Antiallergic Drugs » Brompheniramine

Drugs used for the temporary relief of the symptoms and allergy caused by allergic rhinitis, hay fever and allergy symptoms.

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July 11, 2011 – 12:27 pm

Allergen avoidance

Antihistamines

TABLE. Relative Adverse-Effect

Profiles of Antihistamines

Medication

Relative Sedative Effect

Relative Anticholinergic Effect

Alkylamine class,

nonselective

Brompheniramine

maleate

Low

Moderate

Chlorpheniramine

maleate

Low

Moderate

Dexchlorpheniramine

maleate

Low

Moderate

Ethanolamine

class, nonselective

Carbinoxamine

maleate

High

Clemastine

fumarate

Moderate

High

Diphenhydramine

hydrochloride

High

Ethylenediamine

class, nonselective

Pyrilamine maleate

Low

Low to none

Tripelennamine

hydrochloride

Moderate

Low to none

Phenothiazine

class, nonselective

Promethazine

hydrochloride

High

Piperidine class,

nonselective

Cyproheptadine

hydrochloride

Low

Moderate

Phenindamine

tartrate

Low to none

Moderate

Phthalazinone

class, peripherally selective

Azelastine (nasal

only)

Low to none

Piperazine class,

peripherally selective

Cetirizine

Low to moderate

Low to none

Piperidine class,

peripherally selective

Desloratadine

Low to none

Fexofenadine

Low to none

Loratadine

Low to none

TABLE. Oral Dosages of Commonly Used

Antihistamines and Decongestants

Medication

Dosage and Intervala

Adults

Children

Nonselective (first-generation)

anthihistamines

Chlorpheniramine

maleate, plainb

4 mg every 6 h

6-12 yr: 2 mg every 6 h

2-5 yr: 1 mg every 6 h

Chlorpheniramine maleate,

sustained-release

8-12 mg daily at bedtime or 8-12 mg

every 8 h

6-12 yr: 8 mg at bedtime <6 yr: Not recommended Clemastine fumarateb 1.34 mg every 8 h 6-12 yr: 0.67 mg every 12 h Diphenhydramine hydrochlorideb 25-50 mg every 8 h 5 mg/kg/day divided every 8 h (up to 25 mg per dose) Peripherally selective (second-generation) antihistamines Loratadineb 10 mg once daily 6-12 yr: 10 mg once daily 2-5 yr: 5 mg once daily Fexofenadine 60 mg twice daily or 180 mg once daily 6-11 yr: 30 mg twice daily Cetirizineb 5-10 mg once daily >6 yr: 5 mg once daily infants

6-11 monthsc

Oral decongestants

Pseudoephedrine,

plain

60 mg every 4-6 h

6-12 yr: 30 mg every 4-6 h

2-5 yr: 15 mg every 4-6 h

Pseudoephedrine, sustained-released

120 mg every 12 h

Not recommended

Note: Fexofenadine and

cetirizine are available by prescription only.

aDosage adjustment may be needed in

renal/hepatic dysfunction. Refer to manufacturers’ prescribing information.

bAvailable in liquid form.

c0.25 mg/kg orally demonstrated to

be safe.

dControlled-release product

available: 240 mg once daily (60-mg immediate-release with 180-mg

controlled-release).

Decongestants

TABLE. Duration of Action of Topical

Decongestants

Medication

Duration (h)

Short-acting

Phenylephrine

hydrochloride

Up to 4

Intermediate-acting

Naphazoline

hydrochloride

4-6

Tetrahydrozoline

hydrochloride

Long-acting

Oxymetazoline

hydrochloride

Up to 12

Xylometazoline

hydrochloride

Nasal Corticosteroids

TABLE. Dosage of Nasal Corticosteroids

Medication

Dosage and Interval

Beclomethasone

dipropionate

>12 yr: 1 inhalation (42 mcg) per

nostril 2-4 times a day (maximum, 336 mcg/day)

6-12 yr: 1 inhalation per nostril 3 times/day

Beclomethasone

dipropionate, monohydrate

>12 yr: 1-2 inhalations once

daily 6-12 yr: 1 inhalation per nostril (42 mcg) twice daily to start

Budesonide

>6 yr: 2 sprays (64 mcg) per

nostril in AM and PM or 4 sprays per nostril in AM (maximum, 256 mcg)

Flunisolide

Adults: 2 sprays (50 mcg) per

nostril twice daily (maximum, 400 mcg)

