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Actinic Prurigo

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DOI: 10.1007/978-1-4614-6654-3_41

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 Actinic Prurigo
41
Sonia Toussaint-Caire

Abstract
Actinic prurigo (AP) is a chronic photodermatosis that occurs mainly in dark-skinned pop-
ulations with strong Amerindian genetic lineage who live in dry and sunny geographical
areas at altitudes over 1,000 m above sea level. AP usually begins in childhood and is more
frequent in women. Expression of HLA-DR4 and subtype DRB1*0407 have been found to
be related with the disease. Pathogenesis may be related to the production of tumor necrosis
factor alpha (TNF-α) by epidermal keratinocytes, after UVB radiation. Patients usually
have lesions on sun-exposed skin, characterized by extremely pruritic erythematous mac-
ules, papules, and infiltrated plaques. Due to intense scratching, excoriations, lichenifica-
tion, scars, and residual hypo or hyperpigmentation may be seen. Affectation of lips and
conjunctiva is a very characteristic manifestation of the disease. Microscopic study of ver-
million border biopsy shows a very distinctive inflammatory infiltrate with lymphoid fol-
licle formations. Main differential diagnosis includes photosensitivity associated with
atopic dermatitis. Besides adequate photoprotection, thalidomide is the first line medical
treatment with excellent results, although significant side effects should be closely moni-
tored and prevented.

Keywords
Actinic prurigo • Photodermatosis • Cheilitis • Thalidomide

It was first described in 1952 by López González from

Introduction
Actinic prurigo (AP) is an inflammatory, chronic, and idio-
pathic photodermatosis. As its name implies, skin lesions are
photodistributed. Labial and/or conjunctival mucosae can be
affected too, and in more severe cases, the cutaneous rash
may extend to areas not exposed to sun. AP is predominantly
seen in dark-skinned populations with a strong Amerindian
genetic lineage [1] (Fig. 41.1).
Argentina, under the name of Solar Prurigo [2]. Few years
later, in 1954, Escalona and coworkers reported the first
cases in Mexico [3], and from then on, AP has been identi-
fied in other latitudes such as Canada and in Central and
South America [1]. Dr. Fabio Londoño, from Colombia, was
the one who coined the term “actinic prurigo” [4].
Epidemiology

• Begins in childhood between 6 and 8 years of age and

is more common in women.
S. Toussaint-Caire, M.D. (*) • Commonly seen in dark-skinned people, Fitzpatrick’s
Hospital General Dr. Manuel Gea González, phototypes IV and V.
Calzada de Tlalpan 4800, Colonia Sección XVI, Delegación
Tlalpan, México City 14080, México • Patients usually live in high-altitude, dry, sunny geo-
e-mail: tussita@hotmail.com graphical areas.

