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, 5, 6, 7]

See the image below.

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

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.[10] Id reaction has also been noted with BCG therapy.[11]

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

• Papulonecrotic tuberculid[17] and some other tuberculids: These are now thought to be true cutaneous forms of tuberculosis and not id reactions because of the identification (by polymerase chain reaction) of Mycobacterium tuberculosis in lesions. However, id reactions have been reported following BCG vaccination.[18]

Frequency

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.

Race

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

Sex

The condition has no known predilection for either sex.

Age

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:

• 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.[19] )

• 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.

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).[20]

• 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.[21]

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.

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.

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.

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:

• Systemic or topical corticosteroids

• Wet compresses

• Systemic or topical antihistamines

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.

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

Amcinonide (Cyclocort)

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

Fluocinonide (Fluonex, Lidex)

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)

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)

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

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

Diphenhydramine (Benadryl, Benylin, Caladryl, Dermapax)

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)

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