Papular Urticaria

Papular urticaria is a common and often annoying disorder manifested by chronic or

recurrent papules caused by a hypersensitivity reaction to the bites of mosquitoes, fleas,
bedbugs, and other insects. Individual papules may surround a wheal and display a central
punctum. See a Critical Images slideshow, to help identify various skin reactions, recognize
potential comorbidities, and select treatment options.
Although the overall incidence rate is unknown, papular urticaria tends to be evident
during spring and summer months; in some climates, such as that in San Francisco,
California, this condition may affect children throughout the year. In addition, despite no
known racial or sex predisposition, certain ethnic groups (specifically Asians) may be more
predisposed to more intense reactions, and a small Nigerian study reported a slight female
predominance for skin diseases such as papular urticaria and atopic dermatitis. Papular
urticaria was evident in 2.24% of 5250 first-time pediatric patients, with 6029 diagnoses in
one pediatric dermatology service survey. [ A survey of skin disorders in more than a 1000
new pediatric patients at a hospital in Bangalore, India found insect bite reactions and papular
urticaria in 5.1% A Nigerian survey of 491 pediatric dermatoses in 441 patients found
papular urticaria in 6.7% of them.
This eruption is primarily self-limited, and children eventually outgrow this disease, probably
through desensitization after multiple arthropod exposures

Etiologi dan Patophisiology

Papular urticaria is generally regarded to be the result of a hypersensitivity or id

reaction to bites from insects, such as mosquitoes,gnats,
fleas, mites, bedbugs, caterpillars, and moths. Varicella vaccines have also been
implicated. However, it is unusual to identify an actual culprit in any given patient. One
specific mite causing it is Peymotes ventricosus, and it is also known as the grain itch,
barley itch, straw itch, hay itch, prairie itch, mattress itch, and cotton seed itch,
sometimes evident occupationally in farmers, bakers, dock workers, packers, and indoor
workers. These mites are invisible to the n aked eye.
The histopathologic pattern in papular urticaria consists of mild subepidermal edema,
extravasation of erythrocytes, interstitial eosinophils, and exocytosis of lymphocytes. These
findings suggest a pathophysiologic process that is immunologically based.
Morphologic and immunohistochemical evidence suggest that a type I hypersensitivity
reaction plays a central role in the pathogenesis of papular urticaria. The reaction is thought
to be caused by a hematogenously disseminated antigen deposited by an arthropod bite in a
patient who is sensitive. This theory is supported by the fact that these lesions can and often
do occur in areas away from the bites. The putative antigen is unknown.
The presence of immunoglobulin and complement deposits in the skin of some patients with
papular urticaria suggests that the lesions may be due to a cutaneous vasculitis. The deposits
were most frequently seen in lesions within 24 hours of their development. The presence of
granular deposits of Clq, C3, and immunoglobulin M (IgM) in superficial dermal blood
vessel walls suggests that immune complexes (IgM aggregates) may be primarily involved in
the pathogenesis, with complement activation initiated by Clq through the classic pathway. A
T helper 2 (Th2) shift may be present, similar to what is observed in atopy.
In a study of the specific pattern of flea antigen recognition by IgG subclass and IgE
during the progression of papular urticaria caused by flea bite, variations in the antibody
responses of both subclasses to flea antigens were identified. Among these 25 patients, those
with 2-5 years of papular urticaria had more IgE bands than patients with shorter or longer
durations of symptoms. Thus, the predominant specific antibody isotypes appear to vary
according to the time elapsed from the onset of fleabite-induced papular urticaria. The
cellular immune response against whole-flea antigen in patients with papular urticaria by flea
bites may be the result of an impaired dendritic cell population.

clinicial evaluation
Children, adult males, nonlocal inhabitants, and those belonging to urban or periurban
areas may be more vulnerable to papular urticaria. Patients usually report chronic or recurrent
episodes of a papular eruption that tends to occur in groups or clusters associated with intense
pruritus. The most common first appearance is of papules and urticarial plaques in clusters
over exposed and covered parts of the body.
The eruption is characterized by crops of symmetrically distributed pruritic papules and
papulovesicles. The lesions can also appear in an area localized to the site of insect bites, but
they occur on any body part. The lesions tend to be grouped on exposed areas (see the image
below), particularly the extensor surfaces of the extremities. Sometimes, a central
hemorrhagic punctum may be evident with ecchymoses and brownish pigmentation persisting
after resolution. Scratching may produce erosions and ulcerations. Secondary impetigo or
pyoderma is common. Having pets and the use of colognes were identified as predisposing
factors for insect bite dermatitis in one large study, whereas atopy was not.
DD