Children: 1 spray per nostril 3

times a day

Fluticasone

Adults: 2 sprays (100 mcg) per

nostril once daily; after a few days decrease to 1 spray per nostril

Children > 4 yr and adolescents:

1 spray per nostril once daily (maximum, 200 mcg/day)

Mometasone furoate

>12 yr: 2 sprays (100 mcg) per

nostril once daily

Triamcinolone

acetonide

>12 yr: 2 sprays (110 mcg) per

nostril once daily (maximum, 440 mcg/day)

Cromolyn Sodium

Ipratropium Bromide

Montelukast

June 18, 2011 – 7:31 am

Traditionally all H1 antagonists were considered to act via the mechanism of competitive inhibition at the H1 receptor. Recently, the concept of reversed or inverse agonist has been introduced to explain the action of antihistamines. The idea is based on the existence of histamine receptors, at equilibrium, existing in both active and inactive forms. Histamine stabilizes the histamine receptor’s conformation, resulting in a predominantly activated state, whereas antihistamines are thought to be agonists of the inactive conformation at the receptor site. Stimulation by antihistamines at the receptor thus results in the abolition of the effects of histamine. Important regarding this concept is that antihistamines induce the downregulation of histamine receptor activity, both in the presence and the absence of histamine. Most, but not all, first-generation antihistamines have a structural resemblance to histamine in that they contain a substituted ethylamine moiety. It was previously felt that this structural similarity was necessary for competitive inhibition. However, with the development of newer agents, it has been shown that antihistamine activity can occur without an obvious shared structural relationship between histamine and its antagonist. The proposed difference between the mechanisms of action of antihistamines with an ethylamine moiety (thus exhibiting a structural resemblance to histamine) and those without this entity is that the former group may actually bind to the same site on the histamine receptor as histamine, whereas the latter group binds to the seven-chain, G protein-coupled histamine receptor at other sites to sterically hinder the binding of histamine. In addition, the absence of structural similarities adds credence to the inverse agonist hypothesis.

First-generation antihistamines have classically been separated into categories based on the atom linking the ethylamine grouping to aromatic substituents (Fig. 1). For example, if the link is via oxygen, the drugs are classified as ethanolamines; if via carbon, they are called alkylamines; and if via nitrogen, they are called ethylenediamines. Certain biological activities have been attributed to these differences, but clinically it is unclear whether or not these are significant. For example, it is said that alkylamines cause less drowsiness in general than do ethanolamines.

All first-generation H1 receptor antagonists are rapidly absorbed and reach peak serum concentration within 3 h when given in liquid form. All are extensively metabolized in the liver, and little, if any, of these drugs are excreted unchanged in the urine. All of these agents are metabolized through the hepatic cytochrome P450 system. Rates vary from patient to patient and are age dependent, with children having shorter, and the elderly having longer elimination half-lives. Severe hepatic dysfunction can prolong the half-life and require dosing adjustments.

An important principle of the pharmacodynamic activity of these drugs is that their tissue effect is delayed relative to peak serum levels and can extend far beyond the life of the drug in the serum. For example, hydroxyzine can suppress histamine-induced wheal and flare for as long as 60 h despite maintaining a negligible serum concentration at this time.

Table Characteristics of Representative First-Generation H1 Antagonists Based Upon Chemical Classification

Chemical class

Examples

Comments

Ethanolamines

Diphenhydramine

Significant

antimuscarinic effects. Can be potent sedatives, but sedative potential

varies, with clemastine producing the least amount. Low incidence of

gastrointestinal side effects. Can have some anti-motion sickness activity.

Diphenhydramine and clemastine both available over the counter.

Clemastine

Carbinoxamine

Alkylamines

Chlorpheniramine

Relatively

moderate incidence of drowsiness.

Moderate

anticholinergic effect. No antiemetic or antimotion sickness activity. Little

gastrointestinal side effects. All available over the counter. Occasional

paradoxical central nervous system stimulation, especially in children.

Brompheniramine

Dexchlorpheniramine

Tripolidine

Ethylenediamines

Tripelennamine

Mild to

moderate sedation. Slight anticholinergic effect. Some local anesthetic

effect. Pyrilamine

is sold over

the counter and is the oldest antihistamine preparation available today. As a

group, may have more frequent gastrointestinal side effects.

Pyrilamine

Antazoline

Piperazines

Hydroxyzine

has highest sedative activity in group. Meclizine and cyclizine relatively

low sedative activity with main use being for vertigo, anti-motion sickness,

and antiemetic activity. Hydroxyzine has significant anticholinergic

activity.

