THERAPY IN PRACTICE

Drugs Aging 2001; 18 (11): 827-835

1170-229X/01/0011-0827/$22.00/0
Adis International Limited. All rights reserved.

Diagnosis and Treatment of Allergic

Skin Disorders in the Elderly
Susan T. Nedorost and Seth R. Stevens
Department of Dermatology, Case Western Reserve University and University Hospitals of
Cleveland, Cleveland, Ohio, USA

Contents
Abstract
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1. Approach to the Management of the Elderly Patient with Pruritic Dermatitis
2. Allergic Eczematous Dermatitis: Contact Dermatitis . . . . . . . . . . . . . .
2.1 Cellular Basis of Allergic Contact Dermatitis . . . . . . . . . . . . . . . .
2.2 Prevalence of Allergic Contact Dermatitis in the Elderly . . . . . . . . .
2.3 Allergens Causing Contact Dermatitis in the Elderly . . . . . . . . . . . .
2.4 Patch Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.5 Photoallergens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3. Eczematous Dermatoses Not Due to Contact Allergy . . . . . . . . . . . . .
4. Management of Eczematous Dermatitis . . . . . . . . . . . . . . . . . . . . .
5. Allergic Noneczematous Dermatosis . . . . . . . . . . . . . . . . . . . . . . .
6. Investigating Rashes Due to Systemic Allergic Reactions . . . . . . . . . . . .
7. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

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Allergic skin disorders in the elderly may arise from contact with or ingestion
of offending allergens. Itching associated with skin allergy must be distinguished
from other causes of itching in the elderly such as xerosis, itching due to systemic
disease and bullous disease. Although elderly people have somewhat decreased
cell-mediated immunity and may be harder to sensitise under experimental conditions, they have had many years to acquire allergic responses, and therefore
develop contact dermatitis frequently.
Patch testing is a valuable tool to diagnose contact allergy and should be used
often in the elderly, particularly in patients at high risk of contact dermatitis, such
as those with chronic lower extremity dermatitis or ulcers due to venous stasis.
When prescribing topical medications to high risk patients, a knowledge of the
common sensitisers is important. In addition to allergy to medicaments and dressings used to treat stasis ulcers, contact allergy to dental prostheses and medications used to treat ocular disease are common in the elderly as a result of increased
usage and exposure.
Rash caused by ingested allergens is much more commonly due to medications
than to food in the elderly. Allergic noneczematous dermatoses in the elderly are
commonly drug-induced. Urticarial skin reactions are often associated with the
administration of antibacterials, nonsteroidal anti-inflammatory drugs (NSAIDs),
antidepressants or opioids. Morbilliform rashes are a common sign of systemic

828

Nedorost & Stevens

reaction to anticonvulsants, gold, allopurinol or diuretics. Phototoxic reactions

may be associated with the administration of tetracyclines, diuretics, NSAIDs
and antihyperglycaemic agents. Patient-specific variables such as HLA type and
concomitant medication may affect the likelihood of an allergic response to medication.
Many elderly patients take multiple medications, which can make diagnosis
of drug allergy difficult because diagnosis is most commonly accomplished by
observing clinical response once the medication is withdrawn. In the case of
lichenoid cutaneous reactions, clinical improvement may take several months
after withdrawal of the offending drug. Laboratory tests to detect drug-induced
allergic skin disorders may be available in the future.

