10/25/2018
Psoriasis PRIMARY CARE
DERMATOLOGY • 2% of the population
• Biphasic onset: 16-22 years, 50-60 years • Children can develop guttate psoriasis (subtype) precipitated by strep infection
• CHRONIC and intermittent
• Triggers: stress, physical trauma, infection Ashley Wysong MD, MS William W. Bruce MD Distinguished Chair of Dermatology UNMC Department of Dermatology UNMC Otolaryngology, Head & Neck Surgery UNMC DEPARTMENT of DERMATOLOGY
disclosures etiology
• Unpaid Scientific Advisor: Castle Biosciences • Genetics collaborative gene expression profiling study. • HLA-Cw6 (9-15x increased risk) • HLA-B17 (early onset, increased severity) • HLA-B27 (psoriatic arthritis)
• Upregulation of the IL-23 pathway • Dendritic cells secrete IL-23 which stimulates Th17 T cells IL-17 (induces keratinocyte expression of leukocyte chemotactic factor CCL20 and IL-22) downregulates keratinocyte maturation factors (acanthosis)
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DRUG-induced psoriasis
• “BIG LACES” • Beta Blockers Rashes 101 • IFN, IL2 • Gemfibrozil, GCSF, Glyburide Common red scaly rashes • Lithium, Lamisil (terbinafine) • Ace inhibitors, Antimalarials • Calcium Channel Blockers • Steroid (oral) withdrawal
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Clinical findings
• Well-demarcated (sharply circumscribed) erythematous scaly plaques • Vulgaris: large plaques • Guttate: small “drops” papules/plaques
• Distribution • Symmetric • Elbows, knees, scalp, suprapubic area • Inverse • Erythroderma
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Acrodermatitis continua of hallopeau
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Subtypes of psoriasis inverse
• Guttate: small 0.5-1.5cm lesions over trunk and extremities • Often 2/2 strep throat infection in young adults
• Erythroderma: diffuse involvement of > 90% BSA
• Pustular Psoriasis • Generalized: Impetigo Herpetiformis, Von Zumbusch • Localized: Acrodermatitis Continua of Hallopeau, Palmoplantar Pustulosis
• Inverse Psoriasis: in body folds
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Guttate Erythrodermic
• More common in children/adolescents
• Often associated with pre- existing STREP infection (80%) • Chicken pox • Roseola • Rubella
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DDX erythroderma
• Psoriasis • Drug Reactions • Atopic Dermatitis • Bullous -- pemphigus foliaceus, BP, paraneoplastic • Contact Dermatitis pemphigus • Pityriasis Rubra Pilaris • Congenital ichthyoses • Seborrheic Dermatitis • RARE - Hypereosinophilic Syndrome, Crusted scabies, • CTCL/MF – Sezary LP, Tinea, GVHD Syndrome • Erythroderma is a • Leukemia / Lymphoma (paraneoplastic) DERM EMERGENCY!!!
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CLINICAL SIGNS Psoriatic arthritis
• Auspitz Sign: pinpoint bleeding when scale is removed • Asymmetric oligoarthritis – swelling and tenosynovitis of one or a few hand joints (DIPs/PIPs) – 70% • Oil Spot Sign: distal yellowish discoloration of the nail • Other Nail Findings: • Asymetric DIP Disease with nail damage – 16% • Pitting • Symmetric Polyarthritis (RA-like) – 15% • Subungual hyperkeratosis • Spondylitis (axial) HLA-B27+ -- 5% • Koebnerization: eruption of psoriasis in areas of trauma • Arthritis mutilans – 5% • Wornonoff’s Ring: pale blanching around psoriatic plaque
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pitting “Sausage digits”
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Topical treatment biologics
• Emolliation!!! JAK INHIBITORS TNF⍺ inhibitors • Corticosteroids – right amount, right strength, ointment>cream • Hydrocortisone 2.5% face, groin, folds • Triamcinolone 0.1% body • Fluocinolone 0.05% SOLUTION scalp • Calcipotriene (Dovonex, vitamin D analog) • Topical Retinoids (tazarotene)
• Salicylic acid (5-10%) IL-17 inhibitors JAK INHIBITORS • Calcineurin Inhibitors (tacrolimus) – flexural areas IL-23 inhibitors • Tar or Anthralin (old school)
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Phototherapy Psoriatic associations
• nbUVB – up to 3 times per week • Metabolic Syndrome • PUVA (0.6mg/kg 8-MOP or trimethoxypsoralen) • Ischemic Heart • Crosslinks nucleic acids to increase photoinhibition of Disease DNA synthesis • Peripheral • Localized treatment – hand/foot box Vascular Disease • Cerebrovascular Disease (CVD)
UNMC DEPARTMENT of DERMATOLOGY UNMC DEPARTMENT of DERMATOLOGY World J Cardiol. Feb 26, 2016; 8(2): 120-131
Systemic therapies
• Methotrexate + Folic Acid
• Cyclosporine • Can cause renal toxicity, HTN, electrolyte imbalance, TG
• Biologics • Do NOT use systemic steroids!!! Rebound = WORSE!
