CASE REPORTS

Pediatric Dermatology Vol. 24 No. 6 621627, 2007

Pediatric Blaschkitis: Expanding the

Spectrum of Childhood Acquired
Blaschko-linear Dermatoses
Brian R. Keegan, Ph.D.,* Hideko Kamino, M.D.,* William Fangman, M.D.,*
Helen T. Shin, M.D.,* Seth J. Orlow, M.D., Ph.D.,* and Julie V. Schaer, M.D.*
*Ronald O. Perelman Department of Dermatology and Departments of Pathology and Pediatrics, New York
University School of Medicine, New York City, New York, Departments of Dermatology and Pediatrics,
Hackensack University Medical Center, Hackensack, New Jersey

Abstract: We describe two young children who developed relapsing,

pruritic, papulovesicular eruptions in multiple bands along Blaschko lines
on the neck, trunk, and extremities. Skin specimens in both revealed
spongiotic dermatitis. This represents the first report of blaschkitis in
children, providing further evidence that lichen striatus and blaschkitis are
related acquired Blaschko-linear dermatoses that exist on a spectrum rather
than as the childhood and adult form of a single disease entity. We highlight
the features that differentiate blaschkitis from lichen striatus, review the
potential roles of cutaneous mosaicism, environmental triggers, and background immunologic state in their pathogenesis, and discuss the spectrum
of inflammatory dermatoses that can follow Blaschko lines.

Lichen striatus (LS), a self-limited acquired inammatory dermatosis that follows Blaschko lines, was rst
described by Balzer and Mercier in 1898 (1). It most
often occurs in children, with a mean age at onset of
4 years (28). Lichen striatus is characterized by an
eruption of discrete, hypopigmented to erythematous,
at-topped, 24 mm papules with a smooth or slightly
scaly surface. These papules rapidly coalesce to form a
linear band, which progressively extends along an
extremity or, less commonly, across the trunk or face
over a period of days to weeks. The band is typically
narrow (e.g., <12 cm in width), solitary and unilateral, and may be discontinuous. Lichen striatus tends to
be asymptomatic. It resolves spontaneously, usually

within 1224 months and frequently with residual

hypopigmentation (28). Although the histologic
ndings of LS are variable, a lichenoid dermatitis
accompanied by a deeper periappendageal lymphocytic
inltrate, collections of histiocytes in the dermal papillae, and mild epidermal spongiosis with exocytosis is
suggestive of the diagnosis (9,10).
In 1990, Grosshans and Marot (11) described a
relapsing linear inammatory dermatosis that they
termed adult blaschkitis. Since that time, at least 13
further instances of blaschkitis (also referred to as acquired relapsing self-healing Blaschko dermatitis or
acquired Blaschko dermatitis) have been reported in
the world literature (1225). In addition to a later age at

Address correspondence to Julie V. Schaer, M.D., The Ronald

O. Perelman Department of Dermatology, New York University
School of Medicine, 560 First Avenue, Room H-100, New York,
NY 10016, or e-mail: schafj04@med.nyu.edu.
DOI: 10.1111/j.1525-1470.2007.00550.x

 2007 The Authors. Journal compilation  2007 Blackwell Publishing, Inc.

621

622 Pediatric Dermatology Vol. 24 No. 6 November December 2007

TABLE 1. A Comparison of Blaschkitis (1125, this report), Adult Lichen Striatus (2636), and Classic Lichen Striatus (28)
Pediatric Blaschkitis
Adult Blaschkitis
(n = 12)
Age at onset (yr)
Sex
Papulovesicles
Multiple bands
Width of bands
Distribution on trunk
Duration [range]
Relapses
Pruritus
Histologic features

50 (mean)
1.5F:1M
71%
100%
Usually broad
86%
1.5 mo (mean)
[14 mo]
64%
64%
Purely spongiotic
(69%)

Patient 1

Patient 2

3
F
+
+
Broad
+
3 wk

6
M
+
+
Broad
)
1 mo

+
+
Purely
spongiotic

+
+
Purely
spongiotzic

Adult lichen striatus

(n = 12)

Classic lichen striatus

(n = 340)

41 (mean)
3F:1M
0%*
50%**
Variable
75%
5 mo (mean)
[1 mo1 yr]
0%*
50%
Lichenoid spongiotic

3 (mean)
2F:1M
0%*
6%,*
Usually narrow
22%*
7 mo (mean)
[1 mo4 yr]
2%*
20%*
Lichenoid spongiotic

Seven series of >10 patients with lichen striatus.

