eMedicine Specialties > Dermatology > Allergy & Immunology

Id Reaction (Autoeczematization)

Matthew P Evans, MD, Dermatology, Dreyer Medical Group
Darryl Bronson, MD, MPH, Chairman, Program Director, Division of Dermatology, Department of Medicine, Cook County Hospital of Chicago; Professor, Departments of Dermatology and Pathology, University of Illinois at Chicago

Updated: Feb 25, 2009

Introduction

Background

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 or bacterid when associated with a corresponding infectious process. Clinical and histopathological manifestations are variable and depend on the etiology of the eruption.

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,^3,4 (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.

Frequency

United States

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.

Mortality/Morbidity

Morbidity results from symptoms of the id reaction and the acute onset of the primary eruption.

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.

Clinical

History

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, maculopapular, 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.⁵ )
• 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.

Physical

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).
• 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.⁶

Causes

• Etiology of id reactions
  • Infections with dermatophytes, pulmonary histoplasmosis,⁷ mycobacteria,⁸ viruses, bacteria, or parasites (pediculosis)²
  • Contact dermatitis, stasis dermatitis, or other eczematous dermatoses
  • Papulonecrotic tuberculid,⁹ and some other tuberculids, 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.

Differential Diagnoses

Workup

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.

Procedures

• Biopsy for routine hematoxylin and eosin staining may be helpful in excluding noneczematous dermatoses, which may appear morphologically similar to an id reaction.
• Patch testing may be necessary to identify a contact allergen.

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.

Treatment

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 eruption
  • Systemic or topical corticosteroids
  • Wet compresses
  • Systemic or topical antihistamines

Consultations

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

Medication

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

Corticosteroids

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

Amcinonide (Cyclocort)

Suppresses mitotic activity and causes vasoconstriction. Stimulates synthesis of enzymes needed to decrease inflammation.

Dosing

Adult

Apply sparingly bid/qid as severity warrants

Pediatric

Administer as in adults; exercise caution in patients <2 y who have a relatively larger body surface area-to-weight ratio

Interactions

None reported

Contraindications

Documented hypersensitivity; herpes simplex virus infection; fungal, viral, or tubercular skin lesions

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause adverse systemic effects if used over large areas, on denuded skin, under occlusive dressings, or for prolonged treatment periods; systemic absorption may cause Cushing syndrome, reversible HPA axis suppression, and other systemic adverse effects (see below); do not use potent corticosteroids in areas of decreased skin circulation; use weaker-strength topical steroids for facial or intertriginous regions; local adverse reactions include skin atrophy, folliculitis, steroid acne, telangiectasias, and striae; topical steroids have been associated with secondary allergic contact dermatitis

Fluocinonide (Fluonex, Lidex)

High-potency steroid that inhibits cell proliferation. Is immunosuppressive, antiproliferative, and anti-inflammatory. Also has antipruritic and vasoconstrictive properties.

Dosing

Adult

Apply sparingly bid/qid based on severity

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; herpes simplex infection; fungal, viral, or tubercular skin lesions

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause adverse systemic effects if used over large areas, denuded areas, on occlusive dressings, or during prolonged treatment periods

Prednisone (Orasone, Sterapred, Deltasone)

Commonly used oral agent. Indicated for severe, prolonged, or anaphylactic reactions. Decrease late immune-mediated complications. Must be metabolized to the active metabolite prednisolone for effect. Conversion may be impaired in liver disease.

Dosing

Adult

40-60 mg/d PO divided 1-2 doses/d

Pediatric

0.5-2 mg/kg/d PO divided 1-4 doses/d

Interactions

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective-tissue infections, and fungal or tubercular skin infections; GI bleeding or ulceration

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

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

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Indicated for severe, prolonged, or anaphylactic reactions. Decrease late immune-mediated complications.

Dosing

Adult

4-48 mg/d PO
Acetate/Depo-Medrol: 40-120 mg IM single dose

Pediatric

0.16-0.8 mg/kg/d PO divided bid/qid
Sodium succinate/Solu-Medrol: 0.5-2 mg/kg per dose IV/IM repeated at intervals depending on clinical response

Interactions

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics; grapefruit juice increases concentrations; methylprednisolone and cyclosporine mutually inhibit one another, resulting in increased plasma levels of each drug

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Depo-Medrol contains benzyl alcohol, which is potentially toxic when administered locally to neural tissue; administration of Depo-Medrol by other than indicated routes, including the epidural route, has been associated with reports of serious medical events including arachnoiditis, meningitis, paraparesis/paraplegia, sensory disturbances, bowel/bladder dysfunction, seizures, visual impairment including blindness, ocular and periocular inflammation, and residue or slough at injection site

Antihistamines

These agents relieve pruritus. May control itching by blocking effects of endogenously released histamine.

