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Society of DermatologyPHYSICIAN ASSISTANTS

Supplement to the September 2008 issue

Selected presentations from theSociety of Dermatology Physician Assistants5th Annual Fall CME Conference

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[ S e p t e m b e r 2 0 0 8 • V o l u m e 1 • N u m b e r 3 ] S u p p l e m e n t t o 111

The Society of Dermatology PhysicianAssistants (SDPA) wasfounded in 1994 as the onlyprofessional organization torepresent physician assis-tants in the specialty of der-matology. Since that time,the Society membership hasgrown to more than 891Fellow status members, allof whom are employed byboard-certified or board-eligible dermatologists.

The primary mission of theSDPA is to provide continu-ing medical education (CME)that enhances the skills,knowledge, and function ofits members in the field ofdermatology. This mission isfundamentally accomplishedthrough outstanding CMEopportunities, such as theSDPA Fall CME Conference.This broad-based conferencecovers many common anduncommon dermatologic dis-eases that are not routinelyaddressed at similar events.It also attracts the finest andmost highly sought afterthought leaders as speakersand instructors.

The 2007 SDPA Fall CMEConference took place at theGaylord Opryland Resort inNashville, Tennessee. Morethan 400 dermatology physi-cian assistants enjoyed 28hours of CME, on topicsranging from the common

(contact dermatitis) to theuncommon (vasculitis). Thissupplement to the Journalof Clinical and AestheticDermatology highlightssome of the lectures deliv-ered in Nashville. We hopeyou enjoy reading this specialsupplement and appreciatethe relevance and quality ofCME that is provided annual-ly at our conference.

Additional information aboutthe SDPA and the annualconference can be found atwww.dermpa.org.

Terry Arnold, MA, PA-CChairmanSDPA CME Committee

I N T R O D U C T I O N

by Terry Arnold, MA, PA-C

CONTENTS2Therapeutic Update: Drug Actions, Reactions,and Interactionsby James Q. Del Rosso, DO, FAOCD6Unusual Cases of Hair andScalp Disordersby Andrew D. Lee, MD, andAmy J. McMichael, MD15Tips for Combining andTransitioning BiologicalTherapy for Psoriasisby James E. Turner, MD, PhD

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Fax: (610) 325-9906Copyright © 2008 Matrix Medical Communications. Allrights reserved. Opinions expressed by authors,contributors, and advertisers are their own and notnecessarily those of Matrix Medical Communications, theeditorial staff, or any member of the editorial advisoryboard. Matrix Medical Communications is notresponsible for accuracy of dosages given in the articlesprinted herein. The appearance of advertisements in thisjournal is not a warranty, endorsement, or approval ofthe products or services advertised or of theireffectiveness, quality, or safety. Matrix MedicalCommunications disclaims responsibility for any injuryto persons or property resulting from any ideas orproducts referred to in the articles or advertisements.

The articles publishedin this supplement arebased on selected pre-sentations from theSociety of DermatologyPhysician Assistants5th Annual Fall CMEConference, which washeld October 31 toNovember 3, 2007.

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[ S e p t e m b e r 2 0 0 8 • V o l u m e 1 • N u m b e r 3 ]S u p p l e m e n t t o222

The objective of this article is toprovide a state-of-the-artreview of current informationon the management of common der-matoses as well as to review somedrug reactions and interactions thatare important to recognize, as failureto do so often leads to significantadverse outcomes for the patient.

ORAL ANTIBIOTIC THERAPY FOR ACNE VULGARIS

Dermatologists have been prescrib-ing oral antibiotics such as tetracy-cline, doxycycline, and minocycline foracne vulgaris since the 1950s, 1960s,and 1970s, respectively, based on clinicalexperience and a scattered collection ofsmall clinical studies.1 However, extend-ed-release minocycline (Solodyn,Medicis, Scottsdale, Arizona) is the onlyoral antibiotic that is approved by theFood and Drug Administration (FDA)for the treatment of acne vulgaris basedon large-scale, Phase 3, pivotal trialsdemonstrating efficacy and safety.Importantly, the extended-release for-mulation of minocycline produces aslower time-to-peak plasma level(Cmax) and a reduction in total cumu-lative exposure to minocycline as com-pared to immediate-release minocy-cline formulations.2 Data from Phase 2and 3 trials substantiate therapeuticequivalence for acne vulgaris withextended-release minocycline whendosed at 1mg/kg/day, as compared tohigher daily doses (2mg/kg/day and3mg/kg/day), with a marked reductionof acute vestibular side effects such asdizziness.1,2 This is likely due to the factthat minocycline provides a more opti-mal partition-coefficient in terms oflipophilicity, which is believed to relate

to a greater ability to penetrate thesebaceous gland when compared toother tetracyclines.1

An enteric-coated tablet of doxycy-cline (Doryx, Warner Chilcott,Rockaway, New Jersey) appears to pro-vide reduced gastrointestinal (GI)upset as compared to immediate-release doxycycline formulations.However, enteric coating is not synony-mous with extended-release and servesonly to delay initial gastric dissolution inan attempt to reduce GI upset. Entericcoating may allow for once-daily admin-istration in some patients when using150 to 200mg of doxycycline daily. Withthe exception of anti-inflammatory-dose doxycycline administered oncedaily (doxycycline 40mg delayed-release capsule [Oracea, CollaGenexPharmaceuticals, Inc., Newtown,Pennsylvania]), all other formulationsof doxycycline produce antibiotic activ-ity. There is no scientific evidence thatpill splitting of any tablet formulation ofdoxycycline produces anti-inflammato-ry activity without an antibiotic effect.4

ORAL THERAPY FOR ROSACEAThe only FDA-approved oral therapy

for rosacea is anti-inflammatory-dosedoxycycline (Oracea). Administeredonce daily, this formulation has beenproven to be effective and safe for thetreatment of rosacea in pivotal Phase 3trials and in Phase 4 studies.5 Themechanism of anti-inflammatory-dosedoxycycline appears to relate, at leastpartially, to downregulation of the activ-ity of several matrix metalloproteaseenzymes (MMPs).6 Advantages ofanti-inflammatory-dose doxycyclineinclude efficacy; presence of long-term, nine-month safety data (includ-

ed in approved product labeling); andlack of antibiotic activity. The latterfactor is supported by the absence ofvaginal candidiasis in 180 female sub-jects who were actively treated in thepivotal Phase 3 studies, suggestinglack of antibiotic-selection pressureagainst normal vaginal flora.5

The lack of antibiotic effect of anti-inflammatory-dose doxycycline hasbeen confirmed based on multiplepharmacokinetic and longitudinalmicrobiologic studies completed overnine months with sequential culturesand antibiograms performed on oral,gastrointestinal, vaginal, and skin spec-imens. Unlike anti-inflammatory-dosedoxycycline, doxycycline 100mg dailyadministered over a two-week periodhas been shown to select for multipleresistant organisms within sevendays, with over 32.2 percent of organ-isms obtained on nasopharyngeal cul-tures demonstrating resistance todoxycycline (4μg/mL) as compared to2.2 percent at baseline.7 Doxycycline50mg once daily achieves serum lev-els that exceed the minimum inhibito-ry concentration (MIC) of severalbacteria for 2 to 4 hours.5

A controlled study of the combina-tion of metronidazole gel 1%(MetroGel 1%, Galderma Laboratories,Fort Worth, Texas) and anti-inflamma-tory-dose doxycycline (Oracea), bothonce daily, confirmed the augmentedtherapeutic benefit of the combinationregimen as compared to topical treat-ment alone in patients with inflamma-tory rosacea.8 After four weeks, thecombination regimen produced a sim-ilar reduction of inflammatory lesionsas metronidazole gel 1% achievedover 12 weeks.

T H E R A P E U T I C U P D A T E :D R U G A C T I O N S , R E A C T I O N S ,A N D I N T E R A C T I O N S

by James Q. DelRosso, DO, FAOCD

DISCLOSURE: Dr. Del Rosso is a consultant to, speaker for, and performs research for Allergan, Amgen, Coria, Galderma, Intendis, Medicis,OMP, Ortho Neutrogena, QLT, Ranbaxy, SkinMedica, Stiefel, Triax, Unilever, and Warner Chilcott.ADDRESS CORRESPONDENCE TO: James Q. Del Rosso, DO, FAOCD; e-mail: [email protected]

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A recent controlled study demon-strated that azelaic acid (AzA) gel15% once daily is therapeuticallyequivalent to twice-daily applicationin subjects with inflammatoryrosacea.9 Study endpoints includedquantitative, qualitative, and staticassessments including lesion-countevaluations and global assessments.Once-daily use of AzA gel 15% pro-duces greater convenience and animproved cost benefit.

TOPICAL RETINOID THERAPYFOR ACNE VULGARIS

Topical retinoids are a fundamen-tal component of acne therapy,exhibiting the ability to reduce bothnoninflammatory and inflammatorylesions through multiple modes ofaction (Figure 1).

