A 7-year-old African American girl was brought to her pediatrician by her mom who was worried that she was itching and that her skin was getting darker. The pediatrician knew the girl well as a patient with asthma and allergic rhinitis. In fact, the girl performed the allergic salute more than once in the office as she rubbed her itchy nose. Morgan-Dennie lines were seen under her eyes (Figure 168-1A). The mom undressed the girl to show the dark patches of skin around her knees (Figure 168-1B). Atopic dermatitis is common in the popliteal fossae and this girl clearly demonstrated the atopic triad: atopic dermatitis, asthma, and allergic rhinitis. The darkening of the skin around the knees and also seen on the neck is related to the scratching and rubbing of the skin secondary to the pruritus of atopic dermatitis. The pediatrician explained to the mom and child about the need to more aggressively treat the atopic dermatitis with emollients and topical steroids. No promises were made about the reversibility of the hyperpigmentation as each patient will respond differently to treatment.
A. Atopic triad in a 7-year-old girl with Dennie-Morgan lines and a nasal crease. B. Postinflammatory hyperpigmentation around the knees in the same girl. (Used with permission from Richard P. Usatine, MD.)
Postinflammatory hyperpigmentation (PIH) is an accumulation of melanin in response to chronic inflammation that usually appears as brown, black, or grey macules or patches in the pattern of an underlying inflammatory condition. Postinflammatory hyperpigmentation can result from any kind of irritant to the skin, but is more common in conditions resulting in chronic irritation and inflammation, and is more common in individuals with darker Fitzpatrick Skin Types IV, V, and VI. It is more severe and longer lasting if the underlying inflammatory condition goes untreated though most PIH will fade within 6 to 12 months of treating the underlying inflammatory condition. For the girl in the preceding case, the PIH may resolve without treatment after her atopic dermatitis clears up, but if the atopic dermatitis persists then the PIH will continue until the resolution of the underlying condition.
The prevalence of disorders of hyperpigmentation including post-inflammatory hyperpigmentation in the general population ranges from 0.42 percent in Kuwait to 55.9 percent in a sample population from Michigan.1
The prevalence in children in the US is around 22 percent based on a sample of hospitalized children in Kentucky.2
Postinflammatory hyperpigmentation (PIH) is one of the most common types of cutaneous hyperpigmentation, and although there are no good estimates of its prevalence in the children of the US, studies in Nigeria estimate PIH to represent 49.5 percent of skin lesions present in hospitalized children.3 In studies of adults, “dyschromia” is often used to combine disorders of hyperpigmentation, which would include melasma, lentigines, and PIH so true prevalence is difficult to obtain. In one study dyschromia was the second most common diagnosis among African American patients, but failed to make it into the top 10 for Caucasian patients.4
The distribution of PIH is equal among males and females of all ages.5
PIH is more common in dark-skinned individuals (Fitzpatrick skin types IV, V, and VI), and therefore is frequently found in individuals from Asia, Africa (Figure 168-2), South America, and Native Americans.6
The age at which a child could present with a hyperpigmented lesion varies, and PIH, erythema ab igne, and confluent and reticulated papillomatosis (CARP) are more common in older children and young adults versus young children (Figure 168-3).7
Other hyperpigmented lesions such as “linear and whorled hypermelanosis,” nevus of Ota, and Café au Lait spots are linked to embryologic mosaicism or genetic abnormalities, and may be seen at birth or within a few weeks after birth (Figures 168-4 and 168-5). Mongolian spots are nearly always present at birth (Figure 168-6).7
Just as PIH is most common in darker-skinned individuals, Nevus of Ota, Mongolian spot, Café au Lait macules, and CARP are more common in Asians and Blacks.7 Conversely, linear and whorled hypermelanosis shows no racial predilection.8
An African boy with a long history of atopic dermatitis and newly diagnosed scabies. Note how the postinflammatory hyperpigmentation is concentrated around the waist and forearms. (Used with permission from Richard P. Usatine, MD.)
Confluent and reticulated papillomatosis (CARP) in an obese 15-year-old boy with gynecomastia. (Used with permission from Richard P. Usatine, MD.)
Café au lait macule in a girl found to have tuberous sclerosis. (Used with permission from Richard P. Usatine, MD.)
Nevus of the Ota with a blue-gray coloration around the eye. (Used with permission from Richard P. Usatine, MD.)
