Pigment International

: 2019  |  Volume : 6  |  Issue : 2  |  Page : 59--66

Role of chemical peels in postinflammatory hyperpigmentation: a comprehensive review

Surabhi Dayal, Priyadarshini Sahu, Bhavya Sangal, Shruti Sharma 
 Department of Dermatology, Venereology, and Leprology, Pt. B. D. Sharma University of Health Sciences, Rohtak, Haryana, India

Correspondence Address:
Priyadarshini Sahu
Department of Dermatology, Venereology, and Leprology, Pt. B. D. Sharma University of Health Sciences, Rohtak, Haryana


Postinflammatory hyperpigmentation (PIH) is an acquired hypermelanosis arising after inflammation or injury to the skin and can develop in all skin types especially in Fitzpatrick skin phototypes III to VI. In higher skin phototypes, chances of PIH following procedures using laser and other light sources are high. Therefore, it is becoming increasingly important to manage this unforeseen condition. Wide variety of treatment options are available for PIH, but there is limited literature regarding efficacy and safety of chemical peels in PIH. Hence, a thorough systematic review was performed by searching Pubmed, Scopus, Medline, and Cochrane databases in English language involving studies on PIH. Thus, this article is an attempt to bring together all the possible ways of using chemical peels (alone, in combination with other peels or topical agents) for the management of PIH.

How to cite this article:
Dayal S, Sahu P, Sangal B, Sharma S. Role of chemical peels in postinflammatory hyperpigmentation: a comprehensive review.Pigment Int 2019;6:59-66

How to cite this URL:
Dayal S, Sahu P, Sangal B, Sharma S. Role of chemical peels in postinflammatory hyperpigmentation: a comprehensive review. Pigment Int [serial online] 2019 [cited 2020 Feb 21 ];6:59-66
Available from: http://www.pigmentinternational.com/text.asp?2019/6/2/59/273458

Full Text


Postinflammatory hyperpigmentation (PIH) is an acquired hypermelanosis occurring after cutaneous inflammation or injury that can arise in all skin types.[1] It is often complained by persons having darker skin that can lead to their negative self-esteem. The severity of PIH is determined by number of factors including inherent skin color (especially Fitzpatrick skin phototypes, i.e., SPT III and IV), degree and depth of inflammation, degree of dermoepidermal junction disruption, and the stability of melanocytes leading to epidermal and dermal pigment deposition.[2] The higher levels of melanin in skin of color can lead to greater susceptibility to PIH. It is difficult to treat in patients of darker races as aggressive therapy in these patients leads to greater PIH.

Prevention of inciting inflammation, sun avoidance, and topical depigmenting agents (especially topical hydoquinone) are the mainstay of therapy. Conventional treatment modalities also include superficial and medium depth peels, topical tretinoin, topical steroids, topical kojic acid, lasers, and various combination therapies. Among this wide variety of treatment options, chemical peeling is one of the safe modalities for management of PIH. Although the efficacy of most of the chemical peels have not been studied specifically for PIH, salicylic acid (SA) and glycolic acid (GA) chemical peels have shown good efficacy for the treatment of facial hyperpigmentation. This article is an attempt to discuss and review the use of various chemical peels in PIH.


Multiple epidemiological studies have shown that PIH tends to occur more commonly among skin of color patients compared to Caucasian patients.[2] El-Essawi et al. in 2007[3] reported that uneven skin tone and skin discoloration are two of the most concerning skin problems among Arab Americans, with more than 50% of the survey participants expressing such concerns. Among 3000 Latino patients, the incidence of hyperpigmentation and melasma was reported to be between 6% and 7.5%.[3] In another study conducted in Singapore, PIH tended to occur among Asians with darker skin, showing the importance of the degree of constitutive cutaneous pigmentation in the development of PIH.[4]

In higher SPTs, chance of PIH following procedures using laser and other light sources is also high. The same is reported by Chan et al.[5] who recorded PIH in 92% of SPT IV patients compared to a low of 23% patients of SPT I to III who underwent ablative fractional carbon dioxide laser treatments.

