CAZURI CLINICE

CLINICAL CASES

RETICULOIDUL ACTINIC

ACTINIC RETICULOID
MONICA COSTESCU*,**, DIANA ANA-MARIA NIÞESCU**, IULIA IOANA ANDRONACHE**,
SIMONA-ROXANA GEORGESCU*,**, OANA-ANDREIA COMAN*, **

Rezumat Summary
Reticuloidul actinic reprezintã o dermatozã rarã, Actinic reticuloid is a rare, persistent, sometimes
persistentã, uneori debilitantã, a pielii din zonele debilitating dermatosis of the sun exposed skin areas, which
fotoexpuse, ce afecteazã de obicei persoanele expuse cronic la usually affects persons with chronic sun exposure. The
soare. Particularitatea importantã a acestei patologii derivã particular feature of this pathology derives from the
din asemãnarea cu un limfom cutanat atât din punct de similarity with cutaneous lymphoma both clinically and
vedere clinic cât ºi histologic, prezentând totuºi un risc mic histologically, yet presenting a small risk of malignant
de transformare malignã [1]. Clinic, erupþia din dermatita transformation [1]. Clinically, the eruption of chronic
actinicã cronicã este pruriginoasã, confluentã sau în plãci, actinic dermatitis is pruritic, confluent, or in separated
în principal pe zonele fotoexpuse, la nivelul tegumentului plaques, mainly in sun exposed areas, affecting normal
intact, la pacienþii cu istoric de dermatitã sau rar, dupã skin, in patients with a history of dermatitis or rarely after
consumul cronic de medicamente fotosensibilizante. chronic consumption of photosensitizing drugs.
Raportãm un caz de reticuloid actinic, forma severã de We report a case of actinic reticuloid, the severe form of
dermatitã actinicã cronicã, la o pacientã de 49 de ani, cu chronic actinic dermatitis, in a 49-year-old female patient
istoric de expunere moderatã la soare. Diagnosticul a fost with a history of moderate sun exposure. The diagnosis was
susþinut de aspectul clinic ºi confirmat ulterior de aspectul supported by the clinical aspect and subsequently
histopatologic. confirmed by the histopathological aspect.
Cuvinte cheie: dermatitã actinicã cronicã, reticuloid Key words: chronic actinic dermatitis, actinic
actinic, fototerapie. reticuloid, phototherapy.
Intrat în redacþie: 13.07.2017 Received: 13.07.2017
Acceptat: 29.08.2017 Accepted: 29.08.2017

Introducere Introduction
Primele referinþe despre o patologie sugestivã The first references to a suggestive pathology
pentru dermatita actinicã cronicã dateazã din for chronic actinic dermatitis date back to 1933,
anul 1933, când a fost denumitã reacþie per- when it was called persistent light reaction. It
sistentã la luminã. Abia în anul 1969, forma sa was not until 1969 that its severe form, named
severã, ºi anume reticuloidul actinic, ºi mai apoi actinic reticuloid, and then the moderate variant,
varianta moderatã, denumitã dermatitã foto- called photosensitising dermatitis, were intro-
* Universitatea de Medicinã ºi Farmacie ‘‘Carol Davila’’, Bucureºti.
‘‘Carol Davila’’ University of Medicine and Pharmacy Bucharest, Romania.
** Clinica de Dermato-Venerologie, Spitalul Clinic de Boli Infecþioase ºi Tropicale ‘‘Prof. Dr. Victor Babeº’’, Bucureºti.
Clinical Hospital of Infectious and Tropical diseases‘‘Prof. Dr. Victor Babeº’’, Department of Dermato-Venereology, Bucharest.

