Medical CareThe treatment of postinflammatory hyperpigmentation (PIH) tends to be a difficult and prolonged process that often takes 6-12 months to achieve the desired results of depigmentation. Each of these treatment options potentially improves epidermal hypermelanosis, but none is proven effective for dermal hypermelanosis. Daily use of a broad-spectrum sunscreen (sun protection factor [SPF] 15 or greater) is an essential part of any therapeutic regimen. Show A variety of topical treatments have been used to treat epidermal postinflammatory hyperpigmentation, with varying degrees of success. These agents include hydroquinone, tretinoin cream, corticosteroids, glycolic acid (GA), and azelaic acid. [8] Lightening of hyperpigmented areas may be achieved with one of the previously named topical agents; however, a combination of topical creams and gels, chemical peels, and sunscreens may be necessary for significant improvement. [9] They are only effective for epidermal hyperpigmentation. In one study, the combination of salicylic acid peel and topical tretinoin treatment was better than either treatment alone. [10] Another study showed combining glycolic acid peels with a modified Kligman formula of hydroquinone 2%, tretinoin 0.05%, and hydrocortisone 1% was of particular benefit in facial postinflammatory hyperpigmentation in dark-skinned Indians. [11] Topical tretinoin 0.1% has been effective in treating postinflammatory hyperpigmentation. GA peels, in combination with tretinoin and hydroquinone, are an effective treatment of postinflammatory hyperpigmentation in dark-complexioned individuals. [12] All-trans retinoic acid aqueous gel 0.1-0.4% may be applied concomitantly with hydroquinone–lactic acid ointment for bleaching. [13, 14] After sufficient improvement of the hyperpigmentation is achieved, a corticosteroid may be applied topically with hydroquinone to promote healing. This combination of various topical therapeutic agents has been shown to be beneficial, especially on the face. Topical azelaic acid, which has been approved for the treatment of acne vulgaris, is useful for postinflammatory hyperpigmentation as well. [15] In acne patients who are prone to postinflammatory hyperpigmentation, azelaic acid may be a good treatment option. The efficacy of tazarotene 0.1% cream for the treatment of dyschromia associated with photoaging and for acne vulgaris may also be beneficial, particularly in people with dark skin tone. [16] Early and efficacious treatment of acne in patients with dark-toned skin helps minimize pigmentary abnormalities. [17] Other treatment modalities include use of trichloroacetic acid and gentle cryotherapy with liquid nitrogen. Each method must be used with extreme caution to avoid necrosis or blistering of the treated skin. These 2 methods of treatment should be avoided in dark-skinned patients because of the risk of permanent depigmentation and scarring. Pigmented makeup creams have also been successfully used to camouflage hyperpigmented skin to a hue similar to that of the surrounding unaffected skin. More options will be available in the future. Retinaldehyde (RAL) has shown depigmenting activity, while GA decreases the excess of pigment by a wounding and reepithelization process. A combination of RAL 0.1% and GA 6% (Diacneal) in the treatment of acne vulgaris and postinflammatory hyperpigmentation has been reported. [18] The peroxidase inhibitor methimazole, a noncytotoxic inhibitor of melanin production, is a possible agent for topical use in the years ahead. [19] The efficacy and safety of a combined treatment regimen including serial GA peels, topical azelaic acid cream, and adapalene gel in the treatment of recalcitrant melasma was evaluated in 28 patients in a prospective, randomized, controlled trial lasting 20 weeks. [20] Those receiving chemical peels underwent serial GA peels in combination with topical azelaic acid 20% cream (twice daily) and adapalene 0.1% gel (4 times daily, applied at night). Combined treatment with serial GA peels, azelaic acid cream, and adapalene gel may be an effective and safe therapy for recalcitrant melasma. Choi et al report that Lepidium apetalum is a potential inhibitor of hyperpigmentation caused by UV radiation. [21] Other studies suggest that decapeptide-12 was 17-fold more potent than hydroquinone at inhibiting tyrosinase in vitro. . [22, 23] Decapeptide-12 was shown not to be cytotoxic to melanocytes, making it a safer alternative to hydroquinone. A pilot study by Hantash and Jimenez showed that twice a day treatment for 4 months with decapeptide-12 formulated in a topical emulsion also resulted in a 50% improvement in melasma in patients who had failed 6 months of Tri-Luma therapy. [23] The potential of decapeptide-12 as a therapeutic option for melasma was recently reviewed. [24] Depigmenting agents abound in a variety of formations. Aloe vera leaf extract and its active ingredient aloin are considered potent skin depigmenting agents. [25] Delivery too can be important. Glabridin microsponge-loaded gel may be beneficial in treating hyperpigmentation. [26] Patients should never be treated with monobenzyl ether of hydroquinone because of the risk of developing disfiguring depigmented patches of skin either at the application site or at distal cutaneous sites. Topical application of epidermal growth factor reduces laser-induced postinflammatory hyperpigmentation. [27] Use of sunscreen for both ultraviolet and visible light protection is important to inhibit exacerbation of hyperpigmentation and to improve the appearance. [28] Also see Skin Lightening and Depigmenting Agents.  