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Atopic dermatitis “eczema”
• Very common – 10-20% of school aged children • Typically begins in infancy (90% by age 5) • About half resolve by age 5 • Severity typically decreases with age
• 5-10% of adults
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CLINICAL FINDINGS adults
• Often ill-defined erythematous thin scaly plaques
• Acute: intensely pruritic, erythematous, edematous papules and plaques • +/- vesicles, oozing, and serous crusting • Often secondary excoriations
• Subacute/Chronic: erythematous papules and plaques with scaling and excoriation • +/- lichenification (thickening)
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Distribution ACUTE
• Infants: • Face & Scalp • EXTENSOR surfaces • Diaper area spared (moist)
• Adolescents/Adults: • FLEXURAL areas (popliteal and antecubital fossae), • Chronic hand dermatitis
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Chronic IMPETIGINIZATION lichenification
• Secondary Infection • HSV – “Eczema Herpeticum aka Kaposi’s Varicelliform Eruption” • MSSA/MRSA – staph aureus in up to 90% of lesions • Honey crusting, folliculitis, pyoderma • Molluscum • HPV • Trichophyton Rubrum
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HAND DERMATITIS Impetiginized eczema
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DDX Hand DERMATITIS Eczema herpeticum
• Atopic Dermatitis
• Contact Dermatitis – Irritant vs. Allergic vs. Photo
• Psoriasis
• Tinea Manuum
• Rheumatologic Conditions – SLE, DM
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Other findings etiology
• Hyperlinear Palms • It’s complicated
• Dennie-Morgan lines (infraorbital folds) • Barrier defect (Filaggrin mutation) causing • Ichthyosis Vulgaris sensitization to environmental antigens • Keratosis Pilaris • TH2 cells have increased secretion of IL4/5 IgE • Xerosis synthesis histamine release, CD8 T cell and IFN-gamma secretion by TH1 cells • Atopy (asthma, allergic rhinitis) • Pityriasis Alba • Chelitis
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Four Pronged Other findings approach
• Hyperlinear Palms 1. Treat xerosis (dry skin) – Emollients
• Dennie-Morgan lines (infraorbital folds) 2. Treat inflammation – Corticosteroids • Ichthyosis Vulgaris 3. Treat pruritus (itching) – Antihistamines • Keratosis Pilaris a. Benadryl 25mg, Hydroxyzine 25-50mg, Doxepin
• Xerosis 4. Treat any underlying infection – ABX, Antivirals • Atopy (asthma, allergic rhinitis) a. Bleach baths (1/2 cup / tub) b. Bacterial Keflex (kids 25-50mg/kg divided into BID dosing), • Pityriasis Alba Augmentin / Clindamycin c. Viral Acyclovir/Valacyclovir • Chelitis
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Other findings Dry skin care
• Hyperlinear Palms • Emolliation!!! • Dennie-Morgan lines (infraorbital folds) • Frequent emolliation with CREAM (eucerin, cetaphil) or OINTMENT (Aquaphor, Vasoline) ALL OVER body! • Ichthyosis Vulgaris • Keratosis Pilaris • Short luke warm baths (don’t over dry) • Xerosis • Gentle cleansers (Cetaphil, Dove) • Bland, fragrance free • Atopy (asthma, allergic rhinitis) • Pityriasis Alba • Wet wraps • www.eczemacenter.org • Chelitis
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Favorites!!! Topicals
C • Corticosteroids are the MAINSTAY!!! R • Desonide 0.05% or Hydrocortisone 2.5% to the face, E A groin, armpits M • Triamcinolone 0.1% to body S • Clobetasol to TOUGH spots (hands, etc)
O • Calcineurin Inhibitors (tacrolimus, pimecrolimus) to I sensitive areas (face, body folds) N • Both are topical FK506 derivatives; bind calcineurin to prevent T activation of T cells via transcription factor NF-AT M E • Most efficacious on thinner skin, not lichenified plaques N • FDA black box warning T S UNMC DEPARTMENT of DERMATOLOGY UNMC DEPARTMENT of DERMATOLOGY
Steroids Systemics for severe/recalcitrant eczema
• Low potency = for face, genitalia, folds • Phototherapy – nbUVB • Hydrocortisone 2.5% • Cyclosporine • Desonide 0.05% • Inhibits T-cell activation • Mid Potency = trunk/extremities • Cellcept • Triamcinolone 0.1% • Immunosuppressant, inhibits IMPDH (de novo purine synthesis) • High Potency = hands, short contact severe patches • Azathioprine • Clobetasol 0.05% • Immunosuppressant, decreases purine metabolism • OINTMENT >>> CREAM • Prednisone • Immunosuppressant
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Steroids
IL-4 and IL-13 receptor inhibition (Th2)