Etiology and pathogenesis

Pigment alteration from preceding inflammatory dermatoses can lead to either hyperpigmentation, hypopigmentation, or both depending on the number and activity of melanocytes after inflammation. Inflammation that affects the dermoepidermal junction tends to develop dyspigmentation.[2]

Cutaneous inflammation results in generation of eicosanoids from cell membrane that include prostaglandins E2 and D2, leukotrienes B4, C4, D4, and E4, and thromboxane B2. In vitro, these metabolites have been found to increase the size of melanocytes and stimulate melanocyte dendritic proliferation, although this response of melanocytes to inflammatory mediators is genetically determined. Leukotriene C4 has been shown to increase tyrosinase activity.[2]

PIH within the dermis results from inflammatory damage to basal keratinocytes, which then releases large amounts of melanin. The free pigment is then phagocytosed by macrophages, now called melanophages, in the upper dermis that produces a blue–gray appearance to the skin at the site of injury.[1] The various causes of PIH are compiled in [Table 1].{Table 1}

Clinical presentation

PIH typically manifests as macules or patches in the same distribution as the initial inflammatory process. On the basis of location of pigment deposition, it can be classified as follows[2]:
  1. Epidermal
  2. Dermal

Epidermal PIH will appear dark brown to tan in color and may take months to years to resolve without treatment. Hyperpigmentation within the dermis will give a blue–gray appearance due to Tyndall effect[2] and may take even longer time to resolve if left untreated. PIH is directly proportional to SPT and can even worsen with ultraviolet irradiation or with persistent or recurrent inflammation. Wood’s lamp is a simple diagnostic modality that can distinguish between epidermal or dermal PIH. Epidermal PIH is enhanced and appears darker compared with unaffected normal skin and dermal PIH is not highlighted during Wood’s lamp examination. In patients with Fitzpatrick skin types IV to VI, Wood’s lamp examination may show ambiguous results because of constitutively high concentration of melanin in the epidermis.[6] In such cases, skin biopsy is our rescue to exclude other conditions that can cause hyperpigmentation. The objective scoring systems for evaluating PIH include hyperpigmentation area and severity index (HASI)[7] and Taylor hyperpigmentation scale.[8]
  • HASI[7]: It is described by Burns and colleagues. The HASI score is a measure of the severity of hyperpigmentation; a higher HASI score indicates severe hyperpigmentation. It is calculated as follows:

HASI = 0.3 (DF + HF) AF + 0.3 (DMR + HMR) AMR + 0.3 (DML + HML) AML + 0.1 (DC + HC) AC

The face is divided into four zones: forehead (F), right malar region (MR), left malar region (ML), and chin (C). The area of involvement (A) of each zone is graded 0, no involvement; 1 is <10%; 2 is 10% to 29%; 3 is 30% to 49% involvement; 4 is 50% to 69% involvement; 5 is 70% to 89% involvement; and 6 is >90% involvement. The degree of pigmentation is based on two factors: darkness (D) and homogeneity (H), each having a scale of 0 to 4. A grading of 0 corresponds to no pigmentation and minimal homogeneity, whereas a score of 4 corresponds to severe hyperpigmentation and complete homogeneity.
  • Taylor hyperpigmentation scale[8]: It is a new scale introduced to assess skin color and monitor improvement in hyperpigmentation following therapy. The tool consists of 15 uniquely colored plastic cards with the full range of skin hues and is applicable to individuals with Fitzpatrick skin types I to VI. Each card contains 10 bands of increasingly darker gradations of skin hue that represent progressive levels of hyperpigmentation.


The course and outcome of PIH is generally unpredictable and relapses are frequent after treatment. Prevention and treatment of underlying inflammatory conditions are the primary treatment of PIH. It is suggested to start with medical therapy initially, which include topical depigmenting agents (such as hydroquinone, tretinoin, or azelaic acid), retinoids, and low-potency corticosteroids.[9] If an adequate resolution is not achieved, the treatment can be switched to chemical peeling or lasers.