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sensibilizantã, au fost introduse în cadrul duced into skin rashes induced by sun exposure
erupþiilor cutanate induse de expunerea la category.[1]
soare.[1] Actinic reticuloid is the most severe variant of
Reticuloidul actinic reprezintã cea mai severã the chronic actinic dermatitis spectrum. Etiology
variantã din spectrul dermatitei actinice cronice. is still unknown, but is likely multifactorial,
Etiologia este încã necunoscutã, dar este probabil involving contact allergy, photoallergy,
multifactorialã, implicând alergia de contact, phototoxicity, immunological and metabolic
fotoalergia, fototoxicitatea, factori imunologici ºi factors.
metabolici. Pentru diagnosticul de sindrom Three criteria are required for the diagnosis of
reticuloid sunt necesare 3 criterii: reticuloid syndrome:
1. Papule persistente ºi plãci pe zone 1. Persistent papules and plaques on sun
fotoexpuse cu extensie pe zonele acoperite sau exposed areas with extension on covered areas or
eritrodermie generalizatã, generalized erythroderma,
2. Fotosensibilitate la un spectru larg de 2. Photosensitivity to a wide range of
ultraviolete, incluzând UV-B, UV-A ºi o parte din ultraviolet, including UV-B, UV-A and some part
spectrul vizibil of the visible spectrum
3. Examenul histopatologic cu infiltrat dermic 3. Histopathological examination with
ºi celule atipice limfoide. dermal infiltration and lymphoid atypical cells.

Prezentare de caz Case presentation

Raportãm cazul unei femei în vârstã de 49 de We report the case of a 49-year-old woman
ani care se prezintã pentru o erupþie imprecis presenting for a poor defined eruption consisting
delimitatã, constituitã din papule brun- of brown-erythematous papules on the neck,
eritematoase pe zona gâtului, toracelui posterior anterior and posterior thorax, accompanied by a
ºi anterior, însoþitã de o erupþie eritematoasã, fin erythematous, finely squamous eruption located
scuamoasã, la nivelul obrajilor ºi a frunþii, on the cheeks and forehead, pruritic, with an
pruriginoasã, cu evoluþie de aproximativ 2 ani. evolution of about 2 years. Blood tests were
Analizele sangvine au fost în limite normale iar within normal limits and immunological tests

Fig. 1. Reticuloid actinic, afectarea facialã Fig. 2. Reticuloid actinic, afectarea toracelui posterior
Fig. 1. Actinic reticuloid, facial involvement Fig. 2. Actinic reticuloid, posterior thorax involvement

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Fig. 3. Reticuloid actinic, afectarea toracelui anterior

Fig. 3. Actinic reticuloid, anterior thorax involvement

Fig. 4. Imagine de ansamblu, obiectiv 4x, coloraþie

hemalaun-eozinã. Se observã dilataþia chisticã a ostiului
acoperitã de o crustã, acantozã neregulatã, parakeratozã
Fig. 4. Overall image, 4x lens, hemalaun-eosin staining.
Cystic dilation of the ostium covered by a crust, irregular
acanthosis and parakeratosis are observed

Fig. 5. Obiectiv 10x, detaliu. Se observã acantoza

neregulatã, hipergranulozã, minima exocitozã, minima
spongiozã, colagenul dermic degradat
Fig. 5. 10x lens, detail. Irregular acanthosis,
hypergranulosis, minimal exocytosis, minimal spongiosis
and degraded dermal collagen are observed

testele imunologice au relevat anticorpi anti-vas Fig. 6. Obiectiv 40x. Se observã tipul de infiltrat
prezenþi cât ºi anticorpi anti Scl-70. S-a practicat limfoistiocitar ºi colagenul degradat
Fig. 6. 40 x Objective. The type of lymphocytic infiltrate
biopsia leziunii de la nivelul toracelui posterior.
and degraded collagen are observed
Examenul histopatologic a evidenþiat ortoke-
ratozã, epiderm cu acantozã neregulatã, hiper-
granulozã focalã, minimã spongiozã ºi exocitozã; revealed anti-vascular antibodies as well as anti-
central cu dilataþie chisticã a ostiumului folicular, scl-70 antibodies. Biopsy of the lesion from the
acoperitã de parakeratinã ºi crustã cu serofibrinã. posterior thorax was performed. The
În derm, apar vase dilatate, înconjurate de histopathological examination revealed
infiltrat dens constituit din limfocite, histiocite ºi ortokeratosis, irregular epidermic acanthosis,
rare eozinofile, dispus perianexial ºi perivascular. focal hypergranulosis, minimal spongiosis and
Diagnosticul histopatologic confirmã diagnos- exocitosis; centrally with cystic dilation of the
ticul clinic de sindrom reticuloid sau dermatitã follicular ostium, covered by parakeratine and
actinicã cronicã. crust with serofibrin. In the dermis, dilated
De menþionat cã pacienta primise cu vessels appear, surrounded by dense infiltration
aproximativ 6 luni anterior internãrii terapie cu of lymphocytes, histiocytes and rare eosinophils,

