te (EGIEA TEE Cano) 7D pasic inronmarion DEFINITION ‘ene vulgaris isa chronic disorder othe plseba- caous apparatus caused by abnormal desquama- ton of foliar epithelium leading to obstucton of the plosebaceous canal resulting in inlaeation and subsequent formation of papules, pustules, nodules, comedones, and scaring. Based on thor appearance, the acne lesion can be divided into Intammatery (presence of papules, pustules, and nodules) or nonnfammatory (open and ciosed ‘umedones) For inlammatory acne sons can be classied ss papulopustular, nodular. or both The ‘American Academy of Dermatology clasicaton seme fr aoe denotes the flowing tre levels: 1. Mild acne: Characterized by the presence of comedanes (Fis. and £2) (nonnflaryma- ‘ory lesions), few papules and pustules (gen- erally <10), but no nodules. Moderate acne: Presence of several to many papules and pustules (10 to 40) along with ‘omedanes (10 to 40}, The presence of >40 papules and pustules along with larger, deep- nodular inflamed lesions (Figs. 3 and £4) (up to fv) denotes moderately savere acne, Severe acne: Presence of umerous or exten- sve papules and pustules as well as many nodular lesions (9.5). SYNONYM ene |e0-t0cm coves 1700 Acne vulgaris 170.1 Acne conghobata 170.2 Acne varioltormis 1703 Acne topica 170.4 infantile acne 1705 Bene excoriee des junes files 1708 Other acne 170 Acne, unspecified 1730. Aene keloid EPIDEMIOLOGY & DEMOGRAPHICS + ene is the mast common skin isease inthe us. + Iti mast common in teenagers, with 85% of all toonagers being affected to some degree. ‘+ Highest incidence between ages of 18 and 18 yn both genders, « Involution of the disease usually occurs before age 25 yr, but 26% of waren and 12% of men will continue to have clinical acne until the mi-<0s, PHYSICAL FINDINGS & CLINICAL PRESENTATION + Open comesenes (blackheads, dosed com- eres whtcheads) Greases (oy sk) Presence of scars fom prior acne esis Various tages of development and sevety may be present eoncomtartiy Common cision of acne face, back and upper chest Infammatory papules, pustules, and ecaic pores ETIOLOGY «+ Aone vulgaris is exclusively a folicular dis ease, with the principal abnormally being comodone ‘formation, Overactvty of the sebaceous glands and blockage inthe ducts. The obstruction lads to the formation of comednes, which can become inflamed because of overgrowth of Propionibacterium acnes. Eracerbated by environmental factors (rot humid, topical ciate), medicatons (eg Indie in cough murs, hal greases), nus. ‘val exposure to halogenated hydrocarbons Mechanical or fctonal frees can aggravate eristing acne (eg. excessive washing by some patents to spr them oftheir black: heads or aiiness) (}VbiaGNosis DIFFERENTIAL DIAGNOSIS. Gram-negative focus Staphylocoeal pyoderma ‘ene rosacea Drug eruption Sebaceous hyperplasia ‘Angiooromas, basal call carcinomas, osteo mma cutis (Occupational exposures to ais or grease Steroid acne Hiradenits suppurativa Perioal dermatitis Psoudtolicults barbae ilar Sebortheie darmattis WORKUP History ad physical examination: + Inquire about previous treatment + Careful drug history (hncluding all OTC products) Family history history of joe menstrual fares History of use of cosmetics and cleansers Oral contraceptive use Use of medeations that may worsen acne such as corticosteroids, anabolic steroids, Ithium, neuroleptics, yeosporine Consider the possibility of hyperancrogenic state in all women (sus, regular men 8s, androgenic alopecia) or cilien (ebor ‘hea, acanthosis nigricans, onset of acne between ages 1 and 7 yr and no obvious external factors) LABORATORY TESTS * Laboratory evaluation is generally nat help ful Patients who are candidates for ther apy with isotretinoin should have baseline lver enzymes, cholesterol, and tigyerides checked because ths mediation may result in elevation of lipids and iver enzymes. ‘+ A negative serum pregnancy test or two negative urine pregnancy tests should also be obtained in females 1 wi before inttion of isotretinoin: if also imperative to main tain effective contraception during and + mo after therapy wi isoteioin ends because of its teratogenic effects. Preanancy status shouldbe rechecked at monthly visi, +t hyperandrogenism is suspected in female pallens, levels of dehydroepiandrosterone sulfate (OHEAS), testosterone (otal and tee), land androstenedione should be measured For women with regular menstrual cycles, serum androgen measurements generally ‘aro nat necessary, a TREATMENT NONPHARMACOLOGIC THERAPY * Blue ght (CleasLight therapy system) can be sed for eatment of moderate inflammatory ‘acne vulgaris. Light in the vileUblue range can cause bacterial death bya photoeaction inti porphyrins react with oxygen to gen- ‘erate reactive oxygen species, which damage the cell membranes of P acres. Testment usually consists of 15-nin exposures twice weekly for 4 wk, Phototherapy may be effec tive for short-term treatment of acne, but Jongéterm efcacy and how it compares with conventional acne therapy is unclear. Diet: in obese patients, dietary counseling recommended, high-gheemic diet may worsen acne, although the strength ofits ifuence is controversial ACUTE GENERAL Rx Treatment generally varies with the type of lesions (comedones, papules, pustules, cystic lesions) and the severty of acne. Table 1 sum- Imarizes an acne treatment algorithm. Fisting treatment for mid acne vulgaris icudes ben- 209 peroxide, topical retinoid ora combination tf topieal medications, inusing topical antbiot- les, Use of topical treatments for 6 to 8 weeks Is required to judge their efcacy. Table £2 Aesctbes prescription topical therapes for acne + Comedones (nonnlammatory acne) can be treated with retinoids or retinoid. analogs Topical retinoid are comedolyc and work by ‘normalizing fliclrkeratnizaton, Commonly avaiable agents are Adapalene (Dien, 0.1% gl or cream, applied once of twice daly tararotone Tazorac 0.1% cream or gel applied ai, tretinoin (Retin-A 01% cream or 0.025 gel applied once daly), tretinoin mirosphere {Retin-A Micro, 01% gel, applied at bedtime. Tretinoin i inactivated by ultraviolet ight and cxiized by benzoyl peroxide; therfore it should only be applied at right and not used concomitant wih benzoyl peroxide. + Tretinoin is pregnancy category C and taza tene is pregnancy category X Salicylic acid preparations (eg, Neutrogena 2% wash) have keratlyte and antinlammatory orop- etios and are also useful in the treatment of ‘comedones. Large, open comedones (lack- has) shouldbe expressed, Pationts shoud be roovaluated ater 4 to 6 wk, Benzoyl peroxide gel (2.5% or 5%) may be added i the comedanes become inflamed ‘or form pustules, The most common adverse fects are dryness, erythema, and pooling. ‘Topical anites (erynromycn, clindamycin lotions or pads) can also be used in patients with signicant inflammation, They reduce P acnes inthe pllasebaceous flicle and have@ Acne Vulgaris 17 TABLE 1 Acne Treatment Algorithm ‘Severity (Lesion Type) Ta avon ot Save niente? Sr wan Ban Me nmin ASS ay epeal caps 5 sbsan ef nvacangares 2 swat eseitans ay be condi pla of ucla. neces era yoann sn bul stan. a Zagt Teas OM Beet cate et clay neal oes aap 0% nominate Dae, rc a rape Pea, 05 hat Da a ae st ae thugs erat 765-8208: Cae Hea argent oer arepar am 2 Gna Aire snore Ozone ite, JA ced Dera Sap 1-3 2003. ‘some antiammatory effects. The combina tion of S% benzoyl peroxe and 3% enytro- mycin (Benzaryci) or 1% clindamycin with 5% benzoyl peroxide (BenzaCln) is highly effective in patents who have a mixture of ‘comedanal and irlammatary acne lesion. + Fixed-dose combinations. of clindamycin phosphate 1.2% and totinoin 0.025% are availble (Velin gel, Ziana) and are more effective than ether product used alone: however. they ae much more expensive than the individual goneric component. + Pustular acne can be tested with tretinoin ‘and benzoyl peroxide gel applied on atemate evenings; orying agents (sulacetamide-sufa lotions [Novacet, Sufacat) are also effec: tive wnen used in combination with benzoyl peroxide; orl antibiotics (dxyeyclne 100 img qd or enjtromycin 1 ad given in 2 to 3 did doses) ae effective in patents with moderate to severe pustuar acne. Patents not responding well to these anbiaties can be switched to minocylne 0 to 100mg bid Tablo £3 summarizes oral antics for aene vulgaris. «+ Patients with nodular cystic acne and those with moderate to severe inflammatory acne unresponsive to topical drugs can be treated with systemic agents: anbioties (erthromy- cin, tevacyaine, doxyeyeline, minocycie), isotretinoin (avaliable on a restricted bass). (oF oral contraceptives. Periodic intalesionl ‘riamcinolone Kenalog) injections by a der Imatologst are also effective. The possibilty ‘of endoctinopathy should be considered in patients responding poor to therapy. + Isotretinoin isthe mostetfectve drug availabe for treatment of severe naduleyte acne is Indicated fr acne esstant to anit thera- pyand severe ace. tints P aonescolon- “ation by reducing sebum production and has antinflammatory and keatoic effects tis avalable only on a restricted basis. Dosage is 0.5 to 1 mghalday in 2 dvded doses (max- ‘mum of 2 mg/day); duration of therapy is generally 20 wi fora cumulative dose 2120 g/kg for severe ost ane. Before using tis ‘medication paionts should undergo baseline laboratory evaluation see “Laboratory Tests") This drug is absolutly contraindicated during Pregnancy because of is teratogenicity. It Should be used with cautgn in pants with history of depression Physicians, cstrbuos, pharmacies, and patients must reise inthe |PLEDGE program (nm pledgeprooram com) before using isottinon + Aula acid is a bacteriostatic dearboxiie acid used to normalize Kerathization and reduce inflammation. can be used in preg- rant women, + Oral coniraceptves reduce androgen lev- ‘ls and therefore sebum production. They representa useful ajunctve therapy fr all ‘ypes of acne in women and adolescent gs Commonly used agents are norgestimate/ ethinyl estradiol (Otho Tr-Cyclen) and dro- spirenonelethiny estradiol (Yasmin), REFERRAL Referal for intlesional injection and derm- abrasion shouldbe considered in patients with severe acne unresponsive to conventional therapy, Tele E¢ summarizes altemative veat- ments for acne vulgar PEARLS & CONSIDERATIONS ‘+ Gram-negative folicultis should be sus- pected if inflammatory acne worsens after several months of oral antbati therapy. + Acne may worsen during the fist 30 4 wk of retinoid therapy before improving, COMMENTS Indications for systemic therapy of aone are: * Painful dep papules or nodules «+ Extensive lesions = Active acne with hyperpigmentation + Pationts morale Pations shoud be educated tat in most cases ‘acne can be controlled but not cured and trat atleast 4 to 6 wk of inal therapy should bo required before significant improvement is noted, + The nogatve psychological effect of acne ‘may be severe and long-lasting severe scarring of SUGGESTED READINGS ‘valable a ExperConsult com RELATED CONTENT ‘Acne (Patient information) ‘AUTHOR Fred er MDAcne Vulgaris TABLE E2 Prescription Topical Therapies for Acne Vulgaris Drug Brand Formulation ‘sbiotics Clnaamyein Chola 1% seat, gl pleats, ton Cindalax eaten Clidets 1% ples Cindogel Hoe Evoain 1% foun lnc? Beran 1% 61482 gel use 1% (5% 8 gel Deana 12% 25% BP gel Onexon 12% (8.75% 87 gol Dapsone Dezane 5% oa Enitroryen Linge Eel 29a Ener nay, Stat 2% seuton ‘Stan 1.5% sokten ne mycin 2% cirtment TheramyeinZ 2% ston «28 Enptronyen* Benzamycin 