The Practitioner June 2014-258 (1772)27-31

SPECIAL REPORT

Identifying the causes

of contact dermatitis
AUTHORS
Dr Ruth Jones
MRCP
ST3 Damatology

Dr Helen M. Horn
MD FRCP
Associate Specialist in
Dermatology

Department of
Dermatology, Royal
Infirmary of Edinburgh,
Edinburgh, UK

causes of contact diagnosis

be confirmed?
dermatitis?

CONTACT DERMATiTiS
RESULTS FROM SKIN
CONTACT WITH AN
EXOGENOUS SUBSTANCE.

It can be caused by direct skin contact,

airborne particles, vapours or light.
Individuals of any age can be affected.
The condition can lead to disability and
unemployment and is an important
occupational problem.

VARIANTS
The two most common variants are
irritant contact dermatitis (ICD) and
allergic contact dermatitis (ACD).
ICD is more common and has a worse

prognosis. Studies of unselected

populations suggest that the
prevalence of ACD is between
7 and 13%.
Other less common forms of contact
dermatitis include photocontact allergy
and, in food handlers, protein contact
dermatitis.^
Often multiple mechanisms are
involved. For example, an underlying
endogenous eczema or impaired skin
barrier predisposes to ICD which in turn
facilitates penetration of potential
allergens.

are the
management
options?
irritant contact dermatitis

ICD is a form of eczema and is induced

by direct inflammatory pathways
without prior sensitisation. Strong
irritants or caustic agents can cause
acute changes but more often ICD is
chronic and caused by repetitive
exposure to multiple weaker irritants.
These may be either wet, such as water,
soaps, detergents, solvents, weak acids
or alkalis, or dry, such as friction, low
humidity and heat or cold.
Ailergic contact dermatitis

Classical ACD is mediated by type 4

cell-mediated immunity. Sensitisation

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27

 T h e Practitioner June 2014-258 (1772)27-31

SPECIAL REPORT
CONTACT DERMATITIS
FIGURE 1 (LEFT)
Sensitisation phase
of allergic contact
dermatitis
FIGURE 2 (RIGHT)
Elicitation phase of
allergic contact
dermatitis

Hapten

Hapten
I

Allergen is
formed by
hapten-peptide
binding

/-i*r

T^^

Epidermal and
dermal dentritic
cells

Antigen complex is
transported to regional
lymph nodes by activated
dentritic cells

Hapten-specific
. , T cells form
(O) (O) and proliferate

occurs within 5 to 16 days of skin

contact with a potential allergen but at
this first exposure there is no
inflammation, see figure 1, above.
On re-exposure previously sensitised
T cells recognise the antigen and a
cascade of events occurs resulting in
inflammation 12 to 72 hours later, see
figure 2, above.
Metabolism of a substance may be
necessary to allow it to penetrate the
stratum corneum and further
metabolism may be required within the
epidermis before immunological
stimulation can occur. Mutations of
genes encoding enzymes and
cytokines involved in these processes
influence individual susceptibility to
ACD. Frequent exposure and high
concentrations of potential allergens
increase the risk of sensitisation.

Release of
inflammatory
mediators

Lymph node

Some sensitisers, such as sunscreen

ingredients may only become capable
of inducing ACD after they are exposed
to ultraviolet light. Most can also induce
classical ACD.
If eczema is recurrent/persistent, or
occurs in an individual with no previous
history of eczema, contact dermatitis
should be considered, see figure 3,
opposite. As in any eczema, contact
dermatitis is itchy. If acute there will be
erythema, oedema, vesicles, and
exudation. If the condition is chronic,
the skin will be iichenified with scaling
and fissures.
The distribution of an eruption may
provide valuable diagnostic clues.
Dorsal aspects of the hands are the site
most often affected by ICD, usually with
involvement of the finger webs as well,
see figure 4, opposite.

ACD caused by shampoo ingredients

typically involves the face and upper
trunk, usually sparing the scalp. Hair
dyes can elicit intense inflammation
resembling angioedema but scaling or
flaking during resolution indicates an
eczematous process.
An occupational factor should be
sought if eczema deteriorates during
the working week and improves at
weekends or during periods of leave.
Protein contact dermatitis

individuals suffering from protein

contact dermatitis develop vesicles
within minutes at sites of skin contact
with raw meat, fish, enzymes or plant
proteins. Improvement occurs within a
few hours but with repeated exposure
chronic eczema can evolve.
Inflammation is usually confined to

Common causes of allergic contact dermatitis

Allergen
Nickel
Fragrances
Biocides including methylisothiazolinone *

Rubber additives (thiurams,

mercaptobenzothiazole and carbamates)
Potassium dichromate
p-phenylenediamine
Plants (sesquiterpene lactones) *
Colophony *
Topical antibiotics and corticosteroids
Acrylates
Epoxy resins
Sunscreen ingredients $