Meclizine

Cyclizine

Piperadines

Cyproheptadine

Mild to

moderate sedation. Little anticholinergic activity, antiemetic activity, and

anti-motion sickness activity. Cyproheptadine has potent antiserotonin

effect. As a class, has relatively high incidence of paradoxical central

nervous system stimulatory activity.

Phenindamine

Azatadine

Phenothiazines

Promethazine

Usually highly

sedating. Strong antiemetic,

anticholinergic

activity. Main clinical use is as

antiemetics.

Methdilazine

Trimeprazine

The tissue effect, however, is delayed compared to peak serum concentrations. For example, with hydroxyzine, maximal suppression of wheal and flare does not occur until 7 h after peak serum concentrations have been achieved. Based on these pharmacody-namic observations, it can be concluded that it is best to administer H1 antagonists before allergen exposure.

Table Pharmacokinetic and Pharmacodynamic Characteristics of Selected First-Generation H1 Antagonists

Drug

Approximate time

at which peak serum oncentration is reached

after oral dose (h)

Approximate half-life (h)

Approximate duration of biological activity

(suppression wheat and flare)

Route of metabolism

Diphenhydramine

0 .75-2.5

8-9

6-10

Liver

Chlorpheniramine

1.5-2.5

20-24

Liver

Hydroxyzine

1-2.5

Liver

Brompheniramine

2-3

Liver

Tripolidine

1-2

2.1

—

Liver

First-generation antihistamines have a number of pharmacological activities unrelated to their antihistaminic properties. They can exert antimuscarinic, anti-aadrenergic, antidopaminergic, antiserotonergic, local anesthetic, antiemetic, and anti-motion sickness activity.

By far the most common significant side effect of first-generation antihistamines is drowsiness. All first-generation antihistamines cross the blood-brain barrier. The exact mechanism of production of drowsiness by these drugs is unknown, but may include antihistaminic, anticholinergic, antiserotonergic, and antiadrenergic activities. It should be noted that the antihistaminic activity does not necessarily correlate with the sedative potential, suggesting that this is not the sole cause of this side effect. The degree of sedation depends on many factors, including age, the pattern and quality of nocturnal sleep, and concurrent medication. First-generation antihistamines clearly potentiate the activity of other sedative drugs such as alcohol.

Of importance is the fact that the subjective degree of drowsiness does not necessarily correlate with the objective measurement of central nervous system impairment. For example, drowsiness can occur without impairment and impairment without drowsiness. Although drowsiness can be overcome by the exertion of will, impairment of cognitive functions and psychomotor performance cannot, and will persist until the effect of the drug abates.

Paradoxical central nervous system stimulation can occur in some individuals, especially children. Other central nervous system side effects include dizziness, tinnitus, blurred vision, and tremors.

The next most common group of side effects produced by first-generation antihistaminics relate to their antimuscarinic activity. These include dryness of the mouth, urinary retention, blurring of vision, difficulty urinating, and constipation.

Other side effects are uncommon and include loss of appetite, nausea, abdominal pain, and diarrhea. Drug allergy to first-generation antihistamines is extremely rare but has been reported. Leukopenia, agranulocytosis, and hemolytic anemia have all been seen. Teratogenic effects have been noted in animals, but there has been no documentation of this in human beings.

Limitations to the use of the first-generation antihistamines result from their side effects, including sedation, dry mouth, urinary hesitancy, and, in children, paradoxical central nervous system stimulation.

May 6, 2011 – 8:59 am

Antihistamines have been employed in the treatment of allergic rhinitis since the discovery of the first histamine receptor antagonists in 1937. First-generation antihistamines — including diphenhydramine (Pfizer’s Benadryl, generics), chlorpheniramine (Schering-Plough’s Chlor-Trimeton, generics), and brompheniramine maleate (Wyeth’s Dimetane, generics) — are very effective in treating many common allergic rhinitis symptoms (e.g., rhinorrhea, sneezing, itchy nose, itchy eyes). However, first-generation antihistamines are highly lipophilic and can readily cross the blood-brain barrier. Once they penetrate the CNS, first-generation antihistamines bind H1 receptors, as well as cholinergic, dopamin-ergic, and serotonergic receptors, in the brain. This action triggers undesirable and troublesome CNS side effects, including fatigue, drowsiness, performance impairment, and anticholinergic effects (e.g., dryness of the mouth and eyes, constipation, increased ocular pressure).

