Rom J Morphol Embryol 2014, 55(3 Suppl):1171–1179

RJME
CASE REPORT Romanian Journal of
Morphology & Embryology
http://www.rjme.ro/

A rare case of multiple clear cell acanthoma with a relatively

rapid development of the lower legs
MARIA ROTARU1), GABRIELA MARIANA IANCU1), LAURA GHEUCĂ SOLOVĂSTRU2), ROMANIŢA-FIRUŢA GLAJA3),
FLORIN GROSU4), ADRIANA BOLD5), ADRIAN COSTACHE6)
1)
Department of Dermatology, “Victor Papilian” Faculty of Medicine, “Lucian Blaga” University of Sibiu, Romania
2)
Department of Dermatology, Faculty of Medicine, “Grigore T. Popa” University of Medicine and Pharmacy, Iassy, Romania
3)
Department of Pathology, Emergency City Clinical Hospital, Timisoara, Romania
4)
Department of Histology, “Victor Papilian” Faculty of Medicine, “Lucian Blaga” University of Sibiu, Romania
5)
Department of Histology, University of Medicine and Pharmacy of Craiova, Romania
6)
Department of Pathology, “Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania

Abstract
Clear cell acanthoma, firstly described by Degos as “an epidermal tumor with a particular aspect”, although quite a rare lesion, raised an
important interest because it may be easily confused with other dermatologic lesions, in the absence of a histopathological examination.
Its clinical aspect is of a solitary nodule, with a red-brown varying color, with a size of 3 mm to 2 mm, sometimes covered with a thin scall.
We present a case of a multiple rare cell acanthoma (seven nodular formations), having a rapid development (about two months) diagnosed in
a 71-year-old patient within the lower 1/3 of the right shin.
Keywords: clear cell achantoma, tumoral lesions, inflammatory disease, histopathology, immunohistochemistry.