N.B. Silverberg et al. (eds.), Pediatric Skin of Color, 387

DOI 10.1007/978-1-4614-6654-3_41, © Springer Science+Business Media New York 2015
388
AP occurs mainly in children between 6 and 8 years of
age [5, 6] but can be seen at any age group [6]. It is more
common in women, with a ratio of 2:1 compared to men
[5–7] and commonly affects people with darker skin photo-
types (IV and V of Fitzpatrick’s classification) [5, 6, 8] who
live in dry and sunny geographical areas located in high alti-
tudes, usually above 1,000 m above sea level. However, there
have been cases reported to occur in people living at lower
altitudes, even at sea level [5, 6].
Fig. 41.1 Young girl from the Tojolabal community from the State of
Chiapas, Mexico, with early lesions of actinic prurigo (AP)
Fig. 41.2 Well-developed
lesions of AP in two patients
from the Mazahua community
from the State of Mexico,
Mexico
S. Toussaint-Caire
Pathophysiology
Genetic Amerindian ancestry plays an important role in the
pathogenesis of the disease [9], and may explain why AP
predominates in countries, like Guatemala, Colombia,
Honduras, Ecuador, Peru, Bolivia Mexico, that have indige-
nous populations with low cross-cultural influence, where
there is a reported prevalence of the disease of 3.9 % [10]
(Fig. 41.2).
Isolated cases have been reported in Costa Rica,
Venezuela, Argentina, Uruguay, Chile, northern United
States, in Canada’s Inuit population [1, 5, 7] (prevalence of
0.1 %) [10], Australia, Great Britain, and Thailand [1].
Little is known about the exact etiology of this disease.
Some identified factors involved are low socioeconomic sta-
tus, family history [8], living in rural areas, continuous con-
tact with farm animals and exposure to wood smoke [11].
Regarding genetic predisposition, it has been shown that,
in Mexico, 90–92.8 % of patients with AP express HLA-DR4
[12–15] and the allele HLA-DRB1*0407 [1, 7, 10] the most
common subtype (60–80 %) [12, 15].
HLA-DR4 has also been identified in European patients
with AP [1, 10]. Other related alleles associated with the dis-
ease are HLA-A28 and B39 in Mexico [1, 7], HLA-A24,
HLA-Cw4, and DRB1*14 in Canada [7, 10], HLA-Cw4 in
Chimila indians from Colombia [16], and HLA-B40 and
Cw3 in Bogota [1, 7, 10].
Increased expression of HLA-B40 and Cw3 is seen in
populations with strong Amerindian genetic lineage and may
explain why this disease is more common in this ethnic group
[1, 17]. HLA subtype DRB1*0407 has also been found to be
more frequent in Colombian patients with AP [18].
41 Actinic Prurigo
In 1984, Moncada and coworkers [19] suggested that the
skin of patients with AP had an abnormal immune response
characterized by an increased number of T lymphocytes in
peripheral blood, especially T helper cells (CD4+), and also
an increased number of CDIa+ dendritic cells in the dermal
inflammatory infiltrate [5, 20]. It was subsequently observed
that this abnormal response was induced by solar radiation,
particularly the spectrum of ultraviolet radiation A (UVA)
and B (UVB). However, visible light also has an important
role in the pathogenesis of the disease [1, 5, 21].
UVB radiation stimulates the production of tumor necro-
sis factor alpha (TNF-α) by epidermal keratinocytes, espe-
cially those from the suprabasal layer [1, 6]. This cytokine is
able to activate immunoreactivity and expression of adhesion
molecules on keratinocytes, which promote the migration of
inflammatory cells that produce epidermal tissue injury and
necrosis [6, 22]. TNF-α also initiates the activation of tran-
scription factor NF-κβ and programmed cell death (apopto-
sis), so it is very likely that this immune response occurs in
the pathophysiology of AP [23].
B cells in lymphoid follicles express CD80 (B7) and pro-
mote proliferation of Th2 cells that release IL-5 (eosinophil
activator) and IL-4 (which stimulates production of IgE [24]
and the activation of mast cells). This process promotes the
formation of the characteristic ectopic germinal centers (lym-
phoid follicles) on the lips, also documented in other condi-
tions of hypersensitivity, autoimmunity, or infection [25].
On the other hand, lymphocytes T-CD4+ induce the syn-
thesis of IL-2, which activates natural killer cells and pro-
motes the production of IgE antibodies [1] that have been
demonstrated in situ and in serum of patients with AP [26].
Mast cells also play an important role in both inflamma-
tory and allergic reactions. In 2007, a Mexican study has
shown a higher density of mast cells in the lip lesions of
Fig. 41.3 Patients with AP
usually have lesions on sun-
exposed skin of face, neck,
trunk, and extremities and
show a bilateral and symmetrical
distribution. Associated xerosis
can be seen
389
patients with AP, compared to normal and inflamed mucosa
due to other pathologic processes [26].
The presence of increased levels of IgE, eosinophils, and
mast cells suggests a hypersensitivity reaction as one of the
mechanisms in the pathophysiology of AP [25]. Generally,
hypersensitivity reactions occur after exposure to an antigen
that activates effector cells. AP may be classified as a
delayed hypersensitivity reaction [19, 27, 28] type IVa,
because after sun exposure, keratinocytes are able to pro-
duce TNF-α [1, 6]. It can also be regarded as IVb type reac-
tion due to the presence of increased levels of IgE,
eosinophils, and mast cells [29–31].
Clinical Presentation
• Polymorphous dermatitis affecting photoexposed
areas of face, neck, trunk, and extremities.
• Lesions consist of extremely itchy erythematous mac-
ules, papules, infiltrated plaques. excoriations, lichenifi-
cation, scars, and residual hypo or hyperpigmentation
• Characteristically, it affects lips and conjunctiva with
eventual pseudopterygium formation.
AP is a polymorphous photodermatosis. Patients usually
have lesions on sun-exposed skin of face, neck, trunk, and
extremities, and the lesions are distributed in a bilateral and
symmetrical array (Fig. 41.3). This dermatosis predominates
over areas where radiation hits with more intensity, such as
nasal dorsum, zygomatic and superciliary arches, lower lip,
and conjunctiva [5, 12]. Less frequently, lesions can be
observed in non-photoexposed skin [9, 15] (Fig. 41.4).
AP is an inflammatory dermatosis characterized by ery-
thematous macules and papules that converge to form infil-
trated plaques. Because it is extremely itchy, there are also
390 S. Toussaint-Caire

Fig. 41.4 Mild AP. Lesions

predominate over nasal dorsum,
zygomatic and superciliary
arches, lower lip, and
conjunctiva. Hypopigmented
residual lesions can be seen

