Alergi

Alergi
Alergi, juga dikenal sebagai

penyakit alergi, mengacu pada
sejumlah kondisi yang
disebabkan oleh hipersensitivitas
sistem kekebalan terhadap zat
yang biasanya tidak berbahaya di
lingkungan.[ 11] Penyakit-penyakit
ini termasuk demam, alergi
makanan, dermatitis atopik, asma
alergi, dan anafilaksis.[ 1] Gejala
mungkin termasuk mata merah,
ruam gatal, bersin, batuk, pilek,
sesak napas, atau bengkak.[
12] Perhatikan bahwa intoleransi
makanan dan keracunan
makanan adalah kondisi yang
terpisah.[ 3][4]
Alergi
Gatal-gatal adalah gejala alergi

yang umum.
Spesialisasi Imunologi
Gejala Mata merah,

ruam gatal,
muntah, pilek,
sesak napas,
bengkak, bersin,
dan batuk.
Jenis Hay fever, alergi

makanan,
dermatitis atopik,
asma alergi,
anafilaksis[1]
Penyebab Faktor genetik

dan
lingkungan[2]
Metode Berdasarkan
diagnostik gejala, tes
tusukan kulit, tes
darah[3]
Diagnosis Intoleransi
diferensial makanan,
keracunan
makanan[4]
Pencegahan Paparan awal

terhadap alergen
potensial[5]
Perawatan Menghindari
alergen, obat-
obatan,
imunoterapi
alergen yang
diketahui[6]
Obat- Steroid, antihistamin,
obatan epinefrin, penstabil sel
mast,
antileukotrien[6][7][8][9]
Frekuensi Umum[10]
Alergen umum termasuk serbuk

sari dan makanan tertentu.[
11] Logam dan zat lain juga dapat
menyebabkan masalah seperti
itu.[ 11] Makanan, sengatan
serangga, dan obat-obatan
adalah penyebab umum dari
reaksi parah.[ 2] Perkembangan
mereka disebabkan oleh faktor
genetik dan lingkungan.[
2] Mekanisme yang mendasarinya
melibatkan antibodi
imunoglobulin E (IgE), bagian dari
sistem kekebalan tubuh, mengikat
alergen dan kemudian ke reseptor
pada sel mast atau basofil di
mana ia memicu pelepasan bahan
kimia inflamasi seperti histamin.[
13] Diagnosis biasanya didasarkan
pada riwayat medis seseorang.[
3] Pengujian lebih lanjut pada kulit
atau darah mungkin berguna
dalam kasus-kasus tertentu.[
3] Tes positif, bagaimanapun,
mungkin tidak selalu berarti ada
alergi yang signifikan terhadap zat
yang dimaksud.[ 14]
Paparan dini anak-anak terhadap

alergen potensial mungkin
bersifat protektif.[ 5] Perawatan
untuk alergi termasuk
menghindari alergen yang
diketahui dan penggunaan obat-
obatan seperti steroid dan
antihistamin.[ 6] Pada reaksi yang
parah, adrenalin suntik (epinefrin)
direkomendasikan.[ 7] Imunoterapi
alergen, yang secara bertahap
membuat orang terkena alergen
dalam jumlah yang lebih besar
dan lebih besar, berguna untuk
beberapa jenis alergi seperti
demam dan reaksi terhadap
gigitan serangga.[
6] Penggunaannya dalam alergi
makanan tidak jelas.[ 6]
Alergi adalah umum.[ 10] Di negara

maju, sekitar 20% orang terkena
rinitis alergi,[15] sekitar 6% orang
memiliki setidaknya satu alergi
makanan,[3][5] dan sekitar 20%
memiliki atau pernah memiliki
dermatitis atopik di beberapa titik
waktu.[ 16] Tergantung pada
negaranya, sekitar 1-18% orang
menderita asma.[
17][18] Anafilaksis terjadi pada
antara 0,05–2% orang.[
19] Tingkat banyak penyakit alergi
tampaknya meningkat.[
7][20][21] Kata "alergi" pertama kali
digunakan oleh Clemens von
Pirquet pada tahun 1906.[ 2]
Tanda dan gejala

Organ
yang Tanda dan gejala umum
terkena
dampak
Pembengkakan
Hidung hidungmukosa (rinitis alergi
pilek,bersin
Sinus Alergisinusitis
Kemerahan dangatal
Mata darikonjungtiva
(konjungtivitis alergi, berair)
Bersin,
batuk,bronkokonstriksi,mengi
dandispnea, terkadang
Saluran serangan langsung dariasma
Udara dalam kasus yang parah jalan
napas menyempit karena
pembengkakan yang dikenal
sebagaiedema laring
Perasaan kenyang, mungkin

rasa sakit, dan gangguan
Telinga pendengaran karena
kurangnyadrainase tabung
eustachius.
Ruam, sepertieksim
Kulit
dangatal-gatal (urtikaria)
Saluran Sakit perut,kembung,

pencernaan muntah,diare
Banyak alergen seperti debu atau

serbuk sari adalah partikel di
udara. Dalam kasus ini, gejala
muncul di area yang bersentuhan
dengan udara, seperti mata,
hidung, dan paru-paru. Misalnya,
rinitis alergi, juga dikenal sebagai
demam, menyebabkan iritasi
pada hidung, bersin, gatal, dan
kemerahan pada mata.[
22] Alergen yang dihirup juga
dapat menyebabkan peningkatan
produksilendir diparu-paru,sesak
napas, batuk, dan mengi.[ 23]
Selain alergen sekitar ini, reaksi

alergi dapat dihasilkan dari
makanan,sengatan serangga, dan
reaksi terhadap obat-obatan
sepertiaspirin danantibiotik
sepertipenisilin. Gejala alergi
makanan termasuk sakit
perut,kembung, muntah,diare,kulit
gatal, dangatal-gatal. Alergi
makanan jarang
menyebabkanreaksi pernapasan
(asma), ataurinitis.[ 24] Sengat
serangga, makanan,antibiotik, dan
obat-obatan tertentu dapat
menghasilkan respons alergi
sistemik yang juga disebut
anafilaksis; beberapa sistem
organ dapat terpengaruh,
termasuksistem
pencernaan,sistem pernapasan,
dansistem peredaran darah.[
25][26][27] Tergantung pada tingkat
keparahannya, anafilaksis dapat
mencakup reaksi kulit,
bronkokonstriksi,bengkak,tekana
n darah rendah, koma, dan
kematian. Jenis reaksi ini dapat
dipicu secara tiba-tiba, atau
onsetnya dapat ditunda. Sifat
anafilaksis sedemikian rupa
sehingga reaksinya dapat tampak
mereda tetapi dapat kambuh
sepanjang periode waktu tertentu.
[ 27]
Kulit
Zat yang bersentuhan dengan

