Does Hyperpigmented Skin Feel Different
J Clin Aesthet Dermatol. 2010 Jul; 3(7): 20–31.
Postinflammatory Hyperpigmentation
A Review of the Epidemiology, Clinical Features, and Handling Options in Peel of Color
Erica C. Davis
aCallender Skin & Laser Center, Glenn Dale, Maryland
Valerie D. Callender
aCallender Skin & Laser Middle, Glenn Dale, Maryland
bDepartment of Dermatology, Howard University College of Medicine, Washington, DC
Abstruse
Postinflammatory hyperpigmentation is a common sequelae of inflammatory dermatoses that tends to bear on darker skinned patients with greater frequency and severity. Epidemiological studies prove that dyschromias, including postinflammatory hyperpigmentation, are among the about common reasons darker racial/indigenous groups seek the intendance of a dermatologist. The treatment of postinflammatory hyperpigmentation should exist started early to assist hasten its resolution and begins with direction of the initial inflammatory condition. Kickoff-line therapy typically consists of topical depigmenting agents in improver to photoprotection including a sunscreen. Topical tyrosinase inhibitors, such equally hydroquinone, azelaic acid, kojic acid, arbutin, and certain licorice extracts, can effectively lighten areas of hypermelanosis. Other depigmenting agents include retinoids, mequinol, ascorbic acid, niacinamide, N-acetyl glucosamine, and soy with a number of emerging therapies on the horizon. Topical therapy is typically effective for epidermal postinflammatory hyperpigmentation; nonetheless, certain procedures, such as chemical peeling and light amplification by stimulated emission of radiation therapy, may help treat recalcitrant hyperpigmentation. It is also important to use caution with all of the above treatments to prevent irritation and worsening of postinflammatory hyperpigmentation.
Postinflammatory hyperpigmentation (PIH) is an acquired hypermelanosis occurring subsequently cutaneous inflammation or injury that tin arise in all skin types, just more often affects skin-of-color patients, including African Americans, Hispanics/Latinos, Asians, Native Americans, Pacific Islanders, and those of Center Eastern descent. PIH tin take a significant psychosocial touch on peel-of-color patients (Fitzpatrick pare types 4 through Vi), every bit these pigmentary changes tin can occur with greater frequency and severity in these populations 1 and oftentimes exist more obvious in darker skin. However, at that place is a wide multifariousness of prophylactic and effective treatments for PIH in skin of color, including topical depigmenting agents, chemical peels, and laser and light therapy. Therefore, this article reviews the etiology, pathogenesis, clinical manifestations, and handling options for PIH in skin of color.
Epidemiology
Tabular array 1 shows the worldwide prevalence of pigmentary disorders, excluding vitiligo, in various ethnic populations. These figures typically include postinflammatory hyper- or hypopigmentation although melasma and solar lentigines may also be included. Multiple epidemiological studies take shown that PIH tends to occur more normally amidst peel-of-color patients compared to Caucasian patients. 2,3 In 1983, Halder et al 2 published a study comparison the nearly common dermatoses seen in African American and Caucasian patients. Pigmentary disorders, other than vitiligo, were the tertiary most mutual dermatoses among African-American patients (9%), simply were the seventh virtually common among Caucasian patients (i.seven%). A more contempo study in 2007 three confirmed these findings showing dyschromias to be the second virtually common diagnosis among African-American patients, but dyschromias failed to make information technology into the top ten virtually common diagnoses for Caucasian patients. Of involvement, in a study conducted in Singapore, 4 the authors notation that PIH tended to too be more prevalent among Asians with darker peel, such every bit Malays and Indians, than those with lighter peel, such as the Chinese, suggesting that the degree of pigmentation rather than race/ethnicity may be more than contributory to the development of PIH.
