Fisher’s 6 C O N TA C T D E R M AT I T I S Fisher’s 6 C O N TA C T D E R M AT I T I S Robert L. Rietschel, MD Joseph F. Fowler, Jr, MD Professor of Clinical Medicine Clinical Professor of Dermatology University of Arizona College of Medicine Director of Occupational Dermatology Chief, Dermatology Service University of Louisville School of Medicine Southern Arizona VA Health Care System Louisville, Kentucky Tucson, Arizona 2008 BC Decker Inc Hamilton BC Decker Inc P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7 Tel: 905-522-7017; 800-568-7281 Fax: 905-522-7839; 888-311-4987 E-mail: [email protected] www.bcdecker.com ISBN 1-55009-378-9 © 2008 BC Decker Inc Printed in India by Ajanta Offset & Packaging Ltd. Production Editor: Margaret Holmes All rights reserved. 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Box 878 Fax: +61 (2) 9900 1980 E-mail: [email protected] Kimberton, PA 19442 Email: [email protected] Tel: 610-827-1640 Fax: 610-827-1671 Customer Service New Zealand E-mail: [email protected] Tel (Free): +64 (0) 800 449 312 Fax (Free): +64 (0) 800 449 318 Japan Email: [email protected] United Publishers Services Limited 1-32-5 Higashi-Shinagawa Shinagawa-Ku, Tokyo 140-0002 Tel: 03 5479 7251 Fax: 03 5479 7307 Notice: The authors and publisher have made every effort to ensure that the patient care recommended herein, including choice of drugs and drug dosages, is in accord with the accepted standard and practice at the time of publication. However, since research and regulation constantly change clinical standards, the reader is urged to check the product information sheet included in the package of each drug, which includes recommended doses, warnings, and contraindications. This is particularly important with new or infrequently used drugs. Any treatment regimen, particularly one involving medication, involves inherent risk that must be weighed on a case-by-case basis against the benefits anticipated. The reader is cautioned that the purpose of this book is to inform and enlighten; the information contained herein is not intended as, and should not be employed as, a substitute for individual diagnosis and treatment. To Alex and his inspiration, Lillian. You are both missed. Alex, your wit and wisdom live on in the work you created. To Connie, Eric, and Penny, a wonderful supportive family. To Lynn, for all her love, friendship and support. CONTENTS Preface 1. Pathogenesis of Allergic Contact Hypersensitivity 1 2. Practical Aspects of Patch Testing 11 3. Predictive Testing for Human Contact Dermatitis 30 4. Histology of Contact Dermatitis 35 5. Role of Age, Sex, Color of Skin, and Atopic Status 38 6. Regional Contact Dermatitis 66 7. Noneczematous Contact Dermatitis 88 8. Systemic Contact-Type Dermatitis 110 9. Medications and Medical Devices, and Implications for the Medical Community 125 10. Medications from Plants 175 11. Antiseptics and Disinfectants 190 12. Topical Antimicrobials 210 13. Antihistamines 230 14. Local Anesthetics and Topical Analgesics 239 15. Topical Corticosteroids 254 16. Preservatives and Vehicles in Cosmetics and Toiletries 266 17. Hand Dermatitis Due to Contactants: Special Considerations 319 18. Textiles and Shoes 339 19. Medical Devices, Implants, and Equipment 370 20. Fragrance Allergy 393 21. Allergic Sensitization to Plants 405 22. Photocontact Dermatitis 454 23. Paresthesia Due to Contactants 470 24. Occupational Dermatitis 484 25. Cutting Oils, Solvents, Petrolatum, and Coal-Tar Products 520 26. Gases and Propellants 534 27. Plastics, Adhesives, and Synthetic Resins 542 28. Food Additives and Dyes 566 29. Rubber 581 30. Gums, Rosin, and Natural Resins 605 31. Contact Urticaria 615 32. Metals 641 33. Contact Stomatitis and Cheilitis 700 34. Treatment of Contact Dermatitis 722 35. Specific Instructions for Patients with Common Contact Allergens 731 Appendix 743 Subject Index 809 PREFACE T his is the first revision of Alexander Fisher’s book that the original author will not see. We mourn Dr. Fisher’s passing and in this sixth edition we hope to honor his memory. When we took over this task with the production of the fourth edition, Dr. Fisher remarked that we had taken a classic and turned it into a masterpiece. While his very kind words might have been something of an overstatement, his description of this book as a classic remains appropriate and we have endeavored to maintain that tradition. Much of the history of contact dermatitis remains in these pages, and we have changed Dr. Fisher’s original wording as little as possible. The organization of the book has been slightly modified in this edition. We have removed the Aquatic Dermatoses chapter (since it was less an account of contact dermatitis than a reflection of one of Dr. Fisher’s personal interests), and some chapters have been combined in an effort to eliminate redundancy. A substantial amount of new information has been added and is to be found in the body of the text rather than in tables. The "boxes" that were part of the first five