kulit, sepertilateks, juga
merupakan penyebab umum dari
reaksi alergi, yang dikenal
sebagaidermatitis kontak atau
eksim.[ 28] Alergi kulit sering
menyebabkan ruam, atau
pembengkakan dan peradangan
di dalam kulit, dalam apa yang
dikenal sebagai "Karakteristik
reaksi weal and flare" dari gatal-
gatal danangioedema.[ 29]
Dengan sengatan serangga,

reaksi lokal yang besar dapat
terjadi dalam bentuk area
kemerahan kulit yang berukuran
lebih besar dari 10 cm yang dapat
berlangsung satu hingga dua hari.
[ 30] Reaksi ini juga dapat terjadi
setelahimunoterapi.[ 31]
Penyebab
Faktor risiko alergi dapat
ditempatkan dalam dua kategori
besar, yaitutuan rumah danfaktor
lingkungan.[ 32] Faktor tuan rumah
termasukfaktor keturunan,
seks,ras, dan usia, dengan faktor
keturunan sejauh ini yang paling
signifikan. Namun, ada
peningkatan baru-baru ini dalam
kejadian gangguan alergi yang
tidak dapat dijelaskan oleh faktor
genetik saja. Empat kandidat
lingkungan utama adalah
perubahan dalam
paparanpenyakit menular selama
anak usia dini, pencemaran
lingkungan, tingkat alergen,
danperubahan pola makan.[ 33]
Tungau debu
Alergi tungau debu, juga dikenal

sebagai alergi debu rumah,
adalahsensitisasi danreaksi alergi
terhadap kotoran daritungau debu
rumah. Alergi adalah
umum[34][35] dan dapat memicu
reaksi alergi seperti asma,eksim,
ataugatal. Itu adalah manifestasi
dari sebuahparasitosis. Usus
tungau mengandung enzim
pencernaan yang kuat
(terutamapeptidase 1) yang
bertahan dalam tinja mereka dan
merupakan penginduksi utama
reaksi alergi sepertimengi.
Eksoskeleton tungau juga dapat
berkontribusi pada reaksi alergi.
Tidak sepertitungau kudis atau
tungau folikel kulit, tungau debu
rumah tidak menggali di bawah
kulit dan tidak parasit.[ 36]
Makanan
Berbagai macam makanan dapat

menyebabkan reaksi alergi, tetapi
90% dari respons alergi terhadap
makanan disebabkan oleh susu
sapi,kedelai,telur, gandum,
kacang tanah,kacang pohon, ikan,
dankerang.[ 37] Lainnyaalergi
makanan, mempengaruhi kurang
dari 1 orang per 10.000 populasi,
dapat dianggap "langka".[
38] Penggunaan susu
terhidrolisissusu formula bayi
versus susu standar susu susu
bayi tampaknya tidak
mempengaruhi risikonya.[ 39]
Alergi makanan yang paling

umum di populasi AS adalah
sensitivitas terhadapkrustasea.[
38] Meskipun alergi kacang
terkenal karena tingkat
keparahannya, alergi kacang
bukanlah alergi makanan yang
paling umum pada orang dewasa
atau anak-anak. Reaksi yang
parah atau mengancam jiwa
dapat dipicu oleh alergen lain dan
lebih sering terjadi bila
dikombinasikan dengan asma.[ 37]
Tingkat alergi berbeda antara

orang dewasa dan anak-anak.
Anak-anak terkadang bisa
mengatasi alergi kacang. Alergi
telur mempengaruhi satu hingga
dua persen anak-anak tetapi
tumbuh lebih besar oleh sekitar
dua pertiga anak-anak pada usia
5 tahun.[ 40] Sensitivitas biasanya
terhadap protein dalam warna
putih, bukankuning telur.[ 41]
Alergi susu-protein paling sering

terjadi pada anak-anak.[
42] Sekitar 60% dari reaksi susu-
protein adalahimunoglobulin E-
mediated, dengan sisanya
biasanya disebabkan olehradang
usus besar.[ 43] Beberapa orang
tidak dapat mentolerir susu dari
kambing atau domba serta dari
sapi, dan banyak juga yang tidak
dapat mentolerir produk susu
seperti keju. Sekitar 10% anak-
anak dengan alergi susu akan
bereaksi terhadap daging sapi.
Daging sapi mengandung
sejumlah kecil protein yang hadir
dalam kelimpahan yang lebih
besar dalam susu sapi.[ 44]
Intoleransi laktosa, reaksi umum
terhadap susu, sama sekali bukan
bentuk alergi, tetapi karena tidak
adanyaenzim dalamsaluran
pencernaan.[
Mereka yang memilikialergi

kacang pohon mungkin alergi
terhadap satu atau banyak
kacang pohon,
termasukkemiri,pistachio,kacang
pinus, dankenari.[ 41] Sebagai
tambahan,benih, termasukbiji
wijen danbiji poppy, mengandung
minyak di mana protein hadir,
yang dapat menimbulkan reaksi
alergi.[ 41]
Alergen dapat ditransfer dari satu

makanan ke makanan lainnya
melaluirekayasa genetika; namun
modifikasi genetik juga dapat
menghilangkan alergen. Sedikit
penelitian telah dilakukan pada
variasi alami konsentrasi alergen
pada tanaman yang tidak
dimodifikasi.[ 45][46]
Lateks
Lateks dapat memicu reaksi kulit,

pernapasan, dan sistemik yang
dimediasi IgE. Prevalensi alergi
lateks pada populasi umum
diyakini kurang dari satu persen.
Dalam sebuah studi rumah sakit, 1
dari 800 pasien bedah (0,125
persen) melaporkan sensitivitas
lateks, meskipun sensitivitas di
antara petugas kesehatan lebih
tinggi, antara tujuh dan sepuluh
persen. Para peneliti mengaitkan
tingkat yang lebih tinggi ini
dengan paparan petugas
kesehatan ke daerah dengan
alergen lateks udara yang
signifikan, seperti ruang operasi,
unit perawatan intensif, dan suite
gigi. Lingkungan yang kaya lateks
ini dapat menyadarkan petugas
kesehatan yang secara teratur
menghirup protein alergi.[ 47]
Respons yang paling umum

