Allergies, Anaphylaxis, dan Asma

allergi
Dr Budi Enoch SpPD
 Functio
Kalor Rubor Tumor Dolor laesa
 Kata Alergi diajukan pertama kali oleh
seorang sarjana Austria Clement von
Pirquet (1905), berasal dari kata Greek.
 Allos artinya berubah dan Ergos artinya
kerja. Jadi artimya kerja yang berubah
 Alergi adalah suatu gejala atau reaksi
abnormal dari tubuh pada seseorang, bila
kontak dengan suatu zat atau bahan yang
biasanya tidak menimbulkan gejala/reaksi
pada orang normal
(1905 ) YANG BERASAL DARI KATA GREEK
 Atopi / atopos : yang artinya aneh, karena
terdapat berkelompok dalam keluarga dan
diturunkan seperti, asma, rhinitis alergika,
dermatitis atopik
 Bila kedua orang tua atopi, anaknya terkena atopi
sebesar 50 – 75%
 Bila salah satu orang tua atopi, resiko anak
terkena atopi 25 – 50%
The term atopic allergy implies a familial tendency to
manifest such conditions as asthma, rhinitis, urticaria,
and eczematous dermatitis (atopic dermatitis) alone or
in combination, and in association with the presence of
IgE.
However, individuals without an atopic background
may also develop hypersensitivity reactions, particularly
urticaria and anaphylaxis, associated with the presence
of IgE.
Inasmuch as the mast cell is the key effector cell of the
biologic response in allergic rhinitis, urticaria,
anaphylaxis, and systemic mastocytosis, its
developmental biology, activation pathway, product
Th2 T helper
The induction of allergic disease requires sensitization of a predisposed individual
to a specific allergen. The greatest propensity for the development of atopic
allergy occurs in childhood and early adolescence.
The allergen is processed by antigen-presenting cells of the monocytic lineage
located throughout the body at surfaces that contact the outside environment, such
as the nose, lungs, eyes, skin, and intestine. These antigen-presenting cells
present the epitope-bearing peptides via their MHC to T helper cells and
their subsets. The T cell response depends both on cognate recognition and on
the cytokine microenvironment provided by the antigen-presenting dendritic cells,
with IL-4 directing a TH2 subset, interferon (IFN) a TH1 profile, and IL-6 with
transforming growth factor  (TGF) a TH17 subset. Allergens not only present
antigenic epitopes via dendritic cells but also contain pattern recognition ligands
that facilitate the immune response by direct initiation of cytokine generation
from innate cell types such as basophils, mast cells, eosinophils, and others. The
TH2 response is associated with activation of specific B cells that can also present
allergens or that transform into plasma cells for antibody production. Synthesis
and release into the plasma of allergen-specific IgE results in sensitization of
FcR1-bearing cells such as mast cells and basophils, which become activated on
exposure to the specific allergen.
Cara masuk alergen ada 4 macam
 Alergen Inhalan : masuk melalui hirupan seperti
debu, tungau, bulu binatang
 Alergen Ingestan : masuk dengan cara dimakan
