GROUP 8 (Section D)

Members:
Panyapian, Siraprapa
Patalinghug, Ellaine
Ramagalla, Bhuvan
Sala, Arjonel

CASE 8
A 22-year-old medical student presents to the
Dermatology clinic with an itchy rash on the trunk and
extrimities that started to appear 2 days after a camping
trip.

SALIENT FEATURES
Identifying Data:
22 years old
Medical student
Chief Complaint:
Itchy rash on trunk and
extrimities
History of Present Illness:
Rashes appeared 2 days
after a camping trip

Differential
Diagnosis Itchy rash
(trunk and
extrimities)

Duration (2
days after
exposure)

Measles

Urticaria

Allergic
Contact
Dermatitis

Final Diagnosis:

Allergic Contact
Dermatitis (ACD)

CONTACT DERMATITIS
The inflammation of the skin induced by chemicals
that directly damage the skin.
3 TYPES:
Irritant Contact Dermatitis
-erythema, mild edema and scaling of the skin caused
by (1) Chemical Irritants such as solvents, metalworking
fluids, latex, kerosene, etc. and (2) Physical Irritants
caused commonly by low humidity from air conditioning.

 Photocontact Dermatitis
also termed "photoaggravated", divided into two
categories: phototoxic and photoallergic. It is an
eczematous condition triggered by and interaction
between a substance that may or may not be harmful
(ex. sunscreen, fragrances, insecticides) on the skin and
ultraviolet light. The contact activates them.
It manifests itself only in regions where the sufferer
has been exposed to such rays.

Allergic contact dermatitis (ACD)

ACD accounts for approximately
20% of all contact dermatitis
ACD is a type IV, delayed or cellmediated immune reaction that is
elicited when the skin comes in
contact with a chemical to which
an individual has been previously
sensitized

Allergic contact dermatitis. Linear

streaks seen with ACD to poison ivy.

COMMON ALLERGENS:

Skin tattooing and black henna

Plants such as poison ivy and mango, which contain a highly
allergenic substance called urushiol (*related to the patient's case
since he/she went on a camping trip*)
Airborne substances, (from aromatherapy and spray insecticides)

Acute Contact Dermatitis

Key Features
ACD is a pruritic,
eczematous reaction
Acute ACD and many
cases of chronic ACD are
well demarcated and
located to the site of
contact with the allergen
Prototypic reactions are
ACD due to poison ivy
and nickel
This healthy adolescent developed an intensely
pruritic vesiculobullous allergic contact dermatitis
from hair dye.

 Classic picture of ACD is a

well-demarcated erythematous
vesicular and/or scaly patch or
plaque with well defined margins
corresponding to the area of
contact

Chronic allergic contact dermatitis

leading to hand dermatitis. This golfer
wore one leather glove and had positive
patch tests to potassium dichromate and a
piece of his glove.

 Because ICD and ACD

are not always
differentiable clinically,
patch testing is
required to help identify
an allergen or exclude
an allergy to a
suspected allergen.

Allergic contact dermatitis.

Chronic hand dermatitis due to ACD to
mercaptobenzothiazole found in
rubber gloves

EPIDEMIOLOGY
Affects the old and young, individuals of all races, and both sexes
Differences in genders usually based on exposure patterns, such as
nickel allergy being seen more frequently in women, presumably due
to greater exposure to jewelry
Occupations and avocations play an important role
Allergens differ from region to region, e.g. preservatives used in
personal care products can vary based on government legislation

OCCUPATIONAL CONTACT DERMATITIS

rashes resulting from exposure to allergens on the job.
Jobs with a higher risk of contact dermatitis:
Healthcare workers and pharmaceutical agency
employees
Metalworkers
Cosmetologists and hairdressers
Chefs and waiters
Cleaners
Gardeners and Agricultural workers

Plant dermatitis
Toxicodendron dermatitis (poison ivy) is most common form
of ACD and can be readily identified by its streak-like or
linear papulovesicular presentation
caused by urushiol, which is found in saps of this plant
family
Urushiol contained in mango skin,cashew nut oil, ginkgo
(female) leaves, Japanese lacquer, and Indian marking ink

Allergic contact dermatitis to poison ivy (toxicodendron radicans). Note

the linear lesions induced by contact with branches

Signs and Symptoms

Red rash or bumps (*manifested by the patient*)
Itching, which may be severe (*manifested by the
patient*)
Dry, cracked, scaly skin, if the condition is chronic
Blisters, draining fluid and crusting, if your reaction is
severe
Swelling, burning or tenderness
Lesions appear 24-96 hours of exposure to the allergen.
(*Rashes appeared on the patient 2 days/48 hours after
a camping trip*)

Severity of rash depends on:

Length of exposure
Strength of the substance that caused the reaction
The body's response to the allergen.

