Postinflammatory hyperpigmentation (PIH) is a frequently encountered problem and represents the sequelae of various cutaneous disorders as well as therapeutic interventions.  This acquired excess of pigment can be attributed to various preceding disease processes that affect the skin such as infections, allergic reactions, mechanical injuries, reactions to medications, phototoxic eruptions, trauma (eg, burns), and inflammatory diseases (eg, lichen planus, lupus erythematosus, atopic dermatitis).
Postinflammatory hyperpigmentation can also be seen following treatment with a number of electromagnetic devices such as ultrasound, radiofrequency, lasers, light-emitting diodes, and visible light, as well as secondary to microdermabrasion. Typically, postinflammatory hyperpigmentation is most severe in patients whose basal cell layer of the epidermis is disrupted such as lichenoid dermatoses or lupus erythematosus.
Postinflammatory hyperpigmentation is caused by 1 of 2 mechanisms that result in either epidermal or dermal melanosis. The epidermal inflammatory response (ie, dermatitis) results in the release and subsequent oxidation of arachidonic acid to prostaglandins, leukotrienes, and other products. These products of inflammation alter the activity of both immune cells and melanocytes. When 35% trichloroacetic acid (TCA) solution was applied to skin, it was found that TCA-induced postinflammatory hyperpigmentation might serve as a good in vivo model for the study of acne-induced postinflammatory hyperpigmentation. 
Specifically, these inflammatory products stimulate epidermal melanocytes, causing them to increase the synthesis of melanin and subsequently to increase the transfer of pigment to surrounding keratinocytes. Such increased stimulation and transfer of melanin granules results in epidermal hypermelanosis.
On the contrary, dermal melanosis occurs when inflammation disrupts the basal cell layer, causing melanin pigment to be released and subsequently trapped by macrophages in the papillary dermis, also known as pigmentary incontinence.
Fibroblast-derived melanogenic growth factors may be salient in mesenchymal-epithelial interactions modulating melanocyte function. 
Postinflammatory hyperpigmentation can occur with various disease processes that affect the skin. These processes include allergic reactions, infections, trauma, and phototoxic eruptions. Fractional laser photothermolysis occasionally induces postinflammatory hyperpigmentation. [4, 5]
Common inflammatory diseases that result in postinflammatory hyperpigmentation include acne excoriée, lichen planus, systemic lupus erythematosus, chronic dermatitis, and cutaneous T-cell lymphoma, especially erythrodermic variants.
Furthermore, lesions of postinflammatory hyperpigmentation can darken with exposure to UV light and various chemicals and medications, such as tetracycline, bleomycin, doxorubicin, 5-fluorouracil, busulfan, arsenicals, silver, gold, antimalarial drugs, hormones, and clofazimine.
Postinflammatory hyperpigmentation is a universal response of the skin, but it is more common in individuals with darker skin (Fitzpatrick skin types III to VI). Postinflammatory hyperpigmentation can be caused by any inflammatory process of the skin; however, it is more apparent in photo-induced dermatoses and more severe in lichenoid dermatoses.
Internationally, postinflammatory hyperpigmentation is a common inflammatory response of the skin, developing more commonly in darker skin. Despite their lighter skin color, certain Asians (from Pacific rim countries such as Japan, Taiwan, China) are more susceptible to developing PIH following one of the inciting factors listed above.
Although postinflammatory hyperpigmentation occurs in whites, it is more common in darker pigmented individuals including African Americans or Asians.
Postinflammatory hyperpigmentation occurs with equal incidence in males and females; it has no sexual predilection.
Postinflammatory hyperpigmentation can occur in persons of any age.
Morbidity associated with postinflammatory hyperpigmentation is related to the underlying inflammatory process that causes postinflammatory hyperpigmentation. If the hyperpigmentation is located in cosmetically sensitive regions, a significant amount of emotional distress may result.
Postinflammatory hyperpigmentation tends to fade with time and therapy, as previously discussed. Remnants of epidermal hyperpigmentation may persist for indefinite periods, typically 6-12 months, after the initial inflammatory process resolves. Dermal postinflammatory hyperpigmentation may even persist for years.
Educate patients about the cause of postinflammatory hyperpigmentation, prolonged therapy, and persistence of hyperpigmented lesions.
Kaufman BP, Aman T, Alexis AF. Postinflammatory Hyperpigmentation: Epidemiology, Clinical Presentation, Pathogenesis and Treatment. Am J Clin Dermatol. 2017 Dec 8. [Medline].
Isedeh P, Kohli I, Al-Jamal M, Agbai ON, Chaffins M, Devpura S, et al. An in vivo model for postinflammatory hyperpigmentation: an analysis of histological, spectroscopic, colorimetric and clinical traits. Br J Dermatol. 2016 Apr. 174 (4):862-8. [Medline].
