ALLERGIC RHINITIS CLASSIFICATION AND DIFFERENTIAL ...

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Alhabieb. World Journal of Pharmacy and Pharmaceutical Sciences

ALLERGIC RHINITIS CLASSIFICATION AND DIFFERENTIAL

DIAGNOSIS AND MANAGEMENT

Dr. Naser Shamkhi Ali Alhabieb*

M.B.CH.B, Diploma Otolaryngology.

ABSTRACT

Allergic rhinitis (AR) is one of the commonest allergic manifestations

affecting approximately 400 million people worldwide. It is associated

with a reduced quality of life, low productivity in the workplace, and

poor school performance. On the other hand, medical cost increases.

Allergic rhinitis has a considerable effect on the quality of life and can

have significant consequences if left untreated. Many patients

downplay rhinitis symptoms as an inconvenience rather than a disease.

The majority of the patients start visiting their local physician, when

the problem becomes chronic, especially when it is associated with

complications. There is a huge economic burden associated with

treatment by pharmacological agents available currently. The pharmacological agents are also

associated with various side effects and many severe adverse events. That‟s why we look for

the alternative form of treatment for allergic rhinitis with less financial burden and least

adverse reactions associated with medicines presently in use commonly. Method: This study

show prospective study to patient from 2014 to2020. Results: Show by tables.

KEYWORDS: Allergic rhinitis, Nonpharmacological treatment, SCIT, Allergoids.

INTRODUCTION

Allergic rhinitis is a symptomatic disorder of the nose, induced after allergen exposure by an

IgE-mediated inflammation of the nasal mucosa. Allergic rhinitis represents a global health

problem. It is a worldwide disease affecting at least 10–25% of the population, and its

prevalence is increasing. In European countries the prevalence of allergic rhinitis has been

estimated from 17 to 29%. An increase in this prevalence has been observed in the past 40

years. Allergic rhinitis is not a severe disease but it alters a patient‟s social life, affecting

school performance and work productivity; the costs incurred by rhinitis are substantial.

WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES

SJIF Impact Factor 7.632

Volume 10, Issue 7, 167-187 Research Article ISSN 2278 – 4357

*Corresponding Author

Dr. Naser Shamkhi Ali

Alhabieb

M.B.CH.B, Diploma

Otolaryngology.

Article Received on

10 May 2021,

Revised on 30 May 2021,

Accepted on 20 June 2021

DOI: 10.20959/wjpps20217-19282


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Asthma and rhinitis are common comorbidities, suggesting the concept of “one airway, one

disease”.

Guidelines for the diagnosis and treatment of allergic rhinitis have already been published,

but some were not predicated on evidence-based medicine and few, if any, considered the

patients globally in terms of comorbidities. The ARIA (Allergic Rhinitis and Its Impact on

Asthma) initiative has developed a document that is the state of the art, for the specialist as

well as for the general practitioner to:

Update his/her knowledge of allergic rhinitis

Highlight the impact of allergic rhinitis on asthma

Provide an evidence-based documented revision on the diagnosis methods and on the

treatments available

PROPOSE a stepwise approach to the management of the disease

2.8.2 Definition and Classification

Symptoms of allergic rhinitis include rhinorrhea, nasal obstruction, nasal itching, and

sneezing, which are reversible spontaneously or with treatment. Allergic rhinitis was

previously classified as seasonal and perennial. The new ARIA classification of allergic

rhinitis is based on symptoms and quality-of-life parameters. Duration of symptoms is

subdivided into “intermittent” or “persistent” disease, while severity is subdivided into

“mild” or

Fig. b: Classification of allergic rhinitis (ARIA).


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Moderate-severe”, depending on symptoms and quality of life. This classification has been

recently validate.

Pathophysiology of allergic rhinitis

Risk factors associated with allergic rhinitis

Well-recognized risk factors for allergic rhinitis include having atopy, asthma, eczema and

other allergic diseases.

Many recent studies have found that children with a family history of atopic disease or

parents with allergic rhinitis, asthma, hay fever, and pollen allergies had a high risk of

developing allergic rhinitis.