Appropriate skin care is a vitalcomponent in the treatment of acnevulgaris. By improving epidermal bar-rier function, use of a gentle cleanserand moisturizer reduces the potentialfor skin irritation associated with top-ical medications and augments theability of medications to reduce acnelesions. A recent study evaluating theuse of tazarotene cream 0.1%(Tazorac, Allergan, Inc., Irvine,California) and a ceramide-basedmoisturizer cream (CeraVe, CoriaLaboratories, Fort Worth, Texas) insubjects with acne vulgaris demon-strated that initial application of themoisturizer did not interfere with theefficacy of tazarotene.10

Clinical trials of benzoyl peroxide(BPO)/clindamycin gel (Duac, StiefelLaboratories, Coral Gables, Florida)used in combination with eithertazarotene cream 0.1%, tretinoinmicrosphere gel 0.04% or 0.1%(Retin-A Micro, OrthoNeutrogena,Skillman, New Jersey), or adapalenegel 0.1% (Differin, GaldermaLaboratories, Fort Worth, Texas).11–13

In all three studies, the BPO/clin-damycin gel and the topical retinoid

were applied in the morning andevening, respectively. The combina-tion topical regimen of a retinoid usedalong with BPO/clindamycin from theoutset of therapy produced inflamma-tory and noninflammatory lesionreductions after 12 weeks of at least60 percent and 55 percent, respec-tively, with all three retinoids. In onetrial, the study group using bothBPO/clindamycin and tazarotenedemonstrated a marked reduction innoninflammatory lesions at Week 4(34%) and Week 8 (64%), suggestinga rapid augmentation of anticome-donal activity with this topical combi-nation.13 Tolerability results werehighly favorable in all three trials. Acase report series of BPO microspherecream (NeoBenz Micro, SkinMedica,Inc., Carlsbad, California) applied oncedaily in the morning used in combina-tion with tretinoin microsphere gel0.04% once daily at night also provedto exhibit effective results with noreports of skin irritation.14

TROLAMINE-CONTAININGTOPICAL EMULSION

Trolamine-containing topical emul-sion (Biafine, OrthoNeutrogena,Skillman, New Jersey) is an oil-in-water formulation that has been used

for more than three decades in bothEurope and the US. The mechanism ofaction of trolamine-containing topicalemulsion appears to be promotion ofan increase in the number ofmacrophages recruited to the injurysite, thereby decreasing the timeneeded for healing.15 Macrophagesserve to promote wound healing andserve a central role in directing thecourse and progression of the wound-healing process.16 Therapeutic applica-tions for trolamine-containing topicalemulsion include full-thicknesswounds, superficial wounds, includingthose that are postoperative, and der-mal ulcers; radiation dermatitis; minorabrasions; actinic keratosis treatmentsites after cryotherapy; and woundsthat require second-intention healingafter dermatologic surgery.15 The useof trolamine-containing topical emul-sion for the treatment of radiation der-matitis has made it possible to reduceoverall treatment time of chemothera-py and radiotherapy because themodalities could be administeredsimultaneously rather than sequential-ly. Additionally, trolamine-containingtopical emulsion differs from topicalneomycin and bacitracin because thelatter two agents are well-recognizedas common causes of contact allergy.


Figure 1. Topical retinoids: Mechanism of action and impact on pathophysiology



DRUG REACTIONS OF SIGNIFICANCE INDERMATOLOGY

A high index of suspicion is war-ranted when diagnosing significantcutaneous drug reactions. One canonly make the diagnosis if he or sheconsiders the possibility that a drug isthe underlying cause of a patient’scondition.

Drug hypersensitivity syndrome(DHS) is a potentially serious drugreaction characterized by fever,malaise, a diffuse exanthema-likecutaneous eruption, and systemicabnormalities, such as hepatitis,pneumonitis, and nephritis.17

Hepatitis is the most common sys-temic abnormality seen in associationwith DHS. Eosinophilia is commonlynoted. DHS occurs most often within2 to 6 weeks after initial exposure tothe inciting agents. Drugs associatedwith DHS include phenytoin, carba-mazepine, sulfonamides, and minocy-cline. The most important componentof treatment for DHS is discontinua-tion of the causative drug as early aspossible.

Drug-associated subacute cuta-neous lupus erythematosus (SCLE) isindistinguishable from idiopathic LE,occurring most often within 2 to 3months after starting therapy withthe inciting agent. Clinical presenta-

tions include confluent erythema, anannular eruption, or psoriasiformeruption in a photodistributed pat-tern.17 Serologic testing is typicallypositive for antinuclear antibody(ANA) and anti-Ro antibody (anti-SSA); however, antihistone antibodypositivity is not consistent. Affectedpatients may exhibit some systemicmorbidity, such as arthralgias andarthritis; however, significant renaldisease is rare. Drugs that have beenassociated with a SCLE-like eruptioninclude terbinafine and hydro-chlorothiazide. Upon discontinuationof the causative drug, the clinical fea-tures resolve usually within 4 to 8weeks; however, serologic tests mayremain positive for several months.

Pseudoporphyria cutanea tarda(pseudo-PCT) presents similar to PCT,except that there is absence of anincrease in urinary porphyrins on test-ing. The most common drug associatedwith development of pseudo-PCT isnaproxen.18 The agent most commonlyassociated with drug-induced linearIgA disease is vancomycin.19

DRUG INTERACTIONS OF SIGNIFICANCEIN DERMATOLOGY

The two most common mecha-nisms associated with potentially sig-nificant drug interactions are reduc-

tion in GI absorption and alteration ofhepatic metabolism.20 Examples ofdrug interactions related to reductionin GI absorption are:

• Metal ions such as calcium (infoods such as milk and yogurt),iron (in vitamin-mineral supple-ments), aluminum (in antacids),and/ or magnesium (in antacids)chelate tetracycline or quin-olones, such as ciprofloxacin,which reduces GI absorption ofthe antibiotics. Antibiotic treat-ment failure may occur.20

• Reduction in gastric acidity byantacids, H2-blocker antihista-mines, such as cimetidine(Tagamet, GlaxoSmithKline),rantidine (Zantac, GlaxoSmith-Kline), or famotidine (Pepcid,Johnson & Johnson, MerckConsumer Pharmaceuticals Co.,Fort Washington, Pennsylvania),or proton pump inhibitors, suchas omeprazole (Prilosec,AstraZeneca Pharmaceuticals,Wilmington, Delaware), reducesthe GI absorption of ketoconazole(Nizoral, McNeil ConsumerHealthcare, Fort Washington,Pennsylvania) or itraconazole(Sporanox capsules, JanssenPharmaceutica), leading poten-tially to antifungal treatment fail-ure.21 GI absorption of fluconazole(Diflucan, Pfizer, New York, NewYork) or terbinafine (Lamisil,Novartis Pharmaceuticals, EastHanover, New Jersey) are notdependent on gastric acidity.

Examples of drug interactions relat-ed to altered hepatic metabolism are:

• Inhibition of hepatic metabolismof carbamazepine (Tegretol,Novartis Pharmaceuticals) byerythromycin. Carbamazepinetoxicity commonly results.22

• Inhibition of hepatic metabolismof cholesterol-lowering agentssuch as atorvastatin (Lipitor,Pfizer, New York, New York)and simvastatin (Zocor, Merck,Whitehouse Station, New

˚

Figure 2. Significant interaction of several cholesterol-lowering agents with erythro-mycin, ketoconazole, or itraconazole


Jersey) by erythromycin, keto-conazole, or itraconazole maylead to rhabdomyolysis, a veryserious and potentially life-threatening adverse reaction(Figure 2).22

• Inhibition of the metabolism of 6-mercaptopurine, a metabolite ofazathioprine (Imuran, Glaxo-SmithKline), by allopurinol(Zyloprim, Prometheus Labora-tories Inc., San Diego, California).Serious hematologic reactionsmay result.23

Another interaction of majorimportance involves concomitant useof trimethoprim-sulfamethoxazoleand methotrexate. This interactionshould be completely avoided as seri-ous hematologic toxicity may result.23

REFERENCES1. Del Rosso JQ. Recently approved

systemic therapies for acne vulgarisand rosacea. Cutis. 2007;80(2):113–120.

2. Plott RT, Wortzman MS. Keybioavailability features of a newextended-release formulation ofminocycline hydrochloride tablets.Cutis. 2006;78(4S):6–10.

3. Fleischer AB, Dinehart S, Stough D,et al. Safety and efficacy of a newextended-release formulation ofminocycline. Cutis. 2006;78(4Suppl):21–31.

4. Del Rosso JQ. Scientific panel onantibiotic use in dermatology. Cutis.2008 (submitted for publication).

5. Del Rosso JQ, Webster GF, JacksonM, et al. Two randomized Phase IIIclinical trials evaluating anti-inflammatory-dose doxycycline (40-mg doxycycline, USP capsules)administered once daily fortreatment of rosacea. J Am AcadDermatol. 2007;56(5):791–802.

6. Webster G, Del Rosso JQ. Anti-inflammatory activity oftetracyclines. Dermatol Clin.

2007;25(2):185–193.7. Walker C, Webster GF, Del Rosso

JQ. Effect of doxycycline 100mgdaily on emergence of antibioticresistance. Poster presented at: FallClinical Dermatology Conference;October 2007; Las Vegas, NV.

8. Fowler JF. Combined effect of anti-inflammatory-dose doxycycline (40-mg doxycycline, USP monohydratecontrolled-release capsules) andmetronidazole topical gel 1% intreatment of rosacea. J DrugsDermatol. 2007;6(6):641–645.

9. Fleischer AB, Thiboutot D, DelRosso JQ. Comparison of azelaicacid gel 15% once daily versus twicedaily in the treatment of rosacea.Poster presented at: WorldCongress of Dermatology; October2007; Buenos Aires, Argentina.

10. Data on file. Allergan Inc.; Irvine,California; 2008.

11. Del Rosso JQ, Tanghetti E. Theclinical impact of vehicle technologyusing a patented formulation ofbenzoyl peroxide 5%/clindamycin1% gel: comparative assessments ofskin tolerability and evaluation ofcombination use with a topicalretinoid. J Drugs Dermatol.2006;5(2):160–164.