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9 10/25/2018
Seborrheic dermatitis
• COMMON – 2-5% of the population
• Bimodal • Infantile – “cradle cap” • Adults – 30-50 years old
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Clinical features
• Infantile: greasy scale on vertex/anterior fontanelle • Can disseminate to axilla, inguinal folds, umbilicus
• Adult – ill-defined erythematous (pink-yellow) plaques with white or yellow greasy scale • Rarely can cause erythroderma • Associated with HIV, Parkinson’s and other CNS disorders (stroke, spinal cord injury)
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Adult distribution
• Nasolabial Folds
• Scalp/Beard areas
• Medial eyebrows (glabella), Eyelids, Ears
• Chest
• Umbilicus
• Intertriginous Areas
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DDX eyelid dermatitis
• Seborrheic Dermatitis • Atopic Dermatitis Acne • Contact Dermatitis • Airborne Comedones, and pustules, and • Cosmetics/Nails cysts, oh my!
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treatment Acne Vulgaris
• Infants • Epidemiology • Emollients • Topical steroids – HC, Desonide, Dermasmooth • Pathophysiology • Ketoconazole 2% cream • Adults • Clinical Features • Ketoconazole 2% shampoo and/or cream • Other OTC shampoos: zinc pyrithione, tar, Selsun Blue, Head and • Pathology Shoulders, salicylic acid • Steroids • Treatment • Calcineurin Inhibitors • Acne Variants • HIV-associated • Lithium succinate ointment (8%)
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Differentiating… Epidemiology
Clinical Distribution Associations • Common—termed “physiologic” Psoriasis Well- EXTENSORS NAIL findings • 85% adolescents demarcated, -- elbows, knees, Arthritis erythematous scalp, Metabolic, • >40% people in their 20s & >10% in their 40s plaques with intertriginous Cardiac • Ages—neonate, adolescent, adult thick, silvery scale • Familial Atopic Ill-defined FLEXORS Hyperlinear • difficult to assess due to commonality Dermatitis erythematous or -- antecubital Palms, Dennie lichenified and popliteal Morgan lines, plaques with fossa, posterior Atopy • Race/Gender fine scale or neck, hands • more common, earlier and more severe in males crusting • more common in Caucasians Seborrheic Erythematous Scalp, NLF, Dermatitis patches or glabella, UNMC DEPARTMENT ofplaques DERMATOLOGY with eyebrows, hair- UNMC DEPARTMENT of DERMATOLOGY white to yellow bearing areas
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Pathophysiology: Microbial Flora Multifactoral
• 1. Increase in sebum production • Follicular flora: P. acnes, S. epi, M. furfur
• 2. Abnormal keratinization • P. acnes in patients with acne • bacterial levels ≠ severity of acne • 3. Abnormal microbial flora • Pro-inflammatory products of bacteria • 4. Inflammation • free fatty acids generated by follicular lipases • extracellular enzymes • proteases, hyaluronidases, chemotactic factors • Immune System Changes • TLRs • β-Defensins
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Increase in Sebum Production
• Sebum is the “fodder” for inflammation • Sebum lipidsmetabolized by P.acnes FFAs • Alter keratinization to faciliate comedone formation • Chemotactic for PMNs = Inflammation • Hormonal Influence • Onset at puberty/androgen excess • estrogens seb activity / androgens activity • sebum ≠ worse acne, but is necessary for acne • Drugs which sebaceous activity acne
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Keratinization Changes Clinical Features
• Normal keratinization within follicle • Understanding MORPHOLOGIES!!! • loosely organized with large lamellar granules and few keratohyaline granules • Comedonal • Keratinization in acne • comedone is primary lesion of acne • proliferation/retention/cohesion = comedo formation • non-inflammatory • Keratinacous material • open comedone: blackheads -- flat-slightly raised lesion with central follicular impaction of keratin and • more dense lipid • decreased number of lamellar granules • closed comedone: whitehead -- pale, slightly elevated • increased number of keratohyaline granules small papule without visible orifice • increased cell turnover
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Clinical Features
• Inflammatory • small papules or pustules with erythematous rim • Nodulocystic • not true cysts--large, fluctuant nodules • sinus tracts between cysts may form • Scars • Hyper/hypo- pigmented macules • punched out pits (“ice pick” scars), can occur with comedones only • keloids-- form primarily on trunk • calcification
