAL CORTICOSTEROIDS
▪ Oral antihistamines ▪ Lowest potency steroid ▪ Discuss more with itch discussion ▪ Fluocinolone acetonide topical oil, 0.01% ▪ Topical ▪ Derma-Smoothe FS Body Oil ▪ Ice or cool compresses ▪ Mineral oil and ultra-refined peanut oil based ▪ Moisturizers containing menthol, phenol, or pramocaine. ▪ Approved down to three months of age. AD: TREATMENT AD: TREATMENT TOPICAL CORTICOSTEROIDS TOPICAL CALCINEURIN INHIBITORS
Mid potency steroid ▪ Tacrolimus (Protopic) ▪ Triamcinolone 0.1% ointment (cream) twice daily. ▪ 0.03% twice daily in children 2-15 yo ▪ 0.1% twice daily in 16 years and up High potency steroid ▪ ▪ Betamethasone dipropionate augmented 0.05% ointment twice Pimecrolimus (Elidel) daily. ▪ 1% twice daily ages 2 and up
Black Box Warning: ▪ Use under moist wraps increases absorption Increased risk for malignancies including skin and lymphoma. ▪ Use the right size hose for the right size fire Warning applied to the whole class instead of just oral. REASSURE PARENTS!!!! ▪ Caution in areas of double absorptions ▪ Striae and atrophy with chronic or overuse
AD TREATMENT AD TREATMENT SYSTEMIC
▪ Crisaborale ointment 2% (Eucrisa) ▪ Systemic Treatments ▪ PDE 4 inhibitor ▪ Oral steroids ▪ Apply twice daily ages 2 years and older ▪ Limit use to only acute exacerbations ▪ Three weeks or less ▪ Osteoporosis ▪ Phototherapy ▪ Immunosuppresants ▪ Narrow band UVB three times weekly ▪ Cyclosporine ▪ Challenging for patients to make it that often ▪ Azathioprine ▪ Mycophenolate mofetil ▪ Methotrexate AD TREATMENT AD TREATMENT PLANS
▪ Dupilumab (Dupixent) ▪ Interleukin 4/13 antagonist ▪ 300 mg SC every 2 weeks GREEN LIGHT YELLOW LIGHT RED LIGHT Stable Beginning to flare Exacerbated
▪ Don’t be afraid to refer to dermatology. Day to day Add TCIs or Higher potency management Crisaborale steroids
Moisturizers Low potency Seek treatment for steroids if needed systemic options if Avoiding irritants not improving etc.
* Advise patients if normal treatments not working think infection
CONCLUSION ATOPIC DERMATITIS SHAMELESS PLUG
▪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 DEFINITION OF ITCH
▪An unpleasant sensation of the skin leading to the desire to scratch
ITCH PATHOPHYSIOLOGY OF ITCH
▪Complex and Multifactorial ▪Skin does not contain dedicated receptors for itch. Acute Chronic ▪Itch transmitted through unmyelinated C fibers just as pain. ▪Keratinocytes release a variety of mediators in •Less than six •Greater than response to the pruritic stimuli. ▪Neurons may be located more superficially and are weeks in six weeks in more sensitive to pruritogenic substances than pain duration duration receptors. PATHOPHYSIOLOGY OF ITCH IMPACT OF ITCH ACTIVATORS OF THE NEURONS ▪No matter the cause of the itch it can be ▪ Histamines ▪ Neuropeptide Substance P disabling both physically and emotionally. ▪ Cytokines ▪ Serotonin ▪Chronic itch as bad as chronic pain. ▪ Leukotrienes ▪ Proteases ▪Impacts not only the patient but the entire ▪ mast cell tryptase ▪ Opioids family. ▪ Endothelin ▪ Kinins ▪ Stimulates release nitric oxide ▪Loss of sleep and work time ▪ Prostaglandins ▪Stress to patient and family that treatment and diagnosis is a process.