3% (5% 8) gel pa Sulfacatarice Kron 10% tion Pein 10% (6% sully clots, wash Ciena 10% (3% sult era, wash Pasula 10% 4 sur wash oa ais Drlex 20% ream Retinoids Posen iter 0.1% ream, ge, ton 03% gl aaoabene BP! Epidve 01% (2.5% BP gal Taartene Taree 005, 0.1% cream 005, 0.1% gel Fable 01% foam Tretnon Fetnek 0,028,005, 0.1% cream 101, 0025% gel fati-A Mico 004,0.1% gel ta (0.028% ream, gel Dale 0.08% gel Tretnocnsanycin Zana 0.028% (0.2% cladamycn ge vain (10254 (1.2% cladanycr gel 7 ero pre ie ale ‘ted ae nat: a sve Many ese rps hve ert enti ‘onan bey pot. "a Pale, ae Hawt eines pete mabey» bok af i oe ot ads asco 5 Pei, 20, Che 171Acne Vulgaris 1722 TABLE E3. Oral Antibiotics for Acne Vulgaris: Drug Usual Dosage" ‘Comments/Side-Etfects Commonly wed Tetacjine 250-500 m9 Dental taining <9 yt Dairy produce decreas absarpton upset, hoses, teratogenic, PTC, WE, 8D Mireyane 50-100 mg Dental taning <2 55,65, 20,105,118 mp ER airy produce decease absorption it mpg once dit ‘artigo (ower incidence wi E preparation) lyse. ue-ay skin pigmentation, severe dg reactions ‘th epaspreumentis,Lpuslke rasta, 8, teralaganc, heats, PTC, WC, BO Dowyeytne 50-100 mg Dna taing <2 yr 75,100, 150 mgER. once aly produce deraase abserton sai 20mg (‘subantimcotial ——_—Photosnstvty.pholoaychaysi, Gl upset fare teratogenic, PTC, WE IBD dese’) Enthromn 250-500 m9 6 upset (commor, WC rug-cugmaractons, logan ofthe GT rt no longer reammanded by tet experts gen Iceated eitance Lass commonly used Trimetboprin 0/400 m, 160/800 mg Severe drug resctons 48, bone marion supeston, heats, upset, NC had drug exupton: une tullameiocazoe se for acre stony scauaged ‘ncamyein 75.150 m9 Pseuderembranous colts upset, drug reactions, WE Cephalexin 280-500 m5 upset, rug eaions We [ede ese rn: gastos 8D, itera bowl eae PT “Guay ee day or ace rs cows rtd le From Plo Ai A Mr clncl ed ati tek kn srs of cn and ascent , hse, 206 Ee, rome coer 55 Snare one VE wll cand, TABLE E4 Alternative Treatments for Acne Vulgaris ‘Treatment Comment ‘oecone extractor Perermed win eomedeneoxarlor Inectons Invalesona tiancioiore ected to ge ots notes Unt teapy Bue ight ray potoinatvae acres Aaclight (nay have atinlanmatory tect Combination eed ight bense pulse ght PL) Proiodynasc therapy POT) Laser therapy A pulsed dye ase araly use) Reuraing leer nsing bah naralatve and bli recuracing hes) uel for acne cating Dermaarasenidemasinng eet for aoe seating Colagn jctn Use for acne searing Chae! pets Use for acne seating and yperpimentatin Punch gratsssueaugmen set fr ace scaring ‘Wehbreacte ais set for aopic ane sear Fasten tetany ‘Outdated medaty [Panam ton pep From Pater AS Mand A acne ped emriey atc kn srs of chishn and dolce, 5, heb, 206, Ese7D pasic inronmarion DEFINITION ‘Nopic dermatitis is @ genetically determined ‘ezematous eruption that is pur, symmet, and associated with personal amily istory of allorge manifestations (atopy) Box | sum- marzes criteria fr atopic dermattis, Modified criteria for children with atopic dermatitis are Aeserbed in Box 2 SYNONYMS, Eczema ‘pic neurodermatis ‘pic eczema |ep-t0cm coves 1208 Atopic dermatitis, unspecified 120.89 other atopic dermatiis EPIDEMIOLOGY & DEMOGRAPHICS + Incidence is between 5 and 25 cases/1000, persons Highest incidence is among children (10% to 2094) accounts for 4% of acute care pal- ave visits, I affects 1% to 3% ofthe adult Population. Onset of disease before age yr in 85% of patents ‘+ More than $0% of children with generalizes atopic dermatitis develop asthma and allergic ‘hints by age 13 yc + Concordance in monozygotic twins is 77%, PHYSICAL FINDINGS & CLINICAL PRESENTATION + AMopic dermis presentation can be subi vided nt three phases: 1. cue: Vescular, crusting, weeping erup tion 2 ‘Subacute: Dry, sly, erythematous pap- ules and plaques. 3. Chronic: Liceniication fom repeates seratching + The lesions are typically onthe neck, face Upper trunk, and bends of elbows and knees (eymmetsc on flexural surfaces of extrem ties) (Fo. 1, A. and Fig. 2). Atopic derma. Its lesions are usualy ciscrete but vaguely delineated, scaly and erythematous. ‘There is dryness, thickening ofthe involved areas, discoloration, blistering, and oozing Papular lesions are frequently found in the antecubital and popliteal fosae, In chien, red scaling plaques are often confined to the cheeks and the perioral ana perinasal areas. ‘+ Hertoghe sign: Loss of the outer eyebrow ftom ehranc ubbing (ig. 1.8, + Constant scratching may result in areas af hypapigmentzion or hyperpigmentation (ore common in backs). BOX 1 Criteria for Atopic Dermatitis, Major erteria Must have tvee ofthe followin: © Pras + Typical morphology and distribution + Flenaral ichenieaton in aduts + Facal and extensor involvement In infancy + Chronic or enrerically relapsing dermatits * Personal or family history of stop disease (e.,, asthma, allergic rhinitis, atopic der mattis) Minor criteria Must algo have thee othe following = Xerosis + htyosis or hyperlnear palms or keratosis pars * IgE react (mediate skin test reactivity, RAST test positive) * Elovatod serum IgE + Early age of onset + Tendency for cutaneous infections (especially Staphyloceccus aureus and HSV) * Tendency to nonspecific handioot dermattis + Nipple eczema © Chel + Recurrent conjunctivitis ‘+ Dennie-Morganinfrarotal fold * Keratoconus * Anterior subcapsular cataracts + Orbital darcening «+ Facil pallor or facil erythema + Piyriasis aba * ch when sweating + Intolerance to Woo! and tp sovents * Porifolicuaraccentuation + Food hypersensitvity ‘+ Course inuenced by environmental or emotional factors * White dermatographism or delayed blanch to cholinergic agents Sw Herpes apes its: I, erunoghbuln E: AAS! rasalergoenent asa, From les WD st at Arcos" dresser! she 12, Phsdpie, 216, Saunders, In adults, redness and scaling in the dorsal aspect ofthe hands or about the finger are the mast common expression of atopic dr- malis; oozing and crusting may be present + Secondary stin infections may be present (Staphylococcus aureus, dermatophytosis, herpes simplex. ETIOLOGY Unknown; elevated T-ymphocyte activation, Aetectve cell immunity, and B-cell gE overpro- ction may play a significant rok. (}yoIeNosis DIFFERENTIAL DIAGNOSIS. * Scabies * Psoriasis Dermat herpetiorm Contact dermatitis Photosonsitity Seborheie dermatitis Candidiasis, tea Lichen simplex cronicus Other: Xerosis, impetigo, Wiskot-Aldrich syndrome, phenyketonuria, ichthyosis, HN Germatiis, nonummular eczema, histo- cytasis X, malignancies (T-cell iymphomal mycosis fungoides, LettererSive disease), raft-versus-host disease, metabole and hutrtional deficiencies (zinc, niacin, pyt- oxine deficiencies) BOX 2 Modified Criteria for Children with Atopic Dermatitis Essential = Prtus + Eczema, + Typical morphology and age- specie pattern + Chronic or relapsing history Important features * Ear age at onset + Atopy ‘Personal or fay history + IgE reactivity = Narosis Associated features + Alypicl vascular responses (eg. facial pall, white dermstographism) + keratosis paris, ichthyosis, or hyperin- ear pains. + Orbital or periorbital changes = other regional findings (e.g. perioral changes, peraurcua lesions) + Perifolicuaraccentuation,lchentieatio, or peurigo lesions atures@ Atopic Dermatitis FIG. 1 A, Fiesral atopic dermatitis wth ichanicaton, Many ofthe skin changes are secondary to scratching. Linear eheniteation, as shown here, and excoratons are ype B, Hertoghe sign: Los ofthe outer yebron may occur in haat paint a a result of cri ubting. rom We GM, Cox NA eds: Diseases of the ‘shin coor atas and texted 2, St Lui, 2008, Mosby) Table 1 summarizes characteristics and c= cal features of disorders in the dferental agnosis of atopic dermatis WORKUP Diagnosis is based on the presence of tree of te folowing major features and three minor featus, [MAJOR FEATURES: Prius Personal or family history of atopy: Asthma, allergic rhinits, atopic dermatitis Facial and extensor involvement in infants and children Flexural ichenifistion in aduts [MINOR FEATURES: Elevated IgE Exzema-pertolicularaccentuaion Recurrent conunctvtis letnyosis Nope dermattis Woo! intlerance Cutaneous $. aureus infectons or herpes simplex infections Food intolerance Hand dermatis (nonalergic rian Facial allo, facil erythema nels White dermographism Ely age of onset (after 2 mo of age) LABORATORY TESTS Lab tests are generally not helpful Elevated I levels are found in 80% to 90% of atopic dermatits + Cans by ony t et shew teanen (Qi reearmenr NONPHARMACOLOGIC THERAPY © Gp al decrease arson sn + frucnc of tary te 1 Sulion tongue aes, sweating low hay Oe wer 2. Sone wth tag ssace wot tole ome sap ad ort tne) 3. Feds tt poke excels 9 toon peau fn oy wet 4 Stoo 5 Hlogens an at & Sete ns esting « Putoray uray maybe fects invent aoe ACUTE GENERAL Rx + Emollonts can be. used to provent dry- ness. Severely fected skin canbe optimally hydrated by occlusion in adaton to apolea- tion of emolients. + Low-potony topical corticosteroids (0.9. 1% to 25% hycrocortisone) may be helpfl and fare generally considered first-line therapy. Use intemedite-poteney steroids (e.9. i- amcinoioe, fuocinolone) for more. severe cases and limit potent corticosteroids (e9 belametrasone, desoximetasone, clobetasol to severe cases. Tale 2 summaries relative potencies of topical corticosteroids. (rsaborole 2% ointment i a phosphodi- esterase typed (PDE) inhibitor modesty effective for shor-term ‘reatment of mild to moderate atopic dermatitis Oral antihistamines (@.9.hydroxyzine, tiphenhydramine) are effective in controling paris and inducing sedation, restful seep, and prevention of seratcing during sleep. Doxopin and other teylic antidepressants also have antihistamine eect, induce sleep, and reduce pratus The topical Immunomodulators pimecrolus and tacrolmus are especialy useful or reat- ment of the face and inertginous sts, where steoidinduced atrophy may occur However, due to concems about carsnogenic potential the FDA recommends imiing ther use for short periods in patients who are Intolerant or unresponsive to other weatments Pimecroimus cream 1% applied bid and has antinlammatory eects secondary to block- age of activated T-call cytokine production Tacrolimus ointment (0.03% or 0.1%) applied bid is @ macrolide that suppresses: humoral and cell-mediated immune responses, ‘+ al prednisone, niramusculrtiamcinolone Goeckerman regimen, psoralen and utavioit Aight therapy are generally reserved for severe cases, ‘+ Cyclosporne, azathioprine, mycophenolate and interferon gamma are sometimes ted ‘or recalcitrant disease in adults by physi- cians wo specialize in severe inflammatory skin condos. ‘+ The human monocional antbody dupiumab is effective in adults with moderate to sovere atopic dermatitis that have not responded to topical therapies. tt can be used with or without corticosteroids. tis injected subeu- taneously. Cost isa lmiting factor. 