Other confusing risk factors that may contribute to disease risk but are not well understood

include vitamin D, obesity, exposure to cigarette smoke, increased total serum IgE, increased

blood eosinophils and other environmental exposures common in urban settings.

It is generally accepted that atopic diseases are the results of inappropriate immunological

responses to common environmental allergens in genetically susceptible individuals.

Understanding the underlying immune inflammatory mechanisms is central to developing

better and more targeted therapies.

Changes at the microscopic level: The pathological changes of nasal mucosa from allergic

rhinitis and nonallergic rhinitis have been observed by light and electron microscope. The

results showed that the general characteristic was vascular dilatation with increased

permeability and glandular proliferation with increased secretory activity. The pathological

difference between mucous membranes of allergic and vasomotor rhinitis was mainly cellular

infiltration and degree of damage on the vascular wall. In allergic rhinitis, there were more

eosinophils, basophils, neutrophils and some mast cells and plasma cells in the nasal mucosa.

Gap formation in the capillary wall was found in the allergic nasal mucosa, there was less

cellular infiltration in nonallergic rhinitis. Cardinal symptoms and pathophysiologic

mechanisms are described graphically in The inflammatory response in the nasal mucosa in

subjects with allergic rhinitis challenged intranasally with an allergen includes an immediate

IgE-mediated.


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Figure 1: Sensitization to aeroallergen.

Figure 2: Early-and-Late-Phase response on physiopatology of allergic rhinitis.

Mast cell response as well as a late-phase response characterized by recruitment of

eosinophils, basophils, and T cells expressing Th2 cytokines including IL-4, a switch factor

for IgE synthesis, and IL-5, an eosinophil growth factor. Recent advances have suggested that

additional pathways may contribute to the pathophysiology of allergic rhinitis including local

synthesis of IgE in the nasal mucosa, the epithelial expression of cytokines that regulate Th2

cytokine responses (i.e., thymic stromal lymphopoietin, IL-25, and IL-33), and the activation

of histamine receptors other than H1 and H2 such as H4-histamine receptors,[17]

seasonal

increases in the antigen presenting cell (Langerhans' cell) are also evident. Investigations into


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the mechanisms involved in cell accumulation and activation reveal upregulation of leucocyte

endothelial adhesion molecules and an increase in interleukin-4 (IL-4) in naturally occurring

rhinitis, while mRNA for IL-4, IL-5 and granulocyte macrophage colony stimulating factor

activity and lavage tumour necrosis factor-alpha (TNF alpha) levels are increased following

local allergen challenge. These cytokines may be derived from a variety of sources, including

mast cells, eosinophils, and T-lymphocytes, and contribute to the underlying inflammatory

process in rhinitis. In both seasonal and perennial rhinitis, there is epithelial mast cell

accumulation and tissue infiltration by eosinophils. Activation of these cells can be observed

by electron microscopy and by elevated levels of tryptase and eosinophil cationic protein in

nasal lavage fluid, these levels of eosinophil cationic protein and albumin were also

significantly higher than those of the normal non-rhinitis. In the perennial allergic rhinitis, the

levels of tryptase, eosinophil cationic protein and albumin were higher than the normal non-

rhinitis. The levels of tryptase and histamine were higher in the perennial allergic rhinitis than

the seasonal allergic rhinitis. These changes in mediator levels were accompanied by a

significant influx of into the nasal mucosa of both the symptomatic seasonal rhinitis,

compared with asymptomatic and the perennial rhinitis compared to normal controls.

Mechanisms underlying the neuronal-based symptoms of allergy: Persons with allergies

present with symptoms that often are the result of alterations in the nervous system.

Neuronally based symptoms depend on the organ in which the allergic reaction occurs but

can include red itchy eyes, sneezing, nasal congestion, rhinorrhea, coughing,

bronchoconstriction, airway mucus secretion, dysphagia, altered gastrointestinal motility, and

itchy swollen skin. These symptoms occur because mediators released during an allergic

reaction can interact with sensory nerves, change processing in the central nervous system,

and alter transmission in sympathetic, parasympathetic, and enteric autonomic nerves . There

is a definite relation between the symptoms of hyperparasympathetic nervous system and

allergic rhinitis as one study results have indicated that patients with intermittent and mild

AR have hypervagal activity and hyposympathetic activity, and the predominance lessens in

patients with more persistent AR and severe symptoms.

