REAKSI HIPERSENSITIVITAS Y Y
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REAKSI HIPERSENSITIVITAS
Y Y
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Hipersensitivitas adalah suatu reaksi yang tidak diharapkan
dari respon imun tubuh.
Coombs dan Gell membagi menjadi 4 tipe (mekanisme dan
waktu):
Rx. Hipersensitivitas tipe I Rx. Hipersensitivitas tipe II
Rx. Hipersensitivitas tipe III
Rx. Hipersensitivitas tipe IV
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(hives)
Allergies
4 types of hypersensitivity reactions
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Delayed-type hypersensitivityImmune
complex
disease
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Reaksi Hipersensitivitas tipe I
Reaksi Hipersensitivitas tipe cepat atau anafilaktik
Diperantarai IgE
Alergenproduksi IgEberikatan spesifik dengan reseptor di
permukaan sel mast dan basofil tersensitisasi
Kontak berikutnya sederetan reaksi biokimia degranulasi dan
pelepasan mediator2 (histamin, leukotrien dan sitokin) reaksi alergi
15-30 menit setelah terpapar antigen, kadang keterlambatan (10-12 jam)
Dapat melibatkan kulit (urtikaria dan eksema), mata (konjungtivitis),
nasofaring (rinitis), jaringan bronkopulmoner (asma), dan GI tract
(gastroenteritis)
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Contoh: reaksi anafilaksis terhadap bisa hewan, hay fever , urtikaria akibat
makanan, dermatitis atopik, rhinitis alergika, konjungtivitis, asma, dll
Gejala : ketidaknyamanan ringan sampai kematian
Berat ringan gejala dipengaruhi : antibodi IgE
jumlah alergen
faktor-faktor lain yang dapat meningkatkan respon (infeksi virus
dan polutan)
Reaksi Hipersensitivitas tipe I……….
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Biologic effects of mediators
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Table 1. Pharmacologic Mediators of Immediate Hypersensitivity
MEDIATOR Preformed mediators in granules histamine bronchoconstriction, mucus secretion,
vasodilatation, vascular permeability tryptase proteolysis
kininogenase kinins and vasodilatation, vascular permeability,
edema ECF-A
(tetrapeptides) attract eosinophil and neutrophils
Newly formed mediators leukotriene B4 basophil attractant leukotriene C4, D4 same as histamine but 1000x more potent prostaglandins D2 edema and pain PAF platelet aggregation and heparin release:
microthrombi
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Tes diagnostik
Skin test (prick dan intradermal)
Kadar total IgE dan IgE spesifik terhadap alergen yang
dicurigai (ELISA) IgE tinggi pada kondisi atopik
Terapi:
Antihistamin, adrenalin, bronkodilator, kortikosteroid,menghindari paparan alergen dan immunoterapi
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Ragweed
Control negative (saline)
Control positve (histamine)
Skin test for allergy
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Type I hypersensitivity reaction
12
Capillary dilation
Pressure ofexudate
Release of
chemical
mediators :
Histamine
SRS-A
Kinins
Prostaglandins
Increased
BloodVolume
Increased
Capillary
permebiality
Exudation of
Cell, fluid protein
Nerve
irritation
Constriction
of smooth
muscle
Antigen
Ingestants
Food
Drugs
Pollens
Dusts
Molds
Injectants
DrugsStings
Vaccines
Serum
Allergen
interacts
with
IgE on mast cell
CAUSES MECHANISM PATHOPHYSIOLOGY
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Type I hypersensitivity reaction (continued)13
Respiratory tract
1. Upper “sinus headache”
itching of eyestearing, sneezing,
watery nasal discharge,
itching of nose,
throat irritation
2. Lungs wheezing, dyspnea,
dry cough, tightness in chest
MANIFESTATIONS CLINICAL EXAMPLES
Gastrointestinal
Glossitis, cardiospasm
Nausea, vomitting
Irritable bowel
Diarrhea, pruritus ani
Skin
Urticaria, pruritus,
Angioedema, weeping erthematosus vesico-papular lessions
Respiratory tract
1. Upper “sinus headache”
itching of eyestearing, sneezing,
watery nasal discharge,
itching of nose,
throat irritation
2. Lungs wheezing, dyspnea,
dry cough, tightness in chest
Conjunctivitis
Asthma
Food allergies
Atopic dermatitis
Urticaria
Allergic rhinitis
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Reaksi Hipersensitivitas tipe II
Reaksi hipersensitivitas sitotoksik
Waktu reaksi : menit - jam
Contoh: reaksi transfusi, drug-induced hemolytic anemia,
granulositopenia, dan trombositopenia
Diperantarai IgM atau IgG dan komplemen
Fagosit dan sel K punya peran
Interaksi antigen-antibodi pd permukaan sel, IgM atau IgGdgn antigen yang juga merupakan bagian integral membran
sel atau telah terserap atau menyatu menjadi membran.
