erythrodermic) psoriasis (and generalized pustular psoriasis) may cause severe systemic ups et (fever, \200\200 WCC, dehydration) \200\224also triggered by rapid with- drawal of syst emic steroids. Other signs: K bner phenomenon (p584); Auspitz sign: pinpoint bleeding on s cale removal; pepper pot nail pitting; \200\230grease-spots \200\231. Systemic signs 7% de velop a seronegative arthropathy \200\2245 types: 1 Monoar- thritis or oligomonoarthritis 2 Psoriatic spondylitis 3 Asymmetrical polyarthri- tis 4 Arthritis mutilans (destructive) 5 Rheumatoid-like polyarthritis. Tests None is routine; histology: epidermal keratinocyte hyp erproliferation, parakeratosis intra-epidermal neutrophil microabscesses (of Munro). 99 \201 \201 Eczema; tinea (solitary or few lesions; asymmetrical; expanding); mycosis fung oides (asymmetric, less scaling, do biopsy); seborrhoeic dermatitis. Management Education i s vital; control, not cure, is realistic. Assess severity and proportion of skin aff ected. Find out what he/she \201 nds most distressing. Encourage a support group (Psoriasis Ass ociation) Remove triggers (above). If mild: Creams are mostly used, eg the vitamin D analog calcipotriol + betamethasone 0.05% (once daily Dovobet ;1 it \200\200quality of life). 1 00 Others: Tar: Messy (esp. ointments \200\224reserve for inpatient use); Alphosyl HC , tw ice daily, is cleaner). Dithranol: Available in creams for use in short-contact regimens (a p- ply carefully to aff ected skin; wash off after h): start at low concentrations (0.1%) ; increase as tolerated (eg 0.25%, 0.5%, 1%). SE: burning (avoid \202 exures); staining ( avoid on face). Tacalcitol may be applied once daily before going to bed (max 5g/day, and o nly up to two 12-week courses/yr). For \202 exural disease, topical steroid/antibiotic/an tifungal preparations can be useful (Trimovate ). Psoriatic arthropathy: 2 Consider etaner cept, in \202 iximab, 101 or methotrexate. 102 Moderate to severe psoriasis: Risk:bene \201 t ratio seems most favorable for Goeckerman PUVA (see BOX), followed by etanercept or adalimumab (BOX). 103 y g o o t a m r e D l Fig 1. Psoriasis aff ecting the nails. Courtesy of Dr J Bowling. \201\201 Recalcitrant psoriasis1 Be holistic! This is a biological as well as a social inj unction. 60% of patients with psoriasis are depressed. Cytokine levels correlate with depre ssion and TNF antagonists (below) directly reduce depressive symptoms in psoriasis. 104 Taz arotene (once daily topical retinoid): for mild/moderate psoriasis af- fecting <10% skin su rface. Avoid in pregnancy. Wash hands after use. Avoid contact with eyes, face, intertrigin ous areas, hair-covered scalp, in \202 amed skin; avoid exposure to UV light/PUVA etc. Don \200\231t use emollients or cosmetics within 1h of use. NB: clobetasol 0.05% cream was bet ter in one trial. 105 595 Phototherapy with a selective broadband ultraviolet (UV) source with lit- tle emission <290 nanometres is less photocarcinogenic than narrowband UVB; 106 avoid if history of photosen sitivity; most suitable for guttate/small plaque psoriasis. PUVA: UVA + oral/topical psoral en; suitable for extensive large plaque disease (oral psoralen) and localized psoriasis (to pical pso- ralen); limit total dose to 1000J/150 treatments to avoid undue skin ageing and risk of skin cancer (esp. squamous cell carcinoma); can be combined with oral retinoids (re -PUVA) to \200\201light dose needed to clear lesions. Goeckerman regimen: hospital day-bas ed \200\224 for 3 weeks with coal tar applied once or twice daily then washed off before t otal body UVB (then shower to wash off scales). Non-biologic oral drugs Severe psoriasis of ten needs oral drugs (get help). \200 Methotrexate 10 \200\22320mg/week PO; most useful i n elderly patients; avoid if \200\235 . s u o i g a t n o c m \200\231 I y g o o t a m r e D l s k n i h t e h t c e p x e young in view of long-term risk of hepatic \201 brosis. Monitor FBC & LFT. \200 Ciclosp orin: 2.5 \200\2235mg/kg/day PO; good, but SE bad (BP \200\200; renal dysfunction). \200 Acitretin: Oral retinoid; useful for moderate/severe disease; SE: teratogen- ic; dry skin a nd mucosae; \200\200lipids; glucose \200\200; \200\200LFT (reversible). Check lipids, glu cose, LFT at start, then every 2wks for 8wks, then every 12wks. In the UK, use is limited t o hospitals. Starting at 25 \200\22330mg/24h PO; typical mainte- nance: 25 \200\22350mg/day ; adjust according to response. Exclude pregnancy, and avoid donating blood for >1yr and pr egnancy until >2yrs after the last dose. \200 Hydroxycarbamide: 0.5 \200\2231.5g/24h PO. SE: marrow suppression. 