atau diminum, seperti susu sapi, telur, ikan dll
 Alergen Injektan : masuk melalui tusukan dikulit,
seperti suntikan obat atau gigitan serangga dan
ikan
 Alergen kontaktan : terjadi melalui kontaqk kulit,
seperti logam nikel, kosmetik dll
beberapa gejala allergi
Anaphylactic reaction
Urticaria and Angioedema
Allergic Rhinitis
Anaphylaxis, reaksi tubuh
yang paling ditakuti
 Treatment anaphylactic reaction
Early recognition of an anaphylactic reaction is mandatory, since death
occurs within minutes to hours after the first symptoms.
Mild symptoms such as pruritus and urticaria can be controlled by
administration of 0.3 to 0.5 mL of 1:1000 (1 mg/mL) epinephrine SC or
IM, with repeated doses as required at 5- to 20-min intervals for a severe
reaction.
If the antigenic material was injected into an extremity, the rate of
absorption may be reduced by prompt application of a tourniquet proximal
to the reaction site, administration of 0.2 mL of 1:1000 epinephrine into the
site, and removal without compression of an insect stinger, if present.
An IV infusion should be initiated to provide a route for administration
of 2.5 mL epinephrine, diluted 1:10,000, at 5- to 10-min intervals, volume
expanders such as normal saline, and vasopressor agents such as
dopamine if intractable hypotension occurs. Replacement of intravascular
volume due to postcapillary venular leakage may require several liters of
saline
Epinephrine provides adrenergic effects, resulting in
vasoconstriction, bronchial smooth-muscle relaxation, and
attenuation of enhanced venular permeability.
When epinephrine fails to control the anaphylactic reaction,
hypoxia due to airway obstruction or related to a cardiac
arrhythmia, or both, must be considered.
Oxygen alone via a nasal catheter or with nebulized albuterol may
be helpful, but either endotracheal intubation or a tracheostomy is
mandatory for oxygen delivery if progressive hypoxia develops.
Ancillary agents such as the antihistamine diphenhydramine, 50-
100 mg IM or IV, and aminophylline, 0.25-0.5 g IV, are
appropriate for urticaria-angioedema and bronchospasm,
respectively.
Intravenous glucocorticoids, 0.5-1 mg/kg of medrol, are not
effective for the acute event but may alleviate later recurrence
of bronchospasm, hypotension, or urticaria
 Definition
 Urticaria and angioedema may appear separately or together
as cutaneous manifestations of localized nonpitting edema; a
similar process may occur at mucosal surfaces of the upper
respiratory or gastrointestinal tract.
 Urticaria involves only the superficial portion of the dermis,
presenting as well-circumscribed wheals with erythematous
raised serpiginous borders and blanched centers that may
coalesce to become giant wheals.
 Angioedema is a well-demarcated localized edema involving
the deeper layers of the skin, including the subcutaneous
tissue. Recurrent episodes of urticaria and/or angioedema of
less than 6 weeks' duration are considered acute, whereas
attacks persisting beyond this period are designated chronic.
 Wheal and Flare
Flare Wheal Flare

