PDF | 10+ minutes read | On Jan 1, , Neil Blumberg and others published Manual of Clinical Immunology. Laboratory methods in genitourinary medicine. Techniques used in clinical immunology. A G Bird. Introduction. A wide variety of techniques are used in clinical. Clinical Immunology publishes original research on the molecular and cellular bases of .. The system converts your article files to a single PDF file used in.
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autoimmune diseases through clinical immunology are of great interest Immunology begins with the basic concepts and then details the immuno-. Immunology. Clinical. Immunology. The Spectrum of Clinical Immunology. Basic. Immunology. Inflammation. Immune Response. Loss of Tolerance. Deficiency. PDF | On Jan 1, , J David M Edgar and others published Clinical Immunology.
Specialized forms of dendritic cells are: The antigen is degraded and a peptide fragment is attached to class II MHC molecules 8 is exported to the surface. The presence of normal flora in the skin and gut preventing colonization by pathogenic organisms. The Latin "immunis" means free from burden. Possess B antigen on R. Local IgE in non-allergic rhinitis.
Within the PAL. Which is called periarterial lymphotic sheath PAL predominantly T cells zone. Candida" and worms "multicellular parasites e. Bacteria pyogenic organisms. The Latin "immunis" means free from burden. Non specific.
Mechanical removal also by coughing and sneezing. Granulocytes and natural killer cells. Adaptive immunity. Colonization resistance: The presence of normal flora in the skin and gut preventing colonization by pathogenic organisms. Physical barriers: Skin and mucosae. Non specific immune response: There is considerable interaction is innate and specific immune response. It is an essential component of the cellular innate system involved in killing bacteria and fungi. The migration into tissues is unidirectional.
They are abundant in bone marrow and blood. Innate Immunity: Cellular Mechanisms Several cellular mechanisms are present and functional at birth and constitute the innate cellular immune system. Polymorphnuclear cell PMN is a highly specialized microbial phagocyte. They are released from the bone marrow in large numbers during infections and new cells are produced by the action of granulocyte colony stimulating factor GMCSF.
Complement components C Their functions include cell activation. Cytokines e. FMLP a peptide which is a bacterial product. Leukotrien B4 LTB4 which are macrophage derived products of the lipooxygenase pathway of arachidonic acid metabolism. Adhesion molecules: These are surface proteins which facilitates intercellular adhesion.
These activators cause up regulation of adhesion molecules on the surface of neutrophils and endothelial cells. When large numbers of phagocytes are involved in an infective process. Two major mechanisms of killing occur in neutrophils: The directed movement of a cell along a gradient of increased concentration of the attracting molecule i. C-reactive protein and antibody i. Opsonins are factors that coat microorganisms and enhance neutrophil's ability to engulf them. Neutrophils have the capacity to ingest more than one bacterium or fungus at once.
The ability to ingest and kill microorganisms is a key component in host defence. Then the intracellular phagosome becomes fused to neutrophil granules which releases its contents. The best opsonins are complementing component C3b. There are 3 main families: IL8 and LTB4. The most potent chemoattractant are C5a. The eosinophil cationic proteins are: They are a feature of infiltrate in tissues involved in allergic responses e.
They are more abundant in tissues where they survive for several weeks. Recurrent bacterial and fungal infections occur in conditions associated with failure of neutrophil's action e. They share many features in common. The major granule products are histamine and leucotriens which have profound effects on blood vessels and bronchial smooth muscles.
They have histamine containing granules and high affinity receptors for IgE. C4a and C5a activate basophils and may activate mast cells.
They are activated in allergic and inflammatory conditions by IgE. The effects of these granule release products depend on the site and the stimulus. The majorities are soluble but some are membrane bound.
The term complement was proposed by Paul Ehrlich to describe the ability of these proteins to complete or augment the actions of immunoglobulins during bacterial destruction. The soluble proteins circulate in an inactive state and each must be activated sequentially for the reaction to proceed. The complement proteins are formed mainly in the liver. The final common pathway must be activated via the classic or alternative pathway. Proposed by WHO. The alternative pathway is relatively primitive and a part of the innate system while the classic pathway combines with antibody to initiate activation and therefore it is associated with acquired adaptive immunity.
Capital C followed by the number for the classic and common pathway e. Other activators include: The classical pathway: The letter I prefix e. C4b 2a. Capital letter followed by the number for the alternative pathway e.