Itching, with or without a rash, is the most common cutaneous complaint in the elderly. The prevalence of itching and of dry skin continues to increase from the young elderly aged in their sixties
to the very elderly aged in their nineties.[1,2] Xerosis is the most common cause of itching in the elderly. Other common causes of itching include allergic and irritant contact dermatitis, seborrhoeic
dermatitis, stasis dermatitis with or without autoeczematisation and medication reactions (table
I). Systemic causes such as thyroid disease, malignancy, renal or biliary disease, or HIV infection are
of particular concern when a patient has generalised itching without a cutaneous rash.
1. Approach to the Management of the
Elderly Patient with Pruritic Dermatitis
Elderly patients with pruritic dermatitis should
be instructed to avoid frequent washing and the use
of skin irritants such as harsh, deodorant-type
soaps, astringents and lotions. Bathing should be
followed immediately by the application of a bland
emollient ointment or a cream emollient, if an oint-

ment is not acceptable to the patient. Lotions are

more popular with patients, but require many more
ingredients to formulate compared with bland
emollients containing only water in petrolatum or
mineral oil. Lotions are less effective as moisturisers
than bland emollients of the cream type and contain
potential contact sensitisers and therefore should
be avoided if possible. Extremely low humidity
should be corrected with environmental controls,
where possible. If stasis oedema of the lower extremities is present, this should be corrected with
compression. Stasis dermatitis can cause generalised dermatitis which is now increasingly understood as a manifestation of immune autoreactivity.[3] If asteatosis and stasis dermatitis are not
present (or have been corrected), and the patient
still has dermatitis, then the possibility of allergic
contact dermatitis should be considered; this is best
investigated by a dermatologist familiar with patch
testing. If there are morbilliform, urticarial or lichenoid lesions present in addition to eczematous
dermatitis, then systemic drug allergy should be
considered.

Table I. Characteristics of the rashes discussed in this article

Type of dermatitis

Morphology

Distribution

Allergic contact dermatitis

Oozing in acute form; red scaly

Pattern corresponds to exposure

Seborrheic dermatitis

Red, dandruff-like scale

Scalp, central face and upper torso

Atopic dermatitis

Like other dermatitis forms above, often

lichenified when chronic

Commonly affects hands, face and neck in adults

Urticaria

Smooth-surfaced welts

Any part of skin or mucous membranes

Morbilliform rash

Red macules and papules

Usually starts on torso and spreads to extremities

Lichenoid rash

Purple, thin plaques with fine scale

Can involve any area but often volar wrist and legs

Cutaneous vasculitis

Purple, non-blanching

Favours gravity-dependent areas such as legs

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Drugs Aging 2001; 18 (11)

Allergic Skin Disorders

829

2. Allergic Eczematous Dermatitis:

Contact Dermatitis
2.1 Cellular Basis of Allergic
Contact Dermatitis

Elderly patients can develop allergic contact

dermatitis despite the fact that cell-mediated immunity is decreased as a result of unknown mechanisms. Absolute T and B cell counts are not reduced with age.[4] Age does not seem to affect the
number of Langerhans cells in the elderly skin
compared with the nonelderly skin,[5] although
there are reports to the contrary.[6] However, allergic contact sensitivity to poison ivy appears to decrease with age[7] and elderly men are harder to
sensitise with dinitrochlorobenzene compared with
younger men.[8] Susceptibility to some,[9] but not
all,[10] cutaneous irritants decreases with age. It is
possible that this decreased irritation reduces the
production of cytokine danger signals that are necessary for the cutaneous sensitisation process. Because sensitisation, once acquired, is long-lasting,
and years of potential exposure and cumulative acquisition of allergens produces a high incidence of
contact dermatitis in the elderly.
2.2 Prevalence of Allergic Contact
Dermatitis in the Elderly

In a group of healthy volunteers aged 68 to 87

years and without skin disease, the prevalence of
positive patch test reactions to a standard screening
tray was 37% compared with a prevalence of 15%
in a young comparator population with a mean age
of 24 years.[11] This is consistent with the persistence of acquired allergies over many years. In patients aged >60 years and referred for evaluation
of dermatitis, patch test reactions have been reported to be positive in as many as 75% of patients,
with the highest percentage of positive reactions
reported in patients aged >70 years.[12] However,
other studies have shown a peak prevalence of positive patch test reactions in young women (due to
nickel sensitivity in jewellery) and in adults aged
40 to 50 years (due to occupational sensitisation)
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Fig. 1. A patient with venous stasis ulcers of the lower limb who
has multiple contact allergies resulting in dermatitis.