vasodilatation & activated

leakage of plasma congestion mast cell
fluid and protein
(edema)

vasodilatation at vasodilatation at
edge of lession edge of lession
Abbas ea, Cellular & Molecular Immunology, W B Saunders, 4 th ed, 2000 : 427
 Predisposing Factors and Etiology
Urticaria and angioedema probably occur more frequently
than usually described because of the evanescent, self-
limited nature of such eruptions, which seldom require
medical attention when limited to the skin.
Although persons in any age group may experience acute
or chronic urticaria and/or angioedema, these lesions
increase in frequency after adolescence, with the highest
incidence occurring in persons in the third decade of life;
indeed, one survey of college students indicated that 15-
20% had experienced a pruritic wheal reaction.
The classification of urticaria-angioedema presented in
Table 317-1 focuses on the different mechanisms for
eliciting clinical disease and can be useful for differential
diagnosis; nonetheless, most cases of chronic urticaria are
idiopathic.
Urticaria and/or angioedema occurring during the
appropriate season in patients with seasonal respiratory
allergy or as a result of exposure to animals or molds is
attributed to inhalation or physical contact with pollens,
animal dander, and mold spores, respectively.
However, urticaria and angioedema secondary to
inhalation are relatively uncommon compared to urticaria
and angioedema elicited by ingestion of fresh fruits,
shellfish, fish, milk products, chocolate, legumes including
peanuts, and various drugs that may elicit not only the
 Additional etiologies include physical stimuli such as cold, heat, solar rays, exercise, and
mechanical irritation. The physical urticarias can be distinguished by the precipitating event
and other aspects of the clinical presentation.
 Dermographism, which occurs in 1-4% of the population, is defined by the appearance of a
linear wheal at the site of a brisk stroke with a firm object or by any configuration appropriate
to the eliciting event (Fig. 317-3). Dermographism has a prevalence that peaks in the second
to third decades. It is not influenced by an atopic diathesis and has a duration generally of <5
years.
 Pressure urticaria, which often accompanies chronic idiopathic urticaria, presents in response
to a sustained stimulus such as a shoulder strap or belt, running (feet), or manual labor
(hands).
 Cholinergic urticaria is distinctive in that the pruritic wheals are of small size (1-2 mm) and
are surrounded by a large area of erythema; attacks are precipitated by fever, a hot bath or
shower, or exercise and are presumptively attributed to a rise in core body temperature.
 Exercise-related anaphylaxis can be precipitated by exertion alone or can be dependent on
prior food ingestion. The clinical presentation can be limited to flushing, erythema, and
pruritic urticaria but may progress to angioedema of the face, oropharynx, larynx, or intestine
or to vascular collapse; it is distinguished from cholinergic urticaria by presenting with wheals
of conventional size and by not occurring with fever or a hot bath.
 Cold urticaria is local at body areas exposed to low ambient temperature or cold objects (ice
cube) but can progress to vascular collapse with immersion in cold water (swimming).
 Solar urticaria is subdivided into six groups by the response to specific portions of the light
 Pathophysiology and Manifestations
Urticarial eruptions are distinctly pruritic, may involve any area of the body
from the scalp to the soles of the feet, and appear in crops of 12- to 36-hour
duration, with old lesions fading as new ones appear. Most of the physical
urticarias (cold, cholinergic, dermatographism) are an exception, with individual
lesions lasting less than 2 hours. The most common sites for urticaria are the
extremities and face, with angioedema often being periorbital and in the
lips. Although self-limited in duration, angioedema of the upper respiratory tract
may be life-threatening due to laryngeal obstruction, while gastrointestinal
involvement may present with abdominal colic, with or without nausea and
vomiting, and may result in unnecessary surgical intervention. No residual
discoloration occurs with either urticaria or angioedema unless there is an
underlying process leading to superimposed extravasation of erythrocytes.
The pathology is characterized by edema of the superficial dermis in urticaria
and of the subcutaneous tissue and deep dermis in angioedema. Collagen
bundles in affected areas are widely separated, and the venules are sometimes
dilated. Any perivenular infiltrate consists of lymphocytes, monocytes,
