A 67-year-old Black woman presented with a long-standing history of pruritus and “scaly thick bumps” on the lower extremities. Upon further questioning, she reported a 30-year history of placing her feet by an electric space heater and daily baths in “very hot” water. A review of systems and medical history were unremarkable, and the patient was not on any medications. Initial physical examination of the lower extremities demonstrated lichenified plaques and scattered, firm, ulcerated nodules surrounded by mottled postinflammatory hyperpigmentation with sharp demarcation at the midcalf bilaterally (Figure 1).
Subsequently, the patient was shown to have multiple actinic keratoses and SCCs, both in situ and invasive, within the areas of EAI (Figure 2). The patient had no actinic keratoses or other cutaneous malignant neoplasms elsewhere on the skin. Management of actinic keratoses, SCC in situ, and invasive SCC on the lower extremities included numerous excisions, treatment with liquid nitrogen, and topical 5-fluorouracil under occlusion. The patient continues to be monitored frequently.
Presentation of EAI
Erythema ab igne is a cutaneous reaction resulting from prolonged exposure to an infrared heat source at temperatures insufficient to cause a burn (37 °F to 113 °F [2.78 °C to 45 °C]). Initially presenting as transient blanchable erythema, chronic heat exposure induces persistent areas of reticular erythema, often accompanied by hyperpigmentation, epidermal atrophy, and telangiectases.1 Erythema ab igne is most commonly reported on the anterior shins, inner thighs, and back, and it is historically associated with open fires and coal stoves. More recently, other implicated causes include heating pads, laptop computers, heated furniture, and electric space heaters.2,3 Erythema ab igne often is asymptomatic but can present with pruritus and a burning sensation. Treatment involves removal of the inciting heat source, which might allow resolution of early-stage lesions. Long-term exposure leads to permanent skin discoloration and on occasion predisposes patients to malignant transformation.3
Histopathology of EAI
Histologically, later stages of EAI can demonstrate focal hyperkeratosis with dyskeratosis and increased dermal elastosis, similar to actinic damage, with a predisposition to develop SCC.2 Notably, early reports document various heat-induced carcinomas, including kangri-burn cancers among Kashmiris, kang thermal cancers in China, and kairo cancers in Japan.2,4,5 More recent reports identify cutaneous carcinomas arising specifically in the setting of EAI, most commonly SCC3; Merkel cell carcinoma and cutaneous marginal zone lymphoma are less commonly reported malignancies.6,7 Given the frequency of malignant transformation within sites of thermal exposure, chronic heat exposure may share a common pathophysiology with SCC and other neoplasms, including Merkel cell carcinoma and cutaneous marginal zone lymphoma.
SCC in Black Individuals
Squamous cell carcinoma is the most common skin cancer in Black individuals, with a notably higher incidence in high-risk subpopulations (immunosuppressed patients). Unlike White individuals, SCCs frequently occur in non–sun-exposed areas in Black individuals and are associated with unique risk factors, such as human papillomavirus, as demonstrated in Black transplant patients.8 A retrospective study examining the characteristics of SCC on the legs of Black individuals documented atypical hyperkeratotic neoplasms surrounded by abnormal pigmentation and mottling of surrounding skin.9 Morphologic skin changes could be the result of chronic thermal damage: Numerous patients reported a history of leg warming from an open heat source. Other patients had an actual diagnosis of EAI. The predilection for less-exposed skin suggests UV radiation (UVR) might be a less important predisposing risk factor for this racial group, and the increased mortality associated with SCC in Black individuals might represent a more aggressive nature to this subset of SCCs.9 Furthermore, infrared radiation (IRR), such as fires and coal stoves, might have the potential to stimulate skin changes similar to those associated with UVR and ultimately malignant changes.
Compared to UVR, little is known about the biological effects of IRR (wavelength, 760 nm to 1 mm), to which human skin is constantly exposed from natural and artificial light sources. Early studies have demonstrated the carcinogenic potential of IRR, observing an augmentation of UVR-induced tumorigenesis in the presence of heat. More recently, IRR was observed to stimulate increased collagenase production from dermal fibroblasts and influence pathways (extracellular signal-related kinases 1/2 and p38 mitogen-activated protein kinases) in a similar fashion to UVB and UVA.10,11 Therefore, IRR might be capable of eliciting molecular responses comparable to those caused by UVR.
Although SCC in association with EAI is uncommon, historical reports of thermal cancers and scientific observations of IRR-induced biological and molecular effects support EAI as a predisposing risk factor for SCC and the important need for close monitoring by physicians. Studies are needed to further elucidate the pathologic effects of IRR, with more promotion of caution relating to thermal exposure.