 Introduction within the Emergency Hospital of Sibiu, Romania, there

was admitted a female patient, aged 71-year-old, from the
The clear cell acanthoma (CCA), also known as the rural area, presenting seven pink-red nodular formations
“Degos acanthoma” or as the “pale acanthoma” [1], is a of 1–2 cm in the lower 1/3 of the right leg. The patient
rare benign lesion, with a variable clinical aspect and stated that the lesions had a relatively rapid evolution of
distinct histopathological characteristics. Firstly described about two months. The symptoms presented by the
in 1962 by Degos et al. [2] as “an epidermal tumor with patient were unspecific, such as mild pain, sensation of
a particular aspect”, the rare clear cell acanthoma discomfort and local exudation. In the medical history,
presented a special interest, because, clinically, it may there could not be signaled any local traumas, insect
be easily be confused with other skin lesions. Most stings, scratching lesions or other dermatologic affections.
often, it is confused with seborrheic keratosis, nummular The dermatologic examination showed that all the
eczema, pyogenic granulomas, psoriasis, epidermic nevus, lesions had a nodular aspect, with a clear, slightly
skin hemangioma, histiocytoma, poroma, basal cell carci- irregular aspect, with moist surface, covered by scalls,
noma or squamous carcinoma [3–5]. Clinically, CCA with a tendency to form peripheral cholerets, painful under
presents as a solitary papule or node, with a red-brown moderate pressure (Figures 1 and 2).
varying color, with a size of 3 mm to 2 mm, sometimes
covered with a thin scall. Sometimes, it may have a
polypoid or pedunculated aspect [6–8]. Most often, CCA
is diagnosed in middle-aged or old-aged individuals, but
it may also be found in children [1]. The lesions are
usually localized at lower limbs level, but there were also
reported localizations at the level of the inguinal area,
scrotum, face, scalp, hand, trunk, nipple, buttock, forearm,
head, etc. [5]. Regarding the sex, it seems that the lesion
affects both sexes at the same rate. Most often, the clear
cell acanthoma (CCA) is a single lesion, but there have
also been reported multiple lesions [5, 9–11].
We present a case of a multiple clear cell acanthoma,
with particular aspects and rapid evolution in a 71-year-
old patient.
Figure 1 – Macroscopic aspect Figure 2 – Clinical aspect
 Patient, Methods and Results of skin lesions localized on the of lesions localized on the
In November 2010, in the Clinic of Dermatology dorsal side of the 1/3 inferior internal side of the right
part of the right calf. calf.
ISSN (print) 1220–0522 ISSN (on-line) 2066–8279
1172 Maria Rotaru et al.
The general clinical examination highlighted the Table 1 – Antibodies used in the immunohistochemical
presence of various associated affections: chronic venous study
insufficiency, high blood pressure and liver steatosis Antibody Code Clone
Antigen
Specificity DilutionSource
retrieval
associated with moderate hepatomegaly.
Sodium
The laboratory tests showed a moderate leukopenia citrate B-
CD20 M0755 L26 1:100 Dako
(3970 leukocytes/mm3), a slight increase of blood urea buffer, lymphocytes
(52 mg/dL), cholestasis (gamma glutamyl transpeptidase pH 6
Sodium
292 U/L), slight hypercholesterolemia (seric cholesterol citrate T-
216 mg/dL) and lambliasis. CD3 A0452 F7.2.38 1:100 Dako
buffer, lymphocytes
The pulmonary X-ray highlighted the presence of a pH 6
hypertrophy in the heart left ventricle, a diameter increase Sodium
citrate
and thoracic aorta calcifications. The abdominal echo- CD68 M0814 KP1
buffer,
Macrophages 1:200 Dako
graphy confirmed liver steatosis and hepatomegaly and pH 6
it also showed the presence of two hepatic hemangiomas: Sodium
CD34 QBEnd citrate Vascular
one of 3.4 cm in the 5th segment and another of 3.2 cm M7165 1:50 Dako
class II 10 buffer, endothelium
in the 7th segment. pH 6
In order to establish a positive and differential Sodium
diagnosis, we proceeded to a skin biopsy from a single OV-TL citrate
CK 7 M7018 Cytokeratin 7 1:50 Dako
12/30 buffer,
lesion. After obtaining the patient’s informal consent, pH 6
there was performed a local anesthesia with 1% Xyline Sodium High
and there were harvested two samples of about 3/4 mm CK
M0630
34β citrate molecular
1:50 Dako
that were immediately fixed in 10% neutral formalin 34βE12 E12 buffer, weight
pH 6 cytokeratins