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prednison în doze moderate (30mg/zi), pe o disposed perianexially and perivascularly.

perioadã de 1 lunã, cu dispariþia erupþiei, dar cu Histopathological diagnosis confirms the clinical
reapariþia acesteia treptat, dupã oprirea diagnosis of reticuloid syndrome or chronic
corticoterapiei sistemice. Evoluþia a fost favo- actinic dermatitis.
rabilã sub tratament sistemic cu antihistaminice, It should be noted that the patient had
sedative, suplimente vitaminice ºi local cu received prednisone at moderate doses (30mg /
dermatocorticoizi cu potenþã mare (clasa aIIIa) ºi day), over a period of one month, about 6 months
emoliente. Pacientei i s-a recomandat evitarea prior to admission, with the disappearance of the
expunerii la soare ºi utilizarea cremelor ecran eruption, but with a gradual recurrence after
solar (SPF 50+) cu revenire la control periodic systemic corticotherapy was stopped. The
pentru urmãrire. evolution was favorable under systemic
treatment with antihistamines, sedatives, vitamin
Discuþii supplements and under topical treatment with
high potency dermatocorticoids( class III a) and
Spectrul dermatitei actinice cronice cuprinde emollients. The patient was advised to avoid
reacþia persistentã la luminã, reticuloidul actinic, sunlight exposure and the use of sun screens (SPF
eczema fotosensibilizantã ºi dermatita atopicã 50+) with periodic follow-up control.
fotosensibilizantã. Reacþia persistentã la luminã a
fost raportatã încã din anii 1960 la indivizii cu
Discussions
dermatitã fotoalergicã asociatã cu expunerea la
saliciliaþi halogenaþi, persistând ºi dupã încetarea Chronic actinic dermatitis spectrum
expunerii.[2] Reticuloidul actinic prezintã un comprises persistent light reaction, actinic
model identic cu al reacþiei persistente la luminã reticuloid, photosensitizing eczema and
cu particularitatea cã la examenul histopatologic photosensitising atopic dermatitis. Persistent
descrie limfocite atipice. Eczema fotosen- light reaction has been reported since 1960 in
sibilizantã este asemãnãtoare cu reacþia persis- individuals with photo-allergic dermatitis
tentã la luminã cu excepþia absenþei unui istoric associated with exposure to halogenated
de fotoalergie.[2] salicylates, persisting even after the exposure was
Spectrul solar implicat în declanºarea stopped [2]. Actinic reticuloid presents an
dermatitei actinice cronice este reprezentat de identical pattern as the persistent light reaction
UVA ºi UVB. Teoria conform cãreia dermatita with the particularity that at histopathological
actinicã cronicã este un rãspuns de tip examination atypical lymphocytes are described.
hipersensibilitate întârziatã, comun ºi pentru The photosensitising eczema is similar to the
dermatita alergicã de contact, este confirmatã de persistent light reaction except for the absence of
infiltratul dermic cu limfocite CD 8 pozitive dar ºi a history of photoallergy.[2]
de cãtre pattern-ul de molecule de adeziune The solar spectrum involved in triggering
implicate în acest proces. chronic actinic dermatitis is represented by UVA
Dermatita actinicã cronicã afecteazã de obicei and UVB. The theory that chronic actinic
persoanele expuse cronic la soare, prin natura dermatitis is a delayed hypersensitivity response
profesiei sau nu, care prezintã o dermatitã common to allergic contact dermatitis is
fotoalergicã de contact la sensibilizanþi exogeni confirmed by the dermal infiltrate with CD8
de tipul compoziþilor sau cremelor de protecþie positive lymphocytes and by the pattern of
solarã. Este astfel posibil ca fotodistrugerea adhesion molecules involved in this process.
cronicã sã diminueze imunosupresia cutanatã Chronic actinic dermatitis typically affects
normalã la aceºti indivizi iar pe de altã parte sun exposed people, whether by their job nature
dermatita de contact exogenã sã creascã or not, having a pre-existing photo-allergic
rãspunsul imun împotriva unui fotoantigen contact dermatitis to exogenous sensitizers such
endogen slab, nonimunogen în mod fiziologic. as compositae or sunscreen creams. It is thus
Efectele nocive ale razelor ultraviolete derivã possible that chronic photo-destruction to
din capacitatea acestora de a fi absorbite la diminish normal skin immunosuppression in
nivelul pielii ºi implicit de modificãrile pe care these individuals and on the other hand,

