Содержание

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Allergy definition Type of hypersensitivity reactions of the immune system. may

Allergy definition

Type of hypersensitivity reactions of the immune system.
may involve more

than one type of reaction.
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Important factors Host factors; heredity, gender, race, and age. Environmental factor;

Important factors

Host factors; heredity, gender, race, and age.
Environmental factor; infectious diseases during early

childhood, environmental pollution, allergen levels and dietary changes.
Site specific factors (peculiarities of the local receptors)
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Gel and Coombs classification of hypersensitivities Type I -immediate hypersensitivity -

Gel and Coombs classification of hypersensitivities

Type I -immediate hypersensitivity - IgE-mediated.


Type II - antibody-dependent cytotoxic hypersensitivity ( with participation of natural killer cells, eosinophils, macrophages), complement
Type III - immune complex disease) - circulating antigen-antibody immune complexes deposited in vessels or tissue
Type IV - delayed hypersensitivity - T-cell–mediated;
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Gel and Coombs classification of hypersensitivities.

Gel and Coombs classification of hypersensitivities.

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Sell et al. classification Inactivation/activation antibody reactions Cytotoxic or cytolytic antibody

Sell et al. classification

Inactivation/activation antibody reactions
Cytotoxic or cytolytic antibody reactions
Immune-complex

reactions
Allergic reactions
T-cell cytotoxic reactions
Delayed hypersensitivity reactions
Granulomatous reactions

Immediate Hypersensitivity Reactions
Updated: Feb 09, 2015 
Author: Becky Buelow, MD, MS; Chief Editor: Michael A Kaliner, MD  more...
https://emedicine.medscape.com/article/136217-overview

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Pathogenesis Allegren processing and presenting peptides from allergens on MHCII class:

Pathogenesis

Allegren processing and presenting peptides from allergens on MHCII class: dendritic

cells in mucosal surface
MHC class II molecule+antigen complex: ligand of T-cell receptors on Naive CD4+ T cells
Naive CD4+ T cells differentiation to allergen-specific Th2 cell
Th2 cells: cytokines, promoting isotype switching of B cells to produce specific IgE and proliferation of eosinophils, mast cells and neutrophils
Produced antigen-specific IgE binds to high-affinity IgE receptors on mast cells or basophils.
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I

I

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Type I Antigen binds to IgE bound to tissue mast cells

Type I

Antigen binds to IgE bound to tissue mast cells and

blood basophils
release of preformed mediators (histamine, proteases, chemotactic factors)
synthesis of other mediators (prostaglandins, leukotrienes, platelet-activating factor, cytokines).
mediators cause vasodilation, increased capillary permeability, mucus hypersecretion, smooth muscle spasm, and tissue infiltration with eosinophils, type 2 helper T (TH2) cells, and other inflammatory cells.
atopic disorders (allergic asthma, rhinitis, conjunctivitis), anaphylaxis, some cases of angioedema, urticaria, and latex and some food allergies. Type I reactions develop < 1 h after exposure to antigen.
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Main mediators: Pre-existing Histamine (H1, H2 receptors): smooth muscles contraction in

Main mediators: Pre-existing

Histamine (H1, H2 receptors): smooth muscles contraction in airways

and GI, vasodilation and leakage (incl.skin), increased mucus production, itching
Tryptase: released by mast cells; cleave C3, C3a, airways remodeling
Proteoglycans: inclheparin and chondroitin sulfate
Chemotactic factors:
eosinophilic chemotactic factor of anaphylaxis - Eos chemotaxis
inflammatory factor of anaphylaxis - neutrophil chemotaxis
major basic protein (released by Eos)
THIUS - tissue damage in the later phases of allergic reactions.
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Main mediators: newly synthesized Leucotriens: B4 (Neutrophils, vessels permeability); C4, D4

