Glucocorticoids are steroids with 21 carbon atoms. They are derived from sterane, pentacyclic carbure. Paradoxically, although widely used for inflammatory and allergic manifestations, they can cause allergic symptoms.
Uncommon for systemic reactions: fewer than one hundred cases reported since 1957 (10 deaths published after methylprednisolone pulse therapy).
Common for contact dermatitis: 0.2 to 4.8% prevalence in patients attending clinics for patch testing (corticosteroid contact dermatitis will be explored in the next chapter).
Risk factors
Female gender.
Age 30 to 60 years.
Aspirin intolerance (for bronchospasm due to hydrocortisone).
Intravenous administration.
Atopic background (controversial).
Chronic dermatitis requiring topical therapy over an extended period (for corticosteroid contact allergy).
Clinical manifestations
Drugs involved: hydrocortisone (46%), methylprednisolone (31%), prednisolone (11%), dexamethasone (9%), prednisone (3%).
Immediate: anaphylactic shock, urticaria, angioedema, bronchospasm.
Generalized delayed systemic reactions: generalized dermatitis, exanthematous rashes with focal bullae and purpura.
Allergic contact dermatitis: worsening or lack of response of dermatitis to treatment, perinasal dermatitis, worsening of perennial rhinitis.
Diagnostic methods
Cutaneous testing.
Skin-prick tests: sometimes positive.
Intradermal skin-tests: positive in 50% of the cases with immediate hypersensitivity.
Patch-tests: budesonide (1% eth) + tixocortol pivalate (1% pet) positive in 91.3% of corticosteroid contact allergic subjects.
Skin-tests with the excipient may be positive (carboxymethylcellulose).
Specific IgE antibodies: one case (methylprednisolone).
Challenge tests may be useful but hazardous.
IgE-mediated hypersensitivity: one case report.
Preservatives and excipients have been implicated: parabens, sulfites, carboxymethylcellulose.
Possible role of contaminants and metabolites.
Possible role of steroid salts (hydrocortisone esters).
Most cases involve a non-allergic mechanism.
In patients with aspirin intolerance, hydrocortisone inhibits arachidonic acid release by phospholipids and thus deprives the airways of the cycloxygeneation products (PGE2, prostacycline) which play an important role in bronchodilatation.
Do not use hydrocortisone in patients with aspirin intolerance.
When possible, administer orally rather than intravenously.
If use is absolutely necessary, perform desensitization to hydrocortisone starting with 15 µg and ending with 100 mg in 46 days.


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As in all diagnostic testing, the diagnosis is made by the physican based on both test results and the patient history.