Since 1981, numerous second-generation antihistamines (e.g., fexofenadine [Sanofi-Aventis’ Allegra / Telfast], cetirizine [Pfizer / UCB / Daiichi / / Sumitomo’s Zyrtec / Virlix / Cirrus, generics], desloratadine [Schering-Plough’s Clarinex / Aerius / Neoclarityn], levocetirizine (UCB’s Xyzal / Xusal]) have entered the market, and these agents have all but replaced first-generation antihistamines in the prescription allergic rhinitis market. Second-generation antihistamines are equally effective in controlling the common symptoms of allergic rhinitis, but they offer numerous advantages over their predecessors. Because second-generation antihistamines are larger molecules, possess a different ionic charge, and are more lipophobic than the first-generation agents, they do not cross the blood-brain barrier as readily as the original antihistamines. Thus, they lack the unwanted CNS effects of the first-generation agents. Additionally, second-generation antihistamines are highly specific for histamine H1 receptors, with little affinity for cholinergic, dopaminergic, and serotonergic receptors. As a result, they cause mild or no sedation, do not affect performance, and have no anticholinergic effects.

The discussion here focuses on four of the top-selling second-generation antihistamines — fexofenadine, cetirizine, desloratadine, and levocetirizine — as representatives of this crowded class. These four antihistamines offer comparable efficacy. Some of the product characteristics that differ between agents include the following: indications and age of patients for which each drug is approved; formulations in which the drug is available; and the potential to cause sedation.

There are four types of histamine receptors in the human body — H1, H2, H3, and H4 — although H1 is the receptor through which histamine exerts most of its effects in allergic disease. The H1 receptor demonstrates constitutive activity in the human body — even in the absence of ligand binding — because two states of the H1 receptor (the active state and the inactive state) exist in equilibrium. Histamine preferentially binds to the active form of the receptor, shifting the balance between the two receptor states toward the active form. The active form of the receptor then initiates a G protein-mediated signal transduction cascade that results in the degranulation of FceRI+ cells. Antihistamines bind to the inactive form of the H1 receptor and stabilize this conformation, thereby inhibiting the signal transduction cascade that ultimately results in degranulation of mast cells and basophils. H1 antihistamines, previously viewed as H1 receptor antagonists, have been reclassified as inverse agonists owing to enhanced understanding of their molecular pharmacology.

The degranulation of mast cells and basophils initiates a host of physiological changes leading to allergic rhinitis’s early-phase symptoms (e.g., sneezing, itching, rhinor-rhea, ocular irritation). However, antihistamines are less effective at controlling nasal congestion, as histamine is not the primary mediator of this symptom. Instead, mediators such as kinins, prostaglandins, leukotrienes, and, in the late-phase allergic response, leukocyte infiltration are more intimately involved in nasal congestion.

Numerous in vitro and in vivo studies have shown that antihistamines possess a range of anti-inflammatory properties, including down-regulation of adhesion protein expression, inhibition of eosinophil and other inflammatory cell migration

and activation, and inhibition of the generation and activity of various proinfiammatory cytokines and mediators. However, further studies are needed to determine the clinical relevance of these anti-inflammatory effects in allergic rhinitis patients during natural exposure to allergens at typical therapeutic doses of oral antihistamines.

Most second-generation antihistamines are delivered orally; the exceptions are azelastine (MedPointe’s Astelin, Viatris’ Allergodil / Rhinolast / Afluon) and levocabastine (Janssen Cilag’s [a Johnson & Johnson subsidiary] Livostin), which are administered intranasally. Because of patient preference for oral formulations, azelastine and levocabastine are used far less frequently than oral antihistamines for the treatment of allergic rhinitis.

April 13, 2011 – 6:08 am

Immediate and delayed reactions to airborne allergens, beginning with

the generation and presence of specific antigen-responsive IgE antibody

receptors on mast cells of the nasal mucosa

• An antigen-antibody chemical union initiates a cascade of events in

the mast cell culminating in its degranulation and production of a

melange of inflammatory mediators including histamine, heparin,

leukotrienes, prostaglandins, proteases and platelet activating factor

• An immediate symptomatic response occurs followed by a more

prolonged, persistent late phase reaction. This involves the

infiltration into the reactive region of eosinophils, neutrophils,

basophils and mononuclear cells

• May be seasonal or perennial depending on climate and individual response and the offending antigens