Sources of exposure

Metal jewellery, buckles, studs on clothing, coins

Cosmetics, toiletries, wet wipes, room fresheners, fabric conditioners,
household products, scented candles, incense sticks, aromatherapy oils
Cosmetics, toiletries, wet wipes, fabric conditioners, household
products, pharmaceutical creams, industrial oils and cooling fluids,
water-based paints
Natural and synthetic rubber gloves and other rubber articles
Tanned leather, cement
Permanent and semi-permanent hair dyes
Compositae species, tulips and many others
Adhesive in fabric dressings, rosin, solder, pine trees
Pharmaceutical creams and ointments
Artificial nails
Adhesive systems
Sunscreens, cosmetics, toiletries

" Can also cause airborne contact dermatitis $ Can also cause photocontact allergy
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the hands and is often of such severity

that a change of occupation may be
necessary. The mechanism of protein
contact dermatitis is poorly understood.^

COMMON CULPRITS
Irritants

FGURE3
Allergic contact dermatitis caused by flavouring agents
in toothpastes

FIGURE 4
Sparing of the finger webs suggests that this chronic eczema
might not be ICD. Patch testing is required

FIGURE 5
Linear streaks indicate that this bullous eruption was caused
by plants

Cumulative effects of water, soaps and

detergents are the most common cause
of ICD which affects the hands more
often than any other site. Frequent hand
washing associated with the arrival of a
new baby is often responsible for new
onset hand eczema in a young mother.
ICD is common in occupations
involving frequent hand washing such
as hairdressing, healthcare, and
catering. Because of their impaired skin
barrier function atopic individuals
working in these occupations are at
especially high risk.

'If eczema is
recurrent,
persistent, or
occurs in a patient
with no previous
history of eczema,
contact demratitis
should be
considered*
Sweat and caustic substances
trapped next to the skin by waterproof
gloves or protective clothing can all
cause ICD. Incontinent patients are at
risk of developing ICD of the perineum.
Cosmetics often contain abrasive
particles capable of inducing ICD.
Airborne irritants include abrasive dusts,
especially dry cement, as well as caustic
vapours. Organic solvents, acids and
alkalis, low humidity, heat and cold are
also important causes of ICD.
Allergens

FIGURE 6
Stasis eczema. Patch testing is indicated

Nickei, fragrances, rubber accelerators

and biocides are the most common
sensitisers, see table 1, p28. Biocides are
added to products to prevent growth of
pathogens. Methylisothiazolinone, a
biocide, is responsible for a current
epidemic of ACD involving numerous
well known brands of cosmetics and
toiletries. Sensitised individuals entering
rooms freshly decorated with
water-based paints containing
methylisothiazolinone can develop

airborne ACD on exposed skin.

More common causes of airborne
ACD include fragrances in room
fresheners, scented candles or incense
sticks. Seasonal eczema on exposed
skin suggests allergy to plants, see
figure 5, below left. Acrylate vapours
released during application or sculpting
of artificial nails are an increasingly
common cause of airborne ACD
eczema in beauticians and their clients.
Patients with leg ulcers and stasis
eczema are at especially high risk of
developing allergies to ingredients of
their topical treatments, dressings and
bandages, see figure 6, below left.
It is important to remember that
topical antibiotics and corticosteroids
can cause ACD. SIGN guidelines
recommend that bandages and
compression hosiery should be latex
free to avoid inducing allergy to rubber
accelerators.^
Carers applying topical treatments to
individuals already sensitised to these
chemicals should wear accelerator-free
gloves. Wool alcohols (lanolin) and
parabens, once common sensitisers in
leg ulcer patients, have become
infrequent causes of ACD now that
they are seldom found in dressings and
bandages.
In the UK, sunscreen ingredients are
the most frequent cause of
photocontact allergy but in sunnier
latitudes allergy to topical NSAIDs in
sports gels is an increasingly common
problem. It can be difficult to
differentiate between photocontact
allergy, photosensitivity and airborne
ACD, see figure 7, p30. Involvement of
the posterior auricular areas suggests
that eczema at an exposed site is
caused by an airborne substance, not
light, see figure 8, p30.
If relevant allergens can be identified
there is a realistic prospect of cure.

INVESTIGATIONS
A careful history is important, enquiring
about exposure at work and at home,
hobbies, cosmetics and toiletries and
timing of the eruption.

'Age should not

be a deterrent
to patch testing*
If ACD is suspected the patient
should be referred to secondary care
for patch testing. Age should not be a
deterrent to patch testing. This involves
applying standardised concentrations
of suspected substances to the skin

29

. T h e Practitioner June 2014-258 (1772)27-31

SPECIAL REPORT
CONTACT DERMATITIS

FIGURE 7 (LEFT)
Exposed site
eczema,
Photosensitivity or
contact dermatitis?

