Philippine Dermatological Society - The Filipino Eczema.pdf · Philippine Dermatological Society Officers…

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<p>Philippine Dermatological Society</p> <p>Officers and Board Members 2001 - 2002</p> <p> PresidentVice President</p> <p>SecretaryTreasurer</p> <p>Members of the Board</p> <p>Immediate Past President</p> <p>Rm. 1015 Front Tower, Cathedral Heights Complex, St. Lukes Medical Center, E. Rodriguez Sr., Ave., Quezon CityEmail: Website: No.: 727-7309; Fax No.: 932-9269</p> <p>Elizabeth Amelia V. Tianco, M.D.Francisca C. Roa, M.D.Benjamin B. Bince, M.D.Georgina C. Pastorfide, M.D.</p> <p>Ma. Lorna F. Frez, M.D. Daisy K. Ismael, M.D. Evelyn R. Gonzaga, M.D. Sylvia S. Jacinto, M.D. Vermen M. Verallo-Rowell, M.D.</p> <p>Clarita C. Maao, M.D.</p> <p>ECZEMA CpM4THEDITION</p> <p>Guidelines in the Diagnosis &amp; Treatment of EczemaPrepared byVermn M. Verallo-Rowell, M.D.Board Member and Past President, Philippine Dermatological Society</p> <p>Eczema and eczematous dermatitis refer to an in-flammatory condition of the skin characterized by the exudation of serous matter in lesions that appear and evolve in a very similar manner. These skin changes frequently rank among the top 5 - 10 that bring patients to a doctors office. A wide variety of unrelated causes produce eczema. Each of these have different pathoge-netic characteristics that differentiate one type of eczema from all the others. Treatment becomes successful when the guidelines are targeted towards specific aspects of Pathogenesis. CommonFeaturesofEczematousDermatitis(ED)</p> <p>The primary clinical presentation of acute ED begins with an itchyedematousandredpatch which then develops tiny bumps or bubbles within the patch. These bumps/bubbles become fluid-filled vesicles or larger bullae, which break down, become eroded, often with more itching, sometimes pain, redness and edema of the patch, Fig. 1: </p> <p>Figure 1</p> <p>Almost immediately, secondary changes develop. The fluid filled vesicles or blisters turn into a wet crust,then into adryscab,resulting in adry,scalypatch.The inevitable scratching and excoriations of the itchy </p> <p>patch lead to varying degrees of infection which further lead to thickening or lichenification, and post-inflam-matoryhyperorhypopigmentationoftheinvolvedskin,Fig.2:</p> <p>Figure 2</p> <p>The series of primary and secondary changes re-occur at the initial patch, or spread to other areas depending on the continued activity or presence of the primary cause in subacute ED, Fig. 3: </p> <p>Figure 3</p> <p>Common conditions with these sequence of skin events, but with different causes, pathogenesis, and clinical evolution, are: Atopic Dermatitis Contact Dermatitis Photosensitivity Dermatitis Palmo-plantar Vesicular Eczema Nummular Eczema Asteatotic Eczema of the elderly, and Gravitational Eczema. 1,2,3</p> <p>Itchy edematousand red patch</p> <p>Vesicle</p> <p>Bumps or bubbles</p> <p>Crust</p> <p>open, eroded blister</p> <p>Vesicles</p> <p>ECZEMA</p> <p>CpM4THEDITION ECZEMA</p> <p>DIsEAsEs</p> <p>ATOpICDErMATITIs(Eczema)(AD)</p> <p>primaryCause/pathogenesisFamilial Inheritance Pattern, autosomal dominant Polygenic Flare-ups associated with Allergens which act </p> <p>either as Antigens (need cellular processing), or as superantigens (no prior processing), induc-ing IgE synthesis, TH2-like cell expansion, mast cell degranulation, and injury to keratinocytes. All contribute to the inflammation and cutaneous hyperresponsiveness in AD</p> <p> Allergensare: Environmental contactants by direct skin contact: </p> <p>on the face of babies: tomatoes, citrus fruits; soaps, detergents, wool, acrylics. Inhalants by airborne exposure, Indoors/Outdoors: Dander, housedust mites, pollens</p> <p> Foodallergens - a subset is known to exist but in most, this is unsubstantiated</p> <p> Microbes - Staphylococci, P. ovate, T. rubrum</p> <p>CONTACTDErMATITIs(CD) </p> <p>primaryCause/pathogenesis Acquired and specific Reaction to a substance in direct contact with the </p> <p>skin. AllergicCD:the contactant is processed by antigen </p> <p> presenting cells at the epidermis, followed by a TH-1 or delayed type immune response</p> <p> CommonContactAllergens: Metals: Chrome, Nickel. Perfume ingredients. </p> <p>Rubber chemicals. Dyes; Formaldehyde resins formaldehyde releasing preservatives.