Bar over symbols e. The cleavage of C3 by C4b 2a forms two fragments C3a which has powerful biological properties and C3b which becomes bound to the membrane and to C3b 2a. Activators of the alternative pathway include endotoxin found in gram negative bacterial cell walls.
The main components of the alternative pathway are factor B. The alternative pathway. C2 is then cleaved by activated C1 into C2b and C2a which combines with C4b to form the classic pathway C3 convertase C4b 2a. C3b is formed as a result of low grade hydrolysis of C3.
Activated C1 causes cleavage of C4 to C4b which continues the reaction process and C4a which has other biological activities. It coats the bacterial wall and becomes bound to complement receptors on neutrophils leading to more efficient engulfment of the pathogen by neutrophils. The C3b fragment accounts for the most opsonic activity of the complement. Cell activation: Anaphylatoxins as C3a. C5a and C4a can directly activate basophils and mast cells through specific receptors leading to their degranulation and release of inflammatory mediators as histamine.
Then the complex C5b67 becomes bound to the membranes. Cell recruitment to inflammatory sites chemotaxis: This starts by cleavage of C5 by either the classic or the alternative pathway leading to the formation of the small fragment C5a which is biologically active and the larger fragment C5b which continues the reaction by binding C6 which then binds C7. The membrane attack pathway. This maintains the solubility of antigen antibody complexes. Removal of immune complexes: The binding of C3b to antibody in a complex inhibits lattice formation.
C1 esterase C1 inhibitor which inactivates activated C1 by combining with it irreversibly. Factor H binds C3b and accelerates its destruction by factor H. The antibody coated C3b can attack to complement receptors found on many cells including R. Regulatory proteins include circulating or membrane bound inhibitors. C4 binding protein: It is also responsible for regulation of other plasma enzyme systems e.
Carboxypeptidase N: Cleaves C3a. Control is achieved by the lability of active molecules. Control mechanisms are important because complement activation may cause extensive tissue damage through the mediators of inflammation produced. Bind C4b and accelerates its destruction by factor I. Treatment of acute attack: Fresh frozen plasma. Laryngeal oedema may be fatal. Acute phase reactants are proteins that are synthesized in response to infection.
CRP is produced in the liver and binds phosphorylcholine moieties which constitute a major component of bacterial cell wall constitute a major component of bacterial cell wall teichoic acid. A protein which has the property of binding of the Cpolysaccharide of pneumococci.
They are secreted by the liver under the effect of certain cytokines e. Since it has a relatively short half life. Its blood levels raise folds within hours of the starts of infective or inflammatory process. When CRP is bound. It cleaves bacterial cell wall at a precise point. Some antigens act as tolegens i. The molecular target of the acquired immune response is the antigen.
Is a bactericidal enzyme secreted in saliva. In general. Acquired Immunity The cardinal features of acquired immune response are specificity. Most biological materials serve as antigens which function as immunogens i.
Whether exposure to an antigen results in an immune response or not is dependent on a variety of factors: A Nature of the antigen: The animals usually do not respond to self antigens except in pathological states e. The more complex the molecule, the greater the likelihood of being immunogenic in most individuals. Large homopolymers are not immunogenic. Virtually all proteins are immunogenic. In general they are multideterminant antigens. Polysaccharides are potentially not always.
Glycoproteins are immunogenic. B Exposure to the antigen: C Nature of recipient: Haptens to grasp Low molecular weight antigens which are not capable of inducing an immune response by themselves i. The immune response elicited by antigen generates antibodies or lymphocytes that react specifically with that antigen. The smallest portion of the antigen that binds specifically with the binding site of an antibody or a receptor on a lymphocyte is called antigenic determinant or "epitope".
Compounds may have one or more epitopes capable of reacting with immune components. The part of the antibody which contacts the antigen is called paratope. They cannot interact directly with soluble antigens i. The antigen must be degraded, held and presented to the T-cells by other glycoprotein molecules MHC molecules. The T-cell recognizes both MHC and the peptide antigen.
Major histocompatibility complex hold peptide antigens enclosed within a groove. The T-cell receptor recognizes a combination of the shapes formed by the peptide antigen and the wall of the groove in the MHC molecule. The binding may involve electrostatic interactions, hydrogen bonds and Van der Waals forces. The strength of binding of antibody to a single combining site antigen determinant site.