terhadap lateks adalah dermatitis
kontak alergi, reaksi hipersensitif
yang tertunda yang muncul
sebagai lesi kering dan berkerak.
Reaksi ini biasanya berlangsung
48-96 jam. Berkeringat atau
menggosok area di bawah sarung
tangan memperburuk lesi,
mungkin menyebabkan ulserasi.[
47] Reaksi anafilaksis paling sering
terjadi pada pasien sensitif yang
telah terpapar sarung tangan
lateks ahli bedah selama operasi
perut, tetapi lainnyapaparan
mukosa, seperti prosedur gigi,
juga dapat menghasilkan reaksi
sistemik.[ 47]
Sensitivitas lateks dan pisang

dapat bereaksi silang. Selain itu,
mereka yang memiliki alergi lateks
mungkin juga memiliki kepekaan
terhadapalpukat, buah kiwi, dan
kastanye.[ 48] Orang-orang ini
sering memilikigatal perioral dan
lokalurtikaria. Hanya sesekali
alergi yang diinduksi makanan ini
menyebabkan respons sistemik.
Para peneliti menduga bahwa
reaktivitas silang lateks dengan
pisang,alpukat,buah kiwi,
dankastanye terjadi karena
protein lateks secara
strukturalhomolog dengan
beberapa protein nabati lainnya.[
47]
Obat-obatan
Sekitar 10% orang melaporkan

bahwa mereka alergi
terhadappenisilin; namun, 90%
ternyata tidak.[ 49] Alergi serius
hanya terjadi pada sekitar 0,03%.
[ 49]
Sengat serangga
Biasanya, serangga yang

menghasilkan respons alergi
adalah serangga menyengat
(tawon,lebah,lebah dansemut)
atau serangga yang menggigit
(nyamuk,centang). Serangga
menyengat menyuntikkan racun
ke korbannya, sementara
serangga yang menggigit
biasanya diperkenalkananti-
koagulan.[
Racun berinteraksi dengan

protein
Reaksi protein non-makanan

lainnya,dermatitis kontak yang
diinduksi urushiol, berasal setelah
kontak denganpoison ivy,pohon
ek beracun timur,pohon ek
beracun barat, atauracun
sumac.Urushiol, yang bukan
protein itu sendiri, bertindak
sebagaihapten dan bereaksi
secara kimia dengan, berikatan
dengan, dan mengubah
bentukprotein membran integral
pada sel kulit yang terpapar.
Sistem kekebalan tubuh tidak
mengenali sel-sel yang terkena
sebagai bagian normal dari tubuh,
menyebabkan aDimediasi sel-
Trespon imun.[ 50] Dari tanaman
beracun ini, sumac adalah yang
paling ganas.[ 51] Respons
dermatologis yang dihasilkan
terhadap reaksi antara urushiol
dan protein membran termasuk
kemerahan,
pembengkakan,papula,vesikel,lec
et, dan melesat.[ 52]
Perkiraan bervariasi pada

persentase populasi yang akan
memiliki respon sistem kekebalan
tubuh. Sekitar 25 persen dari
populasi akan memiliki respons
alergi yang kuat terhadap
urushiol. Secara umum, sekitar 80
persen hingga 90 persen orang
dewasa akan mengalami ruam
jika mereka terpapar .0050
miligram (7,7×10−5 gr) urushiol
murni, tetapi beberapa orang
sangat sensitif sehingga hanya
perlu jejak molekuler pada kulit
untuk memulai reaksi alergi.[ 53]
Genetika
Penyakit alergi sangat

kuatfamilial:kembar identik
cenderung memiliki penyakit
alergi yang sama sekitar 70% dari
waktu; alergi yang sama terjadi
sekitar 40% dari waktu dikembar
yang tidak identik.[ 54] Orang tua
yang alergi lebih cenderung
memiliki anak yang alergi,[55] dan
alergi anak-anak tersebut
cenderung lebih parah daripada
anak-anak dari orang tua yang
tidak alergi. Beberapa alergi,
bagaimanapun, tidak konsisten
bersamasilsilah; orang tua yang
alergi kacang mungkin memiliki
anak yang alergi
terhadapragweed. Kemungkinan
mengembangkan alergi
adalahdiwariskan dan terkait
dengan ketidakteraturan dalam
sistem kekebalan tubuh, tetapi
spesifikalergen tidak.[ 55]
Risiko alergisensitisasi dan
perkembangan alergi bervariasi
seiring bertambahnya usia,
dengan anak kecil yang paling
berisiko.[ 56] Beberapa penelitian
telah menunjukkan bahwa kadar
IgE tertinggi di masa kanak-kanak
dan turun dengan cepat antara
usia 10 dan 30 tahun.[ 56] Puncak
prevalensi demam tertinggi pada
anak-anak dan dewasa muda dan
kejadian asma tertinggi pada
anak-anak di bawah 10 tahun.[ 57]
Etnisitas mungkin memainkan

peran dalam beberapa alergi;
namun, faktor rasial sulit
dipisahkan dari pengaruh dan
perubahan lingkungan
karenamigrasi.[ 55] Telah
disarankan bahwa berbedalokus
genetik bertanggung jawab atas
asma, untuk lebih spesifik, pada
orang-orang
dariEropa,Hispanik,Orang Asia,
danAsal-usul Afrika.[ 58]
Hipotesis kebersihan
Penyakit alergi disebabkan oleh

respons imunologis yang tidak
tepat terhadap tidak
berbahayaantigen digerakkan
olehRespon imun yang dimediasi
TH2. Banyak bakteri dan virus
menghasilkanRespon imun yang
dimediasi TH1, yang menurunkan
regulasi respon TH2. Mekanisme
aksi pertama yang diusulkan dari
hipotesis kebersihan adalah
bahwa stimulasi yang tidak
memadai dari lengan TH1 dari
sistem kekebalan tubuh
menyebabkan lengan TH2 yang
terlalu aktif, yang pada gilirannya
menyebabkan penyakit alergi.[
59] Dengan kata lain, individu yang
hidup di lingkungan yang terlalu
steril tidak terpapar patogen yang
cukup untuk menjaga sistem
kekebalan tubuh tetap sibuk.
Karena tubuh kita berevolusi
untuk menghadapi tingkat
tertentu dari patogen tersebut,
ketika mereka tidak terpapar pada
tingkat ini, sistem kekebalan akan
menyerang antigen yang tidak
berbahaya, dan dengan demikian
biasanya benda mikroba jinak—
seperti serbuk sari—akan memicu
respons imun.[ 60]
Hipotesis kebersihan
dikembangkan untuk
menjelaskan pengamatan
bahwademam daneksim, kedua
penyakit alergi, kurang umum
pada anak-anak dari keluarga
besar, yang, diduga, terpapar lebih
banyak agen infeksi melalui
saudara kandung mereka,
daripada anak-anak dari keluarga
dengan hanya satu anak.
Hipotesis kebersihan telah
diselidiki secara ekstensif olehahli
imunologi danahli epidemiologi
dan telah menjadi kerangka
teoretis yang penting untuk studi
gangguan alergi. Ini digunakan
untuk menjelaskan peningkatan
penyakit alergi yang telah terlihat
sejak industrialisasi, dan insiden
penyakit alergi yang lebih tinggi di
negara-negara yang lebih maju.
Hipotesis kebersihan sekarang
telah diperluas untuk mencakup
paparan bakteri dan parasit
simbiosis sebagai modulator
penting dari perkembangan
sistem kekebalan tubuh, bersama
dengan agen infeksi.[
Data epidemiologis mendukung