When evaluating a patient with papular urticaria, the following conditions should also be
considered:
Dermatitis Herpetiformis
Id Reaction (Autoeczematization)
Impetigo
Insect Bites
Pityriasis Lichenoides
True cellulitis

Histopathologic differentials
The histopathologic differential diagnosis of papular urticaria includes other
spongiotic dermatitides, pityriasis lichenoides et varioliformis acuta, the pruritic papular
eruption of human immunodeficiency virus (HIV) disease, and papulonecrotic tuberculid.
Papular urticaria with marked spongiosis and a dense inflammatory cell infiltrate cannot be
reliably distinguished from arthropod bites on clinical and histopathologic grounds.
Histologic features
In a prospective study of papular urticaria that evaluated the histopathologic
features of 30 affected patients, more than 50% of patients had mild acanthosis, mild
spongiosis, exocytosis of lymphocytes, mild subepidermal edema, extravasation of
erythrocytes, superficial and deep mixed inflammatory cell infiltrate of moderate
density, and interstitial eosinophils. [13] Immunohistochemical analysis revealed
abundant T lymphocytes (CD45RO, CD3) and macrophages (CD68). B lymphocytes
(CD20) and dendritic antigen-presenting cells (S100) were not seen. [13]Direct
immunofluorescence staining did not demonstrate immunoglobulin A (IgA),
immunoglobulin G (IgG), IgM, C3, or fibrin.
 The occasional overlapping in histologic pattern between papular urticaria
exhibiting the histologic features of pseudolymphoma and a true lymphoma can
cause problems. Persistent nodules may suggest the possibility of a lymphoma, not
papular urticaria, and require a skin biopsy specimen.

Management and prevention

The treatment of papular urticaria should be conservative and is symptomatic
in most cases. Mild topical steroids and systemic antihistamines for relief of the
itching that often accompanies this condition may be used. On occasion, papular
urticaria may be severe enough to warrant the use of short-term systemic
corticosteroids. If secondary impetigo occurs, topical or systemic antibiotics may be
needed. Note that the use of insect repellents while the patient is outside and the
use of flea and tick control on indoor pets are necessary when these individuals are
being treated for papular urticaria.
Rigorous use of an effective insecticide may prevent insect bites and,
accordingly, papular urticaria. Insecticides containing diethyltoluamide (DEET) are
among the most beneficial. For safety purposes, topical insecticides used on infants
and children should be in accordance with their age. DEET, picaridin, PMD (para-
menthane-3,8-diol), and IR3535 are suitable for protection against arthropod bites;
IR3535 is not suitable for Anopheles mosquitoes. [26] Use of protective clothing,
insecticide-treated bed nets, and insecticide-treated clothing is desirable.
An oral desensitization vaccine has been attempted, but the vaccine was deemed
ineffective and the study sample size was too small for statistical significance

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papular Urtikaria

urtikaria papular adalah gangguan umum dan sering mengganggu

dengan manifestasi berupa papula kronis atau berulang yang disebabkan
oleh reaksi hipersensitivitas terhadap gigitan nyamuk, kutu, kutu busuk,
dan serangga lainnya. Papula tunggal dapat mengelilingi luka dan
menampilkan punctum pusat.