Genetic basis for allergic rhinitis: Large-scale genome- wide association strategies are

underway to discover new susceptibility variants for allergic rhinitis and allergic phenotypes.

Characterization of the underlying genetics provides us with an insight into the potential

targets for future studies and the corresponding interventions. The last decade has been


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marked by the publication of more than 20 Genome-wide association studies (GWASs)

GWASs employing common single-nucleotide polymorphism of allergic rhinitis and the

associated allergic phenotypes. Allergic diseases and traits have been shown to share a large

number of genetic susceptibility loci, of which IL33/IL1RL1, IL-13-RAD50 and

C11orf30/LRRC32 appear to be important for more than two allergic phenotypes. GWASs

have further reflected the genetic heterogeneity underlying allergic phenotypes.

Etiology

Allergens

Aeroallergens are very often involved in allergic rhinitis.[12]

The increase in domestic

allergens is responsible in part for the increase in the prevalence of rhinitis, asthma and

allergic respiratory diseases. In the home, the main allergens are mites, domestic animals,

insects or those derived from plant origin. Outdoor allergens include pollens and moulds.

Occupational rhinitis is less well documented than occupational asthma is but is often

associated with asthma.

Latex allergy has become an increasing concern to patients and health professionals, who

should be aware of the problem and develop strategies for prevention and treatment.

Pollutants

Pollutants are involved in the aggravation of nasal symptoms in patients with allergic and

nonallergic rhinitis. The interaction between pollutants and rhinitis is suggestedby

epidemiological evidence, although the mechanism is not well understood. Indoor pollution,

including domestic allergens and indoor gas pollutants (tobacco smoke), is of great

importance, since in industrialised countries people spend over 80% of their time indoors.

Urban-type pollution is in many countries primarily of automobile origin, and the principal

atmospheric oxidant pollutants include ozone, nitric oxides, and sulphur dioxide. Diesel

exhaust fumes may also enhance IgE formation and allergic inflammation.

Mechanisms of action

In allergic rhinitis, the understanding of the mechanisms of the disease provides a framework

for its rational therapy, based on the complex inflammatory reaction rather than on the

symptoms alone. Allergy is classically considered to result from an IgE-mediated allergy

associated with nasal inflammation of variable intensity.[15]

Allergic rhinitis is characterised

by an inflammatory infiltrate made up of different cells, including: Chemotaxis, activation,


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Differentiation, and survival prolongation of various cell types including eosinophils, T

cells, mast cells and epithelial cells

Release of mediators by these activated cells: cytokines, chemokines, histamine and

cysteinyl leukotrienes (cys-LT) as the major mediators

Communication with the immune system and the bone marrow

Nonspecific nasal hyperreactivity is an important feature of allergic rhinitis and is defined as

an increased nasal response to normal stimuli, resulting in sneezing, nasal congestion and/or

secretion. Intermittent rhinitis can be mimicked by nasal challenge with pollen allergens, and

an inflammatory reaction occurs during the late-phase reaction. In persistent allergic rhinitis,

allergic triggers interact with an ongoing inflammatory reaction, and symptoms are due to

this complex interaction. The concept of “minimal persistent inflammation” has been

confirmed in perennial allergic rhinitis. In patients with persistent allergic rhinitis, allergen

exposure varies throughout the year, and there are periods in which there is little exposure.

Although symptom free, these patients still present with nasal inflammation.

