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Successful Treatment of Tinea Versicolor With Salicylic Acid 30% Peel
Successful Treatment of Tinea Versicolor With Salicylic Acid 30% Peel
Tinea versicolor (TV) is a common, chronic, and recurrent superficial fungal infection caused by Malassezia species, most commonly Malassezia furfur (M. furfur)—a dimorphic fungus that is a part of the normal skin flora and resides in the stratum corneum.1 TV manifests as hypopigmented, hyperpigmented, or erythematous macules and patches with scaling, typically found on the trunk and proximal upper extremities. The condition is most common among young to middle-aged individuals exposed to high temperatures and humidity.1
While many cases respond to topical antifungal treatment, application can be cumbersome, particularly in large areas that are difficult to reach. An efficient and cost effective in-office treatment option could alleviate patient burden and improve satisfaction. This article presents a case of TV successfully treated with an in-office salicylic acid (SA) 30% peel, an uncommon application of this medication.
Case Presentation
An 18-year-old female active-duty US Army service member with a history of acne vulgaris presented to a dermatology clinic with a mildly pruritic rash that had been present for several weeks. An examination revealed hyperpigmented macules and patches with overlying fine scales across the patient’s back and bilateral arms (Figures 1 and 2). She reported no history of similar lesions. The patient had recently completed a military basic training course during which she wore a uniform jacket and trousers daily in hot and humid conditions. A skin scraping was obtained. Microscopic examination with potassium hydroxide preparation revealed hyphae and spores, consistent with TV.
The diagnosis of TV and treatment options (topical ketoconazole 2% shampoo, topical terbinafine, or oral fluconazole) were discussed with the patient. Due to military training-related constraints, residence in the barracks, and personal preference, the patient felt unable to regularly apply topical medications to the entirety of the affected area and preferred to avoid oral medication. The decision was made to pursue in-clinic treatment with a SA 30% peel. The affected areas (back and bilateral arms) were thoroughly cleansed and prepped with alcohol. SA 30% in hydroethanolic solution was applied evenly to the affected area. The patient was observed for pseudofrosting, a precipitation of SA crystals that indicates peel completion (Figure 3). The peel was left in place, as it is self-neutralizing, and the patient was instructed to shower that same day with a gentle cleanser. This procedure was repeated 10 days later. Both treatments were well tolerated, with only a transient burning sensation reported during the application. At 3-week follow-up, the patient presented with complete resolution of her arm lesions and significant improvement of the back lesions (Figures 4 and 5). She also reported improvement in the acne vulgaris on her back.
Discussion
SA 30% is a lipid-soluble hydroxybenzoic acid with comedolytic and desmolytic qualities. This results in the disruption of epidermal cell cohesion and promotes exfoliation.2 Lipophilic properties allow SA to penetrate sebaceous glands and disrupt sebum production, making it particularly effective in seborrheic conditions such as acne. This mechanism may have increased therapeutic effect in this case.3 Additionally, as a salicylate, SA possesses anti-inflammatory properties, though this effect is most pronounced at lower concentrations. SA 30% is considered a superficial peel, as the depth of chemexfoliation is limited to the epidermis.3 A modified SA preparation is a safe and effective treatment for moderate-to-severe acne vulgaris. The apparent pseudofrost during application is due to precipitated SA, rather than the precipitation of dermal proteins seen in deeper peels, such as trichloroacetic acid.2 Unlike glycolic or pyruvic acid peels, SA does not require neutralization.
SA is cost-effective and has been used safely in all skin types to treat various epidermal conditions, including acne vulgaris, melasma, photodamage, freckles, lentigines and postinflammatory hyperpigmentation (PIH).2 Mild adverse effects occur in about 15% to 30% of patients and include prolonged erythema, intense exfoliation, dryness, crusting, and pigmentary dyschromias. Rare adverse effects include systemic toxicity (salicylism) and hypoglycemia. Contraindications to SA 30% peels include history of allergy to salicylates, active bacterial or viral infection, dermatitis in the treatment area, pregnancy, and skin malignancy.2
Chemical peels are typically used with caution in patients with skin of color due to a higher risk of PIH. However, SA 30% has been shown to be safe and effective in these populations.4 A study by Grimes found that 88% of patients with Fitzpatrick skin types V and VI experienced significant improvement in PIH, melasma, or enlarged pores with minimal to no adverse effects.4 Subsequent larger studies have reinforced these findings. In a study involving 250 patients with Fitzpatrick skin types IV and V, no patients experienced PIH, confirming the safety of SA in darker skin tones. This is likely due to the superficial nature of the peel, which does not affect the basal layer of the epidermis where melanocytes reside, reducing the risk of pigmentary complications. Additionally, SA peels are self-neutralizing, unlike glycolic or trichloroacetic acid peels, which require manual neutralization and carry a higher risk of PIH if not neutralized properly.5
SA has been as shown to be a moderately successful treatment for PIH. The Grimes study found that 4 of 5 patients with Fitzpatrick skin types IV and V saw a 75% improvement in PIH after SA peels.4 Davis et al found a nonsignificant trend toward skin lightening in Korean adults treated for acne and PIH, with significant decreases in erythema and improvements in greasiness, dryness, and scaliness.6 Importantly, the risk of PIH following TV is higher in patients with skin of color.7 SA may be effective in treating TV and PIH, offering a multifactorial approach by addressing both conditions while posing a low risk for causing PIH.8
TV and other Malassezia spp infections are common concerns in dermatology and primary care, with Malassezia-associated superficial mycoses (eg, dandruff, pityriasis versicolor, and folliculitis) affecting up to 50% of the population worldwide.9 Despite this, there has been little recent advancement in antifungal treatments. Ketoconazole, terbinafine, and fluconazole have been in use since the 1980s and 1990s.8 Most antifungal drugs target ergosterol, a component of the fungal cell wall.10 Additionally, Malassezia spp have been increasingly reported to cause invasive infections in immunocompromised patients.11 Given the rise in antifungal resistance, the judicious use of antifungals and implementation of novel treatment strategies is essential.
While SA lacks intrinsic antifungal properties, different combinations (Whitfield ointment consisting of 3% SA and 6% benzoic acid; 2% sulfur and 2% SA) have been effective in the treatment of TV.1 It is theorized that the effectiveness of SA against TV is due to its ability to exfoliate and acidify the stratum corneum, the natural habitat of M. furfur.
SA also reduces sebum production by downregulating sebocyte lipogenesis via the sterol regulatory element-binding protein-1 pathway and suppressing the nuclear factor κB (NF-κB) pathway, a key pathway in inflammation.12 These mechanisms make SA an effective acne treatment. Additionally, M. furfur is a lipid-dependent yeast, thus the decreased lipogenesis by sebocytes may be beneficial in treating TV as well.12 A study of 25 patients with TV in India found that 88% achieved clinical and microbiological cure after 4 once-weekly treatments of a SA 30% peel.8
In a study of deployed military personnel, fungal infections affected about 11% of participants.13 Contributing factors to the development of fungal infections included excessive sweating, humid conditions, and limited access to hygiene facilities. In such settings, traditional antifungal therapies may be less effective or challenging to adhere to, making alternative treatments more desirable. SA peels could offer a practical solution in these circumstances, as they are easily applied in the clinic, require no neutralization or downtime, and do not require the patient to apply medications between visits.
In this case, the patient demonstrated significant improvement with 2 SA peels, with noted improvement in her acne. SA 30% peel was highlighted as a useful treatment option for patients with TV who struggle with topical medication adherence; furthermore, it may be particularly beneficial for patients with concomitant acne.
Conclusions
This case demonstrates the successful use of in-office SA 30% peel as a treatment for TV. The rapid improvement and resolution of lesions with minimal adverse effects suggest that SA peel may serve as a valuable alternative for patients with extensive disease in difficult-to-reach affected areas, or those who are dissatisfied with traditional therapies. Additionally, the concurrent improvement of the patient’s back acne underscores the dual therapeutic potential of this treatment. Given the ease of application, cost effectiveness, and favorable safety profile, SA 30% peel is a viable option in the management of TV, especially in cases where topical or oral antifungals are impractical. Further studies could help establish standardized protocols and assess long-term outcomes of this treatment modality.
- Leung AK, Barankin B, Lam JM, et al. Tinea versicolor: an updated review. Drugs Context. 2022;11:2022-9-2. doi:10.7573/dic.2022-9-2
- Arif T. Salicylic acid as a peeling agent: a comprehensive review. Clin Cosmet Investig Dermatol. 2015;8:455-461. doi:10.2147/CCID.S84765
- Shao X, Chen Y, Zhang L, et al. Effect of 30% supramolecular salicylic acid peel on skin microbiota and inflammation in patients with moderate-to-severe acne vulgaris. Dermatol Ther. 2022;13(1):155-168. doi:10.1007/s13555-022-00844-5
- Grimes PE. The safety and efficacy of salicylic acid chemical peels in darker racial-ethnic groups. Dermatol Surg Off Publ Am Soc Dermatol Surg Al. 1999;25(1). doi:10.1046/j.1524-4725.1999.08145.x
- Kang HY, Choi Y, Cho HJ. Salicylic acid peels for the treatment of acne vulgaris in Fitzpatrick skin types IV-V: a multicenter study. Dermatol Surg. Published online 2006. doi:10.1111/j.1524-4725.2006.32146.x.
