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Clinical dermatology • Review article CED

Clinical and Experimental Dermatology


Postinflammatory hypopigmentation
V. Vachiramon and K. Thadanipon
Division of Dermatology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand


Summary Postinflammatory hypopigmentation is a common cause of acquired hypopigmentary

disorders. It can be a result of cutaneous inflammation, injury or dermatological
treatment. There are also many specific conditions that present with hypopigmentation
other than postinflammatory hypopigmentation. Most cases of postinflammatory
hypopigmentation improve spontaneously within weeks or months if the primary
cause is ceased; however, it can be permanent if there is complete destruction of
melanocytes. This article reviews the aetiology, pathogenesis, clinical features,
differential diagnosis and therapeutic options for postinflammatory hypopigmentation.

Table 1 shows the incidence of postinflammatory hypo-

pigmentation in particular conditions.2–9
Postinflammatory hypopigmentation is an acquired
partial or total loss of skin pigmentation occurring after
cutaneous inflammation. The distribution and severity
of pigment loss is related to the extent and degree of the Many cutaneous inflammatory conditions lead to
inflammation. With certain inflammatory skin diseases, postinflammatory hypopigmentation. Some, such as
some individuals develop hyperpigmentation, while pityriasis lichenoides chronica (PLC) and lichen striatus
others develop hypopigmentation, and some individuals (LS), tend to induce postinflammatory hypopigmenta-
develop both. When there is severe cutaneous inflam- tion rather than hyperpigmentation. Cutaneous injuries
mation, loss rather than dysfunction of melanocytes from burns, irritants and dermatological procedures
occurs, resulting in depigmentation.1 (e.g., chemical peels, dermabrasion, cryotherapy, laser
therapy) can also lead to postinflammatory hypo-
pigmentation (Table 2).
Patients with atopic dermatitis (AD) may present with
Postinflammatory hypopigmentation is a very common postinflammatory hypopigmentation. The pigmentary
pigmentary disorder. It can occur in all skin types. changes are more common and intense if potent topical
However, it is more common and prominent in people corticosteroids are used. Vitiligo-like depigmentation
with darker skins, possibly because of the colour contrast has been reported as a consequence of severe AD.10
with their normal skin. There is no gender difference in LS is another common cause of postinflammatory
the incidence of postinflammatory hypopigmentation. hypopigmentation, with an incidence of up to 59%.4
The dermatosis resolves spontaneously within 2 years,
leaving a transient hypopigmentation, especially in
Correspondence: Dr Vasanop Vachiramon, Division of Dermatology, Faculty dark-skinned people. In addition, the inflammatory
of Medicine Ramathibodi Hospital, Mahidol University, 270 Rama VI Road, phase may be undetectable, and hypopigmentation
Rajthevi, Bangkok 10400, Thailand
may be the sole feature.
In many dark-skinned patients, PLC may present with
Conflict of interest: none declared. extensive hypopigmentation with few characteristic
Accepted for publication 14 February 2011 scaly papular lesions.2

 The Author(s)
708 CED  2011 British Association of Dermatologists • Clinical and Experimental Dermatology, 36, 708–714
Postinflammatory hypopigmentation • V. Vachiramon and K. Thadanipon

Table 1 Incidence of postinflammatory hypopigmentation.

Incidence of
Patients, postinflammatory Study
Disease ⁄ condition n ⁄ skin type hypopigmentation, % location Ref.
PLC 5 ⁄ dark-skinned 100 USA
LyP 9 ⁄ NA 23 Spain
Lichen striatus 23 ⁄ NA 59.1 Spain
Cryotherapy 135 ⁄ NA 75 Italy
Dermabrasion 65 ⁄ NA 63 India
QS ruby 101 ⁄ NA 16.8 Japan
QS alexandrite 58 ⁄ NA 10.5 Hong Kong
QS Nd:YAG 105 ⁄ NA 7.6 Hong Kong
Alexandrite laser hair removal Hundreds ⁄ phototypes II–IV 0.5–3 USA

LyP, lymphomatoid papulosis; NA, data not available; ND:YAG, neodymium:yttrium–aluminium–garnet; PLC, pityriasis lichenoides
chronica; QS, Q-switched.