Dermal melanocytosis (Mongolian spot) over the buttocks of a newborn. (Used with permission from Richard P. Usatine, MD.)
Etiology and Pathophysiology
The most common causes of postinflammatory hyperpigmentation are acne vulgaris, atopic dermatitis (Figure 168-7), and impetigo, but any insult to the skin from bug bites and minor burns to drug reactions and other rashes can result in postinflammatory hyperpigmentation.1,5
Postinflammatory hyperpigmentation may be divided based on whether the pigment accumulates in the epidermis or in the dermis. This can be helpful in terms of understanding the pathophysiology, characteristic appearances, and treatment modalities associated with the two categories.
Epidermal hyperpigmentation is thought to be in part caused by the release of inflammatory molecules such as prostanoids, cytokines, chemokines, and other products of arachidonic acid which leads to increased melanocyte activity, increased melanin production and release, and accumulation of melanin in adjacent keratinocytes.1,5,9,10
Dermal hyperpigmentation is thought to result from inflammatory mediated destruction of keratinocytes, which results in melanin release and its accumulation within macrophages in the upper dermis.1 Histologically this is described as “pigment incontinence.”
The distinction between accumulation of pigment in the epidermis and accumulation of pigment in the dermis is reflected in the appearance of the lesion on the skin. Dermal lesions tend to be a blue-gray color with indistinct boundaries and epidermal lesions tend to be tan, brown, or dark brown and with more sharply demarcated borders.1,11
In other disorders of hyperpigmentation the connection between the pathophysiology and the cutaneous appearance also exists; the color and shape of the pigment generally reflects both the location of melanin and the degree of melanocytic hyperplasia or release of melanin.7
Postinflammatory hyperpigmentation over the legs in a black child with severe atopic dermatitis. (Used with permission from John Browning, MD.)
The degree of pigmentation is strongly correlated with the total duration of the inflammatory process, where chronic or relapsing inflammatory processes cause darker and longer lasting hyperpigmentation.1
Darker-skinned individuals have larger and more densely distributed melanin pigment in their skin. In turn, they tend to react to inflammation with more accumulation of pigment, and therefore PIH tends to present with darker lesions that last longer.1,12
UV exposure is also associated with darkening and persistence of hyperpigmented lesions.13
The location of the pigmentation in the skin also effects the persistence of PIH, and dermal hyperpigmentation tends to last longer since the dermis does not continuously turnover like the epidermis.13
A Wood’s lamp examination can be used to distinguish between epidermal and dermal hyperpigmentation, where epidermal lesions will have distinct margins and a prominent border whereas dermal lesions will have fluffy, indistinct margins.5
In general, skin biopsies are unnecessary, but if the etiology is uncertain a 4-mm punch biopsy can help determine the underlying cause of PIH. The Fontana-Masson stain is used to identify melanin in the skin and is useful in distinguishing between epidermal and dermal hyperpigmentation.5
CARP is characterized by hyperkeratotic or verrucous scaly brown papules that coalesce into plaques, with peripheral reticular pattern with or without pruritus (Figure 168-8). It is generally first seen in inframammary region or interscapular region, and often spreads to the chest or abdomen (Figure 168-3). It can be found on the face, neck, extremities, flanks, or gluteal cleft. The etiology is unknown, but potential causes include a keratinization disorder, a reaction to a fungal or bacterial infection, photosensitivity, amyloidosis, and genetic factors.14,15
Confluent and reticulated papillomatosis (CARP) on the back of an African American girl. (Used with permission from Richard P. Usatine, MD.)
CARP can be distinguished from PIH both clinically and by its unique histology. CARP is raised and keratotic papules and plaques on the torso while PIH is typically flat macules or patches where there were previous lesions. Tinea versicolor occurs in a similar distribution to CARP (on the torso) but tinea versicolor is scaly patches and responds to oral or topical antifungal therapy (Figures 168-9 and 168-10).
Tinea versicolor on the back of a 16-year-old boy. Note the pinkish brown coloration. (Used with permission from Richard P. Usatine, MD.)
Tinea versicolor with a cape-like distribution over the chest in a black teenage boy. Note how the Malassezia furfur has caused a brown hyperpigmentation. (Used with permission from Richard P. Usatine, MD.)