Cardinali G, Kovacs D, Picardo M. Mechanisms underlying post-inflammatory hyperpigmentation: lessons from solar lentigo. Ann Dermatol Venereol. 2012 Dec. 139 Suppl 4:S148-52. [Medline].
Graber EM, Tanzi EL, Alster TS. Side effects and complications of fractional laser photothermolysis: experience with 961 treatments. Dermatol Surg. 2008 Mar. 34(3):301-5; discussion 305-7. [Medline].
Harari Z, Sommer I, Knobel B. Multifocal contact dermatitis to nitroderm TTS 5 with extensive postinflammatory hypermelanosis. Dermatologica. 1987. 174(5):249-52. [Medline].
Breathnach AS. Melanin hyperpigmentation of skin: melasma, topical treatment with azelaic acid, and other therapies. Cutis. 1996 Jan. 57(1 Suppl):36-45. [Medline].
Pandya AG, Guevara IL. Disorders of hyperpigmentation. Dermatol Clin. 2000 Jan. 18(1):91-8, ix. [Medline].
Mohamed Ali BM, Gheida SF, El Mahdy NA, Sadek SN. Evaluation of salicylic acid peeling in comparison with topical tretinoin in the treatment of postinflammatory hyperpigmentation. J Cosmet Dermatol. 2017 Mar. 16 (1):52-60. [Medline].
Sarkar R, Parmar NV, Kapoor S. Treatment of Postinflammatory Hyperpigmentation With a Combination of Glycolic Acid Peels and a Topical Regimen in Dark-Skinned Patients: A Comparative Study. Dermatol Surg. 2017 Apr. 43 (4):566-573. [Medline].
Burns RL, Prevost-Blank PL, Lawry MA, Lawry TB, Faria DT, Fivenson DP. Glycolic acid peels for postinflammatory hyperpigmentation in black patients. A comparative study. Dermatol Surg. 1997 Mar. 23(3):171-4; discussion 175. [Medline].
Yoshimura K, Harii K, Aoyama T, Shibuya F, Iga T. A new bleaching protocol for hyperpigmented skin lesions with a high concentration of all-trans retinoic acid aqueous gel. Aesthetic Plast Surg. 1999 Jul-Aug. 23(4):285-91. [Medline].
Yoshimura K, Harii K, Aoyama T, Iga T. Experience with a strong bleaching treatment for skin hyperpigmentation in Orientals. Plast Reconstr Surg. 2000 Mar. 105(3):1097-108; discussion 1109-10. [Medline].
Del Rosso JQ. The use of topical azelaic acid for common skin disorders other than inflammatory rosacea. Cutis. 2006 Feb. 77(2 Suppl):22-4. [Medline].
Grimes P, Callender V. Tazarotene cream for postinflammatory hyperpigmentation and acne vulgaris in darker skin: a double-blind, randomized, vehicle-controlled study. Cutis. 2006 Jan. 77(1):45-50. [Medline].
Shah SK, Alexis AF. Acne in skin of color: practical approaches to treatment. J Dermatolog Treat. 2010 May. 21(3):206-11. [Medline].
Katsambas AD. RALGA (Diacneal), a retinaldehyde and glycolic acid association and postinflammatory hyperpigmentation in acne–a review. Dermatology. 2005. 210 Suppl 1:39-45. [Medline].
Kasraee B, Handjani F, Parhizgar A, et al. Topical methimazole as a new treatment for postinflammatory hyperpigmentation: report of the first case. Dermatology. 2005. 211(4):360-2. [Medline].
Erbil H, Sezer E, Tastan B, Arca E, Kurumlu Z. Efficacy and safety of serial glycolic acid peels and a topical regimen in the treatment of recalcitrant melasma. J Dermatol. 2007 Jan. 34(1):25-30. [Medline].
Choi H, Ahn S, Lee BG, Chang I, Hwang JS. Inhibition of skin pigmentation by an extract of Lepidium apetalum and its possible implication in IL-6 mediated signaling. Pigment Cell Res. 2005 Dec. 18(6):439-46. [Medline].
Abu Ubeid A, Zhao L, Wang Y, Hantash BM. Short-sequence oligopeptides with inhibitory activity against mushroom and human tyrosinase. J Invest Dermatol. 2009 Sep. 129(9):2242-9. [Medline].
Kassim AT, Hussain M, Goldberg DJ. Open-label evaluation of the skin-brightening efficacy of a skin-brightening system using decapeptide-12. J Cosmet Laser Ther. 2012 Apr. 14(2):117-21. [Medline].