Table 2 Causes of postinflammatory hypopigmentation. keratinocytes and melanocytes are separated by oede-
Inflammatory skin diseases
ma. Thereafter, melanocytes migrate into the lesion,
Allergic contact dermatitis resulting in an area of hypopigmentation with a
Atopic dermatitis hyperpigmented rim. The pigmentary changes persist
Chronic graft versus host reaction for at least 6 months. After prolonged freezing, there is
Discoid lupus erythematosus
hypopigmentation with absence of melanosomes in
Insect-bite reactions
Lichen planus
keratinocytes, which may be due to a decrease in
Lichen striatus melanocyte number, reduction in melanosome synthe-
Lymphomatoid papulosis sis or block in melanosome transfer.13
Pityriasis lichenoides chronica Postinflammatory hypopigmentation is also a possible
complication of chemical peels. The use of Baker phenol
peel in the past was associated with porcelain-white
Stevens–Johnson syndrome (alabaster) skin. The likelihood of hypopigmentation
Infections depends on the quantity of phenol applied, the level of
Chickenpox occlusion, skin type (Fitzpatrick type I has a greater
Herpes zoster
likelihood) and existing photodamage.14 Savant6
reported a study on dermabrasion in 65 patients
Pinta with different facial conditions; 41 had permanent
Pityriasis versicolor hypopigmentation.
Syphilis Laser resurfacing commonly induces hypopigmenta-
tion, which seems to be related to the depth of resurfac-
Chemical peels
ing, and it may be permanent. It usually occurs 3–
Dermabrasion 10 months after the procedure. In one study, the
Laser incidence was up to 22% after CO2 laser resurfacing.15
Miscellaneous For pigment-specific laser, the rates of hypopigmentation
after treatment of naevus of Ota with Q-switch ruby, Q-
switch alexandrite, Q-switch neodymium:yttrium–alu-
Pigmentary changes are common after thermal burns minium–garnet (Nd:YAG) and a Q-switch alexan-
and freezing. In superficial burns, postinflammatory drite ⁄ Q-switch Nd:YAG combination are 16.8%,
hyperpigmentation commonly occurs, whereas deep 10.5%, 7.6% and 40%, respectively. Factors associated
burns may produce postinflammatory hypopigmenta- with higher risk include the number of treatment
tion.11 Melanocytes are very sensitive to cold, and sessions and the absorption spectrum of melanin; mel-
irreversible damage can occur at )4 to )7 C.12 After anin absorbs ruby laser (694 nm) better than alexan-
skin freezing, transient hypopigmentation is seen, drite laser (755 nm) or QS-Nd:YAG laser (1064 nm).7,8
caused by the blockage of melanin transfer from Pigmentary changes have also been associated with
melanocytes to keratinocytes, probably because alexandrite laser hair removal. Weisberg9 reported seven

 The Author(s)
CED  2011 British Association of Dermatologists • Clinical and Experimental Dermatology, 36, 708–714 709
Postinflammatory hypopigmentation • V. Vachiramon and K. Thadanipon