- Davis EC, Callender VD. Postinflammatory hyperpigmentation. J Clin Aesthetic Dermatol. 2010;3(7):20-31.
- Kallini JR, Riaz F, Khachemoune A. Tinea versicolor in dark-skinned individuals. Int J Dermatol. 2014;53(2):137- 141. doi:10.1111/ijd.12345
- Saoji V, Madke B. Efficacy of salicylic acid peel in dermatophytosis. Indian J Dermatol Venereol Leprol. 2021;87(5). doi:10.4103/ijdvl.IJDVL_853_18
- Arce M, Gutiérrez-Mendoza D. Pityriasis versicolor: treatment update. Curr Fungal Infect Rep 2018;12(11):195–200. https://doi.org/10.1007/s12281-018-0328-7
- Leong C, Kit JCW, Lee SM, et al. Azole resistance mechanisms in pathogenic M. furfur. Antimicrob Agents Chemother. 2021;65(5):e01975-20. doi:10.1128/AAC.01975-20
- Chang HJ, Miller HL, Watkins N, et al. An epidemic of Malassezia pachydermatis in an intensive care nursery associated with colonization of health care workers’ pet dogs. N Engl J Med. 1998;338(11):706-711. doi:10.1056/NEJM199803123381102
- Lu J, Cong T, Wen X, et al. Salicylic acid treats acne vulgaris by suppressing AMPK/SREBP1 pathway in sebocytes. Exp Dermatol. 2019;28(7):786-794. doi:10.1111/exd.13934
- Singal A, Lipner SR. A review of skin disease in military soldiers: challenges and potential solutions. Ann Med. 2023;55(2):2267425. doi:10.1080/07853890.2023.2267425
Tinea versicolor (TV) is a common, chronic, and recurrent superficial fungal infection caused by Malassezia species, most commonly Malassezia furfur (M. furfur)—a dimorphic fungus that is a part of the normal skin flora and resides in the stratum corneum.1 TV manifests as hypopigmented, hyperpigmented, or erythematous macules and patches with scaling, typically found on the trunk and proximal upper extremities. The condition is most common among young to middle-aged individuals exposed to high temperatures and humidity.1
While many cases respond to topical antifungal treatment, application can be cumbersome, particularly in large areas that are difficult to reach. An efficient and cost effective in-office treatment option could alleviate patient burden and improve satisfaction. This article presents a case of TV successfully treated with an in-office salicylic acid (SA) 30% peel, an uncommon application of this medication.
Case Presentation
An 18-year-old female active-duty US Army service member with a history of acne vulgaris presented to a dermatology clinic with a mildly pruritic rash that had been present for several weeks. An examination revealed hyperpigmented macules and patches with overlying fine scales across the patient’s back and bilateral arms (Figures 1 and 2). She reported no history of similar lesions. The patient had recently completed a military basic training course during which she wore a uniform jacket and trousers daily in hot and humid conditions. A skin scraping was obtained. Microscopic examination with potassium hydroxide preparation revealed hyphae and spores, consistent with TV.
The diagnosis of TV and treatment options (topical ketoconazole 2% shampoo, topical terbinafine, or oral fluconazole) were discussed with the patient. Due to military training-related constraints, residence in the barracks, and personal preference, the patient felt unable to regularly apply topical medications to the entirety of the affected area and preferred to avoid oral medication. The decision was made to pursue in-clinic treatment with a SA 30% peel. The affected areas (back and bilateral arms) were thoroughly cleansed and prepped with alcohol. SA 30% in hydroethanolic solution was applied evenly to the affected area. The patient was observed for pseudofrosting, a precipitation of SA crystals that indicates peel completion (Figure 3). The peel was left in place, as it is self-neutralizing, and the patient was instructed to shower that same day with a gentle cleanser. This procedure was repeated 10 days later. Both treatments were well tolerated, with only a transient burning sensation reported during the application. At 3-week follow-up, the patient presented with complete resolution of her arm lesions and significant improvement of the back lesions (Figures 4 and 5). She also reported improvement in the acne vulgaris on her back.
Discussion
SA 30% is a lipid-soluble hydroxybenzoic acid with comedolytic and desmolytic qualities. This results in the disruption of epidermal cell cohesion and promotes exfoliation.2 Lipophilic properties allow SA to penetrate sebaceous glands and disrupt sebum production, making it particularly effective in seborrheic conditions such as acne. This mechanism may have increased therapeutic effect in this case.3 Additionally, as a salicylate, SA possesses anti-inflammatory properties, though this effect is most pronounced at lower concentrations. SA 30% is considered a superficial peel, as the depth of chemexfoliation is limited to the epidermis.3 A modified SA preparation is a safe and effective treatment for moderate-to-severe acne vulgaris. The apparent pseudofrost during application is due to precipitated SA, rather than the precipitation of dermal proteins seen in deeper peels, such as trichloroacetic acid.2 Unlike glycolic or pyruvic acid peels, SA does not require neutralization.
SA is cost-effective and has been used safely in all skin types to treat various epidermal conditions, including acne vulgaris, melasma, photodamage, freckles, lentigines and postinflammatory hyperpigmentation (PIH).2 Mild adverse effects occur in about 15% to 30% of patients and include prolonged erythema, intense exfoliation, dryness, crusting, and pigmentary dyschromias. Rare adverse effects include systemic toxicity (salicylism) and hypoglycemia. Contraindications to SA 30% peels include history of allergy to salicylates, active bacterial or viral infection, dermatitis in the treatment area, pregnancy, and skin malignancy.2
Chemical peels are typically used with caution in patients with skin of color due to a higher risk of PIH. However, SA 30% has been shown to be safe and effective in these populations.4 A study by Grimes found that 88% of patients with Fitzpatrick skin types V and VI experienced significant improvement in PIH, melasma, or enlarged pores with minimal to no adverse effects.4 Subsequent larger studies have reinforced these findings. In a study involving 250 patients with Fitzpatrick skin types IV and V, no patients experienced PIH, confirming the safety of SA in darker skin tones. This is likely due to the superficial nature of the peel, which does not affect the basal layer of the epidermis where melanocytes reside, reducing the risk of pigmentary complications. Additionally, SA peels are self-neutralizing, unlike glycolic or trichloroacetic acid peels, which require manual neutralization and carry a higher risk of PIH if not neutralized properly.5
SA has been as shown to be a moderately successful treatment for PIH. The Grimes study found that 4 of 5 patients with Fitzpatrick skin types IV and V saw a 75% improvement in PIH after SA peels.4 Davis et al found a nonsignificant trend toward skin lightening in Korean adults treated for acne and PIH, with significant decreases in erythema and improvements in greasiness, dryness, and scaliness.6 Importantly, the risk of PIH following TV is higher in patients with skin of color.7 SA may be effective in treating TV and PIH, offering a multifactorial approach by addressing both conditions while posing a low risk for causing PIH.8
TV and other Malassezia spp infections are common concerns in dermatology and primary care, with Malassezia-associated superficial mycoses (eg, dandruff, pityriasis versicolor, and folliculitis) affecting up to 50% of the population worldwide.9 Despite this, there has been little recent advancement in antifungal treatments. Ketoconazole, terbinafine, and fluconazole have been in use since the 1980s and 1990s.8 Most antifungal drugs target ergosterol, a component of the fungal cell wall.10 Additionally, Malassezia spp have been increasingly reported to cause invasive infections in immunocompromised patients.11 Given the rise in antifungal resistance, the judicious use of antifungals and implementation of novel treatment strategies is essential.
While SA lacks intrinsic antifungal properties, different combinations (Whitfield ointment consisting of 3% SA and 6% benzoic acid; 2% sulfur and 2% SA) have been effective in the treatment of TV.1 It is theorized that the effectiveness of SA against TV is due to its ability to exfoliate and acidify the stratum corneum, the natural habitat of M. furfur.
SA also reduces sebum production by downregulating sebocyte lipogenesis via the sterol regulatory element-binding protein-1 pathway and suppressing the nuclear factor κB (NF-κB) pathway, a key pathway in inflammation.12 These mechanisms make SA an effective acne treatment. Additionally, M. furfur is a lipid-dependent yeast, thus the decreased lipogenesis by sebocytes may be beneficial in treating TV as well.12 A study of 25 patients with TV in India found that 88% achieved clinical and microbiological cure after 4 once-weekly treatments of a SA 30% peel.8
In a study of deployed military personnel, fungal infections affected about 11% of participants.13 Contributing factors to the development of fungal infections included excessive sweating, humid conditions, and limited access to hygiene facilities. In such settings, traditional antifungal therapies may be less effective or challenging to adhere to, making alternative treatments more desirable. SA peels could offer a practical solution in these circumstances, as they are easily applied in the clinic, require no neutralization or downtime, and do not require the patient to apply medications between visits.
In this case, the patient demonstrated significant improvement with 2 SA peels, with noted improvement in her acne. SA 30% peel was highlighted as a useful treatment option for patients with TV who struggle with topical medication adherence; furthermore, it may be particularly beneficial for patients with concomitant acne.