PATHOPHYSIOLOG
Y

DIAGNOSIS

Patch Testing
The mainstay of diagnosis of contact dermatitis.
Has a sensitivity and specificity between 70-80%.
The standard method involves the application of the
antigen to the skin at standardized concentrations.

Patch test technique

applied to upper or middle back areas (2.5 cm lateral to
midspinal reference point) free of dermatitis and hair
kept in place for 48 hours
read 30 minutes after removal of patches
second reading should be done 3 to 5 days after initial
application
Metals , topical antibiotics , topical orticosteroids, and PPD
can elicit positive reactions after 7 days
Nonstandardized patch tests tested at 1:10 to 1:100
dilutions

ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER,

MANAGEMENT

Treatment
Allergen identification to improve contact avoidance
Alternatives and substitutes to cosmetics should be offered
to patient to increase compliance
supportive care and relief of pruritus, cold compresses with
water or saline, Burrow solution , calamine, and colloidal
oatmeal baths might help acute oozing lesions
Excessive handwashing should be discouraged in hand
dermatitis, and nonirritating or sensitizing moisturizers must
be used after washing

Treatment
TOPICAL CORTICOSTEROIDS is first-line treatment for
ACD
For extensive(>20% BSA) and severe CD, systemic
corticosteroids might offer faster relief (12-24hr)
recommended dose is 0.5 to 1 mg/kg daily for 5 to 7 days,
and only if patient is comfortable at that time is dose
reduced by 50% for next 5 to 7 days

J Allergy Clin Immunol 2010;125:S138-49.

Corticosteroids
0.2-6%
Patients with worsening of previous dermatitis or initial
improvement followed by deterioration of dermatitis after
application of corticosteroids should be evaluated
Cross-reactivity between groups A and D2 and groups B
and D2 also has been reported
optimal patch test concentration not worked out for most
corticosteroids
30% of ACD to corticosteroids be missed if delayed 7-day
reading not done

Antibiotics and Antiseptics

Neomycin and nitrofurazone are potent sensitizers
Neomycin sulfate can cross-sensitize with gentamicin,
kanamycin, streptomycin, spectinomycin,
tobramycin,and paromomycin

Treatment
topical T-cell selective inhibitors
efficacy in ACD or ICD not been established
antibiotics should be used for secondary infections of ACD
or ICD
antihistamines have been used for relief of pruritus
associated with ACD, generally ineffective
diphenhydramine not be used in patients with ACD to
Caladryl and hydroxyzine hydrochloride in
ethylenediamine-sensitive patient
Other modes of therapy : UV light treatment and
immunomodulating agents, eg.MTX,AZA, and MMF

Prevention
Primary prevention
In high-risk industries and professions, preventive
surveillance programs are possible, especially for
apprentices or newly hired workers
Secondary prevention
Once diagnosis of ACD or ICD is established, emollients,
moisturizers, and/or barrier creams may be instituted

Prognosis
Individuals with allergic contact dermatitis may have
persistent or relapsing dermatitis, particularly if the
material(s) to which they are allergic is not identified or if
they continue to practice skin care that is no longer
appropriate.

GUIDE TO
DISCUSSION

1. What is the nature of the pathologic

process occurring in this patient's skin and
what is a likely etiology of this pathology?
Inflammation manifested in hypersensitivity reaction
Allergen incurred in the camp site
Toxicodendron
Bilobol

2. What is the primary leukocyte type

responsible for this lesion? What factors are
necessary for this cell type to cause this
pathology?

T lymphocytes are responsible for this lesion.

Haptens or haptenated self-proteins are recognized by innate
immune mechanisms in the skin, and this leads to the elaboration of
a number of proinflammatory mediators that activate effector T cells
back to the initial site of antigen encounter in the skin. The effector T
cells release proinflammatory cytokines, such as interferon-, and
promote the killing of haptenated cells, resulting in the development
of the classic inflammatory rash seen in allergic contact dermatitis.