CARP is a rare disorder, but it is most commonly seen in young adults (ages 18 to 21), and people with skin of color. In the US, it is more common in females than in males, but the gender distribution varies in different parts of the world. Minocycline is considered the first line treatment, but azithromycin, clarithromycin, fusidic acid, and retinoic acid have also been effective in case reports and case studies.14
Linear and Whorled Hypermelanosis (LAWH; Figure 168-11) is characterized by linear and whorled patches that occur along the lines of Blaschko (lines of embryological development).16 The lesions can occur anywhere on the body, but typically spare the mucous membranes, palms, soles, and eyes.16 LAWH appears within a few weeks of birth and will progressively expand and darken until the child is 1 to 2 years of age. The exact cause of LAWH is unknown, but it may be associated with underlying genetic mosaicism.8 There have been a few cases where LAWH was associated with neurologic abnormalities, but the association is very rare.16,17 In general, there is no need to do neurologic testing or brain imaging if the child seems normal and healthy.8
Segmental Hyperpigmentation presents at birth or in early childhood as a hyperpigmented patch on the truck with a characteristic delineation at midline, usually ventral giving them a dermatomal appearance (Figure 168-12). They are typically not Blaschkoid like LAWH and are more geometric than CALMs. There are no known associated abnormalities and is thought to be due to a somatic mosaicism.18
Erythema ab igne is reticular tan-brown pigmented patch (Figure 168-13). It is most commonly caused by prolonged exposure to heat or infrared.19 Although it is rare in children, it has been reported in children who use laptop computers directly on their laps.19 Other common causes include hot-water bottles, heating pads, and heated blankets. It is generally a self-limited condition, but prolonged exposure and recurrence of the lesions may predispose to squamous cell carcinoma or Merkel cell carcinoma.19
Café au Lait Macules (CALMs) are evenly pigmented light brown macules or patches (Figure 168-14). They are commonly solitary and present at birth though they can appear any time in the first few years of life.20 CALMs are also more common in blacks than whites. If CALMs continue to appear into adulthood or are multiple this warrants further investigation as these characteristics increase the likelihood of a coexisting condition like neurofibromatosis, tuberous sclerosis, McCune-Albright, or Noonan syndrome (Figures 168-4 and 168-14).20 There is no medical reason to treat CALMs. These lesions are caused by epidermal melanin, giant melanosomes, and increased melanocyte density. Skin lightening creams are not effective, but several lasers have been used with variable responses including Pulsed Dye, Erbium:YAG, Q-Switched Nd:YAG, QS Ruby, and QS Alexandrite. The risks of laser surgery include hypo/hyperpigmentation, scarring, incomplete removal, and recurrence.21
Dermal Melanocytosis (Mongolian Spot) is a blue-gray hyperpigmented patch that can vary in size, but is most commonly found on the gluteal region of newborns and infants (Figure 168-15).22 It is most prevalent in individuals of Asian and African ancestry, but it can occur in individuals of any race. The lesion is benign, has no known association with other congenital abnormalities, and will disappear in most children by the age of 4 but sometimes persists.22 Given the likelihood of spontaneous regression, there is no need for treatment.
Ashy Dermatosis (Erythema Dyschromicum Perstans [EDP]) is characterized by blue-gray macules that may have a raised erythematous border.23 They are most often found on the trunk, extremities, and neck (Figures 168-16 and 168-17). These lesions of unknown etiology are chronic and may grow larger and multiply over time. The prevalence is highest among Latin Americans though other races can be affected. EDP most commonly presents between the ages of 10 and 30, but can occur at any age.23 The treatment of EDP is limited and lesions are often permanent. Many therapies have been attempted but none are very effective.24
Nevus of Ota (oculodermal melanocytosis) is a speckled blue-gray or brown macular lesion that follows a dermatomal distribution usually unilaterally within the distribution of the ophthalmic and maxillary branches of the trigeminal nerve. In addition to skin, it may involve ocular and oral mucosal surfaces (Figure 168-18).25 These lesions represent a hamartoma of dermal melanocytes. Nevus Of Ito is the same process on the body and usually found on the shoulder. These lesions are often present at birth and tend to darken and expand with age. It is more commonly seen in Asian children, but can occur in any race and shows no gender predilection. The risk of malignant transformation in Nevus of Ota/Ito is extremely rare but there is up to 10 percent risk of glaucoma if the eye is involved. Nevus of Ota have also been associated with Sturge-Weber, Klippel-Trenaunay-Weber, and neurodevelopmental abnormalities.25 These risks make close follow-up important in pediatric patients. This dermal pigmentation responds well to laser therapy with the Q-switched ruby, Q-switched alexandrite, or Q-switched Nd:YAG lasers for cosmesis but they do not require treatment.26–28
In children with pigmented lesions, it is especially important to consider and rule out child abuse as a possibly cause.12 Bruising or PIH that is linear or geometric in nature should raise concern for abuse. Also, lesions of abuse on the back or buttocks in a child can mimic EDP or dermal melanocytosis (Figure 168-19); however, traumatic lesions will fade quickly compared to the latter.