with a decline in the prevalence of positive patch

reactions in patients >60 years of age.[13]
This variation in the prevalence of positive
patch test reactions among the young and the elderly patients may be a function of study methodology. Variables include number and type of allergens patch tested and the time interval between the
application of the patch test and the final reading.
Other contributory factors include differences in
the study population including regional variation
in occupation and the use of personal care items
and topical medication, and inclusion or exclusion
of patients with high risk diseases such as venous
stasis ulcers.
2.3 Allergens Causing Contact Dermatitis in
the Elderly

Nickel and fragrance/Balsam of Peru are the

two most common contact allergens detected with
patch testing in the elderly. Nickel sensitivity
peaks in youth and declines with age, while allergy
to fragrance gradually increases with age.[14] Fragrance allergy may become more common with increasing use of moisturisers to treat xerosis associated with aging; the majority of elderly Americans
use such moisturisers.[2]
Many elderly people dye their hair. Allergy to
paraphenylenediamine used in dark hair dyes gives
a severe reaction with swelling of the face and periDrugs Aging 2001; 18 (11)

830

orbital region beginning hours to days after the dye

exposure. Patients with this allergy must avoid permanent hair dyes. They may, however, tolerate
temporary (rinse out) dyes or metallic dyes that are
applied daily.[15]
Venous stasis ulcers are associated with a high
incidence of multiple contact allergens.[16] Figure
1 shows a woman with venous stasis and superficial lymphocytic vasculitic ulcers who developed
redness and itching of the skin surrounding the ulcers. Patch testing revealed reactions to fragrance,
the preservatives DMDM hydantoin and imidazolidinyl urea, and the topical antibacterials neomycin and bacitracin, all of which were currently or
previously applied to her leg ulcers. Avoidance of
these ingredients resulted in resolution of her dermatitis.
In addition to the allergens noted in the case
described above, patients with venous stasis ulcers
may also become allergic to materials used to provide compression. Allergy to rubber chemicals
(thiurams, carba, mercaptobenzothiazole, black
rubber) were found in 15% of the patients with venous stasis ulcers who were patch tested.[17] Allergy to preservatives in Unna boots has also been
reported.[18]
Elderly patients who have undergone ostomies
for gastrointestinal or urinary disorders often develop irritant or allergic stomal dermatitis. Allergens causing ostomy dermatitis include adhesives,
fragrances, rubber chemicals and acrylates.[15]
Chronic conjunctivitis may be due to or complicated by contact allergy to topical medications or
preservatives in topical medications in about onethird of the patients.[19] When the offending ingredient is an antibacterial or preservative, the patch
tests are readily positive, but patch testing with
ophthalmic -blockers may give false negative results even when higher than usual concentrations
of the= -blockers and larger patch sizes are used.
In these cases, use testing or withdrawal of the
medication may be necessary to confirm diagnosis.[20]
Cheilitis and stomatitis in the elderly may be
due to contact dermatitis to flavourants in denti Adis International Limited. All rights reserved.

Nedorost & Stevens

frices or to sunscreens. Less commonly, these

symptoms may be due to denture materials; acrylic
allergy is much more common in workers with occupational exposure to uncured acrylics than in
denture wearers exposed only to the final product.[21]
2.4 Patch Testing

Patch testing in the elderly does not usually differ from that in younger patients. Elderly patients
may require assistance to remove their patches at
48 hours if they are not returning to the clinic at
that time; many patients lack the flexibility to reach
the patches on their back. Many elderly patients
prefer sponge bathing to full baths or showers and
are less inconvenienced by the bathing restrictions
inherent in the patch test process than are younger
patients. Topical medications are a common cause
of allergic contact dermatitis in the elderly and several of these medications, including neomycin and
the corticosteroids, often give late positive reactions. It is therefore important to perform delayed
readings at 7 to 10 days in patients tested for allergy
to these materials. Corticosteroid allergy, in particular, may be missed if a late delayed reading is not
performed.[22]
2.5 Photoallergens