</p> <p> IrritantCD: Non-immunologic, based on the ir-ritability of the skin and amount of the contactant present.</p> <p> strongContactIrritants: Ethylene Oxide used for gas sterilizations; Hy-</p> <p>drofluoric acid used in electronics/semi-conduc-tors; Wet cement</p> <p> MildtomoderateContactIrritants Soaps, solvents, detergents, fiberglass, metalwork-</p> <p>ing fluids, bleaches, grease removers, insecticides, fertilizers, rodenticides, waxes and polishers </p> <p> someallergensinhighconcentrations</p> <p>pHOTOsENsITIvITyDErMATITIs(pD)CON-TACT(CpD)&amp;Drug(DpD) </p> <p>primaryCause/pathogenesis Acquired and specific Reaction to a contactant or drug which is stimulated </p> <p>by light exposure Common Contact photoallergens: Dyes and fragrance ingredients in household </p> <p> products, toiletries, and cosmetics Therapeutic tars, pitch, creosote Some plants:celery, lime, lemon, garlic, chrysanthemum, dill, parsnip Halogenated salicylanilides used as anti-</p> <p>bacterial ingredients Whiteners in household products Sunscreens Common Drug photoallergens: Antibiotics: Griseofulvin, nalidixic acid, sulfanilamide, tetracyclines, doxycycline, quinolones: cipro-, oflo-, norfloxacin, urologi-</p> <p>cals NSAIDS: Benoxaprofen, piroxicam, naproxen, ketoprofen, mefenamic acid Anti-diabetic drugs:Sulfonylureas Diuretics: Furosemide, thiazides Cardiac medicines: Quinidine, amiodarone BP medicines: Enalapril, diltiazem Antidepressants Anxiolytics Antipsychotics Chemotherapeutic drugs: Dacarbizine, 5-FU,vinblastine Lipid lowering drugs: Fenofibrate, benzofi-</p> <p>brate</p> <p>PAlmo-PlAntAr VesiculAr eczemA(ppvE):This includes the broadened concept of Pom-pholyx or Dyshidrotic Eczema</p> <p>primaryCause/pathogenesisAcquiredandMultifactorial Atopic history as in AD allergens acting as an-</p> <p>tigens or superantigens. Atopichistory20-30%, Familyhistory59%</p> <p> Contact Dermatitis Most commoncontactants: Nickel, chrome, PPDA, fragrance Ingested allergens: Ni, Cobalt, chromates Balsams Neomycins, other drugs Foods Poison oak or poison ivy related to mango, lac-</p> <p>quer tree oil for furniture (Japan, China, India), cashew nut shells and oils. </p> <p> Implanted metals Contact with proteins</p> <p> table 1 - DIFFErENTCAusEsANDpATHOgENETICFEATurEsOF 7COMMONECZEMATOusDErMATOsEs</p> <p>ECZEMA</p> <p>ECZEMA CpM4THEDITION</p> <p> Secondary to distant focus of infections which clear when primary is treated. Fungal Infection: Dermatophytid Bacterial: Bacterid</p> <p>NuMMulArECZEMA(NE)Or[DIsCOIDECZEMA]</p> <p>primaryCause/pathogenesis AcquiredandMultifactorial Unrelated to Atopy IgE level Normal Bacteria as primary cause or through hypersensitiv-</p> <p>ity, but actual role of staphylococcus or streptococ-cus not definite</p> <p> Related to dry skin from obsessive use of soap several times a day, long hours of direct fan expo-sure or low-set air conditioning</p> <p> Some worsen in the summer, exacerbated by heat and humidity</p> <p> Other associations of flare-ups: wool, topical medicines including topical steroids varicosities, autosensitization</p> <p> Drugs: Gold, methyldopa, streptomycin, aminosali-cylic acid, INH </p> <p>AsTEATOTICECZEMA(AE)orECZEMACrAquElATuM</p> <p>primaryCause/pathogenesis Acquired,duetoXerosiscausedby: Aging Post-inflammatory change</p> <p>ATOpICDErMATITIs(ECZEMA)(AD)</p> <p> Infants and children: Facial (Figure 4a) and extensors (Figure 4b) with secondary staphylococcal impetig-inization of lesions.