Linear and whorled hypermelanosis has been present since birth in this otherwise healthy child. (Used with permission from Kane KS, Lio P, Stratigos AJ, Johnson RA. Color Atlas and Synopsis of Pediatric Dermatology, 2nd edition, Figure 12-8, New York, NY: McGraw-Hill, 2009.)
Segmental hyperpigmentation in a healthy 8-year-old boy. Lesion appeared shortly after birth as a faint patch and became more apparent in early childhood. (Used with permission from Jennifer Krejci-Mannwaring, MD.)
Erythema ab igne caused by repeated straddling of a place heater in an attempt to keep warm in a home without central heating. (Used with permission from Richard P. Usatine, MD.)
Café au lait macule in a child with neurofibromatosis. (Used with permission from Richard P. Usatine, MD.)
Dermal melanocytosis (Mongolian spot) in a black infant. (Used with permission from Richard P. Usatine, MD.)
Ashy dermatosis (erythema dyschromicum perstans) in an 8-year-old boy that was confirmed by a punch biopsy. (Used with permission from Richard P. Usatine, MD.)
Ashy dermatosis (erythema dyschromicum perstans) in a 4-year-old girl. (Used with permission from Richard P. Usatine, MD.)
Nevus of Ota around the eye with blue-gray scleral hyperpigmentation. (Used with permission from Richard P. Usatine, MD.)
Multiple patches of dermal melanocytosis (Mongolian spots) on the back and buttocks of a young black child. (Used with permission from Richard P. Usatine, MD.)
The first step in the management of PIH is to ascertain the underlying cause of cutaneous inflammation or trauma and rule out other causes of pigmented lesions.
The shape and distribution of the lesions should mirror the pattern of the underlying disorder and most patients with PIH will have a history of chronic skin disease or trauma. When there is no history of a chronic skin condition it is important to consider congenital diseases or other causes of hyperpigmentation, see differential diagnoses, which was previously discussed.
If the underlying cause is a treatable condition then prompt treatment is essential. Decreasing the development of additional PIH requires controlling the source of cutaneous inflammation.12
The first line of therapy for PIH is daily sunscreen use. Daily use of sunscreen with an SPF of 30 or greater has been shown to decrease the duration of postinflammatory hyperpigmentation and to prevent darkening of existing lesions.1 Any gains made with topical or other therapies can quickly be undone by short exposures to ultraviolet light. Behavior modification often requires additional patient/parent education. While darker skin types are more prone to pigmentary disorder they may not be as familiar sun protection behaviors given that they have a lower propensity for sunburn. “Physical sunscreens” (ones that are zinc or titanium based) are preferred, however, on darkly pigmented skin they may leave a gray or violaceous hue when applied and therefore an aesthetically acceptable product may be tricky. Sun protection should also include avoidance of peak sun hours (10 am to 4 pm), the use of wide brimmed hats, and long sleeves or pants depending on the body part affected.
