What causes the inflammation of nasal mucosa that is seen in allergic rhinitis?

Rhinitis describes inflammation of the nasal mucosa and is clinically defined by symptoms of nasal discharge, itching, sneezing, and nasal blockage or congestion.

From: Probiotics, 2022

Allergic and Nonallergic Rhinitis

A. Wesley Burks MD, in Middleton's Allergy: Principles and Practice, 2020

Rhinitis related to the workplace is characterized by intermittent or persistent nasal symptoms attributable to exposures incurred in a particular work environment.60 Work-related rhinitis may be related to immunologic hypersensitivity, including the presence of IgE, or may be nonallergic in etiology. The first type of work-related rhinitis is occupational rhinitis, in which the primary cause of nasal symptoms arises from exposures occurring in the work environment. The second type, referred to aswork-exacerbated rhinitis, occurs in persons with preexisting or concurrent rhinitis that is worsened by workplace exposures. Occupations that carry a high risk for development of work-related rhinitis include laboratory workers, furriers, and bakers and many others (Table 40.1).

Work-related rhinitis may be divided into three main categories defined by the types of implicated substances: irritant-induced, corrosive, and immunologic (Box 40.2).Irritant-induced rhinitis is caused by small airborne substances not typically categorized as allergens and not shown in appropriate studies to elicit a specific immune response.61 Irritant rhinitis may be associated with exposure to a wide variety of substances, including volatile organic compounds (e.g., perfume, paint fumes), particulates (e.g., chalk dust, coal dust, construction dust), and smoke (e.g., wood-burning fire, tobacco). Whereas irritant-induced rhinitis due to volatile organic compounds may cause transient symptoms that abate once the exposure is stopped, exposure involving cleaning fluids, particulates, and smoke may lead to more persistent symptoms. The second category of work-related rhinitis,corrosive rhinitis, results from exposure to a high concentration of such chemical gases, causing sufficient nasal inflammation that the mucosa may break down and ulcerate.62 Substances that have been linked to this condition include chlorine, sulfur dioxide, and ammonia. Some patients have reported that a single large exposure to these types of gases resulted in long-lasting symptoms of rhinitis; this clinical entity has been termedreactive upper airways dysfunction syndrome (RUDS). The final category of work-related rhinitis,immunologic rhinitis, is characterized by a specific immune response to a substance found in the workplace. Substances that most commonly cause immunologic rhinitis are proteins that elicit an IgE response, such as animal danders (e.g., in laboratory workers) or grains (e.g., in bakers). Low molecular weight substances, such as anhydrides (e.g., plastics manufacturers), act as haptens and induce an immunologic response similar to that seen in persons with occupational asthma.63

Diagnosis of work-related rhinitis relies heavily on a history of symptomatic worsening during the work week, with improvement over the weekend and during vacations, when the putative trigger is absent. Symptom diaries and self-administered assessments of nasal peak flow may establish a clinical pattern suggesting that the workplace is causing or aggravating symptoms. Eventually, however, symptoms may eventually persist during periods away from work as mucosal inflammation becomes more established, making the diagnosis more difficult to establish. In many situations, skin or blood testing for specific IgE may be very helpful, and occasionally a provocative nasal challenge may be required to identify a specific causative agent.

Rhinitis

Anastasia Rowland-Seymour MD, in Decision Making in Medicine (Third Edition), 2010

A.

