eMedicine Specialties > Dermatology > Allergy & Immunology

Id Reaction (Autoeczematization): Treatment & Medication

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

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.

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

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

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.

Adult

Apply sparingly bid/qid based on severity

Pediatric

Apply as in adults

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

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.

Adult

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

Pediatric

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

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

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

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.

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

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

Documented hypersensitivity; viral, fungal, or tubercular skin infections

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.

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

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

Documented hypersensitivity; MAOIs

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.

Adult

10 mg/d PO on empty stomach

Pediatric

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

Ketoconazole, erythromycin, procarbazine, and alcohol may increase levels

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

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

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.

  26. Trattner A, David M. Tefillin dermatitis. J Am Acad Dermatol. May 2005;52(5):831-3. [Medline].

Further Reading

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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