Main mediators: newly synthesized

Leucotriens: B4 (Neutrophils, vessels permeability); C4, D4 –

bronchoconstriction, vessels permeability, arteriolar constriction; E4 bronchial responsiveness; vascular permeability
Prostaglandins: bronchoconstriction, peripheral vasodilation, coronary vasoconstriction; D2 also pulmonary artery constriction, increase of histamine release
Thromboxane A2 – broncho- and vasoconstriction, platelet aggregation
Platelet-activating factor (PAF): bronchoconstriction, increases vascular permeability, causes, eosinophils and neutrophils chemotaxis and degranulation
Adenosine: bronchoconstrictor, potentiates IgE-induced mast cell mediator release.
Cytokines: IL-4 (maintains TH2 cell proliferation, B cells switch to IgE synthesis); IL-5 - maturation, chemotaxis, activation, and survival of eosinophils. primes basophils for histamine and leukotriene release; IL-6 (mucus production) IL-13 (same effects as IL-4)
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Type II antibody-dependent cytotoxic hypersensitivity antibody binds to cell surface antigens

Type II antibody-dependent cytotoxic hypersensitivity

antibody binds to cell surface antigens or

to a molecule coupled to a cell surface.
antigen-antibody complex activates cells that participate in antibody-dependent cell-mediated cytotoxicity (natural killer cells, eosinophils, macrophages), complement, or both.
hyperacute graft rejection of an organ transplant, Coombs-positive hemolytic anemias, Hashimoto thyroiditis, and anti–glomerular basement membrane disease (eg, Goodpasture syndrome)
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Type III reactions (immune complex disease) circulating antigen-antibody immune complexes deposited

Type III reactions (immune complex disease)

circulating antigen-antibody immune complexes deposited

in vessels or tissue.
activate the complement system or bind to and activate certain immune cells, resulting in release of inflammatory mediators.
immune complexes deposite in various tissues ( glomeruli, blood vessels)
isotype of induced antibodies changes, and glycosylation, size, and charge of the complex’s components contribute to the clinical response.
serum sickness, SLE, RA, leukocytoclastic vasculitis, cryoglobulinemia, hypersensitivity pneumonitis, and several types of glomerulonephritis.
develop 4 to 10 days after exposure to antigen and, if exposure to the antigen continues, can become chronic.
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Type IV reactions (delayed hypersensitivity) T cells, sensitized after contact with

Type IV reactions (delayed hypersensitivity)

T cells, sensitized after contact with

a specific antigen, are activated by reexposure to the antigen
tissue damage by direct toxic effects/cytokines release
Activation of eosinophils, monocytes and macrophages, neutrophils, or natural killer cells.
contact dermatitis (poison ivy), hypersensitivity pneumonitis, allograft rejection, immune response to TB, and many forms of drug hypersensitivity.
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Type I: Atopic and Allergic Disorders Allergy: is any abnormal immune

Type I: Atopic and Allergic Disorders

Allergy:  is any abnormal immune response

to a foreign antigen regardless of mechanism.
Atopy: IgE-mediated abnormal immune response; all atopic disorders are type I hypersensitivity disorders.
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Spectrum of atopic diseases Nose - allergic rhinitis Eyes - allergic

Spectrum of atopic diseases

Nose - allergic rhinitis
Eyes - allergic conjunctivitis
Skin: extrinsic

atopic dermatitis, immune-mediated urticaria, immune-mediated angioedema, acute latex allergy
Bronchi and lungs: (some cases of asthma, IgE-mediated components of allergic bronchopulmonary aspergillosis)
allergic reactions to venomous stings
Systemic: anaphylaxy, hay fever
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Latex Sensitivity Abnormal immune response to water-soluble proteins in latex products

Latex Sensitivity

Abnormal immune response to water-soluble proteins in latex products (rubber

gloves, dental dams, condoms, tubing for respiratory equipment, catheters, enema tips with inflatable latex cuffs)
acute (IgE-mediated)/delayed (cell-mediated).
Acute: urticaria, anaphylaxis
Delayed: dermatitis.
Skin may be irritated and crusted - not allergy, usually chemical irritation
Diagnosis: history; assays for detecting IgE antilatex antibodies are available; skin testing is available in Europe and Canada, but not routinely in the US.
Treatment: avoidance of latex, latex-free gloves
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Etiology: multifactorial Environment Genetic Site specific

Etiology: multifactorial

Environment
Genetic
Site specific

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Genetic: familial inheritance association between atopy and HLA loci (peptides promoting

