Review

Common skin conditions affecting the scalp:Tinea Capitis, Pediculosis Capitis, Seborrhoeic Dermatitis, Dandruff,

Psoriasis

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' Introduction

-fhe structure of the skin anrl its firnction r,arie s in the diII'erent regions o1'the lxrrh'. The scalp urth its higl <lcnsin'

<lf large hair fbllicles :urd :rbunclance o1'sebaceous glancls runstitutes ir unirlue ar-ea. The sca$ is apparetrtll' less

l)rone to inllarnmation. Sonre <lernrat<>logical conclitions of'the scalll will be tliscusse<l: clermatophltic inf'eclion(tinca capitis) :rs a common inl'ectious process allbcting lloth thc skin ancl hair; pe<lictrlosis capitis, the trnitlue

parasitic infbstati<xr; an<l inflarnmatory rliseases, seborrhocic dernratitis, danclrtdf ancl psoriasis.

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TINEA CAPITIS

EpidemiologyTinea capitis is caused by a variety ofdermatophytes in the genera Microspo-rum and Trichophyton. In South Africait is caused mainly by Microsporumcanis (white children) and Trichophytonviolaceum (black children).

Tinea capitis affects mostly childrenof primary school age. The increasedincidence of tinea among prepubertalchildren has been attributed to reducedfungistatic properties of the child'ssebum. However, comparison studiesof sebum in prepuberta l versuspostpubertal children failed to revealreal fungistatic diffcrences. Childrencontaminate each other with combs,hats, hair care items and the spread ofsome an th ropoph i l i c spec ies l i keTrichophyton violaceum in this way ismore common in African children. Aninfected cat or dog usually serves as thesource of infection with Microsporumcanis in white children. In familyoutbreaks of th is zoophi l ic speciespostpuberta l ind iv iduals are a lsooccasionally affected. Tinea capitis inadults is rare. It must. however, beconsidered when patients present witha t yp i ca l sca lp l es ions . Th i s i s o fparticular significance in the elderly.Whether this increase in frequency inthe elderly is secondary to differencesin the sebum is soeculative.

Clinical picture (Figures 1-4)The clinical picture of t inea capitisvaries greatly and depends mainly onthe type ofoffending agent. In general,zoophilic species produce much moresevere inflammation than those whichare confined to humans (anthropo-philic). In some cases, the inflammationcan be minimal with delicate scaling andinappreciable hai r loss resembl ings e b o r r h o e i c d e r m a t i t i s o r a t o p i cdermatit is. In some individuals anasymptomatic carrier state occurs. Mostoften scalp dermatophytic infectionmanifests a characteristic loss of hairwith "black dots" which reflects thehair shafts broken within foll icularcanals (main ly in Tr ichophytonviolaceum infection). Microsporumcanis can cause more severely inflamedlesions with pustules - kerion. Thisrepresents an immune reaction to azoophilic fungus and is not a sign ofbacterial superinfection.

Di fferen ti al di agn o si sThe d i f ferent ia l d iagnosis of t ineacapitis includes seborrhoeic dermatitis,pityriasis capitis, atopic dermatit is,psoriasis, furunculosis, alopecia areataand trichotillomania.

DiagnosisThe diagnosis of tinea capitis is basedon typical clinical picture - patchyalopecia, broken hairs, scaling, cervical

adenopathy. Confirmation of t ineacapitis may be made by direct micro-scopic examination of an infected hairand by fungal culture. Only cultureidentifies the species.

TreatmentTinea capitis needs to be treated withan oral agent because the antifungalremedy has to penetrate into the hairfo l l ic le . Sole therapy wi th topicalantimycotic agents is usually ineffective.

Griseofulvin taken orally at a doseof 15-25 mglkglday is still the treatmentof choice for tinea capitis. As a fattymeal enhances griseofulvin absorptionit should be taken during a meal ordirectly after food. Treatment for 6-8weeks usual ly suf f ices but i t isrecommended to perfom cultures everyfew weeks and to continue the treatmentunt i l the cul ture is negat ive.

