Phototoxic dermatitis L56.0

Acute or chronic photochemical light dermatosis of varying degrees of acuteity, induced by internal or external photosensitizers and sharply limited to the exposed skin areas, without immunological basis (important: no previous sensitization). See also Table 1.

Depending on the clinical morphology and the time course of the reaction, 4 types of phototoxic reactions can be distinguished:

1. Immediate or delayed reaction: Urticarial reaction, which is immediate or delayed. Clinical: immediate urticarial erythema with stinging and burning during exposure (smarting); erythema or urticae; triggers: tar, pitch, anthraquinone dyes, benoxaprofen, amiodarone, chlorpromazine.
2. Sunburn-like reaction (corresponds to a dermatitis solaris): Trigger: quinolone, chlorpromazine, amiodarone, benoxaprofen, hydrochlorothiazide, quinidine, demethylchlortetracycline and other tetracyclines.
3. Delayed erythema possibly with blistering: Often subclinical and only noticeable by hyperpigmentation. Trigger: Psoralene (phytophotodermatitis; see below dermatitis pratensis, Berloque dermatitis).
4. Pseudoporphyria: Increased vulnerability of the skin with blistering after banal traumas. Triggers: Nalidixic acid, furosemide, tetracyclines, naproxen, amiodarone.

The clinical symptoms vary with the triggering agent, its mode of application (external, internal) and the intensity of UV exposure. Various photosensitizers (e.g. coal tar, chlorpromazine) can trigger an immediate phototoxic reaction with an erythematous to urticarial local reaction sharply limited to the light-exposed areas, with stabbing or burning pain.

Other phototoxins induce a delayed, sunburn-like reaction (starting about 6-8 hours after exposure). These include: tetracyclines, non-steroidal anti-inflammatory drugs. Tetracyclines can induce distal phototoxic onycholysis.

In the case of furanocoumarins, dermatitis may occur after several hours or, less frequently, only after several days.

In various reactions the acute phase is regularly followed by sharply defined hyperpigmentations (stimulation of melanin synthesis) which can persist for years (e.g. amiodarone). Often it is only the "cosmetically disturbing" residual hyperpigmentations that lead to a visit to the doctor. Amiodarone leads to grey-blue colour changes of the skin. This is caused by degradation products of amiodarone which accumulate in the skin as a function of radiation and lead to toxic melanocyte damage with melanocyte damage(pigment incontinence).

Medium strength glucocorticoid creams such as 0.1% triamcinolone cream R259, 0.05% betamethasone V lotio R030, 0.25% prednicarbate cream (e.g. Dermatop), methylprednisolone cream (e.g. Advantan).

Important phototoxic substances

1. Ferguson J, Addo A. A, Jones S et al (1985) A study of cutaneous photosensitivity induced by amiodarone. Br J Dermatol 113:537-549
2. Hölzle E, Plewig G (1982) Photoallergic contact dermatitis caused by benzophenone-containing sunscreen preparations. Dermatologist 33:391-393
3. Jackson R. T., Nesbitt L. T. Jr, DeLeo V. A (1980) 6-Methylcourmarin photocontact dermatitis. J Am Acad Dermatol 2:124-12
4. Mahler V (2015) Contact eczema. Act Dermatol 40: 95-107
5. Schauder S, Ippen H (1986) Photoallergic and allergic contact dermatitis from dibenzoylmethanes. Photodermatolgy 3:140-147