4 Table 3 summarizes the management of topic dermatits DISPOSITION + Resolution occurs in approximately 70% of patents by adulthood. ‘+ Most patints have a course characterized by remissions and intermittent fares. SUGGESTED READINGS Avalable at ExpertConsultcom RELATED CONTENT Dermatitis Patient information) Eczema (Patent Information) AUTHOR: red er MD 185 sioposia pue1s Atopic Dermatitis @ TABLE 1 Differential Diagnosis of Atopic Dermatitis (AD) Main Age Group Affected Frequency” (Characteristics and Clinical Features seer bats common ‘Saimor-red greasy sa lesions, often on te scalp (rae cp) cate ‘and raphe are: geeraly oresens in th frst 8 we af: ‘peal lars win weaks saber esate common tamalous patches wth allow, white or rash scales in seb- amats trae sens, paricllythe sap cenval face and eter chest rma Chere ane aus common ‘Coin-shaped scaly eles, masty on es and butecks usualy emats ravten tant contact Chen an acu common out t tri ezemateus lesan, mst confined tothe sie ermatts of exposure; story of lal appl inant is a sk facto righ coos wih AD Alegl onact den ane suits common Eczema rsh with masinum expression at shes o ares xp. eats sce but might pread story of cay apie rani 2 Fak acer, might coma with AD Lieto sine este common (ne or more cae ckcumscribed,cherifes plaques tht cronies result rm repelive seractng or bing because of itanse teh Asti eczema ate common ‘Sealy sured pate of crate ovryng dy sin, mos ten on over les Infectious Skin Diseases Dermatopyte Chen ane ate common ne or more demarcated scaly plagues with cent clearing and inecton slg ried redaneseage vara eh Ingetiga criden common Demarco ertematous patches wth ster or honey yl crusting sealer eriden common! ety sper turows and pustules on gals and sola, Between fingers, and on geal ig produce secondary tezoratous changes HY (here ane ats Uncommon Sebathestke ash Keratinzation Diss Tentyossvalgaris fants and alts common Ory skin with ne sealing, pata onthe lower abdomen an ‘censors; perfolicuar skin augheing: paar hyper~ linen: fal form (2 FLGmtatons uncommon: cen coon wre ad Nutritional Deficioney-Matabolie Disorders dine efiency Children Uncommon Eryharatous scaly palches an plaques, mas ofn around the (acotematis mouth and ana rae congenital frm accompanied by ahaa Ferteropatica) and abpeca Bion decency bons Uncommon ‘Sealy perioral deat, ape, conjunc, tary (euro or Typotnia Dtinaredaiceney) Palogra iain Mages Uncommon Sealy crusted epidermis, desquamato, sun-exposed areas, ar celery, hea wasboton bats anderen oogrptic lak say dermatits, swollen in with races pong patches ‘oendent Prenshetonuia bats seamen ematous rash, hypesigmentatn, onde ha, developmental ‘alay Neoplastic Disease Culnonue Te ats Uncommon Etyemalous ps troan acu and lags witha fies lymphoma pry espnsive otal caress val ite ery stages) Langerhans cot bats Uncommon ‘Sealy and pupurie dermal, nepalosplnamepay cjopeiar Fistoyais ‘Caen appetinaty ih otoT ie commen = 1a 12011 00: are 1 100 tin 10.00% 1 in 9000. From Mgmnt Nan Tak Peds 21, Peis, 2020, Shave,@ Atopic Dermatitis 17 TABLE 2 Relative Potencies of Topical Corticosteroids rom Most Potent to Weakest) wa Class Drug Dosage Form(s) ‘Strength (%) Tiara Ange vanes cx os Se cx pre ce nt os seme per ‘prt etre com tos uy seamen Spon cram iu en os p ees tem rer re i nesses er vos Davee ste oan oes | Psa Ga re tn eos vane ce eam ne 08 14 om ty brace let crams i en os Poca mee Oran ime oor fro em oe tos tone eos oem o Trane ie am ie EB ‘awe eto ay rete ne oe rn 2 Pecans com ow ny ence Ge gm eo tos Pcie ete rm ston oo one pny a oean 03 weer Ge i in oases Pere so one ro os From Fair AS, Monee Hn inal pated a ebook an arr of ison and gee, 5,201, Ee TABLE 3 Management of Mild, Moderate, and Severe Forms of Atopic Dermatitis, wi Moderate Severe ating and baer par ating ad barre par Bathing ard baie par ‘ccane oferta and Serge ogee ‘rose of wan and serge ogee Aceanee ofan nd lege Wiggers btemiterehoeterm usecase Var top-_Inarmtent, tartar ue of he IV topical Clas I top tro fr ae; cae S- tap terie + sted + top caineven ino ‘sods = toplal acneun nibs ‘azrolms omen fr maliennce Treatment of suprnecton Tweament of suprnecton Treatment of supernecton Oral aninstamiee Oral anthstamines ‘Systemic aninammatry agents, revi ight therapy "Bark epar maybe aarp by plein ot fei eas 9 ar reap ae From Por AS Mace A art al pets drmty nk kn adr ae and decency, 5,201, EeeBullous Pemphigoid Ezrs PHYSICAL FINDINGS & CLINICAL enon, cast! (nd ay te CD BASIC INFORMATION) Prescirarion trgotri cowering ene nb) rsront poncho dees, tem DEFINITION Tsenes ate pacing cpr Bullous pemphigoid (BP) is a chronic, autoim- 1, Non-bullous phase: Starts as excoriat- ‘ins, sulfasalazine, acetylsalicylic acid, non- mune, subepidermal blistering disease com- ed, eczematous, papular, or urticarial ‘steroidal antiinflammatory drugs (NSAIDs), ‘monly seen in the elderly. Itis the most common plaques characterized by extreme pruritus: dipeptidy! peptidase IV inhibitors (gliptins), sree tent hoe sions ore: 2. Bil pase ecu tay monhe Tse mrad vcs ‘toses. Other related diseases in the pemphi- later and is characterized by formation of * Additionally, there are several reports of UV- OF atl time ences amsebltan is rhb on ince etadan Pare nuces BP cicatricial pemphigoid (MMP), anti-laminin 332 flaccid after rupture '* BP patients are significantly more likely pont, Buty amp ot, PANSIEAL FHS 1 fae Youn eno rg laminin gamma-1 (anti-p200) pemphigoid, and —* Anatomic distribution: sclerosis having the strongest association; Str napountSoneemeacainte 1"Hsurtcs of he ams ad legs, sor Dprdaorr denen soa IgA bullous dermatosis (LABD) and epidermoly- groin, axilla, chest, and abdomen; gener and Parkinson disease are also associated Shuts scusta G98 ote ome aM Sy esther mk ina? sedate eal hrecercedty aes; 2. Wein nentane mene een in Groulecsemeicsnnenancenes| "tow low apaens foam pent (DIAGNOSIS Srbtonet mere te pal ieee he omar wih ara ft) Digs Is based on a contnton ef svmonves ‘+ Lesion configuration: clinical, histologic, and immunotluorescence & {Pay bebeled np t 20% fees fining Dec inmneuorecenes Penh (ecteiies neateapron ar tosne isos ste go sed fea fronted medal toy ning tea oe ee 2, Berta jae an emo oneal pans of pa ase te-toe cone ster andmayraolesyoaromt ae hevlpe aye disses and 120 Bulls pempnins fiome semoeen mlances, and medication hisry over + Let maha ope Cron, sab coe BF EPIDEMIOLOGY & PRMT eC tue meaning 93 Sd be Ngan‘. oon DEMocnaPnics tin lett an eg Gecroe_ sity pater peng wi aeertaed "tat common e te ainnute buss “Song Chenaernemalor__ fer fontearig iss wie mozota Somos dred eas iia se rele reer and yg te hee nck cee eer ate yay 2 Re ten Tgnre Wo send of Th dagen be nee wi he Weslo ncating owns yon endetbusastctsrupun nda on pt ‘satis mat nea 9 Myo eg Tate BP ctr: Tee of ew de STEGUEC Rian deta apne 3. Hea wine seri bt may nw "fees (ae S75, rc, nes Metmetevate a's cae Seem guctntanmaty hpenbmaraton o,f shane of Bla sone on Itoposonyrin te US andor fon teem fan rd ne ps enn ete 96 2.4 to 42.8 cases per 1 million person-yr in and/or C3 deposits along basement mem- Europe. person ETIOLOGY brane on DIF microscopy «Eee seminary rxsin con, = Atcmmane dase wh munegbu- 2 Sn bp) Evans 60a atemet caer Sy cy'aettene "bn. andl C3 complet ey matic aothoge on eto Se se andesncond en BPISO a BBEID)_mureers (mee a ea tng ne! end h be oleral bueno new”. Sknbepy eon ae BF0 an entot te ecioningeing cast _ bare roe erat thao ye ctatncesonenme seinimaateceerttueccr + Bpindaed pemphigoid. athoagh Ink immuraon sy LN age 80, luncommon, can occur in patients "2k EEERENTIAL DIAGNOSIS + Bullous arthropod bites * Linear 1g bulous dermatosis, * Dermatits herpetiformis «+ Aati-laminin amma-t(an-p200) pemphigois Brunsting-Pery pemphigoid Bulous systomic lupus erythematosus Mucous membrane or cicatricial pemphigoid Epidermalysis bulls acquista Pemphigoid gestainis Bullous erythema muttforme Generalized fxed drug eruption Impetigo Porphyria cutanea tarda Blous lichen planus Pemphigus wulgars Paraneoplastic pemphigus Table Ef compares some ofthese immuno- bullous aiseases FIG, E1 duilous pemphigoid. Large, tense bullae ae seen onthe lower region ofthe abgomen inthis 18-year-old boy. Tom Pall AS, Manca Al Hurt cna pedlae damatology textbook o kn car. © LABORATORY TESTS rs of childhood and adlescence, a8, 201, Philadelphia, Elsevier) * Histology of lesional skin27406 Bullous Pemphigoid @ TABLE E1 Immunobullous Skin Diseases Immunobullous Targeted Protein or Tissue Disease Clinical Prosentation Sorum Autoantibodies Structure Immunotiuoresconco* Pemphigus Dermatoses Pemphigus wigs Flaccid bullae on nonin- flamed skin, crusting, postive Nis sign} ‘commonly atfets scalp, chest intertiginous areas, and oral mucosa Superficial bulla, erosions, ‘and scale with cresting, Epidermal IgG and C3 call surface staining IgG epthtal cel suiace; conelates with disease activity Desmoglin 3 and desmoglein 1 ofthe desmasome Pemphigus foliaceous IgG epithelia cel surtace comelates with disease Desmoglein 1 of the desmasome Epidermal IgG and C3 cell surface Staining positive Nikolsky sign? activty Paraneoplastic. Flaccid bulla, lchenoid or g6 epithelia el sutace Desmoglin 3, desmo- Epidermal IgG and C3 cell sur pemphigus erythema muitforme and basement membrane pak 1, desmopla- fae and basement mem- ike, usually inoWes 2one anng on kin 2, PAG, envo- brane zone staining mucosa, often exten- rodent bladder eitielum paki, perpaki, sively includes esopha- is charactersto):cove- ater proteins ofthe geal and respiratory Ines wih cseaseactvty —_desmasome and areas hemigesmosome 9A pemphigus Faccid bul, similar to ighelthlia cell surface: Desmocolin ofthe Epidermal igh call surface pemphigus vulgaris corelates with disease desmasome staining actviy Pemphigold Dermatoses Bullous pemphigoid Tense bulla, offen on urt- IgG basement membrane _—_-BPAG2, BPAGI Linear basement membrane ‘carl base, prominent one, epidermal hemidesmosome, zone IgG and C3 pruritus amin Wcida Mucous membrane or Tense bullae and erosions, IgG basement membrane BPAG2, laminin 382 Linear basement membrane teal scaring sequelae Zone, epidermal (previously known zone IgG and C3 empnigoid as laminin § or epi- gti), hemidesma- some, lamina lucida Pemphigoid Tense bullae, similar to bul- Complement xing, base-_BPAG2, BPAGI Linear basement membrane gestationis lous pemphigoid; onset ‘ment membrane zone, hemidesmosome, zone C3 uring or immediatly epidermal Tamina lucida ater pregnancy Tense bullae; commonly ‘curs in areas of ta sma arin orl mucosa Linear basement membrane zone IgG and C3; may show linear igh and gM Epidermolysisbulosa scmusta IgG basement membrane zone, dermal: ‘Type Wt collagen, anchoring fons Linear igh butous Tense bulla, similar to IgA basement membrane __97-K0 portion of LUnear basement membrane dermatosis and bullous pemphigoid oral zone, epidermal rarely BPAG2, hemides- zone IgA chronic bullous dis invoWement common in derma ‘mosome lamina ease of childhood ‘adult disease Tucida Dermattishorpat Small bulze on extensor ‘IgA endomysial and vans- Epidermal ransgluta- Granular basement membrane formis| surfaces (elbows and slutaminase antibodies; mminase zane IgA with siping in ven) markedly prurt- correlates with disease oral papilae ic; assocated wit ines-_actvty and compliance tial gluten senitvity with gluten-free det Bulous lupus Tense bulla, photodstib-WyG basement membrane Type Vi collagen near basement menbrane erythematosust uted zone, dermal ‘anchoring fois zone gf may stow grrr IgM and C3 basement mer rane ze asin bps band Sp) 2204 ml prin a | G2, Dba pr ati canna ange ca et snatuinera Gp bt rags ant ee seer Serie ts "wala sata eben tn Raman pl ny ae! rere om From inant os ln alr esa pte oP, 2016 Sura, 1. Light microscopy: Subepidermal bullae wth eosinophils and/or neutrophils with associted eosinophil andor neutrophil ‘ermal ntitvate 2, Direct immuncfuorescence (DIF) miros- copy (gold standard}: Linear and or C3 deposits along dermoepidermal junction + Immune serological tests. sot: Only confi matory with DIF