Allergic rhinitis is by far the most common type of rhinitis. Estimates suggest 9%–40% of the U.S. population have some degree of allergic rhinitis. In 80% of cases, allergic rhinitis develops by age 20 years. Incidence wanes as we age, and it is much less common in the geriatric population. History of eczema and family history of atopy may help in the diagnosis. Symptoms occur in individuals who produce an immunoglobulin E (IgE)–mediated response to particular allergens. Allergens may be one or many, seasonal or perennial. Common seasonal allergens are trees, grasses, and weeds. Common perennial allergens include dust mites, cockroaches, animal proteins, dander, and molds. Diagnosing occupational rhinitis can be challenging because symptoms may occur several hours after exposure. Additionally, with chronic exposure, symptoms may not improve on weekends, requiring longer periods of avoidance. With occupational rhinitis, patients typically present with concomitant occupational asthma. Physical examination may reveal allergic shiners; injected conjunctivae; clear nasal discharge; pale, bluish boggy turbinates; and cobblestoning in the posterior pharynx. Allergen avoidance is of utmost importance. Maintaining indoor humidity to ≤50% to limit house dust mite and mold growth may be helpful. First-line treatment of allergic rhinitis is topical intranasal steroids. Additional treatment choices include oral or intranasal antihistamines as a good second choice. Intranasal cromolyn started several weeks prior to allergy season may be effective, leukotriene inhibitors alone or in conjunction with antihistamines are useful, and oral decongestants can be effective. Topical decongestants must be used sparingly because of the development of tachyphylaxis after 3–7 days of use. With prolonged use a resulting rebound nasal congestion and rhinitis medicamentosa develop. Hypertonic saline rinsing of the nares can be used for additional benefit in both acute and chronic rhinosinusitis. If medical maneuvers fail, skin testing and immunotherapy remain an option. Perennial allergic rhinitis appears to be a predisposing factor for acute bacterial rhinosinusitis by causing ostial obstruction.

B.

NARES accounts for 15%–20% of patients with rhinitis. It is characterized by perennial symptoms of nasal congestion, nasal itching, rhinorrhea, hyposmia, and sneezing. These symptoms are milder than in patients with perennial allergic rhinitis, but they are still bothersome. Nasal secretions contain 25% eosinophils on smear. IgE antibodies to inhalant allergens are usually absent. Some researchers believe this is a precursor to the triad of asthma, nasal polyposis, and aspirin allergy. The most useful medications have proved to be topical nasal steroids, and if polyps are present, leukotriene inhibitors have also been shown to be helpful.

C.

Vasomotor rhinitis (idiopathic rhinitis) is an umbrella term for many types of nonallergic rhinitis, including gustatory and hormonal rhinitis. Patients with vasomotor rhinitis complain of chronic nasal congestion with or without persistent rhinorrhea, exacerbated by cold air, strong odors, stress, or inhaled irritants. For the most part, vasomotor rhinitis is believed to result from autonomic dysfunction in the nose where the parasympathetic system dominates, resulting in vasodilation and edema of the nasal vasculature. Idiopathic rhinitis is a diagnosis of exclusion. Allergy skin testing is negative. Nasal steroids are useful, and if rhinorrhea is a major factor, ipratropium can be effective.

D.

Imaging (CT scan of sinuses) should be limited to those patients who have persistent symptoms or if symptoms recur. Recurrent rhinosinusitis may also indicate an underlying process such as nasal polyps, other anatomic abnormalities, ciliary dysfunction, cystic fibrosis, immune deficiency, sarcoidosis, Wegener's granulomatosis, or relapsing polychondritis. Last, atrophic rhinitis is a syndrome of progressive atrophy of the nasal mucosa in the elderly debilitated population. Patients report a persistent foul odor that is a result of nasal mucosal colonization with Klebsiella ozaenae. These patients respond best to nasal irrigation.

E.

Prolonged use of intranasal decongestants can result in rebound congestion (rhinitis medicamentosa). The restoration of normal nasal function may take up to 21 days after withdrawal of the sympathomimetics. Additionally, numerous medications can cause rhinitis, including antihypertensives such as angiotensin-converting enzyme inhibitors, reserpine, phentolamine, methyldopa, and beta blockers; chlorpromazine; gabapentin; penicillamine; aspirin; NSAIDs; exogenous estrogens; and oral contraceptives. The use of intranasal cocaine can cause these symptoms as well.

F.

