ABSTRACT CASE REPORT
A Case of Lichen Planus Pigmentosus
Lichen planus pigmentosus is a
with Facial Dyspigmentation
photodistributed dyschromia of
unknown etiology described
Responsive to Combination Therapy
clinically as hyperpigmented
with Chemical Peels and
gray-blue or brown-black
macules or patches in a photo-
Topical Retinoids
distributed pattern. Although
there has been some debate,
lichen planus pigmentosus is
considered by many to be a
separate diagnostic entity from
aMARISA WOLFF, DO; bNINA SABZEVARI, MSIV; cCHARLES GROPPER, MD; dCINDY HOFFMAN, DO
ashy dermatosis or erythema
aChief Resident, New York College of Osteopathic Medicine of New York Institute of Technology, Department of
dyschromicum perstans, which Dermatology, St. Barnabas Hospital, Bronx, New York; bMedical Student, Edward Via College of Osteopathic Medicine,
shares similar characteristics. Blacksburg, Virginia; cChief of Dermatology St. Barnabas Hospital and Associate Professor at Albert Einstein School of
Medicine, Bronx, New York; dResidency Program Director, New York College of Osteopathic Medicine of New York
Various treatment strategies Institute of Technology, Department of Dermatology, St. Barnabas Hospital, Bronx, New York
have been applied to help
resolve or improve the
appearance of lichen planus
pigmentosus lesions; however,
an optimal treatment method is
yet to be elucidated. The
authors present a case of an 18-
year-old Hispanic man with
lichen planus pigmentosus
whose skin findings responded
dramatically to a combined
regimen of daily topical azelaic
acid foam and tretinoin cream
LICHEN PLANUS PIGMENTOSUS Hispanics and African Americans.4,5
L
with twice-monthly chemical
(LPP) is considered a macular variant Lesions can exhibit a range of
peels using glycolic acid and
of lichen planus with an unknown pigmentary dyschromia, from brown-
Jessner’s solution. The authors
etiology. The condition was first blackish to blue or purple-gray
have noted a sparcity of
described by Bhutani et al as a macules and patches, which
therapeutic literature for lichen
condition recognized in India, predominantly involve the sun-
planus pigmentosus, and hope
presenting in the third to fourth exposed aspects of upper extremities,
to aid clinicians in therapeutic
decade of life and manifesting as face, and neck.4 Areas of involvement
management strategy for this
dyspigmented macules or patches.1–4 tend to be asymptomatic, but pruritus
patient subset.
Since its discovery, LPP has often or burning may be present.
been reported in a variety of ages and Histology classically demonstrates
J Clin Aesthet Dermatol.
darker skin typed ethnicities including hyperkeratosis, epidermal thinning,
2016;9(11):44–50
Disclosure:The authors report no relevant conflicts of interest.
Author correspondence: Marisa Wolff, DO; E-mail: mhwolff@gmail.com
44 JCAD journal of clinical and aesthetic dermatology November 2016 • Volume 9 • Number 11
CASE REPORT
vacuolar degeneration of the basal
cell layer, lymphohistiocytic band-
like infiltrate, variable Civatte or
colloid bodies, and melanin
incontinence.3–5 There are several
treatment options that have been
reported with variable efficacy for
improvement of the appearance of
the lesions, but due to the
chronicity of the underlying
disease process, none of these
treatments are curative.
An 18-year-old Hispanic man
CASE REPORT
presented to our Bronx, New York,
clinic in autumn with an eight-
month history of an asymptomatic
dyspigmentation of the skin on his
face, neck, and bilateral forearms
Figure 1. Multiple round-oval blue-gray macules coalescing into patches on right
that had gradually worsened. He
forearm.