12. Del Rosso JQ. Study results ofbenzoyl peroxide 5%/clindamycin1% gel, adapalene 0.1% gel, and usein combination for acne vulgaris. JDrugs Dermatol. 2007;6(6):616–622.

13. Tanghetti E, Abramovits W,Solomon B, et al. Tazarotene versustazaraotene plus clindamycin/benzoyl peroxide in the treatmentof acne vulgaris: a multicenter,double-blind, randomized, parallelgroup trial. Poster presented at:63rd Annual Meeting of theAmerican Academy of Derm-atology; February 18–25, 2005;New Orleans, LA.

14. Bikowski JB, Del Rosso JQ. Results

of a case report series usingtretinoin microsphere cream aloneand in combination regimens foracne vulgaris. J Drugs Dermatol.2008 (accepted for publication).

15. Del Rosso JQ, Bikowski JB.Trolamine-containing topicalemulsion: clinical applications indermatology. Cutis. 2008 (acceptedfor publication).

16. Broughton G II, Janis JE, AttingerCE. The basic science of woundhealing. Plast Reconstr Surg.2006;117(Suppl 7):12S–34S.

17. Knowles SR, Shear NH. Cutaneousdrug reactions with systemicfeatures. In: Wolverton SE, ed.Comprehensive DermatologicDrug Therapy. 2nd ed.Philadelphia, Pa: Saunders-Elsevier;2007:977–983.

18. O’Donoghue NB, Higgins EM.Naproxen-induced pseudoporphyria.Clin Exp Dermatol. 2002;27(4):339–340.

19. Palmer RA, Ogg G, Allen J, et al.Vancomycin-induced linear IgAdisease with autoantibodies toBP180 and LAD 285. Br JDermatol. 2001;145(5):816–820.

20. Marchbanks C. Drug-drug inter-actions with fluoroquinolones.Pharmacotherapy. 1993;13:23–25.

21. Gupta AK, Katz HI, Shear NH. Druginteractions with itraconazole,fluconazole, and terbinafine andtheir management. J Am AcadDermatol. 1999;41:237–249.

22. Shapiro LE, Shear NH. Druginteractions. In: Wolverton SE, ed.Comprehensive DermatologicDrug Therapy. 2nd ed.Philadelphia, Pa: Saunders-Elsevier;2007:965–969.

23. Remlinger KA. Hematologic toxicityof drug therapy. In: Wolverton SE,ed. Comprehensive DermatologicDrug Therapy. 2nd ed.Philadelphia, Pa: Saunders-Elsevier;2007: 899–903.


Dr. Del Rosso is Clinical Associate Professor (Dermatology), University of Nevada School of Medicine andTouro University College of Osteopathic Medicine; Dermatology Residency Director, Valley Hospital MedicalCenter and Las Vegas Skin and Cancer Clinics, Las Vegas and Henderson, Nevada.



Evaluating and treating hair andscalp disorders is a challenging,yet important part of dermatol-ogy. A thoughtful, well-directed histo-ry and physical examination, with theoccasional laboratory test or scalpbiopsy, is necessary to assemble anappropriate differential diagnosis. Inaddition to accurately diagnosing andtreating a myriad of infectious, inflam-matory, autoimmune, neoplastic, andcongenital diseases, the clinician mustalso address the emotional and socialissues involved with scalp disordersand associated hair loss. This paperdescribes the clinical presentation, eti-ology, differential diagnosis, and treat-ment strategies for a number ofuncommon hair and scalp disorders.

Part of the challenge cliniciansface is due to the occasional atypicalpresentation of these disorders,resulting in a narrow differential andsometimes causing a missed diagno-sis; therefore, considering a broadnumber of clinical possibilities isimportant in preventing a delay indiagnosis and treatment. In this arti-cle, we present a series of interestingcases involving the hair and scalp,each followed by a discussion of clini-cal aspects and treatment options.

Case 1. A two-month-old African-American male infant presented withscaling and non-scarring hair loss inone area of his frontal scalp for sever-al months (Figure 1). Alopecia areatacan cause focal areas of non-scarringalopecia, but scaling is typicallyabsent. Non-inflammatory tinea capi-tis can result in nonerythematousfocal areas of hair loss with scaling.

Diagnosis: Noninflammatory tineacapitis.

Case 2. A 12-year-old African-American girl who covered her hairloss with ponytails for four monthspresented with a boggy, purulentplaque on her scalp, cervical andoccipital lymphadenopathy, and non-scarring hair loss (Figure 2).Dissecting cellulitis is characterizedby painful nodules, abscesses, andsinus tracts on the scalp. However,this disorder is most common inyoung African-American men andresults in scarring alopecia. Patientswith bacterial folliculitis can presentwith pustular, folliculocentric lesions.Allergic contact dermatitis, especiallyfrom personal care products, canresult in pruritic, erythematous,vesiculopustular lesions. Both ofthese inflammatory processes canresult in a localized telogeneffluvium. Finally, inflammatory tineacapitis can present with scaling,pustular lesions, and alopecia. Diagnosis: Kerion frominflammatory tinea capitis.

Case 3. A 17-year-old girl present-ed with scales coming off of her scalpfor more than one year without hairloss. She had no erythema of thescalp, no lymphadenopathy, and didnot feel her scalp was particularlyitchy. In her case, the diagnosis ofpsoriasis must be considered becauseof the sheer amount of scale seen,although seborrheic dermatitis canhave this same large, plate-like scale.Tinea amiantacea should be consid-ered because of the density of scale,but the lack of adherence of the scale

to the scalp is rarely seen in this enti-ty. Chronic contact dermatitis cancause scaling, but pruritus is usuallyprominent. The scaling from nonin-flammatory tinea capitis can be quitesignificant, even in the absence offollicular changes or alopecia. Diagnosis: Noninflammatory tineacapitis.

TINEA CAPITISTinea capitis is a dermatophytosis

of the scalp hair follicle. It is mostcommonly found among prepubes-cent children. In a recently completedstudy at Wake Forest University, theannual per capita visit frequency was1.6 percent for African Americansand 0.2 percent for Caucasians inpatients under 19 years of age seen inour dermatology department.1 Forchildren under nine years of age, theannual per capita visit frequency was2.9 percent for African Americansand 0.4 percent for Caucasians. Adultinfection is uncommon, but if seen, isusually found in African-Americanwomen.

The two main genera of dermato-phytes causing tinea capitis areTrichophyton and Microsporum. T. ton-surans is the most common pathogenfor tinea capitis in the United States.2

This dermatophyte is anthropophilicand has been found to be associatedwith low socioeconomic status andovercrowding. M. canis, a zoophilicdermatophyte, is the most commoncause of tinea capitis worldwide.3

The challenge facing clinicians inthe diagnosis of tinea capitis is com-pounded by its variety of clinical pre-

U N U S U A L C A S E S O F H A I R A N DS C A L P D I S O R D E R S

by Andrew D. Lee, MD, and Amy J. McMichael, MD

DISCLOSURE: Dr. Lee identified no conflicts of interest. Dr. McMichael is a speaker for and advisor to Johnson & Johnson; is a consultant to,speaker for, and receives honoraria from Procter & Gamble; is an advisor to, consultant for, speaker for, and receives honoraria from StiefelLaboratories, Inc.; and is a speaker for and receives honoraria from Galderma.ADDRESS CORRESPONDENCE TO: Amy J. McMichael, MD, Department of Dermatology, Wake Forest University School of Medicine, Winston-Salem, NC 27157; E-mail: [email protected]

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sentations. Inflammatory tinea capitis,commonly seen in infection byzoophilic dermatophytes, may mani-fest as scattered scalp pustules, largeabscesses, or a kerion—a boggy, puru-lent, painful mass developing froman exaggerated host response.Noninflammatory tinea capitis, typical-ly manifesting in patients with anthro-pophilic dermatophytosis, can presentas annular patches of alopecia withscaling as well as cervical and occipitallymphadenopathy. In fact, occipitallymphadenopathy, in combination withalopecia and scaling, is highly predic-tive of tinea capitis among children.4

Ectothrix infections cause cuticledestruction and increased hair break-age by arthroconidia on the surface ofthe hair shaft. Most Microsporumspecies cause ectothrix infections andfluoresce under Wood’s lamp examina-tion. Endothrix infections involvearthroconidia invasion within the haircortex, causing breakage at the surfaceof the scalp, leaving the patient with“black dot” alopecia. T. tonsurans is acommon cause of endothrix infections,does not produce much scaling orinflammation, and does not fluoresceunder Wood’s lamp.

Since the clinical manifestations oftinea capitis can be subtle, a fungal

culture should be performed whenev-er a dermatophyte infection is sus-pected.5 Alternatively, a potassiumhydroxide (KOH) prep with skinscrapings and hair can be performed,but this modality is much less reliablethan culture.

The current treatment of choice isgriseofulvin.6 The recommended doseis 20 to 25mg/kg/day of the microsizedformulation, taken with a fatty meal,for eight weeks. Treatment should becontinued for two weeks after clinicalresolution is seen. The most commonside effects are headache and gas-trointestinal discomfort, and, lesscommonly, elevation of liver enzymes.Alternatively, oral terbinafine 3 to6mg/kg/day for 3 to 4 weeks7 or oralitraconazole 5mg/kg/day for 2 to 4weeks8 may be used if no response togriseofulvin is observed. Adjuvanttreatment with topical antifungalshampoos, such as ketoconazole 2%and zinc pyrithione 1% is also recom-mended to avoid transmission ofinfection to others as well as todecrease the risk of a dermatophytecarrier state.9 Hats, brushes, andother hair accessories should be disin-fected or discarded, as they may actas fomites, providing a reservoir ofinfective agents. Finally, children with

tinea capitis may return to schoolonce treatment has been started.