Role of chemical peels in treatment of PIH

Chemical peeling or chemoexfoliation is a popular, relatively cost-effective, and generally safe modality for the treatment of cutaneous pigmentation. It is used to create a controlled chemical injury at specific skin depth with the goal of stimulating new skin growth with improved surface, texture, and appearance. The exfoliative effect of chemical peels results in regulation of epidermal thickness, more uniform dispersion of basal layer melanin, and lying down of new collagen with ground substance in dermis, thus improving pigmentary dyschromias. It is becoming popular in treating a myriad of skin conditions such as melasma, acne, PIH, or scarring.

In cases of PIH, superficial and medium depth peels are used. Superficial are better than medium depth peel as it offers greater flexibility over a range of skin types and maintain a smooth skin texture with minimal to no downtime. Additionally, it is better in darker skin types to avoid further worsening of PIH.[10] Superficial peel include 15% to 20% trichloroacetic acid (TCA), 50% to 70% GA, four to 10 coats of Jessner’s solution, and 20% to 30% SA. Superficial and medium depth peels are safe to use in skin of color patients. Other techniques that are suggested for chemical peeling are spot peeling for PIH and combination peeling especially in acne and photodamaged skin. However, it is seen that epidermal pigmentation responds better than other mixed pigmented lesions.[7] Chemical peels have been used by many workers but there is limited literature available regarding the efficacy and safety of chemical peels in PIH. Various peeling agents and studies related to them are given in [Table 2].{Table 2}


SA peels in combination with 4% hydroquinone or alone have shown to be safe and effective in reducing PIH in darker skin patients (especially SPT IV and V).[11],[12] Although SA peel is often combined with hydroquinone, there is paucity of literature investigating its inclusion in routine patient regimens. Additionally, there are concerns about the safety and adverse effect profile of hydroquinone. In 2009, Joshi et al.[13] conducted a study to assess the efficacy and safety of SA peel in 10 patients of PIH with skin types IV to VI, who received serial SA (20%–30%) peels on one half of the face and no treatment on the other half. The authors concluded that there was nominal clinical improvement in PIH on the treated side as compared to the control side, but this clinical study did not demonstrate statistical significant improvement.[13]

Similar studies were conducted by Grimes[11] and Bari et al.[12] to treat various facial dermatosis including PIH. Grimes[11] used serial SA peel with hydroquinone and later used 30% SA peel alone. Both the studies had shown encouraging results.[11],[12] Ahn and Kim[14] also reported a whitening effect in patients of acne-induced PIH with 30% SA peel, with a significant decrease in erythema and improvement in greasiness, dryness, and scaliness. This whitening effect can be very fascinating, while selecting a chemical peel for dark complexioned races.[14]

Comparison of SA peels with other modalities

In a recent study, comparing the efficacy of 20% to 30% SA peel along with 0.1% topical tretinoin solution vs both treatments alone demonstrated significantly better improvement in combination group due to its higher efficacy as compared to single treatment alone.[15] Furthermore, combination treatment is well-tolerated with lesser adverse effects and low recurrence rate.

Adverse effects: SA peel is usually associated with minimal side effects such as erythema and itching, which usually resolve within 24 hours and postpeel exfoliation that can be relieved by frequent application of emollient cream. It has also been noticed that stinging and burning sensation associated with SA peel rapidly disappears with volatilization of vehicle and self-precipitation of SA peel.[15] Thus, patients can be reassured during the procedure that burning and stinging sensation will end within minutes. Self-precipitation of SA allows little penetration of active agents, thus accounting for good tolerability and safety profile.

Thus, from the above studies, it is concluded that SA peel with strength varying from 20% to 30% is a cheap, safe, well-tolerated, and reasonably safe procedure suitable for PIH in darker skin patients.


