Contact dermatitis accounts for 70-90% of all occupational skin diseases. 1 It is an inflammatory skin condition induced by exposure to an external irritant or allergen (table 1⇓). A prevalence of 8.2% was seen in a recent cross sectional study of 12 377 subjects across five European countries, in which a randomly selected group of 3119 patients were patch tested. 2 The condition can have a detrimental impact on personal and social relationships, quality of life, and even threaten employment. [3][4][5] What are the different types of contact dermatitis?Irritant contact dermatitis is a non-immunologic response that occurs as a consequence of direct damage to the skin, by chemicals or physical agents, faster than the skin is able to repair itself. 6 7 Approximately 80% of cases of contact dermatitis are irritant contact dermatitis. 8 Common irritants include soaps, detergents, water, solvents, cutting oils, and food ingredients. 8 The hands, particularly finger web spaces (fig 1⇓), and the face are commonly affected. 6 Allergic contact dermatitis comprises 20% of cases of contact dermatitis. It is a type IV delayed hypersensitivity reaction to an external allergen, which occurs only in an individual who has previously been sensitised. 6 Re-exposure to the allergen results in circulating memory T cells homing in to the skin and eliciting an immunologic reaction that causes skin inflammation, typically within 48 hours. [9][10][11][12][13] For personal use only: See rights and reprints

A 69-year-old gentleman with non-Hodgkin's lymphoma (stage I), with baseline fibrotic lung changes on CT, received six cycles of R-PMitCebo chemotherapy containing bleomycin. Three months later he presented to the Accident and Emergency Department with progressive dyspnoea, dry cough, pyrexia and generalised lethargy. Chest radiographs showed bilateral lower zone opacities. Clinically, all signs initially pointed to community-acquired penumonia, but he failed to respond to standard treatment for this. Repeat high-resolution CT (HRCT) subsequently showed widespread peripheral interstitial changes consistent with marked fibrotic lung changes. It became apparent that this was in fact bleomycin-induced pulmonary toxicity. The patient rapidly deteriorated and developed type I respiratory failure. Despite intensive steroid treatment, the patient progressively got worse and died in the Intensive Therapy Unit 10 days after admission. Death was directly attributed to pulmonary fibrosis secondary to bleomycin treatment.

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