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 profile, and target tissues will be considered
in the introduction to these clinical disorders.
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, WB Saunders, 4th 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 anaphylactic syndrome with prominent
gastrointestinal complaints but also chronic urticaria.
 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 spectrum.
Vibratory angioedema may occur after years of occupational exposure or can be idiopathic; it may be
accompanied by cholinergic urticaria.
 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, H1 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 H1 antihistamines fail. The
addition of an H2 antagonist such as cimetidine, ranitidine, or famotidine in
conventional dosages may add benefit when H1 antihistamines are
inadequate. Doxepin, a dibenzoxepin tricyclic compound with both H1 and
H2 receptor antagonist activity, is yet another alternative
Allergic Rhinitis
 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 to an intense TH2 inflammatory
response.
 Perjalanan Alamiah Rinitis Alergik
FASE 2
KEADAAN KLINIK

INFLAMASI INFLAMASI
Sel penyaji AWAL LANJUT
Alergen
antigen

Alergen
RESOLUSI
Reaksi fase
IgE lambat
Alergen
Ab INFILTRASI HIPERESPONSIF KOMPLIKASI
Olahan
SEL
CD4 PRIMING
Sel B
sel T
Mastosit Eosinofil PENYAKIT
Basofil IRREVERSIBLE
Monosit
Limfosit
Pembuluh Saraf
darah kelenjar

Sel plasma Ab IgE Bersin

Rinore
Tersum bat

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

 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 of the sinus
membranes demonstrated by radiography.
 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
Alami dan
adalah 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
minimal
 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