CED

Clinical dermatology Review article

Clinical and Experimental Dermatology

CPD

Postinflammatory hypopigmentation
V. Vachiramon and K. Thadanipon
Division of Dermatology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand
doi:10.1111/j.1365-2230.2011.04088.x

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 hypopigmentation in particular conditions.29

Introduction
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
inflammation. With certain inflammatory skin diseases,
some individuals develop hyperpigmentation, while
others develop hypopigmentation, and some individuals
develop both. When there is severe cutaneous inflammation, loss rather than dysfunction of melanocytes
occurs, resulting in depigmentation.1

Epidemiology
Postinflammatory hypopigmentation is a very common
pigmentary disorder. It can occur in all skin types.
However, it is more common and prominent in people
with darker skins, possibly because of the colour contrast
with their normal skin. There is no gender difference in
the incidence of postinflammatory hypopigmentation.

Correspondence: Dr Vasanop Vachiramon, Division of Dermatology, Faculty

of Medicine Ramathibodi Hospital, Mahidol University, 270 Rama VI Road,
Rajthevi, Bangkok 10400, Thailand
E-mail: vasanop@gmail.com
Conflict of interest: none declared.
Accepted for publication 14 February 2011

708

Aetiology
Many cutaneous inflammatory conditions lead to
postinflammatory hypopigmentation. Some, such as
pityriasis lichenoides chronica (PLC) and lichen striatus
(LS), tend to induce postinflammatory hypopigmentation rather than hyperpigmentation. Cutaneous injuries
from burns, irritants and dermatological procedures
(e.g., chemical peels, dermabrasion, cryotherapy, laser
therapy) can also lead to postinflammatory hypopigmentation (Table 2).
Patients with atopic dermatitis (AD) may present with
postinflammatory hypopigmentation. The pigmentary
changes are more common and intense if potent topical
corticosteroids are used. Vitiligo-like depigmentation
has been reported as a consequence of severe AD.10
LS is another common cause of postinflammatory
hypopigmentation, with an incidence of up to 59%.4
The dermatosis resolves spontaneously within 2 years,
leaving a transient hypopigmentation, especially in
dark-skinned people. In addition, the inflammatory
phase may be undetectable, and hypopigmentation
may be the sole feature.
In many dark-skinned patients, PLC may present with
extensive hypopigmentation with few characteristic
scaly papular lesions.2

 The Author(s)
CED  2011 British Association of Dermatologists Clinical and Experimental Dermatology, 36, 708714

Postinflammatory hypopigmentation V. Vachiramon and K. Thadanipon

Table 1 Incidence of postinflammatory hypopigmentation.

Disease condition

Patients,
n skin type

Incidence of
postinflammatory
hypopigmentation, %

Study
location

PLC
LyP
Lichen striatus
Cryotherapy
Dermabrasion
QS ruby
QS alexandrite
QS Nd:YAG
Alexandrite laser hair removal

5 dark-skinned
9 NA
23 NA
135 NA
65 NA
101 NA
58 NA
105 NA
Hundreds phototypes IIIV

100
23
59.1
75
63
16.8
10.5
7.6
0.53

USA
Spain
Spain
Italy
India
Japan
Hong Kong
Hong Kong
USA

Ref.
2
3
4
5
6
7
8
8
9

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

Table 2 Causes of postinflammatory hypopigmentation.

Inflammatory skin diseases
Allergic contact dermatitis
Atopic dermatitis
Chronic graft versus host reaction
Discoid lupus erythematosus
Insect-bite reactions
Lichen planus
Lichen striatus
Lymphomatoid papulosis
Pityriasis lichenoides chronica
Psoriasis
Sarcoidosis
Scleroderma
StevensJohnson syndrome
Infections
Chickenpox
Herpes zoster
Impetigo
Onchocerciasis
Pinta
Pityriasis versicolor
Syphilis
Procedure-related
Chemical peels
Cryotherapy
Dermabrasion
Laser
Miscellaneous
Burns