Asthma

Nasal and bronchial mucosa share many similarities. Epidemiological studies have shown

that asthma and rhinitis often coexist in the same patients. Most patients with allergic (80%)

and nonallergic (50%) asthma have rhinitis, while many patients with rhinitis (20–30%) have

also asthma. Allergic rhinitis constitutes a risk factor for asthma, and many allergic rhinitis

patients have bronchial hyperreactivity.[18]

Pathophysiological studies also suggest that a strong relationship exists between rhinitis and

asthma. Although differences exist between rhinitis and asthma, upper and lower airways

may be considered as a unique entity influenced by a common inflammatory process. Since

bronchial challenge leads to nasal inflammation and nasal challenge leads to bronchial

inflammation, allergic diseases may be considered systemic. Consequently, when considering

a diagnosis of rhinitis or asthma, an evaluation of both the lower and upper airways should be

made.

Diagnosis

The diagnosis of allergic rhinitis is based on the coordination between a clinical history

(allergic symptoms), nasal examination and diagnostic tests.


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Clinical history

It is essential for an accurate diagnosis of rhinitis to assess its severity and response to

treatment. Although not necessarily of allergic origin, the main nasal symptoms are

obstruction, sneezing, itching and rhinorrhea

Nasal examination

In patients with mild, intermittent allergic rhinitis, a nasal examination is optimal, but all

patients with persistent allergic rhinitis need a nasal examination. Anterior rhinoscopy, using

a speculum and mirror, gives limited information. Nasal endoscopy, which can be performed

only by specialists, is more useful.

Diagnostic tests

In vivo and in vitro tests used to diagnose allergic diseases are directed towards the detection

of free or cellbound IgE. The diagnosis of allergy has been improved by allergen

standardisation.

Skin-prick test

The skin-prick test is used to demonstrate an IgE-mediated allergic reaction and represents a

major diagnostic tool in the field of allergy. If properly performed, it gives confirmatory

evidence for the diagnosis of a specific allergy.

Due to the complexity in performance and interpretation of the test, it is recommended that it

be carried out by trained health care professionals.

Serum-specific IgE

Serum-specific IgE has a similar value to that of skin tests

Allergen nasal challenge

The allergen nasal challenge is mainly used in research and, to a lesser extent, in clinical

practice. It is especially useful in the diagnosis of occupational rhinitis.

2.8.6.3.4 Imaging

Imaging is not usually necessary.

Diagnosis of asthma

Guidelines for recognising and diagnosing asthma have been published by the Global

Initiative for Asthma (GINA) and are recommended.


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Measurement of lung function and confirmation of the reversibility of airflow obstruction are

essential steps in the diagnosis of asthma Laboratory diagnosis.

List of diagnostic tests

• Allergen skin testing is recommended as the most comfortable, most sensitive, and least

expensive method to detect allergen sensitization. This is performed by an allergist, who

will place selected allergen solutions on the patient‟s skin and examine for wheal and

flare reactions within 20 minutes. The results are immediately available and often

illustrative and educational for the patient.

• Serum tests for allergen‐specific IgE antibodies are another way to detect allergen

sensitization.

They provide similar information as allergen skin tests, but are more expensive and less

sensitive for diagnosing environmental allergies. Selection and interpretation are best carried

out by an allergist, as ordering excessive or irrelevant allergens can lead to confusion.

Lists of imaging techniques

• A sinus CT scan may be considered for a patient with persistent symptoms refractory to

therapy.

Potential pitfalls/common errors made regarding


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Differential diagnosis

Differential diagnosis features

Upper respiratory infection Relatively short in duration, typically <2 weeks. Nasal

obstruction, rhinorrhea, and sneezing are common, nasal mucosa is typically erythematous,

but nasal and ocular itching are less prominent.

Rhinitis medicamentosa History of vasoconstrictor nasal spray use or cocaine abuse.

Beefy red nasal membranes on examination.

Atrophic rhinitis Elderly patients.

Chronic congestion with perception of bad odor.

Negative allergen skin tests Chronic non‐allergic rhinitis Perennial symptoms without nasal

itching or sneezing.

Symptoms often exacerbated by changes in temperature, humidity, odors, or alcohol.

Negative allergen skin test to environmental allergens.

Rhinitis of pregnancy Pregnant patient. Improvement after pregnancy Nasal polyps Polyps

may be visible on clinical rhinoscopy examination, fiberoptic rhinoscopy, or on imaging.