editions have been replaced by executive summaries to the chapters, since we felt that the boxes were redundant to the text and not as complete. In addition, a mini-atlas has been added to highlight some of the principles noted in various chapters. It is inevitable that a computer search will turn up items that we have failed to include. However, a computer search will not provide the context that this classic attempts to provide. Most of what is "out there" has found a place "in here." We hope you will find this edition a useful alternative to spending valuable hours at your computer in search of relevant information on contact dermatitis. Robert L. Rietschel, MD Joseph F. Fowler, Jr, MD GLOSSARY OF COMMONLY USED ABBREVIATIONS ACD allergic contact dermatitis acet acetone alc alcohol aq aqueous as is undiluted BP balsam of Peru (now called Myroxylon pereirae) chlor chloroform co castor oil eth ethanol FDA Food and Drug Administration ICD irritant contact dermatitis ICU immunologic contact urticaria MP Myroxylon pereirae pdr powder NACDG North American Contact Dermatitis Group oo olive oil pet petrolatum PPDA paraphenylediamine RAST radioallergosorbent test sat saturated ROAT repeated open application test C 1 HAPTER P A ATHOGENESIS OF LLERGIC C H ONTACT YPERSENSITIVITY EXECUTIVE SUMMARY Allergic contact dermatitis is a T cell-driven process that begins when haptens come into contact with Langerhans cells in the epidermis. When properly stimulated, Langerhans cells migrate to regional lymph nodes. Here, antigen is processed by T lymphocytes, which become specifically reactive to the presented allergen. The T cells that respond when the individual is re-exposed to the allergen are now known as CD8+T cells and are under the control of subsets of CD4+ T cells. A role has also been proposed for B cell participation in allergic contact dermatitis, and an animal model devoid of T and B cells has been found to demonstrate allergic contact dermatitis using natural killer cells. Neurologic factors have also been found toplay animportantroleinallergiccontact dermatitis. Destroying the nerve fibers to draining lymph nodes can abolish the reaction. Neuropeptides Substance P, neurokinin A, and calcitonin gene-related peptide and their receptors all play regulatory roles. T regulatory cells play a critical role in downregulating the contact sensitivity reaction. IL-10 production by these cells is one of the mechanisms.Acell-to-cell,contact-dependent,cytokine-independentmechanismisalsofound.Skinmemoryof contactdermatitismaybeduetoachemokine (CCL27) thatcausesretention ofaspecifictypeofTcellinthe skin site where the allergen was encountered. Jadassohn,1 who described contact allergy to mercury in againstforeignantigens,likethosederivedfrombacteria, 1895,canbeconsideredthe‘‘father’’ofcontactdermatitis. fungi, viruses, and foreign tissues, and against autolo- Prior to this time, and indeed for some years thereafter, gous tumor antigens and other undesirable autologous contact hypersensitivity was essentially unknown except antigens. However, although cell-mediated hypersensi- byafewworkersindermatology.2–5In1927,Landsteiner6 tivity to these antigens in general helps to preserve the published studies regarding antigens containing ‘‘simple body’sintegrity,allergic-contacthypersensitivitytosmall chemical compounds.’’ Sulzberger,7 in 1929, published molecular allergens (which, in fact, is hypersensitivity to one of the earliest American works onthe subject. autologousproteinsmade‘‘foreign’’ bycomplexingwith Anotherimportantdevelopmentwastherecognitionthat smallmolecularcompounds)isdamagingtotheskin.In a close similarity existed between contact allergy and a sense, therefore, contact allergy can be considered a delayed-type hypersensitivity to microbial antigens, after deviant form of cell-mediated hypersensitivity. Landsteiner and Chase published their findings that both contactallergytosmallmolecularallergensanddelayed-type hypersensitivity to microbial antigens could be passively Overview transferredwithlymphocytesinguineapigs.8,9Asamatter of fact, this finding precipitated an era in which many Contact allergens almost invariably are small-molecule investigators considered contact allergy and microbial substancesoflessthan500daltons(Da).12Becauseoftheir allergytobebasedonidenticalmechanisms.Despitemany small size, they penetrate the skin barrier, which is rela- importantfundamentalsimilarities,however,certaindiffer- tively impermeable under normal circumstances to large enceswerealwaysevidentbetweentheseformsofallergy.10,11 molecules,andreachthelivinglayersoftheskin.Inorder Teleologically, one assumes that cell-mediated hyper- to induce contact allergy, these substances must be pre- sensitivity serves the purpose of defending the body sented by antigen-presenting cells, principally epidermal 1 2/Fisher’sContactDermatitis Langerhans cells (LCs), and other dendritic cells, to T instances,however,itisdifficulttopredictthesensitizing lymphocytesinanimmunologicallyeffective‘‘processed’’ capacityofasubstanceonthebasisofitschemicalstruc- form. The effector cells, which mediate allergic contact ture. In the past it has not been adequately emphasized hypersensitivity,aredescendantsoftheseTlymphocytes. that some of the most common contact allergens, like Inorder tointeract withantigenpresented bytheLCs nickel, chromates, and other metal salts, do not form in the course of both induction of hypersensitivity and covalentbondswithproteins;thefactthattheycancom- elicitation of a reaction, the T lymphocytes must possess bine in some form with components of LCs provides a surface receptors (‘‘idiotypes’’) that are complementary reasonable explanation for their allergenicity.13 Current to the physicochemical features of that antigen. Further- research suggests that a ‘‘successful’’ contact allergen more, the antigen-presenting cells must bear immune causesanincreaseinthesizeofLCsalongwithanincrease response–associated antigens for which the T lympho- of Ia (major histocompatibility complex) molecules on cytes possess receptors. The T lymphocytes must also be theLCsurfaces.Inaddition,theallergenmay induce LC activated by interleukin-1 (IL-1), which is released from migrationtolymphnodes.14Langerhanscellsmigrateout LCs and keratinocytes. oftheepidermisnotonlywhenexposedtoallergens,but Under ordinary conditions, exposure to contact aller- alsowhenexposedtotoxicconcentrationsofirritants.15 genssetsinmotiontwocompetingmechanisms,theone mediated by effector T lymphocytes and leading to a GENETIC FACTORS state of hypersensitivity that becomes clinically manifest asaneczematousskinreaction.Theotherismediatedby Susceptibilitytothedevelopmentofcontactsensitivityis suppressor cells and leads to relative or complete toler- geneticallycontrolled.Themodeofinheritanceinguinea ance of the allergen. The state of reactivity of the skin at pigs is autosomal and irregularly dominant.16 Different anyparticulartimeandsiteisprincipallytheresultofthe strains of guinea pigs can make an immune response to existing balance between the effector and the suppressor different contact allergens. For example, one strain cells present. responds to potassium dichromate and beryllium fluor- ide,butnottomercuricchloride,whereasanotherstrain makes a response to mercuric chloride but responds Contact Allergens poorly to potassium dichromate and beryllium fluor- ide.17 These differences apparently relate to different Normally, only small molecular compounds (<500 Da) hapten–amino acid linkages. can penetrate through the horny layer into the living Other studies have shown that ultraviolet-B (UVB) layersoftheepidermis. Yet,inordertoinduceandelicit exposure inhibits contact sensitivity in certain strains of contact allergy, an antigen with a molecular weight of at mice, but not in other genetically distinct strains.18,19 It least 5,000 Da is required. Antigenicity is accomplished has beenpostulatedthattumor necrosisfactor-a(TNF-a) by the conjugation of small molecules with autologous may be an important mediator ofthese effects.20 proteins present in the skin. Other requirements for Studies of the mode of inheritance in humans are still antigenicity are the appropriate number of antigenic inadequate,buttheverylimitedavailabledatasuggestthat determinants and the appropriate tertiary structural fea- herealsogeneticfactorscontrolsusceptibilitytosensitiza- tures in the resulting molecule. Activation of the innate tion toparticular allergens.21 A number ofEuropean stu- immune response is also part of this process. Sensitiza- dies have compared the frequency of human leucocyte tion is more easily induced when the skin barrier is antigens (HLA) antigens in patients with allergic contact compromised by dermatitis or ulceration. dermatitis (ACD), usually to nickel, with local con- It was originally thought that such conjugates were trols.22–24Severalstudieshavepurportedtoshowincreased formedwiththefibrousproteinsofprokeratins,keratins, occurrence of one or two HLA types in patients, but for procollagens and collagens, epidermal cell membranes, reasons that are obscure, no two studies have found the orsolubletissue,andserumproteins.Althougharolefor sameHLAantigentobeincreasedinastatisticallysignifi- theseconjugatescannotbedismissed,itnowappearsthat cantfashion.Amongtheantigensreportedtobeincreased conjugation takes place mainly with cell membrane pro- tosomedegreeareHLA-B7,-B21,-B12,-Bw22,-B35,-B40, teins in the course of ‘‘processing’’ by the antigen-pre- -DR4, and -DRw6. Because the expression of the HLA senting LCs. antigensystemisessentialforthedevelopmentofACD,it Linkage to the protein moiety is frequently covalent; istemptingtosearchforHLA-ACDassociations. for example, the epsilon-amino group of lysine and the Gene products of the TAP-1 and TAP-2 genes (trans- sulfhydryl groups of cystine and cysteine have been sug- porter associated with antigen processing) are involved gested as binding sites for certain allergens. In many in antigen processing. A Finnish study showed that