hipotesis kebersihan. Penelitian
telah menunjukkan bahwa
berbagai penyakit imunologis dan
autoimun jauh lebih jarang terjadi
di negara berkembang daripada
negara industri, dan bahwa
imigran ke dunia industri dari
negara berkembang semakin
mengembangkan gangguan
imunologis dalam kaitannya
dengan lamanya waktu sejak tiba
di dunia industri.[ 61] Studi
longitudinal di dunia ketiga
menunjukkan peningkatan
gangguan imunologis ketika
suatu negara tumbuh lebih
makmur dan, dianggap, lebih
bersih.[ 62] Penggunaan antibiotik
pada tahun pertama kehidupan
telah dikaitkan dengan asma dan
penyakit alergi lainnya.[
63] Penggunaan produk
pembersih antibakteri juga telah
dikaitkan dengan insiden asma
yang lebih tinggi, seperti halnya
kelahiran olehOperasi caesar
daripada kelahiran melalui vagina.
[ 64][65]
Stres
Kronisstres dapat memperburuk

kondisi alergi. Ini telah dikaitkan
dengan respons dominan T helper
2 (TH2) yang didorong oleh
penindasaninterleukin 12 oleh
keduasistem saraf otonom
dansumbu hipotalamus-hipofisis-
adrenal. Manajemen stres pada
individu yang sangat rentan dapat
memperbaiki gejala.[ 66]
Faktor lingkungan lainnya
Penyakit alergi lebih sering terjadi

di negara-negara industri
daripada di negara-negara yang
lebih tradisional atau pertanian,
dan ada tingkat penyakit alergi
yang lebih tinggi pada populasi
perkotaan dibandingkan populasi
pedesaan, meskipun perbedaan
ini menjadi kurang jelas.[
67] Secara historis, pohon-pohon
yang ditanam di daerah perkotaan
sebagian besar jantan untuk
mencegah sampah dari biji dan
buah-buahan, tetapi rasio pohon
jantan yang tinggi menyebabkan
jumlah serbuk sari yang tinggi,
sebuah fenomena yang oleh ahli
hortikultura Tom Ogren disebut
"seksisme botani".[ 68]
Perubahan dalam paparan

terhadapmikroorganisme adalah
penjelasan lain yang masuk akal,
saat ini, untuk peningkatanalergi
atopik.[ 33] Paparan endotoksin
mengurangi pelepasan
peradangansitokin sepertiTNF-
α,IFNγ,interleukin-10,
daninterleukin-12 dari sel darah
putih (leukosit) yang bersirkulasi
dalam darah.[ 69] Penginderaan
mikroba tertentuprotein, dikenal
sebagaiReseptor seperti tol, yang
ditemukan di permukaan sel
dalam tubuh juga dianggap
terlibat dalam proses ini.[ 70]
Cacing usus dan parasit serupa

hadir dalam air minum yang tidak
diobati di negara berkembang,
dan hadir di air negara maju
sampai rutinitasklorinasi dan
pemurnian persediaan air minum.[
71] Penelitian terbaru telah
menunjukkan bahwa beberapa
umumparasit, seperticacing usus
(misalnya,cacing tambang),
mengeluarkan bahan kimia ke
dinding usus (dan, karenanya,
aliran darah) yangmenekan
sistem kekebalan tubuh dan
mencegah tubuh menyerang
parasit.[ 72] Ini memunculkan
kemiringan baru pada teori
hipotesis kebersihan—bahwako-
evolusi manusia dan parasit telah
menyebabkan sistem kekebalan
yang berfungsi dengan benar
hanya di hadapan parasit. Tanpa
mereka, sistem kekebalan menjadi
tidak seimbang dan terlalu
sensitif.[ 73] Secara khusus,
penelitian menunjukkan bahwa
alergi mungkin bertepatan
dengan keterlambatan
pembentukanflora usus dibayi.[
74] Namun, penelitian untuk
mendukung teori ini
bertentangan, dengan beberapa
penelitian yang dilakukan di
Tiongkok danEthiopia
menunjukkan peningkatan alergi
pada orang yang terinfeksi cacing
usus.[ 67] Uji klinis telah dimulai
untuk menguji efektivitas cacing
tertentu dalam mengobati
beberapa alergi.[ 75] Mungkin
istilah 'parasit' bisa berubah
menjadi tidak pantas, dan bahkan
sampai sekarang tidak
terdugasimbiosis sedang bekerja.
[ 75] Untuk informasi lebih lanjut
tentang topik ini, lihatTerapi
cacing.
Patofisiologi
Diagram ringkasan yang menjelaskan bagaimana alergi berkembang
Jaringan terpengaruh diperadangan alergi
Respon akut
Proses degradasi pada alergi. Paparan kedua terhadap alergen. 1 – antigen; 2 –
antibodi IgE; 3 – reseptor FcεRI; 4 – mediator yang telah terbentuk sebelumnya
(histamin, protease, kemokin, heparin); 5 –butiran; 6 –sel mast; 7 – mediator
yang baru terbentuk (prostaglandin, leukotrien, tromboksana,PAF).
Pada tahap awal alergi, reaksi

hipersensitivitas tipe I terhadap
alergen yang ditemui untuk
pertama kalinya dan disajikan
oleh seorang profesionalsel
penyaji antigen menyebabkan
respons dalam jenis sel imun yang
disebut aLimfosit TH2, subset
dariSel T yang menghasilkan
sebuahsitokin disebutinterleukin-
4 (IL-4). Sel TH2 ini berinteraksi
dengan yang lainlimfosit
disebutSel B, yang perannya
adalah produksi antibodi.
Ditambah dengan sinyal yang
diberikan oleh IL-4, interaksi ini
merangsang sel B untuk memulai
produksi sejumlah besar jenis
antibodi tertentu yang dikenal
sebagai IgE. IgE yang
disekresikan beredar dalam darah
dan berikatan dengan reseptor
spesifik IgE (semacamReseptor
Fc disebutFcεRI) pada
permukaan jenis sel kekebalan
lain yang disebutsel mast
danbasofil, yang keduanya terlibat
dalam respons inflamasi akut.
Sel-sel yang dilapisi IgE, pada
tahap ini, peka terhadap alergen.[
33]
Jika kemudian terpapar alergen