Mengaktifkan sistem komplemen dan sel yang terlibat
dihancurkan.
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Type II hypersensitivity reaction 17
CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL
EXAMPLES
Susceptability
to infections
Antigen
Transfusion
reaction
Erythroblastosis
fetalis
Drugs
Autoantibodies
Unknown
Antigeninteracts
with body
cell i.e :
•Erythrocyte
•Leucocyte
•Platelet•Vascular
endothelium
Agranulocytosis
Thrombocytopenia Purpura
Vesicular
purpura
Vasculitis
Erytrhrocyte
hemolysis
Hemolytic
anemia
Reaction of IgG or
IgM antobody withantigen on cell
Activates
complement
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Reaksi Hipersensitivitas tipe III
Reaksi hipersensitivitas kompleks imun / reaksi Arthus
3-10 jam setelah terpapar antigen
Diperantarai kompleks imun (antigen-antibodi)
Antigen eksogen (bakteri, virus, atau parasit)/endogen (SLE)
Contoh: serum sickness,SLE,rx Arthus,lupus nephritis,RA,dll
Terbentuk kompleks antigen-antibodi (toksik terhadap
jaringan di tempat mereka diendapkan seperti ginjal / paru-paru) infiltrasi dinding pembuluh darah kecil aktivasi
kaskade komplemen pelepasan bahan aktif secara
biologis, termasuk faktor-faktor yang menarik sel-sel fagosit
yang akan menfagositosis kompleks tersebut
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Type III hypersensitivity reactions (Arthus Reaction) - Ab-Ag Complexes
Critical mediators appear to be C5a-receptor and FcgRIII--probably present on mast cells
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Type III hypersensitivity reaction20
CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL
EXAMPLES
Tissue
destruction
Inflammation
Antigen and
antibody form
an immune
complex
Antigen
Autoantibodies
Drugs
Serum
ChemicalsForeign antigen
Bacteria
Virus
Glomerulo-
nephritis
Vasculitis
Arthus reaction
Rheumatoid
diseases
Serum sickness
Deposits on vessel walls
or basement membrane
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Diagnosis:
Biopsi jaringan (endapan Ig dan komplemen)
Kompleks imun pada darah dan penurunan
jumlah komplemen
Terapi:
Anti-inflamasi
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Reaksi Hipersensitivitas Tipe IV
tipe seluler atau tipe lambat (delayed type hypersensitivity)
> 12 jam
Contoh klasik: reaksi tuberkulin (Mantoux) yang memuncak48 jam setelah injeksi antigen
Contoh lain: dermatitis kontak, penyakit autoimun dan infeksiseperti tuberkulosis, lepra, granulomatosa, toksoplasmosis,dll
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Biological effects of Eosinophil
mediators
Late stage of an allergic response includes therecruitment of eosinophils and Th2 cells contrast with
a DTH (type IV) response which includes infiltration ofmacrophages and Th1 cells
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Table 3 - Delayed hypersensitivity reactions Type Reaction time Clinical
appearance Histology Antigen and site
contact 48-72 hr eczema lymphocytes,
followed by
macrophages;
edema of epidermis
epidermal ( organic
chemicals, poison
ivy, heavy metals,
etc.)
tuberculin 48-72 hr local induration lymphocytes,
monocytes,
macrophages intradermal
(tuberculin,
lepromin, etc.)
granuloma 21-28 days hardening macrophages,
epitheloid and giant
cells, fibrosis
persistent antigen or
foreign body
presence
(tuberculosis,
leprosy, etc.)
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Mekanisme perusakan melibatkan limfosit T dan monosit
dan/atau makrofag
Sel t sitotoksik (Tc) menyebabkan kerusakan langsung
sedangkan sel T helper (TH1) mensekresi sitokin
aktivasi Tc, makrofag serta monosit kerusakan
Diagnosis:- Mantoux test dan patch test
Terapi:- Kortikosteroid dan agen imunosupresif
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Type IV hypersensitivity reaction
26
CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL
EXAMPLES
Release of :
Lymphokines
Migration inhibition
factorInterferon
Killer cells
Transfer factor
Injury and
destruction oftarget organ
Antigen
Tuberculin
Poison IvyChemical
Fungi
Transplanted
organs
Virus
Contact
dermatitis
Graft vs host
reactions
Viral infection
Autoallergic
disease
Sensitized
Lymphocytereacts with
antigen
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