GA peel is an alpha-hydroxy acid with smallest molecular weight so that it can penetrate easily into the skin. It is available in various concentrations ranging from 20% to 70%; 50% to 70% GA applied for 2 to 5 minutes is classified as superficial and 70% GA applied for 3 to 15 minutes as medium depth peel. The possible mechanism of depigmentation in patients of PIH may be due to epidermolysis of pigmented skin, the reepithelization of new less-pigmented skin as well as coverage of dermal color by new less-pigmented epidermis. Furthermore, it may have a possible direct depigmentary effect on the skin due to its structural similarity to ascorbic acid. Its keratolytic effect with complete sun avoidance is crucial for its skin brightening effect.

According to Sharad,[16] GA peels are excellent when used for postacne pigmentation in Indian skin with Fitzpatrick’s skin types III and IV. Furthermore, she suggested that serial GA peel, that is, 20% followed by 35% for 8 to 10 sessions done at 15 days interval are associated with clearance of lesions, without any adverse effects.[16] In a pilot study by Burns et al.,[7] PIH was treated with a series of GA peels in skin types IV to VI and was proved to be efficacious with no adverse effects in dark-skinned patients. This was further confirmed in another study done by Grover and Reddu,[17] in which PIH and scarring both showed excellent improvement in skin types III to V with overall improvement in skin texture. They had also commented that the results were not encouraging in patients with PIH secondary to superficial burns or drugs.[17] Wang et al.[18] also reported its beneficial effect in PIH in addition to its skin whitening effect.

Comparison of GA peels with other modalities

In a study by Garg et al.,[19] comparing the efficacy and tolerability of 35% GA peels and 20% salicylic-10% mandelic acid (SMPs) peels in active acne and postacne scarring and hyperpigmentation found that SMPs had a higher efficacy for active acne and postacne hyperpigmentation with lesser side-effect profile. In yet another study by Godse and Sakhia,[20] who had studied triple combination of 2% hydroquinone, 0.05% tretinoin, and 0.01% flucinolone acetonide cream with GA peels in treatment of postacne hyperpigmentation, revealed that addition of GA peel with triple combination enhances the overall improvement in hyperpigmentation. Furthermore, in a recent study by Sarkar et al.,[10] comparative evaluation of safety and efficacy of combination of GA peel with modified Kligman formula (MKF) containing hydroquinone 2%, tretinoin 0.05%, and hydrocortisone 1% vs MKF alone in facial PIH in Indian patients (Fitzpatrick skin types III–V) was done. Results were evaluated at the end of 21 weeks (3 weeks after treatment completion) using objective scoring system HASI score and clinical photography. There was a statistically significant difference in results between the peel group vs MKF alone group at 12 and 21 weeks. Minimal side effects were observed in both the groups that were managed with emollients and no patient dropped out of the study as a result of the side effects. Thus, this study demonstrated that serial GA peels in combination with MKF is an efficacious and safe treatment of facial PIH in dark-skinned patients.

Adverse effects: GA peel is most widely used peel with minor side effects such as erythema, stinging/tingling sensation, mild burning, postpeel desquamation, and transient hypopigmentation or PIH. In rare cases, hypopigmentation, persistent erythema, and acne flare-up have been reported.[7]


TCA peels are being performed in cases of various conditions such as PIH, postacne pigmentation, melasma, and frictional dermal melanosis; 70% GA followed by 35% TCA peels performed in cases of pigmentary dyschromias such as PIH, postacne pigmentation, and melasma have been found to produce a deeper and more uniform peel than TCA alone.[21] In another study by Sachdeva,[22] comparative assessment of efficacy of 10% to 20% TCA and 35% to 70% GA peel in PIH showed that GA peel was safer and more effective than TCA peel although the difference was not statistically significant. In a recent study by Sacchidanand et al.,[23] comparing 15% TCA peel with 50% GA peel in frictional melanosis, it was found that both the peeling agents were equally effective. However, response with TCA was better than GA peel, and the difference in response was not statistically significant.[23] TCA peel is also associated with significant erythema and burning sensation as compared to GA peel. Furthermore, TCA peel is associated with frosting reaction that is completely absent in GA peel. GA and TCA peels both may themselves be associated with PIH. However, it is more common with TCA peel as compared to GA peel. This particular side effect is ironical as PIH can be further worsened if not done under proper supervision and sun protection.



