Correspondence
CsA treatment contributed to the ADFK and gingival
overgrowth in this case. This is the first known case of
ADFK associated with CsA treatment reported in the
English literature.
Although the treatment of choice for CsA-associated
ADFK and gingival overgrowth is discontinuation of CsA,
this approach is often not possible and therefore excision is
the appropriate and preferred treatment for ADFK.
J. Qiao, Y. H. Liu and K. Fang
Department of Dermatology, Peking Union Medical College Hospital,
Peking Union Medical College and Chinese Academy of Medical
Sciences, Shuaifuyuan, Wangfujing, Beijing 100730, China.
E-mail: yuehualiu@263.net
Conflict of interest: none declared.
Accepted for publication 13 January 2008
References
1 Bart RS, Andrade R, Kopf AW et al. Acquired digital
fibrokeratomas. Arch Dermatol 1968; 97: 120–8.
2 Pinkus H, Cited by Bart RS, Andrade R et al. Acquired
digital fibrokeratomas. Arch Dermatol 1968; 97: 120–8.
3 Goldman MH, Barnhart G, Mohanakumar T et al. Ciclo-
sporin in cardiac transplantation. Surg Clin North Am 1985;
65: 637–59.
4 Allman SD, McWhorter AG, Seale NS. Evaluation of cyclo-
sporin-induced gingival overgrowth in the pediatric trans-
plant patient. Pediatr Dent 1994; 16: 36–40.
5 Schincaglia GP, Forniti F, Cavallini R et al. Ciclosporin-A
increases type I procollagen production and mRNA level in
human gingival fibroblasts in vitro. J Oral Pathol Med 1992;
21: 181–5.
Anetoderma accompanying microscopic panniculitis
in a patient with antiphospholipid syndrome and
systemic lupus erythematosus
doi: 10.1111/j.1365-2230.2008.02826.x
Anetoderma is a rare cutaneous disease characterized by a
loss of normal elastic tissue; however, its pathophysiology
is still unknown. We describe a case of anetoderma
associated with microscopic panniculitis in a patient with
antiphospholipid syndrome (APS) and systemic lupus
erythematosus (SLE).
An 18-year-old Japanese girl was referred to us for
evaluation of skin lesions on her neck, which she had
noticed 10 days previously. She had been diagnosed
6 years previously with SLE complicated with APS. Her
medical history included cerebral infarction, alveolar
haemorrhage and nephropathy. Results of laboratory tests
at that time were positive for antinuclear antibody
(1 : 320), anti-double-stranded DNA antibody and lupus
anticoagulant. The patient had been taking oral prednis-
olone 24 mg ⁄ day.
 2008 The Author(s)
Journal compilation  2008 Blackwell Publishing Ltd • Clinical and Experimental Dermatology, 34, 240–266
The patient then visited our department 5.5 years after
this diagnosis (6 months before the latest presentation),
reporting tenderness on the back, and again 4 months
later (2 months before the latest presentation), reporting
tenderness on the cheeks. In both cases, there was
subcutaneous induration with normal surface appearance,
and a biopsy was taken from the relevant area at each
presentation to exclude subcutaneous infection. The biop-
sies showed panniculitis with membranous fat necrosis.
Physical examination at the latest presentation revealed
multiple linear, flaccid, protuberant skin lesions measuring
5–30 mm in diameter on the right side of the neck along the
direction of the neck wrinkles (Fig. 1). The lesions had a
translucent appearance without any sign of blistering and
were associated with dilated blood vessels on the surface. A
biopsy was taken from one of these lesions.
Histopathological examination of the area revealed
depletion of elastic fibres in the dermis without infiltration
of inflammatory cells (Fig. 2a,b). Furthermore, in the
subcutaneous fat underlying the affected dermis, lipomem-
branous changes with giant cells and histiocytes were
found, consistent with lobular panniculitis (Fig. 2c,d). We
diagnosed these skin lesions as anetoderma associated with
microscopic panniculitis.
A simple classification1 of anetoderma has been
proposed. Primary anetoderma is idiopathic or associated
with positive antiphospholipid antibodies (APAs) in
conditions such as APS, SLE, human immunodeficiency
virus infection, or other autoimmune conditions. Second-
ary anetoderma follows, preceding skin lesions of specific
dermatoses. Stephansson and Niemi reviewed a group of
patients with SLE with and without APAs and revealed
that 15% of those with positive APAs developed aneto-
derma, whereas none of those without APAs did.2
Although the causative mechanism of anetodermic
lesions is unclear, it could possibly be caused by
microthromboses in the dermal vessels inducing devel-
opment of local ischaemia and leading to degeneration of
Figure 1 Multiple protuberant, flaccid skin lesions on the neck.
259
Correspondence

(a) (b)

(c) (d)

Figure 2 (a) Histopathology of a lesion on the neck (haematoxylin and eosin, original magnification · 100). (b) On the left side of the
specimen, the lesion had no elastic fibres (elastic van Gieson, original magnification · 200). The arrow indicates the boundary of the
lesion. (c) Lobular granulomatous panniculitis underlying the anetodermic lesion in the same specimen (haematoxylin and eosin, original
magnification · 200). (d) Giant cells and membranous fat necrosis in the fat tissue (haematoxylin and eosin, original magnification · 400).

