Id reaction, also known as autoeczematization, secondary dermatitis, autosensitization dermatitis, and generalized eczema, occurs when eczema develops at sites not affected by a primary, inciting dermatosis. In adults, the primary dermatosis is typically allergic contact dermatitis with or without underlying stasis dermatitis, but id reaction is also seen in association with stasis dermatitis without allergic contact dermatitis, other forms of eczematous dermatitis, and inflammatory bullous tinea pedis. The reaction usually appears a few days to weeks after the primary dermatitis and can be severely pruritic. It shows a symmetric distribution and has a predilection for the palms, soles, and extensor surfaces of the upper extremities. All ages and populations, and both sexes, are equally affected.

Autoeczematization is thought to result from a lower threshold for developing an eczematous hypersensitivity reaction in patients with preceding or concurrent inflammatory processes of the skin. Memory T-cells are thought to play a role in the cases of id reaction associated with allergic contact dermatitis. In the case of tinea, id reaction can develop after the institution of effective therapy and can be mistaken for an allergic reaction to the medication.