Thursday, June 25, 2009
Hipersensitivitas
1. Faktor Penyebab Reaksi Hipersensitifitas (Anafilaktif)
Anaphylaxis is a severe, whole-body allergic reaction. After an initial exposure ("sensitizing dose") to a substance like bee sting toxin, the person's immune system becomes sensitized to that allergen. On a subsequent exposure ("shocking dose"), an allergic reaction occurs. This reaction is sudden, severe, and involves the whole body.
Some drugs (polymyxin, morphine, x-ray dye, and others) may cause an "anaphylactoid" reaction (anaphylactic-like reaction) on the first exposure.[6] This is usually due to a toxic reaction, rather than the immune system mechanism that occurs with "true" anaphylaxis. The symptoms, risk for complications without treatment, and treatment are the same, however, for both types of reactions. Some vaccinations are also known to cause "anaphylactoid" reactions.[7] Antitoxins and antivenins may cause similar reactions.
Anaphylaxis can occur in response to any allergen. Common causes include insect bites/stings, food allergies (peanuts and tree nuts are the most common, though not the only), and drug allergies. Pollens and other inhaled allergens rarely cause anaphylaxis. In opthamology, the dye fluorescein used in some eye exams is a well known trigger. Some people have an anaphylactic reaction with no identifiable cause (idiopathic).
The most common cause of anaphylaxis is food, which is followed by insect venom. Allergy to latex rubber is becoming a rapidly increasing problem because the use of latex rubber gloves in the medical field and also an increase in atopy. Exercise, vaccines, and semen account for rare causes of anaphylaxis. In addition, allergen immunotherapy(desensitization) may cause anaphylaxis (Ewan, 1998). See the following table outlining common causes of anaphylaxis.
Common causes of anaphylaxis
· Foods
· Bee and wasp stings
· Drugs
· Latex rubber
A. Foods commonly causing anaphylaxis
· Peanuts
· Tree nuts (eg, brazil nut, almond, hazelnut)
· Fish
· Shellfish
· Egg
· Milk
· Sesame
· Pulses (other than peanuts)
B. Drugs causing anaphylaxis or anaphylactoid reactions
· Antibiotics (especially penicillin)
· Intravenous anesthetic drugs
· Aspirin
· Non-steroidal anti-inflammatory drugs
· Intravenous contrast media
· Opioid analgesics
2. Mekanisme Respon Immun Reaksi Anafilaktif
Immunological Mechanism of Anaphylaxis follow a lot of steps :
(1) Antigen-presenting cell internalizes antigen.
(2) The APC processes the internalized antigen.
(3) The APC presents the processed peptide to CD4+ T lymphocytes via MHC II.
(4) After the peptide is presented, the T cell differentiates into TH2 lymphocytes and produces IL-4, IL-5, IL-9, and IL-13.
(5) IL-4 and IL-13 cause B cell immunoglobulin isotype switching to IgE.
(6) The circulating IgE binds to the IgE receptors on mast cells.
(7) Antigen similar to the original antigen cross-links the mast cell surface-bound IgE, resulting in cellular degranulation. Degranulation releases histamine, tryptase, and other mediators that produce the symptoms of anaphylaxis (Anaesthesia UK, 2005).
Anaphylaxis occurs when a person is reexposed to a specific antigen that cross-links antigen- specific IgE molecules, which are bound to mast cells and basophils. This leads to activation and degranulation of mast cells and basophils. Preformed mediators, such as histamine and tryptase, within the mast cell and basophil are released in degranulation. The metabolism of arachidonic acid in the cell membrane produces other mediators, such as prostaglandins and leukotrienes.
Anaphylaxis is a severe, whole-body allergic reaction. After an initial exposure ("sensitizing dose") to a substance like bee sting toxin, the person's immune system becomes sensitized to that allergen. On a subsequent exposure ("shocking dose"), an allergic reaction occurs. This reaction is sudden, severe, and involves the whole body.
Some drugs (polymyxin, morphine, x-ray dye, and others) may cause an "anaphylactoid" reaction (anaphylactic-like reaction) on the first exposure.[6] This is usually due to a toxic reaction, rather than the immune system mechanism that occurs with "true" anaphylaxis. The symptoms, risk for complications without treatment, and treatment are the same, however, for both types of reactions. Some vaccinations are also known to cause "anaphylactoid" reactions.[7] Antitoxins and antivenins may cause similar reactions.
