Erythema Ab Igne Workup

  • Author: Laila I Alotaibi, MD, MSc; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Apr 23, 2010
 

Laboratory Studies

Laboratory findings may be abnormal if the erythema ab igne is associated with a systemic disease.

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Procedures

Perform a 3- or 4-mm punch biopsy if the diagnosis of erythema ab igne is uncertain.

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Histologic Findings

Microscopic changes in erythema ab igne depend on the type of heat, the length of exposure, and the area of the body involved.[13]

Epidermis

Histologically, erythema ab igne is similar to actinic keratoses, with the epidermis showing squamous atypia.[13] Early erythema ab igne shows atrophy of the malpighian layer and increased epidermal and upper dermal melanin with dermal vasodilatation.[12] Advanced cases show epidermal vacuolation, focal hyperkeratosis, and dyskeratosis.[12] Epidermal dysplasia within abnormal elastic tissue may also be seen.[12] In early erythema ab igne lesions, epidermal atrophy with loss of the rete ridges is seen. Some patients show focal or confluent hyperkeratosis, dyskeratosis, keratinocyte atypia, and, occasionally, melanocyte atypia.[30] Hyperpigmentation, with focal degenerative changes of basal keratinocytes, is seen.[30] Similar alterations can be observed in chronic actinic skin damage.[30]

Dermis

Melanin incontinence occurs with melanophages present in the upper dermis.[30] Collagen degeneration and a relative increase in dermal elastic tissue are seen. In contrast to solar elastosis, this is not basophilic on hematoxylin and eosin–stained specimens.[30] Telangiectasis within the papillary dermis and occasional hemosiderin may be seen more commonly on the legs in patients with erythema ab igne.[30] An apparent functional activation of melanocytes with numerical increase of dendritic processes is also observed.[30] Abundant melanophages and occasional elastic fiber alterations as seen, similar to actinic elastosis. No alterations consistent with preneoplastic skin conditions are observed.[30]

Increased elastosis with fragmented collagen fibers are seen.[12] Minimal basophilia and homogenization of elastic fibers, which are prominent in solar elastosis, are seen in erythema ab igne.[12] Both melanophages and hemosiderin are seen in the dermis.[12] Varying degrees of dermal lymphohistiocytic infiltration are present.[12] Extravasation of red blood cells in inconsistent.[12] Accumulation of dermal elastic tissue can be seen, which is an early sign of both UV radiation- and heat-induced skin damage.[13]

Other considerations

Squamous cell carcinoma and Merkel cell carcinoma may arise in the lesions of erythema ab igne on rare occasions.[13] The most common thermally induced cancer, squamous cell carcinoma, tends to occur after a long latent period of more than 30 years.[13] Squamous cell carcinoma in burn scars often begins as a chronic ulcer, which slowly enlarges and tends not to heal. Although these carcinomas tend to be of low-to-intermediate grade histologically, they may also be aggressive, with metastases and a poor prognosis reported in greater than 30% of cases.[13] Merkel cell carcinoma is an aggressive neoplasm, characterized by local recurrence in approximately 30% of cases and up to 30% mortality.[13]

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Contributor Information and Disclosures
Author

Laila I Alotaibi, MD, MSc  Dermatologist, Rashid Hospital, Dubai Health Authority, United Arab Emirates

Disclosure: Nothing to disclose.

Coauthor(s)

Anwar Al Hammadi, MD, FRCPC  Consultant and Head of Dermatology, Rashid Hospital, Dubai Health Authority; Clinical Assistant Professor of Dermatology, University of Sharjah, United Arab Emirates

Anwar Al Hammadi, MD, FRCPC is a member of the following medical societies: American Academy of Dermatology, Canadian Dermatology Association, Royal College of Physicians and Surgeons of Canada, and Skin Cancer Foundation

Disclosure: Nothing to disclose.

Specialty Editor Board

Marjan Garmyn, MD, PhD  Professor, Faculty of Medicine, Katholieke Universiteit Leuven, Belgium; Chair and Adjunct Head, Department of Dermatology, University of Leuven, Belgium

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Edward F Chan, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine

Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

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.

References

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