microscopy findings 1. Indrectimmunatuarescenc Crating IgG ant-basement antibodies using mai NaC-separated normal skin as sustate 2. EUSA: Test for ant-BP180 IgG; if nega- tive, test for an-8P230 gd a TREATMENT Bullous pemphigoid may be a sel-limited ds aso, but Is course may last ftom months to yrs, Treatment is based on the degree of isease invoWement and the rate of dsease@ Bullous Pemphigoid 27-7 progression; however, there is no general con- sonsus on how to determine disease severity A European guideline defines severity by percent skin involvement, with ess than 10% defined as nil, between 10% and 20% defined as mader- ate, and grater than 30% defined as severe, NONPHARMACOLOGIC THERAPY + Mild soaps with emolients to wt skin after bathing + Use ofronadhernt kes nth case fon ‘Se eos lesions to prevent betel supe ‘ecton minimize pai ar prorat reaing > Only ran larger blisters and leave the biter toof intact as a natural essing; remove fue tering skin only in broken bistrs + Avoid mechanical trauma tothe skin ‘STAGE-SPECIFIC THERAPY * Mild: Topical cass | steroids daly + Moderate: Class | topical steroids dally sys temic therapy may be added as needed ‘TREATMENT-RESISTANT ‘THERAPY, ‘THERAPY ‘Once dsease contl is achioved with oral storolds, begin tapering corticosteroids by 25th at 7- to TM-day intervals; if induction tose is less than 20 may, taper over 2- to 4-wook intervals, + Severe: Clas topical steroids daly in com- + If relapse occurs, return to dose given two reduction intervals prior can resume taper ator 14 days of disease control lesions. bination wih systemic immunosuporessants + Inalesional tiameinolone acetonide to 0- lated lesions “© May adé or switch to adjuvant agents as + Oral antihistamines to contro pruritus needed. TETRACYCLINES + Daxyoydne 100 mgtwiedalyissinfarinefoc. lesions tiveness to oral prednisone, with decreased ‘Se eft compared wth ol steroids. + Tetacyeline 500 mg four times dally pls rico tinamie $00 mg thoe tims daly had simi ceflectveness as predrisone 40 to 80 mg dally. SYSTEMIC STEROID INDUCTION THERAPY * Prednisone (or equivalent) 0.5 mg/kg per ay, which can be combined with adjuvant + Disease contrl is defined 28 no new lesion {ormaton concurrent with healing of exsing DISPOSITION SUGGESTED READINGS BageIS et al: Bulbus rerpig,Atoimmun Rev 185} 445-455, 2017 Baan & et a: Pemphigus wiya Is the most common auonmune bulous lsease in Norhuestrn Romani, int J Dermatol 49(7:788-774, 2070. Baum $ et a: Diagnosis and easteaton of auoimmure Misting sare, ‘Autorun Re 144-5) 482-£88, 018 Bene J ela Bullous pemphigoid and dipepyl peptidase W iis: a case- nenease study in te French Pharmacoglance Databese, Br J Dermat! 1752286-201, 2016 Bia WP et a Localzs buleus pemphigoit on sts of raaterapy and lymphedema inte sare patent Inan Dermatol Onn J Supp 23S101— 3103, 2014 Brick KE ela Icdence of bulous pemphigoid and mortally of pts with bullous pemphigoid in Ose County, Mnnesca, 1860 through 208, J Am ‘Acad Dermatol 82-88, 2014 Cots B et al: Atommune bullous disease Swiss stusyG: morality of bulous ompignid in Switzerland: a prospectvestuty, Br J Dermatol 1652) 388- 374,201, ia Funte Set a: Postracaton bulouspemphiel ininfany- report of tree new cases an trate review, edt Dermat 308)74-744, 2013 Di Zanzo Geta: Bullous pamphigot rm the nc ate bench, Clin Demate) s0()16, 2012 immunasuppressve therapy, including aza- thioprin, dapsone, doxyeycie, methotrex- ate, and mycophenolate mofetil + Ina doses greater than 1.0 mgikg of pred- risolone show Ite added beneft «+ Intravenous immunoglobulin therapy 2 g/kg er oft (4- to 6-week intervals) ‘+ Immunoadsorton or plasmapheresis “+ Rituximab (ani-cD20) 1000 mg W on day 1 then day 14 or 875 mgimé IV administered four times at weekly intervals SYSTEMIC CONSOLIDATION + Relapse is defined as greater than three new lesions per mont or one lesion greater tan 40m that does not heal spontaneously in one week or progression ofthe exsing lesions or emergence of daly purus. In the Unites States, moray rates are est- mated at between 11% to 23% after 1 yt, Standardized morality ratios range trom 1.90 to 6.6. BP isa chronic disease; exacerbations and relapses are not uncommon, even in success- fully treated indviuals, A recent prospective study reported 45% relapse rate of the evalu- able patents a 12 months, with the majority of felapses occuring in te frst 6 months afer cessation of therapy n this study, an ELISA ther soore thee times higner than the normal cutoff valu at time of therapy cessation was the main predicting factor for 8P relapse within the next Dementia and intial extensve disease may be two additonal independent risk factors asso- ciated with relapse during the fist ro harap. REFERRAL Dermatology PEARLS & CONSIDERATIONS COMMENTS: * Pruttus can be the presenting complaint and can precede the appearance of any skin + Bullous pemphigoid should be high on the diferental in paints over 70 yr old with tense bullae, + Exemely prrtc uricaral plaques can pre- ‘cede onset of tense bulla by months + Doxyeycine 100 mg twice daily is equally effective tool prednisolone, RELATED CONTENT Bullous Pemprigos Patent Information) ‘AUTHORS: Sara Mora Tuehayl, MO, snd achiuC Lee, MD, MPH ming ta: 5 guidelines for he treatment of pompigus vgersotacous and bullous penphiat isch Dermat Ges 13)8833-844, 2015. Falcin tat Management of buleus pemphigt the European Dermatology Forum consosut in calibeaton with the European ade Of Deacon) ‘ed Vneresogy, Br J Demata 172 887-877, 2015. Feel Feta: Cinical and immroloi ators ascorited wit bllous peg ‘goirelapse curing the first year of treament a muiceie, prospecive study JAMA Dermatol 1501) 25-38, 014 lsohashi Fo aA case of bulls pemphigoid exaoerbstad by iadaion ate breast conservative radteray, J Cin Oncol 811-813, 2011 ily Petal: Incidence and mortal of balous pemphigoid in France, J vest Dermata13281898-2004, 012. LYE, Yew YW Lambert WC: Bulous pmghigaé adits association wth eo loi eeeaser 8 systamati review and mela-nais, J ur Acad Demalal Venere! 30(12 2007-201, 2018 ‘sha 0, Lprtay 6, Grenae T: Bulous pemphigl folowing ajant radio ‘therapy fr breast cancer, Beast J 172:204-205, 201, ‘Sear ta Buloue pomprigndinauces by easoterapy recur on recha: lenge, cn Exp Dermat! 87(8)916-817, 2012 Wiams HC aa Dorje versus predaisoln as an intalweabrant stony for bulois pemphigod: a pragmatic, norinerory, randomised controled a, ance 380079)1630-1638, 2017fm Dermatitis Herpetiformis 49 © 7D pasic inronmarion DEFINITION Dermatitis herpetiformis (DH) i an autoimmune bisterng disease that Is considered to be a cutaneous mantestaton of celia disease (CD). Its associated with gliton-sonsitve enter- ‘pathy in near all cases though only 20% of Patients have gastrointestinal symptoms. 15% to 25% of patents with CD vill have DH SYNONYMS, DH Dunring disease |ep-10cm cove 113.0 Dermatitis herpetiformis EPIDEMIOLOGY & DEMOGRAPHICS PREVALENCE (IN US): 11 cases per 100,000 persons per yr prevalence for CD is one in 133 adults PREDOMINANT SEX: Male predominance (2:1), however, female predominance in chien PREDOMINANT AGE: Fourth decade a Ie, but can occur at any age PREDOMINANT RACE: Most common in Caucasians of Northern European ancestry GENETICS: oth CD and Di have a stong genetic component. 10% to 15% of patients with DH have a frst-dogree relative with ether DH or CD. Specific HLA genes (involved in process- ing giadn angen in geneteally susceptible Indviauals) have also been shown to predispose to developing DH (HLA-DQ2 in 90%, DOS in the remaining 10%). However, les than 50% of genetic predisposition i atbuted to HLA genes. PHYSICAL FINDINGS & CLINCIAL PRESENTATION ‘Classically, the lesions of OH aro small, ‘rouped,“herpetiorm” vesicles that are ds- ‘rbuted symmeticaly on extensor surfaces (elbows, knees (Fig. £1], scalp, back, and buttocks). However, due to Intense prurtus and scratching, pinpoint erosions and exco- riations in the above distribution are often ‘he most prominent fndings on examination, wth ntact vesicles rarely seen, “Spontaneous improvement with oytc exac- ebation is common, + Celiac-type enamel defects to permanent teeth oral vesicles, or palmoplantar purpura have boon ropored as potential associated ‘indings PATHOGENESIS (0 and DH are both autoimmune-mediated by immunoglobulin A (ig) class autoantibodies. Dietary glten is carta tothe pathogenesis in both. In genetialy predisposed individual, tis hypothesized thatthe gluten by-product, an, complexes with tssue ranslutaminase (6) in ‘the gut binging a8 an antigen to HLA-DQ2 on T calls, creating an immune response that results in antTG IgA antibodies (Le. atiendomysial antibodies) in the blood. 176 cross-reacts with ‘epidermal TS (eT). The blood of CD patents with and without skin disease is found to have both skin and gut ant-T6Ig8 antibodies. Ye, t is thought thatthe high-affiity Ig against eT {erm complexes that are responsible for i. The deposition of lgA-eTS complexes inthe papillary dermis triggors an immunologic cascace result ing in neutrophil recruitment and complement acivation (}ybiaeNosis Physical examination and routine histopatho ‘ogy ae often suggestive of DH; however, ect immunofluorescence (OIF ofa perlesional skin biopsy has pathognomonic findings and is the gold standard for diagnosis. Fig. 2 describes an approach othe pation with suspected derma ‘tis herpetiformis. DIFFERENTIAL DIAGNOSIS + Cinically and histologically, the etferential dagns's includes: 1. Linear igh dermatosis 2. Bullous pemphigoid 5. Bullous lupus Those diagnases canbe differentiated by DIF on prisionl skin biopsy Other ania diagnoses to consider 4 Scabies (check for inesigitl burrows and invclverent of genitalia) 2 Arthropod bite (papular urtcaria over exposed areas) 3. Eczematous dermaits ll-defined weep- Ing erythematous plaques) 44 Herpes simplex or zoster infection (pain ful not symmetric) 5. Generalized prurtus (no blter history) WORKUP AND LABORATORY TESTS * Evaluation for gastrointestinal. symptoms, family history of DH or CD and prurts shoud be sought in patents with suspcted DH + Lesional skin biopsy: Wil demonstrate 2 noutopti-rch subeplermal bulla and rule out many conditions. ‘+ DIF of normal-appearing perilesional skin biopsy: Wil demosstate pathognomonic Ink epost localized to the dormal papillae and dermal-pidermal junction ina granular patter + Serology (enzyme-linked. immunosorbent assay [ELISA for Ig tissue transgltamin ase, ELISA for Igh epidermal transgltamin ase, if avalable, and indirect immuno. rescence for yA endomysialaniboces (otal IgA) can be used to aid in the agnosis of DH in cases where the OIF is negatve or ‘equivocal, or for monitoring disease activity response to treatment. hough these ci culating antibodies n the blood exist, there is high false-positive rate for antssue TS and fo antiendorysal antibodies (one tia of DH patients are negate for aniendo- mysial antibodies}, and their absence does not exclude the diagnosis. Also, IA-defcient DH patents may aso nave negative serologic results. Those with th prosence of circulat- ing antibodies wil have a reduction in levels in response to treatment adnerence a TREATMENT [A gluten-tee det (GFD) and dapsone are con- sidered first-line therapy and are often started in connection + GED mproves symptoms ofboth Gland skin dis- ease, wih Gl responding queker (kin responds attr 2 mo. A reespectv study showed rmis- Son 2 yr witht symptoms) in 12% Dapsone results inimproverent of skin mani- festations within days but does nat teat Gl manifestations. Dapsone is typically tapered cover time, while felong gluten avoidance is oten necessary + One study demonstrated GFD alone was comparable to GFD plus dapsone in the ‘weatment of DH; hence GFD is an essanil ‘component inthe treatment of Di. NONPHARMACOLOGIC THERAPY + Fist line: GD: 1. Avoid barley, re, wheat (can consume ric, com, and oats) 2. Consultation with a cletitan is recom- mended ‘3. Most patents need to follow let indet- ritely; however, cases of spontaneous remission have been reported, + Second line: Elemental it (controversa 1. Can consider elemental det aveidance of hole proteins) in those patents wo do not adequately respond to a stict GFD; however, data are limited. ACUTE GENERAL Rx «Fist lne:Dapsone: 1. Inia dose 25 to S0 mg PO daily with (gradual increase to an average mainte- nance dose af 0.5 to 1 mg/kg daly ten maintenance dose of 100-mg dal. 2, Glinical_ monitoring weekly is recom- mended to aptmize dose (optimal dose is when 1 to 2 new lesions ‘3, auton: Dapsone may produce hemalyis (especialy if G8PD deficiensy),agranu- locytosis, methemoglobinemia, systemic tug hypersensitivity reaction (DRESS), and a peripheral neuropathy. 