An animal model for altering the irritability threshold of normal skin.

Theory behind conditioned hyperirritability (autoeczematization) predicts the lowering of the irritation threshold in the presence of a pre-existing dermatitis. We have attempted to develop an animal model that parallels the syndrome seen in man. Groups of 10 guinea pigs were shaved and depilated; irritation thresholds to benzalkonium chloride and trichloroacetic acid were determined using 1 cm diameter open patches. Reactions were scored 24 h later on the basis of erythema and induration. Animals having as little as 1.56 cm2 of skin acutely inflamed with a known irritant had lowered irritation thresholds to the same irritant on normal skin at remote sites (p less than 0.01). Mild irritation of a much larger surface area produced the same effect (p less than 0.01). More extensive, severe dermatitis did not lower the irritation threshold further. Acute dermatitis induced by a contact allergen (DNCB) lowered the irritation threshold of normal skin to the same level as that obtained with irritants (p less than 0.01). Induction of chronic cutaneous ulcers 3-4 cm in diameter lowered the irritation threshold of normal skin to the same point defined by the acute studies (p less than 0.01). These results indicate that an acute irritant or contact dermatitis, as well as chronic skin ulceration, may alter the reactivity of unaffected normal skin to exhibit a heightened response to irritation. This model appears to differ from that seen in humans, in that a more extensive or chronic dermatitis did not further heighten the susceptibility to irritation.