Glucocorticosteroid allergy

Incompatibility reactions to glucocorticoids such as contact allergic dermatitis, immediate reactions with anaphylactic phenomena, immunological and non-immunological exanthema or occur repeatedly and are described for almost every glucocorticoid. Anaphylactic reactions to administered glucocorticoids may be responsible for some unsuccessful use in emergency medicine. Multiple sensitizations or cross allergies must be expected. Risk groups cannot be identified.

Topical glucocortiosteroids are divided into 4 groups according to their allergological relevance (see also glucocorticoseroid epicutaneous test series):

• A(hydrocortisone type)
• B (acetonide type)
• C(betamethasone type)
• D (ester type - esterifications in the C16 position)

Due to their low molecular weight and high lipophilicity, glucocorticoids penetrate the horny layer very well. The metabolism of glucocorticoids takes place in the skin and the most important step is hydrolysis. A halogenation in C6-position reduces the risk of sensitization. Moderate sensitization accumulations are found with amcinonide, hydrocortisone-17-butyrate and budesonide.

According to an older European study, the incidence of contact allergic reactions is (amazingly!) 0.2-5.0%. 85% of these patients are sensitized to more than one glucocorticoid (Wurpts G 2018).

Diagnosis often requires extensive testing of the suspected glucocorticoid (see glucocorticoids, epicutaneous test series below) including other derivatives as well as excipients. The assessment of an epicutaneous reaction is complicated by the fact that the opposing anti-inflammatory effect of the glucocorticoid tested suppresses the type IV reaction. In addition, the vasoconstrictor effect of the glucocorticoid causes the test site to fade. The epicutaneous test can be falsely negative!

Marker substances are: tixocortol pivalate for hydrocortisone, prednisolone, and methylprednisolone sensitization, budenoside for triamcinolone acetonide, hydrocortisone, hydrocortisone-17-butyrate and prednicarbate. A DKG glucocorticoid test series is available. In cases of doubt, a tear-off epicutaneous test or the ROAT (repeated open application test) is recommended.

Incompatibility reactions to glucocorticoids should always be considered if the underlying disease worsens under treatment or incompatibilities occur for the first time. It is often difficult to recognise symptoms or a worsening of the condition as a result of glucocorticoid administration, e.g. an increase in bronchospasm in asthma patients or the exacerbation of dermatitis under a glucocorticoid externum.

In addition to the glucocorticoid as the active substance, excipients are also considered as triggers, in the case of externals also basic components or other added pharmaceuticals (e.g. neomycin).

A 64-year-old woman developed reversible anaphylactic shock after injection of diclofenac and a preparation containing prednisolone and dexamethasone.

The anaphylactic reaction of a 43-year-old man after amoxicillin and dramatic deterioration of the anaphylaxis situation after intravenous administration of methylprednisolone was attributed to an amoxicillin allergy or reaction to methylprednisolone.

A 37-year-old asthmatic suffered a status asthmaticus after the injection of 40mg triamcinolone, presumably triggered by the excipient sulphite.

In a 32-year-old woman a severe generalized urticaria with angioedema occurred for the first time after taking prednisolone.

1. Castela E et al (2012) Topical corticosteroids in plaque psoriasis: a systematic review of risk of 11adrenal axis suppression and skin atrophy. J Eur Acad Dermatol Venereol 26: Suppl 3, 47-51
2. Dooms-Goossens A et al (1996) Corticosteroid contact allergy: an EECDRG multicentre study. Contact dermatitis 35:40-44.
3. Goossens A (2000) Reactions to corticosteroids: some new aspects regarding cross-sensitivity. Cutis 65:43-45.
4. Wurtps G (2018) Contact allergy to glucocorticoids. Allergo J 27: 13-15