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Treatment: Goals
• Correct altered pattern of keratinization
• Decrease sebaceous gland activity
• Decrease P. acnes Decrease inflammation
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Therapeutic Options: Therapeutic Options: Oral Topicals Antibiotics
• Benzoyl Peroxide • Indications: mild/mod inflammatory acne • Mechanism: • Mechanism: α-microbial and α-inflammatory • Cidal to P.Acnes, no known resistance • Use in COMBO with topical antibiotics (clinda/erythromycin) • Options: • Mild keratolytic • Tetracyclines, Macrolides, Cephalsporin, Sulfas • Mild Comedolytic • Side effects: • RX: 2-10% lotion, gel and wash- daily • Watch out for interactions with OCP • SE: dryness/irritation, Contact Derm, irritation, Bleaching
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Therapeutic Options: Topicals Therapeutic Options: Oral Retinoids
• Isotretinoin (Accutane) • Retinoids (tretinoin, adapalene, tazarotene) • Indications: Severe cystic acne, moderate acne • Normalizes follicular keratinization + comedolysis resistant to other therapy • 0.01-0.1% Gel/Cream/Washes QHS • Can worsen before it gets better = induce flare • Side effects Mechanism: • irritation • • increase sun sensitivity • sebaceous gland activity/size then… • NO evidence of systemic levels or teratogenicity (although • decreases P. acnes colonization topical tazarotene is Category X) • anti-inflammatory • effects keratinization of follicle
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SUMMARY Hormonal Agents
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Procedural Therapeutic Options
• Comedone extraction
• Intralesional Steroids: for cystic lesions Bilateral Cellulitis • Chemical Peels : Comedone clearance • Light and Lasers – short term clearance Is it real? • Photodynamic therapy • IPL? • Red light therapy?
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Photodyamic therapy
• Can help for short-term/quick clearance
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Acne pearls Venous Insufficiency
• Topical retinoids are the mainstay of treatment • Inability of the leg veins to effectively return blood from the legs to the heart • No topical antibiotics alone due to antibiotic resistance • Most commonly 2/2 malfunctioning valves due to aging, (combine with benzoyl peroxide) genetics, hormones/pregnancy, and other risk factors • All acne topicals are for ENTIRE face – no SPOT treatments • Common: • Acne often gets WORSE initially, and can take some – 50-55% of F time 6-8 weeks to improve – must handhold patients and warn about pushing through side effects – 40-45% of M
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pathophysiology Exam findings
• Veins are thin walled and distensible • Varicose Veins • 3-8mm • Uni-directional flow, aided by VALVES to return blood to the heart • >2/3 with underlying SF/SP/IP reflux • Reticular Veins • Store 60-75% of total blood volume • 2-4mm, blue • Factors that effect venous flow • Telangiectasias / “Spider Veins” • Intrinsic – venous contractions, arterial inflow, thoracic/abdominal pressure, valve integrity, vein wall • 0.2 – 1mm, red recoil • CHECK ARTERIAL PULSES!!! • Extrinsic – gravity, atmospheric pressure, centrifugal force, compression • Requirement prior to compression
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anatomy CEAP Classification
• C0 No signs of venous disease Typically • Deep System • C1 Telangiectatic / reticular spider veins only ASYMPTOMATIC • Popliteal/Femoral • C2 Simple varicose veins only • Saphenous System • C3 Ankle edema of venous origin • C4 Skin changes, no ulcerations • GSV • C5 Healed venous ulcers • SSV Femoral External Iliac • C6 Open venous ulcers • Perforators
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Clinical presentation
• Symptoms • Aching/tiredness in leg (Most Common) • Pain – throbbing, burning, pulling, stretching • Swelling (most SPECIFIC symptom) • Tenderness over a vein • Restless legs
• Exacerbating/Alleviating • Worse with prolonged sitting/standing • Improves with exercise, leg elevation, NSAIDs, compression
UNMC DEPARTMENT of DERMATOLOGY UNMC DEPARTMENT of DERMATOLOGY
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EVALUATION ALGORHTHM EVALUATION ALGORHTHM
Is the patient symptomatic? Is the patient symptomatic?