Conclusions
This case demonstrates the successful use of in-office SA 30% peel as a treatment for TV. The rapid improvement and resolution of lesions with minimal adverse effects suggest that SA peel may serve as a valuable alternative for patients with extensive disease in difficult-to-reach affected areas, or those who are dissatisfied with traditional therapies. Additionally, the concurrent improvement of the patient’s back acne underscores the dual therapeutic potential of this treatment. Given the ease of application, cost effectiveness, and favorable safety profile, SA 30% peel is a viable option in the management of TV, especially in cases where topical or oral antifungals are impractical. Further studies could help establish standardized protocols and assess long-term outcomes of this treatment modality.
Tinea versicolor (TV) is a common, chronic, and recurrent superficial fungal infection caused by Malassezia species, most commonly Malassezia furfur (M. furfur)—a dimorphic fungus that is a part of the normal skin flora and resides in the stratum corneum.1 TV manifests as hypopigmented, hyperpigmented, or erythematous macules and patches with scaling, typically found on the trunk and proximal upper extremities. The condition is most common among young to middle-aged individuals exposed to high temperatures and humidity.1
While many cases respond to topical antifungal treatment, application can be cumbersome, particularly in large areas that are difficult to reach. An efficient and cost effective in-office treatment option could alleviate patient burden and improve satisfaction. This article presents a case of TV successfully treated with an in-office salicylic acid (SA) 30% peel, an uncommon application of this medication.
Case Presentation
An 18-year-old female active-duty US Army service member with a history of acne vulgaris presented to a dermatology clinic with a mildly pruritic rash that had been present for several weeks. An examination revealed hyperpigmented macules and patches with overlying fine scales across the patient’s back and bilateral arms (Figures 1 and 2). She reported no history of similar lesions. The patient had recently completed a military basic training course during which she wore a uniform jacket and trousers daily in hot and humid conditions. A skin scraping was obtained. Microscopic examination with potassium hydroxide preparation revealed hyphae and spores, consistent with TV.
The diagnosis of TV and treatment options (topical ketoconazole 2% shampoo, topical terbinafine, or oral fluconazole) were discussed with the patient. Due to military training-related constraints, residence in the barracks, and personal preference, the patient felt unable to regularly apply topical medications to the entirety of the affected area and preferred to avoid oral medication. The decision was made to pursue in-clinic treatment with a SA 30% peel. The affected areas (back and bilateral arms) were thoroughly cleansed and prepped with alcohol. SA 30% in hydroethanolic solution was applied evenly to the affected area. The patient was observed for pseudofrosting, a precipitation of SA crystals that indicates peel completion (Figure 3). The peel was left in place, as it is self-neutralizing, and the patient was instructed to shower that same day with a gentle cleanser. This procedure was repeated 10 days later. Both treatments were well tolerated, with only a transient burning sensation reported during the application. At 3-week follow-up, the patient presented with complete resolution of her arm lesions and significant improvement of the back lesions (Figures 4 and 5). She also reported improvement in the acne vulgaris on her back.
Discussion
SA 30% is a lipid-soluble hydroxybenzoic acid with comedolytic and desmolytic qualities. This results in the disruption of epidermal cell cohesion and promotes exfoliation.2 Lipophilic properties allow SA to penetrate sebaceous glands and disrupt sebum production, making it particularly effective in seborrheic conditions such as acne. This mechanism may have increased therapeutic effect in this case.3 Additionally, as a salicylate, SA possesses anti-inflammatory properties, though this effect is most pronounced at lower concentrations. SA 30% is considered a superficial peel, as the depth of chemexfoliation is limited to the epidermis.3 A modified SA preparation is a safe and effective treatment for moderate-to-severe acne vulgaris. The apparent pseudofrost during application is due to precipitated SA, rather than the precipitation of dermal proteins seen in deeper peels, such as trichloroacetic acid.2 Unlike glycolic or pyruvic acid peels, SA does not require neutralization.
SA is cost-effective and has been used safely in all skin types to treat various epidermal conditions, including acne vulgaris, melasma, photodamage, freckles, lentigines and postinflammatory hyperpigmentation (PIH).2 Mild adverse effects occur in about 15% to 30% of patients and include prolonged erythema, intense exfoliation, dryness, crusting, and pigmentary dyschromias. Rare adverse effects include systemic toxicity (salicylism) and hypoglycemia. Contraindications to SA 30% peels include history of allergy to salicylates, active bacterial or viral infection, dermatitis in the treatment area, pregnancy, and skin malignancy.2
Chemical peels are typically used with caution in patients with skin of color due to a higher risk of PIH. However, SA 30% has been shown to be safe and effective in these populations.4 A study by Grimes found that 88% of patients with Fitzpatrick skin types V and VI experienced significant improvement in PIH, melasma, or enlarged pores with minimal to no adverse effects.4 Subsequent larger studies have reinforced these findings. In a study involving 250 patients with Fitzpatrick skin types IV and V, no patients experienced PIH, confirming the safety of SA in darker skin tones. This is likely due to the superficial nature of the peel, which does not affect the basal layer of the epidermis where melanocytes reside, reducing the risk of pigmentary complications. Additionally, SA peels are self-neutralizing, unlike glycolic or trichloroacetic acid peels, which require manual neutralization and carry a higher risk of PIH if not neutralized properly.5
SA has been as shown to be a moderately successful treatment for PIH. The Grimes study found that 4 of 5 patients with Fitzpatrick skin types IV and V saw a 75% improvement in PIH after SA peels.4 Davis et al found a nonsignificant trend toward skin lightening in Korean adults treated for acne and PIH, with significant decreases in erythema and improvements in greasiness, dryness, and scaliness.6 Importantly, the risk of PIH following TV is higher in patients with skin of color.7 SA may be effective in treating TV and PIH, offering a multifactorial approach by addressing both conditions while posing a low risk for causing PIH.8
TV and other Malassezia spp infections are common concerns in dermatology and primary care, with Malassezia-associated superficial mycoses (eg, dandruff, pityriasis versicolor, and folliculitis) affecting up to 50% of the population worldwide.9 Despite this, there has been little recent advancement in antifungal treatments. Ketoconazole, terbinafine, and fluconazole have been in use since the 1980s and 1990s.8 Most antifungal drugs target ergosterol, a component of the fungal cell wall.10 Additionally, Malassezia spp have been increasingly reported to cause invasive infections in immunocompromised patients.11 Given the rise in antifungal resistance, the judicious use of antifungals and implementation of novel treatment strategies is essential.
While SA lacks intrinsic antifungal properties, different combinations (Whitfield ointment consisting of 3% SA and 6% benzoic acid; 2% sulfur and 2% SA) have been effective in the treatment of TV.1 It is theorized that the effectiveness of SA against TV is due to its ability to exfoliate and acidify the stratum corneum, the natural habitat of M. furfur.
SA also reduces sebum production by downregulating sebocyte lipogenesis via the sterol regulatory element-binding protein-1 pathway and suppressing the nuclear factor κB (NF-κB) pathway, a key pathway in inflammation.12 These mechanisms make SA an effective acne treatment. Additionally, M. furfur is a lipid-dependent yeast, thus the decreased lipogenesis by sebocytes may be beneficial in treating TV as well.12 A study of 25 patients with TV in India found that 88% achieved clinical and microbiological cure after 4 once-weekly treatments of a SA 30% peel.8
In a study of deployed military personnel, fungal infections affected about 11% of participants.13 Contributing factors to the development of fungal infections included excessive sweating, humid conditions, and limited access to hygiene facilities. In such settings, traditional antifungal therapies may be less effective or challenging to adhere to, making alternative treatments more desirable. SA peels could offer a practical solution in these circumstances, as they are easily applied in the clinic, require no neutralization or downtime, and do not require the patient to apply medications between visits.
In this case, the patient demonstrated significant improvement with 2 SA peels, with noted improvement in her acne. SA 30% peel was highlighted as a useful treatment option for patients with TV who struggle with topical medication adherence; furthermore, it may be particularly beneficial for patients with concomitant acne.
Conclusions
This case demonstrates the successful use of in-office SA 30% peel as a treatment for TV. The rapid improvement and resolution of lesions with minimal adverse effects suggest that SA peel may serve as a valuable alternative for patients with extensive disease in difficult-to-reach affected areas, or those who are dissatisfied with traditional therapies. Additionally, the concurrent improvement of the patient’s back acne underscores the dual therapeutic potential of this treatment. Given the ease of application, cost effectiveness, and favorable safety profile, SA 30% peel is a viable option in the management of TV, especially in cases where topical or oral antifungals are impractical. Further studies could help establish standardized protocols and assess long-term outcomes of this treatment modality.
- Leung AK, Barankin B, Lam JM, et al. Tinea versicolor: an updated review. Drugs Context. 2022;11:2022-9-2. doi:10.7573/dic.2022-9-2
- Arif T. Salicylic acid as a peeling agent: a comprehensive review. Clin Cosmet Investig Dermatol. 2015;8:455-461. doi:10.2147/CCID.S84765
- Shao X, Chen Y, Zhang L, et al. Effect of 30% supramolecular salicylic acid peel on skin microbiota and inflammation in patients with moderate-to-severe acne vulgaris. Dermatol Ther. 2022;13(1):155-168. doi:10.1007/s13555-022-00844-5
- Grimes PE. The safety and efficacy of salicylic acid chemical peels in darker racial-ethnic groups. Dermatol Surg Off Publ Am Soc Dermatol Surg Al. 1999;25(1). doi:10.1046/j.1524-4725.1999.08145.x
- Kang HY, Choi Y, Cho HJ. Salicylic acid peels for the treatment of acne vulgaris in Fitzpatrick skin types IV-V: a multicenter study. Dermatol Surg. Published online 2006. doi:10.1111/j.1524-4725.2006.32146.x.