eosinophils, and neutrophils that are present in varying combination and
numbers.
Perhaps the best-studied example of IgE- and mast cell-mediated urticaria and angioedema
is cold urticaria.
Cryoglobulins or cold agglutinins may be recognized in up to 5% of these patients.
Immersion of an extremity in an ice bath precipitates angioedema of the distal portion
with urticaria at the air interface within minutes of the challenge.
Histologic studies reveal marked mast cell degranulation with associated edema of the
dermis and subcutaneous tissues. The histamine level in the plasma of venous effluent of
the cold-challenged and angioedematous extremity is markedly increased, but no such
increase appears in the plasma of effluent of the contralateral normal extremity. Elevated
levels of histamine have been found in the plasma of venous effluent and in the fluid of
suction blisters at experimentally induced lesional sites in patients with dermographism,
pressure urticaria, vibratory angioedema, light urticaria, and heat urticaria.
By ultrastructural analysis, the pattern of mast cell degranulation in cold urticaria
resembles an IgE-mediated response with solubilization of granule contents, fusion of the
perigranular and cell membranes, and discharge of granule contents, whereas in a
dermographic lesion there is additional superimposed zonal (piecemeal) degranulation.
Elevations of plasma histamine levels with biopsy-proven mast cell degranulation have
also been demonstrated with generalized attacks of cholinergic urticaria and exercise-
related anaphylaxis precipitated experimentally in subjects exercising on a treadmill while
wearing a wet suit; however, only subjects with cholinergic urticaria have a concomitant
decrease in pulmonary function.
 Diagnosis
The rapid onset and self-limited nature of urticarial and
angioedematous eruptions are distinguishing features.
Additional characteristics are the occurrence of the urticarial crops in
various stages of evolution and the asymmetric distribution of the
angioedema. Urticaria and/or angioedema involving IgE-dependent
mechanisms are often appreciated by historic considerations
implicating specific allergens or physical stimuli, by seasonal
incidence, and by exposure to certain environments.
Direct reproduction of the lesion with physical stimuli is particularly
valuable because it so often establishes the cause of the lesion. The
diagnosis of an environmental allergen based on the clinical history can
be confirmed by skin testing or assay for allergen-specific IgE in
serum. IgE-mediated urticaria and/or angioedema may or may not be
associated with an elevation of total IgE or with peripheral
eosinophilia. Fever, leukocytosis, and an elevated sedimentation rate
are absent.
Urticaria and angioedema can be differentiated from contact
sensitivity, a vesicular eruption that progresses to chronic
thickening of the skin with continued allergenic exposure.
They can also be differentiated from atopic dermatitis, a condition
that may present as erythema, edema, papules, vesiculation, and
oozing proceeding to a subacute and chronic stage in which
vesiculation is less marked or absent and scaling, fissuring, and
lichenification predominate in a distribution that characteristically
involves the flexor surfaces. In cutaneous mastocytosis, the reddish
brown macules and papules, characteristic of urticaria pigmentosa,
urticate with pruritus upon trauma; and in systemic mastocytosis,
without or with urticaria pigmentosa, there is episodic systemic
flushing with or without urtication but no angioedema.
 Treatment
Identification of the etiologic factor(s) and subsequent elimination provide
the most satisfactory therapeutic program; this approach is feasible to
varying degrees with IgE-mediated reactions to allergens or physical
stimuli.
For most forms of urticaria, H 1 antihistamines such as chlorpheniramine
or diphenhydramine effectively attenuate both urtication and pruritus, but
because of their side effects, nonsedating agents such as loratadine,
desloratadine, and fexofenadine, or low-sedating agents such as cetirizine
or levocetirizine generally are used first.
Cyproheptadine in dosages beginning at 8 mg and ranging up to 32 mg
daily and especially hydroxyzine in dosages beginning at 40 mg and
ranging up to 200 mg daily have proven effective when H 1 antihistamines
fail. The addition of an H2 antagonist such as cimetidine, ranitidine, or
famotidine in conventional dosages may add benefit when H 1 antihistamines
are inadequate. Doxepin, a dibenzoxepin tricyclic compound with both H 1
and H2 receptor antagonist activity, is yet another alternative
Allergic Rhinitis
 Hubungan Mediator Alergik dengan Gejala Rinitis Alergik