107 Biological drugs inhibit T-cell activation and function, or neu tralize cyto- kines. They also can potentially \200\201 adverse systemic side eff ects bec ause of their high speci \201 city for pathogenic cells without aff ecting cells of other or- gans. 95 If psoriasis hasn \200\231t improved eg with ciclosporin, methotrexate and PUV A or these have had side eff ects, consider ustekinumab or etanercept (eg 25mg SC, twice we ekly for \211 24wks). 108 This tumor necrosis factor (TNF- \200 ) inhibitor can also help joints in psoriatic arthropathy (and \200\201radiographic pro- gression). 109 It is usuall y well tolerated. SE: vomiting, oesophagitis, cholecysti- tis, pancreatitis, GI bleeds, isc haemia, emboli, BP \200\200 \200\201, dyspnoea, demyelination, seizures. Specialist use on ly. Alternatives: in \202 iximab, adalimumab. \200 110 I e m t a g n i r a t s s p e e k e H : d e z i t a m g i t s l e e f I \200\234 Fig 2. Onycholysis. Nail pit- ting may also be present. Fig 4. Psoriasis of elbow. Fig 3. Plaques on hand. Figs 2, 3, & 4 Dr S Baron. 1 In stable plaque psoriasis, apply Dovobet to <30% of body surface for \211 4wks; max 1 5g/day or 100gwk; repeat if needed after \211 4wks. Avoid face, genitals and scalp. Dermov ate shampoo can help the scalp. 2 Psoriatic arthropathy may signify endothelial dysfuncti on and impaired coronary microcirculation, so consider a vigorous approach to controlling c ardiovascular risk factors. 111 Eczema (dermatitis) Acute eczema causes a rash with less scale and less demarcated than pso ria- sis. Eczema may be atopic, hypersensitive (type VI), or be caused by irritants or veno us stasis. See also discoid eczema (p602 & \201 g 5, p586). Diff erent types may co-exist . Ask about work, hobbies, and other exposures to allergens. Atopic eczema ( \201 g 1) Cau ses: Multifactorial: Genetic: A family history of atopy is common (70%); Overactive TH2 lym phocytes produce IL4 & IL5, stimulating IgE production. Infection: Staphs colonize lesions and toxins act as a superantigen. Allergens: \200\200IgE is common. RAST (radioallergo- so rbent testing) identi \201 es speci \201 c antigens, eg house dust mite or animal dander. Altered microbial exposure may have a role (probiotics improve this, see BOX). Diet: Some atopic chil- dren have food allergies, eg dairy products egg Fig 1. Atopic eczema. Dr S Baron which exacerbate eczema. Although infantile eczema is common ( 2% of UK infants), m ost grow out of it before 13yrs old. \201\227: \200 Management involves control, not cur e. Dry skin itches and is susceptible to irritants, so use emollients liberally, even when eczema is less active. They treat dryness and act as a barrier. Ditto for bath emollients, eg Oilatum or Aveeno (oat oils). Use soap substitutes such as emulsifying ointment. 596 y g o o t a m r e D l Emollients (use at least twice a day). In severe eczema, greasy emollients are best, eg 50/ 50 emulsifying ointment and liquid paraffi n ( 3/week); Epa- derm costs 7/week. In l ess severe eczema, less greasy preparations are more acceptable, eg Diprobase ( 7/week) . \200 Daily 112 steroid ointment for active sites. Strength depends on severity, site, a nd age. Face, \202 exures, groins: 1% hydrocortisone. Potency of clobetasone 0.05% is one step above hydrocortisone (use on face for <1wk, under super- vision). 113 Elsewhere: Get control in \200\2051wk with higher-potency betametha- sone 0.1% ointment; \200\201strengt h soon (betamethasone 0.025%). Clobetasol is jolly potent; use brie \202 y only on thick s kin ( \200\223 skin thinning, telangiectasia, adrenal suppression). Haelan tape ( \202 u droxycortide) is good at healing \201 ssured digits. Oral anti-staph antibiotics (topical fusidic acid helps little compared to \202 uticasone or tacrolimus). 114 If systemic \200\224 needed, ciclosporin may be best (get help). Irritant dermatitis We are all susceptible to irritants. Hands are often af- fected; rednes s weeping precedes dry \201 ssuring. Common irritants: deter- gents, soaps, oils, solv ents, alkalis; water (if repeated). It often aff ects bar staff and cleaners. \201\227: Av oid all irritants; hand care (soap substitutes; regular emollients; careful drying; cotton or cotton-lined rubber gloves for dry and wet work respectively; as-needed use of topical s teroids for acute \202 are-ups). Allergic contact dermatitis (Type IV reaction) Common al lergens: nickel (jewelry, watches, coins, keys); chromates (cements, leather); lanolin (cre ams, cosmetics); rubber (foam in furniture); plants (primulas); topical neo mycin, framycet in, antihistamines, or anesthetics (haemorrhoid creams). The pattern of contact gives clues to the allergen. There is often a sharp cut- off where contact ends. Secondary spread else where is frequent (auto-sensi- tization). \201\227: Consider patch testing and avoidance o f implicated allergens; topical steroid appropriate for severity ( \200\201 strength and st op as it settles). Adult seborrhoeic dermatitis This common red, scaly rash aff ects scalp (dandruff ), eyebrows, nasolabial folds, cheeks, and \202 exures. Cause: eg over- growth of skin yeasts (Malassezia). It can be severe if HIV+ve. \201\227: Mild topical steroid/an tifungal preparations, eg Daktacort or ketoconazole 2% cream or shampoo (or metronidazole 0.75% gel). Treat intermittently, as needed. 