A 67-year-old woman seen in clinic for unrelated concerns is incidentally noted to have a “rash” on her flank. She says it appeared in adulthood and has been stable for some years. On the right lower back, there is an asymptomatic reticulated erythema without scale or ulceration (Figure). The patient admits to regular heating pad use on her lower back for pain. The remainder of the skin examination is within normal limits.
Answer: C – Erythema Ab Igne (EAI)
Erythema Ab Igne: A Quick Review
EAI is also known as “toasted skin syndrome” and in recent years has been referred to as “laptop thigh.” The condition arises from prolonged exposure to heat—infrared radiation. This well-established diagnosis has been known for centuries. Historically, EAI resulted from sitting in front of heated brick beds in northern China (kang cancers). It was also associated with exposure to coal-burning baskets in Kashmir and India (Kangri cancers).1 Continuous thermal radiation can lead to sequelae that range from reticulated erythema and scaling to hyperpigmentation and telangiectasia. Mild pruritus and burning may be evident, but EAI often is asymptomatic.2
Common sources of infrared radiation include heating blankets, heated car seats, and laptop computers (“thigh burn”). Hazardous exposure to heat affects occupations such as jewelers (facial exposure) and bakers (arm exposure). EAI may be the only cutaneous manifestation of splenomegaly, pancreatitis, and peptic ulcer disease, where topical heat is used for pain management. Recently, it was reported that the bullous variant of EAI can be associated with normochromic normocytic anemia and subclinical hypothyroidism.5 Currently, however, the pathogenesis of this association is unclear.5
There are several theories regarding the pathogenesis of EAI. The prevailing hypothesis suggests that thermal radiation induces damage to superficial blood vessels. Local vasodilation of the superficial subcutaneous plexus in the papillary dermis results in a reticular “net like” patterned erythema. Chronic heat injury to these vessels results in vascular damage, extravasation of red blood cells and deposition of hemosiderin, resulting in chronic hyperpigmentation.3
EAI has become less common in the U.S. since the advent of central heating.1 It is still seen where fireplaces are in routine use. Classically, EAI was found in women who spent a significant amount of time in front of a stove or open flame; lesions would be found on the inner thighs and legs. With the introduction of heating pads and, most recently, laptop computers, the relevant demographics are shifting to younger persons.4
Chronic EAI can lead to the development of dysplastic keratinocytes, ultimately resulting in thermal keratosis and squamous cell carcinoma. Typically, these are latent complications that appear 2 to 3 decades after skin damage is incurred.2
The differential diagnoses for EAI include cutis marmorata, livedo reticularis, livedoid vasculitis, poikiloderma atrophicans vasculare, and poikiloderma vasculare atrophicans (parapsoriasis variegata). Cutis marmorata is seen in the newborn infant with exposure to low environmental temperatures. The lacy reticulated red or blue cutaneous pattern presents in a generalized pattern. Livedo reticularis also is a more generalized presentation than EAI; it is a blanching dermatitis that results from numerous underlying pathologies including hypercoagulability. Poikiloderma atrophicans vasculare is a rare variant of mycosis fungoides. If the diagnosis is unclear, a skin biopsy may confirm.2
No definitive medical care is available for EAI. If detected early, discontinuation of exposure can result in spontaneous resolution of dyschromia. Advanced cases have been successfully treated with tretinoin and 5-fluorouracil. Overall, prognosis is good, although rarely squamous cell carcinoma may result.4
EAI has been recognized as a skin complication of heat exposure for years, but as our specific exposures change, so does its distribution and epidemiology. Education and prevention are important as well as recognizing complication of skin exposure.
1. Nordlund JJ, Boissy RE, Hearing VJ, King RA, Oetting WS, Ortonne J-P, eds. The Pigmentary System. 2nd ed. Wiley-Blackwell. New Jersey.
2. Dvoretzky I, Silverman NR. Reticular erythema of the lower back. Erythema ab igne. Arch Dermatol. 1991;127:405-6, 408-9.
3. Rapini RP, Bolognia JL, Jorizzo JL. Dermatology. 2-Volume Set. Mosby. ISBN 1-4160-2999-0: St. Louis; 2008: Chapter 87.
4. Roth D, London M. Acridine probe study into synergistic DNA-denaturing action of heat and ultraviolet light in squamous cells. J Invest Dermatol. 1977;69:368-372.
5. Arrington JH 3rd, Lockman DS. Thermal keratoses and squamous cell carcinoma in situ associated with erythema ab igne. Arch Dermatol. 1979;115:1226-1228.
6. Turan E, Cimen V, Kutlu Haytoglu NS, Göde ED, Gürel MS. A case of bullous erythema ab igne accompanied by anemia and subclinical hypothyroidism. Dermatol Online J. 2014;20:22336.