solution for 24 hours. After that, the biopsy samples Low
were included in paraffin according to the standard CK MNF EDTA molecular
M0821 1:100 Dako
histological protocol. The sectioning of the biological MNF116 116 pH 9 weight
cytokeratins
material was performed in the Microm HM350 rotary
microtome, equipped with a transfer system of the sections The histological study highlighted an epidermis
on a water bath (STS, Microm). thickness, with an increase of the spinous layer thickening
For the histopathological study, there were used the (acanthosis) associated with hyperkeratosis areas, but
classical stainings with Hematoxylin–Eosin (HE), Goldner– with the reduction of the granulous layer thickening.
Szekely (GS) trichromic and PAS–Hematoxylin (Periodic The interpapillary epithelial apex appeared long and
Acid Schiff). thickened, deeply entering the conjunctive tissue of the
For the immunohistochemical study, there were dermis (Figures 3 and 4). The epidermis thickening was
performed sections of a 4-μm thickness, collected on irregular; from place to place, the epidermis appeared
poly-L-Lysine covered blades in order to increase the quite thin, formed only of 2–3 keratinocyte rows, while
adherence of the biological material to the slide blade, in the superficial dermis there was identified quite a
after which they were kept in a thermostat at 370C for developed network of congested blood vessels (arterioles,
24 hours. Then, after the deparaffinization and hydration capillaries and venules) (Figure 5). This microscopic aspect
of histological sections, the biological material was may explain the moist aspect of the acanthoma surface
incubated for 30 minutes in a 3% hydrogen peroxide and the scall formation on its surface.
solution. After that, the sections were washed in tap water,
boiled for antigen retrieval in the microwave oven in a
sodium citrate solution pH 6 for 21 minutes (seven cycles
of three minutes). For the MNF116 antibody, the antigen
retrieval was performed by boiling it in an EDTA, pH 9
solution for 21 minutes. After boiling, they were left to
cool down for 15 minutes, followed by their wash-up in
a buffering solution of phosphate-buffered saline (PBS),
and then in 2% free-fat milk for 30 minutes, in the stage
of blocking the unspecific sites. The sections were
incubated with primary antibodies, for 18 hours over
night, in a refrigerator at 40C. In the second day, on the
sections of skin biopsy there was applied the biotinylated
secondary antibody (αMs/αRb) for 30 minutes, followed
by the passing to the HRP Streptavidin for 30 minutes.
The signal was detected with 3.3’-diaminobenzidine (DAB) Figure 3 – Overall microscopic image of the lesions
(Dako) after which there was performed a Hematoxylin where there could be observed the presence of
acanthosis and hyperkeratosis at epidermis level,
contrasting, alcohol dehydration, xylene clarification and
formation of multiple epithelial deep and thickened
fixing the blades in the DPX environment (Fluka). In our apex in the superficial dermis and the presence of an
study, we used the following markers (Table 1). abundant inflammatory infiltrate. HE staining, ×40.
 A rare case of multiple clear cell acanthoma with a relatively rapid development of the lower legs
With the classical histological stainings (HE, GS
trichromic), the keratinocytes in the spinous layer presented
a slight increase of their size, with a more pale and
sometimes heterogeneous cytoplasm. The intercellular
gaps appeared larger, which allowed the highlighting of
desmosomes (Figure 6). In some areas of the epidermis
there were highlighted some intra-Malpighian leukocyte
aggregates (lymphocytes and granulocytes) or diffusely
disseminated leukocytes in the epidermis thickness. In the
areas where there were identified more abundant leukocyte
infiltrations there could also be observed a tendency of
keratinocyte acantholysis and necrosis (Figure 7).
Figure 4 – Histological aspect of an acanthoma area
with clear cells of accentuated acanthosis and hyper-
keratosis and with numerous disseminated leukocytes
in the epidermis structure. HE staining, ×100.
Figure 6 – Keratinocytes with heterogeneous, clear or
vacuolar cytoplasm, with large intercellular spaces where
there are highlighted numerous diffusely disseminated
leukocytes. HE staining, ×200.
1173
The PAS–Hematoxylin staining, used for highlighting
the glycogen presence, showed a heterogenous arrange-