115 \201\201 Holistic care of children with atopic eczema Identify triggers (irritants, infect ions, inhalants, ingest substances/foods). Find out how family life works to harmonize regi mens with daily lifestyles. Say to report any severe weeping rash eg around the mouth: this may be eczema herpeticum (Kaposi \200\231s varicelliform eruption):1 \200 IV aciclovir ma y be needed. \200\207Also get help if: nightly loss of sleep; \200\201social functioning; incessant itch; bleeding; oozing; extensive skin thickening/redness/excoriation. Tacrolimu s, bandages, phototherapy systemic therapy may be needed. Dermatology nurses play a big role in giving practical support for parents. They can show how to apply creams and occlusi ve dressings, eg stockinet suits, which aid emollient absorption, and prevent drying and sc ratching. If less severe \200 \200 Dry skin is itchy, so scratching is a big problem; it may become a habit (distraction therapies/star charts can help). Use leave-on emollients o ver the whole body often (500g/week). Turn down the heating (avoids drying). \200 Sedatin g antihistamines help, eg hydroxyzine or alimemazine. High doses 597 y g o o t a m r e D l may be needed in breaking the itch \200\223scratch cycle, and in enabling sleep. \200 Enc ourage joining a national eczema association (in UK, 020 7388 4097). \200 Discourage elim ination diets. Only occasionally is there a clear trigger (eg con \201 rm a dairy allergy with a RAST test; if +ve, get a dietician \200\231s help). Reducing exposure to house dust mite may help (high \201 ltration vacuuming of mattresses, limiting of carpet use; Gore-tex mattress covers). Use mild potency topical steroids; for severe \202 ares moderate potency ster- oids (for \211 5 days if on face; for <2wks for axillae/groins) may be needed. \200 116 Non-steroid al immunomodulation: Pimecrolimus 1% cream and tacrolimus 0.03% ointment have a role if >2y rs old; use sparingly twice daily on any skin, including face & \202 exures, for \211 3w ks (usually by a dermatologist, if topical steroids have failed or skin thinning would be a problem). Stop if no eff ect after 2wks. SE: pruritus, burning, acne (not skin atrophy). O ne advantage is that bene \201 ts keep developing even after treatment stops. 117 It does help itch. 118 Cautions: Infection at treatment site; UV exposure. CI: Erythroderma; pregna ncy/lactation. SE: Tingling, pruritus, folliculitis, acne, herpes simplex, \200\200sensiti vity to hot and cold, alcohol intolerance. NB: tacrolimus ointment is said to be better, wi th faster onset of action than pimecrolimus in atopy. 119 Preventing infantile eczema Exclu sive breastfeeding for the 1st 3 months associates with less atopic ec- zema in children wi th a 1st degree relative with atopy. 120 Antigen avoidance diets in high-risk women in preg nancy has little eff ect 121 but during lactation this might \200\201 infant atopic eczema . If a mother wants to try antigen avoid- ance, point out that it may not work. Prenatal di ets rich in \201 sh oil (n-3PUF) may help. 122 If breastfeeding is impossible, many try s oya milk, but this doesn \200\231t work; milk with hydrolysed casein (Nutramigen ; Pregest imil ) does.123 Probiotics are dietary supplements containing potentially bene \201 cial bacte- ria to assist developing body \200\231s gut \202 ora. The idea is that altered mic robial exposure may underlie the rise of allergic diseases in affl uent areas. Probiot- ics have been found to \200\201 incidence of IgE-associated eczema in infancy. 124 Reducing e xposure to house dust mite: High- \201 ltration vacuuming of mat- tresses; acaricidal spra ys, eg benzyltannate; Gore-tex mattress covering; washing bedding at 55 C. NB: meta-anal yzes doubt the effi cacy of these. 125 Abbreviated Williams diagnostic criteria for atopic eczema 126 A child must have an itchy skin (or parents report scratching) + \211 3 of: 1 O nset before 2yrs. 2 Past skin crease involvement. 3 History of generally dry skin. 3 Person al history of other atopy or history of atopy in 1st degree relative. 5 Flexural dermatitis or on cheeks/forehead and outer side of limbs if <4yrs. N=595 1 This is a primary herpes infection in skin traumatized by eczema; it may be fatal Skin infections Fungi Super \201 cial mycoses are the commonest of human fungal infections \200\224 and are limited to skin, hair, nails, and mucous membranes. They include der- mat ophytes (ringworm), super \201 cial candidosis, and Pityrosporum infections. 