Aktivasi Mediator Jaringan Respon

sel mast alergi target fisiologis

Histamin Saraf Bersin

Lekotrin Pembuluh darah Kongesti
Antigen + Prostaglandin
sel mast Kinin Kelenjar mukus Rinore
Tromboksan Leukosit Inflamasi
 Definition
Allergic rhinitis is characterized by sneezing;
rhinorrhea; obstruction of the nasal passages;
conjunctival, nasal, and pharyngeal itching; and
lacrimation, all occurring in a temporal relationship to
allergen exposure.
Although commonly seasonal due to elicitation by
airborne pollens, it can be perennial in an environment
of chronic exposure.
In North America, the incidence of allergic rhinitis is
about 7%. The overall prevalence in North America is
nearly 20%, with the peak prevalence of nearly 40%
occurring in childhood and adolescence.
 Predisposing Factors and Etiology
Allergic rhinitis generally occurs in atopic individuals, i.e., in
persons with a family history of a similar or related symptom
complex and a personal history of collateral allergy expressed
as eczematous dermatitis, urticaria, and/or asthma.
Up to 40% of patients with rhinitis manifest asthma, whereas
70% of individuals with asthma experience rhinitis.
Symptoms generally appear before the fourth decade of life
and tend to diminish gradually with aging, although complete
spontaneous remissions are uncommon. A relatively small
number of weeds that depend on wind rather than insects for
cross-pollination, as well as grasses and some trees, produce
sufficient quantities of pollen suitable for wide distribution by
air currents to elicit seasonal allergic rhinitis
The dates of pollination of these species generally vary little from year
to year in a particular locale but may be quite different in another
climate. In the temperate areas of North America, trees typically
pollinate from March through May, grasses in June and early July, and
ragweed from mid-August to early October.
Molds, which are widespread in nature because they occur in soil or
decaying organic matter, may propagate spores in a pattern that
depends on climatic conditions. Perennial allergic rhinitis occurs in
response to allergens that are present throughout the year, including
desquamating epithelium in animal dander, cockroach-derived
proteins, mold spores, or dust, which has mites such as
Dermatophagoides farinae and D. pteronyssinus.
Dust mites are scavengers of flecks of human skin and coat the
digestate with mite-specific protein for excretion. In up to one-half of
patients with perennial rhinitis, no clear-cut allergen can be
demonstrated as causative. The ability of allergens to cause rhinitis
rather than lower respiratory tract symptoms may be attributed to their
large size, 10-100 m, and retention within the nose.
 Pathophysiology and Manifestations
Episodic rhinorrhea, sneezing, obstruction of the nasal passages
with lacrimation, and pruritus of the conjunctiva, nasal mucosa,
and oropharynx are the hallmarks of allergic rhinitis. The nasal
mucosa is pale and boggy, the conjunctiva congested and
edematous, and the pharynx generally unremarkable.
Swelling of the turbinates and mucous membranes with obstruction
of the sinus ostia and eustachian tubes precipitates secondary
infections of the sinuses and middle ear, respectively.
Nasal polyps, representing mucosal protrusions containing edema
fluid with variable numbers of eosinophils, can increase
obstructive symptoms and can concurrently arise within the
nasopharynx or sinuses. Nasal polyps may occur independent of
allergic rhinitis in patients with the aspirin-intolerant triad of
rhinosinusitis and asthma and in patients with chronic
staphylococcal colonization, which produces superantigens leading
 Perjalanan Alamiah Rinitis Alergik
FA SE 2
K E A D A A N K L IN IK

IN F L A M A S I IN F L A M A S I
S e l p e n y a ji AW AL LA N J U T
A le r g e n
a n t ig e n

A le r g e n
R E S O LU S I
R e a k s i fa s e
Ig E la m b a t
A le rg e n
O la h a n Ab IN F ILTR A S I H IP E R E S P O N S IF K O M P L IK A S I
SEL
C D4 P R IM IN G
Se l B
se l T
M a s t o s it E o s in o f il P E N Y A K IT
B a s o f il IR R E V E R S IB L E
M o n o s it
L im f o s it
P e m b u lu h S a ra f
d a ra h k e le n ja r

S e l p la s m a A b Ig E B e rs in
R in o re
Te rs u m b a t

Sumber: Naclerio RM. N Eng J Med 1991;325:860-9

 Sel mast Gejala konjungtivitis
YY Histamin Mata gatal
Lekotrin Kemerahan

YY
Prostaglandin Keluar air mata
Y Bradikinin, PAF
Y
IgE
Gejala rinitis segera
Alergen Limfosit B Hidung gatal
Bersin, berair,
Hidung tersumbat
ICAM
IL-4

MBP Gejala rinitis kronik

Limfosit T EPO
Hidung tersumbat kronik
IL-3, IL-5 ECP Penciuman berkurang
GM-CSF eosinofil Hidung hipereaktif