Table 1
Worldwide prevalence of pigmentary disorders (excluding vitiligo) in peel of color
| Writer | YEAR | Report POPULATION | PREVALENCE | RANK | LOCATION |
|---|---|---|---|---|---|
| Halder ii | 1980–1983 | two,550: 78.4% African Americans, 21.half-dozen% Caucasian | 9% black; ane.seven% white | 3/13 black, 7/ten white | Washington, DC |
| Chua-Ty four | 1989–1990 | 74,589: 77.2% Chinese, 9.nine% Indian, 7.6% Malay, 5.3% Other | 1.8% Chinese, 2.vii% Malay, 2.3% Indian, ane.two% other | x/10 | Singapore |
| Nanda 116 | 1992–1996 | 10,000: 88% Kuwaitis, eight% other Arabs, 4% not-Arabs; all children | 0.42% | 33/74 | Kuwait |
| Child 117 | 1996 | 461: blackness (African, Afro-Caribbean, mixed race); 187 children, 274 adults | 1.6% children, 3.iv% adults | viii/14 children, vii/29 adults | London, England |
| Hartshorne 118 | 1999 | 7,029: 76.1% black, 10.9% Caucasian, 6.vii% Indian, 6.one% colored (mixed race) | 0.vii% black, 0.1% Caucasian, 0.three% Indian, 0.v% colored (mixed race) | 22/91 overall | Johannesburg, S Africa |
| Dunwell 119 | 2001 | 1,000: 95.half-dozen% Afro-Caribbean, 0.eight% Caucasian, two.2% Indian, 1.4% Chinese | 22.8% * (includes PIH, melasma, solar lentigines) | 3/18 | Kingston, Jamaica |
| Sanchez 120 | Published 2003 | three,000: Latino (i,000 individual practice, 2,000 infirmary-based clinic) | six% private exercise, 7.5% hospital-based dispensary | 7/12 private, 6/12 hospital | New York, New York |
| Arsouze 121 | 2004 | 1,064: black (African, Afro-Caribbean; FST V and Vi); 228 children, 836 adults | 6.1% children, 9.ii% adults | 6/16 children, two/20 adults | Paris, France |
| Alexis 3 | 2004–2005 | 1,074: black and white | xix.9% of diagnoses in blacks # , not in whites | 2/xiv | New York, New York |
| El-Essawi 122 | Published 2007 | 401: Arab Americans (33.7% Lebanese descent) | 56.4% uneven skin tone, 55.9% skin discoloration | Acme 2 peel concerns out of 10 | Detroit, Michigan |
Etiology
Many types of inflammatory dermatoses or cutaneous injuries tin cause pigmentary changes; nevertheless, there are some diseases that show a proclivity to develop PIH rather than hypopigmentation. A wide range of etiologies for PIH exists including infections such as dermatophytoses or viral exanthems, allergic reactions such as those from insect bites or a contact dermatitis, papulosquamous diseases similar psoriasis or lichen planus, medication-induced PIH from hypersensitivity reactions, or cutaneous injury from irritants, burns, or corrective procedures (Figure 1). v However, very common causes of PIH in skin of colour include acne vulgaris, atopic dermatitis, and impetigo. In fact, PIH is a particularly common sequela after acne in dark-skinned patients (Figure 2). A study in 2002 evaluating acne in skin of color establish that 65.3 percentage of African-American (N=239), 52.seven percent of Hispanic (Due north=55), and 47.iv pct of Asian (Northward=19) patients developed acne-induced PIH. six Pseudofolliculitis barbae (PFB) is another common inflammatory dermatosis, particularly among African Americans, that results in PIH and is estimated to have a prevalence charge per unit between 45 and 83 percentage. 7,viii In a study by Perry et al 9 of 71 African American and Hispanic patients with PFB, 90.1 per centum of patients reported hyperpigmentation; therefore, the authors suggest that PIH may exist a major clinical finding in PFB (Effigy 3).