Case 4. A 55-year-old African-American man presented with a one-year history of scalp ulcers, whichbecame worse after using topicalsteroids (Figure 3). Nonmelanomaskin cancer should be considered inolder individuals with persistent,poorly healing ulcers in sun-exposedareas. Bizarre ulcerations with angu-lar borders are seen in patients withneurotic excoriations; obsessive-com-pulsive behavior is common, but gen-eralized anxiety disorder or depres-sion may also be seen. Discoid lesionsof chronic cutaneous lupus erythe-matosus, when localized, commonlyappear on the head and neck and cancause scarring alopecia. Patients withpemphigus foliaceus develop flaccidbullae with scaly, crusted erosions,commonly in a seborrheic distribu-tion. While localized disease may bepersistent, these lesions are superfi-cial and do not heal with much scar-ring. A localized variant of cicatri-cial pemphigoid, common amongelderly men, involves the head andneck and manifests as tense, bul-lous lesions that ulcerate and causescarring and hair loss. A scalp biop-sy is a critical part of the diagnostic


Figure 1. A two-month-old African-American male infant withscaling and nonscarring hair loss in one area of his frontalscalp for several months

Figure 2. A 12-year-old African-American girl with a boggy,purulent plaque on her scalp, cervical and occipital lym-phadenopathy, and nonscarring hair loss



work-up in a patient presentingwith chronic scalp ulcerations.Diagnosis: Cicatricial pemphigoid.

CICATRICIAL PEMPHIGOIDCicatricial pemphigoid is a chronic,

autoimmune, blistering disease asso-ciated with autoantibodies directedprimarily against BPAG2 (collagenXVII) and epiligrin (laminin-5) foundwithin the basement membranezone.10 It predominantly affects themucous membranes, commonlyinvolving the mouth and eyes.Lesional skin heals with scarring,often leading to vision problems, air-way obstruction, and dysphagia. Theskin is involved approximately 25 to30 percent of the time, manifested bytense vesicobullous lesions that healwith scarring and milia. This is helpfulin differentiating cicatricial pem-phigoid from linear immunoglobulinA (IgA) bullous dermatosis and bul-lous pemphigoid, both of which donot tend to scar.11

The Brunsting-Perry variant oflocalized bullous pemphigoid is acutaneous form of cicatricial pem-phigoid involving the head and neckwithout mucosal involvement.12

Elderly male patients are typicallyaffected. These patients present withrecurrent vesiculobullous lesions onthe face, neck, and scalp that heal

with scarring and alopecia.Diagnosing cicatricial pemphigoid

requires a clinical presentation of ablistering process that heals with scar-ring; histology demonstrating a nonin-flammatory, subepidermal blisteringprocess; and direct immunofluores-cence on uninvolved, perilesional skinshowing deposits of immunoglobulin G(IgG), IgA, and/or C3 along the base-ment membrane zone.

Treatment depends upon theseverity and location of the disease.First-line treatment consists of topi-cal, intralesional, and systemic corti-costeroids.13 Dapsone, cyclosporine,azathioprine, mycophenolate mofetil,and cyclophosphamide may be usedfor recalcitrant or severe disease.Even if eyes are not visibly affected,an ophthalmologic examination at ini-tial diagnosis is suggested to note anysubclinical involvement.14 Despitetherapy, cicatricial pemphigoid is aprogressive disorder that typicallyresponds poorly to therapy. Whilesome patients enjoy long-term remis-sions, many experience intermittentexacerbations of this scarring, blister-ing process.

Case 5. A 13-year-old Caucasiangirl presented with localized, erythe-matous areas of crusting and hair lossafter a cheerleading competition towhich she wore a tight ponytail

(Figure 4). She demonstrated focalareas of nonscarring alopecia charac-terized by irregular, angular bordersand mild erythema. No scaling or fol-licular changes were observed, and ahair-pull test was negative. Tightponytails can result in traction alope-cia with symmetric hair loss typicallyinvolving the temples and postauricu-lar areas. Patients with alopecia area-ta present with patchy, nonscarringhair loss; exclamation-point hairs;and a positive hair-pull test withactive disease (a positive pull test isconfirmed by grasping 20 to 30 hairsfirmly between the forefinger andthumb and yielding 4 to 6 club hairsupon applying firm traction). Anotherconsideration, especially in the sexu-ally active individual, is secondarysyphilis, characterized by irregularlydistributed patches of alopecia with a“moth-eaten” appearance. Thebizarre pattern of hair loss observedin this patient, however, suggests anexogenous etiology.Diagnosis: Trichotillomania.

TRICHOTILLOMANIATrichotillomania is listed in the

Diagnostic and Statistical Manualof Mental Disorders (DSM-IV) as animpulse-control disorder manifestedby an urge to recurrently pull outone’s hair. Trichotillomania is associat-

Figure 3. A 55-year-old African-American man with a one-yearhistory of scalp ulcers, which became worse after using topi-cal steroids

Figure 4. A 13-year-old Caucasian girl with localized, erythe-matous areas of crusting and hair loss after a cheerleadingcompetition to which she wore a tight ponytail


ed with pleasure, gratification, orrelief, and results in hair loss thatcauses marked distress or impairmentin occupational or social situations.15

However, many patients whodemonstrate chronic hair pulling donot meet DSM-IV criteria, complicat-ing diagnosis. In fact, nonclinical hair-pulling behavior was present among15.3 percent of university studentswho responded to surveys, withoutthe associated-DSM-IV criteria ofnoticeable hair loss or sense of ten-sion prior to pulling behavior.16

The incidence of trichotillomaniahas been estimated to affect 0.6 to 3.4percent of the US population, with alifetime risk of up to 10 percent.17 Thisdisorder usually presents in prepuber-tal children, with a mean age of 11.3years and appears to be more com-mon among girls. This is in contrast tobenign hair-pulling behavior seen pre-dominantly in boys during infancy orearly childhood (age

disorders less likely. Loose anagenhair, common among blonde-hairedgirls, can be associated with wooly-appearing hair. These hairs may bepulled out easily, and a “rumpledsock” cuticle is observed on lightmicroscopy. Our patient had a nega-tive hair-pull test, suggesting abenign, congenital, hair-shaft defect,rather than a problem with the root.Diagnosis: Uncombable hairsyndrome.

UNCOMBABLE HAIR SYNDROMEUncombable hair syndrome, also

known as spun-glass hair, is character-ized by blonde, dry, shiny hair that isdifficult to comb into place.22 Hairbreakage frequently occurs, usually asa result of excessive manipulation ofthe hair rather than inherent hair-shaft fragility. The entire scalp is typi-cally involved, and eyebrows and eye-lashes are conspicuously spared. Thiscondition presents within the firstthree years of life, with boys and girlsequally affected. Both sporadic andinherited cases have been reported.

Examination of affected hair bylight microscopy may be normal.Electron microscopy demonstratescharacteristic longitudinal depres-sions along the shaft as well as trian-gular-shaped cross-sections known aspili trianguli et canaliculi. These

changes may also be observed intransverse sections of scalp biopsies.This syndrome may be caused by adefect in the configuration of theinner root sheath, which keratinizesbefore the hair shaft and ultimatelydetermines its shape.23

Treatment is limited to cosmeticmanagement. Patients who wear theirhair longer may achieve better man-ageability. Biotin 0.3mg three timesdaily has been reported to improvehair quality as well.24 Finally, somepatients experience spontaneousimprovement with age.

Case 7. A 58-year-old Caucasianman presented with persistent ulcerson his scalp and body that he has hadfor years (Figure 7). Persistentulcers and erosions may be seen inbullous pemphigoid, an autoimmune,subepidermal blistering disease.Chronic ulcers with undermined bor-ders are seen in patients with pyo-derma gangrenosum. These patientsusually have an underlying condition,such as inflammatory bowel disease,leukemia, or viral hepatitis. Rarelyare the head and neck involved.Nonmelanoma skin cancer typicallypresents as poorly healing, ulceratedlesions in photodistributed areas.Metastatic cancer may also presentas ulcerated lesions, usually in thesetting of systemic symptoms, such

as fever, night sweats, and uninten-tional weight loss. Finally, lym-phomas may affect the skin, either asa primary cutaneous process or sec-ondary to systemic disease.Diagnosis: Mycosis fungoides.

MYCOSIS FUNGOIDESMycosis fungoides is the most

common form of cutaneous T-celllymphoma. It is a slowly progressivecutaneous disorder of malignant CD4T-cells that typically affects the skin,but can progress internally overtime.25 Its etiology remains unknown,but viral infections as well as environ-mental and occupational exposuresare suspected to play a role in thisdisease.

Patients initially present with ery-thematous, scaly, mildly infiltratedpatches and plaques that may be gen-eralized or localized to one area beforespreading. In richly pigmented individ-uals, these lesions may be hypo- orhyperpigmented. Pruritus is common.When the scalp is involved, it is oftenaccompanied by hair loss.26 Wheninvolvement is advanced, lym-phadenopathy may be appreciated. Intumor-stage disease, large ulceratednodules appear on infiltrated plaques.Finally, there may be progression ofmycosis fungoides to an erythroder-mic state, with generalized exfoliation,

[ S e p t e m b e r 2 0 0 8 • V o l u m e 1 • N u m b e r 3 ]S u p p l e m e n t t o10 [ S e p t e m b e r 2 0 0 8 • V o l u m e 1 • N u m b e r 3 ]

Figure 7. A 58-year-old Caucasian man with persistent ulcerson his scalp and body that he has had for years

Figure 8. A 51-year-old Caucasian woman with a three-monthhistory of hair loss and a history of squamous cell carcinoma(SCC) in situ on the scalp


palmoplantar hyperkeratosis, and ony-chodystrophy. Visceral involvement inadvanced disease commonly affectsthe lungs, liver, and bone marrow.