Pigmentary changes are common after thermal burns

and freezing. In superficial burns, postinflammatory
hyperpigmentation commonly occurs, whereas deep
burns may produce postinflammatory hypopigmentation.11 Melanocytes are very sensitive to cold, and
irreversible damage can occur at )4 to )7 C.12 After
skin freezing, transient hypopigmentation is seen,
caused by the blockage of melanin transfer from
melanocytes to keratinocytes, probably because

keratinocytes and melanocytes are separated by oedema. Thereafter, melanocytes migrate into the lesion,
resulting in an area of hypopigmentation with a
hyperpigmented rim. The pigmentary changes persist
for at least 6 months. After prolonged freezing, there is
hypopigmentation with absence of melanosomes in
keratinocytes, which may be due to a decrease in
melanocyte number, reduction in melanosome synthesis or block in melanosome transfer.13
Postinflammatory hypopigmentation is also a possible
complication of chemical peels. The use of Baker phenol
peel in the past was associated with porcelain-white
(alabaster) skin. The likelihood of hypopigmentation
depends on the quantity of phenol applied, the level of
occlusion, skin type (Fitzpatrick type I has a greater
likelihood) and existing photodamage.14 Savant6
reported a study on dermabrasion in 65 patients
with different facial conditions; 41 had permanent
hypopigmentation.
Laser resurfacing commonly induces hypopigmentation, which seems to be related to the depth of resurfacing, and it may be permanent. It usually occurs 3
10 months after the procedure. In one study, the
incidence was up to 22% after CO2 laser resurfacing.15
For pigment-specific laser, the rates of hypopigmentation
after treatment of naevus of Ota with Q-switch ruby, Qswitch alexandrite, Q-switch neodymium:yttriumaluminiumgarnet (Nd:YAG) and a Q-switch alexandrite Q-switch Nd:YAG combination are 16.8%,
10.5%, 7.6% and 40%, respectively. Factors associated
with higher risk include the number of treatment
sessions and the absorption spectrum of melanin; melanin absorbs ruby laser (694 nm) better than alexandrite laser (755 nm) or QS-Nd:YAG laser (1064 nm).7,8
Pigmentary changes have also been associated with
alexandrite laser hair removal. Weisberg9 reported seven

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Postinflammatory hypopigmentation V. Vachiramon and K. Thadanipon

patients who developed similar pigmentary changes,

described as initial hyperpigmented rings, followed by a
wafer-like crust, hypopigmentation and finally resolution within 2 weeks to 6 months.

Pathogenesis
There is limited information about the mechanism and
pathogenesis of postinflammatory hypopigmentation.
The variation in individual response to cutaneous
inflammation or trauma is not well understood. RuizMaldonado16 proposed the term individual chromatic
tendency to describe this variation. Melanocytes can
react with normal, increased or decreased melanin
production in response to cutaneous inflammation or
trauma. The chromatic tendency is genetically determined, and inherited in an autosomal dominant
pattern. People with weak melanocytes, which have
high susceptibility to damage, are more likely to develop
hypopigmentation, whereas those with strong melanocytes tend to develop hyperpigmentation. However,
dark-skinned people do not always have strong melanocytes, and those with weak melanocytes are prone to
develop hypopigmentation.
Melanogenesis is a complex process, which includes
melanin synthesis, transport and release to
(a)

(c)

keratinocytes. It is controlled by multiple mediators

(e.g., growth factors, cytokines) acting on melanocytes,
keratinocytes and fibroblasts. Through the release of
these mediators, cutaneous inflammation may cause
aberration of melanogenesis. A study using histopathological examination of hypopigmented lesions occurring after laser resurfacing found variation in the
quantity of epidermal melanin and number of melanocytes. It is suggested that hypopigmentation may result
from inhibition of melanogenesis rather than destruction of melanocytes;17 however, severe inflammation
may lead to loss of melanocytes or even melanocyte
death, and thus permanent pigmentary changes.