- Davis EC, Callender VD. Postinflammatory hyperpigmentation. J Clin Aesthetic Dermatol. 2010;3(7):20-31.
- Kallini JR, Riaz F, Khachemoune A. Tinea versicolor in dark-skinned individuals. Int J Dermatol. 2014;53(2):137- 141. doi:10.1111/ijd.12345
- Saoji V, Madke B. Efficacy of salicylic acid peel in dermatophytosis. Indian J Dermatol Venereol Leprol. 2021;87(5). doi:10.4103/ijdvl.IJDVL_853_18
- Arce M, Gutiérrez-Mendoza D. Pityriasis versicolor: treatment update. Curr Fungal Infect Rep 2018;12(11):195–200. https://doi.org/10.1007/s12281-018-0328-7
- Leong C, Kit JCW, Lee SM, et al. Azole resistance mechanisms in pathogenic M. furfur. Antimicrob Agents Chemother. 2021;65(5):e01975-20. doi:10.1128/AAC.01975-20
- Chang HJ, Miller HL, Watkins N, et al. An epidemic of Malassezia pachydermatis in an intensive care nursery associated with colonization of health care workers’ pet dogs. N Engl J Med. 1998;338(11):706-711. doi:10.1056/NEJM199803123381102
- Lu J, Cong T, Wen X, et al. Salicylic acid treats acne vulgaris by suppressing AMPK/SREBP1 pathway in sebocytes. Exp Dermatol. 2019;28(7):786-794. doi:10.1111/exd.13934
- Singal A, Lipner SR. A review of skin disease in military soldiers: challenges and potential solutions. Ann Med. 2023;55(2):2267425. doi:10.1080/07853890.2023.2267425
- Leung AK, Barankin B, Lam JM, et al. Tinea versicolor: an updated review. Drugs Context. 2022;11:2022-9-2. doi:10.7573/dic.2022-9-2
- Arif T. Salicylic acid as a peeling agent: a comprehensive review. Clin Cosmet Investig Dermatol. 2015;8:455-461. doi:10.2147/CCID.S84765
- Shao X, Chen Y, Zhang L, et al. Effect of 30% supramolecular salicylic acid peel on skin microbiota and inflammation in patients with moderate-to-severe acne vulgaris. Dermatol Ther. 2022;13(1):155-168. doi:10.1007/s13555-022-00844-5
- Grimes PE. The safety and efficacy of salicylic acid chemical peels in darker racial-ethnic groups. Dermatol Surg Off Publ Am Soc Dermatol Surg Al. 1999;25(1). doi:10.1046/j.1524-4725.1999.08145.x
- Kang HY, Choi Y, Cho HJ. Salicylic acid peels for the treatment of acne vulgaris in Fitzpatrick skin types IV-V: a multicenter study. Dermatol Surg. Published online 2006. doi:10.1111/j.1524-4725.2006.32146.x.
- Davis EC, Callender VD. Postinflammatory hyperpigmentation. J Clin Aesthetic Dermatol. 2010;3(7):20-31.
- Kallini JR, Riaz F, Khachemoune A. Tinea versicolor in dark-skinned individuals. Int J Dermatol. 2014;53(2):137- 141. doi:10.1111/ijd.12345
- Saoji V, Madke B. Efficacy of salicylic acid peel in dermatophytosis. Indian J Dermatol Venereol Leprol. 2021;87(5). doi:10.4103/ijdvl.IJDVL_853_18
- Arce M, Gutiérrez-Mendoza D. Pityriasis versicolor: treatment update. Curr Fungal Infect Rep 2018;12(11):195–200. https://doi.org/10.1007/s12281-018-0328-7
- Leong C, Kit JCW, Lee SM, et al. Azole resistance mechanisms in pathogenic M. furfur. Antimicrob Agents Chemother. 2021;65(5):e01975-20. doi:10.1128/AAC.01975-20
- Chang HJ, Miller HL, Watkins N, et al. An epidemic of Malassezia pachydermatis in an intensive care nursery associated with colonization of health care workers’ pet dogs. N Engl J Med. 1998;338(11):706-711. doi:10.1056/NEJM199803123381102
- Lu J, Cong T, Wen X, et al. Salicylic acid treats acne vulgaris by suppressing AMPK/SREBP1 pathway in sebocytes. Exp Dermatol. 2019;28(7):786-794. doi:10.1111/exd.13934
- Singal A, Lipner SR. A review of skin disease in military soldiers: challenges and potential solutions. Ann Med. 2023;55(2):2267425. doi:10.1080/07853890.2023.2267425
Successful Treatment of Tinea Versicolor With Salicylic Acid 30% Peel
Successful Treatment of Tinea Versicolor With Salicylic Acid 30% Peel
Managing Contact Dermatitis Related to Amputee Care
Managing Contact Dermatitis Related to Amputee Care
Amputees who use prosthetic devices are particularly susceptible to contact dermatitis due to moisture, irritation, and prolonged contact with components of the device. Contact dermatitis accounts for approximately one-third of the dermatoses encountered by amputees who wear a prosthesis.1 Diagnosing allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD) is challenging due to errors of omission from the differential and the substantial clinical overlap with other eczematous dermatoses. Diagnosis relies on patient history, clinical examination, exposure assessment, diagnostic testing, and a high index of suspicion. Conventionally, ACD comprises approximately 20% of all contact dermatitis cases, whereas ICD accounts for 80%.2 Symptoms vary between the 2 conditions, with pruritus more common in ACD and burning and soreness more common in ICD.3 Onset of dermatitis relative to exposure is crucial, with ICD often manifesting more quickly and ACD requiring an initial sensitization phase.4 Additionally, the complexity of ICD as a condition with variable features adds to the diagnostic difficulty, especially when allergens also have irritant effects.
Understanding these 2 primary types of contact dermatitis is crucial for effective management and prevention strategies in amputees who use prosthetics. In this article, we describe common causes of ACD and ICD related to amputee prosthetics and propose a tailored patch testing panel in order to better diagnose ACD in this patient population.
Allergic Contact Dermatitis
Allergic contact dermatitis occurs when the skin comes into contact with a substance to which the individual is sensitized. In amputees who use prosthetics, the socket and sock liner materials are frequent culprits for triggering allergic reactions. Components such as rubber, metals (eg, nickel), adhesives, and various plastic monomers can induce ACD in susceptible individuals. Additionally, chronic friction and sweat augment hapten penetration, increasing the risk of developing ACD.5
Contact allergens (typically small molecules under 500 Da) penetrate the skin, engage dendritic cells, activate T lymphocytes, and trigger the immune response and memory.6 The skin contains a substantial population of memory T cells, with CD8+ T cells in the epidermis and CD4+ T cells in the dermis, expressing markers that facilitate skin reactivity. The balance between effector and regulatory T cells, which can produce suppressive cytokines such as IL-10, promotes clinical tolerance to allergens such as nickel.
Textile-driven ACD presents with a distinct clinical pattern, often manifesting as patchy generalized dermatitis that coincides with sites where garments fit most snugly. This presentation can mimic other forms of dermatitis, such as nummular or asteatotic dermatitis. The skin beneath undergarments such as underwear or prosthetic socks may be spared, as these act as shields from contact allergens. Notably, the face and hands typically are spared unless the patient has a cross-reaction to formaldehyde-based preservatives found in personal care products.4
Allergy to Components of the Prosthetic Socket and Sock Liner
A prosthesis consists of several key components, including a socket, sleeve, liner, and stump shrinker (eFigure 1). The prosthetic socket, custom-made to fit the residual limb, is the upper part of the prosthesis, while the lower part consists of prosthetic components such as joints and terminal devices ordered to meet individual needs. Prosthetic sleeves provide suspension by securely holding the prosthetic limb in place, while liners offer cushioning and protection to the residual limb, enhancing comfort and reducing friction. Stump shrinkers aid in reducing swelling and shaping the residual limb, facilitating a better fit for the prosthetic socket. Together, these components work in harmony to optimize stability, comfort, and functionality for the user, enabling them to navigate daily activities with greater ease and confidence. Common allergens found in components of the socket and sock liner include rubbers and other elastomers, metals, plastics, adhesives, and textiles.