The average age of onset is 50 yearsof age for patients with patch andplaque disease, while patients withtumor-stage disease, erythroderma, orSezary syndrome present over 60years of age. The incidence of mycosisfungoides is one in 300,000 per year. Itis more common among AfricanAmericans and occurs more frequent-ly in men than in women (2:1).27

Diagnosis is usually made by skinbiopsy.28 Histologic features suggestiveof mycosis fungoides include epider-motropism of atypical lymphocytes,sometimes with cerebriform nuclei,forming aggregates within the epider-mis (Pautrier microabscesses), and alichenoid infiltrate without interfacechange, a grenz zone, or papillaryedema. Immunohistochemistry revealslymphocytes that are CD4+, CD7-, andCD26-. Polymerase chain reaction stud-ies may demonstrate clonal T-cell recep-tor gene rearrangements.29

Treatment is based on the stage ofdisease as well as prior treatment his-tory.30 Early patch and plaque diseasemay be treated with topical corticos-teroids, retinoids, nitrogen mustard,carmustine (BCNU), and ultraviolet(UV) light therapy (either PUVA ornarrow band UVB). These may beused in combination for greater effi-cacy. Total skin electron beam radia-tion can be used for early diseaserefractory to topical treatment.31 Withmore severe or recalcitrant disease,systemic treatments, including oralbexarotene, conventional chemother-apy, and diphtheria-IL-2 fusion toxintreatment may be necessary.32

Case 8. A 51-year-old Caucasianwoman presented with a three-monthhistory of hair loss and a history ofsquamous cell carcinoma (SCC) insitu on the scalp that was treatedwith imiquimod (Aldara, GracewayPharmaceuticals, LLC, Bristol,Tennessee) (Figure 8).

This patient presented with focal,nonscarring alopecia, without scalingor erythema. Female patterned hairloss commonly affects the vertexscalp with sparing of the frontalscalp and is noninflammatory. Theacute onset of her hair loss makesthis cause less likely, although anacute process often unmasks andro-genetic alopecia. Alopecia areatamust be considered wheneverpatchy, nonscarring alopecia isobserved. Trichoteiromania, or com-pulsive hair rubbing, can result in africtional alopecia in a patient withfocal areas of hair loss as well asshortened, broken hairs.33 Since herlocalized hair loss began just weeksafter initiating imiquimod therapy tothe same area, a contact reactionseemed plausible. Within months ofterminating imiquimod therapy,hair regrowth was observed.Diagnosis: Localized telogeneffluvium.

TELOGEN EFFLUVIUMTelogen effluvium presents as

excessive shedding of normal hairs inthe setting of premature conversionof anagen to telogen hairs. This canbe caused by drugs, surgery, parturi-tion, severe illness, dieting, or localinflammation.34 In addition, iron defi-ciency, thyroid disease, and papu-losquamous disease can exacerbatethis condition.

Clinically, patients present withdiffuse nonscarring alopecia. A posi-tive pull test is highly suggestive oftelogen effluvium. Light microscopyof these hairs demonstrates visible,depigmented, club-shaped bulbswithout root sheaths. Histologically,transverse sections reveal >15 to 20percent of terminal follicles in telogenphase.35

Drug-induced telogen effluviumhas been reported with the use ofbeta-blockers, nonsteroidal anti-inflammatory drugs, anticonvulsants,anticoagulants, hormone replacementtherapy, retinoids, and lithium.36 In

addition, topical minoxidil oftenresults in mild telogen effluvium uponinitiation of therapy. Other topicalmedications that induce local irrita-tion or an allergic contact dermatitis,such as imiquimod, may produce sim-ilar effects.37

In most cases, no specific therapyis required, and patients will noticespontaneous resolution within a fewmonths, with regrowth of hair.Medications associated with telogeneffluvium should be avoided and awell-balanced diet should be encour-aged. Iron deficiency, thyroid dys-function, or papulosquamous scalpdisease should be addressed if identi-fied, especially if telogen hair loss isprolonged.

Case 9. A 31-year-old Caucasianman presented with scaly scalp andpruritus for five years. No hair losswas noted, although the patient didpresent with his head shaved for easeof examination and application ofmedication (Figure 9).

This patient presented with scaly,red-brown, folliculocentric papuleswithout alopecia. Chronic bacterial orpityrosporum folliculitis could presentin such a fashion as well as inflamma-tory tinea capitis. Scaling and pruritusare common features of seborrheicdermatitis and psoriasis and should beconsidered as well. The chronicnature of the scalp papules and pruri-tus in this patient is worrisome for fol-licular mucinosis, which is associatedwith cutaneous T-cell lymphoma,especially when observed in olderpatients. Very rarely, localized vari-ants of histiocytosis X present on thescalp and intertriginous areas withchronic, scaly, folliculocentric papulesthat sometimes ulcerate and scar.Diagnosis: Langerhans cellhistiocytosis.

LANGERHANS CELL HISTIOCYTOSISLangerhans cell histiocytosis, or

histiocytosis X, is a group of disorderscharacterized by an abnormal prolifer-ation of Langerhans cells. The disease




primarily affects children from 1 to 3years of age and is more common inboys than girls (2:1). The skin is mostcommonly affected (approximately50%), but involvement of bone, lymphnodes, lungs, liver, spleen, endocrineglands, and the nervous system canalso be seen.38 There are several over-lapping syndromes comprisingLangerhans cell histiocytosis, includ-ing Letterer-Siwe disease, Hand-Schuller-Christian disease, Hashimoto-Pritzker disease, and eosinophilicgranuloma. Letterer-Siwe disease,characterized by disseminated dis-ease, is associated with the worstprognosis (mortality rate >50%).39

Patients afflicted with other histiocy-toses in this group, characterized bylocalized, multifocal, and chronic dis-ease, tend to fair much better.

Patients with cutaneous involve-ment present with red-brown, fol-liculocentric papules that favor thescalp and intertriginous areas. Hairloss is common with scalp involve-ment. Noduloulcerative lesions mayalso be observed in these areas aswell as in the anogenital region.Histiologically, the dermis is filledwith a dense infiltrate of Langer-hans cells. Epidermotropism ofLangerhans cells, dermal edema,hemorrhage, and ulceration are com-mon. Immunohistochemically, the

Langerhans cells stain positively forS-100 and CD1a. Birbeck granules,which appear like tennis rackets, aredetected within these cells with elec-tron microscopy.

Treatment is not always necessary,especially for localized disease. Fordisease limited to the skin, topicalcorticosteroids, antibacterials, nitro-gen mustard, and PUVA therapy maybe effective.40 For multifocal or dis-seminated disease, chemotherapyagents and systemic corticosteroidsare typically used. Bone marrow orstem cell transplantation are reservedfor patients with a very poor progno-sis (

decision can be made regarding pro-phylactic surgical excision. Full-thickness excision is favored overlocal destruction, as superficial scar-ring can mask deep malignantchanges that may arise. Early removalmay be preferred due to cosmetic orsocial issues associated with larger,more conspicuous lesions.

SUMMARYEvaluation of hair and scalp disor-

ders can be very interesting and chal-lenging for the dermatologist. The cli-nician must rely upon a well-directedhistory and physical examination inorder to assemble an appropriate dif-ferential diagnosis. Laboratory testsare rarely necessary, but a well-per-formed scalp biopsy, with evaluationof vertical and transverse sections, isoften helpful in making a diagnosis.Finally, developing a comprehensivetherapeutic plan, providing patientswith thoughtful explanations regard-ing treatments and prognosis, anddemonstrating a compassionate atti-tude will result in appreciativepatients who will be left with a senseof caring and trust.

REFERENCES1. Tack A, Fleischer AB Jr, McMichael A,

Feldman SR. The epidemic of tineacapitis disproportionately affectsschool-aged African Americans.Pediatr Dermatol. 1999;16(1):75.

2. Suh DC, Friedlander SF, Raut M, etal. Tinea capitis in the United States:diagnosis, treatment, and costs. JAm Acad Dermatol. 2006;55(6):1111–1112.

3. Ginter-Hanselmayer G, Weger W, IlkitM, et al. Epidemiology of tinea capitisin Europe: current state and changingpatterns. Mycoses. 2007;50(Suppl2):2–6.

4. Hubbard TW. The predictive value ofsymptoms in diagnosing childhoodtinea capitis. Arch Pediatr AdolescMed. 1999;153(11):1150–1153.

5. Friedlander SF, Pickering B,Cunningham BB, et al. The use of

the cotton swab method indiagnosing tinea capitis. Pediatrics.1999;104:276–279.

6. Gupta AK, Cooper EA, Bowen JE.Meta-analysis: griseofulvin efficacy inthe treatment of tinea capitis. J DrugsDermatol. 2008;7(4):369–372.

7. Elewski BE, Caceres HW, DeLeon L,et al. Terbinafine hydrochloride oralgranules versus oral griseofulvinsuspension in children with tineacapitis: results of two randomized,investigator-blinded, multicenter,international, controlled trials. J AmAcad Dermatol. 2008;59(1):41–54.

8. Mohrenschlager, M, Schnopp C, FesqH, et al. Optimizing the therapeuticapproach in tinea capitis ofchildhood with itraconazole. Br JDermatol. 2000;143(5):1011–1015.