Infectious rhinitis can be caused by both viruses and bacteria (bacterial rhinitis), with the common cold being the most common cause of infectious rhinitis. Acute infectious rhinitis is often considered in conjunction with acute sinusitis. Symptoms statistically associated with culture-proven acute bacterial sinusitis include nasal congestion, purulent rhinorrhea, postnasal drip, facial or dental pain, and cough. The guidelines recommend that a diagnosis of acute bacterial rhinosinusitis (ABRS) is appropriate in patients who have had symptoms of a viral upper respiratory infection who have not improved after 10 days or worsen after 5–7 days. Streptococcus pneumoniae and Haemophilus influenzae account for 50% of rhinosinusitis bacterial isolates. Moraxella catarrhalis, other streptococcal species, Staphylococcus aureus, and anaerobic bacteria each account for a small proportion of cases. Of symptomatic patients, 30% have negative bacterial cultures, suggesting either viral or allergic disease. Because it is not possible to predict which cases of ABRS will resolve spontaneously, the use of an antimicrobial is recommended.

Prior antibiotic use is a major risk factor for infection with antimicrobial-resistant strains. For patients with mild disease who have not received antibiotics in the prior 4–6 weeks, initial therapy should include amoxicillin-clavulanate, amoxicillin, cefpodoxime, cefuroxime, or cefdinir. Fluoroquinolones or high-dose amoxicillin-clavulanate is recommended as first-line therapy for patients with mild disease who have had recent antibiotics or for patients with moderate disease. Treatment with a macrolide after treatment failure with amoxicillin or a cephalosporin will result in a second treatment failure in about 60% of cases as a result of high rates of resistance to macrolides in penicillin-resistant S. pneumoniae and H. influenzae.

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Rhinitis

Rick D. Kellerman MD, in Conn's Current Therapy 2021, 2021

Introduction

Rhinitis is defined as inflammation of the nasal mucous membranes. Rhinitis presents as nasal congestion, sneezing, itching, rhinorrhea, and postnasal drainage; it can be divided into allergic and nonallergic rhinitis. Mixed rhinitis has components of both allergic and nonallergic disease. Allergic rhinitis is nasal inflammation that is mediated by IgE to environmental allergens. Nonallergic rhinitis is defined by non–IgE-mediated perennial symptoms. Nonallergic rhinitis shares symptoms with allergic rhinitis, but is only distinguishable by negative allergy tests. Nonallergic rhinitis is also known as perennial nonallergic rhinitis, idiopathic rhinitis, and vasomotor rhinitis.

Most research still classifies allergic rhinitis according to its seasonality or its perennial nature. Seasonal allergic rhinitis is commonly caused by pollen allergens; perennial allergic rhinitis is mainly caused by dust mites and animal dander. Allergic rhinitis can be further classified as mild, moderate, or severe. Mild rhinitis is rhinitis that does not impair work, school, daily functioning, or sleep. Moderate to severe rhinitis interferes with activities of daily living, quality of life, and/or sleep. Severe rhinitis is so marked that normal functioning cannot take place without treatment. Episodic allergic rhinitis occurs with sporadic inhalant aeroallergen exposure not typically encountered by the patient’s usual indoor and outdoor environments. An example of episodic allergic rhinitis is a child who is allergic to cats but is not normally exposed, but then visits a household with cats and develops symptoms.

The Allergic Rhinitis and its Impact on Asthma Guidelines: Revised 2010 (ARIA) discouraged the use of the terms seasonal and perennial rhinitis in favor of intermittent and persistent rhinitis. Intermittent rhinitis can be defined as nasal symptoms lasting less than 4 weeks’ duration and fewer than 4 days per week. Persistent rhinitis is rhinitis lasting more than 4 weeks’ duration or more that 4 days per week.

No standard classification exists for nonallergic rhinitis. A variety of conditions present with similar symptoms and are called nonallergic rhinitis. Nonallergic rhinitis includes vasomotor rhinitis, gustatory rhinitis, nonallergic rhinitis with eosinophilia syndrome (NARES), occupational rhinitis, hormonal rhinitis, drug-induced rhinitis, and atrophic rhinitis. Another entity classified in or out of nonallergic rhinitis is infectious rhinitis.