Postinflammatory hyperpigmentation afterward lite electrodessication for dermatosis papulosa nigra
Acne-induced PIH in a patient with Fitzpatrick skin type V
African-American female person with hirsutism and pseudofolliculitis barbae with PIH
Pathogenesis
PIH results from the overproduction of melanin or an irregular dispersion of pigment after cutaneous inflammation. 10 When PIH is bars to the epidermis, there is an increase in the production and transfer of melanin to surrounding keratinocytes. Although the exact mechanism is unknown, this rise in melanocyte activity has been shown to be stimulated by prostanoids, cytokines, chemokines, and other inflammatory mediators equally well every bit reactive oxygen species that are released during the inflammatory process. Multiple studies have demonstrated the melanocyte-stimulating properties of leukotrienes (LT), such every bit LT-C4 and LT-D4, prostaglandins E2 and D2, thromboxane-2, interleukin (IL)-1, IL-vi, tumor necrosis factor (TNF)-α, epidermal growth gene, and reactive oxygen species such as nitric oxide. one,5,11,12
PIH within the dermis results from inflammation-induced damage to basal keratinocytes, which release large amounts of melanin. The free paint is then phagocytosed by macrophages, at present called melanophages, in the upper dermis and produces a blue-gray appearance to the skin at the site of injury. 13,14
Clinical Manifestations
PIH typically manifests every bit macules or patches in the same distribution as the initial inflammatory process. The location of the excess paint inside the layers of the skin will determine its coloration. Epidermal hypermelanosis will appear tan, dark-brown, or dark brown and may take months to years to resolve without treatment. 1 Hyperpigmentation inside the dermis has a blue-gray appearance and may either exist permanent or resolve over a protracted period of fourth dimension if left untreated. i,xv The intensity of PIH may also correlate with higher pare phototypes (Figures 4A and 4B), although studies are needed to ostend this finding. In improver, PIH can worsen with ultraviolet (UV) irradiation or with persistent or recurrent inflammation. 16
Postinflammatory hyperpigmentation in Fitzpatrick skin type IV (A) versus VI (B). Annotation the greater intensity of pigmentation in darker skin.
Treatment
The management of PIH should brainstorm starting time with addressing the underlying inflammatory dermatosis. Initiating treatment early on for PIH may help hasten its resolution and forbid further darkening. Even so, it is important to always be mindful of the potential the handling itself has to crusade or exacerbate PIH by causing irritation. 17 There are a variety of medications and procedures in improver to photoprotection that can safely and effectively care for PIH in darker skinned patients. Topical depigmenting agents, such as hydroquinone, azelaic acid, kojic acrid, licorice excerpt, and retinoids, can be effective lone or in combination with other agents, and procedures such as chemexfoliation and laser therapy can also be incorporated into the direction strategy if needed (Table 2). Of notation, topical agents are typically used to treat epidermal PIH as deeper pigmentation does non respond well to these agents. 16
Table 2
Management strategy for postinflammatory hyperpigmentation in skin of colour
| USE | THERAPY |
|---|---|
| First-line therapy | Hydroquinone 4% * |
| Sunscreen | |
| Additional treatment needed after viii–12 weeks of therapy | Combination therapy: HQ plus other depigmenting agents # OR |
Chemexfoliation
| |
Laser/lite therapy
| |
| First-line therapy for HQ allergy or prior long-term use | Other depigmenting agents
|
| Sunscreen | |
| Additional handling needed after 8–12 weeks of therapy | Chemexfoliation or laser/light therapyas above |
Photoprotection. An integral office in the treatment of PIH that should not be overlooked or underestimated is the importance of photoprotection to forbid the worsening of PIH. Patients should be educated on the use of daily broad-spectrum sunscreen with a sun protection cistron (SPF) of 30 and sun-protective measures, such as avoidance and protective wear. This is peculiarly truthful for those with higher skin phototypes who may not normally wear sunscreen, just as well may not realize the darkening effects UV irradiation has on hyperpigmentation. In fact, a study analyzing data from the 1992 National Health Interview Survey of 1,583 African Americans regarding dominicus-protection behaviors found that only a minority of the respondents were very probable to use sunscreen (9 vs. 81% who were unlikely to use it), wear protective clothing (28%), or stay in the shade (45%). 18
Although clinical studies have shown that serum vitamin D levels are reduced in sunscreen users compared to nonusers, these levels are nevertheless within normal range. 19,20 This is especially of import for dark-skinned individuals who may already be at gamble for vitamin D deficiency due to inherently higher melanin concentrations in the peel. 21 The American University of Dermatology has released a position statement on vitamin D, which states that groups at chance for vitamin D deficiency, including dark-skinned individuals, may need a daily total dose of 1000IU of vitamin D, through nutrition and supplementation, according to the current United States Section of Agriculture Dietary Guidelines. 22 Therefore, proper counseling and education involves encouraging the daily utilise of a broad-spectrum sunscreen with an SPF of thirty; dominicus-protective measures, such every bit avoidance and protective article of clothing; the intake of foods rich in vitamin D, such equally salmon, fish liver oils, and fortified foods; and vitamin D supplementation.