Photopatch testing should be carried out whenever there is a photodistributed eczematous rash.
Photopatch test allergens include plant derivatives
that are often photoactive, as well as sunscreens
and other allergens from the standard tray such as
fragrance, some of which may cause a rash and give
positive patch test results only after exposure to
ultraviolet light.
Chronic actinic dermatitis is a condition seen
primarily in elderly dark-skinned men who have a
hypersensitivity response to ultraviolet and visible
light. These patients almost always have positive
patch tests to airborne allergens or photoallergens,
which in some way must stimulate subsequent development of sensitivity to light even in the absence of the allergen. Immunosuppressants are ofDrugs Aging 2001; 18 (11)

Allergic Skin Disorders

831

ten needed to control this severely debilitating disease.[23]

3. Eczematous Dermatoses Not Due to
Contact Allergy
Seborrhoeic, nummular and atopic dermatitis
occur in the elderly and can mimic allergic disease.
Seborrhoeic dermatitis may affect a more widespread area of skin in the elderly patient compared
with younger adults. Figure 2 shows seborrhoeic
dermatitis of the back and neck in an elderly
woman patient who also had more classic scalp
dermatitis and blepharitis and who had negative
patch testing to rule out contact dermatitis to personal care products including shampoo.
Atopic dermatitis is much less common in the
elderly compared with children and young adults.[24]
Atopy is associated with seasonal mucosal allergies, asthma, positive prick tests to various protein
allergens and positive atopy patch tests to aeroallergens such as dust mite. Food allergy is far
less common in adults than in children with atopic
dermatitis. Some adults, however, may benefit by
avoiding pseudoallergens which release histamine such as salicylates and benzoates which occur
naturally and as additives in the diet.[25] Interestingly, elderly patients with nummular eczema are
more likely than age-matched controls to show
positive atopy patch tests to dust mite. [26] Lateonset atopic dermatitis, without the usual history
of atopy, may explain the occurrence of dermatitis
in some adult patients referred for patch testing
who have negative patch test results and appear to
have endogenous eczema of unknown origin.[27]
Scabies should enter the differential diagnosis
in generalised dermatitis: institutional acquisition
of scabies is common in the elderly.[28]
4. Management of
Eczematous Dermatitis
A thorough history and physical examination,
with patch testing if indicated, will allow classification of the type of eczema.
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Fig. 2. A patient with seborrhoeic dermatitis involving the back

and neck. Patch tests were negative.

Allergic contact dermatitis is best treated by patient education and avoidance of identified allergens.
Stasis dermatitis is treated with compression of
the oedematous lower extremity.
Seborrhoeic dermatitis is treated with anti-yeast
medications.
Asteatotic dermatitis is treated with emollients.
Atopic dermatitis, and all of the other forms of
dermatitis that are recalcitrant to other therapies, can be treated with topical or systemic corticosteroids.
Topical corticosteroids should not be used continuously, as they often cause tachyphylaxis as well
as adverse effects such as atrophy and striae. Topical corticosteroids, when applied on the face, may
cause steroid rosacea. Cataracts or glaucoma can
occur through application of topical corticosteroids in the periorbital area. Systemic corticosteroids contribute to osteoporosis and weight gain,
and can aggravate peptic ulcer disease, hypertension and diabetes mellitus. If adverse effects preclude the use of corticosteroids, or if they are
ineffective, treatment with the new nonsteroidal
topical immunosuppressive drug tacrolimus, phototherapy, or systemic immunosuppressives such
as cyclosporin may be required.
The desire to prevent allergic contact dermatitis
in the elderly patient does have implications for
prescribing. Potent sensitisers like neomycin
Drugs Aging 2001; 18 (11)