NO YES Are there worrisome Are there worrisome findings on examination? findings on examination? - LE swelling - LE swelling • Detailed bilateral Duplex - Extensive varicosities - Extensive varicosities - Skin changes Ultrasound by Registered Vascular Technologist - Skin changes
• Medical Management Exercise, Elevation, Compression
Surgical/Minimally Invasive Sclerotherapy Management
CEAP Classification VEIN EVALUATION
• C0 No signs of venous disease Typically • C1 Telangiectatic / reticular spider veins only • Consultation ASYMPTOMATIC • C2 Simple varicose veins only • IMAGING: Detailed bilateral • C3 Ankle edema of venous origin Duplex Ultrasound by Registered • C4 Skin changes, no ulcerations Vascular Technologist • C5 Healed venous ulcers SCLEROTHERAPY • C6 Open venous ulcers • Medical Management = EEE • Exercise, Elevation, Compression
• 3 month follow-up
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Tip of iceberg imaging
• 29% of patients with leg • Bilateral Venous Duplex telangiectasias / “spider veins” Ultrasound ONLY have underlying venous • Gray scale to evaluate: insufficiency • Vein size • GSV >/= 4mm • 84% of those that fail • SSV >/= 3mm sclerotherapy • PV >/= 3.5mm • Vein Anatomy • Mapping • Evaluate for Congenital Anomalies • r/o obstruction (clot)
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imaging
• Bilateral Venous Duplex Ultrasound • Gray scale to evaluate vein size and anatomy • Color flow/Duplex + compression to r/o DVT/obstruction in deep system and to assess reflux Sun Safety • Color Doppler = direction of flow/frequency shifts • Pulsed Wave Doppler = evaluates reflux • ABNORMAL/reflux • >0.5s in superficial venous system • >1s in deep system • >0.35s in perforators
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Sun safety
• SPF > 30
• Broad-spectrum
• Re-apply every 2 hours
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Endovenous Laser Ablation UNMC Comprehensive Vein Clinic
TREATMENT ALGORITHM Endovenous Chemical Ablation
Ambulatory Sclerotherapy Phlebectomy
(Overlying bony prominences) JAMA Dermatol. UNMC DEPARTMENT of DERMATOLOGY UNMC DEPARTMENT of DERMATOLOGY 2018;154(3):380.
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Face -- TINTED
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reapplication
• POWDERS!!!
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Face -- MEN
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Reactive / sensative Final pearls
• There’s really no such thing as bilateral cellulitis.
• It’s RARELY a spider bite
• Medrol dose packs don’t work for the skin
• Four pronged approach to atopic dermatitis is KEY!
• Psoriasis is a systemic disease
• For poison ivy or acute contact dermatitis, TOPICAL steroids >>> oral steroids (unless really widespread)
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BODY ACTIVE EXTRAS!!
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The Vitamin D Conundrum
• Association not causation • Low vitamin D levels have been associated with Final Thoughts increased risk of most cancers UV • Sun AVOIDANCE (shade, long sleeves) but NOT sunscreen use is associated with lower vitamin D levels DNA 7 Dehydrocholesterol • POSSIBLE role for vitamin D supplementation • 600 IU daily for most adults • 1000-4000 IU daily for thoseMutations with strict photoprotection Vitamin D3
Promotes Inhibits Tumor tumor UNMC DEPARTMENT of DERMATOLOGY UNMC DEPARTMENT of DERMATOLOGY 123
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The Vitamin D Sunscreen Conundrum Controversies
• Clinical studies have identified both a positive • The chemicals used in sunscreens routinely undergo a correlation and inverse association between vitamin rigorous safety assessment to explore the possibility of D3 intake and melanoma risk. UV local and systemic toxicity, such as sensitization, • Vitamin D production in the skin: irritation, phototoxicity, and carcinogenicity. • Protects against irradiation and likely suppresses melanomagenesis. DNA 7 Dehydrocholesterol • Reduces UV- induced DNA damage, including oxidative and genotoxic DNA damage, and induces DNA damage repair. Mutations Vitamin D3 • Inhibits proliferation and invasion of melanoma cells in vitro and in vivo. Promotes Inhibits Tumor tumor UNMC DEPARTMENT of DERMATOLOGY UNMC DEPARTMENT of DERMATOLOGY
Sunscreens Antioxidants Hormonal Distruption • Topical/systemic antioxidants can help supplement • Concern over “estrogen like effects” of sunscreen comes UV protection and skin repair from a study performed in rats, where the rats were fed • Vitamin C/D/E, beta-carotene, others supratherapeutic doses of sunscreen increased weight of uterus in immature rats and “significant dose • Polyphenols (green tea) have been shown to provide dependent estrogenic activity on MCF-7 breast cancer some benefit in the reduction of UVA induced damage cells in in vitro culture (highest in oxybenzone).
