Diagnosis and mangement of

Skin allergy diseases

Fajar Waskito
 An overview

Allergic Contact Dermatitis

Drug Eruptions
Cutaneous Vasculitis
Immunodermatology and Viral Skin
Infection
Bacterial Infections
Parasitic Infections
Fungal Infections
Allergic Urticaria
Contact Dermatitis . . . 01
Contact dermatitis is one of the most prevalence dermatitis
Irritant and allergic contact dermatitis are the two major
variants
Different mechanisms, can be difficult to distinguish at the
clinical, histologic and even molecular levels.
Allergic contact dermatitis is biphasic, with an sensitization
phase and an elicitation phase.
Cutaneous antigen-presenting cells (Langerhans cells) play a role in
trafficking and presenting hapten-self complexes
to T lymphocytes.
CD8+ T lymphocytes are thought to be the major effector cells
CD4+ T lymphocytes may play a role as regulatory cells
Patch testing plays a critical role in the management
Irritant contact dermatitis is a nonimmunologic response to
chemicals that are damaging to the skin (surfactants,
solvents, hydrocarbons, strong acids/bases, and others).
Contact Dermatitis . . . 02
Eczema (Greek = boiling): Tiny vesicles
Dermatitis = inflammation of the skin
Dermatitis: acute-sub acute-chronic
Dermatitis: Exogenous, endogenous
 Allergic Contact Dermatitis . . . 01
3 phase mechanisms
Sensitization
Elicitations
Resolution
 Sensitization
Penetrated hapten into the skin
To form hapten-protein complexes
Allergen presentation on the surface LCs
(I, II)
Interaction LCs Naive T cell
Generation of 2 memory T cells:
MHC II class-restricted CD4+T cells
MHC I class-restricted CD8+ T cells
 Elicitation
occurs in sensitized individuals after additional skin
contact with the same antigen.
ACD develops within 24 hours or longer after antigen
exposure.
The elicitation response is caused by the
inflammatory effects of cytokines (TNF- and IL-1)
which are potent inducers of
Endothelial adhesion molecules (ICAM-1)
Selectins
Integrins
Leukocyte functional antigen-1 (LFA-1)
Very late antigen-4 (VLA-4)
 Resolution
Antigen exposure activates two opposing
pathways.
The first is mediated by effector T cells, leading
to a state of hypersensitivity manifested as an
eczematous skin reaction (i.e., ACD).
The other leads to production of suppressor T
cells, which mediate antigen tolerance.
Suppressor T cells have been shown to be CD4+
and CD25+
Allergic Contact Dermatitis . . . 01
Haptens, simple chemicals, small mol. weight
(500 dalton), electrophilic molecules that
bind to carrier proteins via covalent bonds to
form a complete antigen before they can
sensitize
Class I and II molecules on the surface of the
antigen-presenting cells (APC) act as the
binding site (carrier) for contact allergens
Allergic Contact Dermatitis . . . 02
Cause
The mechanism: delayed (type IV)
hypersensitivity
It has the following features:
The individual must be genetically susceptible
Previous contact is needed to induce allergy.
It is specific to one chemical and its close relatives.
After allergy has been established, all areas of skin
will react to the allergen
Sensitization persists indefinitely.
Desensitization is seldom possible.
 Allergic Contact Dermatitis . . . 03
Allergic contact dermatitis should be suspected if:
Certain areas are involved, e.g. the eyelids,
external auditory meati, hands or feet, and
around gravitational ulcers
There is known contact with the allergens
mentioned
The individuals work carries a high risk, e.g.
hairdressing, working in a flower shop, or
dentistry.
Allergic Contact Dermatitis . . . 04

Clinical feature
 Allergic Contact Dermatitis . . . 05
Treatment
Avoidance of the relevant allergen
Reducing exposure by active steps have to be taken to avoid the
allergen completely.
Job changes .
In ACD cause by Ni, Decreasing Nickel in the diet, avoid Ni release
from cans or steel saucepans may rarely be helpful.
Topical corticosteroids
suppress recruitment of polymorphonuclear leukocytes
reversing capillary permeability.
Topical tacrolimus (Protopic ointment 0.03% or 0.1%) and
pimecrolimus (Elidel cream)
Phototherapy
Systemic immunosuppressive agents
 Hapten-carrier complex is processed by Langerhans cells: (a & b)
After migrating to draining lymph nodes, Langerhans cells present the complex to CD4+
cells. (c)
Activated CD4+ cells then secrete cytokines, which induce expression of adhesion
molecules and MHC on keratinocytes and endothelial cells, as well as activation of
keratinocytes to secrete pro-inflammatory cytokines. (d)
Other T cells and pro-inflammatory cells then undergo chemotaxis to the site of cytokine
secretion.