DISEASES ASSOCIATED WITH DISEASES ASSOCIATED WITH PRURITUS: DERMATOLOGIC PRURITUS: DERMATOLOGIC
Inflammatory • Atopic dermatitis, psoriasis, contact • Bullous dermatoses, dermatitis dermatitis, dry skin, drug reactions, scars, Autoimmune herpetiformis, bullous pemphigoid, dermatoses “invisible dermatoses” dermatoses dermatomyositis
• Mycotic, bacterial and viral infections and • Darier’s disease, Hailey-Hailey disease, Infectious folliculitis, scabies, pediculosis, arthropod Genodermatoses ichthyoses, Sjögren-Larsson syndrome, dermatoses reactions, insect bites epidermal bullosa pruriginosa DISEASES ASSOCIATED WITH DISEASES ASSOCIATED WITH PRURITUS: PRURITUS: DERMATOLOGIC SYSTEMIC DISEASE
•Polymorphic eruption of • Chronic renal failure, liver diseases with or Dermatoses Endocrine and without cholestasis, hyperthyroid, pregnancy, pemphigoid gestationis, hypothyroid, malabsorption, of pregnancy prurigo gestationis metabolic perimenopausal pruritus
•Cutaneous T-cell-lymphoma, Neoplasms cutaneous B-cell lymphoma, Infectious • HIV infection, helminthiasis, parasitosis leukemic infiltrates of the skin
DISEASES ASSOCIATED WITH DISEASES ASSOCIATED WITH PRURITUS: PRURITUS: SYSTEMIC DISEASE : DRUG ASSOCIATED SYSTEMIC DISEASE
Common Drugs ▪ Opioids Hematologic and • Iron deficiency, polycythemia vera, Hodgkin disease, ▪ ACE Inhibitors Lymphoproliferative Non-Hodgkin lymphoma, plasmocytoma ▪ Amiodarone ▪ Hydrochlorothiazide ▪ Estrogens Visceral • Solid tumors of the cervix, prostate, or colon, ▪ Statins carcinoid syndrome ▪ Hydroxyethyl starch ▪ Allopurinol
Pregnancy • Pruritus gravidarum with and without cholestasis DISEASES ASSOCIATED WITH PRURITUS PRURITUS Workup Pruritus NEUROLOGIC AND PSYCHIATRIC As Indicated + ROS H&P,H ROS
Localized: Generalized • Multiple sclerosis, neoplasms, abscesses, cerebral Yes No or spinal infarcts, brachioradial pruritus, nostalgia •Consider biopsy Pruritus with Neuropathic parastethica, postherpetic neuralgia, vulvodynia, •Consider Primary small fiber neuropathy dermatologic Skin undetermined Lesion condition origin Generalized: •Consider • Psychiatric/psychosomatic diseases, depression, dermatologic cause anxiety disorders, obsessive-compulsive •Drug eruption Somatoform • disorders, schizophrenia, tactile hallucinosis, Atopic Dermatitis Distinguish fatigue •Scabies Primary & •Lichen Planus Secondary • Etc Lesions
CONSIDERATION FROM HISTORY CONSIDERATION FROM HISTORY TO TO DETERMINE CAUSE OF ITCH DETERMINE CAUSE OF ITCH
▪ Itch With or Without Skin Lesions? ▪Age : Xerosis? Neuropathy? Neurodegeneration? ▪ Primary or secondary itch lesion? Distribution? Morphology? Metabolic? Cancer? Infection? Immunosuppression? ▪ Alloknesis? (itch produced by innocuous mech stim) ▪Trigger factors: Temp changes? Water? Chemicals? ▪ Dermatographism: White? Red? Urticarial? Haptens? Medication? ▪ Quality and quantity (on a scale from 0 to 10) of the itch? ▪Signs for systemic cause: anemia, cholestasis, jaundice, wt. ▪ Impact on the quality of life? loss, signs for neoplasia or paraneoplastic syndrome, nerve ▪ compression, neurological symptoms, signs of psychiatric Allergies (subtype?) disease ▪ Medications? ▪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 Generalized pruritus with undetermined origin PRURITUS Workup Pruritus As Skin Care Improved Indicated + ROS Topical: coolants, anesthetics, corticosteroids, calcineurin inhibitors, and doxepin H&P,H ROS Continue good skin Oral: antihistamines care. Taper Localized: Generalized antihistamines. No Improvement: Consider underlying cause •Consider biopsy Yes No