The main cause of tinea capitis inSouth African white children, Micro-sporum canis, appears to be highlysensitive to griseofulvin. Griseofulvinis a safe medication and the routinemonitoring of hepatic and haemopoieticparameters is rarely necessary in healthychildren.

Itraconazole (Sporanox@) has beenfound to be very ef fect ive in t ineacapitis. Itraconazole should be dosedaccording to body weight at about 3 to5 mgkglday. A continuous therapy withitraconazole ( l00mg/day) for 4-6 weeks

SA liarn Plact 2(X)3; trri(ll)

has been reported as very effective.r'2Availability of itraconazole in a liquidformula (Sporanox@ oral solution)permits the administration of a moreprecise dose than using the non divisiblecapsules. Gupta et a1.3 used intermittentpulse therapy, Smglkglday; each pulselasted one week, with two weeks off thedrug between the first and second pulsesand three weeks off between the secondand third pulses. The third pulse wasnot necessary in every patient. In thisstudy, itraconazole was found to beeffective and resulted in both clinicaland mycologic cure. In itraconazolepulse therapy the drug is largelyeliminated from the plasma within 7 tol0 days, thereby reducing the potentialfor adverse effects. Itraconazole shouldnot be used with terfenadine or othernonsedating antihistamines owing topotential combined cardiac toxicity.

Fluconazole (Diflucan@), anotherazole antifungal, was also found to be apromising drug for tinea capitis.a Acontinuous treatment with a dose of 5mglkglday for 4 weeks was foundeffective in cases oftinea capitis causedby Trichophyton species. Availabilityof f luconazole in ora l suspension(Diflucan@ susp.) makes it a usefulalternative in paediatric patients.

Terbinafine (Lamisil@), a member ofthe allylamine family, is also a usefulagent in tinea capitis. It appears veryeffective in infections with Trichophy-ton violaceum. The dose of 62,5-250mglk{day for 4-6 weeks, depending onbody weight, is usually required ininfect ions caused by th is fungus.Microsporum canis usually requireshigher doses and a longer period ofadminis t rat ion, l0 to l2 weeks.Terbinafine, initially considered free ofany side-effect potential, lost a bit ofitsimocuous image since with wide useseveral unwanted effects have beenreported (most often blood dyscrasisiasand hepatotoxicity). It is neverthelessa safe drug and there do not seem to beany absolute contraindications.

PEDICULOSIS CAPITIS

(HEAD LICE)

Head lice (Pediculosis humanus capitis)are transmitted among persons living inunhealthy, crowded conditions and

sharing hats, brushes and combs. Longhair and elaborate styles ofhairdressingwhich prevent f requent washingincrease the susceptibility. Head lice ismost common in children but no age isimmune. The eggs are attached to thehair and when they hatch, numerous nits,resembling dandruff, are left behind.These are seen mainly in the occipitaland postauricular regions. Pruritus isthe most characteristic manifestation.Scratching often leads to secondaryinfection and the occipital lymph nodesare frequently enlarged. The diagnosisis often missed when the possibility isnot considered. Nits firmly attached tothe hair shafts are not easily pulled off.This differentiates them from dandruffscales.

The treatment of choice is to applyPermethrin lo/o cream rinse. Applica-tion of Permethrin should be precededby a regular shampooing and toweldrying. Permethrin has to be applied tothe hair and scalp for l0 minutes andthen rinsed off with water. A singlet reatment is usual ly suf f ic ient .Permethrin is safe for children over 2years ofage.

An alternative therapy is to apply10% Crotamiton cream (Eurax). It isleft on the scalp for 24 hours and thenshampooed. This treatment can berepeated in 7-10 days, if necessary.