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acestea le pot determina. Astfel, razele UVA (400- exogenous contact dermatitis to increase the
315nm) sunt absorbite la nivel dermic pânã în immune response against a weak, physi-
porþiunea profundã, UVB ( 315-290 nm) la nivel ologically non-immunogenic endogenous photo-
epidermic ºi UVC (290-200nm) în stratul cornos ºi antigen.
în straturile superficiale ale epidermei. Odatã The harmful effects of ultraviolet rays derive
absorbite de cãtre biomolecule, acestea from their ability to be absorbed into the skin
declanºeazã un lanþ de reacþii fotochimice ºi and, implicitly, by the changes they can cause.
fotobiologice. Cromoforii, definiþi ca molecule cu Thus, UVA rays (400-315nm) are absorbed as far
putere de absorbþie a energiei luminoase, sunt as the profound dermis, UVB (315-290 nm) in
transformaþi fie în mod direct prin reacþii epidermal layer and UVC (290-200nm) in the
fotochimice, fie indirect printr-o moleculã stratum corneum and superficial layers of the
intermediarã, în cadrul unei reacþii foto- epidermis. Once absorbed by biomolecules, they
sensibilizante. Celula afectatã reacþioneazã astfel trigger a chain of photochemical and photo-
prin modificãri vizibile clinic. Prin citokinele biological reactions. Chromophores, defined as
proinflamatorii implicate în acest proces pot fi light-absorbing molecules, are transformed either
afectate ºi alte straturi ale pielii. directly by photochemical reactions or indirectly
Efectele razelor ultraviolete asupra siste- through an intermediate molecule in a
mului imun sunt atât proinflamatorii cât ºi photosensitizing reaction. The affected cell reacts
imunosupresive. Fotoreceptorii care declanºeazã by clinically visible changes. Other layers of the
activarea cãilor de semnalizare ale rãspunsului skin may be affected as a result of the pro-
imun sunt: ADN-ul (prin produºii de degradare), inflammatory cytokines involved in this process.
acidul urocanic (prin izomerizare de la forma The effects of ultraviolet light on the immune
trans la forma cis) din stratul cornos ºi lipidele system are both pro-inflammatory and
membranare (prin alterarea potenþialului redox immunosuppressive. Photoreceptors that trigger
membranar).[1] Forma cis a acidului urocanic the activation of the immune response signalling
induce transcripþia genelor si sinteza de pathways are: DNA (by degradation products),
mediatori imunomodulatori la keratinocitele urocanic acid (by isomerization from the trans
umane in vitro, conform unor studii recente.[3] form to the cis form) of the stratum corneum, and
De asemenea, alte studii au arãtat cã razele membrane lipids (by altering the redox
ultraviolete activeazã sistemul imun înnãscut membrane potential).[1] According to recent
prin stimularea producþiei de peptide studies, the cis form of urocanic acid induces
antimicrobiene în tegumentul uman, cum e cazul gene transcription and the synthesis of
psoriasinei, de aici derivând efectele benefice pe immunomodulatory mediators in human
imunitate.[3] De altfel, un grad controlat de keratinocytes in vitro.[3] Also, other studies have
imunosupresie UV indusã a imunitãþii adaptative shown that ultraviolet rays activate the innate
poate fi benefic în prevenþia rãspunsului imun la immune system by stimulating the production of
fotoantigeni, ca în cazul erupþiei polimorfe la antimicrobial peptides in the human skin, as is
luminã. the case of psoriasin, thereby deriving beneficial
Din punct de vedere clinic, reticuloidul effects on immunity.[3] In fact, a controlled
actinic apare în general la bãrbaþii de vârstã degree of induced immunosuppression of
medie, în special pe timpul verii ºi se prezintã sub adaptive immunity may be beneficial in
forma unei eczeme pruriginoase (papule, noduli preventing immune response to photo-antigens,
sau plãci) la nivelul zonelor fotoexpuse (obraji, as in the case of polymorphic light rash.
urechi, gât, feþele posterioare ale antebraþelor), cu From a clinical point of view, actinic
respectarea pleoapelor superioare ºi a pliurilor reticuloid generally occurs in middle-aged men,
tegumentare. Uneori poate apãrea ºi afectarea especially during summer, and appears in the
zonelor neexpuse, fenomen explicat fie de form of pruritic eczema (papules, nodules or
sensibilitatea accentuatã la luminã, cu penetrare plaques) in the exposed areas (cheeks, ears,
prin materialul hainelor, fie de reacþiile throat, posterior forearms), sparing the upper
imunologice propagate la nivelul pielii neexpuse. eyelids and skin folds. Occasionally, unexposed

