Id reaction
| Id reaction | |
|---|---|
| Other names | Cutaneous autosensitization |
| Specialty | Dermatology |
Id reactions(also known as "disseminated eczema",[1]and "generalized eczema"[1]) are types of acutedermatitisdeveloping after days or weeks at skin locations distant from the initial inflammatory or infectious site. They can be localised or generalised.[2][3]This is also known as an 'autoeczematous response'[4]and there must be an identifiable initial inflammatory or infectious skin problem which leads to the generalised eczema. Often intensely itchy, the redpapulesandpustulescan also be associated withblistersand scales and are always remote from the primary lesion.[5]It is most commonly a blistering rash with itchyvesicleson the sides of fingers and feet as a reaction tofungal infectionon the feet,athlete's foot.[6]Stasis dermatitis,allergic contact dermatitis,acute irritant contact eczemaandinfective dermatitishave been documented as possible triggers, but the exact cause and mechanism is not fully understood.[7]Several other types of id reactions exist includingerythema nodosum,erythema multiforme,Sweet's syndromeandurticaria.[3]
Presentation
[edit]Complications
[edit]Id reactions left untreated may become infected with bacteria.[2]
Causes
[edit]Causes include infection withdermatophytosis,Mycobacterium,viruses,bacteria and parasites. Eczematous conditions including contact allergic dermatitis andstasis dermatitisas well asstitchesand trauma have also been associated with id reactions.[2]Radiation treatmentoftinea capitishas been reported as triggering an id reaction.[8]
Pathogenesis
[edit]Potential explanations include
- Atypical immune recognition of autologous skinantigens
- Stimulation of normalT cellsby changing skin constituents
- Lower threshold for skin irritation
- Spreading of infectious antigens causing a secondary response
- Hematogenous dissemination ofcytokinesfrom the primary site of inflammation[2]
Diagnosis
[edit]Although there are a multitude of varying appearances, the id reaction often presents with symmetrical red patches of eczema with papules and vesicles, particularly on the outer sides of the arms, face and trunk which occur suddenly and are intensely itchy occur a few days to a week after the initial allergic or irritant dermatitis. Most commonly, athlete's foot can lead to localised vesicles on hands, bacterial infections toerythema nodosumandherpes simplex virustoerythema multiforme.[2][3]
The diagnosis is frequently made by treating the initial triggering skin problem and observing the improvement in the eczematous rash. Both the initial skin problem and the id reaction must be observed to make the diagnosis.[5][6]
Not alldyshidroticrashes are id reactions, but id reactions are often dyshidrotic-like.[2]
Initial tests may include isolating a fungus by taking a swab and sending it for culture.Patch testingmay be considered if there is suspicion of allergic contact dermatitis.[2]
A skin biopsy is rarely necessary,[2]but if done mostly shows an interstitial granulomatous dermatitis, somelesionsbeing spongiotic.[4]Id reactions cannot be distinguished from other skin diseases by histopathology. However, they can be distinguished from other id reactions by histopathology.[3]
Differential diagnosis
[edit]Other rashes that occur in a widespread distribution can look like an id reaction. These includeatopic dermatitis,contact dermatitis,dyshidrosis,photodermatitis,scabiesanddrug eruptions.[2]
Treatment
[edit]Id reactions are frequently unresponsive tocorticosteroidtherapy, but clear when the focus of infection or infestation is treated.[9][5]: 81 Therefore, the best treatment is to treat the provoking trigger. Sometimes medications are used to relieve symptoms. These includetopical corticosteroids,andantihistamines.Ifopportunisticbacterial infection occurs,antibioticsmay be required.[2]
Prognosis
[edit]A full recovery is expected with treatment.[2]Recurrent id reactions are frequently due to inadequate treatment of the primary infection or dermatitis and often the cause of recurrence is unknown.[3]
Epidemiology
[edit]With no particular affinity to any particular ethnic group, seen in all age groups and equally amongst males and females, the precise prevalence is not known.[2]
History
[edit]The suffix-idhas its origins inGreek,referring to a father–son relationship. German dermatologistJosef Jadassohn(1863–1936), who coined the termid,had observed a dermatophytosis causing a secondary allergic skin dermatitis. In 1928, Bloch recorded that the peak of the dermatophyte infection corresponded with the id reaction.[3]
See also
[edit]References
[edit]- ^abRapini RP, Bolognia JL, Jorizzo JL (2007).Dermatology: 2-Volume Set.St. Louis: Mosby. p. 224.ISBN978-1-4160-2999-1.Archived fromthe originalon 2020-08-22.Retrieved2018-06-15.
- ^abcdefghijklFerri FF (2018).Ferri's Clinical Advisor 2018: 5 Books in 1.Philadelphia, PA: Elsevier. p. 690.ISBN978-0-323-28049-5.OCLC989151714.
- ^abcdefIlkit M, Durdu M, Karakaş M (August 2012). "Cutaneous id reactions: a comprehensive review of clinical manifestations, epidemiology, etiology, and management".Critical Reviews in Microbiology.38(3): 191–202.doi:10.3109/1040841X.2011.645520.PMID22300403.S2CID43906095.
- ^abPatterson JW, Hosler G (2014-12-07).Weedon's skin pathology(Fourth ed.). pp. 103–134.ISBN978-0-7020-6200-1.OCLC900724639.
- ^abcFitzpatrick JE, High WA (2017-07-28).Urgent care dermatology: symptom-based diagnosis.Philadelphia, PA: Elsevier. pp. 135–162.ISBN978-0-323-48553-1.OCLC994056971.
- ^abHabif TP (2016).Clinical Dermatology: A color guide to diagnosis and therapy(Sixth ed.). St. Louis, Mo.: Elsevier. pp. 90–125.ISBN978-0-323-26607-9.OCLC911266496.
- ^"International Classification of Diseases 11th Revision".World Health Organization.
- ^Evans MP, Bronson D, Belsito D (October 2020). Vinson RP, Callen JP, Elston DM (eds.)."Id Reaction (Autoeczematization) Clinical Presentation: History, Physical Examination, Causes".emedicine.medscape.com.Retrieved2017-11-25.
- ^James WD, Berger T, Elston D (2006).Andrews' diseases of the skin: clinical dermatology(10th ed.). Philadelphia: Saunders Elsevier.ISBN978-0-7216-2921-6.