Lichen planus actinicus is a photodistributed variant of lichen planus that most often occurs in dark-complexioned young adults of Middle Eastern descent. (1) Other names for this disorder include: summertime actinic lichenoid eruption, lichen planus atrophicus annularis, lichen planus subtropicus, lichen planus tropicus, and lichenoid melanodermatitis (2). Although the etiology of this disease has not been determined, sunlight appears to be the triggering factor in most cases. The lesions often are exacerbated by sun exposure and may improve spontaneously in the winter months (3-4). The lesions of lichen planus actinicus usually occur on the forehead, face, neck, and the extensor surfaces of the arms and hands. The lateral aspect of the forehead is the most common site of presentation. (5). Unlike classic lichen planus, lichen planus actinicus has an earlier age of onset, a longer course, a predilection for dark-complexioned females, and a seasonal occurrence. Additionally, pruritus, scaling, nail involvement, and the Köbner reaction frequently are absent.
Differential diagnosis of lichen planus actinicus includes discoid lupus erythematosus, granuloma annulare, melasma, secondary syphilis, fixed drug eruption, polymorphous light eruption, and erythema dyschronicum perstans. (5) The clinician also must exclude the possibility of a drug-induced photosensitive lichenoid eruption by taking a complete medication history.
The histologic features of lichen planus actinicus are consistent with findings in classic lichen planus. (2-5) Hyperkeratosis of the stratum corneum, hypergranulosis, basal cell vacuolization, and Civatte bodies usually are present. Although clinically similar to cutaneous lupus and polymorphous light eruption, lichen planus actinicus can be distinguished histologically from these photodermatoses. Lichen planus actinicus lacks follicular plugging, thickening of the basement membrane, and the periadnexal inflammatory infiltrate seen in cutaneous lupus erythematosus.
Variable treatment responses have been reported with bismuth, grenz rays, arsenic compounds, and topical corticosteroids under occlusion. 4,6 Hydroxychloroquine, intralesional corticosteroids, and topical sunscreens have been used with success. (5-8) Acitretin, used in combination with topical steroids and sun avoidance, also has resulted in complete resolution of lesions without recurrence. (9) Although psoralen-UVA, isotretinoin, systemic corticosteroids, cyclosporine, and dapsone have been used to treat classic lichen planus, there are currently no reports of their use in lichen planus actinicus.(10-11) Some cases may remit spontaneously with sun avoidance and use of sunblock. (11)
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Dr. Treacy's Dermatology Casebook No 1
1. 43
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Aesthetic Medicine • April 2014
S K I N / D E R M AT O L O G Y
A
51-year-old Indian man presented with a three-year history of asymptomatic
hyperpigmentationonthefrontalisareaofhisface.Thelesionwasviolaceousin
colour,hadanirregularmargin.Hewasarestaurantownerwhowentbackhome
to India for a few months every summer. The patient was otherwise healthy
and denied any history of infection or trauma. He carried a previous laboratory
examination,whichshowedafullbloodcountandbloodchemistrywithinnormalrange.The
patient had seen many previous doctors who had prescribed hydroquinone preparations
and topical steroids without improvement in the pigmentation. He had no other medical
problems and was not taking any systemic medications. Also anti-nuclear antibody and
othersystemiclupuserythematosusprofileswereallnegative.
On physical examination, there were violaceous hyperpigmented patches on his
forehead (Figure 1), eyelids and temporal areas. He also had hyperpigmented lesions in the
dorsalsurfacesandcleftareasofhishands(Figure2).Alltheseareasofhyperpigmentation
were noted to be in areas of sun exposure. There was no associated mucous membrane or
nailinvolvement.
A punch biopsy was taken from the margin of
lesion on the forehead to aid in the diagnosis. Low
power magnification of the specimen showed
hyperplasia of the epidermis with a band-like
inflammatory infiltration in the upper dermis.
Histological examination demonstrated an
atrophicepidermiswithmildhyperkeratosis
and orthokeratosis (Figure 3). Basilar
vacuolization, a band like lymphocytic
infiltrate, and marked pigmentary
incontinencewerepresent.>
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S K I N / D E R M AT O L O G Y
COMMENT
Based on the clinical findings
in his fingers a provisional
diagnosis of Lichen Planus was
made. Additionally, because
the violaceous lesions
developed on his forehead,
which is a sun exposed area,
andwasatrophicinappearance
the suspicion of LPA (lichen
planus actinicus) existed. This is
a photodistributed variant of lichen
planus that most often occurs in dark-
complexioned young adults of Middle
Eastern descent. (1) Four morphologic
patterns have been clinically described in the literature including:
summertime actinic lichenoid eruption, lichen planus atrophicus annularis,
lichen planus tropicus, and lichenoid melanodermatitis (2). Although the
etiology of this disease has not been determined, the lesions often are
exacerbated by sun exposure and may improve spontaneously in the
winter months (3).The lesions of lichen planus actinicus usually occur on the
forehead,face,neck,andtheextensorsurfacesofthearmsandhands.(3-4).
Thelateralaspectoftheforeheadisthemostcommonsiteofpresentation.