Rubbers and Other Elastomers—Consumables, including liners, knee sleeves, and socks, are tailored to each client and utilize materials such as silicone and natural and synthetic rubbers for comfort and secure fit. Allergic reactions to natural rubber latex, more commonly used in earlier prosthetics, are associated with both type I and type IV hypersensitivity reactions.4 Proteins inherent to natural rubber are overwhelmingly associated with an immediate urticarial eruption, whereas chemical additives used to produce latex are mostly linked to delayed hypersensitivity reactions, manifesting as allergic reactions ranging from mild itching to severe skin blistering.4
Vulcanization is the process of using heat and other accelerators to manufacture rubber. Common rubber accelerators include thiurams (the most common allergen associated with rubbers and other elastomers), carbamates/carba mix, 1,3-diphenylguanidine, and mercaptobenzothiazole.4 Thiourea is an implicated cause of ACD to neoprene rubber.7 These sensitizing chemicals are all included in the North American 80 Comprehensive Series; only thiuram mix, carba mix, and mercaptobenzothiazole are available in the T.R.U.E. TEST (SmartPractice). Sensitization often occurs due to repeated exposure, particularly in individuals who have undergone multiple prosthetic fittings. Many modern prospective liners utilize a medical-grade silicone as an elastomer for its high flexibility; silicone is considered biologically nonreactive and generally is considered a rare cause of ACD.8
Metals—Nickel, a ubiquitous allergen found in metal alloys used in prosthetic hardware, can cause localized itching, redness, and even blistering upon contact with the skin. Other metals, such as cobalt and chromium, also may trigger allergic reactions in susceptible individuals. Though many elastic fitting prosthetic socks contain silver fibers to reduce odors and friction-causing blisters, pure silver used in clothing or jewelry rarely causes dermatitis.4
Plastics and Adhesives—Leg prosthesis sockets typically are finished with the application of varnish, plastics, and/or resins—all potential allergens—to improve the appearance of the device and protect it from external agents.9 Polyester plastics themselves can cause ICD, only rarely leading to ACD.4 Incomplete curing during their manufacture may result in inadvertent exposure to epoxy resins or other phenol- formaldehyde resins such as 4-tert-butylcatechol and 4-tert-butylphenol formaldehyde, demonstrated causes of ACD in amputees.10 Adhesives used in sock liners or tapes to secure prosthetic devices can contain ingredients such as acrylates (a well-known cause of nail allergens) and other formaldehyde resins.4 Additionally, benzophenone commonly is added to paints and rubbers as a UV light absorber, reducing UV degradation and enhancing the material’s durability under light exposure.11
Textiles—Cotton, a common component in prosthetic sock liners, is almost 100% cellulose and typically does not cause ACD; however, synthetic fibers such as polypropylene and elastane (spandex) can elicit allergic reactions.4 Allergy to textiles often is driven by the chemicals used in the manufacturing process, particularly textile finishes, dyes, and formaldehyde resins, which are commonly used as fabric treatments. Disperse dyes are another common cause of allergic reactions. Para-phenylenediamine, a dye found in permanent hair dye and other darkly colored fabrics, is a potent sensitizer that may cross-react with other compounds that also contain similar amine groups, such as ester anesthetics, sunscreens containing para-aminobenzoic acid, other para dyes, and sulfonamides.12 Sweat can exacerbate these reactions by causing allergens to leach out of textiles, increasing skin exposure. Additionally, prosthetics containing leather may trigger allergies to potassium dichromate and other chromium compounds used in the leather-tanning process.12
Allergy to Personal Care Products
Skin protectants and prosthetic cleansers are crucial in dermatologic care for amputees, working together to safeguard the skin and maintain prosthetic hygiene. Skin protectants form a barrier against irritation, friction, and moisture, protecting the residual limb from damage and enhancing comfort and mobility. Meanwhile, prosthetic cleansers remove sweat, oils, and bacteria from the prosthetic socket, reducing the risk of infections and odors and ensuring the longevity and optimal function of the prosthetic device. Together, they support skin health, comfort, and overall quality of life for amputees.
The socket should be cleaned with warm water prior to use, but more importantly, immediately after removing the prosthesis. If cleaning products are used at night, residual haptens may remain on the device, increasing the risk of sensitization. Common contact irritants found in personal care products utilized in amputee care include sulfates, surfactants, preservatives, and fragrances (eTable 1).4 Additionally, common household cleaners and disinfectants can damage the prosthesis, leading to breakdown and the release of the monomers, precipitating ACD.
Patch Testing to Identify Causative Allergens
Patch testing is a valuable tool for identifying specific allergens responsible for ACD in amputees. This procedure involves applying small amounts of suspected allergens to the patient’s skin under occlusion and leaving the patches in place for 48 hours. After removal, the skin is assessed for reactions at 48 hours, with additional assessments conducted according to International Contact Dermatitis Research Group guidelines, typically at 72 and 96 hours, to identify delayed responses. This diagnostic approach helps pinpoint the substances to which the individual is allergic, enabling targeted avoidance strategies and treatment recommendations. Two widely used patch tests—the T.R.U.E. TEST, a preassembled patch test encompassing 35 allergens, and the North American 80 Comprehensive Series, which includes 80 allergens—demonstrate a sensitivity range between 70% and 80%.13,14 eTable 2 shows a recommended custom contact dermatitis panel to assess the most common causes of ACD related to amputee care.
Irritant Contact Dermatitis
Irritant contact dermatitis occurs when the skin’s protective barrier is damaged by repeated exposure to a particular irritant. In amputees, perspiration, friction, and pressure from prosthetic devices can exacerbate irritant reactions, leading to skin maceration, breakdown, and increased transepidermal penetration. Sweat accumulation within the prosthetic socket creates a moist environment conducive to ICD. The combination of sweat and friction can strip the skin of its natural oils, leading to dryness, chafing, and maceration. Continuous exposure to moisture also can exacerbate existing dermatitis and compromise skin integrity.4 Additionally, chronic irritation may increase transepidermal penetration of haptens, potentiating the development of ACD.15
Management of ICD in amputees involves a combination of treatments aimed at reducing friction, reducing sweating, and restoring barrier protection. Strategies to minimize mechanical trauma to the skin include ensuring proper socket fit, managing moisture, and protecting the skin. Using moisture-wicking sock liners and breathable prosthetic materials can help keep the skin dry. Topical antiperspirants containing aluminum chloride or similar compounds that help to block sweat glands often are the first line of treatment. Oral anticholinergics may be prescribed to reduce overall sweating, though they can have systemic side effects. Iontophoresis, a procedure where the affected area is exposed to a mild electrical current, can also be effective, especially for sweating of the hands and feet, though its application in amputees might be more limited.14
Recently, 2 treatments have emerged as options for managing excessive sweating (hyperhidrosis) in amputees: botulinum toxin injections and laser hair removal. By inhibiting the release of acetylcholine from sweat glands, botulinum toxin effectively reduces sweat production, thereby alleviating perspiration-induced skin irritation. Approximately 2 to 3 units of botulinum toxin at a dilution of 100 units in 1 mL of bacteriostatic saline 0.9% are injected transdermally at 1-cm intervals in a circumferential pattern on the skin covered by the prosthesis socket (typically a total of 300-500 units are utilized in the procedure)(eFigure 2).16 Laser hair removal can assist amputees with hyperhidrosis by reducing hair in the residual limb area, which decreases sweat retention and the potential for skin irritation due to friction.
Final Thoughts
In amputee dermatologic care, individuals with limb loss are particularly prone to contact dermatitis due to moisture, friction, and prolonged contact with prosthetic components. Diagnosing ACD and ICD is challenging due to overlapping symptoms and the potential for simultaneous occurrence. Distinguishing between these conditions is crucial for effective management. Understanding their causes, particularly in relation to prosthetic use, is essential for developing targeted prevention and treatment strategies, including the use of tailored patch testing panels to better diagnose ACD in amputees.
- Lyon CC, Kulkarni J, Zimersonc E, et al. Skin disorders in amputees. J Am Acad Dermatol. 2000;42:501-507.
- Bains SN, Nash P, Fonacier L. Irritant contact dermatitis. Clin Rev Allergy Immunol. 2018;56:99-109.
- Angelini G, Bonamonte D, Foti C, eds. Clinical Contact Dermatitis: A Practical Approach. Springer; 2021:57-92.
- Fisher AA, Rietschel RL, Fowler JF. Fisher’s Contact Dermatitis. BC Decker Inc; 2008.
- Johansen JD, Frosch PJ, Lepoittevin JP. Contact Dermatitis. Springer; 2010:43-90.
- Eisen HN, Orris L, Belman S. Elicitation of delayed allergic skin reactions with haptens: the dependence of elicitation on hapten combination with protein. J Exp Med. 1952;95:473-487.
- Johnson R. Wrist dermatitis: contact allergy to neoprene in a keyboard wrist rest. Am J Contact Dermat. 1997;8:172-174.
- Adams RM. Occupational Skin Disease. WB Saunders; 1999:501-551.
- Requena L, Vázquez F, Requena C, et al. Epoxy dermatitis of an amputation stump. Contact Dermatitis. 1986;14:320.
- Freeman S. Contact dermatitis of a limb stump caused by p-tertiary butyl catechol in the artificial limb. Contact Dermatitis. 1986;14:68-69.
- Heurung AR, Raju SI, Warshaw EM. Benzophenones. Dermatitis. 2014;25:3-10.
- Manneschi V, Palmerio B, Pauluzzi P, et al. Contact dermatitis from myoelectric prostheses. Contact Dermatitis. 1989;21:116-117.
- Heinrich D, Altmeyer P, Brasch J. “New” techniques for more sensitive patch testing? J Dtsch Dermatol Ges. 2011;9:889-896.
- James WD. Contact dermatitis update. Presented at: Walter Reed National Military Medical Center; April 18, 2024.
- Smith HR, Basketter DA, McFadden JP. Irritant dermatitis, irritancy and its role in allergic contact dermatitis. Clin Exp Dermatol. 2002;27:138-146.
- Lannan FM, Powell J, Kim GM, et al. Hyperhidrosis of the residual limb: a narrative review of the measurement and treatment of excess perspiration affecting individuals with amputation. Prosthet Orthot Int. 2021;45:477-486.