• Seasonal responses usually to grasses, trees and weeds

• Perennial responses usually house dust mites, mold antigens and animal body products

System(s) affected: Pulmonary, Skin/Exocrine, Hemic/Lymphatic/lmmunologic

Genetics: Complex, but strong genetic determination present

Incidence/Prevalence in USA: 10-25% of the population affected

Predominant age:

• Onset usually in first 4 decades with declining tendency with advancing age

• Mean age onset approximately 10 years

Predominant sex: Male = Female

• Nasal stuffiness and congestion

• Rhinorrhea usually clear

• Pruritus of nose, eyes and palate

• Sneezing, often paroxysmal

• Injection and watering of eyes

• Postnasal drainage

• Mouth breathing

• Fatigue or malaise

• Dark circles under eyes, “allergic shiners”

• Transverse nasal crease from rubbing nose upwards

• Inhalant allergens:

– Perennial: house dust mites, molds, animal dander.

cockroach

– Seasonal: tree, grass and weed pollens

– Occupational: latex, plant products (such as baking flour), sensitizing chemicals

Risk Factors

• Family history

• Repeated exposure to offending antigen

• Exposure to multiple offending allergens

• Presence of other allergies, e.g., atopic dermatitis, asthma, urticaria

• Non-compliance to appropriate therapeutic measures

Differential Diagnosis

• Nonallergic rhinitis with eosinophilia syndrome (NA-RES)

• Vasomotor rhinitis

• Chronic sinusitis

• IgA deficiency with recurrent sinusitis

• Nasal polyps and tumor

• Reactive rhinitis of recumbency

• Cribriform plate defect with cerebrospinal fluid leakage (rule out by testing watery discharge for sugar)

• Foreign body

• Hormonal: pregnancy, thyroid disorder, oral contraceptives

• Medications

– Rebound effect associated with continued use of topical decongestant drops and sprays

– Aldosterone converting enzyme inhibitors

– Chronic aspirin use

• Septal/anatomical obstruction

• Chronic rhinitis digitorum

Laboratory

• CBC with differential. May have slight increase in eosinophils but often normal with uncomplicated rhinitis.

• Nasal probe smear with cytologic exam for eosinophils

• Increase IgE level. Determine specific allergen sensitivity with allergen skin testing or RAST.

Drugs that may alter lab results:

• Corticosteroids will ablate eosinophilia

Disorders that may alter lab results:

• Secondary infections may alter differential and decrease nasal eosinophils

• Parasitic infestations with more marked eosinophilia

Pathological Findings

• Nasal washing/scraping

– Eosinophils predominate

– Basophils

– May see mast cells

• Nasal mucosa

– Submucosal edema but intact without evidence of destruction

– Eosinophilic infiltration

– Granulocytes to lesser extent

– Increased amount of tissue waterwith poor staining of ground substance

– Congested mucous glands and goblet cells

Special Tests

• Skin tests using suspected antigens. Either technique manifests a

positive reaction by inducing an expanding wheal and flare reaction.

Special training recommended and available treatment for anaphylaxis

mandatory.

– Prick or puncture: a superficial injury to the epidermis with application of diluted test antigen

– Intradermal: Introduction of diluted material between layers of skin raising a 4 mm wheal using a 25 or 27 gauge needle

• Radioallergosorbent test (RAST)

– More expensive and used especially in cases where skin testing not practical, e.g., in atopic dermatitis and dermatographia

• Audiometry

– For deficits and baseline evaluation

– Rhinoscopy: particularly useful to visualize intra-nasal anatomy,

posterior pharyngeal structures including adenoids and larynx

Imaging

Sinus radiographs when indicated. Check for complete opacity, fluid

level and mucosal thickening. Sinus imaging using CT may be preferable.

Diagnostic Procedures

Appropriate diagnostic prick test kits available.

Appropriate Health Care

Outpatient

General Measures

• Patient education, assurance and understanding important

• Limit exposure to offending allergen

• Try to establish specific cause(s) — history and appropriate skin testing

• Intensity of treatment determined by severity of disease

• Allergen immunotherapy (allergy shots/desensitization)

– Usually reserved for seasonal allergies uncontrollable with drugs and not responding to environmental adjustment.

– Specific allergen extract is injected subcutaneously in increasing doses to patient tolerance as determined by local reaction

– Patient response should be evaluated each season or year

Surgical Measures

Septoplasty when deviation significant enough to interfere with benefits of medication.

Activity

No specific restrictions. Emphasize avoiding activity in areas of allergen exposure.