Surgical CareFractional photothermolysis may be used to treat postinflammatory hyperpigmentation after or in conjunction with ablative carbon dioxide laser resurfacing. [29, 30, 31] Paradoxically, successful treatment of postinflammatory hyperpigmentation after two sessions of fractional carbon dioxide laser has been described. [32] Laser treatment may be able to address dermal pigment deposition. The 1064-nm Q-switched Nd:YAG laser with low-fluence treatment may be considered in the treatment of postinflammatory hyperpigmentation caused by procedures such as laser surgery and chemical peeling in Asian patients. [33] A novel pulse-in-pulse mode intense pulsed light worked well for facial postinflammatory hyperpigmentation for Korean patients, [34] as did a picosecond 755-nm Alexandrite laser for postinflammatory hyperpigmentation. [35] Latanoprost-induced diffuse facial skin hyperpigmentation may be treated with laser. [36] PreventionPatients with postinflammatory hyperpigmentation (PIH) should use sunscreen on a daily basis to prevent any further darkening of lesions. A wound-dressing biomaterial may be used to prevent postinflammatory hyperpigmentation after suction blister epidermal grafting in stable vitiligo patients [37]
Author Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, New York Academy of Medicine, Royal College of Physicians of Edinburgh, Sigma Xi, The Scientific Research Honor Society Disclosure: Nothing to disclose. Coauthor(s) Basil M Hantash, MD, PhD, MBA Medical Director, Advanced Skin Institute Basil M Hantash, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, Sigma Xi, The Scientific Research Honor Society, Society for Investigative Dermatology Disclosure: Nothing to disclose. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape. Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American College of Rheumatology Disclosure: Received income in an amount equal to or greater than $250 from: Genentech as a consultant for a potential study on a drug that has yet to be approved for any use<br/>Received honoraria from UpToDate for author/editor; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for these trust accounts; I served on a safety monitoring committee for Principia Biopharma (ended 9-2021) for: Stocks held in various trust accounts: Allergen; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen; Gilead. Chief Editor Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology Disclosure: Nothing to disclose. Additional Contributors Andrea Leigh Zaenglein, MD Professor of Dermatology and Pediatrics, Department of Dermatology, Hershey Medical Center, Pennsylvania State University College of Medicine Andrea Leigh Zaenglein, MD is a member of the following medical societies: American Academy of Dermatology, Society for Pediatric Dermatology Disclosure: Received consulting fee from Galderma for consulting; Received consulting fee from Valeant for consulting; Received consulting fee from Promius for consulting; Received consulting fee from Anacor for consulting; Received grant/research funds from Stiefel for investigator; Received grant/research funds from Astellas for investigator; Received grant/research funds from Ranbaxy for other; Received consulting fee from Ranbaxy for consulting. Acknowledgements Nadia I Kihiczak, MD Staff Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey Medical School Nadia I Kihiczak, MD is a member of the following medical societies: American Academy of Dermatology Disclosure: Nothing to disclose. What is the fastest way to fade postAccording to Ayodele, a chemical peel is also a great way to fade post-inflammatory hyperpigmentation, as "it will help the skin to exfoliate quickly and fade the discolouration." Alpha-hydroxy-acids such as glycolic, lactic and mandelic acid work by dissolving the 'glue' that holds dead skin cells together, revealing ...
How long does it take for inflammatory hyperpigmentation to go away?The good news is PIH will eventually go away, even if left untreated. Since these spots are caused by melanin production, the affected skin will shed like all skin cells. On its own, PIH will generally resolve within two years.
How do you get rid of postFirst-line therapy typically consists of topical depigmenting agents in addition to photoprotection including a sunscreen. Topical tyrosinase inhibitors, such as hydroquinone, azelaic acid, kojic acid, arbutin, and certain licorice extracts, can effectively lighten areas of hypermelanosis.
How do you know PIH is permanent?Will PIH ever go away? Unlike acne scars, PIH is not permanent, though it may take anywhere from months to years to fade. The more the inflammation, the more obvious the discoloration. And, when the area is manipulated with abrasive treatments or picking the area, the longer the recovery.
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How long does post inflammatory hyperpigmentation last
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