Fig. 41.5 Moderate to severe

AP. Papular lesions become
confluent forming infiltrated
plaques. There are more
exulcerations covered with scale
crusts and lichenified areas, due
to severe scratching

excoriations, scale-crusts, lichenification, scars, and residual
hypo or hyperpigmentation [5–7, 9, 12] (Fig. 41.5).
On the vermilion border of the lips, erythema, edema, fis-
sures, and ulcers covered by serohemorrhagic scales can be
observed. This is a very characteristic manifestation of the
disease and is referred to as actinic prurigo cheilitis (APC).
There is sometimes associated gingival hypertrophy, possi-
bly secondary to mouth breathing due to the uncomfortable
symptoms on the lip [12]. APC is a common clinical mani-
festation and more frequently affects the lower lip. Up to
65 % of children with AP can show labial lesions [1], and in
27.6 %, it could be the only manifestation of the disease [12]
(Fig. 41.6).
Conjunctiva can be affected in approximately 45 % of
patients. Conjunctivitis of AP initially presents with hyper-
emia, photophobia, increased tearing, and subsequent pseu-
dopterygium formation, and in severe cases, there can be
partial loss of the visual fields. It appears that conjunctival
alterations are usually a late manifestation of the disease [5,
9, 12] (Fig. 41.7).
41 Actinic Prurigo 391

Fig. 41.6 Actinic prurigo

cheilitis. Lips can be swollen,
with areas of erythema, fissures
and ulcers covered by
serohematic scales

Fig. 41.7 Actinic prurigo conjunctivitis. Conjunctivitis of AP initially presents with hyperemia, photophobia, increased tearing and subsequent
pseudopterygium formation