The strength of attachment between the antigen and its receptor. It is the functional affinity, e. In an antibody molecule V regions are the variable regions antigen binding sites. The most important features are specificity and biologic activity. Antibodies Definition They are soluble glycoprotein molecules that exhibit antigen binding ability. Each heavy chain is attached to a light chain by interchain disulphide bonds.
The typical Ig molecule has a molecular mass of KDs. The two heavy chains and the two light chains are identical to each other. In an antibody molecule the two heavy chains are linked together by interchain disulphide bonds. Similar structure was found in MHC molecules adhesion molecules. These bonds bend segments back into themselves creating regions called domains. There is a hinge region in the middle of Ig molecule which allows flexibility of the two arms of the Y shaped molecule bearing the antigen binding sites.
T-cell receptors. The C regions are relatively constant in each molecule and hold the effector functions of the molecules e. The variability is critical for generating the potential to bind to more than different antigen structures.
Within the heavy and light chains. This domain structure is very distinctive. This increases the chances of binding two antigens at one time. Opsonization of particles for phagocytosis. Surface Igs on B cells act as antigen receptors to present antigens to T lymphocytes. Binding to prevent adhesion and invasion of organisms.
C In Lab. A In host defence: Antibodies are used in a vast range of diagnostic and research studies. Lysis in combination with complement. B In clinical medicine: It has multiple functional domains.
It does not cross the placenta. IgG is further divided into 4 subclasses IgG Elevated levels of IgM in a newborn infant. It is a large pentamer composed of 5 IgM monomers. There are 5 major classes of Igs according to the heavy chain type: They are responsible for transfusion reactions which arise as a result of ABO incompatibility in which the recipient haemagglutinins react with the donor's R.
This antibody is confined mainly to the intravascular space. It has potential binding sites. Elevated levels indicate recent infection or recent immunization. It is the major antibody formed in primary immune response i. IgM antibodies include "natural isohaemagglutinins" which are naturally occurring antibodies against red cell antigens of the ABO blood groups.
This is the most abundant immunoglobulin in serum. It is the major Ig secreted into external surfaces saliva. It can occur as monomer in serum and as a dimmer where two molecules are joined together by a short peptide J chain.
It is present as a monomer and has a high antigen affinity. It is the only antibody that crosses the placenta in significant amounts. This gives some specific protection on the new born during the period when its own immune system is immature.
GIT secretions. IgG2 and IgG4 are produced in response to polysaccharide antigens e. IgG1 and IgG3 are produced mainly in response to protein antigens such as tetanus toxin and many viruses. This is caused by maternal antibodies to foetal red blood cells. This is the next most abundant Ig molecule.
They are good opsonins. The maternal IgG antibodies produced by Rh —ve mother to Rh antigen. It is the major antibody in secondary immune response. This placental transfer is responsible for the hemolytic disease of the newborn erythroblastosis foetalis. Its protective effect is by preventing the invading organism from attachment to and penetration of epithelial surfaces.
Its serum levels are very low and its function in the serum is not certain.
It has been suggested to have a role in B lymphocyte activation. For IgA responses. After clonal expansion. It is transported by a secretory component to the mucosal surface. It is the largest Ig monomer. It has an important function in protection against bacterial. IgD is present on the surface of B lymphocytes and may have an immune regulatory role.
IgA precursor B cells in the mucosal lymphoid follicles journey to regional lymph nodes. Most of IgE is membrane bound on high affinity receptors on mast cells and basophils. It is present in the serum of healthy individuals at extremely low levels.
This is because after encountering antigen. The first exposure of an individual to an immunogen primary immunization and the measurable response is called the primary response. The first class of the antibodies detected is the IgM sometimes the only class detected. After the second exposure to the antigen. Its levels in the serum rise in response to parasitic infestations especially nemtodes e. Then IgG production occurs with rapid cessation of IgM production. After the latent phase a time before the antibody is detected in serum which is about weeks.
There is a class shift where the IgG appears in large amounts than IgM. Then there is arise in concentration of antibodies which becomes steady and then decline. Human monoclonal antibodies are produced by genetic engineering recombinant DNA technology. Homogenous populations of antibody molecules. Monoclonal antibodies are produced by the hybridoma technique. Most antibody responses to complex macromolecular antigens involve the targeting of multiple epitopes on the antigen. This is called anamnestic memory response.
