Id Reaction (Autoeczematization)



Id reaction, or autoeczematization, is a generalized acute cutaneous reaction to a variety of stimuli, including infectious and inflammatory skin conditions. The pruritic rash that characterizes the id reaction, which is considered immunologic in origin, has been referred to as dermatophytid,[1] pediculid,[2] bacterid when associated with a corresponding infectious process, and tuberculid when associated with tuberculosis.[3] Clinical and histopathological manifestations are variable and depend on the etiology of the eruption, and systemic manifestations may occur.[4]

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Id reaction (autoeczematization). Courtesy of DermNet New Zealand (


While the exact cause of the id reaction is unknown, the following factors are thought to be responsible: (1) abnormal immune recognition of autologous skin antigens, (2) increased stimulation of normal T cells by altered skin constituents,[5, 6] (3) lowering of the irritation threshold, (4) dissemination of infectious antigen with a secondary response, and (5) hematogenous dissemination of cytokines from a primary site. Some cases have been related to medications and intravenous immune globulin.[7] Id reaction has also been noted with BCG therapy.[8]

Etiology of Id Reaction

The etiology of id reactions includes the following:



The exact prevalence of id reaction is not known. Dermatophytid reactions are reported to occur in 4-5% of patients with dermatophyte infections. Id reactions have been reported in up to 37% of patients with stasis dermatitis. Furthermore, an estimated two thirds of patients with contact dermatitis superimposed on stasis dermatitis develop an id reaction.


The condition has no known predilection for any racial or ethnic group.


The condition has no known predilection for either sex.


Predilections according to age group are unknown but are influenced by the primary cause of the reaction.


Prognosis is good once the inciting etiology has been identified and appropriately treated. Morbidity results from symptoms of the id reaction and the acute onset of the primary eruption.


Id reactions result from a variety of stimuli, including infectious entities and inflammatory skin conditions. Dermatological manifestations vary and depend on the etiology of the eruption. General history may include the following:

Physical Examination

Clinical lesions of id reactions are quite variable and are largely predicated on the inciting etiology. Lesions are, by definition, at a site distant from the primary infection or dermatitis. They are usually distributed symmetrically. Clinical forms include the following:

Laboratory Studies

Laboratory workup of id reactions is clearly indicated for dermatophytids. Strict criteria include a proven dermatophyte infection and a positive skin test finding for a group-specific trichophytin antigen. Absence of fungi in the dermatophytid lesions and clearing of the dermatophytid after the fungus is eradicated are necessary to confirm a definitive diagnosis of a dermatophytid reaction.

Other Tests

Patch testing may be needed to exclude primary or secondary allergic contact dermatitis.


Biopsy for routine hematoxylin and eosin staining may be helpful in excluding noneczematous dermatoses, which may appear morphologically similar to an id reaction.

Histologic Findings

Histopathology of the typical papulovesicular lesion reveals a superficial perivascular lymphohistiocytic infiltrate with a spongiotic epidermis, often with vesiculation. Small numbers of eosinophils may be present in the dermal infiltrate. By definition, infectious agents should not be found in the specimens.

Medical Care

The goal is to adequately treat the underlying infection or dermatitis, which should lead to prompt resolution of the id reaction. Recurrences are common, especially if the primary source is not treated adequately.

Treatment of the eruption includes the following:


If a severe underlying infection is present, consult an infectious disease specialist or internist.


Complications can include secondary infection and secondary allergic contact dermatitis from topically applied medicaments/emollients.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Amcinonide (Cyclocort)

Clinical Context:  Amcinonide suppresses mitotic activity and causes vasoconstriction. It stimulates the synthesis of enzymes needed to decrease inflammation.

Fluocinonide (Fluonex, Lidex)

Clinical Context:  Fluocinonide is a high-potency steroid that inhibits cell proliferation. It is immunosuppressive, antiproliferative, and anti-inflammatory. It also has antipruritic and vasoconstrictive properties.

Prednisone (Orasone, Sterapred, Deltasone)

Clinical Context:  Prednisone is a commonly used oral agent. It is indicated for severe, prolonged, or anaphylactic reactions. It decreases late immune-mediated complications. Prednisone must be metabolized to the active metabolite prednisolone for effect. Conversion may be impaired in liver disease.

Methylprednisolone (Depo-Medrol, Medrol, Adlone, Solu-Medrol)

Clinical Context:  Methylprednisolone may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. It is indicated for severe, prolonged, or anaphylactic reactions. It decreases late immune-mediated complications.

Class Summary

Corticosteroids help lesion resolution and provide symptomatic relief of pruritus. The strength and administration of a topical corticosteroid should be chosen based on the extent, location, and morphology of the eruption. Systemic corticosteroids may be used for severe or refractory eruptions.

Diphenhydramine (Benadryl, Benylin, Caladryl, Dermapax)

Clinical Context:  Diphenhydramine is a first-generation antihistamine with anticholinergic effects that binds to H1 receptors in the CNS and the body.

It competitively blocks histamine from binding to H1 receptors. It has significant antimuscarinic activity and penetrates the CNS, which causes a pronounced tendency to induce sedation. Approximately half of those treated with conventional doses experience some degree of somnolence. A small percentage of children paradoxically respond to diphenhydramine with agitation.

It is for symptomatic relief of symptoms caused by the release of histamine in allergic reactions.

Loratadine (Claritin, Alavert)

Clinical Context:  Loratadine selectively inhibits peripheral histamine H1 receptors. It is tolerated well, with a rate of sedation not significantly different from placebo.

Class Summary

These agents relieve pruritus. They may control itching by the blocking effects of endogenously released histamine.

What is id reaction (autoeczematization)?What is the pathophysiology of id reaction (autoeczematization)?What causes id reaction (autoeczematization)?What is the prevalence of id reaction (autoeczematization)?What is the prognosis of id reaction (autoeczematization)?Which history is characteristic of id reaction (autoeczematization)?Which physical findings are characteristic of id reaction (autoeczematization)?What are the differential diagnoses for Id Reaction (Autoeczematization)?What is the role of lab studies in the evaluation of id reaction (autoeczematization)?What is the role of patch testing in the evaluation of id reaction (autoeczematization)?What is the role of biopsy in the evaluation of id reaction (autoeczematization)?Which historical findings are characteristic of id reaction (autoeczematization)?What is included in the medical care for id reaction (autoeczematization)?Which specialist consultations are needed for the treatment of id reaction (autoeczematization)?What are possible complications of id reaction (autoeczematization)?Which medications in the drug class Corticosteroids are used in the treatment of Id Reaction (Autoeczematization)?Which medications in the drug class Antihistamines are used in the treatment of Id Reaction (Autoeczematization)?


Matthew P Evans, MD, Chair, Department of Dermatology, Dreyer Medical Clinic

Disclosure: Nothing to disclose.


Darryl Bronson, MD, MPH, Consultant and Immediate Past Chairman, Division of Dermatology, Department of Medicine, Cook County Hospital of Chicago; Instructor, Department of Dermatology, University of Illinois at Chicago

Disclosure: Nothing to disclose.

Specialty Editors

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD, Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Disclosure: Received honoraria from UpToDate for author/editor; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Allergen; Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Donald Belsito, MD, Professor of Clinical Dermatology, Department of Dermatology, Columbia University Medical Center

Disclosure: Nothing to disclose.


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Id reaction (autoeczematization). Courtesy of DermNet New Zealand (

Id reaction (autoeczematization). Courtesy of DermNet New Zealand (