ment of the glycogen granules in the keratinocytes. The
richest in glycogen were the cells in the spinous and
granulous layers (Figures 8 and 9).
In the dermis there was observed the presence of a
rich inflammatory infiltrate, formed of lymphocytes,
plasmocytes and granulocytes, having a heterogenous
distribution. The trichromic staining allowed us to observe
the presence of large amounts of fibrillary collagen in
the superficial dermis and the intensification of the local
fibroblast activity (Figure 10).
Figure 5 – Superficial dermis with a well-developed
vascular network, mainly formed of arterioles and
capillaries. In the conjunctive tissue there may be
observed an infiltrate with lymphocyte and plasmocyte
cells. GS trichromic staining, ×200.
Figure 7 – Area of infiltrate epidermis with numerous
leukocytes (granulocytes and lymphocytes), with slight
acantholysis. GS trichromic staining, ×400.
1174 Maria Rotaru et al.
Figure 8 – Keratinocytes loaded with glycogen granules.
PAS–Hematoxylin staining, ×100.
For the immunohistochemical study of keratinocytes, we
used three antibodies. The cytokeratin 7 (CK 7) reaction
was completely negative at epidermis level (Figure 11),
but it presented a positive value in the excretory channel
epithelium of the perspiratory glands. In contrast, the
cytokeratin 34βE12 reaction (CK 34βE12) was intensely
positive in all keratinocytes, except for some areas where
there could be observed some keratinocyte acantholysis
and necrosis processes, areas where there were identified
numerous disseminated leukocytes among the epidermis
cells (Figure 12). The keratocyte reaction to cytokeratin
MNF116 (CK MNF116) was an intense one, except for
some keratinocytes whose cytoplasm contained high
amounts of glycogen (Figure 13).
The immunohistochemical study of the inflammatory
infiltrate in the dermis showed that it was mainly formed
of T-lymphocytes. In the papillary dermis, the T-lympho-
cytes appeared diffusely spread into the conjunctive
matrix of this area, among the angiogenesis vessels
(Figure 14). Numerous T-lymphocytes were identified in
the epidermis structure, diffusely disseminated among the
keratinocytes of the basal and spinous layers (Figure 15).
In the deep part of the superficial dermis and into the
deep dermis, the T-lymphocytes were well represented,
sometimes with a tendency of nodule formation (Figure 16).
The B-lymphocytes appeared diffusely arranged,
mainly in the superficial dermis and in a much reduced
number than T-lymphocytes (Figure 17).
The macrophages, similarly to B-lymphocytes,
appeared in a much more reduced number than T-
lymphocytes (Figure 18).
Figure 9 – Glycogen granules present in larger quantities
in the keratinocytes from the spinous and granulous
layers (previous image in detail). PAS–Hematoxylin
staining, ×200.
In order to better highlight the vascular structures at
dermis level, we used the CD34 antibody that marked the
angiogenesis sels (neovascularization). This immuno-
histochemistry technique allowed us to observe that inside
the clear cell acanthoma there developed a large number
of angiogenesis vessels. In the papillary dermis there were
identified low-caliber vessels (capillaries, metarterioles
and venules) (Figure 19), while in the deep dermis there
were highlighted, besides capillaries, a high number of
arterioles and venules (Figure 20).
Based on the clinical and paraclinical data, there was
established the diagnosis of multiple clear cell acanthoma.
The performed treatment included the surgical removal
of larger lesions and the dermatocoagulation of small
lesions. The evolution was a favorable one, the patient
being completely cured when she left the hospital. The
patient did not return to the Clinic of Dermatology as
the lesions did not relapse.
 Discussion
One of our case particularities was represented by
the rapid development of skin nodular lesions, for
approximately two months. Most studies showed that the
clear cell acanthoma generally has a slow development
of about two to 10 years, with reduced or even absent
symptoms [1]. We consider that the rapid development
of the acanthoma lesions were favored by the presence
of various associated diseases, such as chronic venous
insufficiency, which determined edema and stasis at
lower limb level, and liver failure.
 A rare case of multiple clear cell acanthoma with a relatively rapid development of the lower legs 1175