Anaphylaxis can occur in response to any allergen. Common causes include insect bites/stings, food allergies (peanuts and tree nuts are the most common, though not the only), and drug allergies. Pollens and other inhaled allergens rarely cause anaphylaxis. In opthamology, the dye fluorescein used in some eye exams is a well known trigger. Some people have an anaphylactic reaction with no identifiable cause (idiopathic).
The most common cause of anaphylaxis is food, which is followed by insect venom. Allergy to latex rubber is becoming a rapidly increasing problem because the use of latex rubber gloves in the medical field and also an increase in atopy. Exercise, vaccines, and semen account for rare causes of anaphylaxis. In addition, allergen immunotherapy(desensitization) may cause anaphylaxis (Ewan, 1998). See the following table outlining common causes of anaphylaxis.
Common causes of anaphylaxis
· Foods
· Bee and wasp stings
· Drugs
· Latex rubber
A. Foods commonly causing anaphylaxis
· Peanuts
· Tree nuts (eg, brazil nut, almond, hazelnut)
· Fish
· Shellfish
· Egg
· Milk
· Sesame
· Pulses (other than peanuts)
B. Drugs causing anaphylaxis or anaphylactoid reactions
· Antibiotics (especially penicillin)
· Intravenous anesthetic drugs
· Aspirin
· Non-steroidal anti-inflammatory drugs
· Intravenous contrast media
· Opioid analgesics
2. Mekanisme Respon Immun Reaksi Anafilaktif
Immunological Mechanism of Anaphylaxis follow a lot of steps :
(1) Antigen-presenting cell internalizes antigen.
(2) The APC processes the internalized antigen.
(3) The APC presents the processed peptide to CD4+ T lymphocytes via MHC II.
(4) After the peptide is presented, the T cell differentiates into TH2 lymphocytes and produces IL-4, IL-5, IL-9, and IL-13.
(5) IL-4 and IL-13 cause B cell immunoglobulin isotype switching to IgE.
(6) The circulating IgE binds to the IgE receptors on mast cells.
(7) Antigen similar to the original antigen cross-links the mast cell surface-bound IgE, resulting in cellular degranulation. Degranulation releases histamine, tryptase, and other mediators that produce the symptoms of anaphylaxis (Anaesthesia UK, 2005).
Anaphylaxis occurs when a person is reexposed to a specific antigen that cross-links antigen- specific IgE molecules, which are bound to mast cells and basophils. This leads to activation and degranulation of mast cells and basophils. Preformed mediators, such as histamine and tryptase, within the mast cell and basophil are released in degranulation. The metabolism of arachidonic acid in the cell membrane produces other mediators, such as prostaglandins and leukotrienes.
Faktor Penyebab Penyakit Autoimun
Faktor Penyebab Penyakit Autoimun
1. Genetik
Beberapa peneliti menemukan adanya hubungan antara penyakit LES dengan gen Human Leukocyte Antigen (HLA) seperti DR2, DR3 dari Major Histocompatibility Complex (MHC) kelas II. Individu dengan gen HLA DR2 dan DR3 mempunyai risiko relatif menderita penyakit LES 2-3 kali lebih besar daripada yang mempunyai gen HLA DR4 dan HLA DR5. Peneliti lain menemukan bahwa penderita penyakit LES yang mempunyai epitop antigen HLA-DR2 cenderung membentuk autoantibodi anti-dsDNA, sedangkan penderita yang mempunyai epitop HLA-DR3 cenderung membentuk autoantibodi anti-Ro/SS-A dan anti-La/SS-B. Penderita penyakit LES dengan epitop-epitop HLA-DR4 dan HLA-DR5 memproduksi autoantibodi anti-Sm dan anti-RNP.
2. Defisiensi komplemen
Pada penderita penyakit LES sering ditemukan defisiensi komplemen C3 dan atau C4, yaitu pada penderita penyakit LES dengan manifestasi ginjal. Defisiensi komplemen C3 dan atau C4 jarang ditemukan pada penderita penyakit LES dengan manifestasi pada kulit dan susunan saraf pusat. Individu yang mengalami defek pada komponen-komponen komplemennya, seperti Clq, Clr, Cls mempunyai predisposisi menderita penyakit LES dan nefritis lupus. Defisiensi komplemen C3 akan menyebabkan kepekaan terhadap infeksi meningkat, keadaan ini merupakan predisposisi untuk timbulnya penyakit kompleks imun. Penyakit kompleks imun selain disebabkan karena defisiensi C3, juga dapat disebabkan karena defisiensi komplemen C2 dan C4 yang terletak pada MHC kelas II yang bertugas mengawasi interaksi sel-sel imunokompeten yaitu sel Th dan sel B. Komplemen berperan dalam sistem pertahanan tubuh, antara lain melalui proses opsonisasi, untuk memudahkan eliminasi kompleks imun oleh sel karier atau makrofag. Kompleks imun akan diikat oleh reseptor komplemen (Complement receptor = C-R) yang terdapat pada permukaan sel karier atau sel makrofag. Pada defisiensi komplemen, eliminasi kompleks imun terhambat, sehingga jumlah kompleks imun menjadi berlebihan dan berada dalam sirkulasi lebih lama.