Genetic:

familial inheritance
association between atopy and HLA loci (peptides promoting Th2

response).
polymorphisms of genes: for the high-affinity IgE receptor β-chain, IL-4 receptor α-chain, IL-4, IL-13, CD14, dipeptidyl-peptidase 10 (DPP10), and a disintegrin and metalloprotease domain 33 ( ADAM33 ).
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Environmental factors: Allergens Proteins: serum, vaccines Pollen: rye grass, timothy grass,

Environmental factors: Allergens

Proteins: serum, vaccines
Pollen: rye grass, timothy grass, birch trees,

ragweed and lots…
Food: nuts, seafood, eggs, peas, beans, citrus, apples (not green), honey, milk, chocolate, grapes, peaches, nuts, tomatoes…
Epidermal: epidermis of cats, dogs, horses etc
Drugs: penicillin, sulfonamides etc (adverse reactions are not allergy), sometimes even glucocorticosteroids
Insect products (bee, wasp, ant venoms, cocroach calyx, house dist mites etc)
Mold spores
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Environmental factors and Th2 reponce Environmental factors interact with genetic ones

Environmental factors and Th2 reponce

Environmental factors interact with genetic ones to maintain

type 2 helper T (TH2) response
TH2 cells activate eosinophils, promote IgE production, and are proallergic
Late exposure to indoor and outdoor environmental factors in infants
chronic allergen exposure and sensitization
Diet
environmental pollutants.
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Late exposure to indoor and outdoor environmental factors in infants early

Late exposure to indoor and outdoor environmental factors in infants

early childhood

exposure to bacterial and viral infections and endotoxins (lipopolysaccharide etc) shifts TH2-cell responses to TH1–cell responses and suppression of TH2 mediated reactions.
This is mediated by regulatory T (CD4+CD25+Foxp3+; Treg) cells (capable of suppressing TH2-cell responses) and IL-12–secreting dendritic cells (drive TH1-cell responses)
Trends to smaller families, fewer children, cleaner indoor environments, early use of antibiotics may limit children's exposure to the infectious agents/decrease shift to predominantly TH1-cell response
Because of this - increased prevalence of some allergic disorders.
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Indian Journal of Allergy, Asthma and Immunology | Jan-Jun 2013 @BULLET

Indian Journal of Allergy, Asthma and Immunology | Jan-Jun 2013 @BULLET

Volume 27 @BULLET Issue 1 Allergen immunotherapy: Basic concepts
Article
Jan 2013
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Site-specific factors adhesion molecules in bronchial epithelium/ skin molecules in the

Site-specific factors

 adhesion molecules in bronchial epithelium/ skin
molecules in the GI

tract that direct TH2 cells to target tissues.
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Pathophysiology Mast cells are widely distributed but are most concentrated in

Pathophysiology

Mast cells are widely distributed but are most concentrated in skin,

lungs, and GI mucosa
Allergen + IgE-sensitized mast cells/ basophils
Histamine release from intracellular granules
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Phases of allergic reaction (on example of atopic asthma) TRENDS IN

Phases of allergic reaction (on example of atopic asthma)

TRENDS IN IMMUNOLOGY

OPINION| VOLUME 22, ISSUE 7, P372-377, JULY 01, 2001
Th2 responses without atopy: immunoregulation in chronic helminth infections and reduced allergic disease
Maria Yazdanbakhsh Anita van den Biggelaar Rick M Maizels
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Immediate Hypersensitivity Reactions Updated: Feb 09, 2015 Author: Becky Buelow, MD,

Immediate Hypersensitivity Reactions
Updated: Feb 09, 2015 
Author: Becky Buelow, MD, MS; Chief

Editor: Michael A Kaliner, MD  more...
https://emedicine.medscape.com/article/136217-overview
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Other than histamin mediators pre-formed in mast cells granules Cytokines TNF-α,

Other than histamin mediators pre-formed in mast cells granules

Cytokines TNF-α,

IL-1, IL-6.
Chemoattractants for Neutrophils and Eosinophils.
Enzymes
tryptase, chymase, cathepsin.
Changes in connective tissue matrix, tissue breakdown.
Leukotrienes
Prostaglandins
Th2 cytokines- IL-4, IL-5, IL-13, GM-CSF
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Histamine effects Local vasodilation (causing erythema) Increased capillary permeability and edema

