Facial psoriasis in the etiology of prolonged erythema following medium‐depth chemical peels for severe photodamage

Chemical peeling is the controlled wounding of the epidermis and dermis for skin rejuvenation, involving the application of ablative agents to induce keratolysis and regeneration of damaged cell layers. Prolonged erythema is one complication of this procedure. We report the prevalence and probable etiology of prolonged facial erythema in a cohort of patients treated with medium‐depth chemical peels.

Prolonged erythema has been reported to occur in 11% of deep chemical peel patients. 6 Among these patients, it has thus far been attributed to angiogenic factors stimulating vasodilatation and it has been considered an indicator of prolonged stimulation of fibroplasia. 7 When the duration of erythema exceeds 3 weeks and is associated with pruritus, this may indicate hypertrophic scarring and should be treated with standard approaches for this procedural complication, such as pulsed dye laser or topical/intralesional/systemic corticosteroid. 8 To date, such prolonged erythema has been thought to be due to pre-/post-treatment retinoid use, exacerbation of pre-existing skin disease, genetic susceptibility, contact dermatitis, contact sensitization, and consumption of alcohol. 9 The use of cosmetics, sunscreen, emollient, or topical corticosteroids postoperatively may also result in prolonged erythema. Some experts believe that in cases of prolonged erythema with textural change, a true corticosteroid allergy should be excluded. 6 Psoriasis is a chronic, multisystem, inflammatory disease predominantly affecting the skin and joints. 10 Approximately 30% of patients with psoriasis have a positive family history, 11 and prevalence of psoriasis has been quoted as low as 0.27% and as high as 11.4%. 12 Psoriatic plaques are characterized by dysfunctional keratinocyte proliferation and differentiation. 13 Histologically, acanthosis and epidermal hyperplasia overlie an inflammatory infiltrate, while dermal papillae contain dilated, tortuous blood vessels. 14 Currently, the Psoriasis Area and Severity Index (PASI) is the most widely adopted clinical measure for the condition, based on area of involvement and the degree of erythema, induration, and desquamation. 15 Facial involvement is a marker for severe psoriasis, and is associated with longer disease duration, earlier onset, extracutaneous involvement, and the need for more extensive treatment. 16,17 Facial involvement occurs in approximately 29.9% of psoriasis patients. 18 We report the prevalence of prolonged facial erythema in a cohort of 82 patients treated with medium-depth chemical peels (hereafter referred to as peel/s), in whom an etiology of facial psoriasis was uncovered.

| MATERIAL S AND ME THODS
A retrospective audit was conducted of all full-face peels performed at two major teaching hospitals in New South Wales, Australia, between January 2018 and August 2022. All patients had severe facial photodamage affecting at least 75% surface area of the face. Figure 5C, a clinical image taken immediately pre-peel, is representative of the degree of qualifying sun damage in our treatment cohort.

TA B L E 1 (Continued)
Treatment consisted of skin preparation with 70% isopropyl al- including progressing to biologic therapy where indicated.

Details and management summaries of patients affected by such
prolonged erythema are presented in Table 1

| DISCUSS ION
Peels have been used for centuries to improve the signs of photodamage. 1 Ultraviolet radiation, through reactive oxygen species, incurs damage to DNA molecules, fatty acids, carbohydrates, and proteins, including collagen and elastin. 19 The structural framework of cutaneous fibers is severely affected by photodamage, and its degeneration leads to a gradual loss of tissue support with cosmetic ramifications. 19,20 We propose that the clinical signs of facial psoriasis, such as erythema and scale, may be masked by cutaneous changes resulting from ultraviolet radiation. Therefore, the exfoliative effects of peels may uncover underlying facial psoriasis following the shedding of a photodamaged skin layer.
The masking of erythema is explained by the Tyndall effect, which describes how shorter wavelengths (e.g., blue) are dispersed and reflected more than longer wavelengths (e.g., red). 21 When visible light enters a non-homogenous medium, longer wavelengths continue through the medium with less scatter. Therefore, observers do not detect red-orange colors as well. 22 In patients with skin thickening resulting from severe photodamage, erythema appears more fleshcolored due to reduced scatter, in effect masking erythema. While several devices are currently available for specific quantification of skin erythema, 23 we recorded facial erythema visually by standard digital photography, which is most readily available to practitioners. Scale may be masked by a similar increase in skin density and induration due to elastin production being disrupted by ultraviolet radiation, leading to inadequate protein synthesis required for proper assembly of elastic fibers. Hence, loss of cutaneous elasticity is a direct reflection of ultraviolet radiation damage and alterations in elastic fiber production. 19 The epidermis thickens in response to ultraviolet radiation reaching the proliferative basal layer. 24 Typically, photoaged skin exhibits solar elastosis, an accumulation of dystrophic elastotic material in the dermis, 19 in association with altered collagen fibers. 25 This may play a role in increasing thickness and induration, which may be difficult to differentiate from the induration of facial psoriasis.
Cutaneous exposure to ultraviolet radiation can result in changes to intracellular components of the stratum corneum, such as intercellular lipids and corneodesmosomes. These alterations to the mechanical barrier function of the superficial epidermis can lead to severe macroscopic skin damage, including associated inflammation, abnormal desquamation, chapping, and fissuring. 25 Corneodesmosomes are critical to desquamation, an essential protective mechanism by which there is complete stratum corneum turnover in 2-4 weeks. 26 Corneodesmosome damage by ultraviolet exposure may alter normal desquamation, potentially leading to longer-term barrier disruption. 25 Therefore, similar to the masking of psoriatic induration, the desquamation (otherwise described as scale) of psoriasis may also be masked.
Facial psoriasis arising de novo is an alternate mechanism for its occurrence among peel patients, particularly since this may be explained by the Koebner phenomenon in patients with psoriasis, Our data suggest that facial psoriasis is the probable cause of prolonged erythema in the context of peels. Resolution of prolonged erythema was only achieved for each patient by adhering to a conventional treatment ladder for psoriasis. Interestingly, compared with reported prevalence of prolonged erythema in deep peel patients (11%), 6 the prevalence among our patients, in whom this was attributed to facial psoriasis, is strikingly similar (12%).
When patients fail to respond to standard treatments for pro-

| CON CLUS ION
We present the first case series proposing a probable etiology

ACK N OWLED G M ENT
None declared.

DATA AVA I L A B I L I T Y S TAT E M E N T
The data that support the findings of this study are available from the corresponding author upon reasonable request.

E TH I C A L A PPROVA L
Authors declare human ethics approval was not needed for this study.
F I G U R E 5 Patient 10 pre-(A)/post-(B) treatment of facial psoriasis, and immediately pre-peel (C).