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În cazuri severe poate apãrea eritrodermie areas may also be affected, phenomenon
generalizatã.[4] Tegumentul este îngroºat ºi explained either by extreme light sensitivity,with
uneori acoperit cu scuame, chiar cu facies leonin, penetration through the clothes fabric, or by the
în formele mai severe. immunological reactions propagated in the
Diagnosticul diferenþial al reticuloidului unexposed skin. In severe cases, generalized
actinic se face cu dermatozele fotoagravate, cu erythroderma can occur.[4]The tegument is
fotosensibilizarea la anumite medicamente, cu thickened and sometimes covered with sheds,
limfomul cu celule T, cu eritrodermiile de alte even with leonin facies, in more severe forms.
cauze. Rezultatele negative ale fototestelor The differential diagnosis of actinic reticuloid
pledeazã pentru limfom cutanat în timp ce is done with photoaggravated dermatoses, with
infiltratele cu celule CD 8 pozitive ºi rãspunsul photosensitization on certain drugs, with T-cell
prompt la tratament indicã dermatita actinicã lymphoma, with erythroderma of other causes.
cronicã cu formele sale. Deasemenea, pentru Negative results of phototests indicate cutaneous
confirmarea diagnosticului de limfom cutanat cu lymphoma while infiltrates with CD8 positive
celule T sunt necesare teste imunohistochimice ºi cells and the prompt response to treatment
analiza rearanjamentelor genice.[5] indicates chronic actinic dermatitis with its
Fotodermatozele pot duce la scãderea forms. Also, immunohistochemistry and gene
drasticã a calitãþii vieþii pacienþilor [6], de aceea rearrangement assays are required to confirm the
pe lângã tratamentul medicamentos este necesarã diagnosis of T-cell lymphoma.[5]
deprinderea unui stil de viaþã particular ce Photo-aggravated dermatoses can lead to a
presupune evitarea expunerii la soare, utilizarea drastic decrease in the quality of life of patients
îmbrãcãmintei adecvate, utilizarea de creme cu [6], therefore, besides medication it is necessary
fotoprotecþie periodic ºi evitarea expunerii la to learn a particular lifestyle that supposes
alergeni (de menþionat rolul important al avoiding sun exposure, wearing appropriate
parafenilendiaminei ca ºi alergen de contact).[7] clothing, using periodically photoprotective
Tratamentul de primã linie presupune: creams and avoiding exposure to allergens
fotoprotecþie strictã ºi evitarea alergenilor de (mention on the important role of
contact, corticosteroizi topici ºi emoliente. paraphenylendiamine as a contact allergen). [7]
Terapia de a doua linie include: azatioprinã, First-line treatment involves: strict photo-
ciclosporinã, micofenolat, hidroxicarbamidã, protection and avoidance of contact allergens,
fotochemoterapie cu UVA ºi fototerapie cu UVB topical corticosteroids and emollients. Second
în bandã îngustã precum ºi inhibitori topici de line therapy includes: azathioprine, cyclosporine,
calcineurinã.[8] Linia 3 de tratament presupune: mycophenolate, hydroxycarbamide, UVA photo-
hidroxiclorochinã, etretinat, danazol, talidomidã, chemotherapy and narrowband UVB photo-
interferon ºi infliximab.[9] therapy as well as topical calcineurin inhibitors.
Interesant de menþionat este efectul pozitiv [8] Third line treatment includes: hydroxy-
obþinut prin terapia sistemicã cu UVA în doze chloroquine, etretinate, danazol, thalidomide,
mai mici decât cele care declanºeazã practic boala interferon and infliximab [9].
[10]. Foarte importantã este asocierea la aceastã It is interesting to note the positive effect
terapie a corticosteroizilor sau a azatioprinei în achieved by systemic therapy with UVA at lower
perioada de inducþie. Conform studiilor din doses than those that actually trigger the
literaturã, în ciuda beneficiilor clare ale acestui disease.[10] The association at this therapy of
tip de terapie asupra bolii, menþinerea remisiunii corticosteroids or azathioprine, during the
în timp este un deziderat realizabil la un numãr induction period, is very important. According to
relativ limitat de pacienþi [10], [11]. Azatioprina literature studies, despite the clear benefits of this
este deseori medicamentul salvator în cazul type of therapy, maintaining remission over time
multor cazuri refractare, în urma experienþei is a possible achievement in a relatively limited
clinice din studii.[12] number of patients [10], [11]. Azathioprine is
Evoluþia pozitivã a bolii odatã cu adoptarea often the rescue drug in many refractory cases
mãsurilor corecte de tratament este clar admisã following clinical trial experience [12].