Histamine effects

Local vasodilation (causing erythema)
Increased capillary permeability and edema (producing a

wheal)
Vasodilation of surrounding arterioles mediated by neuronal reflex mechanisms (causing flare—the redness around a wheal)
Stimulation of sensory nerves (causing itching)
Smooth muscle contraction in the airways (bronchoconstriction) and in the GI tract (increasing GI motility)
Increased nasal, salivary, and bronchial gland secretions
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Frequent histamine release: potent arteriolar dilator causes extensive peripheral pooling of

Frequent histamine release:

potent arteriolar dilator
causes extensive peripheral pooling of blood and

hypotension
cerebral vasodilation - factor in vascular headache.
loss of plasma and plasma proteins from the vascular space which worsens circulatory shock.
this loss triggers a compensatory catecholamine response
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Non-specific/non-allergic histamin liberation physical disruption of tissue and various substances (tissue

Non-specific/non-allergic histamin liberation

physical disruption of tissue and various substances (tissue irritants,

opiates, surface-active agents, complement components C3a and C5a) can trigger histamine release directly, independent of IgE
This causes pseudoallergic symptoms
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Continuation of sensitization cycle Eosinophils Eosinophils play key role in late

Continuation of sensitization cycle Eosinophils

Eosinophils play key role in late phase reaction.


Eosinophils make
enzymes,
cytokines (IL-3, IL-5, GM-CSF),
Lipid mediators (LTC4, LTD4, PAF)
Eosinophils can provide CD40L and IL-4 for B cell activation.
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Types of allergens Pollen Dust Epidermal Food Drugs Insect – venom, cocroaches etc Latex

Types of allergens

Pollen
Dust
Epidermal
Food
Drugs
Insect – venom, cocroaches etc
Latex

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Pollen Canada (shortened) Moote, W., Kim, H. Allergen-specific immunotherapy. All Asth

Pollen Canada (shortened)

Moote, W., Kim, H. Allergen-specific immunotherapy. All Asth Clin Immun 7, S5

(2011). https://doi.org/10.1186/1710-1492-7-S1-S5
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Common symptoms upper respiratory tract: rhinorrhea, sneezing, and nasal congestion, itching,

Common symptoms

upper respiratory tract: rhinorrhea, sneezing, and nasal congestion, itching,

nasal turbinate edema, sinus pain during palpation
lower respiratory tract: wheezing, dyspnea, stridor (in severe cases)
Skin: itching, urticaria, angioedema, dermatitis, and skin lichenification
Eyes: itching, conjunctival hyperemia and edema.
Systemic: fever (hay fever), hypotension and shock (in anaphylaxis)
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Diagnosis Clinical evaluation CBC serum IgE levels skin testing and allergen-specific

Diagnosis

Clinical evaluation
CBC
serum IgE levels
skin testing and allergen-specific serum IgE testing

(specific tests)
Rarely provocative testing
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Clinical evaluation frequency and duration of attacks and changes over time

Clinical evaluation

frequency and duration of attacks and changes over time
Identification of

triggering factors
Relation to seasonal or situational settings (predictably occurring during pollen seasons; after exposure to animals, hay, or dust; during exercise; or in particular places)
Family history of similar symptoms or of atopic disorders
Responses to attempted treatments
Age at onset: childhood asthma is likely to be atopic and asthma beginning after age 30 is not.
Professional anamnesis: latex products, other allergens
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Allergologic anamnesis 1. Allergic diseases in case history: asthma, pollinosis, urticaria,

Allergologic anamnesis

1. Allergic diseases in case history: asthma, pollinosis, urticaria, quincjedema,

migraine, exema, allertic rhinitis, allergic dermattis etc, other allertic skin diseases, drug allergy, serim diseases (date and manifestations)
2. Allergic diseases in relatives in past and nowadays а) father/relatives
б) mother/relatives
г) children
4. Serum reaction and vaccination reaction (what/when)
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5. Drug reaction (what/when) ; anaphylactic shock, urticaria, quickedema, bronchospasm, dermatites

5. Drug reaction (what/when) ; anaphylactic shock, urticaria, quickedema, bronchospasm, dermatites

of different types, itching, allergic rhinitis, conqunctivitis (dates, type of reaction)
5.1. antibiotics: pelicillines
Aminoglycosides
Streptomycine
Sintomycine, levomycetine
Other antibiotics
5.2. sulfonamides
5.4. local anesthetics
5.5. iodine containing drugs
5.6. В group vitamines
5.7. other drugs
5.8.other side reactions: dizziness, nausea, fever, vomiting, disbiosis etc (with data)
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6. seasonal exacerbations (summer, autumn, winter, spring) 7. climate influence on