Patrizi et al. (7), n = 115 (data not available from other lichen striatus series).

Refers to individual episodes; duration of the disease process ranged from 1 mo to 12 yr.

Remainder had spongiotic and lichenoid features.

*
p 0.001 (chi-square test, for dierence from adult blaschkitis).
**
p 0.01 (chi-square test, for dierence from adult blaschkitis).

onset (mean, 41 years; range, 2470 years), blaschkitis

diers from LS in its papulovesicular morphology,
prominent pruritus, multilinear pattern with relatively
broad bands, predominantly truncal distribution, rapid
resolution, and frequent recurrences. Histologically,
blaschkitis is characterized by a primarily spongiotic
(eczematous) rather than a lichenoid dermatitis. The
features of blaschkitis and LS are compared in Table 1.
Although some authors consider blaschkitis to represent an adult variant of LS (16,31), the papulovesicular
lesions, multiple bands, and relapsing nature dier signicantly from that of adult LS reported in the literature.
Shepherd et al (33) emphasized that all of the typical
features of LS (except young age at onset) can be
observed in adults. We have followed several adults with
classic LS, including a 50-year-old Indian man with a
2-year history of hypopigmented, thin, at-topped papules arranged along Blaschko lines on the upper
extremity and trunk (J.V.S., unpublished observations).
Because childhood LS occasionally develops in a multilinear pattern on the trunk (37,38), has been reported to
relapse (4,5,7), and can exhibit spongiotic as well as
lichenoid features histologically (9,10), Taieb et al (4)
proposed that LS and blaschkitis exist on a spectrum of
Blaschko-linear acquired inammatory skin eruptions
(BLAISE). Determining whether a particular occurrence
is better classied as LS or blaschkitis depends upon the
clinical as well as histologic features, and intermediate
presentations in children (e.g. pruritic, pink, scaly papules in a band on the trunk with prominent spongiosis on
histologic examination) are typically considered as LS.
However, despite some overlap, clearly the two ends of

the spectrum dier substantially in their clinical

appearance, natural histories, histologic ndings and
dierential diagnoses (Fig. 1) (15,18,28,33,39).
Herein we describe two young children who developed relapsing papulovesicular eruptions in multiple
bands following Blaschko lines on the neck, trunk and
extremities, with skin biopsy specimens revealing a
spongiotic dermatitis. To our knowledge, this represents
the rst report of pediatric blaschkitis, providing further evidence that LS and blaschkitis are related but
distinct acquired Blaschko-linear dermatoses (ABLD)
rather than the childhood and adult form of a single
disease entity.

CASE REPORTS
Patient 1
A 3-year-old girl presented with a 1-week history of a
pruritic papulovesicular eruption that rapidly developed
in a linear conguration on the left posterior neck, upper
back, and arm. She had received a 5-day course of oral
acyclovir for a presumptive diagnosis of herpes zoster,
but a viral culture and direct uorescent antibody testing
of vesicular lesions were negative. The patient had no
history of atopy or other medical problems and was
taking no medications. The family history was notable
for allergic rhinitis and atopic dermatitis in her mother
and sibling, respectively.
Physical examination found multiple 23 mm, bright
pink, edematous papules coalescing to form a
well-dened triangular plaque that covered most of the

Keegan et al: Pediatric Blaschkitis

623

Figure 1. The spectrum of inflammatory acquired Blaschko-linear dermatoses.

right posterior neck and upper back, with an extremely

sharp midline demarcation. The plaque extended as a
broad (24 cm), multilinear band over the right shoulder
to the upper arm and exor forearm. Overlying 13 mm
collarettes of scale and serous crusting were evident.
Treatment was initiated with uticasone propionate
0.05% cream twice daily, and the eruption almost completely resolved within 3 weeks. However, despite continuation of the uticasone, 1 week later a second crop of
discrete 34 mm edematous papules and papulovesicles
appeared in an area of prior involvement on the left
upper back (Fig. 2A). This was associated with a recrudescence of pruritus.
A biopsy specimen from an edematous papule
revealed epidermal hyperplasia with spongiosis, hypergranulosis, and ortho- and parakeratosis adjacent to a
focal erosion (Fig. 3A,B). A perivascular lymphocytic
inltrate was evident in the supercial and mid-dermis.
The second outbreak was treated with diorasone
diacetate 0.05% ointment twice daily, and resolved over
the next two weeks. The eruption has not recurred during
a follow-up period of 1 year.
Patient 2
A 6-year-old Hispanic boy presented with a 7-month
history of an extremely pruritic papulovesicular eruption on the right neck and leg. The lesions initially
resolved within one month upon treatment with a class
I topical corticosteroid and a short course of oral