patients who developed similar pigmentary changes, keratinocytes. It is controlled by multiple mediators
described as initial hyperpigmented rings, followed by a (e.g., growth factors, cytokines) acting on melanocytes,
wafer-like crust, hypopigmentation and finally resolu- keratinocytes and fibroblasts. Through the release of
tion within 2 weeks to 6 months. these mediators, cutaneous inflammation may cause
aberration of melanogenesis. A study using histopath-
ological examination of hypopigmented lesions occur-
ring after laser resurfacing found variation in the
There is limited information about the mechanism and quantity of epidermal melanin and number of melano-
pathogenesis of postinflammatory hypopigmentation. cytes. It is suggested that hypopigmentation may result
The variation in individual response to cutaneous from inhibition of melanogenesis rather than destruc-
inflammation or trauma is not well understood. Ruiz- tion of melanocytes;17 however, severe inflammation
Maldonado16 proposed the term ‘individual chromatic may lead to loss of melanocytes or even melanocyte
tendency’ to describe this variation. Melanocytes can death, and thus permanent pigmentary changes.
react with normal, increased or decreased melanin
production in response to cutaneous inflammation or
Clinical features
trauma. The chromatic tendency is genetically deter-
mined, and inherited in an autosomal dominant The size and shape of hypopigmented lesions usually
pattern. People with weak melanocytes, which have correlate with the distribution and configuration of the
high susceptibility to damage, are more likely to develop original inflammatory dermatosis, and the colour
hypopigmentation, whereas those with strong melano- ranges from hypopigmentation to depigmentation
cytes tend to develop hyperpigmentation. However, (Fig. 1a–c). Complete depigmentation is commonly seen
dark-skinned people do not always have strong melano- in cases of severe AD and discoid lupus erythematosus,
cytes, and those with weak melanocytes are prone to and is more obvious in patients with darker skin.
develop hypopigmentation. Pigmentary changes sometimes coexist with the original
Melanogenesis is a complex process, which includes inflammatory lesions, making the diagnosis straightfor-
melanin synthesis, transport and release to ward. However, in some conditions, the inflammatory

(a) (b)

(c) (d)

Figure 1 Postinflammatory hypopigmentation caused by (a) lichen striatus, showing linear distribution of hypopigmented lesions along
Blaschko lines; (b) psoriasis, showing multiple well-demarcated hypopigmented lesions a similar size and shape to the original psoriasis
lesions. (c) Depigmentation secondary to discoid lupus erythematosus. The lesion is obvious in dark-complexioned skin because of the
colour contrast. (d) Hypopigmented and depigmented lesions secondary to low fluence Q-switched 1064-nm Nd:YAG laser therapy for
melasma. The configuration of the lesions corresponds to the size and shape of the laser spot.

 The Author(s)
710 CED  2011 British Association of Dermatologists • Clinical and Experimental Dermatology, 36, 708–714
Postinflammatory hypopigmentation • V. Vachiramon and K. Thadanipon