denied preceding cutaneous
redness, scale, pain, or pruritus. perstans, drug-induced and protective clothing. Following
There was no truncal or lower hyperpigmentation (although biopsy confirmation of the
extremity involvement, but he did denied minocycline use), post- diagnosis, combination therapy
admit to frequent sun exposure and inflammatory pigmentary was added with topical lightening
lack of sun protection. Past medical alteration from a resolved medications and superficial
history was significant only for dermatitis, pigmented contact chemical peels for lightening and
mild facial acne, with no history of dermatitis, and a resolved resurfacing. The authors began the
topical prescription or over-the- phototoxic or photoallergic patient on topical 5% azelaic acid
counter medications. No one in his reaction. foam to face to be applied in the
family had similar lesions, and he A 3mm punch biopsy obtained morning, and tretinoin 0.1% cream
denies any personal or family from the right forearm to face and arms at night.
history of autoimmune disease. demonstrated a patchy vacuolar Chemical peels were applied every
Physical examination interface dermatitis with melanin two weeks, with Jessner’s peel
demonstrated multiple round-to- incontinence, dermal selected for his arms and glycolic
oval blue-gray macules and melanophages, and mild dermal acid peels applied to his face.
patches with some areas of atrophy (Figure 3). These findings, Jessner’s peel requires no
coalescence scattered in the setting of his clinical neutralization and was evenly
symmetrically on lateral aspect of presentation, confirmed the applied to entire upper extremities
his cheeks, neck, and diagnosis of lichen planus with one layer at initial visit, with
circumferentially on his forearms pigmentosus. two layers at each follow-up.
in a photodistributed pattern Initial treatment regimen Glycolic acid peels were
(Figures 1 and 2). included daily sun protection with administered evenly with two
Differential diagnosis included use of sunscreen with a minimal passes on the entire face, sparing
LPP, erythema dyschromia sun protection factor (SPF) of 30 only periocular skin and ears.
JCAD journal of clinical and aesthetic dermatology November 2016 • Volume 9 • Number 11 45
CASE REPORT
Following an even application, the
patient was under physician
observation for redness, itching,
burning, or discomfort to signify
endpoint of treatment of glycolic
acid, with time ranging from 2 to 8
minutes as tolerated
symptomatically by the patient. At
endpoint, the glycolic acid was
neutralized with water, and
sunscreen was applied to face and
arms. Glycolic peel strength was
increased sequentially at each visit,
with two treatments of 35%
followed by two treatments of 50%
glycolic acid. Peels had been
premade by the manufacturer and
were not buffered or altered. After
eight weeks of therapy (four
peels), the authors’ patient noticed
a significant improvement in his
facial dyspigmentation (Figure 4).
Peel frequency then changed to
monthly due to schedule
Figure 2. Multiple round-oval blue-gray macules coalescing into patches along the
limitations, and topical therapy and
temple, cheek, jaw, and neck.
photoprotection measures were
continued daily. He received two
additional chemical peels with
Jessner’s for his arms, and glycolic
acid 70% on his face. After 16 total
weeks of treatment, a marked
improvement in the appearance of
his facial lesions was noted (Figure
5). While the dyschromia on his
arm lesions did mildly improve,
the difference was not as clinically
dramatic as his facial response.
Future therapy will include
neodymium-doped yttrium
aluminium garnet (Nd-YAG) laser
and the addition of tacrolimus
Figure 3. H&E (40x) revealing patchy vacuolar interface dermatitis with melanin ointment.
incontinence, dermal melanophages, and mild dermal atrophy.
Lichen planus pigmentosus is a
DISCUSSION
chronic relapsing and remitting
46 JCAD journal of clinical and aesthetic dermatology November 2016 • Volume 9 • Number 11
CASE REPORT
dyspigmentation of the skin that
has primarily been identified in
darker ethnic skin types commonly
in young-to-middle-aged adults,
particularly in the third to fourth
decade.3,5 LPP was first described
in 1974 by Bhutani et al after they
investigated a subset of Indian
patients with similar dermatologic
findings to erythema
dyschromicum perstans (EDP)
(also known as ashy dermatosis),
except that they also had
associated lichen planus clinically
and histologically.5 They
considered this new entity as a
macular variant of lichen planus.