yang sama terjadi, alergen dapat
mengikat molekul IgE yang
disimpan di permukaan sel mast
atau basofil. Pengikatan silang
reseptor IgE dan Fc terjadi ketika
lebih dari satu kompleks reseptor
IgE berinteraksi dengan molekul
alergenik yang sama dan
mengaktifkan sel yang peka. Sel
mast dan basofil yang diaktifkan
menjalani proses yang
disebutdegranulasi, di mana
mereka melepaskanhistamin dan
mediator kimia inflamasi lainnya
(sitokin,interleukins,leukotrien,
danprostaglandin) dari
merekabutiran ke dalam jaringan
sekitarnya menyebabkan
beberapa efek sistemik,
sepertivasodilatasi,sekresi
lendir,stimulasi saraf,
dankontraksi otot polos. Ini
menghasilkanRhinorea, gatal,
dispnea, dan anafilaksis.
Tergantung pada individu, alergen,
dan mode pengenalan, gejalanya
dapat berupa seluruh sistem
(anafilaksis klasik) atau
terlokalisasi ke sistem tubuh
tertentu. Asma terlokalisasi ke
sistem pernapasan dan eksim
terlokalisasi kedermis.[ 33]
Respon fase akhir

Setelah mediator kimia dari
respons akut mereda, respons
fase akhir sering dapat terjadi. Ini
karena migrasi orang lainleukosit
sepertineutrofil,limfosit,eosinofil,
danmakrofag ke situs awal. Reaksi
biasanya terlihat 2-24 jam setelah
reaksi asli.[ 76] Sitokin dari sel
mast mungkin berperan dalam
persistensi efek jangka panjang.
Respons fase akhir yang terlihat
pada asma sedikit berbeda dari
yang terlihat pada respons alergi
lainnya, meskipun mereka masih
disebabkan oleh pelepasan
mediator dari eosinofil dan masih
bergantung pada aktivitas sel
TH2.[ 77]
Dermatitis kontak alergi
Meskipundermatitis kontak alergi

disebut reaksi "alergi" (yang
biasanya mengacu pada
hipersensitivitas tipe I),
patofisiologinya melibatkan reaksi
yang lebih tepat sesuai dengan
areaksi hipersensitivitas tipe IV.[
78] Pada hipersensitivitas tipe IV,
ada aktivasi tipe tertentu dariSel T
(CD8+) yang menghancurkan sel
target saat kontak, serta
diaktifkanmakrofag yang
menghasilkanhidrolitik enzim.[
Diagnosis
An allergy testing machine being operated in a diagnostic immunology lab

Effective management of allergic
diseases relies on the ability to
make an accurate diagnosis.[79]
Allergy testing can help confirm or
rule out allergies.[80][81] Correct
diagnosis, counseling, and
avoidance advice based on valid
allergy test results reduce the
incidence of symptoms and need
for medications, and improve
quality of life.[80] To assess the
presence of allergen-specific IgE
antibodies, two different methods
can be used: a skin prick test, or
an allergy blood test. Both
methods are recommended, and
they have similar diagnostic
value.[81][82]
Skin prick tests and blood tests

are equally cost-effective, and
health economic evidence shows
that both tests were cost-
effective compared with no
test.[80] Early and more accurate
diagnoses save cost due to
reduced consultations, referrals to
secondary care, misdiagnosis,
and emergency admissions.[83]
Allergy undergoes dynamic

changes over time. Regular allergy
testing of relevant allergens
provides information on if and
how patient management can be
changed to improve health and
quality of life. Annual testing is
often the practice for determining
whether allergy to milk, egg, soy,
and wheat have been outgrown,
and the testing interval is
extended to 2–3 years for allergy
to peanut, tree nuts, fish, and
crustacean shellfish.[81] Results of
follow-up testing can guide
decision-making regarding
whether and when it is safe to
introduce or re-introduce
allergenic food into the diet.[84]
Skin prick testing
Skin testing on arm

Skin testing on back
Skin testing is also known as

"puncture testing" and "prick
testing" due to the series of tiny
punctures or pricks made into the
patient's skin. Tiny amounts of
suspected allergens and/or their
extracts (e.g., pollen, grass, mite
proteins, peanut extract) are
introduced to sites on the skin
marked with pen or dye (the
ink/dye should be carefully
selected, lest it cause an allergic
response itself). A small plastic or
metal device is used to puncture
or prick the skin. Sometimes, the
allergens are injected
"intradermally" into the patient's
skin, with a needle and syringe.
Common areas for testing include
the inside forearm and the back.
If the patient is allergic to the

substance, then a visible
inflammatory reaction will usually
occur within 30 minutes. This
response will range from slight
reddening of the skin to a full-
blown hive (called "wheal and
flare") in more sensitive patients
similar to a mosquito bite.
Interpretation of the results of the
skin prick test is normally done by
allergists on a scale of severity,
with +/− meaning borderline
reactivity, and 4+ being a large
reaction. Increasingly, allergists
are measuring and recording the
diameter of the wheal and flare
reaction. Interpretation by well-
trained allergists is often guided
by relevant literature.[85] Some
patients may believe they have
determined their own allergic
sensitivity from observation, but a
skin test has been shown to be
much better than patient
observation to detect allergy.[86]
If a serious life-threatening
anaphylactic reaction has brought
a patient in for evaluation, some
allergists will prefer an initial blood
test prior to performing the skin
prick test. Skin tests may not be
an option if the patient has
widespread skin disease or has
taken antihistamines in the last
several days.
Patch testing
Patch test
Patch testing is a method used to

determine if a specific substance
causes allergic inflammation of
the skin. It tests for delayed
reactions. It is used to help
ascertain the cause of skin
contact allergy or contact
dermatitis. Adhesive patches,
usually treated with several
common allergic chemicals or
skin sensitizers, are applied to the
back. The skin is then examined
for possible local reactions at
least twice, usually at 48 hours
after application of the patch, and
again two or three days later.
Blood testing
An allergy blood test is quick and

simple and can be ordered by a
licensed health care provider
(e.g., an allergy specialist) or
general practitioner. Unlike skin-
prick testing, a blood test can be
performed irrespective of age,
skin condition, medication,
symptom, disease activity, and
pregnancy. Adults and children of
any age can get an allergy blood
test. For babies and very young
children, a single needle stick for
allergy blood testing is often
gentler than several skin pricks.
An allergy blood test is available