Patofisiologi dari rinitis alergik dan konjungtivitis

 Diagnosis
The diagnosis of seasonal allergic rhinitis depends
largely on an accurate history of occurrence coincident
with the pollination of the offending weeds, grasses, or
trees.
The continuous character of perennial allergic rhinitis
due to contamination of the home or place of work
makes historic analysis difficult, but there may be a
variability in symptoms that can be related to exposure
to animal dander, dust mite and/or cockroach allergens,
fungal spores, or work-related allergens such as latex.
Patients with perennial rhinitis commonly develop the
problem in adult life, and manifest nasal congestion and
a postnasal discharge, often associated with thickening
The nasal secretions of allergic patients are rich in eosinophils, and a
modest peripheral eosinophilia is a common feature.
Local or systemic neutrophilia implies infection. Total serum IgE is
frequently elevated, but the demonstration of immunologic specificity for
IgE is critical to an etiologic diagnosis. A skin test by the intracutaneous
route (puncture or prick) with the allergens of interest provides a rapid and
reliable approach to identifying allergen-specific IgE that has sensitized
cutaneous mast cells.
A positive intracutaneous skin test with 1:10-1:20 weight/volume of extract
has a high predictive value for the presence of allergy. An intradermal test
with a 1:500-1:1000 dilution of 0.05 mL may follow if indicated by history
when the intracutaneous test is negative, but while more sensitive, it is less
reliable due to the reactivity of some asymptomatic individuals at the test
dose. Skin testing by the intracutaneous route for food allergens can be
supportive of the clinical history. A double-blind, placebo-controlled
challenge may document a food allergy, but such a procedure does bear the
risk of an anaphylactic reaction. An elimination diet is safer but is tedious
and less definitive. Food allergy is uncommon as a cause of allergic
rhinitis.
 ASMA ALERGI
ASMA HANYA MENYERANG MEREKA YANG MEMILIKI
SALURAN NAPAS YANG HIPERREAKTIVITAS

HIPERREAKTIVITAS TERSEBUT ( BERMULA DARI FAKTOR

KETURUNAN ), DENGAN PENGARUH FAKTOR-FAKTOR
TERTENTU, BAIK NON-SPESIFIK MAUPUN SPESIFIK, DAPAT
MENIMBULKAN ASMA

FAKTOR-FAKTOR NON-SPESIFIK : DEBU KAPUR, ASAP

ROKOK
DINGIN, KABUT, TEGANG DAN EMOSI

FAKTOR-FAKTOR SPESIFIK : POLLEN, BULU HEWAN, DEBU

RUMAH, RACUN SERANGGA, ATAU ALERGEN LAIN
GEJALA ASMA :
TERDIRI DARI BEBERAPA GEJALA DAN YANG UTAMA
ADALAH SESAK, DAPAT BERUPA MENGI, SESAK MALAM,
SESAK WAKTU MENJALANKAN LATIHAN JASMANI ATAU
BATUK KRONIK.
BILA TERJADI SERANGAN, SALURAN NAPAS MENYEMPIT
OLEH KARENA :
1. SPASME (KONTRAKSI) OTOT POLOS DARI SALURAN
NAPAS.
2. EDEMA YAITU TERKUMPULNYA CAIRAN DISELAPUT
LENDIR SALURAN NAPAS.
3. PRODUKSI MUKUS/LENDIR YANG BERLEBIHAN (TEBAL
DAN PEKAT) OLEH KELENJAR SALURAN NAPAS.

Ke 3 faktor tersebut akan mempersempit saluran napas dan

mengganggu aliran udara melalui saluran napas
pemberian kortikosteroid
Kortikosteroid
Kortikosteroid

Terdiri atas
Kortikosteroid Kortikosteroid
adalah Alami dan
Hormon Buatan
(sintetik)

Kortikosteroid Fungsi
Alami diproduksi utamanya
di Kelenjar
Adrenal,
adalah Anti
tepatnya bagian Inflamasi dan
Korteks (kulit) Imunosupresan
 Kortikosteroid Sintetik
 Kortikosteroid Sintetik tidak dihasilkan oleh tubuh, tetapi hasil sintesis kimia dalam
bentuk obat
 Efek Kortikosteroid Sintetik serupa dengan Kortikosteroid Alami tubuh
 Kortikosteroid Sintetik dikelompokkan berdasarkan Lama Kerjanya

