4 - Reaksi Hipersensitivitas
4 - Reaksi Hipersensitivitas
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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
(hives)
Allergies
hypersensitivity
Reaksi Hipersensitivitas tipe cepat atau anafilaktik Diperantarai IgE Alergenproduksi IgE berikatan 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
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)
Table 1. Pharmacologic Mediators of Immediate Hypersensitivity MEDIATOR Preformed mediators in granules histamine bronchoconstriction, mucus secretion, vasodilatation, vascular permeability proteolysis kinins and vasodilatation, vascular permeability, edema attract eosinophil and neutrophils basophil attractant same as histamine but 1000x more potent edema and pain platelet aggregation and heparin release: microthrombi
tryptase kininogenase ECF-A (tetrapeptides) Newly formed mediators leukotriene B4 leukotriene C4, D4 prostaglandins D2 PAF
Tes diagnostik
Skin test (prick dan intradermal) Kadar total IgE dan IgE spesifik terhadap alergen yang dicurigai (ELISA) IgE tinggi pada kondisi atopik
Terapi:
CAUSES
Antigen Ingestants Food Drugs Pollens Dusts Molds Injectants Drugs Stings Vaccines Serum
MECHANISM
PATHOPHYSIOLOGY
Increased Blood Volume
Capillary dilation Release of Allergen chemical interacts mediators : Exudation of Increased with Histamine Cell, fluid protein Capillary IgE on mast cell SRS-A permebiality Kinins Prostaglandins Pressure of exudate Nerve irritation Constrict ion of smooth muscle
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MANIFESTATIONS Respiratory tract Respiratory tract 1. Upper sinus headache 1. Upper sinus headache itching of eyes itching of eyes tearing, sneezing, tearing, sneezing, watery nasal discharge, watery nasal discharge, itching of nose, itching of nose, throat irritation throat irritation 2. Lungs wheezing, dyspnea, 2. dry cough, tightness in chest Lungs wheezing, dyspnea,
Gastrointestinal Glossitis, cardiospasm Nausea, vomitting Irritable bowel Diarrhea, pruritus ani
CLINICAL EXAMPLES
Allergic rhinitis
Conjunctivitis
Asthma
Food allergies
Atopic dermatitis Skin Urticaria, pruritus, Angioedema, weeping erthematosus vesico-papular lessions Urticaria
Type I hypersensitivity reaction (continued)
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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 IgG dgn antigen yang juga merupakan bagian integral membran sel atau telah terserap atau menyatu menjadi
MECHANISM
PATHOPHYSIOLOGY
CLINICAL EXAMPLES Hemoly tic anemia Susceptabi lity to infections Purpu ra Vesicul ar purpura
Antigen interacts with body cell i.e : Erythroc yte Leucocyt e Platelet Vascular endotheli um
Thrombocytopenia Vasculiti s
Reaksi hipersensitivitas kompleks imun / reaksi Arthus 3-10 jam setelah terpapar antigen Diperantarai kompleks imun (antigenantibodi) 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
CAUSESMECHANISM
Antigen
Antigen and Deposits on vessel walls Autoantibodies Tissue antibody form basement membranedestructio Drugs or an immune Serum n complex Chemicals Inflammat Foreign antigen ion Bacteria Virus
Diagnos is:
Biopsi
jaringan (endapan Ig dan komplemen) Kompleks imun pada darah dan penurunan jumlah komplemen
Terapi:
Anti-inflamasi
tipe seluler atau tipe lambat (delayed type hypersensitivity) > 12 jam Contoh klasik: reaksi tuberkulin (Mantoux) yang memuncak 48 jam setelah injeksi antigen Contoh lain: dermatitis kontak, penyakit autoimun dan infeksi seperti tuberkulosis, lepra, granulomatosa, toksoplasmosis, dll
Late stage of an allergic response includes the recruitment of eosinophils and Th2 cells contrast with
a DTH (type IV) response which includes infiltration of macrophages and Th1 cells
Table 3 - Delayed hypersensitivity reactions Type Reaction time Clinical appearance 48-72 hr eczema Histology Antigen and site epidermal ( organic chemicals, poison ivy, heavy metals, etc.)
contact
tuberculin
48-72 hr
local induration lymphocytes, monocytes, macrophages hardening macrophages, epitheloid and giant cells, fibrosis
intradermal (tuberculin, lepromin, etc.) persistent antigen or foreign body presence (tuberculosis, leprosy, etc.)
granuloma
21-28 days
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:
-
CAUSES
MECHANISM
PATHOPHYSIOLOGY
CLINICAL EXAMPLES Contact dermatiti s Graft vs host reactions Viral infection Autoallerg ic disease
Antigen Tuberculi n Poison Ivy Chemical Fungi Transplan ted organs Virus Sensitized Lymphocy te reacts with antigen
Release of : Lymphokines Migration inhibition factor Interferon Killer cells Transfer factor