Followup 2-4 wks •Consider Primary Pruritus with dermatologic Skin Systemic Psychogenic undetermined Delusions of Parasitosis condition Lesion Renal Disease origin Cholestasis Substance Abuse Generalized: Hematologic Disease OCD •Consider Endocrine Disorder Depression dermatologic cause Lymphoreticular Malignancy Fibromyalgia •Drug eruption Solid Organ Tumor Anorexia Nervosa • Polycythemia Vera Neurogenic Atopic Dermatitis Distinguish •Scabies Aquagenic Itch Brachioradial Primary & •Lichen Planus Pruritus of senescence Notalgia paresthetica Secondary •Etc PHN Lesions Post CVA Multiple Sclerosis
Initial Workup Diagnostic Indications TREATMENT FOR PRURITUS •Detailed drug history of a Systemic Disease •Complete Blood Count •Complete evaluation WITHOUT RASH: FIRST LINE TOPICAL •Creatinine and BUN to confirm underlying THERAPIES •Liver function tests disease or illness •TSH, free T4 Abnormal •Treatment of •Erythrocyte sedimentation rate Findings underlying condition ▪ Good Skin Care •HIV Screening •Chest radiography ▪ Emollients- petrolatum, ceramide-based creams •Fecal occult Topical anti-inflammatory •Age appropriate cancer screenings ▪ ▪ Corticosteroids, calcineurin inhibitors •Other test based on ROS ▪ Cooling agents ▪ Menthol, camphor, ice Normal Findings ▪ Topical anesthetics ▪ Capsaicin, pramoxine, lidocaine/prilocaine Periodic re-evaluation (every 4-6 wks, change of season) ▪ Predominantly nerve modulation •H&P, ROS ▪ Doxepin Consider additional diagnostics: •Hepatitis B&C, Stool for O&P, Ferritin, Imaging (CT chest & abdomen) Consider 2nd and 3rd line therapies TREATMENT FOR PRURITUS TREATMENT FOR PRURITUS SYSTEMIC: ANTIHISTAMINES (AH) OTHER SYSTEMIC AGENTS
▪Low dose ▪First Level ▪Nonsedating AH daily ▪Systemic Glucocorticoids ▪Cetirizine, levocetirizine, fexofenadine, loratidine, ▪Gabapentin desloratidine ▪Pregabalin ▪High dose ▪Selective serotonin reuptake inhibitors (SSRI) ▪Nonsedating AH, BID to QID, or combination with ▪Especially for paraneoplastic, polycythemia vera, or sedating AH at bedtime depression ▪Hydroxyzine, diphenhydramine, cyproheptadine ▪Naltrexone ▪Especially for renal or liver dysfunction
TREATMENT FOR PRURITUS: OTHER CONCLUSION: ITCH SYSTEMIC AGENTS
▪ Second Level ▪Itch can be acute or chronic ▪ SSRI ▪ Mirtazapine ▪The pathophysiology is complex and ▪ Tricyclic and tetracyclic antidepressants multifactorial ▪ Phototherapy: Narrow Band UVB ▪ Third Level ▪Impact of itch can be extreme and impact the ▪ Naltrexone* ▪ Lidocaine 5% patch entire family ▪ Fourth Level ▪There are numerous etiologies for itch ▪ IVIG ▪ Extracorporal Photophoresis ▪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.” CASE # 1, “C.O.”
▪Denies anything new over the last two Treated for allergic contact dermatitis. months, medications or products. ▪Medications ▪No obvious aggravating factors. ▪Levocetirizine 5 mg in am ▪No relieving factors. ▪Fexofenadine 180 mg in the afternoon. ▪Hydroxyzine 10 mg, i, ii, or iii at HS ▪Keeps her awake at night. ▪Triamcinolone 0.1 % ointment BID to affected areas, ▪MISERABLE leaving small area untreated for possible biopsy. CASE # 1, “C.O.” CASE # 1, “C.O.”
▪Other measures Two Week Followup ▪Elimination of all dyes and fragrances ▪Mild improvement. ▪Laundry detergent, fabric softener, cleansers, moisturizers, shampoo, etc. ▪Rash slightly improved, itch still present. ▪Topical emollient twice daily ▪Husband present now. ▪Ceramide based, dye and fragrance free. ▪“Something has got to be done!” ▪Avoid hot showers, scratching, etc. ▪Triamcinolone changed to clobetasol ▪Punch biopsy performed.