Local allergic rhinitis is a newly defined entity found in nonatopic patients. Local allergic rhinitis is characterized by local inflammatory reactions including local eosinophils and localized IgE in response to aeroallergens. Local allergic rhinitis does not show significant skin-prick testing reactions, and patients have negative systemic IgE reactions to aeroallergens.

Rhinitis may be viewed by some as a trivial disease, but it places a significant financial burden on society. The estimated direct and indirect costs to society of rhinitis were around $11.58 billion in 2002.

Rhinitis

Susanna Dowie MA, LicAC, MBAcC, HonMRCHM, MATCM, in Acupuncture, 2009

Western Differentiation: Rhinitis

An inflammation of the nasal mucosa.

Signs and symptoms: excessive mucus production; congestion; sneezing paroxysm; watery eyes; nasal and ocular pruritus.

1.

Allergic rhinitis: associated symptoms are fatigue; malaise; headache; symptoms usually develop before age 20; family history; allergic shiners (blue grey or purple discoloration under lower eyelids); mouth breathing; conjunctivitis.

a)

Co-morbidity with asthma, eczema, chronic sinusitis.

b)

Differential diagnosis:

i.

Occupational rhinitis: exposure to irritants and allergens including laboratory animals, grains, coffee beans, wood dust, tobacco smoke, cold air, formaldehyde, hair spray.

ii.

Perennial rhinitis: allergens may include mould spores, dust mites, animal dander.

iii.

Seasonal rhinitis: allergens may include plant and grass pollens, mould spores.

2.

Non-allergic rhinitis: associated symptoms are postnasal discharge; enlarged tonsils; perennial symptoms. Symptoms aggravated by irritant exposure and weather changes, and usually there is no family history.

a)

Infectious rhinitis: acute (viral) or chronic (rhinosinusitis), accompanied by lymphadenopathy, normally self-limiting.

b)

Hormone-induced rhinitis: hypothyroidism, menstrual cycle, oral contraceptives, pregnancy.

c)

Occupational rhinitis.

d)

Vasomotor rhinitis: temperature changes, humidity, alcohol ingestion, odours.

e)

Gustatory rhinitis: particularly hot and spicy food.

f)

Atrophic rhinitis.

g)

Drug-induced rhinitis: antihypertensive medications, aspirin, NSAIDs, oral contraceptives, rhinitis medicamentosa.

h)

Other types include rhinitis from: emotions, exercise, posture, primary ciliary dyskinesia, reflux or gastro-oesophageal reflux disease.

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Allergy and Immunology of the Upper Airway

Paul W. Flint MD, FACS, in Cummings Otolaryngology: Head and Neck Surgery, 2021

Assessment of Symptom Control in Rhinitis

There has been interest in evaluating rhinitis symptom control on an ongoing basis. To this end, two different tools have been developed. The Rhinitis Control Assessment Test (RCAT) is a 6 item tool that evaluates the frequency of nasal congestion, sneezing, and watery eyes, as well as sleep interference, avoidance of activities, and patient rating of control using a 5 point Likert response scale.325 It utilizes a 1 week recall to assess the symptoms. The responses are graded from 1 to 5 with a score range from 6 to 30, with higher scores indicating better control of rhinitis. To test the tool, a longitudinal study in 402 patients with seasonal, perennial, and nonallergic rhinitis was undertaken.326 The study showed internal consistency and test-retest reliability, as well as good convergent validity between the RCAT and total nasal symptom scores and physician global assessment scores. The RCAT was found to be responsive to change in patient symptom control and was deemed acceptable and appropriate by patients suffering from different forms of rhinitis. A cut-point score of 21 or less was suggested to identify patients experiencing rhinitis control issues. This test should prove useful for adjusting management of patients with rhinitis in physician's offices and will also be useful to patients who self-medicate because many of the mainstay treatments are now available over the counter.