through most laboratories. A
sample of the patient's blood is
sent to a laboratory for analysis,
and the results are sent back a
few days later. Multiple allergens
can be detected with a single
blood sample. Allergy blood tests
are very safe since the person is
not exposed to any allergens
during the testing procedure.
The test measures the

concentration of specific IgE
antibodies in the blood.
Quantitative IgE test results
increase the possibility of ranking
how different substances may
affect symptoms. A rule of thumb
is that the higher the IgE antibody
value, the greater the likelihood of
symptoms. Allergens found at low
levels that today do not result in
symptoms cannot help predict
future symptom development.
The quantitative allergy blood
result can help determine what a
patient is allergic to, help predict
and follow the disease
development, estimate the risk of
a severe reaction, and explain
cross-reactivity.[87][88]
A low total IgE level is not

adequate to rule out sensitization
to commonly inhaled
allergens.[89] Statistical methods,
such as ROC curves, predictive
value calculations, and likelihood
ratios have been used to examine
the relationship of various testing
methods to each other. These
methods have shown that
patients with a high total IgE have
a high probability of allergic
sensitization, but further
investigation with allergy tests for
specific IgE antibodies for a
carefully chosen of allergens is
often warranted.
Laboratory methods to measure

specific IgE antibodies for allergy
testing include enzyme-linked
immunosorbent assay (ELISA, or
EIA),[90] radioallergosorbent test
(RAST)[90] and fluorescent
enzyme immunoassay (FEIA).[91]
Other testing
Challenge testing: Challenge

testing is when tiny amounts of a
suspected allergen are introduced
to the body orally, through
inhalation, or via other routes.
Except for testing food and
medication allergies, challenges
are rarely performed. When this
type of testing is chosen, it must
be closely supervised by an
allergist.
Elimination/challenge tests:
This testing method is used most
often with foods or medicines. A
patient with a suspected allergen
is instructed to modify his diet to
totally avoid that allergen for a set
time. If the patient experiences
significant improvement, he may
then be "challenged" by
reintroducing the allergen, to see
if symptoms are reproduced.
Unreliable tests: There are other

types of allergy testing methods
that are unreliable, including
applied kinesiology (allergy
testing through muscle
relaxation), cytotoxicity testing,
urine autoinjection, skin titration
(Rinkel method), and provocative
and neutralization
(subcutaneous) testing or
sublingual provocation.[92]
Differential diagnosis
Before a diagnosis of allergic

disease can be confirmed, other
plausible causes of the presenting
symptoms should be
considered.[93] Vasomotor rhinitis,
for example, is one of many
illnesses that share symptoms
with allergic rhinitis, underscoring
the need for professional
differential diagnosis.[94] Once a
diagnosis of asthma, rhinitis,
anaphylaxis, or other allergic
disease has been made, there are
several methods for discovering
the causative agent of that allergy.
Pencegahan
Giving peanut products early may
decrease the risk of allergies
while only breastfeeding during at
least the first few months of life
may decrease the risk of
dermatitis.[95][96] There is no
good evidence that a mother's
diet during pregnancy or
breastfeeding affects the risk of
allergies,[95] nor is there evidence
that delayed introduction of
certain foods is useful.[95] Early
exposure to potential allergens
may actually be protective.[5]
Fish oil supplementation during

pregnancy is associated with a
lower risk.[96] Probiotic
supplements during pregnancy or
infancy may help to prevent
atopic dermatitis.[97][98]
Manajemen
Management of allergies typically
involves avoiding the allergy
trigger and taking medications to
improve the symptoms.[6]
Allergen immunotherapy may be
useful for some types of
allergies.[6]
Medication
Several medications may be used

to block the action of allergic
mediators, or to prevent activation
of cells and degranulation
processes. These include
antihistamines, glucocorticoids,
epinephrine (adrenaline), mast
cell stabilizers, and antileukotriene
agents are common treatments of
allergic diseases.[99]
Anticholinergics, decongestants,
and other compounds thought to
impair eosinophil chemotaxis are
also commonly used. Although
rare, the severity of anaphylaxis
often requires epinephrine
injection, and where medical care
is unavailable, a device known as
an epinephrine autoinjector may
be used.[27]
Immunotherapy
Anti-allergy immunotherapy
Allergen immunotherapy is useful
for environmental allergies,
allergies to insect bites, and
asthma.[6][100] Its benefit for food
allergies is unclear and thus not
recommended.[6] Immunotherapy
involves exposing people to larger
and larger amounts of allergen in
an effort to change the immune
system's response.[6]
Meta-analyses have found that

injections of allergens under the
skin is effective in the treatment in
allergic rhinitis in children[101][102]
and in asthma.[100] The benefits
may last for years after treatment
is stopped.[103] It is generally safe
and effective for allergic rhinitis
and conjunctivitis, allergic forms
of asthma, and stinging
insects.[104]
To a lesser extent, the evidence

also supports the use of
sublingual immunotherapy for
rhinitis and asthma.[103] For
seasonal allergies the benefit is
small.[105] In this form the allergen
is given under the tongue and
people often prefer it to
injections.[103] Immunotherapy is
not recommended as a stand-
alone treatment for asthma.[103]
Alternative medicine
An experimental treatment,
enzyme potentiated
desensitization (EPD), has been
tried for decades but is not
generally accepted as
effective.[106] EPD uses dilutions
of allergen and an enzyme, beta-
glucuronidase, to which T-
regulatory lymphocytes are
supposed to respond by favoring
desensitization, or down-
regulation, rather than
sensitization. EPD has also been
tried for the treatment of
autoimmune diseases, but
evidence does not show
effectiveness.[106]
A review found no effectiveness

of homeopathic treatments and
no difference compared with
placebo. The authors concluded
that based on rigorous clinical
trials of all types of homeopathy
for childhood and adolescence
ailments, there is no convincing
evidence that supports the use of
homeopathic treatments.[107]
According to the National Center