832

should be avoided in high-risk patients such as

those with stasis ulcers. In fact, some researchers
have suggested avoiding the routine use of topical
antibacterials even after surgical procedures, as the
reduced risk of contact allergy with white petrolatum alone compared with use of bactitracin may
outweigh the risk of wound infection.[29] When
prescribing topical corticosteroids for patients at
high risk of allergic contact dermatitis, it should be
noted that fluorinated corticosteroids are less likely
to sensitise, and are preferred to non-fluorinated
corticosteroids such as hydrocortisone and hydrocortisone-17-butyrate.[30]
5. Allergic Noneczematous Dermatosis
Sensitisation by the oral route is less common
than topical sensitisation, and more likely to produce drug-specific antibodies rather than delayed-

Fig. 3. Erythroderma and scales in a patient with a severe

morbilliform drug eruption associated with the administration of
carbamazepine.

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Nedorost & Stevens

type hypersensitivity.[31] When urticarial, lichenoid or morbilliform lesions are present with or
without eczema in an elderly person with a pruritic
rash, a reaction to systemic medication is the likely
diagnosis.
Urticarial skin reactions are often caused by antibacterials, nonsteroidal anti-inflammatory drugs
(NSAIDs), antidepressants or opioids.[32] The hives
often resolve promptly after discontinuing the medication, but occasionally may last for weeks. Urticaria may also be caused by contact with rather
than ingestion of the allergen. Common causes of
contact urticaria include latex, as well as proteins
in foods.[33] Histamine H1 receptor antagonists (antihistamines) are very useful in managing the pruritus
of urticaria, in contrast to their limited usefulness
in eczematous pruritus.[34] The dosage of antihistamines may be increased until limited by sedation.
Caution should be exercised to avoid respiratory
suppression in patients also receiving other sedating medications.
Morbilliform (maculopapular) rashes are the
most common sign of systemic reaction to medication (figure 3). Such rashes are often associated
with the administration of antibacterials, anticonvulsants, gold, allopurinol or diuretics,[32] and are
more common in patients with concomitant viral
infection.[31] In the case of Stevens-Johnson syndrome or toxic epidermal necrolysis, suspected
drugs should be withdrawn as soon as possible.
These severe reactions with mucosal involvement
can be fatal, and have an improved prognosis if the
offending drug is withdrawn early in the course[35]
(figure 4).
Lichenoid drug reactions have clinical and histological features of lichen planus, and are often
associated with the administration of quinidine, blockers or thiazides.[36] These reactions may take
months to resolve after discontinuation of the causative drug.
Cutaneous vasculitis may be caused by diuretics, antibacterials and other medications.[32,36]
Phototoxic reaction may be associated with the
administration of tetracyclines, diuretics, NSAIDs
and antihyperglycaemic drugs.[37]
Drugs Aging 2001; 18 (11)

Allergic Skin Disorders

Fig. 4. A patient with toxic epidermal necrolysis who had widespread epidermal loss requiring endotracheal intubation went
on to die from complications of his drug reaction.

Fixed drug eruptions occur in limited areas, often on mucous membranes, as red or vesicular lesions that flare after each ingestion of the causative
medication, with progressive hyperpigmentation
between active episodes. They may be caused by
antibacterials such as cotrimoxazole (trimethoprim-sulfamethoxazole) or analgesics, particularly
NSAIDs. The tendency to develop this eruption
may be linked to the presence of HLA-B22.[38]
6. Investigating Rashes Due to Systemic
Allergic Reactions
There is currently no reliable, routine test to determine the cause of a drug-induced rash when the
patient is receiving multiple medications, as is the
case with many elderly patients. If the reaction is
mild, the most likely medication (often the medication most recently introduced) should be discontinued and substituted with a structurally unrelated
medication. The patient should be observed and if
no clinical improvement is noted after several
weeks, the next most likely medication should be
discontinued and so on until improvement is noted.
If the reaction is severe, all medications should be
substituted with structurally unrelated alternatives.[31]
Prick testing can be used to document some
drug allergies, such as penicillin,[31] and patch testing is sometimes useful when performed on lesio Adis International Limited. All rights reserved.