4, Baseline labs: CBC, LFTs, O6PO levels ‘tar te intition of therapy, monitor CBC every wk x1 mo, then every other Wk x2 smo, montaly 3 mo, then every 3 o 4 ma. Monitor LETS every 3 to & mo, + Seconds aternativs: 1. Sulfpytidine (00 to 1500 mlday, com- Pounded. medication) or sulfasalazine {600 to 1000 mg bd) may be substtuted in cases of dapsone intolerance or inthe rare case that neuropathy develoos. 2. Case reports of efficacy using topical dapsone 5% twice daly In patients who o not tolerate oral dapsone; also report-@® Dermatitis Herpetiformis «us jopsies + Lsional punch biopy for RE + Perfesional punch ropa for DIF biopiy rents Monterey iG. 2 Appr ey te aa ane es Tm Beri, {Aaa A “Screening for associated diseare Del poote SDE ld peocoe st eke " + Ober Buoimmane sera Soved Texan focings «onal bod near + Total + An eae Consider genetic testing + HIADQ2, HAD OS: ipa ‘analysis ach tothe patient with suspected dermatitis herpetiformis, DH, Demattsherpettoeis DIF srctimmunaorescence: eT, epidermal ans- jutamiase; HAE ematonin and eosin; HLA-D02hstocompabailty locus atigen haleype DO2: HLA-DOS, itecompatity lous antigen haplotype DOB; ‘mmunoglouln; 6, tetanus immune globulin, (rom Balatn 0, Petrone-RascV Dermat herpetfornis: ar. Diagnss, mangement. and progress, JA Acad ermata68:1027-1083, 2011} tobe effieacious as an ajuvant oor dapsone. 3. Uncontrolled studies and case reports have suggested eficacy wh tetracy- lines, nicotinamide, cyclosporin, colch cine, and heparin, + Symptomate rele for orurtus: 1. Potent and superpotent topical cortcnste- roids (atrophy with prolonged use, iit to 14 days per mo), nonsedating anis- famines twice dally, sedating anthiste- mines at bedtime, menthalatd lotion ‘CHRONIC Rx ‘As DH Is considered to represent the cute- noous manifestations of CD, Ielong avoié- ance of glen is typically’ recommended Information about educational resources, ‘such as national and local support groups, should be provided (ve.clac.0), + Patients with DH and CD have an increases risk of developing Hashimoto thyroid (60% with thycoid disease). non-Hodgkin Iymphoma, and Gl lymphomas, An increases incidence of other autoimmune dlsoroers (ype 1 abetes melitus, pernicious ane- Ina, Addison disease, viligo, systemic lupus erythematosus, rheumatoid artis, and Sjogren syndrome) and osteoporosis have ‘also been reports. 1. Screening for tyrold disease (TSH, ant- thyrod peroxidase antibody tes) spl cally commended, 2 Screening for autoimmune connective tissue diseases should be considered if there are suspicious signs or symptoms. 3. Routine screening for Gi lymphomas is controversial REFERRAL + Dermatologist for skin biopsy and manage ment of cutaneous disease + Gastoenterologist fr evaluation of CD + Nuttionist to educate patients about glter free diet + National support groups (wwwrcelia.org) and local support groups PEARLS & CONSIDERATIONS + Classic areas invoWed are those that are exposed it ina “fetal poston, Lesions may be worsened by iodides and certain NSAIDs; systemic steroids inetectve + Location of biopsies is IMPORTANT: False- negate DIF can result if biosies are taken from Iesional skin (should be taken trom normal-appeaing skin adjacent to lesion) as agnostic IgA deposits are usualy destoyed by the blistering proces. + GFD results in reduced IgA in skin on DIF (with eventual dsappearance) and reduced antendomysial antibodies in the blood. Hence, serologies (.g.,aniendomysial ant- bodies) can be used to monitor degree of compliance to dietary gluten restition. + Some studies have suggested a possible pro- tectve effect of GFD against intestinal m= phoma. first-degree relatives do not appear to be at increased risk for Gl or systemic lymphomas in the absence of DH or CD. SUGGESTED READINGS Available at ExertConsultcom RELATED CONTENT Cela Disease (Related Key Topic) AUTHOR: Lisa K Pappas-Tater, MO seston sioposa putews Erythema Multiforme (19 © 7D pasic inronmarion DEFINITION Eythema multiforme is an intammatory disease characterized by eruption of annular, maculo- papular lesions with dark raised, erythematous, or vesiculobulous center surrounded by a pale zon. tis believed tobe caused by immune cm- Plex formation and subsequent deposition inthe skin and mucous membranes. It fs considered a byporsonstity reaction to infection or drugs. SYNONYM =m |ep-t0cm copes 51.0 Nonbullous erythema multiforme L518 Other erythema muliforme 51.9 Erythema multiforme, unspecified EPIDEMIOLOGY & DEMOGRAPHICS PREDOMINANT AGE: 20 to 40 yr RISK FACTORS: Often assorated with herpes Simplex and oer infectious agents, drugs, or connective tissue diseases PHYSICAL FINDINGS & CLINICAL PRESENTATION ‘+ Prodrumal symptoms ae mid or absent. thing fr buning atte se of erupton may osc: ‘Symmetric skin lesions (Fig. £1) with a Classic “target” appearance (caused by the centrfugal spread of red’ maculopapules to circumference of 1 to 3em witha purpuric, cyanotic, or vesicular center) ae present (ig. 2), The papules may enlarge into plaques measuring afew centimeters in dameter with a dark or red central parton (Fg. £3) Target lesions. may ot be apparent for several days and generaly heal in 1 to 2 Wk tout scaring, “+ EM lesions are mast common on the face, back of the hands and feet, and extensor aspect ofthe forearms and legs (EM mar. Trunk involvement can occur in severe cases EM majo, + Urticarial papules, vesicles, and bullae may also be present and generaly indicate EM major. ‘+ EM major bullae and erosions may also be present inthe ora eavity. The mast common sites are the Ips and buccal mucosa, ETIoLocy + Immune complex formation and subsequent depostion in the cutaneous microvasculature may ply a role in the pathogenesis of ery: ‘hema mutiorme. 4 The majority of cases folow outbreaks of hetpes simplex vs 1 and 2 + Mycoplasma pneumoniae, fungal infection, medications (bupropion, sulfonamides, pen ellis, nonsteroidal antintammatory drugs, barbiturates, phenothiazines, hyantans). + In >80% of pationts no speci: cause is ident. (}yoIGNosts DIFFERENTIAL DIAGNOSIS. * Chron urticaria Pityriasis rosea Contact cermatits Pompigus vulgaris Lichen planus Serum Sickness Drug eruption Grandloma annlare Polymorphic ight eruption Vial exantema Stevens-Johnson syndrome (8) ‘oxi epidermal nazralysis (TEN) Bulous pemphigoid Vial exantnems. + Leukocytoctastc vascults, «+ Lupus erythematasus Secondary syphilis WORKUP ‘+ Modical history with emphasis on drug ingestion, * Laboratory evaluation in patients with sus pected colagen-vascuar diseases + Skin biopsy whan diagnosis is unclear Fig. E1 Erythema multiforme (EM). Round erthemtous swolen plaques and target lesions on the alms. Tis il developed EW in association wits her systemic pus erythematosus. rom Pall AS, Mancin ‘A: Huns inal petatc dermatology a textbook of skin disorders of childhood and adolescence, ed 8, Philadel, 2016, lav LABORATORY TESTS + Complete blood count wih dierent, ele- vated ESR + Atinucloar antibody + Serology for Mycoplasma pneumoniae, HSV- 1 HSV-2 + Blopsy for atypical cases * Direct immuncfuorescence if suspecting bullous diseases RX} TREATMENT NONPHARMACOLOGIC THERAPY + Mil cases gonraly do nat equ treatment lesions esove spontaneously within mo, + Potential drug preciptants should be ACUTE GENERAL Rx + Treatment of associated diseases (e.g. vala- cycovie oF famecovr for herpes simplex, cexythromycin for Mycoplasma infection), Dapsone, antimalarials, or azathioprine for sovere or resistant cases, Prednisone 40 to 80 mgitay for t to 3 wi effective for decreasing inflammation and pain and may be tried inpatients with many target lesions; however, the role of systemic stores romains controversial LLevamiscle, an immuncmodulator, may be fective in the treatment of patients with chronic or recurrent oral lesions (dose is 150 mglday for 3 consecutive days used alone or in combination vith prednisone. 1V immunoglobulins in severe cases Antimicrobial therapy i indicated if. pneu ‘moniae isthe trigger of EM. DISPOSITION ‘The rash general evolves over a 2-wk period and resolves within 3 to 4 wh without seating ‘A severe bullous form can occur (se entry for *Stevens-Jonnson Syndrome") REFERRAL Hospital admission in patients with suspected Stovens-Johnsonsynrome PEARLS & CONSIDERATIONS COMMENTS ‘The risk of recutence of erytema mutforme exceeds 30%%, Recurrence may be treated with valacylovr 500 to 1000 mgiday, facile 125 to 250 mg/day oracyclr 400 mg bd. Dapsone, antimalarials, azathioprine, or eychosporne use is reserved for cases resistant to antvials, RELATED CONTENT Exyhama Multforme (Patent information) Stovers-Johnson Syndrome (Related Key Tops) AUTHOR: Fre Fee, MO9 sasic inronmaTion DEFINITION Erythema nodosum (EN) is an acute, tender, frythematous, nodular skin eruption resulting ‘rom inflammation of subcutaneous fat, atten associated with bruising Its the most common ‘orm of panniculitis, ‘SYNONYM eN eD-10¢M CODE 152. Erythema nodosum EPIDEMIOLOGY & DEMOGRAPHICS INCIDENCE: ts the most common form of pan- nicultis, Two to three cases/100,000 persons ery PREDOMINANT SEX: Forale:male rato of 3 toa PREDOMINANT AGE: 25 to 40 yr PHYSICAL FINDINGS & CLINICAL PRESENTATION, + Prodromal symptoms of fatgue, malaise, upper respiratory infection symptoms. may precede eruption by 1 to 2 wk + Auto onset of tender nodules typical locat- ‘eon the shins and occasionally seen on the ‘highs and forearms Fg. E), 4 Tho nodules are usvally 1/8 to 1 Inch in dametor but can be as lage as 4 inches; ‘hay begin as lott rd lesions, then become Garker and often ecchymotc. The nodules heal witin 8 w without ulceraton + Assocated findings: 1. Fever (60%) 2. lymphadenopathy (<50%) 3. artralgia (64%) 44. ‘Signs of the underying ines ETIOLOGY Cell- mediated hypersensitivity reaction is seen ‘more ‘requendy in persons with human louko- ct antigen (HLA) BB. The lesion resulls ftom fan exaggerated Ineracon between an antigen and cell-mediated immune mechanisms lead- ing to granuloma formation. Up to 85% of cases Of EN ae idiopathic. Infectons: * Bactera: 1 Campylobacter 8 4 5 6 1 8 8 10. 1 12 13. 