Meskipun tingkat kejadian secara keseluruhan tidak diketahui,

urtikaria papular cenderung terlihat selama musim semi dan musim panas
atau bisa juga anak sepanjang tahun. Selain itu, meskipun tidak ada
kecenderungan ras atau jenis kelamin, kelompok etnis tertentu (khususnya
Asia) mungkin lebih cenderung bereaksi lebih intens, dan sebuah studi di
Nigeria melaporkan perempuan sedikit lebih dominan untuk terkena
penyakit kulit seperti urtikaria papular dan dermatitis atopik. urtikaria
papular terbukti pada 2.24% dari 5250 pasien anak, dengan 6029 diagnosa
dalam satu survei layanan dermatologi anak. Sebuah survei penyakit kulit
di lebih dari 1000 pasien anak baru di sebuah rumah sakit di Bangalore,
India menemukan reaksi gigitan serangga dan urtikaria papular sebanyak
5,1% Sebuah survei Nigeria dari 491 penyakit kulit pediatrik di 441 pasien
ditemukan urtikaria papular sebanyak 6,7% dari keseluruhan pasien.
Erupsi penyakit ini adalah self-limiting atau sembuh sendiri, dan hilang saat
anak-anak tumbuh dewasa.

Etiologi Dan Patophisiology

urtikaria papular umumnya dianggap sebagai hasil dari

hipersensitivitas atau reaksi terhadap gigitan dari serangga, seperti
nyamuk, agas, kutu, tungau, kutu busuk, ulat, dan ngengat. Vaksin
varicella juga terlibat. Namun, itu tidak biasa untuk mengidentifikasi
pelakunya yang sebenarnya pada setiap pasien diberikan. Satu tungau
tertentu menyebabkan itu Peymotes ventricosus, dan juga dikenal sebagai
"gandum gatal", "barley gatal", "jerami gatal", "hay gatal", "padang rumput
gatal", "kasur gatal", dan "biji kapas gatal ", kadang-kadang terlihat
occupationally di petani, tukang roti, pekerja dermaga, pengepakan, dan
pekerja dalam ruangan. tungau ini terlihat n aked mata.

Pola histopatologi di urtikaria papular terdiri dari edema ringan

subepidermal, ekstravasasi eritrosit, eosinofil interstitial, dan eksositosis
limfosit. Temuan ini menunjukkan proses patofisiologis yang imunologis
berdasarkan.
Morfologi dan bukti imunohistokimia menunjukkan bahwa reaksi tipe I
hipersensitivitas memainkan peran sentral dalam patogenesis urtikaria
papular. Reaksi ini diduga disebabkan oleh antigen hematogen disebarkan
disimpan oleh gigitan arthropoda pada pasien yang sensitif. Teori ini
didukung oleh fakta bahwa lesi ini dapat dan sering terjadi di daerah jauh
dari gigitan. Antigen diduga tidak diketahui.

Kehadiran immunoglobulin dan melengkapi deposito di kulit beberapa

pasien dengan urtikaria papular menunjukkan bahwa lesi mungkin karena
vaskulitis kulit. Deposito yang paling sering terlihat pada lesi dalam waktu
24 jam dari perkembangan mereka. Kehadiran deposito granular dari CLQ,
C3, dan immunoglobulin M (IgM) di dinding pembuluh darah dermal
dangkal menunjukkan bahwa kompleks imun (IgM agregat) mungkin
terutama terlibat dalam patogenesis, dengan aktivasi komplemen
diprakarsai oleh CLQ melalui jalur klasik. A T helper 2 (Th2) pergeseran
mungkin ada, mirip dengan apa yang diamati dalam atopi.

Dalam sebuah studi tentang pola tertentu dari kutu pengakuan antigen oleh
IgG subclass dan IgE selama perkembangan urtikaria papular yang
disebabkan oleh gigitan kutu, variasi dalam respon antibodi kedua subclass
untuk antigen loak diidentifikasi. Di antara 25 pasien ini, orang-orang
dengan 2-5 tahun urtikaria papular memiliki band lebih IgE dibandingkan
pasien dengan jangka waktu yang lebih pendek atau lebih dari gejala.
Dengan demikian, isotipe antibodi spesifik dominan muncul bervariasi
sesuai dengan waktu yang telah berlalu dari awal urtikaria papular bekas
gigitan kutu-diinduksi. Respon imun seluler terhadap antigen whole-kutu
pada pasien dengan urtikaria papular oleh gigitan kutu mungkin hasil dari
populasi sel dendritik terganggu.

evaluasi clinicial

Anak-anak, laki-laki dewasa, penduduk nonlokal, dan mereka yang

termasuk daerah perkotaan atau daerah di pinggir kota mungkin lebih
rentan terhadap urtikaria papular. Pasien biasanya melaporkan episode
kronis atau berulang dari erupsi papular yang cenderung terjadi dalam
kelompok atau cluster terkait dengan pruritus intens. yang paling umum
penampilan pertama adalah papula dan plak urtikaria dalam kelompok
lebih terbuka dan tertutup bagian tubuh.