(5).Clinically, lichen planus actinicus resembles the lesions found in discoid
lupus erythematosus (DLE), granuloma annulare, melasma, morphea,
secondarysyphilis,lichenoiddrugeruptionandpolymorphouslighteruption
and should be differentiated by histopathologic and immunofluorescence
(IF) findings (5). In DLE, the liquefaction, degeneration or thickening of the
basal layer is more prominent and IF finding or autoantibody in a blood test
may be the conclusive factor. In melasma, melanin synthesis in epidermal
layerandthenumberofmelanocytesareincreased.
The histologic features of lichen planus actinicus are consistent with
findingsinclassiclichenplanus.(2-5)Hyperkeratosisofthestratumcorneum,
hypergranulosis, basal cell vacuolization, and Civatte bodies usually are
present. Although clinically similar to cutaneous lupus and polymorphous
light eruption, lichen planus actinicus can be distinguished histologically
from these photodermatoses. Lichen planus actinicus lacks follicular
plugging, thickening of the basement membrane, and the periadnexal
inflammatory infiltrate seen in cutaneous lupus erythematosus. (3-4).
Clinical manifestations such as the site of lesion, age or the history of sun
exposure should be examined for final diagnosis. Finally, the patient with
lichenoiddrugeruptionshouldhaveahistoryofmedication.
TREATMENT
The cause of actinic LP is still unknown but sunlight might be the major
precipitating factor. Several modalities such as topical corticosteroid,
4,6 hydroxychloroquine , intralesional corticosteroid injection, grenz
ray, arsenic compounds or antimalarial agent have been applied for the
treatment of actinic LP. (5-8). Acitretin, used in combination with topical
steroids and sun avoidance, also has resulted in complete resolution of
lesions without recurrence. (9) Van der Shroeff et all, induced actinic LP
by using repeated doses of UVB radiation on the back. So sunscreen
is considered necessary for treatment. (10). Although psoralen-UVA,
isotretinoin,systemiccorticosteroids,cyclosporine,anddapsonehavebeen
usedtotreatclassiclichenplanus,therearecurrentlynoreportsoftheiruse
in lichen planus actinicus. (11-12).Recently topical 0.1% pimecrolimus cream
have been reported to be successful in a case of actinic LP (12). This patient
wassuccessfullytreatedwithPIGMANORM®CrèmeWIDMERwithactive
ingredientsHydroquinone5.0g.Tretinoin0.1g.Hydrocortisone1.0g. AM
REFERENCES
1. ZancaA,ZancaA.Lichenplanusactinicus.IntJDermatol.
1978;17:506-508.
2. SalmanSM,KibbiAG,ZaynounS.Actiniclichenplanus.JAm
AcadDermatol.1989;20:226-231.
3 ShannaB.Meads,MD;JoyKunishige,BS;FranciscoA.Ramos-
Caro,MD;AshrafM.Hassanein,MD,PhDCutis.2003;72:377-
381.
4. KatzenellenbogenI.Lichenplanusactinicus(lichenplanusin
subtropicalcountries).Dermatologica.1962;124:10-20.
5. DilaimyM.Lichenplanussubtropicus.ArchDermatol.
1976;112:1251-1253.
6. BediTR.Summertimeactiniclichenoideruption.
Dermatologica.1978;157:115-125.
7. VerhagenAR,KotenJW.Lichenoidmelanodermatitis.a
clinicopathologicalstudyoffifty-oneKenyanpatientswithso-
calledtropicallichenplanus.BritJDermatol.1979;101:651-658.
8. BoydA,NeldnerK.Lichenplanus.JAmAcadDermatol.
1991;25:593-619.
9. JansenT,GambichlerT,vonKobyletzkiL,etal.Lichenplanus
actinicustreatedwithacitretinandtopicalcorticosteroids.J
EurAcadDermatolVenereol.2002;16:174-175.
10 VanderShroeffJG,SchothorstAA,KanaarP.Inductionof
actiniclichenplanuswithartificialUVsources.ArchDermatol
1983;119:498-500.
11. BakerH,AlmeydaJ.Lichenplanusactinicus.BritJDermatol.
1970;82:426-427.
12 EzzedineK,SimonartT,VereeckenP,HeenenM.Facialactinic
lichenplanusfollowingtheBlaschko’slines:successful
treatmentwithtopical0.1%pimecrolimuscream.JEurAcad
DermatolVenereol2009;23:458-459.
HISTOLOGY REPORT
Skin with a prominent lichenoid superficial
dermal infiltrate, composed predominantly
of lymphocytes. Vacuolar interface change
with associated basal apoptotic keratinocytes
and focal lymphocyte exocytosis are present.
The most striking feature is marked pigment
incontinence in the dermis. The features are
those of lichen planus actinus – a variant of
lichen planus in which lesions are limited to sun
exposedareas.
Prof.KieranSheahan,Consultant
Histopathologist,St.Vincent’sUniversity
Hospital,ElmPark,Dublin4.
DrLindaMulligan,PathologyRegistrar,St.
Vincent’sUniversityHospital,ElmPark,
Dublin4.
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