3. Hormon
Pada individu normal, testosteron berfungsi mensupresi sistem imuns sedangkan estrogen memperkuat sistem imun. Predominan lupus pada wanita dibandingkan pria memperlihatkan adanya pengaruh hormon seks dalam patogenesis lupus. Pada percobaan di tikus dengan pemberian testosteron mengurangi lupus-like syndrome dan pemberian estrogen memperberat penyakit.
4. Lingkungan Pengaruh fisik (sinar matahari), infeksi (bakteri, virus, protozoa), dan obat-obatan dapat mencetuskan atau memperberat penyakit autoimun. Mekanismenya dapat melalui aktivasi sel B poliklonal atau dengan meningkatkan ekspresi MHC kelas I atau II.
1. Genetik
Beberapa peneliti menemukan adanya hubungan antara penyakit LES dengan gen Human Leukocyte Antigen (HLA) seperti DR2, DR3 dari Major Histocompatibility Complex (MHC) kelas II. Individu dengan gen HLA DR2 dan DR3 mempunyai risiko relatif menderita penyakit LES 2-3 kali lebih besar daripada yang mempunyai gen HLA DR4 dan HLA DR5. Peneliti lain menemukan bahwa penderita penyakit LES yang mempunyai epitop antigen HLA-DR2 cenderung membentuk autoantibodi anti-dsDNA, sedangkan penderita yang mempunyai epitop HLA-DR3 cenderung membentuk autoantibodi anti-Ro/SS-A dan anti-La/SS-B. Penderita penyakit LES dengan epitop-epitop HLA-DR4 dan HLA-DR5 memproduksi autoantibodi anti-Sm dan anti-RNP.
2. Defisiensi komplemen
Pada penderita penyakit LES sering ditemukan defisiensi komplemen C3 dan atau C4, yaitu pada penderita penyakit LES dengan manifestasi ginjal. Defisiensi komplemen C3 dan atau C4 jarang ditemukan pada penderita penyakit LES dengan manifestasi pada kulit dan susunan saraf pusat. Individu yang mengalami defek pada komponen-komponen komplemennya, seperti Clq, Clr, Cls mempunyai predisposisi menderita penyakit LES dan nefritis lupus. Defisiensi komplemen C3 akan menyebabkan kepekaan terhadap infeksi meningkat, keadaan ini merupakan predisposisi untuk timbulnya penyakit kompleks imun. Penyakit kompleks imun selain disebabkan karena defisiensi C3, juga dapat disebabkan karena defisiensi komplemen C2 dan C4 yang terletak pada MHC kelas II yang bertugas mengawasi interaksi sel-sel imunokompeten yaitu sel Th dan sel B. Komplemen berperan dalam sistem pertahanan tubuh, antara lain melalui proses opsonisasi, untuk memudahkan eliminasi kompleks imun oleh sel karier atau makrofag. Kompleks imun akan diikat oleh reseptor komplemen (Complement receptor = C-R) yang terdapat pada permukaan sel karier atau sel makrofag. Pada defisiensi komplemen, eliminasi kompleks imun terhambat, sehingga jumlah kompleks imun menjadi berlebihan dan berada dalam sirkulasi lebih lama.
3. Hormon
Pada individu normal, testosteron berfungsi mensupresi sistem imuns sedangkan estrogen memperkuat sistem imun. Predominan lupus pada wanita dibandingkan pria memperlihatkan adanya pengaruh hormon seks dalam patogenesis lupus. Pada percobaan di tikus dengan pemberian testosteron mengurangi lupus-like syndrome dan pemberian estrogen memperberat penyakit.
4. Lingkungan Pengaruh fisik (sinar matahari), infeksi (bakteri, virus, protozoa), dan obat-obatan dapat mencetuskan atau memperberat penyakit autoimun. Mekanismenya dapat melalui aktivasi sel B poliklonal atau dengan meningkatkan ekspresi MHC kelas I atau II.
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