9. McGinley KJ, Leyden JJ. Antifungalactivity of dermatological shampoos.Arch Dermatol Res. 1982;272(3-4):339–342.

10. Fleming TE, Korman NJ. Cicatricialpemphigoid. J Am Acad Dermatol.2000;43(4):571–591.

11. Ahmed AR, Kurgis BS, Rogers III RS.Cicatricial pemphigoid. J Am AcadDermatol. 1991;24(6 Pt 1):987–1001.

12. Gibson V, Tschen JA, Bean SF.Localized cicatricial pemphigoid(Brunsting-Perry syndrome). Cutis.1986;38(4):252–253.

13. Sacher C, Hunzelmann N. Cicatricialpemphigoid (mucous membranepemphigoid): current and emergingtherapeutic approaches. Am J ClinDermatol. 2005;6(2):93–103.

14. Bruch-Gerharz D, Hertl M, Ruzicka T.Mucous membrane pemphigoid:clinical aspects, immunopathologicalfeatures and therapy. Eur JDermatol. 2007;17(3):191–200.

15. American Psychiatric Association.Diagnostic and Statistical Manualof Mental Disorders, FourhEdition. Washington, DC: AmericanPsychiatric Press, Inc.; 1994.

16. Stanley MA, Borden JW, Bell GE, etal. Nonclinical hair pulling:phenomenology and relatedpsychopathology. J Anxiety

Disord. 1994;8:119–130.17. Woods DW, Flessner CA, Franklin

ME, et al. The TrichotillomaniaImpact Project (TIP): exploringphenomenology, functional impair-ment, and treatment utilization. JClin Psychiatry. 2006;67(12):1877–1888.

18. Christenson G, Mackenzie T, MitchellJ. Characteristics of 60 adult chronichair pullers. Am J Psychiatry.1991;148:365–370.

19. Hautmann G, Hercogova J, Lotti T.Trichotillomania. J Am Acad Dermatol.2002;46(6):807–821.

20. Bloch MH, Landeros-Weisenberger A,Dombrowski P, et al. Systematic review:pharmacological and behavioral treat-ment for trichotillomania. BiolPsychiatry. 2007;62(8):839–846.

21. Walsh KH, McDougle CJ.Pharmacological strategies forTrichotillomania. Expert OpinPharmacother. 2005;6(6):975–984.

22. Jarell AD, Hall MA, Sperling LC.Uncombable hair syndrome. PediatrDermatol. 2007;24(4):436–438.

23. Mallon E, Dawber RP, De Berker D, etal. Cheveux incoiffables—diagnostic,clinical, and hair microscopic findingsand pathogenic studies. Br JDermatol. 1994;131(5):608–614.

24. Shelley WB, Shelley ED. Uncombablehair syndrome: observations onresponse to biotin and occurrence insiblings with ectodermal dysplasia. JAm Acad Dermatol. 1985;13(1):97–102.

25. Whittaker S. Biological insights intothe pathogenesis of cutaneous T-celllymphomas (CTCL). Semin Oncol.2006;33(1 Suppl 3):S3–S6.

26. Monopoli A, Annessi G, LombardoGA, et al. Purely follicular mycosisfungoides without mucinosis: reportof two cases with review of theliterature. J Am Acad Dermatol.2003;48(3):448–452.

27. Criscione VD, Weinstock MA.Incidence of cutaneous T-celllymphoma in the United States, 1973-2002. Arch Dermatol. 2007;143(7):854–859.




28. Fung MA, Murphy MJ, Hoss DM, et al.Practical evaluation and managementof cutaneous lymphoma. J Am AcadDermatol. 2002;46(3):325–357.

29. Juarez T, Isenhath SN, Polissar NL,et al. Analysis of T-cell receptor generearrangement for predicting clinicaloutcome in patients with cutaneousT-cell lymphoma: a comparison ofSouthern blot and polymerase chainreaction methods. Arch Dermatol.2005;141(9):1107–1113.

30. Horwitz SM, Olsen EA, Duvic M, et al.Review of the treatment of mycosisfungoides and Sezary syndrome: astage-based approach. J Natl ComprCanc Netw. 2008;6(4):436–442.

31. Jones GW, Kacinski BM, Wilson LD, etal. Total skin electron radiation in themanagement of mycosis fungoides:Consensus of the EuropeanOrganization for Research andTreatment of Cancer (EORTC)Cutaneous Lymphoma Project Group.J Am Acad Dermatol. 2002;47(3):364–370.

32. Duvic M. Systemic monotherapy

versus combination therapy forCTCL: rationale and future strategies.Oncology (Williston Park). 2007;21(2Suppl 1):33–40.

33. Banky J, Sheridan A, Dawber R.Weathering of hair in trichoteiromania.Austral J Dermatol. 2004;45:186–188.

34. Harrison S, Sinclair R. Telogeneffluvium. Clin Exp Dermatol.2002;27(5):389–395.

35. Eudy G, Solomon AR. Thehistopathology of noncicatricialalopecia. Semin Cutan Med Surg.2006;25(1):35–40.

36. Tosti A, Pazzaglia M. Drug reactionsaffecting hair: diagnosis. DermatolClin. 2007;25(2):223–231.

37. Tosti A, Piraccini BM, van Neste DJ.Telogen effluvium after allergiccontact dermatitis of the scalp. ArchDermatol. 2001;137(2):187–190.

38. Alston RD, Tatevossian RG,McNally RJ, et al. Incidence andsurvival of childhood Langerhanscell histiocytosis in NorthwestEngland. Pediatr Blood Cancer.2007;48(5):555–560.

39. Bingham EA, Bridges JM, Kelly AM, etal. Letterer-Siwe disease: a study ofthirteen cases over a 21-year period.Br J Dermatol. 1982;106(2):205-209.

40. Satter EK, High WA. Langerhanscell histiocytosis: a review of thecurrent recommendations of theHistiocyte Society. PediatrDermatol. 2008;25(3):291–295.

41. Nagarajan R, Neglia J, Ramsay N, etal. Successful treatment of refractoryLangerhans cell histiocytosis withunrelated cord blood transplantation.J Pediatr Hematol Oncol.2001;23(9):629–632.

42. Jaqueti G, Requena L, Sanchez YusE. Trichoblastoma is the mostcommon neoplasm developed innevus sebaceous of Jadassohn: aclinicopathologic study of a series of155 cases. Am J Dermatopathol.2000;22(2):108–118.

43. Cribier B, Scrivener Y, GrosshansE. Tumors arising in nevussebaceous: a study of 596 cases. JAm Acad Dermatol. 2000;42(2 Pt1):263–268.

[ S e p t e m b e r 2 0 0 8 • V o l u m e 1 • N u m b e r 3 ]

Drs. Lee and McMichael are from the Department of Dermatology, Wake Forest University School ofMedicine, Winston-Salem, North Carolina.



Psoriasis and psoriatic arthritisare dermatologic diseasesaffecting 3 to 5 percent of thepopulation, while a similar disorder,atopic dermatitis, is thought to affect15 to 20 percent of the population.1,2

Both diseases, as well as contact der-matitis and graft-versus-host disease(among others), are T-cell-mediatedskin disorders. The number of psoria-sis cases diagnosed is increasing at arate of about 250,000 per year, 25 per-cent of whom qualify for systemictreatments such as biologics.1,2 Keepin mind that many psoriasis patientsare not being treated at all. Psoriasisaffects every aspect of a patient’s life,including work and family relation-ships. It is disabling, debilitating, anda disease that deserves dermatology’sbest efforts. The best treatment plandepends on the individual patient andhis or her disease. All patients withpsoriasis should receive the mosteffective, safe, and affordable treat-ment options that work best for them.

PATHOGENESISThe pathogenesis of psoriasis is

believed to occur in three areas: thelymph node, along the endothelial lin-ing where T-cells extravasate into thetissues, and out in the psoriasislesions. Initial activation occurs in thelymph node, re-activation occurs atthe endothelial lining of blood vessels,then again out in psoriasis plaques.There are multiple points in the path-way where the process can be inter-rupted or blocked. The purpose ofimmunologic treatment of psoriasis iseither to engage the receptor at theantigen-presenting cell (APC) T-cellcomplex or to block key APC T-cell

interactions down-line, such as at thepoint of T-cell extravasation and/orout in the psoriasis plaque.Immunologic treatment may alsoblock lymphokines such as tumornecrosis factor-alpha (TNF-α), whichis thought to be responsible for ker-atinocyte proliferation, resulting inthe skin lesion we know as psoriasis.1-4

Two classes of biologics are nowapproved for the treatment of psoria-sis: T-cell receptor blockers and TNFblockers. The three types of TNFblockers are very effective for thetreatment of both psoriasis and psori-atic arthritis; whereas, T-cell receptorblockers are less effective for arthritisand therefore only approved for thetreatment of psoriasis.

For a clearer understanding of thepathogenesis of psoriasis and the pro-posed mechanism of action of the twoclasses of biologics, please refer toFigure 1. From this mechanism ofaction, one might propose that a T-cell-receptor biologic, such as efal-izumab or alefacept, which acts veryearly in the process, might have anadvantage over the TNF blockers,which appear to occur downstream inthe pathogenesis of psoriasis.

TNF-ALPHA BLOCKERSAdalimumab is a human, mono-

clonal antibody that is self-injectedsubcutaneously (SC). It specificallybinds TNF-α and inhibits TNF-α-mediated inflammation, cell infiltra-tion, and keratinocyte proliferation.Dosing begins with an 80-mg startingdose, which is reduced to 40mg everyother week.12

Etanercept is a human, soluble,receptor, fusion protein that is self-

injected SC at 50mg twice weeklywith the option of reducing that dosein three or six months to25mg/week.13 Etanercept specificallybinds TNF-α and inhibits TNF-α-mediated inflammation, cell infiltra-tion, and keratinocyte proliferation.Many insurance companies mandate adose reduction and, in some cases,when reduced, the disease showsregression or flares.