for Complementary and
Integrative Health, U.S., the
evidence is relatively strong that
saline nasal irrigation and
butterbur are effective, when
compared to other alternative
medicine treatments, for which
the scientific evidence is weak,
negative, or nonexistent, such as
honey, acupuncture, omega 3's,
probiotics, astragalus, capsaicin,
grape seed extract, Pycnogenol,
quercetin, spirulina, stinging
nettle, tinospora, or guduchi.
[108][109]
Epidemiologi
Penyakit alergi—demam dan
asma—telah meningkat di dunia
Barat selama 2-3 dekade terakhir.
[ 110] Peningkatan asma alergi dan
gangguan atopik lainnya di
negara-negara industri,
diperkirakan, dimulai pada 1960-
an dan 1970-an, dengan
peningkatan lebih lanjut terjadi
selama 1980-an dan 1990-an,
[111] meskipun beberapa
menunjukkan bahwa peningkatan
sensitisasi yang stabil telah terjadi
sejak 1920-an.[ 112] Jumlah kasus
baru per tahun atopi di negara
berkembang, secara umum, tetap
jauh lebih rendah.[ 111]
Kondisi alergi: Statistik dan

epidemiologi
Jenis Britania
alergi Amerika Serikat Raya
35,9 3,3 juta

Rinitis juta[114] (sekitar (sekitar
alergi 11% dari 5,5% dari
populasi[115]) populasi
5,7 juta
(sekitar
9,4%). Pada
usia enam
dan tujuh
10 juta memiliki tahun asma
asma alergi meningkat
(sekitar 3% dari dari 18,4%
populasi). menjadi
Prevalensi asma 20,9%
meningkat 75% selama lima
Asma dari 1980 hingga tahun,
1994. Prevalensi selama
asma 39% lebih waktu yang
tinggi di Afrika sama
Amerika tingkatnya
daripada diOrang menurun
Eropa.[ 117] dari 31%
menjadi
24,7% pada
usia 13
hingga 14
tahun.
Sekitar 9% dari
populasi. Antara
tahun 1960 dan 5,8 juta
Eksim 1990, prevalensi (sekitar 1%
atopik telah meningkat parah).
dari 3% menjadi
10% pada anak-
anak.[ 118]
Setidaknya 40
kematian per
tahun karena
racun serangga.
Sekitar 400
kematian akibat
anafilaksis Antara 1999
penisilin. Sekitar dan 2006,
220 kasus 48 kematian
anafilaksis dan 3 terjadi pada
Anafilaksis kematian per orang mulai
tahun dari lima
disebabkan oleh bulan hingga
alergi lateks.[
119] Diperkirakan 85 tahun.
150 orang
meninggal setiap
tahun karena
anafilaksis
karena alergi
makanan.[ 120]
Sekitar 15%
orang dewasa
memiliki reaksi
alergi ringan dan
terlokalisasi.
Racun Reaksi sistemik Tidak
serangga terjadi pada 3% diketahui
orang dewasa
dan kurang dari
1% anak-anak.[
121]
Reaksi
anafilaksis
terhadap
Alergi Tidak
penisilin
obat diketahui
menyebabkan
400 kematian
per tahun.
5–7% bayi
dan 1-2%
7,6% anak-anak orang
dan 10,8% orang dewasa.
dewasa.[ Peningkatan
122] Kacang 117,3%
tanah dan/atau dalam alergi
Alergi kacang pohon kacang
makanan (misalnyakenari) diamati dari
alergi tahun 2001
mempengaruhi hingga
sekitar tiga juta 2005,
orang Amerika, diperkirakan
atau 1,1% dari 25.700
populasi.[ 120] orang di
Inggris
terpengaruh.
2,3 juta
Beberapa (sekitar
alergi 3,7%),
(Asma, prevalensi
eksim, dan telah
rinitis Tidak diketahui meningkat

sebesar
alergi 48,9%
bersama- antara tahun
sama) 2001 dan
2005.[
Mengubah frekuensi
Meskipun faktor genetik

mengatur kerentanan terhadap
penyakit atopik, peningkatanatopi
telah terjadi dalam waktu yang
terlalu singkat untuk dijelaskan
oleh perubahan genetik dalam
populasi, sehingga menunjuk
pada perubahan lingkungan atau
gaya hidup.[ 111] Beberapa
hipotesis telah diidentifikasi untuk
menjelaskan tingkat peningkatan
ini. Peningkatan paparan alergen
abadi mungkin disebabkan oleh
perubahan perumahan dan
peningkatan waktu yang
dihabiskan di dalam ruangan, dan
penurunan aktivasi mekanisme
kontrol kekebalan umum dapat
disebabkan oleh perubahan
kebersihan atau kebersihan, dan
diperburuk oleh perubahan pola
makan, obesitas, dan penurunan
latihan fisik.[ 110] ItuHipotesis
kebersihan
mempertahankan[124] bahwa
standar hidup yang tinggi dan
kondisi higienis membuat anak-
anak terkena lebih sedikit infeksi.
Diperkirakan bahwa
berkurangnya infeksi bakteri dan
virus di awal kehidupan
mengarahkan sistem kekebalan
yang matang menjauh
dariRespons tipe TH1, mengarah
ke respons TH2 yang tidak
terkendali yang memungkinkan
peningkatan alergi.[ 73][125]
Perubahan tingkat dan jenis

infeksi saja, bagaimanapun, tidak
dapat menjelaskan peningkatan
penyakit alergi yang diamati, dan
bukti terbaru telah memusatkan
perhatian pada
pentingnyalingkungan mikroba
gastrointestinal. Bukti telah
menunjukkan bahwa paparan
makanan danPatogen fecal-oral,
sepertihepatitis A,Toxoplasma
gondii, danHelicobacter pylori
(yang juga cenderung lebih umum
di negara berkembang), dapat
mengurangi risiko atopi secara
keseluruhan lebih dari
60%,[126] dan peningkatan tingkat
infeksi parasit telah dikaitkan
dengan penurunan prevalensi
asma.[ 127] Dispekulasikan bahwa
infeksi ini memberikan efeknya
dengan mengubah regulasi
TH1/TH2 secara kritis.[
128] Elemen penting dari hipotesis
kebersihan yang lebih baru juga
termasuk paparanendotoksin,
paparan hewan peliharaan dan
tumbuh di pertanian.[ 128]
Sejarah
Some symptoms attributable to
allergic diseases are mentioned in
ancient sources.[129] Particularly,
three members of the Roman
Julio-Claudian dynasty
(Augustus, Claudius and
Britannicus) are suspected to
have a family history of
atopy.[129][130] The concept of
"allergy" was originally introduced
in 1906 by the Viennese
pediatrician Clemens von Pirquet,
after he noticed that patients who
had received injections of horse
serum or smallpox vaccine usually
had quicker, more severe
reactions to second
injections.[131] Pirquet called this
phenomenon "allergy" from the
Ancient Greek words ἄλλος allos
meaning "other" and ἔργον ergon
meaning "work".[132]
All forms of hypersensitivity used