Diet

No special diet unless concomitant food reactions suspected and evaluated

Drug(s) of Choice

Most patients present because of inability to control symptoms with

avoidance of allergens or with over the counter medications.

Antihistamines (second generation have a favorable side effects profile)

are considered first line therapy for most patients. Topical nasal

corticosteroids are usually considered second line therapy, but should

be used in patients with more severe nasal symptoms. Consider allergen

immunotherapy when usual pharmaceutical therapy fails or in patients

with comorbidities or complications. Cromolyn is sometimes surprisingly

helpful but a patient may have already tried this OTC agent.

• Antihistamines (H1 antagonists):

– First generation: side effects include sedation, performance impairment, anticholinergic effects. Includes 5 major classes:

• Ethanolamines — diphenhydramine (Benadryl), clemastine (Tavist)

• Alkylamine — chlorpheniramine, brompheniramine

• Ethylenediamines — tripelennamine (PBZ)

• Piperazines — hydroxyzine (Atarax)

• Phenothiazines — promethazine (Phenergan), methdilazine (Tacaryl)

– Second generation (considered non-sedating)

• Loratadine (Claritin)

• Desloratadine (Clarinex)

• Fexofenadine (Allegra)

• Cetirizine (Zyrtec)

– Intranasal: azelastine (Astelin)

• Decongestants

– Oral, e.g., pseudoephedrine

– Topical drops or sprays, e.g., phenylephrine

– Topical ophthalmic for annoying conjunctival itching

• Mast cell stabilizers

– Cromolyn (Nasalcrom)

– Olopatadine (Patanol), cromolyn (Opticrom); topical ophthalmics for conjunctival itching

• Leukotriene antagonist

– Montelukast (Singulair)

• Steroids

– Intranasal

• Beclomethasone (Beconase AQ, Vancenase AQ)

• Flunisolide (Nasalide, Nasarel)

• Triamcinolone (Nasacort)

• Budesonide (Rhinocort)

• Mometasone (Nasonex)

– Fluticasone (Flonase)

– Systemic. Only in urgent, selected cases and only for short-term use.

• Physiologic saline solution may be comforting

Contraindications:

• Antihistamines may precipitate urinary retention in males with prostatism and/or hypertrophy

• Decongestants if congestion is a “rebound” phenomenon

• Discourage decongestants if hypertension a problem

Precautions:

• The elderly often require less aggressive treatment and will more frequently present with non-allergic rhinitis

• Warn patients that first generation antihistamines are associated with somnolence and may impair performance

Significant possible interactions: Refer carefully to manufacturer’s literature for interactions

Alternative Drugs

Combinations with decongestants

• Initiate patient education, supplementing with available videotapes and/or literature

• Avoidance — most patients with inhalant allergy have problems controlling their symptoms totally with allergen avoidance

• Air conditioning and limited outside exposure during season helpful

• Instructions as to the best housekeeping tactics and control for dust mites in patients sensitive to this allergen helpful

• Exposure to all animal contacts minimized. Discourage house pets.

• Avoid environmental irritants, e.g., smoke and fumes

• Air cleaners

• Use of allergy control covers especially on mattresses and pillows

• Secondary infection

• Otitis media

• Sinusitis

• Epistaxis

• Nasopharyngeal lymphoid hyperplasia

• Decreased pulmonary function

• Asthma

• Continue to suspect effects of medications

• Facial changes

• Maximal, beneficially acceptable control of symptoms should be the goal

• Treatment tailored to each individual case.

• Immune system changes overtime often associated with lessening of

symptoms of allergic rhinitis. Therefore early, adequate control

important.

Associated Conditions

• Other IgE mediated conditions, e.g., asthma and atopic dermatitis

Age-Related Factors

Pediatric:

• Consider allergy as principle cause of persistent rhinitis

• Family understanding and involvement important

• Environmental control requires a cooperative effort and may include

carpet and drape removal, removal of house plants, pet control, etc.

Geriatric:

• Increased medication side effects

• Number and specific types of allergens causing symptoms may change

• Symptoms may decrease by 4th-5th decade (not a hard rule)

Pregnancy

Physiological changes of pregnancy may aggravate all types of

rhinitis including allergic, vasomotor, nonallergic rhinitis with

eosinophilia and chronic irritable airways

Synonyms

• Hay fever

• Pollinosis

• IgE mediated rhinitis

International Classification of Diseases

477.9 Allergic rhinitis, cause unspecified