Clinical features
The size and shape of hypopigmented lesions usually
correlate with the distribution and configuration of the
original inflammatory dermatosis, and the colour
ranges from hypopigmentation to depigmentation
(Fig. 1ac). Complete depigmentation is commonly seen
in cases of severe AD and discoid lupus erythematosus,
and is more obvious in patients with darker skin.
Pigmentary changes sometimes coexist with the original
inflammatory lesions, making the diagnosis straightforward. However, in some conditions, the inflammatory
(b)

(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.

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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 dermatosis. Pigmentary changes caused by pigment-specific
laser are seen as small white macules that match the
size and shape of the laser spot (Fig. 1d).

Differential diagnosis
The differential diagnosis of postinflammatory hypopigmentation includes pityriasis alba, progressive
macular hypomelanosis, pityriasis versicolor, leprosy,
sarcoidosis, hypopigmented lesions in acantholytic disorders, hypopigmented lesions in extramammary Paget
disease, hypopigmented mycosis fungoides (MF), infundibulomatosis, and hypopigmentation from medication,
especially potent topical corticosteroids and intralesional corticosteroids. These conditions can be differentiated
by clinical findings (e.g., epidermal changes, induration,
presence of scales and lesion distribution) and histopathological examination.1820
The differential diagnosis of postinflammatory depigmentation includes vitiligo, chemical leucoderma
and depigmented extramammary Paget disease.

Investigations and diagnosis

Examination under Wood lamp accentuates the lesion,
and helps distinguish between hypopigmented and
depigmented lesions. In addition, it may help to exclude
some conditions (e.g., progressive macular hypomelanosis displays punctiform red fluorescence, whereas
pityriasis versicolor is coppery-orange). Confocal laser
scanning microscopy may allow distinction between
different hypomelanotic conditions, based on the melanin content and distribution patterns. Melanophages
have been found in postinflammatory hypopigmentation but not in vitiligo and naevus depigmentosus.
However, the contents of melanin and dermal papillary
rings vary with the degree of the inflammation.21
Histopathology of postinflammatory hypopigmentation shows nonspecific findings, including decreased
epidermal melanin, variable degrees of superficial
lymphohistiocytic infiltration, and presence of melanophages in the upper dermis. In addition, there may be
some histopathological evidence that can help to
establish the diagnosis of the cause of postinflammatory
hypopigmentation, such as in lupus erythematosus.22
Even if the biopsy shows nonspecific findings, it is still
useful in excluding many dermatoses that present with
hypopigmentation only, such as MF, sarcoidosis and
leprosy.

Management
The most important step of management is to identify
the cause. Once the underlying cause is effectively
treated, the hypopigmentation usually improves over
time. To prevent iatrogenic hypopigmentation, dermatological and cosmetic procedures should be performed
carefully, especially in high-risk patients.
Twice-daily application of a medium-potency topical
steroid in combination with a tar-based preparation has
been used to treat postinflammatory hypopigmentation,
although the mechanisms behind this are currently not
well understood. The steroid may affect inflammatory
cells responsible for the inflammation,23 while the tar
may photodynamically induce melanogenesis.24 A
preparation of combined steroid and tar is more effective
in stimulating melanogenesis.23
Topical pimecrolimus cream was reported to be
beneficial in an open-label, pilot trial for the treatment
of seborrhoeic dermatitis with associated postinflammatory hypopigmentation in dark-skinned patients.25
The regimen consisted of twice-daily application of
1% pimecrolimus cream for 16 weeks. The degree of
improvement, assessed by a mexameter, was greatest
during the first 2 weeks after the application.
Sun or ultraviolet (UV) exposure may help in
repigmentation when there are functional melanocytes
in the affected area; however, overexposure may
enhance the colour contrast as a result of tanning of
surrounding skin. Topical application of 0.1% 8-methoxypsoralen, 0.51% coal tar or anthralin followed by
sun exposure can be helpful in the restoring the
pigment.16 Various regimens of topical photochemotherapy (topical psoralen UVA; PUVA) have been used
to treat postinflammatory hypopigmentation caused by
various conditions, with favourable results. The regimen consists of topical application of 0.0010.5% 8methoxypsoralen in aquaphor or hydrophilic ointment
to the affected area for 2030 min, followed by UVA
exposure 13 times per week at an initial dose of 0.2
0.5 J cm2, increasing by 0.20.5 J cm2 weekly.17,23
The 308-nm excimer laser may be used to stimulate
pigmentation in hypopigmented scars, and had a
response rate of 6070% after nine biweekly treatments.
However, regular subsequent treatment is needed every
14 months to maintain the results.26 For extensive
involvement, narrowband UVB phototherapy or oral
PUVA may be used 23 times weekly. The number of
treatment sessions required is higher for repigmenting
vitiligo lesions.23 The ablative fractional CO2 laser has
been reported to be effective in the treatment of hypopigmentation associated with CO2 laser resurfacing.27