FIGURE 8 (RIGHT)
Posterior auricular
involvement
suggests airborne
contact dermatitis,
in this case due to
an epoxy resin in a
floor-laying adhesive

under occlusion leaving them in place

for 48 hours, see figure 9, below.
Readings are taken on removal of the
patches and two days later. It takes
expertise to select allergens and to
interpret results.
Photopatch testing, use tests and
repeated open application tests may
also be appropriate for some patients.
FIGURE 9

Patch testing:
standardised
concentrations of
suspected culprits
are applied to
the skin under
occlusion and
left for 48 hours

MANAGEMENT
Accurate diagnosis, avoidance of
identified allergens and protection from
irritants are the key to successful
treatment, see table 2, below.
Patient information leaflets are
available from the British Association of
Dermatologists, see Useful information
box, p31. Formal hand dressings may be

necessary if hand eczema is severe.

Cotton gloves or dressings can be
covered by waterproof gloves during
unavoidable wet tasks. At home PVC
gloves are a safer choice than rubber or
nitrile as sensitisers in rubber can
penetrate cotton gloves or dressings.
In an occupational setting glove
choice will depend on the nature of the
chemicals involved.
Topical steroids of sufficient potency
should be prescribed as ointments not
creams. The latter are less emollient
than ointments and contain potentially
sensitising excipients usually not
present in the equivalent ointment.

Management of allergic contact

dermatitis
Identify and avoid the cause
Protect affected skin
Prescribe cotton gloves for hand
eczema
Use soap substitutes at home and
at work
Apply emollients frequently at home
and at work
Use topical steroid ointments (not
creams)
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key points
Dr Peter Saul
GP, Wrexham and Associate GP Dean for North Wales

Contact dermatitis results from skin contact with an

exogenous substance. It can be caused by direct contact,
airborne particles, vapours or light. Individuais otany age
can be affected. The two most common variants are irritant
contact dermatitis (ICD) and allergic contact dermatitis
(ACD). ICD is more common and has a worse prognosis.
Other less common forms of contact dermatitis include
photocontact allergy and, in food handlers, protein contact
dermatitis.
ICD is a form of eczema and is induced by direct
inflammatory pathways without prior sensitisation.
Classical ACD is mediated by type 4 cell-mediated
immunity. Sensitisation occurs within 5 to 16 days of skin
contact with a potential allergen but at this first exposure
there is no inflammation. Frequent exposure and high
concentrations of potential allergens increase the risk
of sensitisation.
If eczema is recurrent/persistent, or occurs in an
individual with no previous history of eczema, contact
dermatitis should be considered. Dorsal aspects of the
hands are most often affected by ICD, usually with
involvement of the finger webs. Cumulative effects of
water, soaps and detergents are the most common cause
of ICD which affects the hands more often than any
other site.

Ingredient lists of prescribed topical

treatments should be checked to
ensure that previously identified
allergens are not inadvertently supplied
to the patient.

'If contact
dermatitis
persists
a change of
occupation
maybe
necessary'
Patients with eczema that is in an
unusual distribution, recurrent or
persistent despite appropriate
management should be referred to
secondary care for investigation and
intensive treatment. Patch testing is
especially important for patients
suffering from chronic hand eczema,
facial or stasis eczema.
Treatments available in secondary
care include phototherapy, alitretinoin
for refractory hand eczema,''azathioprine
and ciclosporin. If contact dermatitis
persists a change of occupation may
be necessary.

Nickel, fragrances, rubber accelerators and biocides are

the most common sensitisers in ACD. Patients with leg
REFERENCES
1 Bourke J, Coulson I. Englisin J. Guidelines for the
ulcers and stasis eczema are at especially high risk
management of contact dermatitis: an update. BrJ
of developing allergies to ingredients of their topical
Dermato/2009;160(5):946-954
treatments, dressings and bandages. In the UK, sunscreen 2 Hjorth N, Roed-Petersen J. Occupational protein
ingredients are the most frequent cause of photocontact contact dermatitis in food handlers. Contact Dermatitis
1976;20):28-42
allergy but in sunnier latitudes allergy to topical NSAIDs
3 Scottish Intercollegiate Guidelines Network. SIGN 120.
Management of chronic venous teg ulcers. SIGN.
in sports gels is an increasingly common problem.
If ACD is suspected the patient should be referred to
secondary care for patch testing. Age should not be a
deterrent to patch testing. Accurate diagnosis, avoidance
of identified allergens and protection from irritants are
the key to successful treatment.
Topical steroids of sufficient potency should be
prescribed as ointments not creams. The latter are less
emollient than ointments and contain potentially
sensitising excipients usually not present in the equivalent
ointment. Patients with eczema that is in an unusual
distribution, recurrent or persistent despite appropriate
management should be referred to secondary care for
investigation and intensive treatment.

Edinburgh. 2010
4 Ruzicka T, Lynde CW, Jemec GBE et al. Efficacy and
safety of oral alitretinoin C9-cis retinoic acid) in patients
with severe chronic hand eczema refractory to topicai
corticosteroids: results of a randomized, doube-blind.
placebo-controlled, multicentre trial. BrJ Dermatoi
2008;158(4):808-817

Useful information
British Association of Dermatologists
Patient information leaflets on hand
dermatitis and contact dermatitis
www.bad.org.uk
National Eczema Society
www.eczema.org

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editor@thepractitioner.co.uk

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