</p> <p>Figure 4a</p> <p> Post-use of irritants Low ambient humidity from seasonal change of </p> <p>weather, prolonged airplane flights, air-condition-ing</p> <p> Frequent bathing using soaps with high or alkaline pH.</p> <p> Diminished use of emollients Familial tendency for dry skin Occasionally a presenting sign of hypothy-</p> <p>roidism, Lymphoma, other systemic diseases.</p> <p>grAvITATIONAlECZEMA(gE) oldtermforstasisDermatits</p> <p>primaryCause/pathogenesisAcquired,duetochronic, venous, hypertension from </p> <p>poor venous drainage due to: Obesity Trauma Venous thrombosis from pelvic/lower abdominal </p> <p>operations, prolonged recumbency, leg injuries, varicose veins, thrombophlebitis</p> <p> Multiple pregnancies Heredity for incompetent valves,causing backflow </p> <p>of blood Common in wheelchair bound patients All other situations with decreased muscle pump </p> <p>function for assisting blood return</p> <p>table 2 - DIFFErENTIATINgFEATurEsOFprIMArylEsIONsANDDIsTrIBuTIONpAT-TErNsOF7COMMONECZEMATOusDErMATOsEs</p> <p>Figure 4b</p> <p>ECZEMA</p> <p>CpM4THEDITION ECZEMA</p> <p>Figure 5a, affecting antecubital spaces</p> <p>Figure 5b, affecting popliteal spaces</p> <p> Adult AD: Flexural distributioin, often with licheni-fication is very common, Fig. 5 a and b.</p> <p> Airborne CD due to contactants such as pollens, house-dust, perfume/insecticide sprays, affect exposed areas, spare covered areas. This is similar to the distribution of photocontact dermatitis. The difference is involve-ment of eyelids, inner arms creases of the neck. Fig 6a:</p> <p> Plants: Linear pattern from leaf, or plant markings, Fig. 7:</p> <p> Clothing-related allergens affect covered areas es-pecially posterior aspect of neck, upper back, lateral thorax, flexor surfaces, axilla. Fig. 8 is contact due to exposure to leather below the abdomen bulge.</p> <p>CONTACTDErMATITIs(CD)</p> <p> Involvement of the chin and under the chin areas, Fig 6b:</p> <p>Figure 6b</p> <p>Figure 7</p> <p>Figure 8</p> <p>ECZEMA</p> <p>ECZEMA CpM4THEDITION</p> <p>Dermatitis of the face, ears, neck are often due to com-ponents of facial, scalp cosmetics, other products for grooming on areas of application, Fig. 9:</p> <p>Figure 9</p> <p> Deodorants can also cause CD, Fig. 10:</p> <p> Topical medications commonly produce Contact Dermatitis. These eczematous lesions were produced by allergy to petrolatum, used as a moisturizer and in an ointment : Fig. 11a on the thighs:</p> <p>Figure 10</p> <p>Figure 11a</p> <p>Figure 11b, on the legs</p> <p>CONTACTpHOTOsENsITIvITy(CpD)andDrug(DpD)</p> <p> The pattern in Photosensitivity whether due to a Drug </p> <p>or Contactant, remains the same, and is similar to airborne CD.</p> <p> Exposed areas are affected but differ from airborne CD by sparing the eyelids and the area below the jawline, Fig. 12a:</p> <p> Spares the area under the chin, Figure 12b</p> <p>Figure 12a</p> <p>Figure 12b</p> <p>ECZEMA</p> <p>CpM4THEDITION ECZEMA</p> <p>AsTEATOTICECZEMA(AE)orECZEMACrAquElATuM</p> <p> Older patients: Appearance of a cracked river bed with </p> <p>poorly defined borders Primarily on the extensor aspects of the limbs and </p> <p>trunk (Figure 14).</p> <p>grAvITATIONAlECZEMA(gE) old term forstasisDermatitis</p> <p> Rarely before middle age Scaling, erythema pigmentation, scarring, often with </p> <p>pruritus and eczematous changes from scratching, topical medicines used, Fig. 15a and Fig. 15b </p> <p>Figure 15a</p> <p>Figure 15b</p> <p> Affects the exposed areas of the dorsa of ankles and feet, Fig. 12c</p> <p>Figure 12c</p> <p>NuMMulArECZEMA(NE)or[DIsCOIDECZEMA]</p> <p> In men: 55 - 56 peak age. In women peak age at 15 - 25</p> <p> Rare in children Single, multiple or episodic, and recurrent at previ-</p> <p>ously affected sites Start as discrete vesicles, papules become confluent, </p> <p>coin-shaped usually up to 10 cm. size (Figure 