14 15, Streptococcal pharyngitis (28% to 48%) Salmonelientertis Yorsinta enters Psittacas's Chlamydia pneumonia infection ‘Mycoplasma pneumonia Meningococcal infection Senora Sypils Lymohogranuioma venereum Tularemia Cat-sratch cisease Leprosy Tuberculosis + Fung 1 2, 3 4 Histoplasmosis Coceidnidomyensis Blastomycosis Tichophyton verucesum = Vises: 1 2 3 Cytomegalovirus Hepatitis B Epstein-Barr ius Drugs (3% to 10%): Sulfonylureas Sulfonamides Pencins (ral contraceptives Gold sats Prazosin Aspirin Bromidos Sarcoidosis (11% to 25%) Inflammatory bowel disease Hodgkin disease, non-Hoagkin ymphoma Ankylosing spondylosis and reactive arthrop- athies (eg. associated with inlammetory bowel disease) + Beicet disease Latgrn syndrome + Acute myelogenous leukemia (yoinewosis DIFFERENTIAL DIAGNOSIS + Insect bites Postraumate ecchymases Vasculitis Wober-Chrstian disease Fat necrosis associated with pancreatitis NecrooiassIpoiica Scleroderma Lupus pannicutis Subcutaneous granuloma 16 Erythema Nodosum WORKUP * Physical examination + Diagnass of underyng less. by istry, physical examination, and laboratory tests as Indicated LABORATORY TESTS «+ Erythrocyte sedimentation rate Throat culture and antteptoiysn Other Purid protein derivative Others. depending on index of suspicion (eg, stool euture and evaluation for ova and parasites in patients with diarea and gastointestinal symptoms), Skin biopsy in doubtil cases: 1. Eaty lesion: Inlaation and hemor ‘hag in subcutaneous issue 2, Late lesion: Giant cels and granulomata IMAGING STUDIES Chest radiograph to rule out sarcoidosis and tuberculosis gq TREATMENT ‘Tho disease is sled and treatment is ‘symptomatic, EN nodules develop in pretit- ll locations and resolve spontaneausly over ‘several weeks without scarring or ulceration, Treatment of underyng dsordors, Aidance of contact Iritation of affected areas. Nonsteroidal antinfammatory crus for pan Systemic steroids (prednisone 1 mglkg of body weight/ay, tapered over several days) may be useful in severe cases if underying risk of sopsis and malignancy have been ercluded, Potassium iodide gen as tablet 800 mg ti (oF a5 a supersaturated solution (five drops ‘ree tmesiday in orange juce) has bean reported as etlective for symptom conto + Invalesonalcortcosteoi irjetions for per- sistent lesions PROGNOSIS Typical case: + Pain for 2 vik luton within 8 wk RELATED CONTENT Erythema Nodosum (Patent information) Sarcoidosis (Related Key Topic NoTHOR Fre Fer, MD 539 seston ‘spiosg purFira Folliculitis °16 9 pasic inronmarion DEFINITION Folicults is inflammation ofthe har flice as a result of infection, physical injury, or chemical ination SYNONYM Sycosisbarbae |ep-t0cm coves 1729 Follicular ystof skin and subeuta- neous tissue, unspected 173.1 Pseudoolicults brbae 173.8 Other specie flicuar disorders 166.2 —Folicuts dcalvans 166.4 Folicultsulerytnematosa retouata 166.3 Pesoliclts capitis abscedens EPIDEMIOLOGY & DEMOGRAPHICS PREVALENCE: Staphylococcal flicults is the most common form of infectious folicults: i ‘occurs mast commonly in persons wih diabe- tes. Gram-negative focus occurs in patients who have had moderatly inflammatory acne for long periods and have been teated with long-term anbiotics such as tetracycline. PREDOMINANT SEX: Sycosis barbae occurs most frequent in men who have commenced shaving, PHYSICAL FINDINGS & CLINICAL PRESENTATION ‘+ The lesions generally consist of pabfl yel- low pustules surrounded by erythema: a cen- ral har is presontin the pustules. Furuncles vt pus may be present Patents with sjcosis barbae may intally present with smal flicular papules or pus- ules that increase in size with continued shaving: deep flicular pustules may occur surrounded by erythema and swelling, the Upper lips frequent involves ‘+ “Hot tub" folicultis occurs within 1 to 4 days afer the use ofa hot tub with poor chloe hatin. tis characterized by papules and pustules (Fig. £1) with surrounding erythema (generally affecting the tors, butocks, and limbs (9. £2. ETIoLoay ‘Staphylococcus infection (e. bae), Pseudomonas aeruginosa ‘olicults) Gram-negative folliculitis (Kiebsiel Enterobacter, Proteus) assciateé with ant biotic troatmont a acne Chronic iitation of the hair folie (use of cocoa butter or coconut ol chron itation from workplace) Initial use of systemic corticosteroid therapy (steroid acne), eosinophilic folicultis (ADS patents), Candida albicans mmunocompo- mised patents) + Piyrosporum orbicuare (}ybiaNosis DIFFERENTIAL DIAGNOSIS. ‘+ Pseudotolicultisbarbae (ingrown has) «Acne vulgaris + Dermatophyte fungal infections «+ Keratoss plans * Cutaneous candidiasis + Supericial fungal infections = Wiles WORKUP. ‘Physical examination and medical history (@9., use of hot tub: "hot tub” flicutis adolescent patients vino have started sha: ing: syeosis barbae: use of occlusive topical steroid therapy: Staphylococcus fliclts. + Gram-negative fliculis in acne patents on prolonged antibiotic treatment manifests with superficial pustules 3 to 6 mm in diameter ‘lring ut from anterior nares or futuant, deep-seated nodules. LABORATORY TESTS + General not necessary. * Gram stan i useful to identity the infective organisms in infectious focus and to der erate infectous follculs rom noninfectious, a TREATMENT NONPHARMACOLOGIC THERAPY ‘+ Prevention of chemical or mechanical skin iritation + Gljcemic conto inaiabetcs + Proper chlorination of hot tubs and spas Shaving with a clean razor ACUTE GENERAL Rx + Cleansing ofthe area with chlorhexidine and application of saline compresses to involved sea, + Application of 2% mupiocin ointment or 1% relapamulin ointment for bacteria folios afecting aimted ar (9. sycossbarbae. + Treatment of severe cases of Pseudomonas folicultts with eorotoxaci + Treatment of S aureus flicults with dilx- aca 250 mg qd for 10 days, * Isovetnoin is the treatment of choice in gram-negative flicultis,Amoxiclin or TMS- ‘SMX canbe used whan scretinoin is conta- indicated or canna be tolerated, CHRONIC Rx + Chronic nasal or perineal S. aureus caries With frequent folicults can be treated with rifampin 300 ma bid for 5 days ‘+ Mupitocn or retapamulin ointment appli to ares bids also effective for nasal caries, DISPOSITION + Most cases of bacteral folicults resobe completly wih proper treatment + Steroid foliculits responds to discontinuation ofsterias, PEARLS & CONSIDERATIONS COMMENTS Patonts shouldbe instructed in good personal hygiene and avoidance of sharing razors, tow tls, and washalaths, RELATED CONTENT Folicultis (Patent information) AUTHOR: Fred Fe, MD FG, E2 Pseudomonas hot foot syndrome, Tender papules anépapuloousiuls on tre plentaraspect of te foot Cute of a swab rom ora ofthe pustules grew P seruginasa (Courtesy John J. Van Aa, MD. Frm Palle AS, Mancini A: Hurniz einal pediatric dermatology a txtook of shin cists of eihood and adooscones, 4 5, Placephia, 2016, Elsevier) FIG. E1 Paputes and pustules in het tub fl- eultis, (From Klagman RM eta. Nelson textbook of pais, ed 18, Phacalpia, 2011, Saunders)Em Food Allergies 7D pasic inronmarion DEFINITION Food alleges are divided into IgE-medieted and Immunologicaly mediated non-gE reac- tions. They include & spectrum of cisorders that involve adverse immunologic responses to iotary antigens. leD-10cm coves 780. Adverse food reaction (including anaphylactic shock) 78.1 Other adverse food reactions, not slsewhere classified 1272 _ Dermatitis ue to ingested food 721,010 Allergy o peanuts 791.011 Alergy to milk products 221.012 Alergy o eggs 781.013 Alergy to seafood 291.018 Alergy to other foods 791,02 Food additives allergy status EPIDEMIOLOGY & DEMOGRAPHICS INCIDENCE: Food alergies have a cumulative incidence of 64 to 8% forthe fist 3 yr of If. PREVALENCE: + Overall prevalence is 1% to 2% in general population, -3.9% to 834 in chide, Patont sol-reparted food allergies have a prevalence of 12% to 13%, demonstrating the importance of objecive measures. in assessing fod alrges Nearly 40% of children with food allergy have a history of severe reactions that if not rated immediately with proper medication, can ead to hospitalization or even death There Is insucent evidence to conclude a racial prediction (Greenhava, 2013). GENETICS: Children with parents or close rela- tives with allergies may have a tendency to become allergic to foods PHYSICAL FINDINGS & CLINICAL PRESENTATION ‘+ Iof-mediated reactions: (within minutes to a few hous) Prurtus, urticaria or angioedema, atopic dermatitis, Gi symptoms, conjunctival injection, sneezing, nasal congestion ino ‘hee, bronchospasm, and anaphylaxis Non-igf-mediated reactions: Food-induced fenteocolis, celiac disease, Crohn disease dermatiis herpetiformis, and_ pulmonary reactions such as Heiner syndrome, These lhesses are discussed separately Signs, symptoms, and presentation reflect spectic allergic manifestation, but in food allergies there is @ reproducible temporal relationship to ingested food allergens. ETIoLocy Failure to establish tolerance to food antigens. 1L-33 mediated epithelial permeabity ang Th? Gupta AS at a The prevalence, covery nd at baton of clchand fod algy in he Unies States, Peds 1288217, 2011, skewing result in senstizaton to food proteins which ace presented to primed T cells. Food processing condone that may affect allergenic activity ae described in Table Dx} DIAGNOSIS + Thorough history (o ident specific food's, ‘quantity consumed, timing, and nature of reac tion) and physcal exam shoul be perormed. ‘The temporal relationship and reproduc ily of the symptoms are most important to establishing the diagnos ‘review of Ingredent abels may be helpful Confirmatory testing can include skin testing or in vito testing Skin prick testing (SPT): Postive predictive Value mes pu pezset po soon nse oe ‘sanpadd py esse000 Hn aun ms nen sea aa i n i le EPI ‘ye step see, nen ry pare-yod oo a NBA suopeayduy eaquHg| van su -sods 09 ) ito us ue) ‘puede ‘ez 86 omeg aide yoweg we00y vid ‘uepyng aA POD ane Brseaoa say pun oes aye suoREyDOUL spb pssanad-pu Aianze ue manus puosusuep-aong 204 ue! subse EN SLL pur i) subioye ura p aumongs ap sap uN ‘suse sy pu ‘3 yj anon a 8 "a}0m Bupeca a pat ate ses way yoroute hand ue! ung $2 pu ea] AueBGrs UE ey, ‘onas oiey ago yn Uo sobs 9 “omongs o-apeu ear S47 4 Ale uedns YUE ‘aupoul ae sfouey | a8 age fueadne yea Faupout a sfojuoy 1 meg eT ‘tof an ay w pac sys Yo SoBe Yo #807 bess bu 0 so) ‘sens tuum pa tasune pungsodg "na usu, yt pareduco ou s+ fyb 90) ‘eos tno penta stojuou 1m 9g wash ‘suabsaiy wo Buysseo01g yo yeu onepuztog sepmad ayy 600 panuaises put tu PauuDe nds jase ys su spo jo woes ty pu unseoy og pu ep ay sn pezzeied jo wgaseey pu sat us “ffi fq 220 0 perowy sgn pu nates 1) sodsoune poupoR Buyss20014 Jo ame Sayssoo fapuncas fwsseoi Keung afi Gusseo01g ‘Aunnoy o1ueBioiry iooyy AeW 1eUL suoRIPUOD BuIsse00i4 poos | TEV.sm Food Allergies @ @ ‘pues yr wt 19 sea pr syed ae seagate SKY WH, aNosos 0 Sug ioe 5009 cu oso asp ova 3 feu PEG 9 Aiae aubrey sarge 4G oun ajucwag se spas sue Jago yan uzun w pas ae 2b uy au pu Asa sep Jo aNEU siopeosne3 oad 1u op so yraead pays, ‘sysfs seromgus 64 vonduns.o 14 ES paepsuo ave yo wrens pauyes Aub 2 ‘sun oie om nego sats pu ous 809 sraead ureokos e680 ‘ayn a0 od ao aseseg enue pnesu jo ved Buea 1a, pos Bune ayn ha po teu 658 pauruns “0 paseoodueeg i pepnp 9 Ae spe pony sued spo) passzovtun so. um paseduoopaypou fn ‘om fen safetag Sapo ya pue sabe Su ‘wo fans] pus Ab an usd rosa pu stood Suse Bp porous a 544 ‘9u9pIN3 eRe -ODg ‘suabioiy wo Buyssoo0ug Jo yoeduy 00) poe $00) poe 28 you 0 pape st sp0oy wnt awa 10 sept poo peri Buysse001g Jo oimeN a8 BYSEBO01g ‘Aunnoy o1U06:0ITy you ABW YUL SUORIPUOD BUISSOD0g Pood | TTEVL@® @ Food Allergies 57 eee) Sa hae