Diphenhydramine (Benadryl, Benylin, Caladryl, Dermapax)

First-generation antihistamine with anticholinergic effects that binds to H1 receptors in the CNS and the body.
Competitively blocks histamine from binding to H1 receptors. Has significant antimuscarinic activity and penetrates CNS, which causes 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.
For symptomatic relief of symptoms caused by release of histamine in allergic reactions.

Dosing

Adult

25-50 mg PO q6-8h prn; may administer as single 25- 50-mg qhs dose if somnolence exists; not to exceed 400 mg/d
10-50 mg IV/IM q6-8h prn; not to exceed 400 mg/d
Topical: Apply to affected area tid/qid

Pediatric

>10 lb: 12.5-25 mg PO tid/qid or 5 mg/kg/d or 150 mg/m²/d divided tid/qid; not to exceed 300 mg/d
5 mg/kg/d IV/IM or 150 mg/m²/d divided qid; not to exceed 300 mg/d
Topical: Administer as in adults

Interactions

Potentiates effect of CNS depressants; due to alcohol content, do not give syrup dosage form to patient taking medications that can cause disulfiramlike reactions

Contraindications

Documented hypersensitivity; MAOIs

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, or urinary tract obstruction; xerostomia may occur

Loratadine (Claritin, Alavert)

Selectively inhibits peripheral histamine H1 receptors. Tolerated well, with rate of sedation not significantly different from placebo.

Dosing

Adult

10 mg/d PO on empty stomach

Pediatric

<6 years: Not established
>6 years: Administer as in adults

Interactions

Ketoconazole, erythromycin, procarbazine, and alcohol may increase levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Initiate therapy at lower dose in liver impairment

Follow-up

Complications

• Secondary infection
• Secondary allergic contact dermatitis from topically applied medicaments/emollients

Prognosis

• Prognosis is good once the inciting etiology has been identified and appropriately treated.

Miscellaneous

Medicolegal Pitfalls

• The chance of medical or legal liability is slight provided the inciting etiology is identified and addressed.

References

1. Brown A, Sorey W. To Itch, Perchance to Scratch. Clin Pediatr (Phila). Nov 17 2008;[Medline].

2. Brenner S, Ophir J, Krakowski A. Pediculid. An unusual -id reaction to pediculosis capitis. Dermatologica. 1984;168(4):189-91. [Medline].

3. Cunningham MJ, Zone JJ, Petersen MJ, Green JA. Circulating activated (DR-positive) T lymphocytes in a patient with autoeczematization. J Am Acad Dermatol. Jun 1986;14(6):1039-41. [Medline].

4. Kasteler JS, Petersen MJ, Vance JE, Zone JJ. Circulating activated T lymphocytes in autoeczematization. Arch Dermatol. Jun 1992;128(6):795-8. [Medline].

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8. Choudhri SH, Magro CM, Crowson AN, Nicolle LE. An Id reaction to Mycobacterium leprae: first documented case. Cutis. Oct 1994;54(4):282-6. [Medline].

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11. Belsito DV. Autosensitization dermatitis. In: Freedberg M, Eisen AZ, Wolff K, et al, eds. Fitzpatrick's Dermatology in General Medicine. 5^th ed. New York, NY: McGraw-Hill; 1999:1462-4.

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17. Gonzalez-Amaro R, Baranda L, Abud-Mendoza C, Delgado SP, Moncada B. Autoeczematization is associated with abnormal immune recognition of autologous skin antigens. J Am Acad Dermatol. Jan 1993;28(1):56-60. [Medline].

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Keywords

Id reaction, autoeczematization, autosensitization, pruritic rash, dermatophytids, dermatophytid reactions, dermatophyte infections, stasis dermatitis

Contributor Information and Disclosures

Author

Matthew P Evans, MD, Dermatology, Dreyer Medical Group
Matthew P Evans, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Darryl Bronson, MD, MPH, Chairman, Program Director, Division of Dermatology, Department of Medicine, Cook County Hospital of Chicago; Professor, Departments of Dermatology and Pathology, University of Illinois at Chicago
Darryl Bronson, MD, MPH is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, Illinois State Medical Society, Noah Worcester Dermatological Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Donald Belsito, MD, Clinical Professor, Department of Internal Medicine, Division of Dermatology, University of Missouri at Kansas City; Private Practice, American Dermatology Associates, LLC
Donald Belsito, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Dermatology Foundation, Kansas Medical Society, Noah Worcester Dermatological Society, Phi Beta Kappa, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, Chief, Division of Dermatology, University of Louisville School of Medicine
Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology
Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Honoraria Consulting; Centocor Honoraria Consulting; Genetech Honoraria Consulting; Celgene Honoraria Consulting

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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