Medical therapy. Hydroquinone (HQ). The mainstay of treatment for PIH remains HQ. It is a phenolic compound that blocks the conversion of dihydroxyphenylalanine (DOPA) to melanin by inhibiting tyrosinase. x,23 Its mechanism of action may too involve inhibition of deoxyribonucleic acrid (Dna) and ribonucleic acid (RNA) synthesis, selective cytotoxicity toward melanocytes, and melanosome deposition. 24,25 HQ is unremarkably used at concentrations from 2 to 4% but tin can be prescribed in strengths upwardly to ten% and is bachelor over the counter (OTC) at 2% in the The states.
Hydroquinone monotherapy can be effective in treating PIH, but more than recently HQ has been formulated with other agents, such as retinoids, antioxidants, glycolic acid, sunscreens, and corticosteroids, to increase efficacy. 10 Cook-Bolden et al 26 conducted a 12-week, open up-label study of microencapsulated HQ four% and retinol 0.xv% with antioxidants in the handling of 21 patients (81% Fitzpatrick skin types IV–VI) with PIH (n=17) and melasma (north=4). There were significant decreases in lesion size, pigmentation, and illness severity from Week 4 to the written report endpoint (all P<0.032), and reflectance spectrophotometric analysis showed statistically significant reductions in melanin content as early as Week 4 likewise. A similar written report with a bulk of skin-of-color patients treated with microentrapped HQ 4%/retinol 0.xv% and sunscreen also found this amanuensis to be safe and effective for both PIH and melasma. 27
Irritant reactions can result from long-term daily apply of iv% or higher HQ, particularly when used in combination with other agents that can be irritating, such as retinoids. 28 Nonetheless, concomitant use of a topical corticosteroid tin can reduce irritation, thereby decreasing the gamble of further hyperpigmentation. 16 An early formulation, Kligman's formula containing five% HQ, 0.i% tretinoin, and 0.1% dexamethasone, is 1 such combination that was effective still problematic due to its employ of high concentrations of tretinoin and a stiff fluorinated steroid. 10 More recently, less irritative combination agents have been developed including TriLuma® (Galderma, Fort Worth, Texas), which contains 4% HQ, 0.05% tretinoin, and 0.01% fluocinolone acetonide. This triple combination agent has been shown to be both safe and constructive in the treatment of melasma 29–32 and photoaging 33 in skin of color and is used successfully in clinical practice to treat PIH. However, formal clinical studies are withal needed to further evaluate its use in PIH.
Adverse events reported with HQ utilize include contact dermatitis, nail discoloration, permanent leukoderma, and hypopigmentation of the surrounding normal peel that has been treated with HQ ("halo effect"). 23 Patients may likewise develop exogenous ochronosis (EO) (Figure v) where homogentisic acid accumulates within the dermis causing hyperpigmentation and papules on dominicus-exposed areas where HQ has been applied to the skin. 10,34,35 EO is typically associated with frequent utilise of very loftier concentrations of HQ on a long-term basis although EO tin still occur with short-term utilise of 1 to ii% HQ. 36,37 It is most commonly reported in blacks in Southward Africa, where the prevalence of EO is high. 6 In the United States, a depression number of hydroquinone-induced EO cases take been reported. 38 However, there has been a recent rise in the illicit use of loftier-concentration HQ available OTC in ethnic stores in the United States. 38
In 2006, the United States Nutrient and Drug Administration (FDA) released a statement proposing a ban on all OTC HQ agents based on rodent studies, which suggested that oral HQ may be a carcinogen. 37 All the same, at that place have been no reports of skin cancers or internal malignancies associated with topical HQ use. 23 To engagement, a final ruling by the FDA is nevertheless pending.
Mequinol. A derivative and culling to hydroquinone is 4-hydroxyanisole or mequinol. Although the ii agents are related, mequinol is idea to be less irritating to the peel than HQ. 39 The drug is available by prescription in a 2% concentration and is typically formulated with 0.01% tretinoin, a retinoic acid and penetration enhancer. 40 The mechanism past which mequinol causes depigmentation may involve a competitive inhibition of tyrosinase; yet, the exact pathway is unknown. xl Several big clinical studies have shown that mequinol finer treats solar lentigines in all patients 39,41 including ethnic populations 42 ; even so, merely small-scale clinical studies be that evaluate its effectiveness in the treatment of PIH. 43–45 One such written report 43 compared mequinol two%/tretinoin 0.01% to HQ 4% cream in 61 pare-of-color patients with mild-to-moderate facial PIH. Patients practical each medication to contralateral sides of the face up for 12 weeks. Topical mequinol/tretinoin was shown to be noninferior to 4% HQ as 81 and 85 pct of patients experienced clinical success on the mequinol-treated and the HQ-treated sides of the face up, respectively.