CASE # 1, “C.O.” CASE # 1, “C.O.”
Follow up in 3 months and was still doing well. ▪Pathology Results ▪ ▪ Acute Spongiotic Dermatitis ▪ 6 months later presents with itching of entire upper body for one ▪ Most probably allergic contact dermatitis. week duration, miserable again. ▪Patch Test Allergies ▪ Started Narrow band UVB three times weekly. ▪ Nickel, Paraben mix, Mercapto mix, thimerosol, Gold sodium thiosulfate, ▪ Improved for 6 months disperse blue ▪ Biopsy for H&E and DIF ▪Discussed avoidance ▪ Superficial perivascular dermatitis ▪ Positive Direct Immunofluorescense consistent with bullous pemphigoid ▪Labs all WNL ▪To use pimecrolimus cream BID prn CASE # 1, “C.O.” CASE #2 “J.C.”
▪Treatment ▪35 yo female ▪Prednisone Taper ▪Presents with rash and itch in popliteal area ▪Doxycycline 100mg bid bilateral and lower legs. ▪Niacinamide 500mg tid ▪Duration 5 to 10 years Mycophenolate mofetil (CellCept) 500mg daily, ▪ Biopsy performed: possible psoriasis increased to BID. (Max 1 gram bid) ▪ ▪Histology proven psoriasiform dermatitis with ▪Patient has had lab monitoring and has been eosinophils: most likely contact dermatitis doing quite well. ▪Features of lichen simplex chronicus
CASE #2 “J.C.” CASE #2 “J.C.”
▪ Started ▪T.R.U.E Test Patch Testing ▪ cetirizine 10 mg twice daily ▪Disperse Blue ▪ hydroxyzine 10mg, i,ii, or iii at HS ▪Immunocap ▪ Referred to Allergist ▪Region 8 (Central Midwest, MO, IL, IA) ▪ Did not follow up UNTIL 2 ½ years later. ▪ Still itching and legs lichenified from scratching ▪Multiple moderate to highly allergic ▪ ▪Food Had not seen the allergist. ▪ Discussed proper skin care, restart the antihistamines and topical ▪None steroids, reinforced need for allergist. ▪IgE elevated ▪ Follow up pending CASE #3 “D.B.” CASE #3 “D.B.”
▪ 84 yo female ▪ Elimination of dyes and fragrance ▪ Rash on and off for ten years. ▪ Proper skin care ▪ Located on trunk, arms, legs, feet ▪ OTC anti-itch lotions and cleansers ▪ Erythematous inflammatory papules with excoriations ▪ Levocetirizine 5mg in am ▪ Prior treatment camphor/menthol/triamcinolone/aqua/lact compounded lotion with temporary relief. ▪ Fexofenadine 180 mg in afternoon ▪ Dial soap ▪ Hydroxyzine 10, i,ii, or ii @ HS ▪ No new drugs or products ▪ T.R.U.E. Test in 2 weeks when skin calmed, too flared today ▪ CBC and CMP all WNL
CASE #3 “D.B.” REFERENCES
▪ T.R.U.E Test all negative ▪ Reich, A., Stander, S., & Szepietowski, J. C. (2009). Drug-induced pruritus: A review. Acta Dermato Venereologica, 89, 236-244. doi: ▪ Rash resolved 10.2340/00015555-0650 ▪ Itch improved for now ▪ Stander, S., Weisshaar, E., Mettang, T., Szepietowski, J. C., Carstens, E., ▪ Did well for 6 months then itch returned without the rash. Ikoma, A., et al. (2007). Clinical classification of itch: A position paper of the International Forum for the Study of Itch. Acta Dermato- ▪ TSH, free T4, ANA all WNL Vernereologica, 87, 291-294. ▪ Narrow band UVB three times weekly ▪ Steinhoff, M., Cevikbas, F., Ikoma, A., & G, B. T. (2011). Pruritus: ▪ Patient was improving slowly but sadly suffered a CVA, required long Management algorithms and experimental therpaies. Seminars in term care. Husband reports since CVA no itch. Cutaneous Medicine and Surgery, 30, 127-137.