prednisolone. However, the eruption recurred and extended further down his leg following an episode of
scarlet fever 5 months later. The patient had no history
of atopic dermatitis or other skin conditions. He was a
carrier of sickle cell trait and had a history of recurrent
otitis media. Although he was taking no chronic
medications, he received a course of amoxicillin therapy for the scarlet fever. The family history was signicant for asthma and atopic dermatitis in the
patients mother.
Physical examination found a pink linear plaque with
overlying hemorrhagic and serous crusting on the right
posterior lower extremity, extending from the right
medial buttock to the heel (Fig. 2B,C). Similar plaques
were present along the medial and lateral aspects of the
right foot and on the right posterior neck, in a distribution corresponding to Blaschko lines.
A biopsy specimen from the right calf showed irregular epidermal hyperplasia with marked spongiosis and
exocytosis of lymphocytes as well as a few eosinophils
(Fig. 3C). The granular layer was diminished, with
conuent parakeratosis and a focal crusted erosion.
A supercial and deep perivascular and interstitial inltrate of lymphocytes and eosinophils was present in the
dermis (Fig. 3D). Edema and brosis were noted in the
papillary dermis, with collagen bundles oriented perpendicularly to the cutaneous surface.
The lesions were treated with clobetasol propionate
0.05% ointment, and resolved over the next few weeks.
Several milder recurrences were noted during a follow-up

624 Pediatric Dermatology Vol. 24 No. 6 November December 2007

Figure 2. A relapse of discrete, pink, edematous papules

with hemorrhagic crusting in an area of previous confluent
involvement on the upper back of Patient 1 (A). Pink crusted
plaque in a linear distribution on the leg (B) and thigh (C) of
Patient 2.

period of 2.5 years, always in the same linear distribution

and resolving spontaneously within two weeks.
DISCUSSION
The distribution pattern of ABLD is thought to reect
cutaneous mosaicism (i.e., the presence of two or more
genetically dierent populations of skin cells). When a
somatic mutation or chromosomal non-disjunction
occurring during embryogenesis aects an epidermal
progenitor cell, its daughter cells proliferate and migrate
along Blaschko lines (the normal pathways of ectoder-

mal development) (40). In the case of an ABLD, the

aberrant clone of keratinocytes is not clinically apparent
at baseline. However, a triggering event may lead to
recognition of the clone by the immune system, possibly
via molecular mimicry or by inducing expression of
(unmasking) a unique antigen (4,18); alternatively, the
aected skin may respond to a precipitant with an
excessive inammatory response (19). These mechanisms
could account for the appearance of cutaneous inammation following Blaschko lines. The observation of
abnormalities involving chromosome 18 in cells from
lesional skin, but not in normal-appearing skin, of a
patient with blaschkitis (22) supports the theory that
cutaneous mosaicism underlies ABLD. The functional
mosaicism of the X-chromosome that is present in all
females (Lyon hypothesis) may help to explain the higher
incidence of ABLD in girls and women (41).
The consistent nding of epidermal CD8+ T cells
surrounding necrotic keratinocytes in biopsy specimens
of LS (9,10) implicates cell-mediated cytotoxicity directed against keratinocytes in its pathogenesis. Although
overlap exists, the pattern of inammation in blaschkitis
tends to be primarily spongiotic, without prominent
keratinocyte necrosis (1113,15,17,1921,23). Direct attack on a target antigen and subsequent elimination via
apoptosis of an abnormal keratinocyte clone may explain the lack of recurrences in LS, whereas persistence of
the clone may account for the relapsing nature of blaschkitis (7,39). Perhaps LS results from an obviously
deviant clone that is typically deleted early in life, whereas
a clone with subtle alterations in antigenicity or propensity for inammatory stimulation but a relatively
widespread distribution leads to blaschkitis. Further
studies examining the cellular inltrates and cytokine
proles in blaschkitis may help to better dene this entity
and its pathogenesis.
A tendency for dierent types and distributions of
inammation in LS and blaschkitis may be related to
variability in the triggers and background immunologic
state as well as the abnormal clone itself. Viral infections,
vaccinations (e.g., hepatitis B and BCG), pregnancy, and
trauma have been reported as possible precipitants of LS
(5,7,3335,4144); in addition to viral infections, medications (e.g. metronidazole) and emotional stress have
been implicated in blaschkitis (18,24,25). Descriptions of
the simultaneous occurrence of LS in at least ve sets of
siblings and one motherson pair suggest a role for a
common environmental stimulus (e.g., a viral infection)
in a setting of genetic predisposition (5,7,36,41,43,44).
Observations of seasonal and epidemic clustering of LS
also support a viral trigger (5,45). Lastly, although some
studies have found an increased prevalence of atopy in
patients with LS (2,3,7), indicating that the associated