Retinoids. Retinoids are structural and functional analogues of vitamin A, and are effective alone or in combination with other agents for the treatment of PIH in ethnic patients. Retinoids exert multiple biological effects that result in pare lightening including the modulation of cell proliferation, differentiation, and cohesiveness; induction of apoptosis; and expression of anti-inflammatory properties. 46 Topical tretinoin, all-trans-retinoic acrid, is a naturally occurring metabolite of retinol and first-generation retinoid. 46 Concentrations range from 0.01 to 0.1% and tretinoin can exist formulated in creams, gels, and microsphere gels, which allows for the controlled release of tretinoin leading to less irritation. 47,48 A 40-week, randomized, double-blind, vehicle-controlled clinical trial was conducted with 54 black patients to determine the condom and efficacy of 0.one% tretinoin in the treatment of PIH. Tretinoin was significantly more than effective than vehicle in lightening PIH lesions when assessed by clinical (P<0.001) and colorimetric (P=0.05) analysis. However, 50 percent of patients developed retinoid dermatitis, which is the concern with using retinoids in pare of color. Starting at lower concentrations and titrating up based on handling response and choosing more tolerable formulations, such as creams over gels, may help to subtract the take chances of exacerbating PIH. 17
Third-generation retinoids, adapalene and tazarotene, are synthetic topical agents that are besides effective in the handling of PIH. Adapalene is formulated in creams or gels in 0.1 to 0.iii% concentrations; whereas, formulations of tazarotene include 0.05 and 0.one% creams or gels. Both agents have been shown in clinical studies to safely and finer treat PIH, particularly acne-induced PIH, in darker skinned individuals. 49,50 Isotretinoin (13-cis-retinoic acid) is a naturally occurring, showtime-generation retinoid that is available in both oral and topical formulations. Oral isotretinoin is very effective in the treatment of severe acne; however, there has likewise been a case reported in the literature of significant resolution of PIH afterward oral isotretinoin therapy in an Asian patient. 51
Azelaic acid. Naturally occurring as a dicarboxylic acid isolate from the organism responsible for Pityriasis versicolor, azelaic acid (AA) has been shown to be effective in the treatment of PIH. 10 AA has several mechanisms by which it depigments the skin including tyrosinase inhibition equally well as selective cytotoxic and antiproliferative furnishings toward abnormal melanocytes through the inhibition of DNA synthesis and mitochondrial enzymes. 52,53 Available formulations include a fifteen% gel, typically used in the handling of rosacea, or a 20% foam that is ordinarily used for acne vulgaris and melasma in addition to PIH. Lowe et al 54 conducted a randomized, double-blind, vehicle-controlled trial of 52 patients (Fitzpatrick skin types Iv–Half-dozen) with facial hyperpigmentation including PIH and melasma to determine the safety and efficacy of xx% AA cream. Patients treated with AA showed greater decreases in pigmentary intensity subsequently 24 weeks of treatment versus vehicle as measured past the investigator's subjective scale (P=0.021) and chromometric analysis (P<0.039). Side effects were balmy and transient. Multiple other studies have also shown the safety and efficacy of AA in skin of color for the treatment of melasma 55–57 ; nevertheless, larger studies are needed in this patient population with PIH.