Figure 10 – Superficial dermis rich in collagen fibers, Figure 11 – Image of a clear cell acanthoma with negative
activated fibroblasts and neoformation blood vessels. reaction to CK 7. Anti-CK 7 antibodies immunostaining,
GS trichromic staining, ×200. ×100.

Figure 12 – Intensely positive reaction of keratinocytes
to cytokeratin 34βE12, except for some areas infiltrated
with leukocytes associated with keratinocyte necrosis
and predisposition to acantholysis. Anti-CK 34βE12
antibodies immunostaining, ×200.
Figure 13 – Keratinocytes with intense reaction to cyto-
keratin MNF116, except for the ones containing large
amounts of glycogen. Anti-CK MNF116 antibodies
immunostaining, ×400.
1176 Maria Rotaru et al.

Figure 14 – T-lymphocytes (brown colored) diffusely Figure 15 – Numerous T-lymphocytes present among
disseminated in the inflammatory infiltrate of the the keratinocytes from basal and spinous layers of the
superficial dermis. Anti-CD3 antibodies immunostaining, epidermis. Anti-CD3 antibodies immunostaining, ×200.
×200.

Figure 16 – T-lymphocytes with a tendency of nodular Figure 17 – B-lymphocytes in a relatively small number
aggregation, situated at the limit between the superficial present in the superficial dermis. Anti-CD20 antibodies
and deep dermis. Anti-CD3 antibodies immunostaining, immunostaining, ×200.
×200.
 A rare case of multiple clear cell acanthoma with a relatively rapid development of the lower legs
Figure 18 – Inflammatory infiltrate containing a moderate
number of diffusely disseminated macrophages in the
dermis. Anti-CD68 antibodies immunostaining, ×200.
Figure 20 – Immunohistochemical image of a dense
network of arterioles, capillaries and venules, located
at the limit between the superficial and deep dermis.
Anti-CD34 antibodies immunostaining, ×400.
The sizes of our patient’s lesions were of 1–2 cm,
1177
Figure 19 – Neoformation vessels, mainly capillaries,
present in a large number in the papillary dermis.
Anti-CD34 antibodies immunostaining, ×200.
similar to other cases described up to now [12]. Other
authors detected tumoral lesions with larger sizes, over
3–4 cm present at the level of the legs, buttocks or
perineum [13–15].
The lesions presented by our patient were located on
the inferior 1/3 part of the right calf, with a pale pink
color, moist surface, and covered with scalls. We think
that the color was given by the rich vascularization in
the dermis, and the moist aspect by the presence of a
plasma transudate, which could have also contributed to
the formation of scalls alongside the epidermis hyper-
keratinization in some areas. Most of the CCA cases
described up to now presented a scaly surface, sometimes
with a serous or, occasionally, serosanguinous exudation
[3, 12]. Some authors showed that the CCA lesions, due
to an intense vascularization and the presence of some
pale epidermis area, may bleed at minor traumas [16].
The color of CCA lesions may vary from pale pink, as
in our case, up to black brown. The brown, pigmented
color may be given by the presence of a large number of
melanocytes in the acanthoma structure, these forms
being defined as “melanoacanthomas” [17], “clear cell
melanoacanthomas” [18] or “pigmented clear cell acan-
thoma” (pigmented CCA) [19]. Bugatti and Filosa [20]
described a hemosiderinicum CCA, with a black macula
with a desquamative surface, where the histopathological
examination identified a large number of twisted blood
vessels in the papillary dermis, surrounded by hemosiderin
deposits, because of the extravasation and destruction of
red blood cells.
Another particular aspect of our case was the presence
of seven simultaneous CCA lesions. The first description
1178 Maria Rotaru et al.
of a multiple CCA belongs to Delacretaz (1964) [21].
Various other authors found multiple CCA lesions [5,
22–25]. Burg et al. [26] identified in a 38-year-old patient
the presence of more than 100 CCA spread along the legs,
arms and trunk. In the specialized literature, we found
less than 30 cases of multiple CCA lesions.
Regarding the etiopathogeny of the disease, all the
authors agree that this still remains unknown [8]. At
present, there are two main theories: the first theory
claiming that CCA is an epidermic benign tumor, having
as starting point the epidermis [7, 26, 27], the hair follicle
[28] or the excretory channel of the eccrine sweat glands
