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An allergic reaction develops in 2.4% of patients that use insulin. This ranges in severity from erythema and pruritus to life-threatening anaphylaxis. llergic reactions to insulin usually occur within a few hours after an injection and are usually due to a local or systemic type I IgE-mediated hypersensitivity reaction. Despite considerable research into the immunogenicity of insulin, this has not yet been clarified completely and allergic reactions to insulin still occur. A systematic diagnostic approach is essential for an adequate treatment plan. A blood test for anti-insulin antibodies and intradermal skin tests are of great importance. There are many options available for the treatment of insulin allergy and each patient must therefore be evaluated individually.

Exact data concerning the incidence of cutaneous drug eruptions are lacking due to underreporting. Diagnostics of cutaneous drug eruptions is hampered by the fact that one drug may induce different eruptions while the same cutaneous eruption can be caused by several drugs. Important steps in the diagnostics of cutaneous drug eruptions are: suspicion of the drugs as cause of the eruption, precise history-taking with emphasis on medication use and a complete physical examination. The 'golden standard' in the diagnostics of a drug eruption is the dechallenge-rechallenge procedure, but in severe cutaneous reactions such as Stevens-Johnson syndrome, toxic epidermal necrolysis and vasculitis, this procedure can cause severe, sometimes life-threatening reactions. Reporting suspected adverse drug reactions to pharmaco-vigilance centres is important to identify rare drug reactions.

In six patients (4 women aged 80, 62, 43 and 52 years and 2 men aged 58 and 51 years), who used eyedrops containing beta-blockers for the treatment of glaucoma, allergic contact dermatitis of the eyelids was diagnosed. Three were allergic to metipranolol, 2 to levobunolol and 1 to timolol. In literature, less than 50 cases of hypersensitivity to beta-blockers in eye medication have been reported. There are, however, reasons to assume that sensitization is more frequent: (a) not all patients are referred by the ophthalmologist to the dermatologist; (b) false-negative reactions to patch tests with the commercial preparations and with beta-blockers are not infrequent; (c) they are not routinely tested because beta-blockers are difficult to obtain in pure form; (d) cross-reactions with other beta-blockers are infrequent, and changing to another preparation therefore usually solves the clinical problem. Nevertheless it is advisable to test a battery of beta-blockers (befunolol, levobunolol, metipranolol, timolol) in allergic patients. A test preparation of 2% in water or 3%-10% in petrolatum may be suitable. Control testing in non-exposed individuals is necessary to exclude irritation reactions.

Contact allergy to corticosteroids is not rare. In some studies prevalence rates up to 6% have been observed among patients suspected of allergic contact dermatitis. Hypersensitivity occurs especially in individuals who have been suffering for years from atopic dermatitis, contact dermatitis of the hands and feet, or stasis dermatitis caused by chronic venous insufficiency. The clinical picture is rarely that of acute allergic contact dermatitis, because the reaction is mitigated by the anti-inflammatory properties of the corticosteroid itself; the diagnosis must be suspected when eczema does not improve or spreads during topical corticosteroid therapy. Application to the mucous membranes less frequently leads to sensitisation. Most such cases are caused by nasal sprays containing tixocortol pivalate or budesonide. Oral or parenteral administration of corticosteroids to sensitive individuals causes exacerbation of pre-existing contact dermatitis or widespread allergic cutaneous drug reactions. Allergological investigation with corticosteroids presents some specific problems, the most important being occurrence of false-negative reactions. Nevertheless, most sensitive patients can be identified by testing the 'indicator' allergens, budesonide and tixocortol pivalate, which should be added to the routine series of contact allergens. Cross-reactions to other corticosteroids occur frequently. This should be taken into account when prescribing alternative corticosteroid preparations.

In four patients, three women aged 45, 29 and 52 years and a man aged 45 years, allergic contact dermatitis due to 'tea tree' oil was diagnosed. The case of the man was published before. 'Tea tree' oils are essential oils distilled from the leaves of myrtaceous trees and shrubs occurring in Australia and South-East Asia. The 'tea tree' oil available in the Netherlands is distilled from the Melaleuca alternifolia and mainly contains eucalyptol. Eucalyptol is probably the most important allergen.