Letusan ini ditandai dengan tanaman papula pruritus didistribusikan secara

simetris dan papulovesicles. Lesi juga bisa muncul di daerah lokal ke lokasi
gigitan serangga, tetapi mereka terjadi pada setiap bagian tubuh. Lesi
cenderung dikelompokkan pada daerah yang terpapar (lihat gambar di
bawah), bagian
DD

Ketika mengevaluasi pasien dengan urtikaria papular, kondisi berikut juga

harus dipertimbangkan:

Dermatitis herpetiformis

Id Reaction (Autoeczematization)

Impetigo

Gigitan serangga

Pityriasis lichenoides

Benar selulitis

perbedaan histopatologi

Diagnosis histopatologis urtikaria papular termasuk dermatitides lainnya

spongiotik, lichenoides et varioliformis acuta, letusan papular pruritus
human immunodeficiency virus penyakit pitiriasis (HIV), dan tuberculid
papulonekrotik. urtikaria papular dengan spongiosis ditandai dan infiltrasi
sel radang padat tidak dapat diandalkan dibedakan dari gigitan arthropoda
atas dasar klinis dan histopatologis.

fitur histologis

Dalam sebuah studi prospektif urtikaria papular yang mengevaluasi fitur

histopatologi dari 30 pasien yang terkena, lebih dari 50% dari pasien
memiliki acanthosis ringan, spongiosis ringan, eksositosis limfosit, ringan
subepidermal edema, ekstravasasi eritrosit, dangkal dan dalam campuran
infiltrasi sel radang dari kepadatan moderat, dan eosinofil interstitial. [13]
Analisis imunohistokimia mengungkapkan limfosit berlimpah T (CD45RO,
CD3) dan makrofag (CD68). limfosit B (CD20) dan dendritik antigen-
presenting sel (S100) tidak terlihat. [13] Langsung immunofluorescence
pewarnaan tidak menunjukkan immunoglobulin A (IgA), imunoglobulin G
(IgG), IgM, C3, atau fibrin.

Tumpang tindih sesekali dalam pola histologis antara urtikaria papular

memamerkan fitur histologis dari pseudolymphoma dan limfoma benar
dapat menyebabkan masalah. nodul persisten mungkin menyarankan
kemungkinan limfoma, tidak papular urtikaria, dan memerlukan biopsi kulit
spesimen.
Manajemen dan pencegahan

Pengobatan urtikaria papular harus konservatif dan gejala pada

kebanyakan kasus. steroid topikal ringan dan antihistamin sistemik untuk
menghilangkan gatal-gatal yang sering menyertai kondisi ini dapat
digunakan. Pada kesempatan, urtikaria papular mungkin cukup berat untuk
menjamin penggunaan kortikosteroid sistemik jangka pendek. Jika
impetigo sekunder terjadi, antibiotik topikal atau sistemik mungkin
diperlukan. Perhatikan bahwa penggunaan penolak serangga saat pasien
berada di luar dan penggunaan kutu kontrol pada hewan peliharaan dalam
ruangan yang diperlukan ketika orang-orang sedang dirawat karena
urtikaria papular.

Penggunaan ketat insektisida yang efektif dapat mencegah gigitan

serangga dan, sesuai, urtikaria papular. Insektisida yang mengandung
Diethyltoluamide (DEET) adalah yang paling menguntungkan. Untuk tujuan
keselamatan, insektisida topikal digunakan pada bayi dan anak-anak harus
sesuai dengan usia mereka. DEET, picaridin, PMD (para-mentana-3,8-
diol), dan IR3535 cocok untuk perlindungan terhadap gigitan arthropoda;
IR3535 tidak cocok untuk nyamuk Anopheles. [26] Penggunaan pakaian
pelindung, kelambu berinsektisida, dan pakaian berinsektisida diinginkan.

Vaksin desensitisasi lisan telah dicoba, namun vaksin dianggap tidak

efektif dan ukuran sampel penelitian adalah terlalu kecil untuk signifikansi
statistik