[29, 30]; the second theory, embraced by more and more
authors, suggests that CCA is a reactive inflammatory
dermatosis [8, 10, 31, 32].
The histological and immunohistochemical study
performed by us showed an epidemic hyperplasia, with a
slight increase of the keratinocyte sizes, possibly determined
by the presence of the intracytoplasmic glycogen granules.
The glycogen is responsible for the “clear” aspect of
these cells in the usual histological staining and the
positive reaction to the Periodic Acid–Schiff. The glycogen
accumulation in the keratinocytes could be due to the
absence of phosphorylasis, an enzyme involved in the
glycogen degradation and metabolization [5, 16]. The
presence of glycogen granules in the keratinocyte cyto-
plasm was also confirmed by electronic microscopy studies
[7, 28]. The lack of reactivity to CK 7 of the epidermis
keratinocytes and the positive value of the eccrine sweat
gland cells leads us to the conclusion that CCA does not
have its origin in the eccrine sweat gland epithelium. Also,
the different keratinocyte reactivity to CK MNF116 also
denotes a metabolic character of CCA, the glycogen
granules and the lack of phosphorylasis impeding the
synthesis of some structural cytokeratins.
In our case of multiple CCA, the inflammatory type
alterations were quite intense. The dermis inflammatory
infiltrate was dominated by the T-lymphocytes, B-
lymphocytes, macrophages, neutrophil leukocytes and
plasmocytes. T-lymphocytes and neutrophil leukocytes
have been identified as diffusely scattered also among the
keratinocytes of the basal, spinous and granulous layers.
At dermis level, we highlighted a reactivity of local
fibroblasts, with an increase of conjunctive matrix syn-
thesis, especially of the collagen. Also, we highlighted
quite a developed blood vessels network, with an intensely
positive epithelium to the CD34 antibody, a characteristic
of the angiogenesis vessels. Other authors, as well, showed
that the intense inflammatory reaction and hypervascu-
larization favorize the inflammatory origin of CCA [33–
35].
We consider that, due to a varied clinical aspect,
similar to other dermatological lesions, the lesion biopsy
and the histopathological study are essential for the
positive and differential diagnosis of CCA.
 Conclusions
We described the first case of a multiple CCA in
Romania, with a relatively rapid development, located on
the inferior 1/3 part of the calf, in a 71-year-old female
patient. The positive diagnosis was confirmed by the
histopathological and immunohistochemical examination
that highlighted at epidermis level the microscopic
alterations characteristic for CCA, including the presence
of glycogen granules in the keratinocyte cytoplasm. The
presence of an intense inflammatory reaction at dermis
level, associated with a dense network of angiogenesis
blood vessels and the alterations of the conjunctive matrix
are in favor of the inflammatory origin of CCA in the
studied case.
Acknowledgments
We kindly and sincerely thank Professor Laurenţiu
Mogoantă, Director of the Research Center for Microscopic
Morphology and Immunology within the University of
Medicine and Pharmacy of Craiova, who supported us
in the performance of the histopathological and immuno-
histochemical studies.
Author contribution
All the authors had an equal contribution in the
study performance.
References
[1] Tempark T, Shwayder T, Clear cell acanthoma, Clin Exp
Dermatol, 2012, 37(8):831–837.
[2] Degos R, Delort J, Civatte J, Poiares Baptista A, Tumeur
epidermique d’aspect particulier: acanthome à cellules claires,
Ann Dermatol Syphiligr (Paris), 1962, 89:361–371.
[3] Betti R, Bruscagin C, Inselvini E, Palvarini M, Crosti C,
Successful cryotherapic treatment and overview of multiple
clear cell acanthomas, Dermatol Surg, 1995, 21(4):342–344.
[4] Wang SH, Chi CC, Clear cell acanthoma occurring on the
hallux: the first case report, J Eur Acad Dermatol Venereol,
2006, 20(9):1144–1146.
[5] Monari P, Farisoglio C, Gualdi G, Botali G, Ungari M,
Calzavara-Pinton P, Multiple eruptive clear cell acanthoma,
J Dermatol Case Rep, 2010, 4(2):25–27.
[6] Petzelbauer P, Konrad K, Polypous clear cell acanthoma,
Am J Dermatopathol, 1990, 12(4):393–395.
[7] Nijssen A, Laeijendecker R, Heinhuis RJ, Dekker SK, Polypoid
clear cell acanthoma of unusual size, J Am Acad Dermatol,
2001, 44(2):314–316.
[8] Park SY, Jung JY, Na JI, Byun HJ, Cho KH, A case of polypoid