Amputees who use prosthetic devices are particularly susceptible to contact dermatitis due to moisture, irritation, and prolonged contact with components of the device. Contact dermatitis accounts for approximately one-third of the dermatoses encountered by amputees who wear a prosthesis.1 Diagnosing allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD) is challenging due to errors of omission from the differential and the substantial clinical overlap with other eczematous dermatoses. Diagnosis relies on patient history, clinical examination, exposure assessment, diagnostic testing, and a high index of suspicion. Conventionally, ACD comprises approximately 20% of all contact dermatitis cases, whereas ICD accounts for 80%.2 Symptoms vary between the 2 conditions, with pruritus more common in ACD and burning and soreness more common in ICD.3 Onset of dermatitis relative to exposure is crucial, with ICD often manifesting more quickly and ACD requiring an initial sensitization phase.4 Additionally, the complexity of ICD as a condition with variable features adds to the diagnostic difficulty, especially when allergens also have irritant effects.
Understanding these 2 primary types of contact dermatitis is crucial for effective management and prevention strategies in amputees who use prosthetics. In this article, we describe common causes of ACD and ICD related to amputee prosthetics and propose a tailored patch testing panel in order to better diagnose ACD in this patient population.
Allergic Contact Dermatitis
Allergic contact dermatitis occurs when the skin comes into contact with a substance to which the individual is sensitized. In amputees who use prosthetics, the socket and sock liner materials are frequent culprits for triggering allergic reactions. Components such as rubber, metals (eg, nickel), adhesives, and various plastic monomers can induce ACD in susceptible individuals. Additionally, chronic friction and sweat augment hapten penetration, increasing the risk of developing ACD.5
Contact allergens (typically small molecules under 500 Da) penetrate the skin, engage dendritic cells, activate T lymphocytes, and trigger the immune response and memory.6 The skin contains a substantial population of memory T cells, with CD8+ T cells in the epidermis and CD4+ T cells in the dermis, expressing markers that facilitate skin reactivity. The balance between effector and regulatory T cells, which can produce suppressive cytokines such as IL-10, promotes clinical tolerance to allergens such as nickel.
Textile-driven ACD presents with a distinct clinical pattern, often manifesting as patchy generalized dermatitis that coincides with sites where garments fit most snugly. This presentation can mimic other forms of dermatitis, such as nummular or asteatotic dermatitis. The skin beneath undergarments such as underwear or prosthetic socks may be spared, as these act as shields from contact allergens. Notably, the face and hands typically are spared unless the patient has a cross-reaction to formaldehyde-based preservatives found in personal care products.4
Allergy to Components of the Prosthetic Socket and Sock Liner
A prosthesis consists of several key components, including a socket, sleeve, liner, and stump shrinker (eFigure 1). The prosthetic socket, custom-made to fit the residual limb, is the upper part of the prosthesis, while the lower part consists of prosthetic components such as joints and terminal devices ordered to meet individual needs. Prosthetic sleeves provide suspension by securely holding the prosthetic limb in place, while liners offer cushioning and protection to the residual limb, enhancing comfort and reducing friction. Stump shrinkers aid in reducing swelling and shaping the residual limb, facilitating a better fit for the prosthetic socket. Together, these components work in harmony to optimize stability, comfort, and functionality for the user, enabling them to navigate daily activities with greater ease and confidence. Common allergens found in components of the socket and sock liner include rubbers and other elastomers, metals, plastics, adhesives, and textiles.
Rubbers and Other Elastomers—Consumables, including liners, knee sleeves, and socks, are tailored to each client and utilize materials such as silicone and natural and synthetic rubbers for comfort and secure fit. Allergic reactions to natural rubber latex, more commonly used in earlier prosthetics, are associated with both type I and type IV hypersensitivity reactions.4 Proteins inherent to natural rubber are overwhelmingly associated with an immediate urticarial eruption, whereas chemical additives used to produce latex are mostly linked to delayed hypersensitivity reactions, manifesting as allergic reactions ranging from mild itching to severe skin blistering.4
Vulcanization is the process of using heat and other accelerators to manufacture rubber. Common rubber accelerators include thiurams (the most common allergen associated with rubbers and other elastomers), carbamates/carba mix, 1,3-diphenylguanidine, and mercaptobenzothiazole.4 Thiourea is an implicated cause of ACD to neoprene rubber.7 These sensitizing chemicals are all included in the North American 80 Comprehensive Series; only thiuram mix, carba mix, and mercaptobenzothiazole are available in the T.R.U.E. TEST (SmartPractice). Sensitization often occurs due to repeated exposure, particularly in individuals who have undergone multiple prosthetic fittings. Many modern prospective liners utilize a medical-grade silicone as an elastomer for its high flexibility; silicone is considered biologically nonreactive and generally is considered a rare cause of ACD.8
Metals—Nickel, a ubiquitous allergen found in metal alloys used in prosthetic hardware, can cause localized itching, redness, and even blistering upon contact with the skin. Other metals, such as cobalt and chromium, also may trigger allergic reactions in susceptible individuals. Though many elastic fitting prosthetic socks contain silver fibers to reduce odors and friction-causing blisters, pure silver used in clothing or jewelry rarely causes dermatitis.4
Plastics and Adhesives—Leg prosthesis sockets typically are finished with the application of varnish, plastics, and/or resins—all potential allergens—to improve the appearance of the device and protect it from external agents.9 Polyester plastics themselves can cause ICD, only rarely leading to ACD.4 Incomplete curing during their manufacture may result in inadvertent exposure to epoxy resins or other phenol- formaldehyde resins such as 4-tert-butylcatechol and 4-tert-butylphenol formaldehyde, demonstrated causes of ACD in amputees.10 Adhesives used in sock liners or tapes to secure prosthetic devices can contain ingredients such as acrylates (a well-known cause of nail allergens) and other formaldehyde resins.4 Additionally, benzophenone commonly is added to paints and rubbers as a UV light absorber, reducing UV degradation and enhancing the material’s durability under light exposure.11
Textiles—Cotton, a common component in prosthetic sock liners, is almost 100% cellulose and typically does not cause ACD; however, synthetic fibers such as polypropylene and elastane (spandex) can elicit allergic reactions.4 Allergy to textiles often is driven by the chemicals used in the manufacturing process, particularly textile finishes, dyes, and formaldehyde resins, which are commonly used as fabric treatments. Disperse dyes are another common cause of allergic reactions. Para-phenylenediamine, a dye found in permanent hair dye and other darkly colored fabrics, is a potent sensitizer that may cross-react with other compounds that also contain similar amine groups, such as ester anesthetics, sunscreens containing para-aminobenzoic acid, other para dyes, and sulfonamides.12 Sweat can exacerbate these reactions by causing allergens to leach out of textiles, increasing skin exposure. Additionally, prosthetics containing leather may trigger allergies to potassium dichromate and other chromium compounds used in the leather-tanning process.12
Allergy to Personal Care Products
Skin protectants and prosthetic cleansers are crucial in dermatologic care for amputees, working together to safeguard the skin and maintain prosthetic hygiene. Skin protectants form a barrier against irritation, friction, and moisture, protecting the residual limb from damage and enhancing comfort and mobility. Meanwhile, prosthetic cleansers remove sweat, oils, and bacteria from the prosthetic socket, reducing the risk of infections and odors and ensuring the longevity and optimal function of the prosthetic device. Together, they support skin health, comfort, and overall quality of life for amputees.
The socket should be cleaned with warm water prior to use, but more importantly, immediately after removing the prosthesis. If cleaning products are used at night, residual haptens may remain on the device, increasing the risk of sensitization. Common contact irritants found in personal care products utilized in amputee care include sulfates, surfactants, preservatives, and fragrances (eTable 1).4 Additionally, common household cleaners and disinfectants can damage the prosthesis, leading to breakdown and the release of the monomers, precipitating ACD.
Patch Testing to Identify Causative Allergens
Patch testing is a valuable tool for identifying specific allergens responsible for ACD in amputees. This procedure involves applying small amounts of suspected allergens to the patient’s skin under occlusion and leaving the patches in place for 48 hours. After removal, the skin is assessed for reactions at 48 hours, with additional assessments conducted according to International Contact Dermatitis Research Group guidelines, typically at 72 and 96 hours, to identify delayed responses. This diagnostic approach helps pinpoint the substances to which the individual is allergic, enabling targeted avoidance strategies and treatment recommendations. Two widely used patch tests—the T.R.U.E. TEST, a preassembled patch test encompassing 35 allergens, and the North American 80 Comprehensive Series, which includes 80 allergens—demonstrate a sensitivity range between 70% and 80%.13,14 eTable 2 shows a recommended custom contact dermatitis panel to assess the most common causes of ACD related to amputee care.
