Inflammatory Dermatoses

Definition of Terms
DERMATOSES = Entire spectrum of skin disorders
(inflammatory, congenital, neoplastic, etc.)

DERMATITIS = Inflammatory diseases of the skin ECZEMA asstd with = Inflammatory diseases intraepidermal

ECZEMA
(Greek eksein = to boil out)

Acute/ subacute/ chronic 3 GROUPS:

I. II. III.

Atopic dermatitis Contact dermatitis Other Eczemas

Classification: Eczema
I. ATOPIC DERMATITIS II. CONTACT DERMATITIS a. Allergic CD b. Irritant CD III. OTHER ECZEMAS
a. b. c. d. Nummular/ discoid dermatitis Seborrheic dermatitis Stasis dermatitis Hand and foot dermatitis (palmoplantar pompholyx)

ATOPIC DERMATITIS
A chronic, relapsing inflammatory skin disease affecting up to 20% of the population A multigenic disorder = the genetics of atopy are complex Has a serious impact on the quality of life of patients and their families Increasing prevalence worldwide noted due to 1. environmental factors : house dust mites, airborne allergens, poor air quality, poorly-ventilated homes 2. Western lifestyle factors: Increased urbanization, increasing industrialization in dev. countries stress, dietary changes, travel to new environments, new microbial environment, most time spent indoors, more pets

ATOPIC DERMATITIS
Diagnosis is arrived at by history taking and clinical criteria (based on Clinical criteria as guidelines for dx of AD by Rajka and Hanifin): A. Major criteria (3 or more): 1. Pruritus 2. Typical morphology and distribution - Adults: Flexural lichenification - Children: Facial and Extensor involvement 3. Chronic or chronically relapsing dermatitis 4. Personal/Family Hx of ATOPY (asthma, allergic rhinitis aka hay fever, atopic dermatitis, allergic conjunctivitis, GI allergy)

ATOPIC DERMATITIS
B. Minor features (3 or more)
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. Xerosis (dry skin) Ichthosis/palmar hyperlinearity/ keratosis pilaris Immediate(type I) skin test reactivity Elevated serum IgE Early age of onset Tendency towards skin infections(esp. S.aureus & Herpes simplex) / impaired cellmediated immunity Tendency towards nonspecific hand or foot dermatitis Nipple eczema Cheilitis Recurrent conjunctivitis Dennie-Morgan infraorbital folds Keratoconus Anterior subcapsular cataracts Orbital darkening Facial pallor/erythema Pityriasis alba Anterior neck fold Itch when sweating Intolerance to wool and lipid solvents Perifollicular accentuation Food intolerance Course influenced by environemental and emotional factors White dermographism

IRRITANT CONTACT DERMATITIS

A nonallergic inflammatory reaction - May be induced in any person if sufficiently high concentration of the irritating substance is used - No previous exposure to a substance necessary - Effect is evident within minutes or a few hours at most - Examples of irritating substances: - A. ALKALIS: Dissolve keratin penetrate & destroy deeply (Eg.soaps, detergents, bleaches) Tx: Apply weak acids like vinegar, lemon juice B. ACIDS : Ex. Hydrochloric acid= blisters Nitric & sulfuric acids =corrosive/ can cause deep burns Tx: Rinse with copious amounts of water and alkalinization with sodium bicarbonate/ CaOH (lime)/soap solutions

ALLERGIC CONTACT DERMATITIS

Results when an allergen comes into contact with previously sensitized skin Results from a specific acqquired hypersensitivity of the delayed type a.k.a. cell-mediated immunity or cellmediated hypersensitivity May be induced upon a sensitized area of skin when an allergen is taken internally Patient may have exposure to an allergen for years before developing hypersensitivity e.g. hair dyes, rubber,

TREATMENT
A. Topical Regimen
1. 2. 3. 4. Steroids hydrocortisone, dexamethasone, mometasone, methylprednisolone, triamcinolone, betamethasone, clobetasol, fluocinolone Antibiotics gram-positive coverage, broadspectrum Immunomodulatory drugs tacrolimus Emollients / Moisturizers /hypoallergenic cleansers

A. Systemic Drugs
1. 2. 3. 4. Antihistamines sedating/ nonsedating Antibiotics Steroids prednisone, methylprednisolone, hydrocortisone Immunomodulatory drugs cyclosporine, methotrexate, azathioprine