Kojic acrid. Kojic acid (KA) is a fungal metabolite of certain species of Acetobacter, Aspergillus, and Penicillium. 23,52 Its depigmenting ability originates from a potent inhibition of tyrosinase past chelating copper at the active site of the enzyme. 34 KA is bachelor in 1 to 4% concentrations and can exist formulated with other lightening agents, including glycolic acid and hydroquinone, to increment efficacy. Multiple studies including Caucasian and Asian patients have shown that combination therapy with 2% KA and hydroquinone improves melasma. 58,59 However, clinical studies are still needed to determine its efficacy in the handling of PIH. In the U.s. and parts of Asia, KA is a frequent ingredient in cosmeceutical formulations although contact dermatitis is a common side effect with its use, 10 and multiple clinical studies have demonstrated its increased sensitizing potential. 60,61
Arbutin. Extracted from the dried leaves of the bearberry shrub or pear, cranberry, or huckleberry plants, arbutin is some other derivative of HQ, but without the melanotoxic effects. 40,62 Arbutin causes depigmentation by inhibiting non only tyrosinase activeness but too melanosome maturation. 23 Although its efficacy is dose-dependent, higher concentrations of arbutin tin pb to a paradoxical hyperpigmentation. 63 Synthetic forms of arbutin, blastoff-arbutin and deoxyarbutin, exhibit greater ability to inhibit tyrosinase than the naturally occurring compound. 64,65 A clinical study conducted by Boissy et al 65 showed 3% deoxyarbutin to be constructive in the treatment of solar lentigines in light-skinned patients (n=34), but at that place was no pregnant clinical response in the subset of dark-skinned patients (n=16). Arbutin is also used in a variety of cosmeceutical formulations marketed in the U.s.. 10,23 However, clinical studies evaluating arbutin for the treatment of PIH in higher skin phototypes is lacking.
Niacinamide. Niacinamide is the physiologically active derivative of vitamin B3 or niacin. In-vitro studies show that niacinamide significantly decreases melanosome transfer to keratinocytes without inhibiting tyrosinase action or cell proliferation, and niacinamide may also interfere with the prison cell-signaling pathway between keratinocytes and melanocytes to decrease melanogenesis. 66 One of the advantages of niacinamide is its stability being unaffected by light, wet, acids, alkalis, or oxidizers. 23 The safe and efficacy of niacinamide for PIH in darker skinned individuals has not been studied; however, topical 2 to five% niacinamide has shown some efficacy when used alone or in combination with N-acetyl glucosamine for the handling of melasma and UV-induced hyperpigmentation in fair-skinned patients and Asians. 66–68
N-acetyl glucosamine. N-acetyl glucosamine (NAG) is an amino carbohydrate that is a forerunner to hyaluronic acid and is institute throughout nature and human being tissues. 69 Its depigmenting ability originates from the inhibition of tyrosinase glycosylation, a footstep necessary in the product of melanin. 69 Glucosamine itself has been reported to decrease melanogenesis; however, formulating a topical agent has been hard due to its instability. More than recently, focus has at present shifted to the development of NAG-containing cosmeceuticals given its greater stability, proficient skin penetration, and overall tolerability. 69 NAG is typically used in ii% concentrations as monotherapy or in combination with niacinamide, which may lead to a greater clinical outcome given that there are two different mechanisms of depigmentation at piece of work. 69 Multiple double-blind, controlled clinical trials have shown the safe and efficacy of NAG alone or NAG/niacinamide combination therapy to significantly lighten hyperpigmentation secondary to solar radiation in Caucasian and Japanese patients. 68,69 NAG was generally well tolerated with balmy-to-moderate skin irritation reported in a small number of patients. However, big clinical studies are even so needed to determine the role of NAG in the management of PIH in all skin types.
Ascorbic acid. 50-ascorbic acid (AA) or vitamin C is a naturally occurring antioxidant obtained from certain fruits and vegetables. 23 AA causes pare lightening by interacting with copper ions at the tyrosinase active site and by reducing oxidized dopaquinone, a substrate in the melanin synthetic pathway. 23,70 In addition to pare lightening, other advantages of AA include not simply antioxidant furnishings but some studies also demonstrate anti-inflammatory and photoprotective properties. 71–76 However, early formulations of AA were unstable then esterified derivatives, such every bit ascorbyl-6-palmitate and magnesium ascorbyl phosphate, were created. 71 AA is typically used in 5 to 10% concentrations and tin can be formulated with other depigmenting agents, such as hydroquinone, which is generally well tolerated in pare of colour given the good safety profile of AA. 10,40 AA and its derivatives take been shown to be safe with some efficacy in sure racial/ethnic populations including Latino and Asian patients; however, most studies involved the handling of melasma and did not include PIH. 77,78
Licorice. Licorice root excerpt (Glycyrrhiza glabra, Glycyrrhiza uralensis) is a common ingredient constitute in many pare-lightening cosmeceuticals, 40 and is also used in the handling of a broad variety of diseases even outside the scope of dermatology due to its anti-inflammatory, antiviral, antimicrobial, and anticarcinogenic properties. 79 Some of the active ingredients in licorice root excerpt include glabridin, which inhibits tyrosinase and possesses anti-inflammatory effects, 80,81 and liquiritin, which does non inhibit tyrosinase only causes depigmentation past melanin dispersion and removal. 82 There are very few clinical trials that study the utility of licorice root extracts in the treatment of dermatological conditions. One study conducted in twenty Egyptian women showed that topical liquiritin cream (1g/twenty-four hour period) for four weeks was both safe and constructive in the treatment of melasma. 82 Side effects were minimal. Farther clinical studies with racial/ethnic patients are needed to evaluate the efficacy of licorice root extract in the treatment of PIH.