3. What is the likely outcome of this

case?
RESOLUTION
clearance of injurious stimuli
clearance of mediators and inflammatory cells
replacement of injured cells
normal function

LEARNING OBJECTIVES

1. Compare and contrast acute vs chronic

inflammation with respect to causes, nature of
the inflammatory response and tissue changes.
ACUTE INFLAMMATION

CHRONIC INFLAMMATION

Causes

Infections( bacterial, viral,

fungal or parasitic and microbial
toxins)
Foreign bodies (splinters, dirt,
sutures)
Tissue necrosis ( ischemia,
trauma, physical and chemical
`injury)
Immune reactions

Persitent infections
Immune mediated
inflammatory diseases
Prolonged exposure to toxic
agents(endogenenous or
exogenous)

Nature of
Inflammatory
Response

Immediate and early response

to tissue injury

Inflammation of prolonged
duration(weeks or months)
May follow acute inflammation

Tissue
Changes

Vasodilation
Increased vascular permeability
(leakage and edema)
Leukocyte emigration to
extravascular tissues

Angiogenesis
Mononuclear cell infiltrate
Fibrosis

2. What are the clinical settings in which different types of

inflammatory cells accumulate in tissues? Compare and
contrast the contents of neutrophil and eosinophil granules.
NEUTROPHIL GRANULES

EOSINOPHIL GRANULES

LOBES

3-5

STAIN

Weakly, Neutral

Red or Pink

Primary Granules (A
Granules)
contains lysosomal
enzymes

Large Rounded Vesicles

contain the enzymes
histaminase and
arylsufatase. These
enzymes break down
histamine and leukotrienes
an electron-dense,
proteinaceous crystal

GRANULES
Secondary (B Granules)
contains enzymes with
strong bactericidal action

The process of acute inflammation is initiated by

resident immune cells already present in the involved
tissue, mainly resident macrophages, dendritic cells,
histiocytes, Kupffer cells and mastocytes. At the onset of
an infection, burn, or other injuries, these cells undergo
activation, one of their pattern recognition receptors
(PRRs) recognize a pathogen-associated molecular
patterns (PAMP) and release inflammatory mediators
responsible for the clinical signs of inflammation.

3. Describe differences between the

various cell types in of their regenration
potential (i.e. Lanile, stable, permanent
cells). List examples of each cell type.

TISSUE

REGENERATION

EXAMPLE

Cells proliferate throughout

life
Able to replace cells that
are destroyed

Stratified squamous
epithelium of oral
cavity,skin,vagina,cervix
Lining mucosa of excretory
ducts of the body (salivary
glands,pancreas,biliary tract)
Columnar epithelium
(G.I. tract and uterus)
Transitional epithelium of
urinary tract
Cells of bone marrow and
hematopoietic tissues

Stable(quiescent)

Low level of replication

Can undergo rapid division
in response to stimuli
Capable of reconstituting
the tissue origin

Parenchymal cells of:

Liver,kidneys and pancreas
Mesenchymal cells:
Fibroblast and smooth
muscle cells
Vascular endothelial cells
Lymphocytes and leukocytes

Permanent
(non-dividing)

Cannot undergo mitotic

division in postnatal life

Neurons, skeletal and cardiac

muscles

Labile
(continuously
dividing)

4. What is the most important factor that

determines whether regeneration will
restore normal tissue architecture?
EXTRACELLULAR MATRIX
Tissue repair depends not only on growth factor activity
but also on interactions between cells and ECM components. The ECM
is a complex of several proteins that assembles into a network that
surrounds cells and constitutes a significant proportion of any tissue.
ECM sequesters water, providing turgor to soft tissues, and minerals,
giving rigidity to bone. It also regulates the proliferation, movement, and
differentiation of the cells living within it, by supplying a substrate for
cell adhesion and migration and serving as a reservoir for growth
factors. The ECM is constantly being remodeled; its synthesis and
degradation accompany morphogenesis, wound healing, chronic
fibrosis, and tumor invasion and metastasis.

One function of extracellular matrix is scaffolding for

tissue renewal. Because maintenance of normal tissue
structure requires a basement membrane or stromal
scaffold, the integrity of the basement membrane or the
stroma of parenchymal cells is critical for the organized
regeneration of tissues. Thus, although labile and stable
cells are capable of regeneration, disruption of the ECM
results in a failure of the tissues to regenerate and repair
by scar formation.

Thank You.