Key words: contact dermatitis,
corticosteroids, clinical symptoms, patch-test reactions
The anti-inflammatory activity of a corticosteroid may mask the contact allergic reaction it is causing. This is an important reason why contact allergy to corticosteroids has been frequently missed in the past. The clinical signs of the corticosteroid-allergic patient are rarely spectacular, as the lesions generally present as a chronic eczema. The majority of the corticosteroid-sensitive patients we could observe suffered from stasis dermatitis due to chronic venous insufficiency, irritant and/or allergic dermatitis of the hands, chronic eczema of the feet (sometimes in association with a shoe dermatitis), anal and/or peri-anal dermatitis, (seborrheic) facial eczema, and also atopic dermatitis (even in children). The patients generally report that they simply do not seem to respond to corticosteroid therapy any longer. The failure of the skin lesions to heal leads the attending physician then to prescribe other, still stronger corticosteroid preparations. This often brings no relief of the symptoms and causes other adverse corticosteroid effects (such as atrophy, rosacea, and peri-oral dermatitis that may even dominate the clinical picture). In exceptional cases, the contact allergy may express itself as an id-like reaction elsewhere on the body.
Allergic
reactions may also arise upon the administration of local inhalation
corticosteroids used in the treatment of rhinitis or bronchial asthma. Several reports have been published
regarding the occurrence of eczema located on the face (mainly the eyelids and
the peri-oral and peri-nasal areas) and sometimes also at distant body sites
(even generalized); in some cases, this is associated with endo-nasal
intolerance and broncho-constriction.
The precise allergic mechanisms are not always clear but, in some cases,
even IgE antibodies might be involved.
In these cases, in which such reactions occur already two or three days
after the first administration, a previously existing corticosteroid
sensitivity (i.e. undetected) seems obvious.
Indeed, there have been several cases with tixocortol pivalate, which
indicates a contact allergy to hydrocortisone acetate, prednisolone, etc. and
with budesonide, which indicates contact allergy to other corticosteroids, such
as acetonides (amcinonide, triamcinolone acetonide) as well as to certain
esters (hydrocortisone-17-butyrate, alcomethasone diproprionate, prednicarbate). Thus, such patients may have been sensitized
to a chemically-related corticosteroid and then react to tixocortol pivalate
and budesonide, respectively.
Furthermore,
drug-like eruptions presenting as eczema, exanthema, purpura, urticaria, etc.
may occur following systemic intralesional and also interarticular
administration of corticosteroids in previously sensitized patients.
A
weak concentration of a corticosteroid in a pharmaceutical product can cause a
contact allergy on the treated eczema site while giving a negative patch-test
reaction or even a negative usage test on an intact test site. Moreover, the bio-availability of a
corticosteroid diluted in a test vehicle like petrolatum is generally lower
than in a commercial preparation for which the vehicle has been formulated
intentionally to enhance skin penetration.
However, alternative vehicles may provoke irritant reactions (e.g dimethylsulfoxide)
or give storage problems (e.g. ethanol) because corticosteroids tend to degrade
in them. The occurrence of
false-negative patch-test results has even led certain authors to use
intradermal testing to screen for allergies to hydrocortisone as well as to
other corticosteroids. (One must keep
in mind, though, that the results of intradermal testing are not always
relevant to the patient's contact allergic condition).
Masking
effects frequently occur in patch-test reactions and may produce particular
reactions. A curious reaction that
occurs quite often at the first reading and this primarily with strongly active
corticosteroids is what is called the "edge effect": an eczematous
reaction is only apparent on the edge of the patch-test site and not in the
middle. Probably what is involved is a
suppression by its anti-inflammatory effect in the middle of the patch, where
the concentration is the highest, and a predominating allergenic effect on the
edge just beyond the borders of the test material, where a small concentration
of the corticosteroid has diffused into the surrounding skin. This phenomenon disappears at later
readings, however, and the entire test site becomes eczematous. That this is not simply a pressure effect
caused by the chamber (plastic) is shown by it also occurring when "dry
gels" are used as test vehicles for the corticosteroids.
Another
often occurring phenomenon is a vasoconstrictive or blanching effect at the
first reading, primarily when strong corticosteroids are diluted in an ethanol
solution. This contrasts with what may
be called "reactive vasodilatation" expressed as a faint erythema on
the patch-test site, particularly at the three- or four-day reading. These phenomena, however, only occur in some
of the patients tested, which expresses the individual variability in responses
to local corticosteroids. Weak
erythematous reactions, however, must certainly be checked later, since they
could just as well indicate the beginning of an allergic reaction. Indeed, corticosteroids often react only
after a considerable period of time (5-6 days).
Furthermore,
corticosteroid sensitivity is found to be particularly common among patients
who use vast numbers of topical agents and so tend to develop concurrent
hypersensitivity to several of the ingredients in them. Masking effects can also occur when
corticosteroid preparations are tested, so contact allergies to other
ingredients may be overlooked. In our
experience, we have found that approximately 80 % of corticosteroid-allergic
patients react to other, mainly iatrogenic, allergens, and even to presumably
rare sensitizers. This, too, was a
pitfall for the dermatologist searching for allergens present in such
preparations: one was apt to be satisfied when one could identify an allergenic
ingredient while, in fact, the patient is sensitive to several, including the
corticosteroid itself.
Corticosteroids,
because of their anti-inflammatory effects, often mask the clinical signs of a
patient presenting with a contact dermatitis to a corticosteroid preparation as
well as the patch-test reactions obtained with the corticosteroid molecules
themselves.
Dooms-Goossens
A. Clinical aspects of contact allergy
to corticosteroids. Dermatology 1994,
189 (suppl. 2):54-55.