elastic tissue.3,4 This suggests that a systemic search for
APAs is necessary for patients with anetoderma.
Although our patient had anetoderma associated with
APS and SLE, the presence of lobular granulomatous
panniculitis underlying the anetodermic lesions was
unique. Two previous skin biopsies taken from the tender
lesions at the back and cheek also showed panniculitic
changes. Marzano et al. 5 reported three cases of anetoder-
mic lupus panniculitis and APAs. In these three cases,
anetoderma developed on the previously involved skin or
close to the lupus panniculitis lesions after 1–3 years.
However, in our patient, there were no clinical symptoms
of lupus profundus such as tenderness, induration or
erythema on the neck. We did find panniculitic changes in
the biopsied sample. Thus our patient differs from the
previous patients.
We believe that both the anetoderma and panniculitis
might be caused by common mechanisms, mediated by
ischaemic changes because of APAs. Alternatively aneto-
derma could be secondary to inflammation expanded from
lesions of panniculitis, as seen in other secondary aneto-
derma. In our patient, anetoderma appeared only on the

 2008 The Author(s)

260  Journal compilation  2008 Blackwell Publishing Ltd • Clinical and Experimental Dermatology, 34, 240–266
 Correspondence

neck, although panniculitis was also found on the back and
cheek. This may be a result of site-specific features of the
neck, which has a thinner dermis.
M. Funabiki, M. Tanioka, Y. Miyachi and A. Utani
Department of Dermatology, Kyoto University, 54 Shogoin Kawahara-
cho, Sakyo-ku, Kyoto 606-507, Japan
E-mail: utani@kuhp.kyoto-u.ac.jp
Conflict of interest: none declared.
Accepted for publication 21 December 2007
References
1 Ishida Y, Koizumi N, Shinkai H et al. Primary anetoderma.
A case report and its modified classification. J Dermatol
2005; 32: 982–6.
2 Stephansson EA, Niemi KM. Antiphospholipid antibodies
and anetoderma: are they associated? Dermatology 1995;
191: 204–9.
3 Sparsa A, Piette JC, Wechsler B et al. Anetoderma and its
prothrombotic abnormalities. J Am Acad Dermatol 2003; 49:
1008–12.
4 Hodak E, David M Primary anetoderma and antiphosphol-
ipid antibodies – review of the literature. Clin Rev Allergy
Immunol 2007; 32: 162–6.
5 Marzano A, Vanotti M, Alessi E. Anetodermic lupus pann-
iculitis and antiphospholipid antibodies. Report of three
cases. Acta Derm Venereol 2004; 84: 385–8.
circumferential and localized mainly to the ventral and
both lateral sides of the finger and the ulcer was above the
dorsal side of the proximal interphalangeal joint (Fig. 1a).
Histopathological examination showed a benign neo-
plasm with a predominantly dermal component, consisting
of anastomosing cellular cords of acrosyringeal cells with
focal formation of lumina (Fig. 2a,b). The neoplastic cells
lacked nuclear atypia or mitotic activity. The stroma was
fibroblastic with focal oedema and hyperaemic vessels.
A perivascular lymphoplasmacytic infiltration was also
observed. The surface epithelium was hyperplastic, focally
ulcerated and slightly parakeratotic.
The clinical and histological findings suggested the
diagnosis of ESFA. We offered the patient surgical excision
with flap but she refused. Because of the benign nature of
the lesion, we proposed carbon dioxide (CO2) laser treat-
ment as an alternative option. After regional anaesthesia of
the finger area with lidocaine hydrochloride 2%, we used a
CO2 laser to destroy the lesion. Two passes were performed
in one session using 5 W of power and a spot size of
0.2 mm in continuous wave mode. Postoperative care
(a)

Eccrine syringofibroadenoma treated with carbon

dioxide laser

doi: 10.1111/j.1365-2230.2008.02827.x
Eccrine syringofibroadenoma (ESFA), is a rare benign
tumour that was first described by Mascaro in 1963 (1).
ESFA is typically located on the extremities and presents
as a plaque or a solitary hyperkeratotic nodule in adults
(2–4). We report a 78-year-old woman with ESFA on the (b)
right finger. The patient refused surgical excision; as an
alternative we successfully treated the lesion with a carbon
dioxide laser.
A 78-year-old white Greek woman presented with a
1-year history of a wound on the right ring finger. She did
not recall any trauma or previous inflammation at the site
of the lesion. The wound had progressively enlarged, with
no tendency towards healing. The patient also reported
itching, pain, a burning sensation and occasional bleeding.
She had a history of diabetes mellitus type 2, hypertension
and heart failure, and was taking metformin, acetylsalicylic
acid, captopril, hydrochlorothiazide and diltiazem.
On physical examination, a well-circumscribed, mildly
scaling, hyperkeratotic plaque, 30 mm · 35 mm in size
with a 3 mm deep ulcer in the centre of the lesion, was
visible on the right ring finger. The base of the ulcer was Figure 1 Eccrine syringofibroadenoma of the right ring finger
homogeneously red and clean. The lesion was almost (a) before and (b) after CO2 laser treatment.

 2008 The Author(s)

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