3 genera of d ermatophytes aff ect humans: Epidermophyton, Trichophyton and Microsporum. Spread is from m an to man (anthropophilic, eg T. rubrum, \201 g 2), animal to man (zoophilic, eg M. canis ) or soil to man (geophilic, eg M. gypseum). A ringworm in- fection is a round, scaly, itch y lesion whose edge is more in \202 amed than its center. It is called tinea followed, in Latin, by the part aff ected, eg tinea pedis (foot); cruris (groins); capitis (scalp); ungu i- um (nail); corporis (body, \201 g 1). Infection caused by yeasts of Candida genus (eg C. albicans) are common (esp. in immunocompromised OHCM p441), and mainly aff ect mouth, va gina, glans, skin folds/ toe web; nail areas. They are often pink and moist satellite le sions. Other yeasts causing infec- tion: Malassezia species (eg M. furfur; 11 species are r ecognized and are tricky to distinguish): 127 Pityriasis versicolor (multiple hypo- or hype rpig- Fig 2. Trichophyton rubrum. mented scaly macules on the upper trunk and Courtesy of D r Jonathan Bowling. back). Pityrosporum folliculitis and seborrhoeic dermatitis ( \201\227: once-daily ketoconazole cream). \201 : Skin scrapings from the edge (active margin) of le sion. Collect specimens from hair-pulls and nail clip- pings in folds of black paper (to co ntrast with white scrapings). Wood \200\231s light causes \202 uorescence in some fungi a nd can help diagnosis, and suggest areas for scrapings. Microscopy (added KOH dissolves ker atin) and culture (takes 6 wks) also help. Take skin swabs if candidosis is suspected. \201\227: Dermatophytes: Skin: terbina \201 ne or imidazole creams (eg clotrimazole) twice daily for 2wks. Scalp: griseofulvin or terbina \201 ne PO for children for 2 weeks. Nails : terbina \201 ne PO for 3 months if deemed essential. Explain about SE (headache; dizzine ss; taste disturbance; arthralgia; LFT \200\200; psychiatric illness; vertigo) and interact ions ( \200 -blockers; antidepressants). Candida: Mouth: nystatin (eg oral suspension, 1mL/ 6h for 1 week). Vagina: imidazole cream pessary (eg Canesten Combi ). Pityriasis versic olor: Selenium sulfide shampoo daily for 1 week; wash off after 10mins or twice-daily imida zole creams. Bacteria Impetigo: Contagious super \201 cial infection caused by Staph aureu s ( Strep pyogenes). Peak: 2 \200\2235yrs. Lesions (often well-de \201 ned) usually start around the nose & face with honey-colored crusts on erythematous base ( su- per \201 ci al \202 accid blisters). \201\227: Try topical antibiotics \201 rst (fusidic acid, mup irocin). Give oral antibiotics (eg \202 ucloxacillin 125mg/6h PO, in a child) if more sev ere. 128 Erysipelas: Sharply de \201 ned super \201 cial infection caused by Strep pyogen es. Often aff ects the face (unilateral) with fever and \200\200WCC. \201\227: Systemic p enicillin (see below). Recurrent cases may need prophylactic antibiotics. 129 Cellulitis: A cute infection of skin and soft tissues (eg legs). Cause: \200 -haemolytic streps staph s. It is deeper and less well-de \201 ned than erysipelas. Signs: pain, swelling, erythema , warmth, systemic upset and lymphadenopathy. \201\227: \200\207Elevate the legs. Benzylp enicillin 600mg/6h IV (or penicillin v 500mg/4 \200\2236h PO) + \202 ucloxa- cillin 500mg /6h PO. If penicillin-allergic, try erythromycin 500mg/12h PO. Skin TB: Lupus vulgaris \200 \22455%; a patch of red-brown \200\230apple jelly nodules \200\231 (on white skins) eg on face/leg, which forms a scar in which new nodules may grow; \200 : \200 \200\2062:1. Scr ofuloderma (27%; suppurating nodules over TB foci), TB verrucosa cutis (6%; indolent warty plaques); TB gumma (5%); tuberculids (7%, symmetric generalized exanthems, eg Bazin \200 \231s erythema induratum/lichen scrofulosorum). 130 598 Fig 1. Tinea corporis. Courtesy of Dr Susannah Baron. y g o o t a m r e D l Common viral infections Warts ( \201 g 1) Cause: human papillomavirus (HPV) in keratino- c ytes. Large numbers can occur if immunosuppressed. Com- mon warts: Most common in children/ young adults; often Fig 1. Wart. OUP resolve spontaneously (some are stubborn). Complicatio ns: SCC, p590. Treat- ment: \200\234wait and see \200\235 or salicylic acid (keratolytic, eg Salatac gel); cryother- apy (if \200\2067yrs) or once-daily topical 5- \202 uorouraci l (for 6wks; adults & chil- dren; unlicensed).Glasjo Plantar warts: Large con \202 uent le sions (mosaic warts) often resist treat- ment. T \211\210 2yrs. They are infectious. Avo id excision. After abrading it, try sali cylic acid under an occlusive plaster, eg as Occlu sal . Combination therapy eg topical cantharidin 1% + podophyllotoxin 5% + salicylic acid 30% (CPS) is often better than cryo (double freeze-thaw cycles are better than single ones, but not for hand warts). 133 Recalcitrant warts may respond to photodynamic therapy; use i s non-standard. 