SEBORRHOEIC

DERMA'TITIS OF THE SCALP(FTGURES 5 AND 6)

Seborrhoeic dermatit is is a commonin f l ammato ry cond i t i on p resen t i ngclinically as erythematous, scalingerupt ion, local ized to the scalp,eyebrows, postauricular areas, centralface, central chest and back and flexuralareas, the so-called seborrhoeic areas.Although these lesions are common andare clinically quite distinctive the causeof seborrhoeic dermatit is remainselusive. The seborrhoeic state is asso-ciated with increased susceptibility topyogenic infections and invasion byPityrosporum ovale. Whether Pityro-sporum ovale causes seborrhoeicdermatitis is not clear. Scalp scalesproduced by seborrhoeic dermatitisprovide a good nutrient for the growthof this lipophilic yeast and increased

presence of Pityrosporum ovale maywell be a secondary and not primaryevent.

Clinically seborrhoeic dermatitis ofthe scalp presents as areas of erythemacovered by yel low, greasy scales.Lesions of ten extend beyond themargins of the hair onto the foreheadand behind the ears. Seborrhoeicdermatit is may be associated withtransient alopecia.

TteatmentThe seborrhoeic s tate is probablygenetically determined and eradication(complete prevention ofrelapses) in thepredisposed indiv iduals is ratherunlikely. What can be done is to reduceboth scaling and the inflammation.

The scalp should be shampooedfrequently, daily or every other day insevere acute phase, less often later on.

There are several medicated sham-poos to choose from: selenium sulfide(Selsun@), tar (Polytar@, Alphosyl@),ketoconazole (Nizshampoo@). Altema-t ing d i f ferent types of medicatedshampoos often increases their efficacy.Shampoos should be rubbed into thescalp and left for 5-10 minutes beforerinsed out. The length of t ime theshampoo stays on the scalp appears lessimportant than the f requency ofshampooing. In more resistant cases,topical cor t icostero ids are recom-mended (Procutane@ lotion, Betno-vate@ scalp application, Diprolene@scalp lo t ion, Elocon@ lot ion andothers). The degree of scalp inflamma-tion wil l dictate the potency of thetopical corlicosteroid used.

The t reatment of seborrhoeicdermatitis of the scalp in people ofAfrican descent will differ from theabove general recommendation. Dailyshampooing is too drying for blackpeople hair and rather impractical formany African females with hot-pressedhair. The medicated shampoo shouldbe applied less often, once a week, butfor a longer time, 20 to 30 minutes. Thisshampoo should be fo l lowed by anonmedicated shampoo and the usualmoisturizers or conditioners. When thescalp is considerably inflamed or thereis no response to the shampoos topicalsteroids should be applied. Often morefatty vehicles shouldbe used, ointments

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rather than lotions and gels, particularlyin f-emales with hot-pressed hair.

DANDRUFF (PITYRIASIS

CAPITIS)

In dandruif there is desquamation ofsmall, flaky scales f}om an otherwisenormal scalp. The aetiology of dandruffi s no t c l ea r and the l i t e ra tu re i sconfusing.5 It is usually accepted thatdandrutf and seborrhoeic dermatit isrep resen ts two ends o f a d i seascspectrum. Similarremedies, medicatedshampoos, were fbund equally eftbctivein the treatment of both conditions. Asin seborrhoeic dermat i t is shampooscontaining tar, salicylic acid, seleniumsr"r l f ide and ketoconazole arerecommended. Usually twice weeklyusage controls the scaling.

PSORIASIS OF THE SCALP(FTGURES 7 AND 8)

Psoriasis affects approximately 2%o ofthe wo r ld popu la t i on and sca lp i sinvolved in about 50% ofall psoriatics.Usual ly there are psor iat ic les ionselsewhere but the disease can be limitedto the scalp.