• Polipodium leucotomos • Used with some success in photosensitive cutaneous disease
• Possible role in the prevention of NMSC/melanoma?
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NSAID Debunked Chemoprevention
• Controversial • Sunscreens cause hormonal disruption (estrogen-like effects) • Women in the WHI who used ASA had a 21% lower • A study in 2011 in JAMA Dermatology showed that it risk of melanoma (HR 0.79) relative to non-users. would take 200 years of daily sunscreen application to reach the same amount of exposure as the rats in this • Increased duration of use showed an 11% lower risk of study. melanoma for each categorical increase • Human patients applied more than 3 times the real-life • (Gamba et al., Cancer, 2013) quantity of a high percentage oxybenzone sunscreen (10% oxybenzone, compared to the commercially available 6% oxybenzone) to their whole body daily for one week. Very low levels were detectable in urine, no significant changes in hormone levels. (JID, 2004)
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Debunked Diet & Supplements
• Sunscreen INCREASES risk for skin cancer • Supplementation with specific antioxidants is not • A single toxicology study that suggested that retinal recommended. palmitate (ester of retinol and palmitic acid), a common • Randomized control trials of beta-carotene, selenium, inactive ingredient in sunscreens, may actually increase vitamin A, E, and C have not showed any benefit, and in some cases increased risk of NMSC [Level of evidence your risk for skin cancer by increasing oxidative damage, IA]. or reactive oxidative species (ROS). • Nicotinamide (vitamin B3) has demonstrated • A few epidemiologic studies suggest that individuals my significant benefit in a phase 3, double blinded, inappropriately use sunscreen (i.e. not apply enough, not randomized controlled trial. re-apply) and may increase their overall UV exposure. • 500 mg orally twice daily for one year there was a 23% reduction in new NMSCs and 13% reduction in actinic keratoses [Level of evidence [IB].
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Nanoparticles White Wine & Melanoma!!! absorption?
• Multiple human studies have shown that these particles are unable to penetrate through the skin because, in nature, these nanoparticles aggregate into clumps that are too large to penetrate the skin
UNMC DEPARTMENT of DERMATOLOGY UNMC DEPARTMENT of DERMATOLOGY Semin Cutan Med Surg. 2011 Dec;30(4):210-3.
Diet, supplements, antioxidants
• Topical/systemic antioxidants may help supplement • Nurses Health Study + Health Professionals Follow-up Study UV protection and skin repair • 1,374 cases of invasive melanoma in 3,855,706 person-years of follow-up. • Vitamin C/D/E, beta-carotene, others • Association was seen between higher alcohol intake and incidence of invasive melanoma (pooled multivariate HR 1.14 [1.00–1.29] per drink/day; • Polyphenols (green tea) have been shown to provide • Among alcoholic beverages, white wine consumption was associated with an increased risk of melanoma (pooled multivariate HR 1.13 [1.04–1.24] per drink/day; some benefit in the reduction of UVA induced damage after adjusting for other alcoholic beverages compared to non-drinkers. • Stronger for melanoma in relatively UV-spared sites trunk (HR 1.73[1.25-2.38]) versus • Polipodium leucotomos (tropical fern extract) more UV-exposed sites (head, neck, or extremities)(HR 1.02 [0.64-1.62]) • These findings are similar to those from the Women's Health Initiative, a • Used with some success in photosensitive cohort of postmenopausal women = white wine was associated with cutaneous disease increased risk of melanoma and non-melanoma skin cancer • MECHANISM? UV sensitivity? high levels of pre-existing acetaldehyde carcinogenicity?
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Thank you!!!
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