134 NB: schools expect children to wear verruca socks for swimming. One unc ontrolled study showed pub- lic shower users got more plantar warts than locker room users who didn \200\231t use such showers. 135 Plane warts: Flat skin-colored or brown lesions; t end to K bnerize (p584) in scratch marks; they often resist treatment. Genital warts (cond ylomata acuminata): \201\227: Cryo podophyllin: terato- genic) or imiquimod cream. Scre en for other STI. Women with genital warts (or whose partners have them) may need yearly ce rvical cytology (HPV16 & 18/ cervical cancer, p273). Prevention: p272. If a child, suspect abuse. Other wart treatments: Radiofrequency ablation, infrared coagulation, anti- virals ( cidofovir), bleomycin, interferon intralesional injection, topical 5FU. 136 Molluscum conta giosum (pox virus) These pink papules have an umbili- cated (depressed) central punctum. Wh ite material can be expressed and microscoped to con \201 rm the diagnosis (molluscum bodi es). Common in chil- dren. They resolve spontaneously (may take months). Gentle cryo may be tried. It is more common in atopic eczema. If \202 orid, suspect HIV. Herpes simplex (gi ngivostomatitis or recurrent genital or perioral infec- tion) Infection can be triggered by fevers, sunlight, immunosuppression. Eruption often preceded by symptoms of burning/itchin g. Signs: Grouped painful vesicles on erythematous base which heal without scarring. Treat- ment: Often none needed. Topical aciclovir may prevent or reduce severity of recurrences. Systemic treatment is indicated in certain circumstances (immunosuppressed; frequent recurr ent genital herpes). There is evidence that Bell \200\231s palsy may be related to recurren t herpes infection. Herpes zoster Varicella-zoster virus becomes dormant in dorsal root gan glia. Recurrent infection aff ects one or more dermatomes (p762, esp. if immunosuppressed). Pain and malaise may precedes the rash Signs: Polymorphic red pap- ules, vesicles, pustule s ( \201 g 3). Post- herpetic neuralgia: see OHCM p400. \201\227: If mild, none. If sever e (or immuno- suppressed) try aciclovir 800mg 5 \211\210/ day PO for 1wk (SE: confusion; LF T \200\200; GFR \200\201) or famciclovir 250mg/8h PO for 1wk (SE: headache, confusion). Var icella-zoster vaccine (if >60yrs) and immune globulin (postexpo- sure) are preventives. 137 ! s l i a f 599 n e t f o e s l e g n i h t y r e v e regimen 131 Oral zinc sulfate ( \211 600mg/d) appears to help. 132 d n a y p a r e h t o n u m m y g o o t a m r e D i , s c i t o t i l m i t n a , ) g n i z e e r f , g n i n r u b ( n o i t c u r t s e D . y g o l o t a m r e d f o l l a n i e l u p a p g n i t a r t s u r f t s o m e h t e r a s t r a W Fig 3. Ophthalmic zoster (shingles). Acne vulgaris The 5 pillars of acne (1) Basal keratinocyte proliferation in piloseba- ceous follicles (and rogen- and CRH- driven, p583), (2) \200\200sebum production, (3) Propionib acterium acnes colonization, (4) inflammation, (5) comedones (white- & black-head) blocking secretions, hence papules, nodules, cysts, and scars (face, neck, upper torso). It is almo st universal in teenagers: it causes much angst (nature in one of her darkly ironic moods p icks the fairest skin at its vainest moment for her \201 ercest pustules). Most with acne don \200\231t have \200\200androgens but their sebaceous glands are more sensitive to and rogens (p583). Diff erential diagnosis Acne rosacea \200\224no comedones; diff usely red no se, cheeks, chin, and forehead; telangiectasia; \202 ushing, especially after alcohol. \202\221 Be holistic; subtle doctors use acne consultations to promote mental health by giv ing patients a vocabulary to describe their misery, and so to control it. Dispel myths: it is NOT due to \201 lth, lack of washing, etc. But diet may be important ( \200\200glycaem ic loads may have a role). 138 Ask about mood, fears of social rejection (not always unfoun ded). Suicidal ideation is a red \202 ag. Stress reduction is important (modulates sebace ous gland hormones & cytokines). Mild acne Mainly facial comedones; if to be manually remov ed \200 , do at ovula- tion, before sebaceous ori \201 ces narrow. 139 Topical \200\224: (singly or combined): ben- zoyl peroxide (as low a strength as works, eg 2.5%, or 10% as a twice-weekly wash; more may irritate); azelaic acid (15% gel, twice daily for <6 months); r oll- on antibiotics (clindamycin, as Dalacin T ); with azelaic acid it is synergistic. 140 Moderate acne (in \202 ammatory lesions, face torso): Doxycycline or minocy- cline 141 (erythromycin if pregnant or <12yrs old) for \200\2064 \200\2236 months with topical benz oyl peroxide (start at 2.5%, not 5 or 10% to avoid irritation). 