Anosmia is common

Management

Treatment

Environmental control

A logical approach to treat allergic rhinitis is to avoid allergen exposures. Reducing the

allergic load may significantly decrease symptoms. Methods of reduced exposure to pollen

are to avoid outdoor activities during relevant pollen seasons and to use air conditioning

when possible.[15]

To control dust, mites and mold; household humidity should be reduced,

linens should be washed frequently, carpets and pets should be removed from most used

living areas. Hypoallergenic coverages, HEPA filtration and airborne purifiers can also be

used.[16]

When multiple environmental control techniques are combined, studies have

demonstrated moderate success.


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Pharmacological treatment

Pharmacologic management should take into account to the patient‟s underlying condition,

pathophysiology, the dominant symptoms, the patient‟s age and condition, the coexistence of

airway disorders, the patient‟s preference, and the patient‟s compliance history.

Antihistamines

There are four receptors for histamine; H1 receptors are found on blood vessels, on sensory

nerves, on smooth muscles and in the central nervous system. When histamine binds to H1

receptor; vasodilatation, increased vascular permeability, sneezing, pruritus, glandular

secretion are occured. The contribution of histamine to the early allergic response, largely

mediated by the H1 receptor, large number of H1 antagonists now in clinical use.

Antihistamines are frequently used as a first-line therapy; they block H 1 receptor sites and

prevent histamine releasing, inhibits increased vascular permeability, smooth muscle

contraction, increased mucus production, and pruritus. They also effects the response of skin

testing via preventing the „whale and flare response‟ but in vitro test is not effected.

Antihistamines are effective in early-phase reaction and therefore reduce sneezing,

rhinorrhea, and itching. They have little effect on nasal congestion, a late-phase

phenomenon.[17]

The first-generation antihistamines are effective in the relief of symptoms of allergic rhinitis.

However, first generation antihistamines have some undesirableside effects because of their

lack of selectivity and the resulting nonspecific stimulation of other receptors. It causes

sedation and impair performance and have been associated with a higher risk of both

automobile and work-related accidents, decreased work performance and productivity, and

impaired learning performance. Many have anticholinergic effects and cause dry mouth.

Chlorpheniramine, clemastine, diphenhydramine, hydroxyzine, ketotifen, mequitazine,

oxatomide are the major old generation antihistamines.

Second-generation antihistamines are less lipophilic than first-generation H1 antihistamines

and do not penetrate the blood–brain barrier. Receptor selectivity also reduces the incidence

of anticholinergic side effects. They have no anticholinergic activity and are well mabsorbed,

with a rapid onset of action and symptom relief usually within 1 hour. Acrivastine, azelastine,

cetirizine, desloratadine, ebastine, fexofenadine, levocetirizine, loratadine, mizolastine,

rupatadine are the major new generation antihistamines.


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Azelastine, olopatadine and levocabastine are two local antihistamines. They are quickly

effective against nasal or ocular symptoms. They can produce minor local side effects;

azelastine has bitter taste. These intranasal antihistamines also tend to decrease nasal

congestion more than the oral antihistamines.[18]

Topical steroids

Topical steroids are potent medications for the treatment of allergic rhinitis. These agents

reduce multiple aspects of the inflammatory response to allergen. They relieve sneezing,

itching, and rhinorrhea, and also nasal congestion. Maximal effect may take from 1 to 2

weeks after the onset of their use.

They have minimal systemic absorption with no systemic side effects, and they have been

approved for use in children; and do not affect bone growth in children. The most frequent

side effect is nasal irritation, is manifested as a nasal burning sensation. Thinning of nasal

epithelium, abnormalities in nasal mucosa and septal perforation can be seen after prolonged

use. Local side effects, such as dryness and epistaxis, can be reduced by careful patient

instruction on their use, intranasal saline can also be used concomitantly.[19]

However, when

intranasal antihistamines and intranasal corticosteroids are combined, there is an additive

effect.