6. seasonal exacerbations (summer, autumn, winter, spring) 7. climate influence on

the disease course
8. weather and physical factors influence (cold, heating)
9. physical exercise, negative emotions etc
10. relation to respiratory infections (viral infections, brohcitis, tonsillitis, pneumonia)
11. relation to menstrual cycle, feeding, pregnancy, delivery
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12. where is worse – at home, at the working place,

12. where is worse – at home, at the working place,

in the street, in the forest, at the day or night
13. influence of food, drinks, alcohol, cosmetic, antiinsects, dust, smells, animals, clothes, bad settings
14. situation at home (material of which the home is built, warming, is there a wet surroundings, carpets, furniture, books, bed settings, animals, fishes)
15. working conditions and their changes during the life
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Non-specific tests CBC: eosinophilia (except patients taking corticosteroids); normal eosinophil count

Non-specific tests

CBC: eosinophilia (except patients taking corticosteroids); normal eosinophil count does

not exclude allergy. Total WBC is usually normal.
Anemia and thrombocytosis - not typical, indicate systemic inflammatory disorder.
Conjunctival /nasal secretions/sputum: WBC, formula (eosinophilia suggests probability of TH2-response)
Serum IgE levels: elevated (also in parasitic infections, infectious mononucleosis, autoimmune disorders, drug reactions, hyper-IgE syndrome, Wiskott-Aldrich syndrome, some forms of multiple myeloma.
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Specific tests: Allergen-specific serum IgE tests: enzyme-labeled anti-IgE antibody Performed when

Specific tests:

Allergen-specific serum IgE tests: enzyme-labeled anti-IgE antibody
Performed when

skin testing might be ineffective or risky or in case of skin diseases (eczema/psoriasis) which make skin testing difficult
allergen is immobilized on a synthetic surface, substrate for the enzyme is then added; the substrate provides colorimetric fluorescent or chemiluminescent detection of binding.
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Skin tests standardized concentrations of antigen introduced directly into skin higher

Skin tests

standardized concentrations of antigen introduced directly into skin
higher positive

predictive values for diagnosing allergic rhinitis and conjunctivitis than for diagnosing allergic asthma or food allergy; negative predictive value for food allergy is high.
most commonly used antigens are pollens (tree, grass, weed), molds, house dust mites, animal danders and sera, insect venom, foods, and β-lactam antibiotics.
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Two skin test techniques can be used: Percutaneous (prick) Intradermal

Two skin test techniques can be used:

Percutaneous (prick)
Intradermal

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Percutaneous (prick): drop of antigen extract is placed on the skin

Percutaneous (prick):

drop of antigen extract is placed on the skin
skin

is tented up and pricked or punctured
through the extract with the tip of a 27-gauge needle held at a 20° angle or with a commercially available prick device.
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Intradermal more sensitive less specific can be used to evaluate sensitivity

Intradermal

more sensitive
less specific
can be used to evaluate sensitivity to allergens when

prick test results are negative or equivocal:
typically 0.02 mL is injected intradermally with a 0.5- or 1-mL syringe and a 27-gauge short-bevel needle.
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Necessary for both Negative control: diluent Positive control - histamine (10

Necessary for both

Negative control: diluent
Positive control - histamine (10 mg/mL for

prick tests, 0.01 mL of a 1:1000 solution for intradermal tests)
For patients who have had a recent (< 1 yr) generalized reaction to the test antigen
testing begins with the standard reagent diluted 100-fold
then 10-fold
then the standard concentration.
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Drugs which can interfere with results and should be be stopped

Drugs which can interfere with results and should be be stopped

a few days to a week before testing:
Antihistamines
tricyclic antidepressants,
monoamine oxidase inhibitors;
some recommendations insist on cessation of β-blockers because these patients are more likely to have risk factors for severe reactions.
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Positive test results Diluent – negative Histamin - positive Causative allergen:

Positive test results

Diluent – negative
Histamin - positive
Causative allergen: positive
Postive means
wheal

and flare reaction
wheal diameter is 3 to 5 mm more than that of the negative control after 15 to 20 min.
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Negative test result Diluent – negative Histamin - positive Causative allergen:

Negative test result

Diluent – negative
Histamin - positive
Causative allergen: negative
Skin reacts on

histamin normally, but allergens don’t cause the reaction
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False positive Diluent – positive Histamine – positive Allergen - positive

False positive

Diluent – positive
Histamine – positive
Allergen - positive
Cause may be dermatographism

(a wheal and flare reaction provoked by stroking or scraping the skin).
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False negative Diluent – negative Histamine – negative Allergen - negative

False negative

Diluent – negative
Histamine – negative
Allergen - negative
If used from one

kit
Cause - allergen extracts have been stored incorrectly or are outdated.
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False negative-2 Histamine is positive, allergens are negative, but there is

False negative-2

Histamine is positive, allergens are negative, but there is strong

evidence of allergy
histamine sample is still active or histamine is used from another kit, histamine reaction may be positive
Patient may not react on commersial variant of allergens (some common house dust, common cat’s or dog’s epidermis), but may react on the allergens from his own environment
In case if this is suspected, individual allergens should be performed
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Individual allergens Concrete house dust taken from patients home Epidermis of

Individual allergens

Concrete house dust taken from patients home
Epidermis of the concrete

cat, dog etc
…..
In cases when the anamnestic signs are present, but tests give negative results
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Other specific tests Provocative testing : exposure of the mucosae to

Other specific tests

Provocative testing : exposure of the mucosae to allergen and

is indicated for patients who must document their reaction (for occupational or disability claims) , sometimes for diagnosis of food allergy, cold-induced urticaria etc
Ophthalmic testing: no advantage over skin testing and is rarely used.
Nasal and bronchial challenge: primarily research, but bronchial challenge is sometimes used when the clinical significance of a positive skin test is unclear or when no antigen extracts are available (for occupation-related asthma)
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Treatment Removal or avoidance of allergic triggers H1 blockers Mast cell

Treatment

Removal or avoidance of allergic triggers
H1 blockers
Mast cell stabilizers
Anti-inflammatory corticosteroids and leukotriene

inhibitors
Immunotherapy (desensitization)
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H1 blockers

H1 blockers

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Attention! All sedating antihistamines have strong anticholinergic properties. they should not

Attention!

All sedating antihistamines have strong anticholinergic properties.
they should not be used

in the elderly or in patients with glaucoma, benign prostatic hyperplasia, constipation, delirium, dementia, or orthostatic hypotension.
Commonly cause dry mouth, blurred vision, urinary retention, constipation, and orthostatic hypotension.
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Specific immune therapy Performed in remission only In period without allergens

Specific immune therapy

Performed in remission only
In period without allergens exposure (not

in pollen exposure season)
Allergens used are those which typically cannot be avoided: pollens, house dust mites, molds, and venom of stinging insects.
Individual allergens can be made (dust allergen in patient’s home, epidermis of patient’s pet)
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Indications allergic rhinitis, conjunctivitis, hay fever, atopic asthma of mild course

Indications

allergic rhinitis, conjunctivitis, hay fever, atopic asthma of mild course of

the disease (all with high IgE); stinging insect (venom) hypersensitivity
Asthma should be controlled, FEV1 > 70% of predicted
Atopic dermatitis of mild and moderate course with high degree of sensibilization
The best results are to house dust mites (2++)
Also performed if contact with home pet can’t be avoided
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Contraindications: 3-5 step of asthma treatment (moderate/severe course) Non Th2-variant (non-atopic,

Contraindications:

3-5 step of asthma treatment (moderate/severe course)
Non Th2-variant (non-atopic, low IgE)
Current

use of glucocorticosteroids (suppress immune reactions)
Beta-blockers are relative contraindications in venoms hypersensitivity
Significant comorbidities (cardiovascular etc)
Anaphylactic shock in case history
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Special considerations: • Children

Special considerations:

• Children < 6 yrs • Pregnancy • Elderly • Malignancy, immunodeficiency

and autoimmune diseases (mentioned in some articles, but autoimmune patients usually have glucocorticosteroid treatment which is absolute contraindication); immunodeficiency – depend on nosological units (there are IgE-elevated variants)
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Principle induction of IgG antibodies IgGs compete with IgE for allergen