Irritant Contact Dermatitis
Irritant contact dermatitis occurs when the skin’s protective barrier is damaged by repeated exposure to a particular irritant. In amputees, perspiration, friction, and pressure from prosthetic devices can exacerbate irritant reactions, leading to skin maceration, breakdown, and increased transepidermal penetration. Sweat accumulation within the prosthetic socket creates a moist environment conducive to ICD. The combination of sweat and friction can strip the skin of its natural oils, leading to dryness, chafing, and maceration. Continuous exposure to moisture also can exacerbate existing dermatitis and compromise skin integrity.4 Additionally, chronic irritation may increase transepidermal penetration of haptens, potentiating the development of ACD.15
Management of ICD in amputees involves a combination of treatments aimed at reducing friction, reducing sweating, and restoring barrier protection. Strategies to minimize mechanical trauma to the skin include ensuring proper socket fit, managing moisture, and protecting the skin. Using moisture-wicking sock liners and breathable prosthetic materials can help keep the skin dry. Topical antiperspirants containing aluminum chloride or similar compounds that help to block sweat glands often are the first line of treatment. Oral anticholinergics may be prescribed to reduce overall sweating, though they can have systemic side effects. Iontophoresis, a procedure where the affected area is exposed to a mild electrical current, can also be effective, especially for sweating of the hands and feet, though its application in amputees might be more limited.14
Recently, 2 treatments have emerged as options for managing excessive sweating (hyperhidrosis) in amputees: botulinum toxin injections and laser hair removal. By inhibiting the release of acetylcholine from sweat glands, botulinum toxin effectively reduces sweat production, thereby alleviating perspiration-induced skin irritation. Approximately 2 to 3 units of botulinum toxin at a dilution of 100 units in 1 mL of bacteriostatic saline 0.9% are injected transdermally at 1-cm intervals in a circumferential pattern on the skin covered by the prosthesis socket (typically a total of 300-500 units are utilized in the procedure)(eFigure 2).16 Laser hair removal can assist amputees with hyperhidrosis by reducing hair in the residual limb area, which decreases sweat retention and the potential for skin irritation due to friction.
Final Thoughts
In amputee dermatologic care, individuals with limb loss are particularly prone to contact dermatitis due to moisture, friction, and prolonged contact with prosthetic components. Diagnosing ACD and ICD is challenging due to overlapping symptoms and the potential for simultaneous occurrence. Distinguishing between these conditions is crucial for effective management. Understanding their causes, particularly in relation to prosthetic use, is essential for developing targeted prevention and treatment strategies, including the use of tailored patch testing panels to better diagnose ACD in amputees.
Amputees who use prosthetic devices are particularly susceptible to contact dermatitis due to moisture, irritation, and prolonged contact with components of the device. Contact dermatitis accounts for approximately one-third of the dermatoses encountered by amputees who wear a prosthesis.1 Diagnosing allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD) is challenging due to errors of omission from the differential and the substantial clinical overlap with other eczematous dermatoses. Diagnosis relies on patient history, clinical examination, exposure assessment, diagnostic testing, and a high index of suspicion. Conventionally, ACD comprises approximately 20% of all contact dermatitis cases, whereas ICD accounts for 80%.2 Symptoms vary between the 2 conditions, with pruritus more common in ACD and burning and soreness more common in ICD.3 Onset of dermatitis relative to exposure is crucial, with ICD often manifesting more quickly and ACD requiring an initial sensitization phase.4 Additionally, the complexity of ICD as a condition with variable features adds to the diagnostic difficulty, especially when allergens also have irritant effects.
Understanding these 2 primary types of contact dermatitis is crucial for effective management and prevention strategies in amputees who use prosthetics. In this article, we describe common causes of ACD and ICD related to amputee prosthetics and propose a tailored patch testing panel in order to better diagnose ACD in this patient population.
Allergic Contact Dermatitis
Allergic contact dermatitis occurs when the skin comes into contact with a substance to which the individual is sensitized. In amputees who use prosthetics, the socket and sock liner materials are frequent culprits for triggering allergic reactions. Components such as rubber, metals (eg, nickel), adhesives, and various plastic monomers can induce ACD in susceptible individuals. Additionally, chronic friction and sweat augment hapten penetration, increasing the risk of developing ACD.5
Contact allergens (typically small molecules under 500 Da) penetrate the skin, engage dendritic cells, activate T lymphocytes, and trigger the immune response and memory.6 The skin contains a substantial population of memory T cells, with CD8+ T cells in the epidermis and CD4+ T cells in the dermis, expressing markers that facilitate skin reactivity. The balance between effector and regulatory T cells, which can produce suppressive cytokines such as IL-10, promotes clinical tolerance to allergens such as nickel.
Textile-driven ACD presents with a distinct clinical pattern, often manifesting as patchy generalized dermatitis that coincides with sites where garments fit most snugly. This presentation can mimic other forms of dermatitis, such as nummular or asteatotic dermatitis. The skin beneath undergarments such as underwear or prosthetic socks may be spared, as these act as shields from contact allergens. Notably, the face and hands typically are spared unless the patient has a cross-reaction to formaldehyde-based preservatives found in personal care products.4
Allergy to Components of the Prosthetic Socket and Sock Liner
A prosthesis consists of several key components, including a socket, sleeve, liner, and stump shrinker (eFigure 1). The prosthetic socket, custom-made to fit the residual limb, is the upper part of the prosthesis, while the lower part consists of prosthetic components such as joints and terminal devices ordered to meet individual needs. Prosthetic sleeves provide suspension by securely holding the prosthetic limb in place, while liners offer cushioning and protection to the residual limb, enhancing comfort and reducing friction. Stump shrinkers aid in reducing swelling and shaping the residual limb, facilitating a better fit for the prosthetic socket. Together, these components work in harmony to optimize stability, comfort, and functionality for the user, enabling them to navigate daily activities with greater ease and confidence. Common allergens found in components of the socket and sock liner include rubbers and other elastomers, metals, plastics, adhesives, and textiles.
Rubbers and Other Elastomers—Consumables, including liners, knee sleeves, and socks, are tailored to each client and utilize materials such as silicone and natural and synthetic rubbers for comfort and secure fit. Allergic reactions to natural rubber latex, more commonly used in earlier prosthetics, are associated with both type I and type IV hypersensitivity reactions.4 Proteins inherent to natural rubber are overwhelmingly associated with an immediate urticarial eruption, whereas chemical additives used to produce latex are mostly linked to delayed hypersensitivity reactions, manifesting as allergic reactions ranging from mild itching to severe skin blistering.4
Vulcanization is the process of using heat and other accelerators to manufacture rubber. Common rubber accelerators include thiurams (the most common allergen associated with rubbers and other elastomers), carbamates/carba mix, 1,3-diphenylguanidine, and mercaptobenzothiazole.4 Thiourea is an implicated cause of ACD to neoprene rubber.7 These sensitizing chemicals are all included in the North American 80 Comprehensive Series; only thiuram mix, carba mix, and mercaptobenzothiazole are available in the T.R.U.E. TEST (SmartPractice). Sensitization often occurs due to repeated exposure, particularly in individuals who have undergone multiple prosthetic fittings. Many modern prospective liners utilize a medical-grade silicone as an elastomer for its high flexibility; silicone is considered biologically nonreactive and generally is considered a rare cause of ACD.8
Metals—Nickel, a ubiquitous allergen found in metal alloys used in prosthetic hardware, can cause localized itching, redness, and even blistering upon contact with the skin. Other metals, such as cobalt and chromium, also may trigger allergic reactions in susceptible individuals. Though many elastic fitting prosthetic socks contain silver fibers to reduce odors and friction-causing blisters, pure silver used in clothing or jewelry rarely causes dermatitis.4
Plastics and Adhesives—Leg prosthesis sockets typically are finished with the application of varnish, plastics, and/or resins—all potential allergens—to improve the appearance of the device and protect it from external agents.9 Polyester plastics themselves can cause ICD, only rarely leading to ACD.4 Incomplete curing during their manufacture may result in inadvertent exposure to epoxy resins or other phenol- formaldehyde resins such as 4-tert-butylcatechol and 4-tert-butylphenol formaldehyde, demonstrated causes of ACD in amputees.10 Adhesives used in sock liners or tapes to secure prosthetic devices can contain ingredients such as acrylates (a well-known cause of nail allergens) and other formaldehyde resins.4 Additionally, benzophenone commonly is added to paints and rubbers as a UV light absorber, reducing UV degradation and enhancing the material’s durability under light exposure.11
Textiles—Cotton, a common component in prosthetic sock liners, is almost 100% cellulose and typically does not cause ACD; however, synthetic fibers such as polypropylene and elastane (spandex) can elicit allergic reactions.4 Allergy to textiles often is driven by the chemicals used in the manufacturing process, particularly textile finishes, dyes, and formaldehyde resins, which are commonly used as fabric treatments. Disperse dyes are another common cause of allergic reactions. Para-phenylenediamine, a dye found in permanent hair dye and other darkly colored fabrics, is a potent sensitizer that may cross-react with other compounds that also contain similar amine groups, such as ester anesthetics, sunscreens containing para-aminobenzoic acid, other para dyes, and sulfonamides.12 Sweat can exacerbate these reactions by causing allergens to leach out of textiles, increasing skin exposure. Additionally, prosthetics containing leather may trigger allergies to potassium dichromate and other chromium compounds used in the leather-tanning process.12
Allergy to Personal Care Products
Skin protectants and prosthetic cleansers are crucial in dermatologic care for amputees, working together to safeguard the skin and maintain prosthetic hygiene. Skin protectants form a barrier against irritation, friction, and moisture, protecting the residual limb from damage and enhancing comfort and mobility. Meanwhile, prosthetic cleansers remove sweat, oils, and bacteria from the prosthetic socket, reducing the risk of infections and odors and ensuring the longevity and optimal function of the prosthetic device. Together, they support skin health, comfort, and overall quality of life for amputees.