TREATMENT
C. Phototherapy Use of ultraviolet light: 1. UVA-1 atopic dermatitis 2. Narrow-band UVB D. Intralesional injections of corticosteroids

PSORIASIS
- A chronic, relapsing disease characterized by red, scaling skin lesions of variable forms: 1.PSORIASIS VULGARIS (vulgaris = common) = circular plaques predominantly on scalp (particularly) retroauricular areas , elbows & knees, lower back (lumbar area)

PSORIASIS: Clinical forms

2. INVERSE PSORIASIS = lesions located on flexures axillary vaults, antecubital fossae, popliteal vaults, inguinal/crural creases, inframammary areas 3. GUTTATE PSORIASIS (guttate = droplike) =a.k.a.eruptive psoriasis (sudden/acute onset)

PSORIASIS: Clinical forms

4. PUSTULAR PSORIASIS = lesions are sterile pustules Variant forms of pustular psoriasis: a.Localized: Pustular palmoplantar psoriasis, Acrodermatitis continua of Hallopeau b.Generalized: Von Zumbusch pustular psoriasis

PSORIASIS: Clinical forms

5. Generalized psoriasis 6. Geographic psoriasis (map-like) psoriasis coalesced plaques form irregularly-shaped islands 7. Annular psoriasis (ring-shaped) 8. Follicular psoriasis

PSORIASIS: Epidemiology
Affects about 2% of population (+) Genetic predisposition 1/3 of patients have (+)family history Occurs at ANY AGE PEAKS at 2 age groups: 16-22 y/o and 55-60 y/o

PSORIASIS: Pathogenesis
1. (+)Hyperproliferation of keratinocytes: epidermal cell cycle shortened from 311 hrs to 36 hours = Cells mature more quickly accumulation of scales

PSORIASIS: Pathogenesis
2. Role of immune system mechanisms: Th1-driven disorder (T-cell mediated immune response)

A. Noncutaneous trigger factors: eg. Infection (Streptococci, HIV), e.g.Drugs (lithium, B-adrenergic blockers, ACE inhibitors) generate autoantigens B. Susceptibility genes activated : Most frequently HLA-b13, -B17, -Bw57, -Cw6 C. Th1-Th2 imbalance cytokines, IL-1 Fgf, IL-6 Egf, IL-8 TNF generatedlack of downregulation influx of neutrophils and macrophages/monocytes amplified immune response D. Expression of psoriasis phenotype: = tortuous dilated capillaries (seen clinically as erythema) = presence of microabscesses filled with neutrophils (Munro microabsecesses) : A hallmark of psoriasis

PSORIASIS: Treatment
1. TOPICAL Treatment = applied to skin Glucocotricosteroids Vitamin D3 analogues: calcipotriol Topical retinoid: Tazarotene Tar Anthralin Emollients/ Moisturizers: eg. Petroleum jelly commonly used because cheap but greasiness is uncomfortable

PSORIASIS: Treatment
2. SYSTEMIC Treatment (oral/IM/ IV) Methotrexate Cyclosporine Retinoids (Vit A derivatives)= etretinate, acitretin Biologicals : genetically engineered medication from a living organism (e.g. virus), gene or protein injected or infused intravenously = e.g. etanercept , infliximab

PSORIASIS: Treatment
3. PHOTOTHERAPY Treatment with ultraviolet (UV) light 1.Photochemotherapy : PUVA = a photosensitizer (methoxypsoralen) is ingested and the patient is subjected to UVA light 2.UVB light = broad band UVB = narrowband UVB

EXFOLIATIVE Dermatitis
a.k.a. Erythroderma Inflammatory skin disease in which erythema and scaling is widespread/generalized(GED = generalized exfoliative dermatitis) Due to a preceding skin or systemic dse Drugs implicated May occur as an idiopathic entity w/o preceding dermatitis or systemic

EXFOLIATIVE Dermatitis
SKIN Dses= Eczematous dermatitis, Psoriasis, superficial fungal infections (dermatophytosis), scabies SYSTEMIC Dses = Cancers (leukemia, lymphoma, rectal CA, lungCA), HIV infection DRUGS = allopurinol, NSAIDS, anticonvulsants/ psychotropic drugs(Carbamezapine, Phenytoin, Lithium), antibiotics (penicillin, trimethoprim, sulfonamides,