Soy. The activation of protease-activated receptor 2 (PAR-2) jail cell receptors found on keratinocytes mediates the transfer of melanosomes from melanocytes to surrounding keratinocytes. 83 Soy proteins, such as soybean trypsin inhibitor (STI) and Bowman-Birk inhibitor (BBI), inhibit the activation of these cell receptors, and as a event, phagocytosis of melanosomes into keratinocytes is reduced leading to reversible depigmentation. 83 Soy is now existence formulated alone or in combination with other agents including retinol and sunscreen into cosmeceuticals, particularly moisturizers, to help reduce the signs of photodamage too as PIH in all skin types. 84–86 A 16-week, double-bullheaded, placebo-controlled, clinical written report of African-American, Hispanic, and Asian patients with Fitzpatrick skin types III to Five and acne-induced PIH was conducted to determine the safety and efficacy of an OTC anti-acne treatment containing salicylic acrid, retinol, and total soy. 87 There was a meaning improvement in PIH with the soy formulation from baseline to written report endpoint as well every bit when compared to placebo. Soy-containing products are generally well tolerated. 40 However, more large-scale clinical trials in pare of colour are still needed.
Surgical therapy. Chemical peels. In 2008, chemic peeling was the fourth most common nonsurgical cosmetic procedure performed in the United States, 88 and dyschromias, such every bit PIH, are 1 of the most common indications for this procedure in skin of color. 89 For darker skinned individuals, superficial chemical peels, which penetrate into the papillary dermis, 90 are generally well tolerated with good clinical results. 10 Notwithstanding, care should exist taken in selecting and using the specific chemical peel to avert irritation, which can worsen PIH and lead to other complications, such as new areas of dyspigmentation, keloid formation, and hypertrophic scarring. 91 A detailed history, including other dermatological conditions, current oral and topical medications, history of herpes simplex virus (HSV) infection, past reactions to other cosmetic procedures, and a peel examination should be obtained prior to the procedure. 89,90,92
Glycolic acid (GA), found in sugarcane, is a naturally occurring alpha-hydroxy acid (AHA) that induces epidermolysis, disperses basal layer melanin, and increases dermal collagen synthesis. xc,93 GA concentrations range from twenty to 70%, and neutralization with water or sodium bicarbonate is required to cease the peel. Burns et al 94 conducted a 22-week clinical study of 16 African-American patients with Fitzpatrick skin types IV to VI and facial PIH. Patients were randomized to either the control group receiving 2% hydroquinone/ten% GA gel and 0.05% tretinoin or the peel group receiving the same topical regimen plus six GA peels (l–68%) at iii-week intervals. Significant clinical improvement from baseline was noted in the skin group by subjective measures (p<0.02), and colorimetric analysis also showed a tendency of more than rapid and greater improvement in the peel group. However, in that location were no meaning differences between the two groups by either measure.
Salicylic acid (SA), derived from willow tree bawl, is a beta-hydroxy acid that induces keratolysis by disrupting intercellular lipid linkages between epithelioid cells. 10,90 Superficial SA peels utilize concentrations ranging from 20 to 30% without the need for neutralization. A report of 24 Korean patients with acne-induced PIH underwent 30% SA peels every two weeks for three months. 95 Colorimetric analysis showed a significant improvement in the level of lightness from baseline to the starting time post-peel period (p<0.02), just final levels were not significant. Even so, erythema was significantly decreased (p<0.0001) and improvements were also noted in greasiness, dryness, and scaliness by clinical examination. The safety and efficacy of SA peels in the treatment of PIH has also been demonstrated in even higher skin phototypes 5 and Six. 96
Superficial chemical peels can also be obtained using trichloroacetic acid (TCA) or Jessner's solution, and both agents take been efficacious in the treatment of melasma. 97,98 Even so, clinical evidence supportive of the use of these agents for PIH in skin of color is lacking.