While there is considerable overlap
between EDP and LPP, in 1992,
Vega et al6 reported that these
Figure 4. Decreased blue-gray dyschromia of face after four weeks of biweekly
conditions are distinct entities and
superficial glycolic acid chemical peels and daily azelaic acid foam and tretinoin
presented clinical and
cream.
histopathological differences
between the two. Similarities in the
physical and histologic appearance
of LPP and EDP have made the
diagnosis difficult in the past, but
notable differences identified by
Vega et al has helped clinicians in
distinguishing between the two
diseases.6
Both LPP and EDP are
characterized by dyschromic dark-
brown or slate-gray macules.
Distinction can be made early on,
as lesions of EDP initially present
with an asymptomatic dyschromia
with an erythematous and slightly
elevated margin and often involve
sun-protected areas such as the
trunk and proximal extremities, but
can also include the face, neck, and
upper extremities.6–8 Within several
Figure 5. Markedly improved dyschromia of face and neck after 16 total weeks of
months, this erythematous margin
therapy.
seen in EDP will disappear.
Alternatively, the lesions of LPP
JCAD journal of clinical and aesthetic dermatology November 2016 • Volume 9 • Number 11 47
CASE REPORT
lack erythematous changes that are (Fitzpatrick types IV–VI). This consultations. Inflammatory skin
seen in EDP, can be pruritic hyperpigmentation or reactions all have the ability to
(unlike EDP), and usually effect dyspigmentation in areas of normal disturb the dermoepidermal
sun-exposed areas of the face, sun exposure are classically seen junction, causing melanin to pass
neck, and proximal flexural in conditions such as lichen planus into the dermis and producing
extremities.6–9 It has been reported pigmentosus, erythema persistent hyperpigmentation that
that approximately 20% of patients dyschromia perstans, can make treatment difficult.10
with LPP also have classic lichen photoaggravated atopic dermatitis, Standard initial therapy for any
planus disease.6,10 Both diseases drug-induced photosensitivity, dyschromia includes the removal
are associated with a chronic and pigmented contact dermatitis, and of aggravating factors, vigorous
insidious course. Histopathologic actinic lichen planus.1,2 photoprotection, and a form of
overlap is seen between the two Widespread or localized active pigment reduction with
conditions with shared features of hyperpigmentation is associated topical agents or physical
epidermal atrophy, vacuolar with varieties of conditions and modalities.11 Sun avoidance when
interface dermatitis, and pigment may be due to genetic or systemic possible, and diligent
incontinence with dermal factors, such as metabolic, photoprotection with sunscreen
melanophages.6 When present in endocrine, chemical (drug), and sunblock is of particular
biopsy specimen, a lichenoid physical, nutritional, importance in dark-skinned
infiltrate, hyperkeratosis, and postinflammatory, or neoplastic individuals, as they may be
hypergranulosis can aid in the disease.11 While clinical history unaware of the darkening effects of
diagnosis of LPP. Lichenoid and histologic findings can help ultraviolet (UV) radiation and the
interface reactions and colloid narrow the differential diagnosis, exacerbation of
bodies are more pronounced in similar clinical and histologic hyperpigmentation.11
LPP and only occasionally seen in findings between LPP and Supplementation with daily 1000
EDP.11 Interface lymphohistocytic pigmented contact dermatitis have IU vitamin D is an important
infiltrate is more prominent in been reported. Distinguishing consideration as this patient
EDP, particularly in the early features of pigmented contact population is also at risk of
erythematous phase, however these dermatitis is that it often involves developing a deficiency.11
changes can be present in both the forehead and is preceded by The pathophysiology behind
entities.6 erythema, papules, swelling, and lichen planus-related skin disease
Lesions of LPP initially appear itching, which lead to gradual classically involves a T-cell
as small, ill-defined, oval-to-round hyperpigmentation by frequent and mediated, autoimmune
macules, which later become repeated contact with very small inflammatory response. Although
confluent to form large areas of amounts of the contact sensitizer.11 the exact etiology of LPP remains
pigmentation. Pigmentation varies Contact sensitizers commonly unknown, viral infections, topical
from slate gray to blue to brown to implicated are those within the agents including mustard oil, amla