clear cell acanthoma on the nipple, Ann Dermatol, 2010,
22(3):337–340.
[9] Innocenzi D, Barduagni F, Cerio R, Wolter M, Disseminated
eruptive clear cell acanthoma – a case report with review of
the literature, Clin Exp Dermatol, 1994, 19(3):249–253.
[10] Finch TM, Tan CY, Clear cell acanthoma developing on a
psoriatic plaque: further evidence of an inflammatory aetiology?
Br J Dermatol, 2000, 142(4):842–844.
[11] Portal C, Fang F, Kanner W, Wilson B, Clear cell acanthoma,
Cutis, 2013, 92(2):62,77–79.
[12] Veiga RR, Barros RS, Santos JE, Abreu Junior JM,
Bittencourt Mde J, Miranda MF, Clear cell acanthoma of the
areola and nipple: clinical, histopathological, and immuno-
histochemical features of two Brazilian cases, An Bras
Dermatol, 2013, 88(1):84–89.
[13] Roytman M, Frumkin A, Everett MA, Giant clear cell
acanthoma, J Am Acad Dermatol, 1987, 17(3):513–514.
[14] Murphy R, Kesseler ME, Slater DN, Giant clear cell acanthoma,
Br J Dermatol, 2000, 143(5):1114–1115.
[15] Kim CY, Kim NG, Oh CW, Multiple reddish weeping nodules
on the genital area of a girl. Giant clear cell acanthoma (CCA),
Clin Exp Dermatol, 2010, 35(3):e67–e69.
[16] Fine RM, Chernosky ME, Clinical recognition of clear-cell
acanthoma (Degos’), Arch Dermatol, 1969, 100(5):559–563.
[17] Fanti PA, Passarini B, Varotti C, Melanocytes in clear cell
acanthoma, Am J Dermatopathol, 1990, 12(4):373–376.
[18] Pierard GE, Melanocytes in clear cell acanthoma, Am J
Dermatopathol, 1991, 13(4):430.
[19] Langer K, Wuketich S, Konrad K, Pigmented clear cell
acanthoma, Am J Dermatopathol, 1994, 16(2):134–139.
 A rare case of multiple clear cell acanthoma with a relatively rapid development of the lower legs
[20] Bugatti L, Filosa G, Hemosiderotic clear-cell acanthoma: a
pigmented mimicker, Indian J Dermatol, 2011, 56(4):426–
427.
[21] Delacretaz J, Clear cell acanthomas, Dermatologica, 1964,
129:147–153.
[22] Desmons F, Breuillard F, Thomas P, Leonardelli J, Hildebrand HF,
Multiple clear-cell acanthoma (Degos): histochemical and
ultrastructural study of two cases, Int J Dermatol, 1977,
16(3):203–213.
[23] Trau H, Fisher BK, Schewach-Millet M, Multiple clear cell
acanthomas, Arch Dermatol, 1980, 116(4):433–434.
[24] Kavanagh GM, Marshman G, Burton JL, Multiple clear cell
acanthomas treated by cryotherapy, Australas J Dermatol,
1995, 36(1):33–34.
[25] Morrison LK, Duffey M, Janik M, Shamma HN, Clear cell
acanthoma: a rare clinical diagnosis prior to biopsy, Int J
Dermatol, 2010, 49(9):1008–1011.
[26] Burg G, Würsch T, Fäh J, Elsner P, Eruptive hamartomatous
clear-cell acanthomas, Dermatology, 1994, 189(4):437–439.
[27] Degos R, Civatte J, Clear-cell acanthoma. Experience of 8
years, Br J Dermatol, 1970, 83(2):248–254.
[28] Watanabe S, Wagatsuma K, Takahashi H, Immunohisto-
chemical localization of cytokeratins and involucrin in
calcifying epithelioma: comparative studies with normal skin,
Br J Dermatol, 1994, 131(4):506–513.
1179
[29] Jones EW, Wells GC, Degos’ acanthoma (acanthome à cellules
claires): a clinical and histological report of nine cases, Arch
Dermatol, 1966, 94(3):286–294.
[30] Lindgren AG, Neumann E, Some evidence concerning the
sweat duct origin of clear cell acanthoma, Acta Derm
Venereol, 1973, 53(6):511–514.
[31] Kim DH, Kim CW, Kang SJ, Kim TY, A case of clear cell
acanthoma presenting as nipple eczema, Br J Dermatol,
1999, 141(5):950–951.
[32] Um SH, Oh CW, Three cases of clear cell acanthoma on
nipple and areola, Korean J Dermatol, 2003, 41(1):85–88.
[33] Yamasaki K, Hatamochi A, Shinkai H, Manabe T, Clear cell
acanthoma developing in epidermal nevus, J Dermatol, 1997,
24(9):601–605.
[34] Ardigo M, Buffon RB, Scope A, Cota C, Buccini P,
Berardesca E, Pellacani G, Marghoob AA, Gill M, Comparing
in vivo reflectance confocal microscopy, dermoscopy, and
histology of clear-cell acanthoma, Dermatol Surg, 2009,
35(6):952–959.
[35] Scanni G, Pellacani G, Topical calcipotriol as a new thera-
peutic option for the treatment of clear cell acanthoma, An
Bras Dermatol, 2014, 89(5):803–805.

Corresponding author
Laura Gheucă Solovăstru, Associate Professor, MD, PhD, Department of Dermatology, Faculty of Medicine,
“Grigore T. Popa” University of Medicine and Pharmacy, Dermato-Venereology Clinic, “St. Spiridon” Emergency
Hospital, 111 Ciurchi Street, 700368 Iassy, Romania; Phone +40722–321 377, e-mail: lsolovastru13@yahoo.com

Received: April 6, 2014

Accepted: December 2, 2014