The socket should be cleaned with warm water prior to use, but more importantly, immediately after removing the prosthesis. If cleaning products are used at night, residual haptens may remain on the device, increasing the risk of sensitization. Common contact irritants found in personal care products utilized in amputee care include sulfates, surfactants, preservatives, and fragrances (eTable 1).4 Additionally, common household cleaners and disinfectants can damage the prosthesis, leading to breakdown and the release of the monomers, precipitating ACD.
Patch Testing to Identify Causative Allergens
Patch testing is a valuable tool for identifying specific allergens responsible for ACD in amputees. This procedure involves applying small amounts of suspected allergens to the patient’s skin under occlusion and leaving the patches in place for 48 hours. After removal, the skin is assessed for reactions at 48 hours, with additional assessments conducted according to International Contact Dermatitis Research Group guidelines, typically at 72 and 96 hours, to identify delayed responses. This diagnostic approach helps pinpoint the substances to which the individual is allergic, enabling targeted avoidance strategies and treatment recommendations. Two widely used patch tests—the T.R.U.E. TEST, a preassembled patch test encompassing 35 allergens, and the North American 80 Comprehensive Series, which includes 80 allergens—demonstrate a sensitivity range between 70% and 80%.13,14 eTable 2 shows a recommended custom contact dermatitis panel to assess the most common causes of ACD related to amputee care.
Irritant Contact Dermatitis
Irritant contact dermatitis occurs when the skin’s protective barrier is damaged by repeated exposure to a particular irritant. In amputees, perspiration, friction, and pressure from prosthetic devices can exacerbate irritant reactions, leading to skin maceration, breakdown, and increased transepidermal penetration. Sweat accumulation within the prosthetic socket creates a moist environment conducive to ICD. The combination of sweat and friction can strip the skin of its natural oils, leading to dryness, chafing, and maceration. Continuous exposure to moisture also can exacerbate existing dermatitis and compromise skin integrity.4 Additionally, chronic irritation may increase transepidermal penetration of haptens, potentiating the development of ACD.15
Management of ICD in amputees involves a combination of treatments aimed at reducing friction, reducing sweating, and restoring barrier protection. Strategies to minimize mechanical trauma to the skin include ensuring proper socket fit, managing moisture, and protecting the skin. Using moisture-wicking sock liners and breathable prosthetic materials can help keep the skin dry. Topical antiperspirants containing aluminum chloride or similar compounds that help to block sweat glands often are the first line of treatment. Oral anticholinergics may be prescribed to reduce overall sweating, though they can have systemic side effects. Iontophoresis, a procedure where the affected area is exposed to a mild electrical current, can also be effective, especially for sweating of the hands and feet, though its application in amputees might be more limited.14
Recently, 2 treatments have emerged as options for managing excessive sweating (hyperhidrosis) in amputees: botulinum toxin injections and laser hair removal. By inhibiting the release of acetylcholine from sweat glands, botulinum toxin effectively reduces sweat production, thereby alleviating perspiration-induced skin irritation. Approximately 2 to 3 units of botulinum toxin at a dilution of 100 units in 1 mL of bacteriostatic saline 0.9% are injected transdermally at 1-cm intervals in a circumferential pattern on the skin covered by the prosthesis socket (typically a total of 300-500 units are utilized in the procedure)(eFigure 2).16 Laser hair removal can assist amputees with hyperhidrosis by reducing hair in the residual limb area, which decreases sweat retention and the potential for skin irritation due to friction.
Final Thoughts
In amputee dermatologic care, individuals with limb loss are particularly prone to contact dermatitis due to moisture, friction, and prolonged contact with prosthetic components. Diagnosing ACD and ICD is challenging due to overlapping symptoms and the potential for simultaneous occurrence. Distinguishing between these conditions is crucial for effective management. Understanding their causes, particularly in relation to prosthetic use, is essential for developing targeted prevention and treatment strategies, including the use of tailored patch testing panels to better diagnose ACD in amputees.
- Lyon CC, Kulkarni J, Zimersonc E, et al. Skin disorders in amputees. J Am Acad Dermatol. 2000;42:501-507.
- Bains SN, Nash P, Fonacier L. Irritant contact dermatitis. Clin Rev Allergy Immunol. 2018;56:99-109.
- Angelini G, Bonamonte D, Foti C, eds. Clinical Contact Dermatitis: A Practical Approach. Springer; 2021:57-92.
- Fisher AA, Rietschel RL, Fowler JF. Fisher’s Contact Dermatitis. BC Decker Inc; 2008.
- Johansen JD, Frosch PJ, Lepoittevin JP. Contact Dermatitis. Springer; 2010:43-90.
- Eisen HN, Orris L, Belman S. Elicitation of delayed allergic skin reactions with haptens: the dependence of elicitation on hapten combination with protein. J Exp Med. 1952;95:473-487.
- Johnson R. Wrist dermatitis: contact allergy to neoprene in a keyboard wrist rest. Am J Contact Dermat. 1997;8:172-174.
- Adams RM. Occupational Skin Disease. WB Saunders; 1999:501-551.
- Requena L, Vázquez F, Requena C, et al. Epoxy dermatitis of an amputation stump. Contact Dermatitis. 1986;14:320.
- Freeman S. Contact dermatitis of a limb stump caused by p-tertiary butyl catechol in the artificial limb. Contact Dermatitis. 1986;14:68-69.
- Heurung AR, Raju SI, Warshaw EM. Benzophenones. Dermatitis. 2014;25:3-10.
- Manneschi V, Palmerio B, Pauluzzi P, et al. Contact dermatitis from myoelectric prostheses. Contact Dermatitis. 1989;21:116-117.
- Heinrich D, Altmeyer P, Brasch J. “New” techniques for more sensitive patch testing? J Dtsch Dermatol Ges. 2011;9:889-896.
- James WD. Contact dermatitis update. Presented at: Walter Reed National Military Medical Center; April 18, 2024.
- Smith HR, Basketter DA, McFadden JP. Irritant dermatitis, irritancy and its role in allergic contact dermatitis. Clin Exp Dermatol. 2002;27:138-146.
- Lannan FM, Powell J, Kim GM, et al. Hyperhidrosis of the residual limb: a narrative review of the measurement and treatment of excess perspiration affecting individuals with amputation. Prosthet Orthot Int. 2021;45:477-486.
- Lyon CC, Kulkarni J, Zimersonc E, et al. Skin disorders in amputees. J Am Acad Dermatol. 2000;42:501-507.
- Bains SN, Nash P, Fonacier L. Irritant contact dermatitis. Clin Rev Allergy Immunol. 2018;56:99-109.
- Angelini G, Bonamonte D, Foti C, eds. Clinical Contact Dermatitis: A Practical Approach. Springer; 2021:57-92.
- Fisher AA, Rietschel RL, Fowler JF. Fisher’s Contact Dermatitis. BC Decker Inc; 2008.
- Johansen JD, Frosch PJ, Lepoittevin JP. Contact Dermatitis. Springer; 2010:43-90.
- Eisen HN, Orris L, Belman S. Elicitation of delayed allergic skin reactions with haptens: the dependence of elicitation on hapten combination with protein. J Exp Med. 1952;95:473-487.
- Johnson R. Wrist dermatitis: contact allergy to neoprene in a keyboard wrist rest. Am J Contact Dermat. 1997;8:172-174.
- Adams RM. Occupational Skin Disease. WB Saunders; 1999:501-551.
- Requena L, Vázquez F, Requena C, et al. Epoxy dermatitis of an amputation stump. Contact Dermatitis. 1986;14:320.
- Freeman S. Contact dermatitis of a limb stump caused by p-tertiary butyl catechol in the artificial limb. Contact Dermatitis. 1986;14:68-69.
- Heurung AR, Raju SI, Warshaw EM. Benzophenones. Dermatitis. 2014;25:3-10.
- Manneschi V, Palmerio B, Pauluzzi P, et al. Contact dermatitis from myoelectric prostheses. Contact Dermatitis. 1989;21:116-117.
- Heinrich D, Altmeyer P, Brasch J. “New” techniques for more sensitive patch testing? J Dtsch Dermatol Ges. 2011;9:889-896.
- James WD. Contact dermatitis update. Presented at: Walter Reed National Military Medical Center; April 18, 2024.
- Smith HR, Basketter DA, McFadden JP. Irritant dermatitis, irritancy and its role in allergic contact dermatitis. Clin Exp Dermatol. 2002;27:138-146.
- Lannan FM, Powell J, Kim GM, et al. Hyperhidrosis of the residual limb: a narrative review of the measurement and treatment of excess perspiration affecting individuals with amputation. Prosthet Orthot Int. 2021;45:477-486.
Managing Contact Dermatitis Related to Amputee Care
Managing Contact Dermatitis Related to Amputee Care
PRACTICE POINTS
- Incorporating a tailored patch testing panel that includes common prosthetic-related allergens (eg, rubber, metals, adhesives) can greatly improve the diagnosis and treatment of allergic vs irritant contact dermatitis in amputees.
- Effective management of irritant contact dermatitis in amputees involves reducing moisture and friction in the prosthetic socket with moisture-wicking liners, ensuring proper fit, and utilizing treatments such as topical antiperspirants and botulinum toxin injections.
