Fisher's Contact Dermatitis, 6e

885 Pages·2007·30.29 MB·English

by  Robert L. Rietschel

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
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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