Hantash BM, Jimenez F. A split-face, double-blind, randomized and placebo-controlled pilot evaluation of a novel oligopeptide for the treatment of recalcitrant melasma. J Drugs Dermatol. 2009 Aug. 8(8):732-5. [Medline].
Sadick NS, Palmisano D. Novel synthetic oligopeptide formulation offers nonirritating cosmetic alternative for the treatment of melasma. Cosmet Dermatol. Apr 2010. 23:175-9.
Ali SA, Galgut JM, Choudhary RK. On The Novel Action of Melanolysis by a Leaf Extract of Aloe vera and Its Active Ingredient Aloin, Potent Skin Depigmenting Agents. Planta Med. 2012 May. 78(8):767-71. [Medline].
Park GH, Rhee do Y, Moon HR, Won CH, Lee MW, Choi JH, et al. Effect of an epidermal growth factor-containing cream on postinflammatory hyperpigmentation after Q-switched 532-nm neodymium-doped yttrium aluminum garnet laser treatment. Dermatol Surg. 2015 Jan. 41 (1):131-5. [Medline].
Deshmukh K, Poddar SS. Tyrosinase inhibitor-loaded microsponge drug delivery system: new approach for hyperpigmentation disorders. J Microencapsul. 2012 Apr 3. [Medline].
Rokhsar CK, Fitzpatrick RE. The treatment of melasma with fractional photothermolysis: a pilot study. Dermatol Surg. 2005 Dec. 31(12):1645-50. [Medline].
Huang L. A new modality for fractional CO2 laster resurfacing for acne scars in Asians. Lasers Med Sci. May 2012.
Rokhsar CK, Ciocon DH. Fractional photothermolysis for the treatment of postinflammatory hyperpigmentation after carbon dioxide laser resurfacing. Dermatol Surg. 2009 Mar. 35(3):535-7. [Medline].
Park JH, Kim JI, Kim WS. Treatment of Persistent Facial Postinflammatory Hyperpigmentation With Novel Pulse-in-Pulse Mode Intense Pulsed Light. Dermatol Surg. 2016 Feb. 42 (2):218-24. [Medline].
Lee YJ, Shin HJ, Noh TK, Choi KH, Chang SE. Treatment of Melasma and Post-Inflammatory Hyperpigmentation by a Picosecond 755-nm Alexandrite Laser in Asian Patients. Ann Dermatol. 2017 Dec. 29 (6):779-781. [Medline].
Kim S, Cho KH. Treatment of procedure-related postinflammatory hyperpigmentation using 1064-nm Q-switched Nd:YAG laser with low fluence in Asian patients: report of five cases. J Cosmet Dermatol. 2010 Dec. 9(4):302-6. [Medline].
[Guideline] Morton CA, McKenna KE, Rhodes LE. Guidelines for topical photodynamic therapy: update. Br J Dermatol. 2008 Dec. 159(6):1245-66. [Medline].
Pérez-Bernal A, Muñoz-Pérez MA, Camacho F. Management of facial hyperpigmentation. Am J Clin Dermatol. 2000 Sep-Oct. 1(5):261-8. [Medline].
Taylor MB, Yanaki JS, Draper DO, Shurtz JC, Coglianese M. Successful short-term and long-term treatment of melasma and postinflammatory hyperpigmentation using vitamin C with a full-face iontophoresis mask and a mandelic/malic acid skin care regimen. J Drugs Dermatol. 2013 Jan. 12(1):45-50. [Medline].
Nestor M, Bucay V, Callender V, Cohen JL, Sadick N, Waldorf H. Polypodium leucotomos as an Adjunct Treatment of Pigmentary Disorders. J Clin Aesthet Dermatol. 2014 Mar. 7(3):13-17. [Medline]. [Full Text].
Leyden J, Wallo W. The mechanism of action and clinical benefits of soy for the treatment of hyperpigmentation. Int J Dermatol. 2011 Apr. 50(4):470-7. [Medline].
Woolery-Lloyd HC, Keri J, Doig S. Retinoids and azelaic acid to treat acne and hyperpigmentation in skin of color. J Drugs Dermatol. 2013 Apr. 12(4):434-7. [Medline].
Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration
Disclosure: Nothing to disclose.
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, Society for Investigative Dermatology
Disclosure: Nothing to disclose.
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
Disclosure: Received income in an amount equal to or greater than $250 from: Lilly; Amgen <br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate 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 i inherited these trust accounts; for: Allergen; Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.
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.
Andrea Leigh Zaenglein, MD Professor of Dermatology and Pediatrics, Department of Dermatology, Hershey Medical Center, Pennsylvania State University College of Medicine
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.
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.
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