Nigh superficial chemical peeling agents are well tolerated by Fitzpatrick skin types Iv to VI. Common side effects include erythema, burning sensation, PIH, reactivation of HSV, superficial desquamation, and vesiculation. 89 Other complications include hypopigmentation, hypertrophic scarring, and keloid formation. Patients should too be educated on the importance of photoprotection to foreclose or avoid worsening PIH after chemic peeling.
Laser and low-cal-based therapies. Although topical skin-lightening agents remain the treatment of choice for PIH, lasers and light sources may exist an effective adjunct to therapy or alternative for handling failures. However, there is a paucity of literature specifically evaluating the employ of devices in the treatment of PIH in all pare types. Light-green (510nm, 532nm), carmine (694nm), or most-infrared (755nm, 1064nm) lasers are pigment-specific and generate light used to selectively target intracellular melanosomes. 99 Notwithstanding, due to the broad absorption spectrum of melanin (250nm–1200nm), laser free energy intended for deeper targets can be absorbed within the pigmented epidermis, which tin lead to complications such as dyschromias, baking, and scars. 100
Typically, free energy from brusk wavelength lasers is more efficiently absorbed past epidermal melanin while longer wavelengths penetrate deeper with more selective absorption by dermal targets making them safer to use for darker-skinned patients. 100 The use of longer pulse durations and cooling devices can also provide a greater margin of condom while still maintaining efficacy in darker skinned individuals. 100 There have been case reports of the successful treatment of PIH with bluish calorie-free photodynamic therapy, neodymium-doped yttrium aluminum garnet (Nd:YAG) laser, and fractional photothermolysis in darker pare types 101–103 ; however, larger clinical studies are needed to evaluate the function of these lasers besides as other devices, such as intense pulsed lite, in the handling of PIH.
Cosmetic camouflage. Corrective camouflage may be useful to conceal pigmentary disorders, vascular lesions, scars, and chronic peel conditions that are not acquiescent to medical or surgical treatments. 104 These coverage techniques tin assistance alleviate the patient's distress regarding their appearance and significantly improve quality of life. 105,106 Cover-up can be particularly useful in darker skinned individuals where pigmentary changes may be more noticeable and when highly visible parts of the body are affected by the disease, such as the face, cervix, and hands. 107
The characteristics of a expert cosmetic cover include a natural appearance and not-greasy experience, and the cover should also be waterproof, long lasting, and noncomedogenic with easy awarding. 108 There are four basic foundations: oil-based for dry skin, water-based for dry-to-normal skin, oil-free for oily skin, and water-free, which mixes oils with waxes to form thicker creams that can incorporate higher amounts of pigment to match the patient'due south normal skin color. 104 Cosmetic covers can be applied for subtle coverage up to full concealment, 109 and color correctors utilize the lesion's color opposite to neutralize its intensity. 104
Emerging therapies. Continued research is constantly fueled by the demand for newer, more effective depigmenting agents. Undecylenoyl phenylalanine 2% has been shown to safely and finer care for solar lentigines in a recent randomized, double-blind, vehicle-controlled clinical trial. 110 There have too been instance reports and clinical studies that have shown that topical 5% methimazole, 111 aloesin, 112 and dioic acid 113 tin successfully treat hyperpigmentation secondary to a variety of etiologies. Other agents that accept shown some depigmenting properties but require further research include 4-(1-phenylethyl)1,3-benzenediol, paper mulberry, ellagic acid, quinolines, piperlonguminine, luteolin, calycosin, emblica, and multivitamins. ten,114,115
Conclusion
In skin of color, postinflammatory hyperpigmentation tin be a common yet troubling sequelae of cutaneous inflammation. Yet, there are many rubber and effective treatments for this patient population including a diversity of topical depigmenting agents. It is important to initiate treatment early while at the same fourth dimension use caution with these agents to prevent farther worsening of the hyperpigmentation. Procedures such equally chemical peeling and laser therapy provide alternatives or adjuncts to topical therapy. Adding sunscreen to the treatment regimen and patient instruction regarding sunday protection measures will also exist beneficial in the management of patients with PIH.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921758/
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