Keterangan Lama Kerja (jam) Contoh Kortikosteroid

Short Acting 8-12 Hydrocortisone, Cortisone
Intermediate Acting 12-36 Prednison, Prednisolon,
Metilprednisolon, Triamsinolon
Long Acting 36-54 Paramethasone, Dexamethasone,
Betamethasone
 FLAMICORT
(Triamcinolone)
 Merupakan kortikosteroid masa
kerja sedang (intermediate-
action) dengan efek
antiinflamasi yang kuat
 Mekanisme kerja:
antiinflamasi, antialergi, dan
imunosupresan
 Dosis: 4-48 mg per hari, terbagi
dalam beberapa dosis
 Terapi kronis: Dapat digunakan
secara alternate day
therapy/each other day (EOD)
 Efek supresi HPA Axis
 Indikasi:
Penyakit Inflamasi

DERMATITIS ASMA ARTHRITIS INFEKSI

Inflamasi yang Inflamasi Inflamasi pada Misalnya ISPA :
terjadi pada terjadi pada persendian, Faringitis dan
Kulit Bronkus jika sendi Laringitis ada
sehingga digerakkan inflamasinya
menyebabkan akan nyeri Jika disenter
dada menjadi luar biasa bagian dalam
sesak / nyeri akan berwarna
merah
Mekanisme Anti Radang Kortikosteroid

enzim siklookdigenase (COX)

Radang

Adanya Kortikosteroid menghambat enzim Phospholipase A2 sehingga jalur pembentukan Mediator

(penyebab) Inflamasi menjadi tidak terbentuk
 Indikasi:
Penyakit Alergi

URTIKARIA dan RHINITIS ALERGI INFEKSI

DERMATITIS Alergi terjadi Kasus Infeksi juga
ALERGI pada Hidung. disertai Alergi
Alergi yang Hidung menjadi Misalnya pada
terjadi pada Kulit. kemerahan, gatal Faringitis disertai
Biasa disebut dan berair tenggorokan amat
Eksim atau gatal
Biduran
 Mekanisme Anti Alergi Kortikosteroid

x
x

x
KORTIKOSTEROID
x
Anti alergi :
Inhibisi Aktivasi limfosit B  Mengurangi konsentrasi immunoglobulin E 
mengurangi pelekatan Ig E dengan sel mast  mengurangi pelepasan
mediator alergi seperti Histamin
KORTIKOSTEROID JANGKA
LAMA: SUPRESI HPA AXIS
Penggunaan kortikosteroid dosis besar dalam jangka waktu yang lama
dapat menimbulkan efek supresi HPA axis.
• Tubuh menjadi “malas” memproduksi kortikosteroid sendiri
(alami) karena disuplai terus dari luar (sintetik)
• Ketika suplai berhenti tiba-tiba, tubuh menjadi “kaget” dan timbul
withdrawal syndrome - gejala kekurangan kortikosteroid,
seperti kejang, menggigil, cemas dan gelisah, depresi, dll
• Memproduksi Kortikosteroid butuh waktu yang tidak singkat
Menekan Supresi HPA Axis

Feed
back (-)

Feed
back (-)
 KESIMPULAN
Kortikosteroid adalah hormon yang diproduksi oleh
tubuh (alami) dan buatan (sintetik).
Kortikosteroid sintetik tidak diproduksi tubuh dan
perlu asupan dari luar, seperti triamsinolon
(Flamicort).
Kortikosteroid digunakan sebagai antiradang,
antialergi, dan imunosupresan.
Flamicort merupakan kortikosteroid dengan durasi
kerja sedang yang minimal efek samping dengan
penggunaan yang tepat (tapering).
TERIMA KASIH