833

nal skin to document the cause of fixed drug eruption.[39] Oral provocation testing may be useful
when the reaction has not been severe, but generally should not be used to document severe reactions.
In vitro tests to determine susceptibility to a
drug reaction are being investigated. One severe
drug-induced adverse reaction is the anticonvulsant hypersensitivity syndrome, characterised by a
skin rash, lymphadenopathy and fever and at times
hepatitis, nephritis, pneumonitis or haematological
abnormalities. This rare condition has a delayed
onset after initiation of therapy with aromatic anticonvulsants such as phenytoin, carbamazepine or
phenobarbital (phenobarbitone). The role of the
immune system in this condition remains controversial. However, Shear and colleagues[40] have
developed an in vitro sensitivity test in which murine hepatic microsomal enzymes (e.g. cytochrome
p450) are incubated with the test drug, in order to
convert it to potentially toxic metabolites, and lymphocytes from the patient. Lymphocytes are used
because they are conveniently obtained cells and
they normally contain epoxide hydrolases, not because they are immunocytes. These hydrolases
normally detoxify the toxic areneoxide intermediate metabolite of the drugs. If the patient is deficient in these enzymes, these toxic intermediates
build up and the test lymphocytes die, yielding a
positive test. These authors have shown that a very
similar test can also be used to detect some adverse
reactions to sulphonamides.[41]
In addition to cytotoxicity assays, such as those
described by Shear, Spielberg and colleagues,[40,41]
tests for the in vitro assessment of the true immunological hypersensitivity risk are also available.
The latter tests are largely experimental and incompletely validated. Lymphocyte transformation
assays combine mononuclear leucocytes from the
patient with the suspected allergenic drug.[42] In
the event of a positive reaction, allergen-specific T
cells will undergo activation and growth. Tritiated
thymidine, a radiolabelled DNA precursor, is also
added to the assay, and will be taken up and incorporated into the DNA of daughter cells generated
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834

Nedorost & Stevens

in the assay. Reactivity to the test compound is detected as an increased radioactivity in the tested
cells, reflecting antigen-specific T cell growth.
This test, like the cytotoxicity assay, is still developmental and requires specialised laboratory techniques and is subject to difficulty in interpretation.
Another related approach has been recently described by Yawalker et al.[43] In this report, T cells
derived from positive skin tests were shown to
demonstrate drug specificity manifested as increased tritiated thymidine incorporation, cytokine
production and cytolytic activity.
The tests described above have not yet been validated to the same extent as in vivo skin testing or
tests of humoral immunity such as radioallergosorbent tests. However, they do provide hope that
in the future we will develop the capacity to identify individuals who are at increased risk of developing severe drug eruptions. Alternatively, the antigen specificity testing described by Yawalker et
al.[43] may eventually lead to advanced tests capable of identifying which of the several drugs that
an individual patient may be taking is the cause of
a drug eruption.
7. Conclusion
Allergic skin disease in the elderly patient may
be eczematous if the cause is an environmental
contactant and urticarial or polymorphous if the
cause is an ingested allergen. Patch testing should
be utilised to determine the cause of allergic contact dermatitis. Patient history and discontinuation
of medications may be required to determine the
cause of skin reactions due to systemic allergens.
There are in vitro tests on the horizon that may help
to more rapidly determine the cause of a cutaneous
systemic drug reaction.
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Correspondence and offprints: Dr Susan Nedorost, University Hospital Dermatology Associates, 960 Clague Rd,
Westlake, OH 44145, USA.

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