Keegan et al: Pediatric Blaschkitis

625

Figure 3. Biopsy specimen from an edematous papule (Patient 1) shows epidermal hyperplasia, an erosion, and a perivascular
lymphocytic infiltrate in the upper to mid dermis (A). Note the spongiosis and focal parakeratosis (B). Biopsy specimen from a
crusted plaque (Patient 2) demonstrates epidermal hyperplasia with marked spongiosis, exocytosis of lymphocytes, and confluent
parakeratosis (C) as well as a dermal infiltrate of lymphocytes and eosinophils (D). (Hematoxylineosin; magnification: A, x4; B,
x20; C, x10; D, x40.).

immunologic aberration may represent a predisposing

factor, other series have noted frequencies of atopy
similar to those in the general population (8).
In addition to blaschkitis and LS, which have a
Blaschko-linear pattern by denition, a variety of acquired dermatoses that are usually distributed in a nonmosaic fashion can occur along the lines of Blaschko (see
Fig. 1). These include lichen planus (LP), lichen nitidus,
lichenoid and xed drug eruptions, lichenoid chronic
graft-versus-host disease, lupus erythematosus, psoriasis,
and atopic dermatitis (AD) (39,46,47). Linear LP and
linear lichenoid lupus can sometimes be dicult to distinguish from LS (9,48). Histologically, the presence of a
periadnexal and deeper perivascular as well as a lichenoid
inltrate support a diagnosis of LS rather than LP,
whereas increased dermal mucin or a thickened basement membrane together with the former ndings are
suggestive of lupus (9,10); the presence of mild spongiosis

and focal parakeratosis is also more indicative of LS than

LP. Hladik et al (47) noted that the clinical and histologic
features of linear AD and blaschkitis are similar, with a
history of AD in a typical distribution distinguishing the
former condition. Although the spongiotic dermatitis
with prominent eosinophils observed in the biopsy
specimen from Patient 2 was compatible with AD, he had
no atopic background to support this diagnosis.
The arrangement of a classic dermatosis along Blaschko lines presumably reects a mosaic state in which the
aected clone of epidermal cells has an increased susceptibility to that particular condition. An acquired
dermatosis can also arise superimposed upon an obvious
congenital Blaschko-linear lesion. Examples include the
exanthem of scarlet fever in a distribution limited to areas
of nevoid hypomelanosis (49), linear lupus overlying
nevoid hypertrichosis (39,50), and LS, blaschkitis, LP,
or psoriasis within an epidermal nevus (5,19,39).

626 Pediatric Dermatology Vol. 24 No. 6 November December 2007

Inammatory linear verrucous epidermal nevi (ILVEN)

can usually be distinguished from the latter as well as
from linear psoriasis by their early age at onset (in most
but not all patients), persistence, marked pruritus, and
psoriasiform histologic features with alternating orthoand parakeratosis (51).
Mosaicism for an autosomal dominant genodermatosis represents another occasional cause of inamed
lesions along Blaschko lines, ranging from the keratotic
papules of Darier disease to the crusted erosions of
Hailey-Hailey disease. Inammatory vesicular and
verrucous Blaschko-linear lesions characterize stages 1
and 2, respectively, of the X-linked dominant disorder
incontinentia pigmenti (IP). Although stage 1 of IP typically resolves during infancy, vesicular lesions can recur
in association with childhood illnesses (52). In this situation, residual abnormal keratinocytes are highly susceptible to cytokine-induced apoptosis because of their
lack of NF-jB signaling. The phenomenon of an infection triggering an episode of clonal inammation in
the setting of IP is reminiscent of the relapses associated
with blaschkitis.
The clinical and histologic features of our patients
relapsing, pruritic, papulovesicular eruptions in multiple
bands following Blaschko lines on the neck, trunk, and
extremities were strikingly similar to the instances of
adult blaschkitis previously described in the literature.
This report expands the spectrum of childhood ABLD,
providing further evidence that LS and blaschkitis are
related but distinct entities. The genetic bases and precise
immunologic mechanisms for these patterns of reaction
along Blaschko lines remain to be determined.
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