Currently used topical forms of corticosteroids include flunisolide, beclomethasone,

triamcinolone, budesonide, ciclesonide, mometasone,and fluticasone.

Systemic steroids

These agents are usually administered to patients during intractable and severe exacerbations

of allergic symptoms. They are used successfully in combination with antibiotics for

treatment of sinus infections complicating allergic rhinitis. They can be administered either

by intramuscular injection or orally. The repeated use of these agents can cause serious side

effects.[19]

Decongestants

Decongestants show their effect via α1 and α2 adrenergic receptors present on blood vessels.

They control blood flow and blood volume in capacitance vessels. Increased sympathic

stimulation with adrenergic activity or exercise, nasal mucosa and turbinates are congested.

Topical decongestants are effective in reducing nasal congestion. Prolonged use can bring


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about rhinitis medicamentosa, which is characterized by a reduced duration of action and

rebound nasal congestion after cessation of therapy. So; use of these agents should be limited

to a few days.

Oral decongestants exert their effects directly and by stimulating release of norepinephrine.

Pseudoephedrine and phenylephrine can be used with antihistamines. But in extensive use of

oral decongestants hypertensive crisis and cardiovascular problems can be occured. It should

be carefully prescribed in uncontrolled hypertension, severe coronary artery disease, closed

angle glaucoma, prostatic hypertrophy, urinary retention.[20]

Chromones

Like antihistamines, cromolyn is a mast cell stabilizer; more helpful for sneezing, rhinorrhea,

and nasal itching than for nasal congestion. Its safety profile, however, makes it an attractive

treatment, especially in children and pregnant women. Intranasal cromolyn must be used

before the onset of symptoms to be effective. The recommended dosage is four times daily.

Anticholinergics

Anticholinergic agents inhibit parasympathetic stimulation of glandular secretion by

competing for muscarinic receptors on glands.These agents tend to control only rhinorrhea

and have no other effects on allergy symptoms. One of the most commonly used intranasal

anticholinergics is ipratropium bromide. The side effects of anticholinergics are minor and

local, as there is virtually no systemic anticholinergic activity.

Leukotriene inhibitors

Leukotrienes were detected both in the early and late phase of an allergic reaction.

Leukotrienes stimulate mucous glands, which results in rhinorrhea, and they also have the

ability to increase microvascular permeability and blood flow that result in tissue edema and

subsequent congestion. Introduction of leukotriene modifiers increased the therapeutic

options for patients who have allergic rhinitis. The drugs in this class include montelukast,

pranlukast and zafirlukast, which block cysteinyl leukotriene type receptors. Clinical studies

have shown its efficacy to be greater than that of placebo, but less effective than

antihistamines and intranasal steroids in the treatment of allergic rhinitis.


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Immunotherapy

Allergen-specific immunotherapy is a very effective method of treatment in carefully selected

patients with allergic rhinitis. It is the only treatment that can lead to a life-long tolerance.

Immunotherapy attempts to increase the threshold level of the appearance of symptoms after

exposure. Indications for immunotherapy include long-term pharmacotherapy for prolonged

periods of time, the inadequacy or intolerability of drug therapy, and significant allergen

sensitivities. Before beginning immunotherapy, the physician must first confirm the atopic

diagnosis by testing IgE specific to the offending allergen.

Subcutaneous injection immunotherapy (SCIT) begins with low-dose injections of allergen

extracts and builds to a maintenance dose. Injections usually begin at weekly intervals and

are reduced in frequency when maintenance doses are reached. Allergen injections should be

administered under the supervision of a qualifi ed medical practitioner, and patients should be

observed for at least 30 minutes after every injection. Proper resuscitative equipment should

be present because anaphylactic reactions can occur at any time during treatment.

Sublingual immunotherapy (SLIT) is a new, safe, efficacious and more convenient method

for delivering immunotherapy. SLIT tends to be easy and safe to administer at home by the

patients themselves, and therefore is likely to be more cost-effective. The allergen is kept

under the tongue for one to two minutes and then swallowed. If the vaccine is swallowed

imme

Anti IgE

Omalizumab is a recombinant humanized monoclonal antibody that binds selectively to IgE.