brownish-black; in a single patient, cosmetic, textile, fragrance, and oil, and henna hair dye, as well as
the pigment is generally uniform. dye categories. Unlike LPP, sunlight have been shown to incite
The face and neck are the most pigmented contact dermatitis will reactions; avoidance of these
frequent initial sites, followed by resolve once contact with the triggers is recommended.3 Topical
the upper extremities.2 Coexistent allergen is discontinued, while LPP agents include hydroquinone,
classic lichen planus lesions can be will wax and wane. which is the most commonly used
seen in up to 20 percent of LPP Pigmentary dyschromias occur agent for pigmentary dyschromia,
patients.11 in greater frequency and severity often in combination with topical
Photodistributed dyschromias in darker skin types and are a retinoic acid, corticosteroids,
often occur in darker skin types frequent reason for dermatologic azelaic acid, kojic acid, and
48 JCAD journal of clinical and aesthetic dermatology November 2016 • Volume 9 • Number 11
CASE REPORT
glycolic acid. Additional reported effective therapy can be attributed initial treatment for the authors’
modalities including lightening to modulation of an abnormal cell- patient in combination with daily
agents, such as arbutin, mediated immune response, which lightening and exfoliative topical
niacinamide, N- has been postulated to play a role agents of azelaic acid and
acetylglucosamine, ascorbic acid, in the pathogenesis of both LPP tretinion. The goal of these
licorice, and soy, require further, and EDP.9,10 Topical calcineurin modalities was to reduce further
larger controlled studies inhibitors (tacrolimus, dyschromia and to induce
examining their efficacy.1 pimecrolimus) bind with controlled injury to the epidermis
Literature supporting cytoplasmic immunophilin up to the dermal-epidermal
therapeutic options for LPP have FKBP12 and form a complex that junction with hope to encourage
shown inconsistent efficacy and inhibits the activity of the enzyme keratinocyte turnover and promote
are limited to isolated case reports calcineurin needed for T-cell melanophage clearance. Strict
and few, small-investigative case activation. While tacrolimus photoprotection with daily facial
series. Reported modalities for ointment may be helpful in treating sunscreen with a minimal SPF of
LPP therapy include topical LPP, due to limited data and 30 and long-sleeved shirts were
glucocorticoids, topical inconsistent efficacy, more followed by the patient, with
immunomodulators, topical definitive treatment options are rationale being to prevent further
keratolytics, superficial chemical required. darkening of his dyspigmentation
peels, oral steroids, oral vitamin A, In 2014, Han et al13 reported a by decreasing UV-induced
and Q-switch Nd-YAG laser case study of a patient responding melanogensis. Adherence with
therapy. Oral clofazimine and to low-fluence Q-switch Nd:YAG daily topical 5% azelaic acid foam
dapsone have been reported in laser therapy. This patient initially and nightly tretinoin 0.1% cream
EDP cases, but have not been failed topical therapy with topical were endorsed over the 16-week
reported in LPP. betahydroxy acids and treatment period, and the patient
In a study treating LPP with hydroquinone-tretinoin- had significant improvement of
daily 100,000 IU vitamin A for 15 fluocinolone formulations. This facial lesions. Future therapeutic
days followed by 15 days without patient received low-fluence Q- options the authors plan on adding
treatment, some participants switched Nd:YAG laser every two to the patient’s therapy are
noticed a good-to-excellent weeks for 28 sessions.13 A 6mm tacrolimus cream and Nd:YAG
improvement in hyperpigmentation spot using a fluence of 3J/cm2 and laser. While the patient has noticed
after 10 or more treatments.4 pulse duration of 5ns was used on a decrease in pigmentation with
Systemic vitamin A is believed to the cheek for 10 passes.13 One year his current regimen, the authors
act as a lysosomal labilizer and can following treatment, her cheek hope the addition of these
break melanin in the melanophages maintained the improvement from modalities will also play a role in
of the upper dermis into smaller the laser with very minimal improving the appearance of the
particles.4 macular pigmentation.13 Laser lesions.
An open label, nonrandomized therapy may serve as a promising
study by Al-Mutairi et al 12 therapeutic option in this subset of
reported about half (13 out of 30) patients, and further investigation 1. Wadhwani AR, Sharma VK,
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