13a) extend peripherally (Figure 13b)</p> <p>Figure 13a</p> <p>Figure 13b</p> <p>Figure 14</p> <p>ECZEMA</p> <p>ECZEMA CpM4THEDITION</p> <p>PAlmo-PlAntAr VesiculAr eczemA (ppvE):This includes the broadened concept ofpompholyxorDyshidroticEczema</p> <p> Minor, mainly affects sides of fingers with or without palms or soles Fig. 16a</p> <p> Classic, rare, explosive large coalescent blisters Relapsing, acute, subacute, and chronic Fig. 16b </p> <p>Figure 16a</p> <p>Figure 16b</p> <p>OTHErAssOCIATEDFEATurEs</p> <p>ATOpICDErMATITIs(ECZEMA)(AD) Pruritus, intense Xerosis / Ichtyosis, common, usually severe Cutaneous infections often Pityriasis alba Non-specific hand and feet dermatitis Asthma, allergic rhinitis may develop as AD is out-</p> <p>grown in 30% of children Commonest inflammatory skin disease of childhood </p> <p>(15% in the UK) Less common in adults (1-2%) but more severe and </p> <p>chronic </p> <p>CONTACTDErMATITIs(CD) </p> <p> HighdegreeofawarenessandsuspicionneededtorecognizepatternsofCD</p> <p> Persistent questioning yields results about exposure to contactants</p> <p> Habitually used contactants often least recog-nized</p> <p> Occupational Diseases Contact Dermatitis ranks among the top </p> <p>CONTACT(CpD)andDrug(DpD)pHOTO-sENsITIvITyDErMATITIs(pD) </p> <p> HighdegreeofawarenessandsuspicionneededtorecognizepatternsofpD</p> <p> Persistent questioning yields results about exposure to the photoallergen</p> <p> Familiarity with the generic family of chemicals, needed to recognize cross-reactions.</p> <p>PAlmo-PlAntAr VesiculAr eczemA (ppvE):This condition includes the broadened concept ofDyshidroticEczema(orpompholyx) </p> <p> Affects adolescents and young adults Discomfort and itching precedes development of </p> <p>vesicles, small sago-like Dry out, resolve, often without rupturing Secondary infections common</p> <p>NuMMulArECZEMA(NE)or[DIsCOIDECZEMA] </p> <p> Acute edema exudation Chronic: scaling, lichenification, excoriations, itch-</p> <p>ing, mild to moderate Legs usually, also upper extremities, especially dor-</p> <p>sum of hands, trunk Drug history </p> <p>AsTEATOTICECZEMA(AE)orECZEMACrAquElATuM </p> <p> Bed-ridden or confined indoors especially with con-stant air-conditioning</p> <p>lABOrATOryDATA</p> <p>ATOpICDErMATITIs(ECZEMA)(AD) Elevated serum IgE for foods, aeroallergens, micro-</p> <p>organisms, bacterial toxins KOH of skin scrapings for fungi; fungal culture Microbiology by Giemsa staining, Bacterial culture skinBiopsy: Eczematous Dermatitis with mild to </p> <p>ECZEMA</p> <p>CpM4THEDITION ECZEMA</p> <p>ground KOH skin scrapings for fungi/fungal culture Microbiology by: Giemsa staining, Bacterial culture skinBiopsy: Eczematous Dermatitis with mild Eosi-</p> <p>nophilia</p> <p>NuMMulAr ECZEMA (NE) Or [DIsCOIDECZEMA]</p> <p> Bacterial culture CBC, ASO titer, ESR skinBiopsy: Subacute Eczematous Dermatitis</p> <p>AsTEATOTICECZEMA(AE)OrECZEMACrAquElATuM</p> <p> Thyroidfunction tests Organs check-up as indicated by history and Physical </p> <p>Examination skinBiopsy: Hyperkeratosis with a thin granular layer </p> <p>similar to Ichtyosis</p> <p>grAvITATIONAlECZEMA(gE)oldtermforstasisDermatitis</p> <p> venousultrasonography to rule out DVT in cases with acute onset</p> <p> skinBiopsy shows dilated capillaries with thick walls, abundant melanin and hemosiderin pigment deposi-tion</p> <p>spECIFICTrEATMENTTArgETEDATCAusEsIDENTIFIED</p> <p>ATOpICDErMATITIs(ECZEMA)(AD)</p> <p>Improvementofambienthumidity Avoid over air-conditioning place a bowl of water or a steamer beside the bed Avoiddirect exposure to fansDecreasesweating Improveair circulation Avoidhot baths Takecooling drinks Exercisemoderately, cooldownimmediately Avoidexcesseslessenskindryness Takeshort cool showers usesuperfatted soaps sparingly, and minimally use </p> <p>at the creases usethe mildest non-scented laundry soaps for cloth-</p> <p>ing and beddings Avoi...</p>