Principle

induction of IgG antibodies
IgGs compete with IgE for allergen or block

IgE from binding with mast cell IgE receptors
induction of interferon -γ, IL-12, and cytokines secreted by TH1 cells; or induction of regulatory T cells
In total – switch from Th2 to Th1 responce
Performed by allergen injection in gradually increasing doses (hyposensitization or desensitization)
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Principle: Th2 to Th1 switch Indian Journal of Allergy, Asthma and

Principle: Th2 to Th1 switch

Indian Journal of Allergy, Asthma and Immunology

| Jan-Jun 2013 @BULLET Volume 27 @BULLET Issue 1 Allergen immunotherapy: Basic concepts
Article Jan 2013
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Classification Preseasonal Preseasonal-seasonal Whole year

Classification

Preseasonal
Preseasonal-seasonal
Whole year

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Principle injections are given monthly. Dose: start dose from 0.1 to

Principle

injections are given monthly.
Dose: start dose from 0.1 to 1.0

biologically active units (BAU), depending on initial sensitivity
weekly or biweekly 2 times increase
Until maximum tolerated dose (start of moderate adverse effects)
maximum tolerated dose is given every 4 to 6 wks year-round
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Build-up (induction) phase weekly injections starting with a very low dose,

Build-up (induction) phase

weekly injections
starting with a very low dose,
gradual increases in

dose over the course of 3–6 months
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maintenance phase every 4–6 weeks for venom and every 4 weeks

maintenance phase

every 4–6 weeks for venom and every 4 weeks for inhalant allergens
period

of 3–5 years.
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Principle Observation of patients 30 min postinjection (risk of anaphylaxy) Appearance

Principle

Observation of patients 30 min postinjection (risk of anaphylaxy)
Appearance of blood

during injectionis the protocol violation; the patients are at high risk for anaphylaxy and should be observed more closely
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Specific immune therapy in allergic rhinitis Moote, W., Kim, H. Allergen-specific

Specific immune therapy in allergic rhinitis

Moote, W., Kim, H. Allergen-specific immunotherapy. All

Asth Clin Immun 7, S5 (2011). https://doi.org/10.1186/1710-1492-7-S1-S5
Слайд 74

Sublingual immunotherapy placing a tablet of allergen extract under the tongue

Sublingual immunotherapy

placing a tablet of allergen extract under the tongue until

it is dissolved
available for the treatment of grass and ragweed allergy, as well as house dust mite-induced allergic rhinitis (with or without conjunctivitis).
Tablets: Oralair®, Grastek®, Ragwitek® Acarizax™
(see Table 3) [23–26]. The sublingual route of immunotherapy offers multiple potential benefits over the subcutaneous route including the comfort of avoiding injections, the convenience of home administration, and a favourable safety profile. Like subcutaneous immunotherapy, sublingual immunotherapy is indicated for those with allergic rhinitis/conjunctivitis who have not responded to or tolerated conventional pharmacotherapy, or who are adverse to the use of these conventional treatments.
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Prevention synthetic fiber pillows and impermeable mattress covers Frequently washing bed

Prevention

synthetic fiber pillows and impermeable mattress covers
Frequently washing bed sheets, pillowcases,

and blankets in hot water
Removing upholstered furniture, soft toys, and carpets
Exterminating cockroaches to eliminate exposure
Using dehumidifiers in basements and other poorly aerated, damp rooms
Treating homes with heat-steam
Using high-efficiency particulate air (HEPA) vacuums and filters
Avoiding food triggers
Limiting pets to certain rooms or keeping them out of the house
Frequently cleaning the house
Adjunctive nonallergenic triggers (eg, cigarette smoke, strong odors, irritating fumes, air pollution, cold temperatures, high humidity) should also be avoided or controlled when possible.
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Food allergy Some food antigens stimulate innate immune responses peanut allergen

Food allergy

Some food antigens stimulate innate immune responses
peanut allergen Ara h1

binds to CD209 on DCs
milk sphingomyelin activates type 2 cytokine responses from invariant NKT cells
Changes in microbial flora: associated with allergic sensitization (supporting protection by specific bacteria and their products) through sustaining intestinal Treg population
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