eMedicine Specialties > Dermatology > Allergy & Immunology

Id Reaction (Autoeczematization)

Author: Matthew P Evans, MD, Dermatology, Dreyer Medical Group
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
Contributor Information and Disclosures

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

More on Id Reaction (Autoeczematization)

Overview: Id Reaction (Autoeczematization)
Differential Diagnoses & Workup: Id Reaction (Autoeczematization)
Treatment & Medication: Id Reaction (Autoeczematization)
Follow-up: Id Reaction (Autoeczematization)
References
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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].

  5. Al Aboud K, Al Hawsawi K, Alfadley A. Tinea incognito on the hand causing a facial dermatophytid reaction. Acta Derm Venereol. 2003;83(1):59. [Medline].

  6. Atzori L, Pau M, Aste M. Erythema multiforme ID reaction in atypical dermatophytosis: a case report. J Eur Acad Dermatol Venereol. Nov 2003;17(6):699-701. [Medline].

  7. Crum N, Hardaway C, Graham B. Development of an idlike reaction during treatment for acute pulmonary histoplasmosis: a new cutaneous manifestation in histoplasmosis. J Am Acad Dermatol. Feb 2003;48(2 Suppl):S5-6. [Medline].

  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].

  9. Morrison JG, Fourie ED. The papulonecrotic tuberculide. From Arthus reaction to lupus vulgaris. Br J Dermatol. Sep 1974;91(3):263-70. [Medline].

  10. Ackerman AB, Chongchitnant N, Sanchez J, et al. Allergic contact dermatitis/nummular dermatitis/dyshidrotic dermatitis/id reaction. In: Histologic Diagnosis of Inflammatory Skin Diseases. Baltimore, Md: Williams & Wilkins; 1997:184-6.

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

  12. Brenner S, Wolf R, Landau M. Scabid: an unusual id reaction to scabies. Int J Dermatol. Feb 1993;32(2):128-9. [Medline].

  13. Champion RH, Burton JL, Burns DA, et al. Textbook of Dermatology. Boston, Mass: Blackwell; 1998:650-1,1199-1200,1315,1344.

  14. Elder DE, Elenitsas R, Jaworsky C, et al. Noninfectious vesiculobullous and vesiculopustular diseases. In: Lever's Histopathology of the Skin. Philadelphia, Pa: Lippincott-Raven; 1997:214.

  15. Freedberg IM, Eisen AZ, Wolff K, et al. Superficial fungal infection. In: Fitzpatrick's Dermatology in General Medicine. 5th ed. New York, NY: McGraw-Hill; 1999:2340-1.

  16. Fritsch P, Reider N. Eczematous Group. In: Bolognia JL, Jorizzo J, Rapini R, eds. Dermatology. Vol 1. Mo: Mosby: St. Louis; 2003:221-2.

  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].

  18. Haxthausen H. Generalized ids autosensitization in varicose eczemas. Acta Derm Venereol. 1955;35(4-5):271-80. [Medline].

  19. Heng MC, Allen SG. Predominance of CD8 subset in id eruption of poison oak-induced dermatitis. Australas J Dermatol. 1991;32(2):93-100. [Medline].

  20. Hurwitz S. Eczematous eruptions in childhood. Clin Pediatr Dermatol. 1993;77-8.

  21. Leggiadro RJ, Boscamp JR, Sapadin AN. Temporary tattoo dermatitis. J Pediatr. May 2003;142(5):586. [Medline].

  22. Lian J, Dundas G, Tron V, Lauzon G, Roa W. radiotherapy-induced ID reaction. Am J Clin Oncol. Feb 2005;28(1):105-6. [Medline].

  23. Lu LK, Dunnick CA. Navel history. Am J Med. Mar 2006;119(3):241-3. [Medline].

  24. Roper SS, Jones HE. An animal model for altering the irritability threshold of normal skin. Contact Dermatitis. Aug 1985;13(2):91-7. [Medline].

  25. Suwattee P, Warshaw EM. Self-Assessment examination of the American Academy of Dermatology-Generalized itchy eruption. J Am Acad Dermatol. 2006;55(5):923-5.

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Further Reading

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Keywords

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

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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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