Various topical skin-lightening agents have been used to treat PIH and other disorders of hyperpigmentation. The treatments include topical medication such as hydroquinone, retinoids, mequinol, azelaic acid, kojic acid, and licorice extract, ascorbic acid, niacinamide, N-acetyl glucosamine, and soy.1,12,29 In general, topical skin-lightening agents are most effective on epidermal pigmentation and less effective for dermal hyperpigmentation.12
The first line in topical treatment for PIH is hydroquinone, which can be used at various concentrations though there is no increase in efficacy at concentrations higher than 5 percent.13,30 Controlled trials have shown a decrease in skin hyperpigmentation as compared to baseline by 4 weeks after beginning therapy.31 The potential side effects include allergic dermatitis (most common), the development of a ring of hypopigmentation around the lesions, and rarely paradoxical darkening of the lesions (exogenous ochronosis).32
Combination therapies with hydroquinone show additional efficacy. Small trials of 4 percent hydroquinone and 0.15 percent retinol have shown significant improvement in the degree of pigmentation and the lesion size.31 Triple therapies combining 4 percent hydroquinone, 0.1 percent tretinoin, or 0.5 percent ascorbic acid, and topical steroids (dexamethasone or fluocinolone acetonide) resulted in higher rates of complete skin clearing of melasma than either hydroquinone monotherapy or dual therapy, but there is no such trial on the use of triple therapy in PIH.33
There is some evidence for the efficacy of tretinoin (retinoic acid) as monotherapy in the treatment of PIH. In one randomized control trial, 91 percent of the participants in the treatment group had significant lightening of their lesions compared to 57 percent in the control group based on clinical evaluation.34
There is some limited clinical evidence for the efficacy of such compounds as kojic acid, arbutin, niacinamide, n-acetyl glucosamine, ascorbic acid, licorice extract, and soy in treating hyperpigmentation. Most of the evidence for the efficacy of these naturally occurring chemicals is from trials for the treatment of melasma.29 Of the agents listed, topical soy extract is the only agent with significant evidence in PIH.13 Many of these compounds are marketed in over-the-counter products and may also contain derivatives of retinoic acid such as retinol or retinyl.
The most common procedures used in the treatment of hyperpigmented lesions are chemical peels and laser therapy. Both have been shown to be efficacious in randomized controlled trials, but they remain second-line treatments and are generally only indicated in combination with or after treatment with topical agents have failed.21
Chemical peels are used to treat hyperpigmentation.13 The chemical agents used for these procedures include glycolic acid (GA), salicylic acid, and trichloracetic acid.35,36 In general, superficial peels are recommended for people with skin of color to decrease the risk of additional postinflammatory hyperpigmentation. Side effects of chemical peels include erythema, burning/stinging, hypo/hyperpigmentation, ulceration, scarring, reactivation of HSV, and superficial desquamation. Repeated peels (5 or more) are often needed to achieve results.
A few randomized controlled trials have indicated that the use of GA chemical peels in addition to hydroquinone therapy was as effective in PIH as hydroquinone therapy and tended to work more quickly with more dramatic results.37 There is little data in the current literature assessing the safety of these therapies in children, though there are a few case reports of good outcomes in children with xeroderma pigmentosum and congenital melanocytic nevi.38,39
Lasers are used in the treatment of hyperpigmentation. Q-switch alexandrite, Q-switch ruby, Q-switch Nd:YAG, and nonablative fractional protolysis laser treatments have been effective in treatment of many hyperpigmented lesions including PIH, Mongolian Spots, Nevus of Ota, and Café Au Lait Macules.21,40,41 The wavelength of the system should be correctly matched to the depth of the lesion, and epidermal hyperpigmentation tends to respond best to shorter wavelengths, whereas dermal hyperpigmentation tends to respond best to longer wavelengths.41 Great care must also be taken to avoid increasing the pigmentation of the lesion or inducing postinflammatory hyperpigmentation, as both of these are known potential side effects of laser therapy.40 A review of laser use in children concluded that laser therapies are safe in children and in some cases are more efficacious than in adults.41
The course of postinflammatory hyperpigmentation is strongly dependent on controlling the underlying inflammatory disease. Once the underlying disease is treated most epidermal hyperpigmentation will resolve in 6 to 12 months, and with treatment the lesions may resolve as quickly as 4 weeks.5,31 Dermal hyperpigmentation has a comparatively prolonged course, and lesions can persist for years or be permanent despite treatment.5
The first step for children with PIH is to treat the underlying cause. Once the cause is treated simple reassurance and regular follow-up may be sufficient. More aggressive treatment should be considered for lesions in aesthetically sensitive areas such as the face, or, if the child experiences significant psychological distress.
In children with congenital hyperpigmented lesions that may lead to psychological distress, consider initiating treatment early but to give parents realistic expectations. Most congenital or persistent lesions, if responsive, will do so to more invasive treatments such as laser therapy.
PIH will generally resolve spontaneously over time, and the primary objective is to identify and eliminate the cause of inflammation in the skin.
Strict sun protection may prevent worsening of PIH and can help it fade more quickly.
If PIH persists, there are other treatment options but they have variable effectiveness and side effects and should be reserved for cases that have not resolved with watchful waiting.
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