AP has a chronic clinical course with frequent exacerba- Histopathology

tions after sun exposure. In geographical areas where sea-
sons are well defined, flares usually occur during spring and
summer and decrease in the fall [9, 15]. In contrast, in regions
with tropical climate without marked seasonal variations,
exacerbations may occur year-round related with constant
exposure to sunlight [5].
The microscopic picture of skin lesions shows hyperkerato-
sis, foci of parakeratosis, acanthosis, thickening of the base-
ment membrane, and a superficial perivascular inflammatory
infiltrate of lymphocytes. Sometimes, there are only mild
inflammatory changes with epidermal hyperplasia, suggestive
392
Fig. 41.8 Histopathology of AP. (a) Low power view of a vermillion
mucosa biopsy that shows a nodular lymphocytic infiltrate in the lamina
propria. (b) Higher power magnification of the ectopic lymphoid folli-
of a chronic dermatitis; however, the presence of an intense
nodular inflammatory lymphocytic infiltrate with numerous
eosinophils and mast cells suggests the diagnosis [32].
Unlike other photodermatoses, adnexal structures are not
affected and solar elastosis is not a common finding.
Histology of APC shows hyperkeratosis, scale crusts
covering ulcerated areas, mild acanthosis, spongiosis, and
mild vacuolar alteration of the basal layer. At the superficial
portion of the submucosa, eosinophils and melanophages
can be found, and deeper in the lamina propria, there are
dilated capillary vessels, interstitial edema, and a band-like
or nodular lymphocytic infiltrate. Lymphocytes may aggre-
gate and form well-defined ectopic lymphoid follicles. This
particular histologic picture is named “follicular cheilitis”
and is a very characteristic feature of APC [12] (Fig. 41.8).
S. Toussaint-Caire
cle characteristic in cheilitis of AP. (c) Epithelial spongiosis, exocytosis
of eosinophils and dermal inflammation. (d) Mixed inflammatory infil-
trate with lymphocytes, histiocytes, eosinophils and plasma cells
Conjunctival lesions show epithelial hyperplasia alternat-
ing with atrophy, vacuolation of the basal layer (60 %), capil-
lary dilation, and an inflammatory lymphocytic infiltrate
with eosinophils and melanophages in the lamina propria.
Lymphocytes may also have a follicular arrangement as in
the labial mucosa [5, 7].
Lymphoid follicles can be found in up to 80 % of
vermillion border or conjunctival mucosa biopsies [1, 5, 12].
Immunohistochemical studies of the inflammatory infil-
trate in skin lesions have demonstrated a predominantly T
lymphocyte CD45RO+ population (memory T cells) and
expression of interleukin-2 (IL-2) [1, 6, 33]. It has also been
reported that ectopic lymphoid follicles of lip biopsies are
formed in the periphery by T lymphocytes (CD45+, IL-2),
and in the center, by B (CD20+) lymphocytes [5, 7]. There
41 Actinic Prurigo
are also numerous eosinophils and abundant extracellular
deposits of IgM, IgG, and C3 in the papillary dermis [6, 7].
Diagnosis
The diagnosis of AP is mainly a clinical one and can be sup-
ported by histopathological study [34] preferably of the ver-
million mucosa, where ectopic lymphoid follicles are more
commonly found [32].
Differential Diagnosis
The main clinical differential diagnoses of AP include: atopic
dermatitis with photosensitivity, photocontact chronic der-
matitis, chronic actinic dermatitis, and polymorphous light
eruption (PMLE) [7, 9]. The major diagnostic challenge is
atopic dermatitis with photosensitivity as it also begins in
childhood, is a chronic dermatitis and very often patients are
unaware of their atopic status [35].
PMLE is also a seasonal related idiopathic photodermato-
sis. It is more frequently seen in African Americans and
Caucasians [36] while in Amerindian indigenous popula-
tions, is very rare.
PMLE also differs from AP because its onset is sudden
and it can last hours to days and then subsides. Unlike AP,
lesions in PMLE can be painful, and patients may experience
flu-like symptoms. Skin lesions range from papules, plaques,
and papulovesicles. Vesicles are never found in AP patients
[9]. The characteristic mucosal lesions of the vermillion bor-
der and conjunctiva are not seen in PMLE. Histolopathology
of PMLE is characterized by an almost exclusive lymphoid
Fig. 41.9 Excellent results after 2 months of treatment with oral thalidomide. Skin and conjunctival lesions are almost resolved
393
infiltrate with marked dermal edema. Eosinophils and mast
cells frequently seen in AP are rarely found in PMLE.
Conjunctivitis of AP should be differentiated from vernal
conjunctivitis, which is bilateral, recurrent, pruritic, and highly
prevalent in adolescents with a previous history of atopy [37].
The most important clinical differential diagnosis of APC
is traumatic cheilitis secondary to lip biting, where there is
erythema, atrophy, erosion, and areas of postinflammatory
hyperpigmentation. There is also burning sensation and ten-
dency to chronicity [38]. It is important not to confuse the
terms of APC and actinic cheilitis, as they are completely
different entities [39].
Treatment
As the first-line treatment, it is essential to avoid sun expo-
sure and the appropriate use of sunscreen. Medical treatment
can be used depending on the extent and severity of the dis-
ease [7, 12, 40]. Therapeutic options include topical or sys-
temic corticosteroids, vitamin E, β-carotenes, tetracyclines,
antimalarials, antihistamines, cyclosporine A (topical calci-
neurin inhibitor), and low doses of UVA or UVB photother-
apy. All of these treatment modalities may induce partial
remissions [5, 12, 41].
Thalidomide is a glutamic acid derivative [42]. It was pro-
posed as an optional treatment for AP in 1973 by Londoño
[43], who demonstrated excellent results when treating
patients with AP. These findings were confirmed in 1975 by
Saul [44, 45] and in 1993 by Vega-Memije et al. [17].
Currently, this is the most effective medical treatment [7, 34]
for AP, because it is an immunomodulator that inhibits
TNF-α [6] and IFN [46] (Figs. 41.9 and 41.10).
394
Fig. 41.10 Markedly reduced
papular lesions on upper
extremities after treatment
with thalidomide
The effective oral dose of thalidomide reported for chil-
dren from 9 to 16 years is 0.5–2.5 mg/kg/day [47] and in
adults the initial dose is 100–200 mg daily and this can be
maintained until clinical improvement is observed [7, 12,
46], which usually occurs between 2 and 4 weeks after treat-
ment onset [12]; it can subsequently be decreased to a mini-
mum effective dose usually of 25 mg per week [7, 12].
The main adverse effect of thalidomide is teratogenicity,
making mandatory the use of effective contraception for all
women in the reproductive age [7, 12]. Other reported side
effects include drowsiness, increased appetite [7], headache,
nausea, constipation, skin hypersensitivity [1], and sensory
neuropathy [7]. The latter can be seen in 91 % of the patients
even when asymptomatic, so it should be confirmed by nerve
conduction studies [48].
Conclusions
AP is a chronic photodermatosis most commonly seen in
dark-skinned populations with a strong Amerindian genetic
lineage. Conjunctival and vermillion mucosae are character-
istically affected in AP and are a clue to make the differential
diagnosis between other photodermatoses. Distinctive histo-
logical findings include ectopic lymphoid follicles in the
biopsies of lip mucosa and a mixed inflammatory infiltrate
with eosinophils.
Currently, thalidomide is the most effective medical treat-
ment, although with significant adverse effects.
There is still much to know about the genetics and patho-
genesis of AP. More research studies are needed to fully
understand this disease.
S. Toussaint-Caire
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