It lowers free IgE levels in the circulation. It reducesthe free IgE level in serum, inhibits

allergen-induced circulating and tissue eosinophils.[22]

Surgery

Inferior turbinate hypertrophy appears to be at least partially responsible for nasal congestion

seen with allergic rhinitis. Radiofrequency ablation of the inferior turbinate provided

decreased nasal resistance and improved congestion


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Pregnancy/breastfeeding

• Skin testing should be deferred until after delivery, as there is risk of systemic allergic

reaction with skin testing.

• Non‐pharmacologic therapies should be considered first. Cromolyn sodium nasal spray is

first line for mild allergic rhinitis during pregnancy and breastfeeding given its excellent

safety profile.

Budesonide is the only intranasal glucocorticosteroid with pregnancy category B

classification (other agents are category C). There are no intranasal glucocorticosteroids with

pregnancy category Arating. Loratadine and cetirizine have reassuring human data for drug

safety in pregnant patients.

• Immunotherapy should not be initiated during pregnancy. If a pregnant patient is already

on immunotherapy, then doses should not be increased during pregnancy.

Table a: Of treatment summery.

Conservative

• Allergen avoidance

• Nasal saline irrigation

Medical

• Intranasal glucocorticoids (1–2 sprays once

to twice daily depending on specific agent

and patient‟s age)

• Oral antihistamines

• Diphenhydramine (5 mg/kg/day in divided

doses every 6–8 hours)

• Loratadine (5 mg/day for children 2–5 years,

10 g/day for children ≥6 years or adults)

• Fexofenadine (30 mg twice daily for

children 2–11 years, 60 mg twice daily or

180 mg once daily for children ≥12 years or

adults)

• Cetirizine (2.5 mg once daily for children 6–

12 months, 2.5 mg once or twice daily for

children 12 months to <2 years, 2.5 mg

twice daily or 5 mg once daily for children

2–5 years, 5–10 mg once daily for children

≥6 years or adults)

Intranasal antihistamines

• Azelastine (1–2 sprays to each nostril twice

daily)

• Cromolyn sodium (1–2 sprays to each

nostril up to 4 times daily)


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Montelukast

• Ipratropium bromide (2 sprays to each

nostril 3–4 times daily)

• Immunotherapy (subcutaneous injections of

allergens to which the patient is sensitized,

typically administered weekly during

build‐up to target dose and then monthly

injections of target dose for 3–5 years)

METHOD

This study show prospective study to patient from 2014 to2020.

RESULTS

Table 1: Allergic vs. nonallergic rhinitis.


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Table 4: Strength of evidence for the treatment of allergic rhinitis. Recommendations

are evidence-based on randomisedcontrolled trials (RCT) carried out on studies

performed with the previous classification of rhinitis: seasonal (SAR) and perennial

(PAR) allergic rhinitis. Strength of recommendation: A based on RCT or meta-analysis,

D based on the clinical experience of experts.

DISCUSSION

This prosoective study form more than 200 patient visit to our hospital and fallow up by

mobile or visites Overall, AR is an allergic disease characterized by nasal symptoms, and

when accompanied by ocular symptoms, is called ARC. The disease is common, may start

early in life, and is associated with a high burden of disease that can particularly impair the


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functioning of children in school and other domains of life. Identifying seasonal and

perennial triggers can be helpful, and the first step of treating the patient is avoidance.

Medications are very helpful for treating symptoms and mitigating the disease burden but do

not usually affect the underlying inflammation. IT not only has been shown to improve AR

but also may prevent additional allergic sensitizations and asthma development.

CONCLUSION

As one of the most common chronic conditions in the population that continues to rise in

prevalence, allergic rhinitis needs to be accurately recognized and treated. Appropriate

management may prevent the development of asthma, which often co-exists with allergic

rhinitis, as well as other serious complications. A three-part approach to management, which

includes allergen avoidance, immunotherapy, and pharmacologic treatment, can reduce the

progression of the inflammatory process and improve the patient‟s quality of life.

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