Priming or preparing the skin before a peel is an important adjunctive measure for achieving good results with chemical peeling. This helps in better and uniform penetration of the peeling agent by reducing seborrhea and by thinning the stratum corneum, accelerates reepithelialization, reduces wound healing time, and has skin lightening effect by enhancing the dispersion of melanin granules throughout the epidermis thus reducing the postpeel hyperpigmentation.[24]

This prepeel procedure must be performed for at least 2 to 4 weeks prior to the procedure and should be stopped 1 week before the peeling session.[25],[26] It helps to increase peel efficacy and reduces the risk of PIH. Role of priming in accentuating the efficacy and safety of chemical peels in PIH can be attributed to its various actions including reduction of wound healing time, facilitation of uniform penetration of peeling agent, detection of intolerance to any agent, enhancement of patient’s compliance, and reduction in the risks of complications.

Priming includes application of topical agents such as broad-spectrum sunscreens, hydroquinone (2/4%), tretinoin 0.025%, adapalene 0.1%, GA 6% to 12%, kojic acid, and azelaic acid.

If patients have history of herpes simplex, antivirals (acyclovir or famciclovir) are recommended, beginning 2 days prior to the procedure and continued for 7 to 10 days until complete reepithelialization occurs.[25],[26]
  • There should be minimum interval of 2 weeks between two peeling sessions.
  • Always better to start with a low concentration (20% GA/20% SA) and increase the peel concentration and application time during subsequent sessions.
  • It is very important to neutralize peeling agents of alpha-hydroxy group especially GA peel with water or with basic solutions, such as ammonium salts, sodium bicarbonate, or sodium hydroxide or with neutralizing lotions to avoid postpeel burning and further PIH. Neutralization is usually done after a set duration of 3 to 5 minutes. Peels need to be neutralized to stop acidification of skin. Application of acid to skin saturates the ability of cells to resist acidification, therefore excess acid must be neutralized to avoid burning and PIH.[16] Chemical peels are acids, therefore alkalis such as 10% to 15% sodium bicarbonate and sodium hydroxide are more effective neutralizing agents. Advantage of sodium bicarbonate is that it is a good indicator of complete neutralization, when the fizzing stops. The disadvantage is that heat is produced due to acid–base reaction, which is exothermic in nature.[27]
    • SA, which is a beta-hydroxy acid, does not need neutralization. SA being a lipophilic peel itself is neutralized by skin’s own endogenous lipoproteins.[28]
    • TCA is a medium depth to deep peel, which acts by coagulation of both epidermal and dermal proteins. Its end point is frosting that denotes coagulation of proteins. It is a self-neutralizing peel, hence external application of neutralizing agent is not required.[29]
  • Patients should be instructed to use sunscreen before and after the peel during the daytime and moisturizer at night.
  • It is important to avoid both prepeel and postpeel facial scrubs, depilatory creams, waxing, bleaching, microdermabrasion, and laser hair removal for at least 1 week before and after the procedure.


It is considered as first line in the treatment of PIH and especially in cases with higher SPT. Patients should be educated on the use of daily broad-spectrum sunscreen with a sun protection factor of 30 and sun-protective measures, such as avoidance and protective clothing.


PIH is an often encountered complication, faced in most dermatological procedures. Chemical peeling is a noninvasive yet effective measure to control as well as to treat this unforeseen complication. However, timely initiation of this treatment and caution with these agents is required to prevent further worsening of this side effect. Combination of peeling agents with other modalities such as topical agents as well as lasers can further increase its efficacy.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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