Each epitope may be targeted by more than a single antibody molecule. These are large collection of genes that include those responsible for rejection of transplanted tissues by the immune system. These are present in vertebrate species. Include DR. Each contains 3 classes of genes found on the short arm of chromosome 6. Include genes encoding for complement and TNF. Include HLA. Kupffer cells. This polymorphism creates a difference in tissue compatibility between different subjects which is a barrier to organ transplantation.
Law of MHC restriction: Antigen specific cytotoxic T-cells responses are restricted to kill only target cells that bear the correct MHC molecule. They present peptide antigens from endogenous sources including viral proteins if they are made within the cell presenting antigens to cytotoxic T-cells CD8 cells. They are expressed on the surface of all nucleated cells. B8 DR4.
T-cell receptor makes contact with the lips of the groove within the MHC molecules and the peptide antigen. These are controlled by 3 gene alleles A. Have A antigen on R.
ABO System blood grouping: There are 4 blood groups: The association between inheritance of particular genes in the MHC and higher risk of development of certain diseases has been found. Fat of antigen after penetration of skin or mucosal barriers: A AA or AO.
The system not only traps antigens but also provides sites the secondary lymphoid organs where antigens. Cs but no agglutinins in serum. T-cells and B cells to generate an antigen specific immune response. Possess no A and B antigens on R.
Cs and anti A antibodies in serum which agglutinate group A and AB. Possess A and B antigens on R. Cs but has both anti A and anti B in serum.
Possess B antigen on R. Fate of antigens after penetration: The reticulo endothelial system RES or the mononuclear phagocyte system is designed to trap foreign antigens that have penetrated the body and to subject them to ingestion and degradation by the phagocytic cells of the system. B BB or BO. Lymphocytes also leave the spleen to the circulation. In the LNs. In addition. There it will interact with macrophages and lymphocytes. Antigen specific T and B cells and antibodies also enter the circulation via the thoracic duct and are thereby redistributed to various tissues.
Antibodies synthesized in these organs are deposited in the local tissue. From these tissues.
Present on all mature T-cells. These are individual surface molecules which are assigned a cluster of differentiation CD numbers defined by a cluster of monoclonal antibodies reacting with that molecule.
In other words: It is a surface molecule found on cells according to their lineage and differentiation and identifiable by one or more monoclonal antibodies. A marker for early stem cells. Its function is signal transduction. Unknown function. Act as T-cell co-stimulation molecule. Have a role in B cell activation. CD21 is an EBV receptor.
Present on cytotoxic. Present on activated T-cells. Function as T-cell receptor co-receptor. Present on all mature B cells. Present on mononuclear phagocytes specific. NK cell marker mediates cell adhesion. In recent years, two additional types of rhinitis have been classified that deserve some mention here—occupational rhinitis and local allergic rhinitis.
Occupational rhinitis is defined as an inflammatory disease of the nose characterized by intermittent or persistent symptoms that include airflow limitation, hypersecretion, sneezing and pruritus that are attributable to a particular work environment and not to stimuli encountered outside the workplace [ 6 ].
Although the overall prevalence of occupational rhinitis is unknown, high-risk professions include laboratory or food-processing workers, veterinarians, farmers and workers in various manufacturing industries [ 6 — 8 ]. The condition may be IgE-mediated due to allergen sensitization, or due to exposure to respiratory irritants. Symptoms may develop immediately or several hours after exposure to the inciting stimuli.
Often there are associated ocular and pulmonary symptoms. An evaluation of the patient suspected of having occupational rhinitis should include the usual history and physical examination discussed later , as well as a site visit and skin testing or in vitro testing to inhalants. Treatment primarily involves avoiding exposure to the causative agent and pharmacotherapy as needed. There is little evidence to suggest that occupational rhinitis will progress to occupational asthma with ongoing exposure [ 6 , 8 ], although this is possible.
Therefore, patients are generally not advised to leave their jobs if exposure cannot be eliminated but symptoms are adequately controlled. Local allergic rhinitis LAR is a clinical entity characterized by a localized allergic response in the nasal mucosa in the absence of evidence of systemic atopy [ 9 — 11 ].