142 Make topical antibiotic s the same as the oral drug to \200\201drug resistance. Topical retinoids (creams/gels): a dapalene or isotretinoin used either alone or with benzoyl peroxide (Epiduo gel) or eryth romycin (Isotrexin gel). 142 Severe acne (nodules, cysts, scars): Isotretinoin is 1st cho ice eg 0.5 \200\2231mg/kg/ day for 20wks (to \200\201sebum production and pituitary hormon es). 141,143 Marked bene \201 t occurs in virtually all patients (permanent 65%). SE: ter atogenic (good contraception must be used during and for 1 month after treatment); dry skin , lips, mucosae; myalgia; headache (benign intracranial hypertension reported); depression; 1 hepatitis; \200\200lipids. 144 Monitor triglycerides, AST, ALT, cholesterol, and FBC oft en. 141 Alternative (if \200 and wanting contraception): co-cyprindiol (Dianette ) \200 \224see combined oral contraception, p300. Other putative indica- tions for isotretinoin: m oderate acne not responding to antibiotics; presence of scarring and severe psychological p roblems. Acne rosacea This is a chronic relapsing/remitting disorder of blood vessels and p iloseb- aceous units in convex central facial areas typically in fair-skinned people. Preva lence: 10%. Pre-rosacea features: \202 ushing2 triggered by stress/blushing, alcohol & sp ices. Grade I to III signs: erythemato-teleangiectasies, papulopus- tules, and in \202 amm atory nodules. Severe subtypes: rosacea conglobata; rosacea fulminans; rosacea with lymphoe dema blepharitis/conjunctivitis. In men, rhi- nophyma (swelling + soft tissue overgrowth of the nose) may occur. Cause: Unknown. Chlamydia pneumoniae may have a role. 145 Plan/ \201\227: Avoid irri- tants & sun overexposure. Help with avoiding blushing (CBT, p374) may help social functioning. 146 Topical azelaic acid metronidazole (0.75% gel/12h for 8wks ) for mild/moderate disease, 147 or doxycycline eg 40mg 148 PO for 16wks. Azithromycin 500m g/day PO for 2wks helps (it \200\231s anti-in \202 ammatory and kills C. pneumoniae). 149 Isotretinoin (above) and lasers (eg 532nm) are rarely needed. 600 y g o o t a m r e D l N=88 1 Don \200\231t deny \200\224 if depressed: those with pre-existing depression have most t o gain (eg \200\200quality of life). 2 Flushing \200 \200 : Menopause; alcohol; food int olerances; toxins; drugs (nicotinic acid, bromocriptine, tamoxifen, cyproterone acetate, ci closporin); mastocytosis (p602); carcinoid; pheochromocytoma. 601 Drug eruptions 10% of hospital patients develop a drug eruption during their admission, so. know the main culprits, and how to classify and treat them. Types of reaction Maculopapu lar or ex- anthematous: ( \201 g 1) This is the common- est type, presenting with generali zed ery- thematous macules and papules eg on the trunk fever and eosinophilia \200\224eg within 2wks after onset of therapy. Drugs: Penicil- lins; cephalosporins; anti-epileptics. Urticaria:1 Signs: wheals ( \201 g 2 on p584); rapid onset after taking drug associa- tion with angio-oedema/anaphylaxis. It can result from both immunological and non-immunolog ical mechanisms. Drugs: morphine & codeine cause direct mast cell degranulation; penicillin s & cefalosporins trigger IgE responses; NSAIDs; ACEi. Exfoliative dermatitis: Signs: Wides pread erythema and dermatitis; erythro- derma. Causative drugs: Sulfonamides; allopurinol; carbamazepine; gold. Erythema multiforme major (Stevens \200\223Johnson syndrome): The more se- vere variants of erythema multiforme are usually due to drugs. Signs: Target lesions a nd polymorphic erythema, eg with blistering mucosae (conjunctivae, oral, labial, genital) i f severe. Drugs: Sulfonamides; anticonvulsants. Toxic epidermal necrolysis (TEN): the bad b ad end of the erythema multiforme/ Stevens \200\223Johnson syndrome (SJS) spectrum. Signs: Widespread erythema, then necrosis of large sheets of epidermis. Mucosae se- verely aff ect ed. Risk of TEN in HIV patients is 1000-fold higher. 150 Mortality: 30%. Drug causes: Sulf onamides; anticonvulsants; pen icillins; allopurinol; NSAIDs. Manage in a dermatology or bu rns unit. Short-term dexamethasone pulse therapy, 151 IV Ig. Lichenoid: This is similar to lichen planus but it rarely shows typical signs of idiopath- ic lichen planus. It can be ve ry itchy. Drugs: \200 -blockers; thiazides; gold; antimalarials. Dr Susannah Baron. Fix ed drug eruption: Lesions recur in the same area each time a particular drug is taken. Drug s: paracetamol, tetracyclines, sulfonamides, aspirin. 