to be classified as allergies, and all
were thought to be caused by an
improper activation of the
immune system. Later, it became
clear that several different disease
mechanisms were implicated,
with a common link to a
disordered activation of the
immune system. In 1963, a new
classification scheme was
designed by Philip Gell and Robin
Coombs that described four types
of hypersensitivity reactions,
known as Type I to Type IV
hypersensitivity.[133] With this
new classification, the word
allergy, sometimes clarified as a
true allergy, was restricted to type
I hypersensitivities (also called
immediate hypersensitivity),
which are characterized as rapidly
developing reactions involving IgE
antibodies.[134]
A major breakthrough in
understanding the mechanisms of
allergy was the discovery of the
antibody class labeled
immunoglobulin E (IgE). IgE was
simultaneously discovered in
1966–67 by two independent
groups:[135] Ishizaka's team at the
Children's Asthma Research
Institute and Hospital in Denver,
USA,[136] and by Gunnar
Johansson and Hans Bennich in
Uppsala, Sweden.[137] Their joint
paper was published in April
1969.[138]
Diagnosis
Radiometric assays include the

radioallergosorbent test (RAST
test) method, which uses IgE-
binding (anti-IgE) antibodies
labeled with radioactive isotopes
for quantifying the levels of IgE
antibody in the blood.[139] Other,
newer methods use colorimetric
or fluorescence-labeled
technology in the place of
radioactive isotopes.
The RAST methodology was

invented and marketed in 1974 by
Pharmacia Diagnostics AB,
Uppsala, Sweden, and the
acronym RAST is actually a brand
name. In 1989, Pharmacia
Diagnostics AB replaced it with a
superior test named the
ImmunoCAP Specific IgE blood
test, which uses the newer
fluorescence-labeled technology.
American College of Allergy

Asthma and Immunology (ACAAI)
and the American Academy of
Allergy Asthma and Immunology
(AAAAI) issued the Joint Task
Force Report "Pearls and pitfalls
of allergy diagnostic testing" in
2008, and is firm in its statement
that the term RAST is now
obsolete:
The term RAST became

a colloquialism for all
varieties of (in vitro
allergy) tests. This is
unfortunate because it
is well recognized that
there are well-
performing tests and
some that do not
perform so well, yet
they are all called
RASTs, making it
difficult to distinguish
which is which. For
these reasons, it is now
recommended that use
of RAST as a generic
descriptor of these tests
be abandoned.[14]
The updated version, the

ImmunoCAP Specific IgE blood
test, is the only specific IgE assay
to receive Food and Drug
Administration approval to
quantitatively report to its
detection limit of 0.1kU/L.
Spesialisasi medis
Allergist/Immunologist
Occupation
Names Physician
Occupation Specialty
Occupation Specialty
type
Activity sectors Medicine
Specialty immunology
Description
Education Doctor of
required
Medicine
(M.D.)
Doctor of
Osteopathic
medicine
(D.O.)
Bachelor of
Medicine,
Bachelor of
Surgery
(M.B.B.S.)
Bachelor of
Medicine,
Bachelor of
Surgery
(MBChB)
Fields of Hospitals, Clinics
employment
An allergist is a physician
specially trained to manage and
treat allergies, asthma, and the
other allergic diseases. In the
United States physicians holding
certification by the American
Board of Allergy and Immunology
(ABAI) have successfully
completed an accredited
educational program and
evaluation process, including a
proctored examination to
demonstrate knowledge, skills,
and experience in patient care in
allergy and immunology.[140]
Becoming an
allergist/immunologist requires
completion of at least nine years
of training. After completing
medical school and graduating
with a medical degree, a physician
will undergo three years of
training in internal medicine (to
become an internist) or pediatrics
(to become a pediatrician). Once
physicians have finished training
in one of these specialties, they
must pass the exam of either the
American Board of Pediatrics
(ABP), the American Osteopathic
Board of Pediatrics (AOBP), the
American Board of Internal
Medicine (ABIM), or the American
Osteopathic Board of Internal
Medicine (AOBIM). Internists or
pediatricians wishing to focus on
the sub-specialty of allergy-
immunology then complete at
least an additional two years of
study, called a fellowship, in an
allergy/immunology training
program. Allergist/immunologists
listed as ABAI-certified have
successfully passed the certifying
examination of the ABAI following
their fellowship.[141]
In the United Kingdom, allergy is a

subspecialty of general medicine
or pediatrics. After obtaining
postgraduate exams (MRCP or
MRCPCH), a doctor works for
several years as a specialist
registrar before qualifying for the
General Medical Council
specialist register. Allergy services
may also be delivered by
immunologists. A 2003 Royal
College of Physicians report
presented a case for improvement
of what were felt to be inadequate
allergy services in the UK.[142] In
2006, the House of Lords
convened a subcommittee. It
concluded likewise in 2007 that
allergy services were insufficient
to deal with what the Lords
referred to as an "allergy
epidemic" and its social cost; it
made several
recommendations.[143]
Penelitian
Low-allergen foods are being
developed, as are improvements
in skin prick test predictions;
evaluation of the atopy patch test,
wasp sting outcomes predictions,
a rapidly disintegrating
epinephrine tablet, and anti-IL-5
for eosinophilic diseases.[144]
Lihat juga
Allergic shiner
GWAS in allergy
Histamine intolerance
List of allergens
Oral allergy syndrome
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Alergi, juga dikenal sebagai

Gatal-gatal adalah gejala alergi

Gejala Mata merah,

Jenis Hay fever, alergi

Penyebab Faktor genetik

Pencegahan Paparan awal

Alergen umum termasuk serbuk

Paparan dini anak-anak terhadap

Alergi adalah umum.[ 10] Di negara

Tanda dan gejala

Perasaan kenyang, mungkin

Saluran Sakit perut,kembung,

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Berbagai macam makanan dapat

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Tingkat alergi berbeda antara

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Mereka yang memilikialergi

Alergen dapat ditransfer dari satu

Lateks dapat memicu reaksi kulit,

Respons yang paling umum

Sensitivitas lateks dan pisang

Sekitar 10% orang melaporkan

Biasanya, serangga yang

Racun berinteraksi dengan

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Perkiraan bervariasi pada

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Etnisitas mungkin memainkan

Penyakit alergi disebabkan oleh

Data epidemiologis mendukung

Kronisstres dapat memperburuk

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Perubahan dalam paparan

Cacing usus dan parasit serupa

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An allergy testing machine being operated in a diagnostic immunology lab

Skin prick tests and blood tests

Allergy undergoes dynamic

Skin prick testing

Skin testing on arm

Skin testing on back

Skin testing is also known as

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Patch testing is a method used to

An allergy blood test is quick and

An allergy blood test is available

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Fish oil supplementation during