Psoriasis of the scalp presents as welldemarcated erythemato-squamousplaques covered by thick silvery scales.In severe involvement the plaques cover

the entire scalp. Frequently the psoriaticlesions extend beyond the hairline, rnosto f i en t o t ho f o r chead and i n topostauricular regions. f lair loss is notcommon but does occur cspecially inseve re e ry th rode rm ic and pus tu la rpso r i as i s . I t i s usua l l y t r ans i cn I asresulting fiom increased shedding ofte logen hai rs . l f there are no psor iat icl es ions e l sewhere , i t may be ve rydiff icult to distinguish psoriasis fromseborrhoeic dennatitis. Taking a biopsydoes not help.

Treatmenfl n a pa t i en t w i t h ex tens i ve pso r i as i sinvolv ing several other than scalpregions systemic treatment with well-established modalit ies. i.e. methotre-xate, cyclosporine, acitretin, leads toclearance of the scalp lesions as well.

Local treatment includes usage ofmed ica ted shampoos con ta in ing ta r .salicylic acid, corlicosteroids in lotionsor gels and Vit. D analogr-res.

Firstly, the excess of scales has tobe removed. Salicylic acid 5 to l0%exerts a good keratolytic eff'ect. lt isfonnulated in an ointrnent that can bewashed offeasily. Patients should applythe formulation overnight, preferablyunder a bathing or shower cap to en-hance the absorption of the medication.

Af ter the removal of the scalestopical corticosteroids in lotions, gels

or tbarns should be applied. The usuala p p l i c a t i o n s c h e d u l e c o n s i s t s o finterrnittent applications 3 to 4 timeswcekly. Vitamin D3 analogue calcipo-t r io l (DovonexO) has a substant ia lantipsoriatic efl 'ect. It is available in alotion fbrrnulation for the treatment ofthe scalp lesions. It has to be noted thatmaximum efficacy of calcipotriol lotionis reached after 8 weeks, whereas maxi-mal efticacy of a topical corticosteroidis reached afler 2 to 3 weeks treatment.Calcipotriol can be combined with atopical corticosteroid formulation, afterdescal ing, appears at the moment,optimal therapeutic approach for scalppsoriasis. D

Referencesl. Legendre R. Esola-Macre J. Itracouazole in

the trcatrnent ol tinea capitis. J An ,4cuclDernurto l 1990" 23:559-560.

2. Greer DL. Treatrnent of tinea capitis withitraconazole. J An ,lccrd Dermarol 1996.3 5 :63 7 -63 8 .

l. Gupta AK. Adam P. Dc Doncker P. ltraco-nazole pulse therapy tirr tinea capitis: A newtreatmcnt schcdule. Pecl ia l r i t Dernla lo l1998. l5:225-228.

4. Mercul ico MG. Si lvern, an RA. Elewski BE.Tinea capitis: Fluconazole in Trichophytontonsurans int tct ion. Pediutr ic Dermutol1998. 15:229-232.

5. Shuster S. The aetiology ofdandruffand themode ofact ion of therapeut ic agents. B/ i /JDennutol 198,+. I I l :235-242.

6. Van de Kerkhof PC, Franssen ME. Psoriasisof the scalp. Diagnosis and managcment.Am J ( ; l i n Demn to l 2001 , 2 :159 -165 .

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Figures l-4: Various clinical presentations of tinea

Figure 1: Mildly inflamed, loss ofhair, follicular accentuation.

Infection caused by Trichophytonspecies.

Figure 3: Numerous more inflamedlesions caused by Microsporum

canis.

Figure 6: Seborrhoeic dermatitis.Severe involvement, pyogenic

superinfection.

Figure 2: Small patch of alopeciawith scaling caused by

Microsporum canis.

Figure 4: Kerion (Microsporumcanis)

Figure 7: Psoriasis. Clearly definedinfiltrated patches with white

scales.

Figure 5: Seborrhoeic dermatitis.Small. fine scales. no infiltration.

Figure 8: Psoriasis. Lesions extendbeyond the hair line.

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