Inflammatory Dermatoses

Definition of Terms

• DERMATOSES = Entire spectrum of skin disorders

(inflammatory, congenital, neoplastic, etc.)

• DERMATITIS = Inflammatory diseases of the skin

• ECZEMA = Inflammatory diseases asstd with intraepidermal edema (spongiosis)

vesiculation

ECZEMA (Greek eksein = to boil out)

Acute/ subacute/ chronic

3 GROUPS:I. Atopic dermatitisII. Contact dermatitisIII. Other Eczemas

Classification: Eczema

I. ATOPIC DERMATITISII. CONTACT DERMATITIS

a. Allergic CD b. Irritant CD

III. OTHER ECZEMASa. Nummular/ discoid dermatitisb. Seborrheic dermatitisc. Stasis dermatitisd. 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. Pruritus2. Typical morphology and distribution

- Adults: Flexural lichenification - Children: Facial and Extensor involvement

3. Chronic or chronically relapsing dermatitis4. Personal/Family Hx of ATOPY (asthma, allergic

rhinitis aka “hay fever”, atopic dermatitis, allergic conjunctivitis, GI allergy)

ATOPIC DERMATITISB. Minor features (3 or more)1. Xerosis (dry skin)2. Ichthosis/palmar hyperlinearity/ keratosis pilaris3. Immediate(type I) skin test reactivity4. Elevated serum IgE5. Early age of onset6. Tendency towards skin infections(esp. S.aureus & Herpes simplex) / impaired cell-

mediated immunity7. Tendency towards nonspecific hand or foot dermatitis8. Nipple eczema9. Cheilitis10. Recurrent conjunctivitis11. Dennie-Morgan infraorbital folds12. Keratoconus13. Anterior subcapsular cataracts14. Orbital darkening15. Facial pallor/erythema16. Pityriasis alba17. Anterior neck fold18. Itch when sweating19. Intolerance to wool and lipid solvents20. Perifollicular accentuation21. Food intolerance22. Course influenced by environemental and emotional factors23. 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 juiceB. 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 cell-mediated 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, cosmetics, insecticides

TREATMENTA. Topical Regimen

1. Steroids – hydrocortisone, dexamethasone, mometasone, methylprednisolone, triamcinolone, betamethasone, clobetasol, fluocinolone

2. Antibiotics – gram-positive coverage, broad-spectrum

3. Immunomodulatory drugs – tacrolimus4. Emollients / Moisturizers /hypoallergenic cleansers

A. Systemic Drugs1. Antihistamines – sedating/ nonsedating2. Antibiotics3. Steroids – prednisone, methylprednisolone,

hydrocortisone4. Immunomodulatory drugs – cyclosporine,

methotrexate, azathioprine

C. Phototherapy Use of ultraviolet light:

1. UVA-1 atopic dermatitis2. Narrow-band UVB

D. Intralesional injections of corticosteroids

TREATMENT

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)= “chronic stationary psoriasis” – months/yrs.

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)

= Trunk and proximal extremities most affected

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 psoriasis6. 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. PHOTOTHERAPYTreatment with ultraviolet (UV) light1.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 disease

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, sulfonyureas, INH/Rifampicin, etc.)