The symptoms of LAR are similar to those provoked in patients with allergic rhinitis, and the assumption is that LAR is an IgE-mediated disease based on both clinical findings and the detection of specific IgE in the nasal mucosa. To date, there is no evidence to suggest that LAR is a precursor to allergic rhinitis since follow-up does not show the evolution to typical allergic rhinitis in these patients [ 13 ]; however, patient follow-up may not have been long enough to detect this disease evolution.
The implications for treatment of LAR are not well understood at this time, although some evidence suggests that allergen immunotherapy may be effective in this type of rhinitis [ 9 , 11 ]. Allergic rhinitis is usually a long-standing condition that often goes undetected in the primary-care setting.
Patients suffering from the disorder often fail to recognize the impact of the disorder on quality of life and functioning and, therefore, do not frequently seek medical attention. In addition, physicians fail to regularly question patients about the disorder during routine visits [ 1 , 14 ]. Components of a complete history and physical examination for suspected rhinitis [ 1 ]. Quality of life. Response to previous interventions. Outward signs. Posterior oropharynx. Chest and skin.
During the history, patients will often describe the following classic symptoms of allergic rhinitis: Allergic conjunctivitis inflammation of the membrane covering the white part of the eye is also frequently associated with allergic rhinitis and symptoms generally include redness, tearing and itching of the eyes [ 1 ]. The use of certain medications e. The history should also include patient questioning regarding a family history of atopic disease, the impact of symptoms on quality of life and the presence of comorbidities such as asthma, mouth breathing, snoring, sleep apnea, sinus involvement, otitis media inflammation of the middle ear , or nasal polyps.
Before seeking medical attention, patients often attempt using over-the-counter or other medications to manage their symptoms.
Assessing patient response to such treatments may provide information that can aid in the diagnosis and subsequent management of allergic rhinitis. For example, symptom improvement with newer, second-generation antihistamines e.
However, it is important to note that response to first-generation antihistamines e. Previous response to intranasal corticosteroids may also be suggestive of an allergic etiology, and likely indicates that such treatment will continue to be beneficial in the future [ 1 ]. Outward signs that may be suggestive of allergic rhinitis include: Examination of the nose typically reveals swelling of the nasal mucosa and pale, thin secretions.
An internal endoscopic examination of the nose should also be considered to assess for structural abnormalities including septal deviation, nasal ulcerations, and nasal polyps [ 1 ]. The ears generally appear normal in patients with allergic rhinitis; however, assessment for Eustachian tube dysfunction using a pneumatic otoscope should be considered.
The sinus examination should include palpation of the sinuses for evidence of tenderness or tapping of the maxillary teeth with a tongue depressor for evidence of sensitivity.
The posterior oropharynx should also be examined for signs of post nasal drip mucous accumulation in the back of the nose and throat , and the chest and skin should be examined carefully for signs of concurrent asthma e. Although a thorough history and physical examination are required to establish the clinical diagnosis of rhinitis, further diagnostic testing is necessary to confirm that underlying allergies cause the rhinitis.
Skin-prick testing is considered the primary method for identifying specific allergic triggers of rhinitis. Skin prick testing involves placing a drop of a commercial extract of a specific allergen on the skin of the forearms or back, then pricking the skin through the drop to introduce the extract into the epidermis. A reasonable alternative to skin prick testing is the use of allergen-specific IgE tests e. These in vitro tests can be performed when eczema is extensive, or if the patient cannot stop antihistamine therapy to allow for testing.
However, skin prick tests are generally considered to be more sensitive and cost effective than allergen-specific serum IgE tests, and have the further advantage of providing physicians and patients with immediate results [ 1 , 14 ].
A simplified, stepwise algorithm for the treatment of allergic rhinitis. Treatments can be used individually or in any combination. The first-line treatment of allergic rhinitis involves the avoidance of relevant allergens e.
Pollen and outdoor mould exposure can be reduced by keeping windows closed, using window screen filters, using an air conditioner, and limiting the amount of time spent outdoors during peak pollen seasons. However, compliance with this recommendation is poor and, therefore, the use of high-efficiency particulate air HEPA filters and restricting the animal from the bedroom or to the outdoors may be needed to attempt to decrease allergen levels.