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Postinflammatory hypopigmentation V. Vachiramon and K. Thadanipon

In depigmented lesions with total loss of melanocytes,

epidermal or melanocyte grafting may be considered.28,29 Various methods of camouflage including
high-coverage makeup, tanning products and tattooing
may be an alternative option.

Acknowledgement
We thank Drs P. Suchonwanit and S. Kanokrungsee for
their help in the preparation of the illustrations.

References
Course and prognosis
Minimal hypopigmentation usually resolves within a
few weeks, but severe hypopigmentation and depigmentation associated with lupus erythematosus,
scleroderma or burn may require years to become
repigmented, and may be permanent.

Conclusion
Postinflammatory hypopigmentation is a common
acquired hypopigmented condition that tends to affect
dark-skinned people. There are many disorders that
cause postinflammatory hypopigmentation. The most
important key in its management is to identify and treat
the primary cause. Current treatment options include
topical medication, phototherapy and laser. However,
there are limited data regarding the pathogenesis,
natural course and treatment of postinflammatory
hypopigmentation. Further studies are required to
determine the underlying mechanisms and efficacy of
each treatment.

Learning points
Many types of cutaneous inflammatory conditions and injuries are associated with postinflammatory hypopigmentation.
Some inflammatory conditions have a tendency
to develop postinflammatory hypopigmentation
rather than hyperpigmentation, including PLC
and LS.
Skin biopsy can be of value to exclude dermatoses
that present with hypopigmentation only, such as
MF, sarcoidosis and leprosy.
The most important step of management is to
identify the cause of postinflammatory hypopigmentation. The hypopigmentation usually improves over time after the inflammation is ceased.
Treatment options for postinflammatory hypopigmentation include topical tar, steroids, calcineurin inhibitors, phototherapy, excimer laser, fractional
ablative CO2 laser, grafting and camouflage.

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CPD questions

Question 3

To review recent understanding related to the pathogenesis, causes and differential diagnosis of postinflammatory hypopigmentation, and to demonstrate up-to-date
knowledge relating to the management of postinflammatory hypopigmentation.

Below what temperature does irreversible melanocyte

damage start to occur?
a) 0 C
b) )7 C
c) )30 C
d) )88 C
e) )196 C

Question 1

Question 4

Which of the following diseases may be followed by

postinflammatory hypopigmentation?
a) Psoriasis
b) Lichen striatus
c) Allergic contact dermatitis
d) Pityriasis lichenoides chronica
e) All of the above

Which of the following diseases may present with

hypopigmentation or depigmentation?
a) Leprosy
b) Sarcoidosis
c) Dariers disease
d) Extramammary Paget disease
e) All of the above

Question 2

Question 5

Which of the following diseases may have complete

depigmentation as a sequel?
a) Psoriasis
b) Lichen planus
c) Insect-bite reaction
d) Severe atopic dermatitis
e) All of the above

What would you expect to see under Wood lamp in

progressive macular hypomelanosis?
a) Punctiform red fluorescence
b) Punctiform green fluorescence
c) Diffuse red fluorescence
d) Diffuse green fluorescence
e) None of the above

Learning objectives

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