phase is not always present, and hypopigmentation may

be the only feature. Thus, repeated examinations are
required to identify the primary inflammatory derma- The most important step of management is to identify
tosis. Pigmentary changes caused by pigment-specific the cause. Once the underlying cause is effectively
laser are seen as small white macules that match the treated, the hypopigmentation usually improves over
size and shape of the laser spot (Fig. 1d). time. To prevent iatrogenic hypopigmentation, derma-
tological and cosmetic procedures should be performed
carefully, especially in high-risk patients.
Differential diagnosis
Twice-daily application of a medium-potency topical
The differential diagnosis of postinflammatory hypo- steroid in combination with a tar-based preparation has
pigmentation includes pityriasis alba, progressive been used to treat postinflammatory hypopigmentation,
macular hypomelanosis, pityriasis versicolor, leprosy, although the mechanisms behind this are currently not
sarcoidosis, hypopigmented lesions in acantholytic dis- well understood. The steroid may affect inflammatory
orders, hypopigmented lesions in extramammary Paget cells responsible for the inflammation,23 while the tar
disease, hypopigmented mycosis fungoides (MF), infun- may photodynamically induce melanogenesis.24 A
dibulomatosis, and hypopigmentation from medication, preparation of combined steroid and tar is more effective
especially potent topical corticosteroids and intralesion- in stimulating melanogenesis.23
al corticosteroids. These conditions can be differentiated Topical pimecrolimus cream was reported to be
by clinical findings (e.g., epidermal changes, induration, beneficial in an open-label, pilot trial for the treatment
presence of scales and lesion distribution) and histo- of seborrhoeic dermatitis with associated postinflamma-
pathological examination.18–20 tory hypopigmentation in dark-skinned patients.25
The differential diagnosis of postinflammatory de- The regimen consisted of twice-daily application of
pigmentation includes vitiligo, chemical leucoderma 1% pimecrolimus cream for 16 weeks. The degree of
and depigmented extramammary Paget disease. improvement, assessed by a mexameter, was greatest
during the first 2 weeks after the application.
Sun or ultraviolet (UV) exposure may help in
Investigations and diagnosis
repigmentation when there are functional melanocytes
Examination under Wood lamp accentuates the lesion, in the affected area; however, overexposure may
and helps distinguish between hypopigmented and enhance the colour contrast as a result of tanning of
depigmented lesions. In addition, it may help to exclude surrounding skin. Topical application of 0.1% 8-meth-
some conditions (e.g., progressive macular hypomelan- oxypsoralen, 0.5–1% coal tar or anthralin followed by
osis displays punctiform red fluorescence, whereas sun exposure can be helpful in the restoring the
pityriasis versicolor is coppery-orange). Confocal laser pigment.16 Various regimens of topical photochemo-
scanning microscopy may allow distinction between therapy (topical psoralen UVA; PUVA) have been used
different hypomelanotic conditions, based on the mel- to treat postinflammatory hypopigmentation caused by
anin content and distribution patterns. Melanophages various conditions, with favourable results. The regi-
have been found in postinflammatory hypopigmenta- men consists of topical application of 0.001–0.5% 8-
tion but not in vitiligo and naevus depigmentosus. methoxypsoralen in aquaphor or hydrophilic ointment
However, the contents of melanin and dermal papillary to the affected area for 20–30 min, followed by UVA
rings vary with the degree of the inflammation.21 exposure 1–3 times per week at an initial dose of 0.2–
Histopathology of postinflammatory hypopigmenta- 0.5 J ⁄ cm2, increasing by 0.2–0.5 J ⁄ cm2 weekly.17,23
tion shows nonspecific findings, including decreased The 308-nm excimer laser may be used to stimulate
epidermal melanin, variable degrees of superficial pigmentation in hypopigmented scars, and had a
lymphohistiocytic infiltration, and presence of mela- response rate of 60–70% after nine biweekly treatments.
nophages in the upper dermis. In addition, there may be However, regular subsequent treatment is needed every
some histopathological evidence that can help to 1–4 months to maintain the results.26 For extensive
establish the diagnosis of the cause of postinflammatory involvement, narrowband UVB phototherapy or oral
hypopigmentation, such as in lupus erythematosus.22 PUVA may be used 2–3 times weekly. The number of
Even if the biopsy shows nonspecific findings, it is still treatment sessions required is higher for repigmenting
useful in excluding many dermatoses that present with vitiligo lesions.23 The ablative fractional CO2 laser has
hypopigmentation only, such as MF, sarcoidosis and been reported to be effective in the treatment of hypopig-
leprosy. mentation associated with CO2 laser resurfacing.27

 The Author(s)
CED  2011 British Association of Dermatologists • Clinical and Experimental Dermatology, 36, 708–714 711
Postinflammatory hypopigmentation • V. Vachiramon and K. Thadanipon