These avoidance strategies can effectively improve the symptoms of allergic rhinitis, and patients should be advised to use a combination of measures for optimal results [ 1 ]. The second-generation oral anti-histamines have been found to effectively reduce sneezing, itching and rhinorrhea when taken regularly at the time of maximal symptoms or before exposure to an allergen.
Although the older first-generation sedating antihistamines e. When used regularly and correctly, intranasal corticosteroids effectively reduce inflammation of the nasal mucosa and improve mucosal pathology.
Studies and meta-analyses have shown that intranasal corticosteroids are superior to antihistamines and leukotriene receptor antagonists in controlling the symptoms of allergic rhinitis, including nasal congestion, and rhinorrhea [ 19 — 22 ]. They have also been shown to improve ocular symptoms and reduce lower airway symptoms in patients with concurrent asthma and allergic rhinitis [ 23 — 25 ].
Since proper application of the nasal spray is required for optimal clinical response, patients should be counseled on the appropriate use of these intranasal devices. Ideally, intranasal corticosteroids are best started just prior to exposure to relevant allergens and, because their peak effect may take several days to develop, they should be used regularly [ 4 ].
The most common side effects of intranasal corticosteroids are nasal irritation and stinging. However, these side effects can usually be prevented by aiming the spray slightly away from the nasal septum [ 1 ]. Evidence suggests that intranasal beclomethasone and triamcinolone, but not other intranasal corticosteroids, may slow growth in children compared to placebo.
However, long-term studies examining the impact of usual doses of intranasal beclomethasone on growth are lacking [ 26 — 29 ]. It is important to note that most patients with allergic rhinitis presenting to their primary-care physician have moderate-to-severe symptoms and will require an intranasal corticosteroid.
Bousquet et al. This combination spray has been shown to be more effective than the individual components with a safety profile similar to intranasal corticosteroids [ 31 — 34 ].
The LTRAs montelukast and zafirlukast are also effective in the treatment of allergic rhinitis; however, they do not appear to be as effective as intranasal corticosteroids [ 35 — 37 ]. Although one short-term study found the combination of LTRAs and antihistamines to be as effective as intranasal corticosteroids [ 38 ], longer-term studies have found intranasal corticosteroids to be more effective than the combination for reducing nighttime and nasal symptoms [ 20 , 39 ].
It is important to note that in Canada, montelukast is the only LTRA indicated for the treatment of allergic rhinitis in adults. Allergen immunotherapy is an effective treatment for allergic rhinitis, particularly for patients with intermittent seasonal allergic rhinitis caused by pollens, including tree, grass and ragweed pollens [ 40 — 43 ].
It has also been shown to be effective for the treatment of allergic rhinitis caused by house dust mites, Alternaria, cockroach, and cat and dog dander although it should be noted that therapeutic doses of dog allergen are difficult to attain with the allergen extracts available in Canada.
Allergen immunotherapy should be reserved for patients in whom optimal avoidance measures and pharmacotherapy are insufficient to control symptoms or are not well tolerated. Since this form of therapy carries the risk of anaphylactic reactions, it should only be prescribed by physicians who are adequately trained in the treatment of allergy and who are equipped to manage possible life-threatening anaphylaxis [ 1 ].
Immunotherapy may also reduce the risk for the future development of asthma in children with allergic rhinitis [ 41 ].
After this period, many patients experience a prolonged, protective effect and, therefore, consideration can be given to stopping therapy. Pre-seasonal preparations that are administered on an annual basis are also available [ 1 , 14 ].
Sublingual immunotherapy is a way of desensitizing patients and involves placing a tablet of allergen extract under the tongue until it is dissolved. It is currently available for the treatment of grass and ragweed allergy, as well as house dust mite-induced allergic rhinitis with or without conjunctivitis. At present, four sublingual tablet immunotherapy products are available in Canada: 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 who have not responded to or tolerated conventional pharmacotherapy, or who are adverse to the use of these conventional treatments. The most common side effects of sublingual immunotherapy are local reactions such as oral pruritus, throat irritation, and ear pruritus [ 42 ].
There is a very small risk of more severe systemic allergic reactions with this type of immunotherapy and, therefore, some allergists may offer the patient an epinephrine auto-injector in case a reaction occurs at home.
The risk of systemic allergic reactions is much lower with sublingual immunotherapy compared to traditional injections [ 42 ]. Similar to subcutaneous immunotherapy, sublingual immunotherapy is contraindicated in patients with severe, unstable or uncontrolled asthma.