Infliximab is a chimeric, monoclon-al antibody to TNF-α that is adminis-tered intravenously every 6 to 8weeks during the maintenance periodand is dosed by weight.14 For exam-ple, a patient who weighs 250lb maybe dosed at 5mg/kg every six weeks.Slight changes in dosage and/or fre-quency of infusion may be requiredon a case-by-case basis if a patient’sdisease is not responding accordingto expectations. Infliximab specifical-ly binds TNF-α and inhibits TNF-α-mediated inflammation, cell infiltra-tion, and keratinocyte proliferation.

T-CELL RECEPTOR BLOCKERSAlefacept is a human fusion pro-

tein that is injected intramuscularly inthe office once a week for 12 weeks.11

Alefacept eliminates pathogenic T-cells by binding to natural killer cellsand blocks T-cell activation. Biologicblockage occurs at the APC T-cellinteraction in a similar mechanism asefalizumab. However, alefacept alsocauses apoptosis of T-cells; whereas,efalizumab does not. Patients receiv-ing alefacept are, therefore, moni-tored every other week for CD4counts as per the prescribing infor-mation (PI) label. For the 20 percentof patients in which this treatment

T I P S F O R C O M B I N I N G A N DT R A N S I T I O N I N G B I O L O G I C A LT H E R A P Y F O R P S O R I A S I S

by James E. Turner, MD, PhD

DISCLOSURE: Dr. Turner has no relevant conflicts of interest.ADDRESS CORRESPONDENCE TO: James E. Turner, MD, PhD, Mid-South Dermatology, 6570 Stage Road, Suite 140, Memphis, Tennessee 38134

15_20_SDPA_Turner.qxp 9/2/08 4:39 PM Page 15


works, it works very well. Thesepatients then have a holiday fromtreatment and may not need to beretreated for 3 to 4 months. Thisappears to be a distinct advantageover the other biologics, whichrequire continuous treatment inorder to maintain control over thedisease.11–14

Efalizumab is a monoclonalhumanized antibody that is self-injected SC every week and dosed byweight at 1-mg/kg body weight. Itblocks T-cell activation and reactiva-tion as well as T-cell binding and traf-ficking into dermis and epidermis.Because it is easy to use, patientadherence is very good. In terms ofmonitoring, platelet counts are doneevery three months after a patienthas been receiving the treatment forthree months. Clinical trials showedthat in only 0.3 of one percent of

cases, patients were taken off of efal-izumab because of thrombocytope-nia. With this small number ofpatients, efalizumab was stoppedand, with a short course of steroids,normal platelet counts were observedwithout apparent sequelae.1,3–5

SIDE EFFECTSWhen considering potential side

effects of biologics in the treatment ofpsoriasis, knowing how these medica-tions may affect the immune systemand other organs is crucial. BecauseTNFs are found in so many tissues,TNF blockers could be expected tohave greater potential for efficacy butalso greater side effects.12–14 Blockageof TNF could potentially lead to seri-ous infections, malignancies, or cen-tral nervous system (CNS) demyeli-nating disorders. A few cases of CNS-like disorders have also been report-

ed with the use of efalizumab, whichis now listed in the medication’s pack-age insert.5 Patients with pre-existingheart conditions may be at risk forcongestive heart failure, if placed on aTNF blocker. Since pancytopenia hasbeen reported, as well as tuberculosisand hepatitis B reactivation, appro-priate monitoring should be per-formed.12–14

T-cell receptor agents, such as ale-facept and efalizumab, are much nar-rower in their potential for causingside effects. The most serious poten-tial side effects of T-cell receptoragents may involve bone marrow,lymph nodes, and infections as well aspossible malignancies.3–5 Clinical trialsand post-marketing data have notshown signals for these types of sideeffects to date, however. Rare casesof thrombocytopenia and immune-mediated hemolytic anemia appear to

Figure 1. A comparison of the mechanisms of action of biologics



be the only side effects, not apparent-ly serious.3–5 Psoriasis worseningreported as minor or more seriousflares presents treatment challengesin a small number of patients.5

Efalizumab has the longest historyof efficacy and safety data, going backover 36 months. However, when apatient is given 40mg of adalimumabper week with an induction dose of80mg, this TNF drug appears to be asefficacious as infliximab. When com-paring the efficacy data at one year oftreatment, all TNF and T-cell biologicsshow roughly 50 percent of patientsachieving psoriasis area severity index(PASI) 75-percent improvement,therefore apparently not a great dealdifference in efficacy at the one-yearpoint. This may make it difficult to findthe best treatment for a particularpatient’s disease. It is important toclarify a patient’s treatment expecta-tions and where they expect to be at 6to 12 months when taking a particularbiologic. In my practice, roughly 70percent of patients do extremely wellon biologics. The remaining 30 percentmay be more of a challenge, requiringaugmentative therapy with other con-ventional and/or topical treatments. Asmall percentage may require transi-tioning to another biologic.

WORSENING EVENTSOne problem with the treatment of

psoriasis, particularly with efalizumab,is flares in a small number of patients.Rebound of disease is rarely a problemand occurs when a patient is taken offof a biologic, especially efalizumab, andis manageable if appropriately placedon another systemic treatment. Flarescan occur, even during the course oftreatment and can be managed withaugmentative therapy, such asmethotrexate, cyclosporine, narrow-band ultraviolet B light therapy, or oth-ers depending on the patient’s needs.6–9

TRANSITIONINGHaving the confidence to change

from one agent to another in thetreatment of psoriasis is important. Ifan agent, such as methotrexate orcyclosporine, shows optimal efficacywith no toxicity, it should be contin-ued. However, due to the potentialtoxicity of these drugs, especially ifused for a long period of time, wehave sought better agents, such asbiologics, with at least equal efficacyand safety profiles.

The main strategy in managingpsoriasis is continuing therapy. If thepatient shows a mild flare along theway, a short course of adjunctivetherapy, such as topical steroids, canbe implemented. Topical steroidsalone will usually not work for mod-erate-to-severe flares. In the case ofa major flare, therapy with a conven-tional systemic, such as methotrex-ate, cyclosporine, and/or narrow-band ultraviolet B light therapy,while maintaining the biologic dose,will usually bring the disease undercontrol and not necessitate transi-tioning to another biologic.6–9 If, how-ever, this course is not successful,then transitioning to another biolog-ic, usually in the other class, may bedone. In making this transition fromone biologic to another, augmenta-tive therapy with methotrexate orcyclosporine may be used for a 6- to12-week period of time to help makethe transition a success.

There are no explainable means bywhich one patient may react orrespond to one biologic and notrespond to another. One may be suc-cessful where another one fails, andone may work for a long time, thenfail. A psoriasis patient, without psori-atic arthritis, with a body surface areaof 40 percent, would be an appropri-ate candidate for efalizumab becauseof long-term efficacy, safety, and com-pliance studies on this biologic.1–4

When looking at the general popula-tion, 70 percent of patients who havepsoriasis do not have psoriatic arthri-tis. Therefore, it makes sense to start

this particular patient on a T-cell bio-logic. The patient with signs andsymptoms of arthritis would be bettercandidates for etanercept or adali-mumab. Infliximab, in my practice, isusually used when all else has failed.Phototherapy or isotretinoin may alsobe used with these patients, but usu-ally temporarily to augment the effec-tiveness of a biologic.

DIABETESIf a patient presents with psoriasis

and has diabetes with good control,efalizumab or alefacept would be anappropriate starting treatment. Then,if the patient does not respond downthe line, a TNF blocker could beintroduced. Conventional therapy oflight, methotrexate, cyclosporine, orisotretinoin may also be considered ifthe biologic fails.

HIV PATIENTSPsoriasis in patients with human

immunodeficiency virus (HIV) is diffi-cult to manage. In immunologicallycompromised patients of any kind,including those who have had anorgan transplant and are taking sup-pressive agents, psoriasis may be outof control. In HIV patients under goodcare with HIV medications and whohave low viral load and normal CD4counts, efalizumab is the drug ofchoice. There may be some concernabout the use of TNF blockers inthese patients because of the broadrange of suppression and the poten-tial for infection. An HIV patient whohas “bottomed out” should obviouslybe monitored very closely.

CARDIAC DISEASEIn general, a TNF blocker should not

be used in a patient with heart diseasebecause of the potential for congestiveheart failure.12–14 A patient with cardiacdisease and the potential for congestiveheart failure should be treated withconventional systemics and caution interms of using a TNF blocker.