152 Management A clear history of the onset and duration of the rash is essen- tial. Record all drugs taken (herbal remedies, et c). Stop the likely off ender. If the clinical diagnosis is in doubt, a prick test or skin biopsy may be helpful but is not always so. In order to con \201 rm the suspicion of drug sensitivity, some advocate rechallenge with the suspected drug once the patient has re- cov ered. While this may be the ideal, re-challenge may be dangerous (beware erythroderma and a naphylaxis). Not unreasonably, patients may also object to this. 153 Many drug rashes need no intervention. Give regular emollients for dryness or itch. Very itchy rashes, eg licheno id or dermatitic, may need short courses of topical steroids. Urticaria: prompt antihistami ne with IV hydrocor- tisone/IM adrenaline (=epinephrine, p237) if anaphylaxis. More severe erup- tions, eg erythema multiforme are best managed by specialists. y g o o t a m r e D l Fig 1. Penicillin rash. Fig 2. TEN/Stevens \200\223Johnson syndrome 1 Other triggers of acute urticaria: Animals; rubber; shell \201 sh; nuts; dairy products; stings; viruses. 154 Chronic urticaria: Food additives; autoantibodies which attack mast c ells, which release histamine Miscellaneous skin disorders Lichen planus Lesions (eg on \202 exor aspects of wrists, fo rearms, ankles and legs) are purple, pruritic, poly-angular, planar( \202 at-topped) papul es, seen at any age + white lacy markings (known as Wickham \200\231s striae). Lesions else - where: scalp (scarring alopecia), nails (longitudinal ridges), tongue, mouth (lacy white areas on inner cheeks), and genital lesions. Lesions often arise at sites of trauma. Usuall y persists for 6 \200\22318 months. \201\227: Topical steroids ( topical antifungals) ar e 1st-line (esp. in oral disease, eg \202 uticasone spray). Moderate to potent topical st eroids help itch. Use systemic steroids only if severe. 155 Haemangiomas Strawberry naevae occur in neonates as a rapidly enlarging red spot. Most go by the age of 5 \200\2237 years. No treatment is required unless a vi- tal function is impaired, eg obscuring vision. 156 P yogenic granuloma/lobular haemangioma ( \201 g 1) is a lesion thought to arise as a result of minor trauma, typically occurring on \201 ngers. It is not infectious or granulomatou s. It appears as a moist red lesion which grows rapidly and often bleeds easily. Treatment: Curettage. Pityriasis rosea This is common, often aff ect- ing young adults, and may have a viral cause (eg herpes hominis HHV-6 & HHV- 7). 157 A rash is preceded by a herald patch (ovoid red scaly patch with a scaly edge, similar to but larger than later lesions). Tends to aff ect the neck, trunk, and proximal limbs. There is no good treatment. It is self-limi ting (recovers in 2 \200\22312wks). Oral erythromycin may help treat the rash and decrease the itch. 158 Alopecia Hair loss is scarring or non-scarring. Non-scarring causes may be re versible, but scarring alopecia implies irreversible loss. Scalp disorders may be signs of skin elsewhere: (look for signs of lichen planus, and SLE). 602 y g o o t a m r e D Fig 1. Pyogenic granuloma. Courtesy of Dr Jonathan Bowling. l Non-scarring alopecia: nutritional (Fe or Zn de \201 ciency); androgenetic ( \200 & \200 ) autoimmune (alopecia areata: smooth round patches of hair loss on scalp; hairs like excl amation marks are a typical feature; often spontaneously regrows; total scalp hair loss = a lopecia totalis; total body hair loss = alopecia universalis \200\224its treatment is diffi cult: consider topical or intralesional steroids, or minoxidil, or dinitrochlorobenzene); telogen ef \202 uvium (shedding of telogen phase hairs after period of stress, eg childbir th, surgery, severe illness). Scarring alopecia: lichen planus; discoid lupus erythematosus; trauma. Blistering disorders Infection (eg herpes); insect bites (eg on legs); drugs (ACEi; furosem ide); dermatitis herpetiformis, (p588); friction; discoid eczema;1 Zn \200\201; autoimmune blistering disorders (ABD), eg pemphigoid \200\224the chief ABD in the elderly \200\224due to IgG autoantibodies to basement membrane (bullous pemphi- goid antigens 1 & 2). Signs: Te nse blisters on an urticated base. Skin biopsy: (+ve immuno \202 uorescence; linear IgG an d C3 along the basement membrane). \201\227: clobetasol cream up to 40g/day is better than oral steroids. 159 Pemphigus aff ects younger people (<40yrs) than pemphigoid and is due t o IgG autoantibodies against desmosomal components (desmoglein 1 & 3). This leads to acanth olysis (keratinocytes separate from each other). Drugs may cause it, eg ACEi, NSAID, phenob arbital, L-dopa. Signs: Flaccid blisters which rupture easily to leave widespread erosions. The oral mucosa is often aff ected early. Skin biopsy: +ve immuno \202 uorescence (interc ellular IgG giving a crazy- paving eff ect). \201\227: prednisolone (60 \200\22380mg/day P O, eg life-long in low doses). IVIs of rituximab and immune globulin may have a dramatic ef f ect. 160 1 Discoid (=nummular, ie coin-shaped) eczema may begin with vesicles. 