oop) onder Pawnee becave of “raced wih oil ay ge z peste eae Napa a ‘npleasd food Hered a Tope Tagalog aaa ed ed ed ed Toute alah wai genni as sey =a) ie ewehcon || spony on lod ‘reed ae orig FIG, 1 Algorithm forthe management of food allergy “Testng ndats skin-prck testing radoalergo sorbent ests (RAST) gy a3, anor pach testing Note tat clnical symptoms must be associate with ‘he foot) alts posite before he foots) tou be eliminated frm the dt "Orl foot challenge (OFC) imlvesreincocucng the fod and observing for sins!symptoms of fod allrgy (Treatment of food allergy Imvlves elimination tthe caurate fod} fa theca + Wheat allergy found to resolve by 5 yr of age and soybean alrgy by 2 yrof age PREVENTION + There is conflicting evidence regarding the protoctve effect of breastfeeding on food allergies. + There is no evidence to suggest that exch sive breastfeeding for 6 mo or more is supe- tir to exclusive breastfeeding fr 4 to 6 mo in terms of developing fod alrces. In high-rsk infants wo are not exclusively breastfed, here is limited evgence to sug- gest that feeding with hydrolyzed formula compared to cow's mik formula reduces allergies Currently thee is no evidence to support the use of prebiotics andr probiotics or the prevention of allergic diseases. No current evidence exss to support delay- ing the Introduction ot solid foods beyond 06 mo, ‘+ The eatyinaducton of peanuts significantly decreases the frequency ofthe development of peanut allergy among chilien at high risk for this allergy and modulated immune responses to peanuts.” Enly peanut into- duction (ages 4 to 11 months) lowers the Fisk of developing peanut allergy by 80% ‘compared with peanut introduction after age 5yt ‘In rovent phase 3 tals of oral Immuno- ‘therapy in chilten and adolescents who were highly allergic to peanut. treatment wth ARIOI resulted in Ngner doses of peanut protein that could be ingested without dose- limiting symptoms, PATIENT & FAMILY EDUCATION Information can be found on American ‘Academy of Allergy, Asthma and Immunology "apa RS ot a: The provance covery, and dit but of hood food alargy ine Unites Stats, Plats 122-217, 2011, (owaeachor), the Food Allergy and Anaphylaxis Network (wo. foodallrgy0°), and the Anaphylaxis. Campaign (ww. anapryl avis. 09. REFERRAL Patients maybe referred to an allergyimmunet ‘ogy specialist when the diagnosis is uncertain orf avoidance measures are not success SUGGESTED READINGS ‘Availabe at ExperConsut com RELATED CONTENT Food Allergies Patient Information) ‘AUTHOR Fre. Fer, MD72.02 MU Us male) 7D basic inronmarion DEFINITION Impetigo is highly contagious superficial skin Infection generally caused by Staphyocaccus aureus andor Streptocceus spp ‘Common presentations are bullous impetigo (generally caused by staphylococcal disease) and nonbulous impetigo (rom steptoeaceal Infecon and possible staphylococcal infection) ‘the bullous form is caused by an epldermalytc toxin produced atthe site of infection. SYNONYMS, Impetigo vulgaris Pyoderma Impetigo contagiosa Bullous impetigo |ep-t0cm copes {01.00 Impetigo, unspecified LoT.0t Nonbullous impetigo L0T.02 Bockhart impetigo 1101.03. Bullous impetigo L0T.08 other impetigo EPIDEMIOLOGY & DEMOGRAPHICS + Impetigo isthe mast commen bacterial skin Infection in clr 2 to 5 yr of ago. Bullous impetigo accounts for 30% of cases and non- bullous for 70% of cases. Impetigo is most common in temperate zones, mostly during ‘he summer hot, humid weather. Common souroes for children are dirty fingers, pes, and ater children in school of day care cen- tes. Impetigo often complicates insect ites, pediculoss, scabies, eczema, and poison iv, Bullous impetigo is mast common in infants and children. The nonbullous form is most common in chitren ages 2 to 5 yr wih poor hygiene in arm climates. The overall incidence ot acute nephritis with Impetigo varies between 2% and 5%. PHYSICAL FINDINGS & CLINICAL PRESENTATION ‘+ Nonbullous impetigo begins as a single ed macule or papule that quicdy becomes 2 vesicle. Rupture ofthe vescle produces an feosion of which te contents dry to form honey-clored crusts. Muliple lesions with golden yellow crusts (i. Ei) and weeping areas are often found on the skin around the nose, mouth and lms. Bullous impetigo is manifested by the pres- fence of vesicles that enlarge rapidly to form bullae with contents that vary from clear to cloudy, There is subsequent collapse of the center ofthe bullae (F9. £2); the peipherl areas may retain Mud, and a honey-colored crust may appear in the center (9. £3). AS the lesions enlarge and become contiguous wath the otters, a scaling border replaces the ‘lidtiled rim: there Is minimal erythema surrounding the lesions, ‘+ Regional ymphadenopatry is most common with nonbullous impetigo, + Consttutional symptoms are generally absent, ETIoLocy + . aureus coagulase postive is the dominant microorganism (50% to 70% of cases) 8. pyogenes (group A f-hemolytc strepto- 003) M-T serotypes of his organism asso- ciated with acute nephritis are 2,48, 86,87 and 60. Group B streptococci are associated with newborn Impetige, (}ybiaGNosis DIFFERENTIAL DIAGNOSIS. + Atopic dermatitis «+ Horpes simplex infection * Eethyma + Folicutis + Dermatitis herpetiformis * Insoct bites + Scabies, pediulsis * Tinea corporis, cutaneous candidiasis + Pemphigus vlgais and bullous pemphigoid chickenpox + Thermal burns * Contact dermatitis + Stevens-Jonnson syndrome, Sweet syndrome WORKUP Diagnosis is tinea LABORATORY TESTS Generaly not necessary * Gram stain and culture and sensitiity to confirm the diagnosis when th clinical pre- sentation i unclear + Sedimentation rate oarall to activity of the disease FG. £1 Nonbuious (crusted) Impetigo. Eythemstous papules with honey yelon-colored crusting. From Palle AS, Mancini Al: Hurt cncl paca dermatlegy a txtook of shi sores of chidhood and adolescence, ed, 2016, Elsevier) FIG. E2 Bullous impetigo. Thir-aled vesicles and shalow erosions wth periparlcallareltes and rit crusting onthe butock and posterior thigh Fm Pal AS, Mani Al: Aart cnc! pela dermatigy, {2 lertbook of sin ordre of ehidhocd and adoiescens, eS, 20°6, Fever)Impetigo @ FIG ES Bullous impetige Mull tender, erythematous paches wit apersheral colaret, representing remnant ofthe blister roo. rom Palle AS, Manca Al: Hurt clnical adie dermatology 2 textbook of ‘ski citorers of chldhond and adolescence, e 5, 2076, leet) * Increased ant-DNAse 8 and anthyaluroni- ace + Urinalysis reveating hematuria with erythro cyte casts and proteinuria in pation: with acute nephritis (most tfequenty occuring in chlcren between ages 2 and 4 yr inthe southern part ofthe US) +H recutent staphylococcal impetigo devel- ops. a culture of the anterior nares should be one to rule outa carir state a TREATMENT NONPHARMACOLOGIC THERAPY Remove crusts by soaking with wet coth com- presses (crusts block the penetration of ant- bacterial creams} GENERAL Rx + Treatment consists of topical or oral antbot- 1s that are active against both S. aureus and -hemodti steplocac SUGGESTED READINGS ‘Agpcaton of 2% mugirocn ointment td or 10 days or reiapamalin 1% applied ba for 5 days 0 ‘he tected are or unl allesons have deare, Czenoracin is topical nonfuorinated qu- nolone antibiotic recently FDA-approved for ‘teatment of impetigo In patients 2 mo old Costs a limiting facto, Oral antbiotes are used in severe cases: ‘Commonly used agents are cilorailin 250 1g aid fr 7 to 10 days, cephalexin 250 mg {i for 7 to 10 days, azithromycin 500 mg on day 1, 250 mg on days 2 trough 5, amoxii- lnlevuanate 500 mg ah. Impetigo can be prevented by prompt appl- cation of muprain or tple-antbiaticoint- ment foaitracin, Plyspoin, and neomycin) ‘sites of skin vauma Patents who are carters of S. aureus in ‘ther nares should be treated with mupi- focin ointment applied to theit nares bid for § days or a 10-day course of rifampin, 6600 mg/day, combined with icloxacilin or Banger Set a: Bacal resctance ané impaga werd: 2 review, Petr Dermat 29;481~484, 2012 MarenanAdams ot ak Ingle: sagnsis and treatment, Am Fam Physician 90(:208-235, 2014 methiclin-sensitve Staphylococcus aure- tus [MSSA}) or tvimethoprim-sulfametnox- azole [TMP-SHX} (for methiclin-rsistnt Staphylococcus aureus (MRSA), ‘+ Fingernals shouldbe kept short, and patents should be advised not to scratch any lesions to avoid spread of infection. DISPOSITION Most cases of impetigo resolve promptly with appropriate treatment. Both bullous and nonbul- lous forms of impetigo neal without scaring REFERRAL, Nephrology referral in patients with acute nephritis PEARLS & CONSIDERATIONS COMMENTS: «+ Patients shouldbe instucted on use of ant- bacterial soaps and avoidance of sharing of towels and washeloths because impetigo extremely contagious Children attending “day care should be removed until 48 to 72 hr ale inition of antbatic treatment. + Bulous impetigo may be an early manieste- tion of HV intecton RELATED CONTENT Impetigo Patent information) -NOTHOR Fre, For, MD 782.03feed Lichen Planus fd ©) 7D basic inronmarion DEFINITION Lichen planus (LP) refers to an idiopathic inlammatory disease manifesting with a papu- lar skin eruption characterscaly found over ‘the floxor surfaces ofthe extremities, genital, and mucous membranes, SYNONYMS, LUchon Lichen planus et alrophicus iP |ep-t0cm coves 43 Lichen planus |L43.0 Hypertrophic lichen planus 443.1. Bullous lichen planus L423 Lchen planus, unspecified 14338 Other Vehen planus EPIDEMIOLOGY & DEMOGRAPHICS INCIDENCE: One in every 100 new patients swen in dermatology cline in the United States Is diagnosed with LP PREVALENCE: 440 cases/100,000 persons PREDOMINANT SEX: Found equally between male and feales (1) PREDOMINANT AGE: Usually found in people between the ages of 80 and 60 yr PREDISPOSING FACTORS: + Associated with other autoimmune disorders (e.9., prmary biliary cithosis, myasthenia (avs, ulcerative colts, diabetes) + Associated with hepatitis C infection + Drug-induced form affects any area of the body surface (e.g. beta-blocker, methyl dopa, penicilamine, quinidine, nonstero- al antinflammatory drugs, angiotensin- comerting enzyme inhibitors, sulfonylurea agents) PHYSICAL FINDINGS & CLINICAL PRESENTATION Lichen planus often manifests wth prur, t- ‘opped violaceous papules but tre clrical pre- sentation varies depending onthe aea involve, History Usually stats on an extremity and may remain localized or spread to involve otter areas over a 1 to 4-mo period ++ Puutie Physical findings Anatomie distrbuton: 1, Flexor surface of wrists, forearms, shins, and upper thighs Neck and back area Nalls (6% to 10% of patients) Scalp (lichen planoplrs) Oral mucosa, buccal mucosa, tongue, gingiva, and lps; orl lichen planus can cause extensive desquamatve gngvits 6, Vulva (Fig. £1), penis Fg. £2) Genital mucosa: Lesion configuraton: 1 Unear 2. Annular (more common) 8. Reticular pattern noted on oral mucosa and genital area + Lesion morphology 1, Papules most common presentation (Yat, smooth, shiny (ig 3) 2. Hypertrophic 3. Follculer 4, Vesicular + Color 1. Dark 10d, bluish red, purplsh-vlacoous colors noted in cutaneous LP (Fig. E 2 Individual lesions enaracteritcaly have white lines visible (Wicknam striae) (Fig. 3) 3. Oral and genital LP has a reticular net- work of white lines that may be raised or annular in appearance (ig. £8) * Scalp lesions may result in alopecia, + The plaques of chen planus may be hyper- ‘eophic but show the charactrstic viol .20us coloration an intense hyperpigmenta- ton (Fo. £7. ETIOLOGY LUchen planus is characterized by an immu- ologic reaction mediated by CBs T calls These eels induce keratinocytes to undergo apoptosis. though the inflammatory reaction is believed to be autoimmune, the antigen targeted by these effector T Iymphocytes is unknown, FIG E1 Lichen planus ofthe vulva with a whit, lacelike pattern and erythema. (om Crum C? eta Diagnastic gmecalogc and obstetric pattology,e 3, Philadelphia, 2018, sever) FIG. E2 Lichen planus of the penis. rom Swartz MH: Textbook o pyc! agnosis hstory and eraina- tin 07, Peli, 2014, Saunders)Lichen Planus @® FIG, E3 Flattopped, purple, polygonal papules of lichen planus. (Fon Morell JG: Diseases ofthe ‘dermis, in Kogan RM oa os Nolan tevibok of peda, ed "8, Philadel, 2011, Saunders) FG, E4 Shiny, flttopped, polygonal, violaceous papules of lichen planus. Hote the Wickham striae linear, whitish-gray streaks) on the surface. ron Pale AS, Mancini A Hurwitz cn pediatric dermatology, textbook of skin dsrdesof childhood and adlescence of 5, 2016, sev} + Clinica history and physical findings usually establish the diagnosis of LP. + Skin biopsy (deep shave or punch biopsy of ‘he most developed lesion) can be performed to confirm the diagnosis DIFFERENTIAL DIAGNOSIS: + Drug eruption. psoriasis, Bowen disease, loukoplaka, canditiasis, lupus rash, second ‘ay sypilis, sebortelc dermattis, chronic graftversus-host disease ‘+ Teble El summarizes variants of lichen planus WORKUP Iv the agnosis is questionable, askin biopsy 's performed LABORATORY TESTS Laboratory tests are not speci forthe dagno- ‘is of LP. Lipid panels screening is useful since increases in serum triglycerides and decreases in HDL cholesterol are common in patients with LP IMAGING STUDIES Imaging studies are not helpful in dlagnosing it NONPHARMACOLOGIC THERAPY “+ Avoid seratohing. + Use mild soaps and emolients ater bathing ‘to proventcryness GENERAL Rx FOR CUTANEOUS LP: > Topical steroids (29. ameinoione aceton- ide 0.1%, fluocinonide 0.05%, cobetasol propionate 0.05% cream or ointment) with ‘occlusion used twice daly ‘Acietin 30 ma/day PO for 8 wk + Systemic prednisone 30 to 60 ma/day as a starting dose and tapered to 15 to 20 mg/ day maintenance for 6 wk can be used for widespread lesions ‘+ Inradermal sto tiamcinolone acatoide 5 mg/ml can be ted for thick hyperkeratoc lesions + Hydraxyzine 25 mg PO a6h can be used for prurtus| + Phototherapy: PUA or narrow-band ultavio- Iet B therapy: 2 of 3 times per wr, for a total of 12 sessions (., one cyte) FOR ORAL LP: * Topical steroid uocinonide in an adhesive base used six tmes/day for 9 wk ‘Topical calcineurin in sterold-uwesponsve cases + Topical or systemic retinoids 0.1% retinoic ‘acid in an adhesive base or ge + Etretinate 75 mglday for 2 mo DISPOSITION * Spontaneous remissions of cutaneous LP ‘ur in >65% of cases within the fst year. + Spontaneous remission of oral LP usually ‘ocurs by 5 yr. + Approximately 10% fo 20% of patients wi hhave recurrence. REFERRAL To dermatologist agnosis is unclear COMMENTS: + LP can be remembered as purple, planar prutc, plygona, papules, and plaques (sie Ps, + Lesions can develop at the site of pio skin inury(Keebner phenomenon). + AMthough there Is an increased risk of squa- mous call carcinoma in chronic lesions of mucosal L, ransformation to skin cancer is RELATED CONTENT LUchen Planus Patient information) -NSTHOR Fred Fer, MDLichen Planus @ 83304 FIG. E5 A 2nd B,Lihon planus. Note te ne, eculted whit sales. Swartz NM: Textbook of physical iagnass, history and examination, ed 7, Phadelpra, 2014, Saunders) FIG, E6 Oral lichen planus. Wickham sie onthe buccal mucoss, (rom Palar AS, Mancini Alt Horta clic pediatc dermatology,» textbook o skin dsrdereo chighend and agoescece ed 6, 2016, ever)Lichen Planus @® FIG, E7 Lichen planus. The plaques of licen planus may be hypertepic but stow the etaactersic Vilacous coloration and intense hyperpigmentation (From Pals AS, Marcin Ai: Aural clinca pedi ‘dermatology. textbook o skin aeordersof childhood and adolescence 8, 2018, Ekevier) TABLE E1 Variants of Lichen Planus Variant Type Characteristics ‘Bulan develo on estan LP lesions atous > pamphigeies satne ‘route Pyperphi Arphic emormapetou- ure Un Erosveleerave etapa ees tonue Lehn planar UP bulou pemphigoid wit aucune react, sua agaist type cae lagen ulus pemprignd 180 antigen) nse cui sping, sume, primey sun-exposed surace Pace, neck. desu of ‘rms and hard} fen anrlar canfguratin most common inciéen an young ute (Occur n 10% of patents, een sare ami yl esos ot LP ‘Thick, pruntic, hyperkeratate plagues, expec onthe lege and dorsal repos of he feet pesson May represents resoing hase n whic large plaques become cantly depressed vith esl perpimentaton ‘Shows nonlaching eamponent on scopy LP owen spontanacsly ang tenes of Bsc, presumably reflect somatic resaicem Intensely painful uceaton on he pls and sce; chronic lesan ray avo into squamous celcarcnoms; eave lslons may ozur on mucosal suraces Overiopng features of lupus and LP. sions ae sully acral and patents may show high ters of ANA Foliclar LP; keratote pigs surouned by vlaceos ertrena, especialy on scab but can fect ny hai-bearing ars; usally ests in leat alopecia ‘rc rode: een Hs, From Pale, Maze A Maciel pate mao txook of shins f cheat and aero ote deen SUGGESTED READINGS ‘as Sontag So a Crsvazculr rik factors in patti Hen planus, ‘nS od 124543-548, 2011, Le Cleat, Choséw 0: Lichen planus, M Engl J Med 36:729-72, 2012Fry Lichen Sclerosus 10 ©) 7D pasic inronmarion DEFINITION Lichen sclerosus (LS) isa chronic intammatory condition ofthe skin usually affecting the vulva, pens, perianal area, and ron. SYNONYMS, Lichen scerosus et atrophicus kKraurosis vulae Balai erotica obterans Is |eD-10cm cove 190.0 Lichen sclerosus et atophicus EPIDEMIOLOGY & DEMOGRAPHICS Most common in postmenopausal women and men between ages 40 and 60 yr. More comman in females (female:male ratio of $:1). affects 1.7% ofthe general adult female population ‘Can occur in chidren (usually prepubertal itis with involement of the vulva. and perineum), PHYSICAL FINDINGS & CLINICAL PRESENTATION Exythema may be the only inal sign. A characteriste fnding is the presence of Inoryetite atrophic lesions onthe involved Close inspection of the affected area wil reveal the presence of whit-to-brown fol cular plugs on the surface (ls), When the genitals are involved, the white parchmeni-ke skin assumes an hourglass Coriguraton around the inital and per- anal area (*keyhole” cistibuion; Fig. El Fig. £2) Inflammation, supithalial hemor ages, and chronic ulceration may develop. In males, lesions are atophic and may be hypopigmentedordepigmented,esembingvit- igo. Phimoss and paraphimoss are common ‘complictons in uncrcumesed males wih LS. Lesions may be surrounded by an erythoma- tous to violaceous halo, Dyspareunia, genital bleeding, and anal bleeding ae common, Prutus may be a prominent symptom ETIoLoay Unknown, Tere may be an autoimmune asso- lation and a genetic fala! component (}ybiaenosts DIFFERENTIAL DIAGNOSIS. Localized seerederma (morphea) Cutaneous discoid ypus erythematosus ‘trophic lichen planus Psorias's Lichen simplex eronieus Vulvar intraepithelial neoplasm Extramammary Paget disease ‘Table E1 summarizes the ditferentil dag rosis of common vulvar mucocutaneous dlsordors WORKUP Diagnosis is based on close examination ofthe lesions forthe presonce of Wory-white atrophic lesions and typical locaton LABORATORY TESTS “+ Punch or deep shave biopsy can be used to confirm te dlagnosis, + Autoantibodies to extracellular mate protein 1 (ECW-1) are present in 8% of LS patents and the ECM-1 tier coralates with disease acti g ‘TREATMENT NONPHARMACOLOGIC THERAPY * Aitention to hygione and elimination of i tants o excessive bathing with harsh soaps. ‘Cryotherapy and photodynamic therapy can be used in retractoy cases. GENERAL Rx + Applicaton of cobetasel propionate 0.05% topically bia for up to 4 wk is usualy eter: tive, Repeat courses of corticosteroids may be necessary because ofthe cronic nature of this disorder, Continual application of top cal steroids may lead to atrophy ofthe vula ‘There is no substantial evidence that use of topical sex hormones (e.g. topical tes- tostorane 23) Is effective In gonial lichen solerosus, + Lubricants (eg, Nutraplus cream) are useful to soothe dry tissues + Hydroxyzine 25 ma at bedtime is etective in ecreasing nocturnal itching + Use of intalesional steroids, ebetinate, and sutgieal management is usualy reserved for refractory cases. DISPOSITION + The disease persists in approximately one third of patients + Most prepubertal girls improve spontane- ously at menarche, + Squamous cell carcinoma can dvelop within the lesions in 3% to 10% of older patients therefore periodic examination and biopsy of suspicious areas are indicated. PEARLS & CONSIDERATIONS COMMENTS + Prepubetal lichen sclerosus may be con- fused with sexual abuse in prepubertal gis and may lead to false accusations and rvestigations. + Pregnancy leads to improvement and often ‘complete resolution of lesions, suggesting 2 hormonal component to etiology of lesions. FAG, £1 Lichen selerosus with stenosis ofthe itrelts,fesuring In the posterior fourchette, and erianalinvelvement producing the "key jes" sha BK and Magesson Li: Genital skin sores: agnosis an restment n Disa P et al Cinel gmecolgi oncology ed 8 Phisdphi. 2017, Elser)Lichen Sclerosus 833.07 Lichen sclerosus of the wv (raurosis wulvae) usually occurs ater menopause and is generaly chronic. It can be painful and interfere with sexual activity, * Lichen sclerosus ofthe penis (balanits xerot- ica obliterans) is seen more commonly in Uuncircumesed males. tt affects the glans and prepuce and may lead to sicture if it ‘enroaches into the urinary meatus. RELATED CONTENT Lichen Selerosus Patient Information) -NOTHOR: Fred For, MO FIG EZ A, lsicalapoewance at lchen slrous, Note the stop ofthe fblum mins. , Lichen slerosus wih prominent nourglassappenrance, om Cram OP et a: Dagnoste gynecologic and obsttcpaheegy, 3, Pladephia. 2018, Eker) ‘TABLE E1_Differental Diagnosis of Common Vulvar Mucocutaneous Disorders Diagnosis Aen PK Spong HK LL IDEM Selva top TTR Exchde Len simgex + = + = Cane evoncus 80) Leben semrsus soe * 2 ann as) Eszema * + * Sobol dermatitis Lichen planes * * + Ey Ls Lsc+is + + + an szema + LSC + + ana en : + * Sypits Proasis + + 80, Candida ‘ea eas Ae apy a tee avr wpe shai: Wp Flere Gems EX, nny Zep Leh wa PX peor os Sng apne TT tube maya preset From Gum Gata Dap sracco and bre pay 08, Pea 2018. bev, ‘SUGGESTED READING (fC eta Topica interventions for geal chen sclerosis, Coohrane Database ‘jst Rer 200008240, 2011,9 basic inronmarion DEFINITION Psoriasis is a chronic skin disorer charactr- zed by excessive proleration of keratinocytes, resulting in the formation of thickened scaly plaques, itching, and intammatory changes of the epidermis and dermis. Psoriasis is also associated with cardovascular, metabo, and neuropsychiatric effects. The various forms of psoriasis include plaque (most common), guttate,eryirodermic, pustular, inverse, and arts variants 1eD-t0cm coves Lao. Proriasis 40.0. Psoriasis vulgaris 40.1. Generalized pustular psoriasis, 40.4 Guta psoriasis L40.8 Other psorass 40. Psoriasis unspected [40.54 Psoriatic juvenile arthropathy EPIDEMIOLOGY & DEMOGRAPHICS * Peorisis affects 2% to 4% of the world’s population. Most patients have limited pso- isis involving

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