MULTIPLE SCLEROSISA patient with multiple sclerosis

or another demyelinating diseasemust not be put on a TNF blockerbecause of the potential of diseaseworsening. Methotrexate, cyclo-

sporine, and/or narrowband ultravio-let B light therapy may be the besttreatment options for these patients.If a patient has a first-degree familyhistory of multiple sclerosis or otherdemyelinating diseases, the same

consideration should be made. If thepatient does not respond to thesetreatments, try using efalizumab withcaution (in a few recent cases, numb-ness and signs of neurological prob-lems were reported).5

CASE REPORTFigure 2 shows a 58-year-old Caucasian

male, weighing 290 pounds with a body massindex of 37.2. His comorbidities include obesity,hypertension, myocardial infarction, and asth-ma. He smokes one and a half packs of ciga-rettes per day. He presented with generalizedinvolvement of psoriasis including legs, back,arms, trunk, hands, and feet and a body surfacearea of about 16 percent. Upon presentation, hehad disease duration of eight years, eightmonths and no signs of arthritis. He receivedprior methotrexate therapy with inadequateresponse. He also received topical and systemicsteroids, but reported treatment failure.Efalizumab was the treatment of choice for himbecause of his comorbidities and the necessityfor weight-based dosing. He was started on thestandard 1-mg/kg weight-based dose. Figure 3shows the patient after three months of therapy.The patient also had severe hand and foot pso-riasis, which also responded well to efalizumab.Figure 4 shows that he was practically clearafter six months of therapy. After seven monthsof efalizumab treatment, the patient experienceddisease improvement on trunk, hands, and feetwith plaques responding well; slow, but definiteimprovement in pain and itching; and a bodysurface area of only four percent. At sevenmonths he still had flaking, guttate flare, andsymptoms on his legs, back, and arms. He hasreceived efalizumab therapy for more than oneyear now with continued disease control.

Figure 2. Basline photos of a 58-year-old male with generalizedinvolvement of psoriasis including legs, arms, trunk, hands, and feet

Figure 3. The same patient three months after treatment with efalizumab

Figure 4. The same patient six months after treatment with efalizumab



CANCERIn a psoriasis patient with a history

of cancer, involving the consultingphysician or oncologist in his or hertreatment before placing the patienton efalizumab or TNF blockers is rec-ommended. It is also necessary to beeducated on the patient’s cancer. Ifthe cancer occurred more than fiveyears ago, was not an aggressive car-cinoma, and did not involve lymphnodes, then a biologic may be appro-priate. In cases where biologics can-not be used, conventional systemicscan be used. In a patient with solidtumor or lymphoreticular diseasewith no recurrences, biologics may beused if the patient is monitored veryclosely.

HEPATITIS INFECTIONSIf a patient has had hepatitis B or

C, biologics may be used, but thepatient would need to be monitoredclosely with blood tests. There is noknown clinical data that suggests thatT-cell receptor biologics are con-traindicated in patients with hepatitisB or C. There is data against TNFinhibitors in chronic active hepatitisB, but not in hepatitis C. In my prac-tice, we are treating a patient withhepatitis C who has received biologicsand done well and is now on inflix-imab. She was previously treated withefalizumab and etanercept, separate-ly, with temporary success. No clini-cal trials on the use of biologics in thetreatment of psoriasis patients withhepatitis have been conducted.Conventional therapies, such asmethotrexate and isotretinoin shouldbe used with caution because of theirmetabolism through the liver.

PREGNANCYA pregnant woman should not be

treated with a biologic agent. If apatient becomes pregnant while on abiologic, the biologic should bestopped and the psoriasis treatedwith a safer topical agent. Many skin

diseases, including psoriasis andatopic dermatitis, improve with preg-nancy. Topical therapy along withnarrowband light phototherapy (notPUVA) if indicated may be the besttreatment option in pregnant womenwith psoriasis. Methotrexate and/orcyclosporine should certainly not beused.

PRE-PUBESCENTTNF blockers have been approved

for the treatment of some childhooddiseases, including juvenile rheuma-toid arthritis, pediatric Crohn’s dis-ease, and psoriasis. Efalizumab andalefacept are not approved to treatchildren, but have been used off label.Narrowband ultraviolet B light thera-py can be used in children underclose watch. In dire situations,methotrexate and cyclosporine havebeen used in pre-pubescent childrenwith success.

TUBERCULOSIS TESTINGIf a patient tests positive for tuber-

culosis (TB), an infectious diseasespecialist will need to ensure that thepatient receives proper treatment. Inpre-treatment screening, all patientsreceiving TNF blockers should havetesting at least once a year if they aregoing to be maintained on biologics.When using any immune modulator, itis probably wise to test for TB.

VACCINATIONSAlthough there are no rules and

regulations regarding vaccinationsand biologics, there are some strongsuggestions. With a non-live vaccine,if a biologic is not stopped for a 2- or3-week period, the patient may notdevelop a sufficient immune responseto the vaccine they are receiving.Thus, it is probably wise to stop thebiologic for a couple of weeks beforeand after the vaccine. In a normal sit-uation, psoriasis should not flare intwo or even four weeks.

When using a live vaccine, such as

MMR, polio, varicella, or smallpox,biologics should be stopped for 2 to 4weeks because they may put thepatient at risk for dissemination ofthe infection.

BRIDGING To initiate control of psoriasis,

one may place a patient oncyclosporine or methotrexate for 6to 8 weeks as a starter while waitingfor approval of a biologic, then taperthe patient off the conventional sys-temic while maintaining the biologic.

Etanercept at 50mg twice a weekprovides good control of psoriasis, butwhen the dose is reduced to onceweekly, approximately 40 percent ofpatients lose efficacy, particularly ifthey are obese. When this happens,augmentation or bridging can beaccomplished by placing the patienton methotrexate or cyclosporine—thedosage depending on the severity ofpsoriasis. If the patient does notrespond sufficiently with the augmen-tation, then consider bridging toanother biologic. Then, once the dis-ease is controlled, methotrexateand/or cyclosporine should be taperedslowly over a 10- to 12-week period,while maintaining the biologic towhich the patient was transitioned.8,9,15

Weight-based dosing. If apatient weighs 200lb or more, effica-cy scores decrease considerably if onetanercept.15 In this case, and/or ifthere is a lack of efficacy initially, onemay use methotrexate as an exampleto augment or bridge the transition oftreatment from etanercept to sayefalizumab. Once you determine thatpsoriasis is under control, slowlytaper methotrexate while maintain-ing the correct biologic, eventuallymaintaining monotherapy with thatbiologic.

HAND AND FOOTIn hand and foot psoriasis, efal-

izumab is the first line of therapybecause it has been shown to be more


effective than other biologics.16

Patients with severe hand and footpsoriasis may be put on eithermethotrexate or cyclosporine, with orwithout narrowband ultraviolet Blight therapy, then transitioned toefalizumab monotherapy.

CONCLUSION Older treatment paradigms in the

management of psoriasis start withtopical steroids, tar, and light. Whenthat fails, conventional systemic agentsmay be used. Efficacy, safety, compli-ance, and cost issues have dictated aneed to develop more cost- and safety-effective measures for the treatment ofthis dreadful disease. The developmentof biologics have enabled us to betterunderstand the pathogenesis of psoria-sis and, to a degree, find a better cost-effective way to treat this disorder.Conventional treatment regimens arestill used for selective patients and sit-uations where the use of biologics maynot be appropriate or adequate.

Choice of therapy depends on theindividual patient as well as on thedoctor and his or her comfort level andexperience with a specific therapy.Combination therapy certainlybecomes desirable with some patients.

REFERENCES1. Gottlieb AB, Gordon KB, Lebwohl

MG, et al. Extended efalizumabtherapy sustains efficacy withoutincreasing toxicity in patients withmoderate-to-severe chronic plaquepsoriasis. J Drugs Dermatol.2004;3:614–624.

2. Peters BP, et al. Pathophysiology andtreatment of psoriasis. Am J HealthSyst Pharm. 2003;57:645–659.

3. Gottlieb AB, Krueger JG, WittkowskiK, et al. Psoriasis as a model for T-cellmediated disease; immunobiologicand clinical effects of treatment withmultiple doses of efalizumab, an anti-CD11a antibody. Arch Dermatol.2002;138(5):591–600.

4. Lebwohl M, Tyring SK, HamiltonTK, et al. A novel targeted T-cellmodulator, efalizumab, for plaquepsoriasis. N Engl J Med. 2003;349(21):2004–2013.

5. Raptiva [package insert]. South SanFrancisco, CA: Genentech Inc; 2005.

6. Lebwohl M, Ellis C, Gottlieb A, et al.Cyclosporine consensus conference:with emphasis on the treatment ofpsoriasis. J Am Acad Dermatol.1998;39(3):464–475.

7. Roenigk HH Jr, Auerbach R, MaibachH, et al. Methotrexate in psoriasis:

consensus conference. J Am AcadDermatol. 1998;38(3):478–485.

8. A consensus report: cyclosporinetherapy for psoriasis. Br JDermatol. 1990;122:1–3.

9. Kuijpers AL, van de Kerkhof PC. Risk-benefit assessment of methotrexate inthe treatment of severe psoriasis. AmJ Clin Dermatol. 2000;1:27–39.

10. Leonardi CL, Papp KA, Gordon KB,et al. Extended efalizumab therapyimproves chronic plaque psoriasis:results from a randomized phase IIItrial. J Am Acad Dermatol.2005;52(3 Pt 1):425–433.

11. Alefacept [package insert]. Deerfield,IL: Astellas Pharma; 2006.

12. Adalimumab [package insert]. NorthChicago, IL: Abbott Laboratories;2007.

13. Etanercept [package insert].Thousand Oaks, CA: Amgen Wyeth;2004.

14. Infliximab [package insert]. Malvern,PA: Centocor, Inc.; 2006.

15. Data on file; South San Francisco,CA; Genentech, Inc.

16. Leonardi CL, et al. Poster 532presented at: 65th AmericanAcademy of Dermatology Meeting;February 2007; Washington, DC.

Dr. Turner is Clinical Professor of Dermatology at the University of Tennessee and in private practice,Midsouth Dermatology and Skin Cancer Center, Memphis, Tennessee.

S u p p l e m e n t t o [ S e p t e m b e r 2 0 0 8 • V o l u m e 1 • N u m b e r 3 ]20


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