161 Typical patient: \200 50 \200\22370yrs or \200 20 \200\22330, with somewhat symmetrical round/oval very itchy vesicles, or papular plaques often on legs (or trunk/arm, not face) with well-de \201 ned irregular margins (p587 \201 g 5). They may crust and get infected by staphs bef ore \202 attening into hyperpigmented macules. It recurs at the same sites. Sunlight may improve it. Cause: unknown; patch test +ve in 50% (if +ve, avoid culprits). 162 \200\224: lukewarm baths + moisturizers + steroid ointment (eg high-potency, preceded by a 20min wat er-soak 163) + oral antihistamine. Photosensitivity For classi \201 cation of susceptibility to ultraviolet, see p593. Photos ensitivity denotes conditions triggered by light (eg solar urticaria; poly morphic light er uption). Photoaggravation describes disorders worsened by light but not due to abnormal sen sitivity to light (eg recurrent herpes la- bialis; rosacea). Photosensitivity can occur to visible light, UVA (320 \200\223400nm) or UVB (290 \200\223320nm). \200\207Usually a caref ul history allows accurate diagnosis. \200 A rash every summer, for example, suggests tha t uv has a role. \200 How long does the rash take to appear? Within 30min suggests solar urti- 603 caria; polymorphic light eruption may take days to appear. \200 Itching suggests polymorp hic light eruption or solar urticaria. \200 Face rashes, including the V of the neck, but sparing periorbital skin. \200 The dorsum of the hands and the arms are other typical si tes. \200 As hands are usually relaxed in the semi- \202 exed position, skin around DIP y g o o t a m r e D joins is less aff ected than that around the knuckles and PIP joints. l Is there a family history? If so, refer to genophotodermatologist. Is it xero- derma pigmentosum, Bloom \200\231s syndrome, or Cockayne \200\231s syndrome? \200 Pain ( family history) suggests erythropoietic protoporphyria (sun may hurt so much that a child quickly avoids it, so there is pain but no rash). \200 Was the rash related to starting a drug (eg nalidixic acid)? See below. \200 Are there papules: this suggests polymorphic light eruption. \200 Any blisters or linear marks where plants have scratched the skin (p hyto- photodermatitis from furocoumarins)? Ask about hobbies/work. Polymorphic light eruption: This is a common idiopathic disorder typically aff ecting young women in spring. After light exposure, itchy red papules, vesicles, and plaques develop on exposed sites, often improving over the sum- mer due to a phenomenon called \200\230harde ning \200\231. Smoking and alcohol may trig- ger it. 164 \201\227: Sun-avoidance; sun-prot ection (high factor UVA + UVB sunscreen). Acute attack: potent topical steroids a short course of systemic steroids. Severe cases: desensitization (UVB phototherapy or PUVA therap y). 165 Porphyria cutanea tarda: (The commonest porphyria) The 1 ab nor mality is \200 \201uroporphyrinogen decarboxylase in liver. Causes/triggers: some alleles of haemochromato sis gene; HIV; hepatitis C; alcohol; estrogen, \200\200iron, \200\201ascorbic acid. Signs: Vesicles/bullae in sun-exposed sites, hypertrichosis, hyperpigmen- tation, skin fragility, and scarring (milia). Tests: \200\200LFT; \200\200ferritin; \200\200plasma, fecal & urin ary porphyrins (protect urine from the light and ensure it gets analyzed promptly; phone la b). \201\227: Remove precipitants; sun-avoidance/protection; reg- ular venesection until f erritin in normal range; chloroquine, ascorbic acid. 166,167 Systemic lupus erythematosus: (OHCM p556) Light exposure often triggers erythematous rashes, with systemic \202 are. A variant of lupus, subacute LE, is associated with marked photosensitivity and anti-Ro antib odies. Drugs often cause of photosensitivity, so \200\207look up details of all drugs take n. Frequent off enders: thiazides (sunburn-like or lichenoid rash); tetracyclines/ sulfonam ides (sunburn-like); tricyclics; phenothiazines; NSAIDs; amiodarone (sunburn-like eruptions ). It may take months to settle, after drug withdrawal. Ordinary urticaria Acute: Rash (eg to latex) lasts <6wks. Skin prick or blood RAST tests (p596) may help. Chronic: Idiopathic, but can be auto immune in 45 % of patients (IgG against IgE receptor, 168 causing degranu lation, p610) or seen with collagen, thyroid or sinus disease. Physical urticaria is caused within minutes by an external trigger, eg heat, cold, exercise, or trauma (dermato- graphi sm). Contact urticaria arises eg on contact with food, insect bites, or pet saliva. Urticar ia pigmentosa ( \201 g 1, p610) May be caused by H. pylori. Urticarial vasculitis Cutaneou s lesions resemble urticaria, but histologically show features of a vasculitis. Also: \202 itting arthralgia, GI symptoms obstruc- tive lung disease especially in smokers. If co mplements are low, it may be as- sociated with SLE, Sj gren \200\231s syndrome, or cryoglo bulinaemia. \201\227: Antihistamine, NSAIDs, but some patients may need immunosuppressive therapy. 169