Id Reaction (Autoeczematization)

Practice Essentials

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]  Noninfectious etiologies include stasis dermatitis, dyshidrotic eczema, medications and topical creams, tattoo ink, sutures, and radiotherapy.^[4]

 Clinical and histopathologic manifestations are variable and depend on the etiology of the eruption, and systemic manifestations may occur.^{[5, 6, 7]}  (See the image below.)

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Id reaction (autoeczematization). Image from DermNet New Zealand (http://www.dermnetnz.org/assets/Uploads/dermatitis/a-ecz2.jpg).

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Pathophysiology

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,^{[8, 9]} (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 (IVIG).^[10] Id reaction has also been noted with bacille Calmette-Guérin (BCG) therapy.^[11]

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Etiology

The etiology of id reactions includes the following:

• Infections with dermatophytes, pulmonary histoplasmosis,^[12]  mycobacteria,^[13] viruses,^[14] bacteria, or parasites (pediculosis)^[2]
• Contact dermatitis, stasis dermatitis, or other eczematous dermatoses^{[15, 16]}
• Immunization reactions - Id reactions have been reported following BCG therapy^[11]
• Miscellaneous noninfectious reactions - Medications and topical creams, sutures, and radiotherapy^[4]

With the growing popularity of tattoos, id reactions to red tattoo ink have been increasingly noted, as well as an id reaction reported following laser tattoo removal.^{[17, 18]}  Neosporin was found to be the trigger for an id reaction in an immunocompromised patient.^[19]

No consensus has been reached on whether papulonecrotic tuberculid^[20]   represents a true hypersensitivity reaction rather than the result of a local cutaneous tuberculosis infection because of the identification (by polymerase chain reaction) of Mycobacterium tuberculosis in some lesions.^{[7, 21]}   

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Epidemiology

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.

Predilections according to age group are unknown but are influenced by the primary cause of the reaction. The condition has no known predilection for either sex. The condition has no known predilection for any racial or ethnic group.

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Prognosis

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.

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History

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

• Varying degrees of pruritus are typically noted.
• An acute onset of an extremely pruritic, erythematous, morbilliform, or papulovesicular eruption occurs 1-2 weeks after primary infection or dermatitis. Id reactions associated with stasis dermatitis are usually symmetrical and, in descending order of frequency, involve the forearms, thighs, legs, trunk, face, hands, neck, and feet.
• Id reactions are usually preceded by exacerbation of the preexisting dermatitis induced by infection, scratching, or inappropriate therapy. (Id reaction to tinea incognito has been reported.^[22] )
• Reactions have previously been reported after radiation treatment of tinea capitis.
• Vesicles may be present on the hands or feet.
• Fingers may be tender.
• Travel history relating to infectious agent exposure may be relevant.
• A history of cultural or religious practices may indicate possible contact allergens leading to an id reaction.

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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:

• A widespread symmetrical eruption of small follicular papules associated with a kerion and a pompholyxlike eruption are usually associated with inflammatory tinea pedis (common).^[23]
• An acute, intensely pruritic, symmetric maculopapular or papulovesicular reaction that involves the forearms, thighs, legs, trunk, face, hands, neck, and feet (in descending order of frequency) is typical of the id reaction with stasis dermatitis (common).
• Erysipelaslike eruption on the anterior leg secondary to a dermatophytosis may occur (less common).
• Extracutaneous manifestations include fever, anorexia, generalized adenopathy, splenomegaly, and leukocytosis (uncommon).
• The clinical picture may rarely mimic erythema multiforme.^[24]

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Laboratory Studies

Laboratory workup of id reactions (autoeczematization) is clearly indicated for dermatophytids (id reactions from dermatophytes). 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. Laboratory investigations require suspicion of the underlying cause and must be designed accordingly, as in the case of syphilid or tuberculid.

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Other Tests

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

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Procedures

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

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Histologic Findings

Histopathologic evaluation 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.

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Medical Care

The goal of medical care is adequate treatment of the underlying infection or dermatitis, which should lead to prompt resolution of the id reaction (autoeczematization). Recurrences are common, especially if the primary source is not treated adequately. The id reaction itself can be treated with topical steroids, systemic steroids, or antihistamines, but such treatment should not be instituted before infectious causes are eradicated.

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Complications

Complications can include secondary infection resulting from excoriation, as well as secondary allergic contact dermatitis from topically applied medicaments or emollients and the use of medications targeting etiologies and symptoms.

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Consultations

If a severe underlying infection is present, consultation with an infectious disease specialist or an internist is warranted.

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Amcinonide (Cyclocort)

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Fluocinonide (Lidemol, Lidex, Lyderm)

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Prednisone (Deltasone, Prednisone Intensol, Rayos)

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Methylprednisolone (A-Methapred, DepoMedrol, Medrol)

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Diphenhydramine (Alka-Seltzer Plus Allergy, Benadryl, Benadryl Allergy Dye-Free LiquiGels)

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Loratadine (Alavert, Claritin, Claritin RediTabs)

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