In depigmented lesions with total loss of melanocytes,

epidermal or melanocyte grafting may be consid-
ered.28,29 Various methods of camouflage including We thank Drs P. Suchonwanit and S. Kanokrungsee for
high-coverage makeup, tanning products and tattooing their help in the preparation of the illustrations.
may be an alternative option.
Course and prognosis
1 Papa CM, Kligman AM. The behavior of melanocytes in
Minimal hypopigmentation usually resolves within a inflammation. J Invest Dermatol 1965; 45: 465–73.
few weeks, but severe hypopigmentation and de- 2 Lane TN, Parker SS. Pityriasis lichenoides chronica in
pigmentation associated with lupus erythematosus, black patients. Cutis 2010; 85: 125–9.
scleroderma or burn may require years to become 3 Martorell-Calatayud A, Hernandez-Martin A, Colmenero I
et al. Lymphomatoid papulosis in children. Report of 9
repigmented, and may be permanent.
cases and review of the literature. Actas Dermosifiliogr
2010; 101: 693–701.
Conclusion 4 Peramiquel L, Baselga E, Dalmau J et al. Lichen striatus.
Clinical and epidemiological review of 23 cases. Eur J
Postinflammatory hypopigmentation is a common Pediatr 2006; 165: 267–9.
acquired hypopigmented condition that tends to affect 5 Rusciani L, Paradisi A, Alfano C et al. Cryotherapy in
dark-skinned people. There are many disorders that the treatment of keloids. J Drugs Dermatol 2006; 5:
cause postinflammatory hypopigmentation. The most 591–5.
important key in its management is to identify and treat 6 Savant SS. Facial dermabrasion in acne scars and geno-
the primary cause. Current treatment options include dermatoses – a study of 65 patients. Indian J Dermatol
topical medication, phototherapy and laser. However, Venereol Leprol 2000; 66: 79–84.
7 Kono T, Nozaki M, Chan HH, Mikashima Y. A retrospective
there are limited data regarding the pathogenesis,
study looking at the long-term complications of Q-switched
natural course and treatment of postinflammatory
ruby laser in the treatment of nevus of Ota. Lasers Surg Med
hypopigmentation. Further studies are required to 2001; 29: 156–9.
determine the underlying mechanisms and efficacy of 8 Chan HH, Leung RS, Ying SY et al. A retrospective analysis
each treatment. of complications in the treatment of nevus of Ota with the
Q-switched alexandrite and Q-switched Nd:YAG lasers.
Dermatol Surg 2000; 26: 1000–6.
9 Weisberg NK, Greenbaum SS. Pigmentary changes after
Learning points
alexandrite laser hair removal. Dermatol Surg 2003; 29:
• Many types of cutaneous inflammatory condi- 415–19.
tions and injuries are associated with postinflam- 10 Larregue M, Martin J, Bressieux JM et al. Vitiligoid achro-
matory hypopigmentation. mias and severe atopic dermatitis. Apropos of 4 cases. Ann
Dermatol Venereol 1985; 112: 589–600.
• Some inflammatory conditions have a tendency
11 El-Bishry MA, Nassar AM, El-Maghraby MZ. Tattooing, a
to develop postinflammatory hypopigmentation
new hope for secondary leukoderma. Scand J Plast Reconstr
rather than hyperpigmentation, including PLC Surg 1979; 13: 147–53.
and LS. 12 Gage AA, Meenaghan MA, Natiella JR, Greene GW Jr.
• Skin biopsy can be of value to exclude dermatoses Sensitivity of pigmented mucosa and skin to freezing
that present with hypopigmentation only, such as injury. Cryobiology 1979; 16: 348–61.
MF, sarcoidosis and leprosy. 13 Burge SM, Bristol M, Millard PR, Dawber RP. Pigment
• The most important step of management is to changes in human skin after cryotherapy. Cryobiology
identify the cause of postinflammatory hypo- 1986; 23: 422–32.
pigmentation. The hypopigmentation usually im- 14 Brody HJ. Complications of chemical resurfacing. Dermatol
proves over time after the inflammation is ceased. Clin 2001; 19: 427–38, vii–viii.
15 Bernstein LJ, Kauvar AN, Grossman MC, Geronemus RG.
• Treatment options for postinflammatory hypo-
The short- and long-term side effects of carbon dioxide laser
pigmentation include topical tar, steroids, calcineu-
resurfacing. Dermatol Surg 1997; 23: 519–25.
rin inhibitors, phototherapy, excimer laser, fractional 16 Ruiz-Maldonado R, Orozco-Covarrubias ML. Postinflam-
ablative CO2 laser, grafting and camouflage. matory hypopigmentation and hyperpigmentation. Semin
Cutan Med Surg 1997; 16: 36–43.