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de cele mai multe studii însã vindecarea per se The positive evolution of the disease with the
este practic dificil de prevãzut.[13] adoption of the right treatment measures is
clearly admitted by most studies but per se
Concluzii healing is practically difficult to predict.[13]
Am raportat un caz atipic de reticuloid actinic
Conclusions
la o femeie în vârstã de 49 de ani, cu istoric de
expunere moderatã la soare pe timpul anului, We have reported an atypical actinic
care s-a prezentat pentru exacerbarea afecþiunii în reticuloid case in a 49-year-old woman, with a
lunile de iarnã, ceea ce sugereazã o sensibilitate moderate history of sun exposure during the
crescutã la razele ultraviolete. Deºi riscul year, who presented for an exacerbation of the
cunoscut de transformare malignã este mic, se disease in the winter months, suggesting
recomandã monitorizarea periodicã a pacientei. increased sensitivity to ultraviolet rays. Although
the known malignant transformation risk is
low, periodic monitoring of the patient is
recommended.

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11. Masood Q, Sameem F, Hassan I, Khan D, Majid I, Bhat T, Singh G. PUVA therapy in chronic actinic dermatitis: A
preliminary study. Indian J Dermatol 2005;50:212-5
12. LEIGH, I.M. and HAWK, J.L.M. (1984), Treatment of chronic actinic dermatitis with azathioprine. British Journal
of Dermatology, 110: 691–695. doi: 10.1111/j.1365-2133.1984.tb04706.x
13. Robert S. Dawe, MRCP; Iain K. Crombie, PhD; James Ferguson, FRCP, The Natural History of Chronic Actinic
Dermatitis, Arch Dermatol. 2000;136(10):1215-1220.

Conflict de interese Conflict of interest

NEDECLARATE NONE DECLARED

Adresa de corespondenþã: Diana Ana-Maria Niþescu

Spitalul Clinic de Boli Infecþioase ºi Tropicale ‘‘Prof. Dr. Victor Babeº’’,
Bucureºti, ªos. Mihai Bravu nr. 281
E-mail: drnitescudiana@gmail.com

Correspondance address: Diana Ana-Maria Niþescu

Clinical Hospital of Infectious and Tropical diseases ‘‘ Prof. Dr. Victor Babeº’’
Bucharest, Mihai Bravu Street, no 281
E-mail: drnitescudiana@gmail.com

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