ARTICLE
Post-traumatic iatrogenic aggravation of eruptive collagenomas
in a child
Auteur(s) : Brigitte CORAS, Alexander ROESCH, Lars
KOSCHORRECK, Michael LANDTHALER, Thomas VOGT
Department of Dermatology
University of Regensburg
Franz-Josef-Strauss-Allee 11
93042 Regensburg
Germany
Fax: (+49) 941 944-9608
<brigitte.coras@klinik.uni-regensburg.de>
Eruptive collagenomas are defined as acquired connective tissue
nevi of the collagen type [1]. The eruption presents with
skin-colored multiple asymtomatic papules and nodules up to
3 cm. Histologically, thickening and homogenisation of
collagen fibers and degenerative changes of elastic fibers are
present [2]. Here we report a 12 year old girl with a sudden
eruption of 0.5-2.5 cm sized collagenomas after curettage of
‘mollusca contagiosa’.
‘Traumatic’ triggers of eruptive collagenomas have not been
described before. Therefore, this report sheds a new light on the
formal pathogenesis of eruptive collagenomas as ‘inducible’ nevoid
lesions.
A 12 year old patient presented with multiple asymptomatic
white to flesh-coloured small papules. Reportedly, those small
lesions had developed spontaneously in the axillae, flanks, knee
and elbow bends.
In the left axilla, however, where ‘molluscs’ had been previously
removed by curettage, dermal nodules up to 2.5 cm in diameter
were found (figure
1A).
There was no history of associated disease in this patient and
patient’s family.
A X-ray image of the left hand neither revealed sclerotic tissue
nor isolated areas of increased bone density indicating
osteopoikilosis.
Histopathological examination showed a dermal nodule with
condensed, largely increased swollen collagen fibres. Subtle
perivascular lymphocytic infiltrations were also present. Elastica
staining revealed thin fibres with a relative reduction compared to
the collagen compound. Alcian blue staining was negative (not
shown). Electron microscopy confirmed an increase of collagen
fibers. Interestingly, 10-15% of the fibrillar component showed
elevated diameters. Elastic fibers were normal (figure 1B).
Connective tissue nevi are classified according to their main
dermal component (collagen, elastin, proteoglycan) and are further
subdivided into inherited and acquired forms [1].
Hence, nevi of the collagen type can be subdivided in eruptive
acquired collagenomas, familial cutaneous collagenomas, shagreen
patches and isolated collagenomas [3].
Eruptive collagenomas (EC) usually appear in the first or second
decade with cutaneous nodules or scattered papules appearing on the
upper trunk and proximal arms. In a few cases an extended eruption
covering the whole body has been described [4]. Patients with EC
show no corresponding family history or associated systemic
findings [5, 6].
To our knowledge this is the first report on a posttraumatic
aggravation of EC. Although an induction of collagen by trauma can
not be proven, this case indicates that any traumatic treatment
should be avoided in EC if possible. Our hypothesis is that a
traumatic induction of focal collagen overexpression is possible in
EC. Alternatively, the mollusca contagiosa themselves may have
caused the enlargement of EC. Interestingly, the first report in
the world literature documented EC after a syphilitic eruption.
Therefore, infective agents may also contribute to this ‘nevoid’
overproduction of collagen [2].
The most important differential of EC is familial cutaneous
collagenoma.
Papular elastorrhexis (PE) should not be confused with EC. PE is a
rare entity characterized by multiple 1-5 mm nonfollicular
white papules scattered over the trunk, shoulders and mainly the
upper extremities [7]. The lesions of PE are uniformly sized and
much smaller than in EC [2]. The disorder was first described by
Bordas et al. in 1987 as a variant of ‘nevus anelasticus’
because of its typical reduction and fragmentation of the elastic
fibres [8]. Sears et al. (1988) reported two similar cases
which they believed to be variants of connective tissue nevi
[2].
Schirren et al. (1994) considered a case with familial PE
as an abortive variant of the Buschke-Ollendorf syndrome (BOS),
dermatofibrosis lenticularis disseminata [9]. In contrast to
Schirren’s view, Buechner et al. (2002) pointed out that in
BOS the papules mostly present with an accumulation of elastin and
should therefore be considered to be distinct from PE [7]. This is
further supported by experimental data showing that fibroblasts
from BOS patients reveal increased elastin mRNA levels consistent
with a phenotype of abnormal high elastogenesis and elastin
production [10]. Also Uitto et al. 1981 demonstrated an
accumulation of elastin in BOS [11].
No possible therapy of EC has been described yet. Assuming a
formal pathogenetic homology with spontaneous keloids or
hypertrophic scars, we are currently trying to influence the EC in
this patient with a silicon gel (Dermatix®). In keloid
treatment, several studies [12-14] reported successful reduction of
collagen production after a mean application time of
2-4 months. Since reactive elements in the pathogenesis of
nevoid EC seem possible on the basis of this report, such
conservative strategies of EC treatment and strict avoidance of
iatrogenic traumas seem to make sense. n
References
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