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712 CED  2011 British Association of Dermatologists • Clinical and Experimental Dermatology, 36, 708–714
Postinflammatory hypopigmentation • V. Vachiramon and K. Thadanipon

17 Grimes PE, Bhawan J, Kim J et al. Laser resurfacing- 23 Halder RM, Richards GM. Management of dyschromias in
induced hypopigmentation: histologic alterations and ethnic skin. Dermatol Ther 2004; 17: 151–7.
repigmentation with topical photochemotherapy. Dermatol 24 Urbanek RW. Tar vitiligo therapy. J Am Acad Dermatol
Surg 2001; 27: 515–20. 1983; 8: 755.
18 Verma S, Patterson JW, Derdeyn AS et al. Hypopigmented 25 High WA, Pandya AG. Pilot trial of 1% pimecrolimus
macules in an Indian man. Arch Dermatol 2006; 142: cream in the treatment of seborrheic dermatitis in African
1643–8. American adults with associated hypopigmentation. J Am
19 Rowley MJ, Nesbitt LT Jr, Carrington PR, Espinoza CG. Acad Dermatol 2006; 54: 1083–8.
Hypopigmented macules in acantholytic disorders. Int J 26 Alexiades-Armenakas MR, Bernstein LJ, Friedman PM,
Dermatol 1995; 34: 390–2. Geronemus RG. The safety and efficacy of the 308-nm
20 Yang CC, Lee JY, Wong TW. Depigmented extramam- excimer laser for pigment correction of hypopigmented
mary Paget’s disease. Br J Dermatol 2004; 151: scars and striae alba. Arch Dermatol 2004; 140: 955–60.
1049–53. 27 Tierney EP, Hanke CW. Treatment of CO2 laser induced
21 Xiang W, Xu A, Xu J et al. In vivo confocal laser scanning hypopigmentation with ablative fractionated laser resur-
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comparison of confocal images in vitiligo, nevus depig- Dermatol 2010; 9: 1420–6.
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Med Sci 2010; 25: 551–8. Oncol 1987; 13: 44–8.
22 Franca AF, de Souza EM. Histopathology and immuno- 29 Suvanprakorn P, Dee-Ananlap S, Pongsomboon C, Klaus
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CPD questions Question 3

Below what temperature does irreversible melanocyte

Learning objectives
damage start to occur?
To review recent understanding related to the pathogen- a) 0 C
esis, causes and differential diagnosis of postinflammato- b) )7 C
ry hypopigmentation, and to demonstrate up-to-date c) )30 C
knowledge relating to the management of postinflamma- d) )88 C
tory hypopigmentation. e) )196 C

Question 1 Question 4

Which of the following diseases may be followed by Which of the following diseases may present with
postinflammatory hypopigmentation? hypopigmentation or depigmentation?
a) Psoriasis a) Leprosy
b) Lichen striatus b) Sarcoidosis
c) Allergic contact dermatitis c) Darier’s disease
d) Pityriasis lichenoides chronica d) Extramammary Paget disease
e) All of the above e) All of the above

Question 2 Question 5

Which of the following diseases may have complete What would you expect to see under Wood lamp in
depigmentation as a sequel? progressive macular hypomelanosis?
a) Psoriasis a) Punctiform red fluorescence
b) Lichen planus b) Punctiform green fluorescence
c) Insect-bite reaction c) Diffuse red fluorescence
d) Severe atopic dermatitis d) Diffuse green fluorescence
e) All of the above e) None of the above

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Postinflammatory hypopigmentation • V. Vachiramon and K. Thadanipon

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714 CED  2011 British Association of Dermatologists • Clinical and Experimental Dermatology, 36, 708–714