It should ideally be avoided in patients on beta-blocker therapy as well as in those with active oral inflammation or sores [ 46 — 50 ]. Sublingual immunotherapy should only be administered using the Health Canada approved products discussed above. A simplified, stepwise algorithm for the treatment of allergic rhinitis is provided in Fig.
Note that mild, intermittent allergic rhinitis can generally be managed effectively with avoidance measures and oral antihistamines. However, as mentioned earlier, most patients presenting with allergic rhinitis have moderate-to-severe symptoms and, therefore, will require a trial of intranasal corticosteroids. Oral and intranasal decongestants e.
However, the side-effect profile associated with oral decongestants i. Furthermore, these agents are contraindicated in patients with uncontrolled hypertension and severe coronary artery disease. Oral corticosteroids have also been shown to be effective in patients with severe allergic rhinitis that is refractory to treatment with oral antihistamines and intranasal corticosteroids [ 1 , 4 ]. Although not as effective as intranasal corticosteroids, intranasal sodium cromoglycate Cromolyn has been shown to reduce sneezing, rhinorrhea and nasal itching and is, therefore, a reasonable therapeutic option for some patients.
The anti-IgE antibody, omalizumab, has also been shown to be effective in seasonal allergic rhinitis and asthma [ 1 ], however, it is not currently approved for the treatment of allergic rhinitis.
Surgical therapy may be helpful for select patients with rhinitis, polyposis, or chronic sinus disease that is refractory to medical treatment. Most surgical interventions can be performed under local anesthesia in an office or outpatient setting [ 1 ]. It is important to note that allergic rhinitis may worsen during pregnancy and, as a result, may necessitate pharmacologic treatment. The benefit-to-risk ratio of pharmacological agents for allergic rhinitis needs to be considered before recommending any medical therapy to pregnant women.
Intranasal sodium cromoglycate can be used as a first-line therapy for allergic rhinitis in pregnancy since no teratogenic effects have been noted with the cromones in humans or animals. Antihistamines may also be considered for allergic rhinitis in pregnancy. Starting or increasing allergen immunotherapy during pregnancy is not recommended because of the risk of anaphylaxis to the fetus.
However, maintenance doses are considered to be safe and effective during pregnancy [ 1 ]. Given the popularity of complementary and alternative medicines CAM in the general population, it is reasonable for physicians to ask patients about their use of CAM in a nonjudgmental manner. Given the limited number of well-designed clinical trials examining the efficacy of CAM in allergic rhinitis, it is difficult for clinicians to evaluate these therapies and provide guidance.
Nonetheless, since there will be patients who wish to pursue CAM for the management of allergic rhinitis, it is advisable to provide some information about these therapies including a discussion of the lack of high-quality studies evaluating some of these therapies. In a number of studies, acupuncture has been shown to provide modest benefits for patients with allergic rhinitis [ 52 , 53 ]. However, acupuncture is time consuming. Allergic rhinitis is a common disorder that can significantly impact patient quality of life.
The diagnosis is made through a comprehensive history and physical examination. Further diagnostic testing using skin-prick tests or allergen-specific IgE tests is usually required to confirm that underlying allergies cause the rhinitis. The therapeutic options available for the treatment of allergic rhinitis are effective in managing symptoms and are generally safe and well-tolerated.
Second-generation oral antihistamines and intranasal corticosteroids are the mainstay of treatment for the disorder. Allergen immunotherapy as well as other medications such as decongestants and oral corticosteroids may be useful in select cases. Allergen skin testing is the best diagnostic test to confirm allergic rhinitis. Intranasal corticosteroids are the mainstay of treatment for most patients that present to physicians with allergic rhinitis.
Allergen immunotherapy is an effective immune-modulating treatment that should be recommended if pharmacologic therapy for allergic rhinitis is not effective or is not tolerated. T helper 2. Allergic Rhinitis and its Impact on Asthma. All authors read and approved the final manuscript. The authors would like to thank Julie Tasso for her editorial services and assistance in the preparation of this manuscript.
Data sharing not applicable to this article as no datasets were generated or analyzed during the development of this review.
Ethics approval and consent to participate are not applicable to this review article. Practical guide for allergy and immunology in Canada