Another more recent assessment tool was developed through the Mobile Airways Sentinel Network for AR (MASK-rhinitis), which is a patient-centered information and communication technologies system. A mobile phone application allows the users to click on 5 consecutive visual analog scale (VAS) measures (VAS global, VAS nasal, VAS ocular, VAS asthma, and VAS work) at levels ranging from 0 (not at all bothersome) to 100 (very bothersome). The mobile phone application is available in 22 countries and the tool has been validated and found to be an easy and effective method of assessing symptoms of AR.327-330 A VAS score of 50 to 60/100 mm is suggestive of moderate to severe AR.331,332 In a study where the MASK tool was coupled to reported medication intake on the mobile application, it allowed differentiation between treatments within or between classes (intranasal corticosteroids and oral antihistamines).333

Endotype-Driven Approach in Rhinitis

Peter W. Hellings, in Implementing Precision Medicine in Best Practices of Chronic Airway Diseases, 2019

Abstract

Rhinitis can be subdivided into three main phenotypes based on history and clinical examination: allergic rhinitis (AR), infectious rhinitis (IR), and nonallergic noninfectious rhinitis (NAR). Different treatment approaches need to be considered given the different etiology of the rhinitis phenotypes. Four pathophysiological mechanisms have been identified as key drivers of the disease: Th2 inflammatory type, Th2 inflammatory type, neurogenic type, and epithelial endotype. The Th2 inflammatory type is predominantly seen in AR patients, whereas the Th2 inflammatory type is mainly found patients with infectious rhinitis. The neurogenic type has been associated with nonallergic rhinitis. Epithelial dysfunction has been demonstrated in AR patients. In real-life, patients might have different endotypes causing rhinitis symptoms, hence making their identification by the use of biomarkers crucial in order to move toward an endotype-driven treatment approach.

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Occupational Allergy

Catherine Lemière, Olivier Vandenplas, in Middleton's Allergy Essentials, 2017

Occupational Rhinitis

Occupational rhinitis (OR) has been defined as an inflammatory disease of the nose, which is characterized by intermittent or persistent symptoms (i.e. nasal congestion, sneezing, rhinorrhea, itching) and/or variable nasal airflow limitation and/or hypersecretion due to causes and conditions attributable to a particular work environment and not to stimuli encountered outside the workplace.4

As with work-related asthma (Fig. 14-1), the broad spectrum of rhinitis syndromes related to the work environment can be broken down into the following categories: (1) allergic OR; (2) non-allergic OR; and (3) work-exacerbated rhinitis.

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Infectious Diseases

Harold Merriman, in Acute Care Handbook for Physical Therapists (Fourth Edition), 2014

Rhinitis.

Rhinitis is the inflammation of the nasal mucous membranes and can result from an allergic reaction or viral infection. Allergic rhinitis is commonly a seasonal reaction from allergens, such as pollen, or a perennial reaction from environmental triggers, such as pet dander or smoke. Viral rhinitis, sometimes referred to as the common cold, is caused by a wide variety of viruses that can be transmitted by airborne particles or by contact.

Clinical manifestations of allergic and viral rhinitis include nasal congestion; sneezing; watery, itchy eyes and nose; altered sense of smell; and thin, watery nasal discharge. In addition to these, clinical manifestations of viral rhinitis include fever, malaise, headache, and thicker nasal discharge.

Management of allergic rhinitis includes antihistamines, decongestants, nasal corticosteroid sprays, and allergen avoidance. Management of viral rhinitis includes rest, fluids, antipyretics, and analgesics.44-46

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Approach to the Patient with Nose, Sinus, and Ear Disorders

Andrew H. Murr, in Goldman's Cecil Medicine (Twenty Fourth Edition), 2012

Definition

Rhinitis is generally defined as any inflammatory process in the nose, with the common result being a sensation of excess mucous or nasal congestion. The patient may have a sensation of fluid dripping from the nose, either coming from the nose anteriorly or coming from the nose posteriorly. Anterior nasal drainage may be perceived by the patient as being accompanied by an activity such as eating (gustatory rhinitis) and may be visible to an observer. Posterior nasal drainage is more nebulous and subjective, but it is very common and is referred to as postnasal drip.

In general, acute rhinitis and sinusitis describe inflammatory conditions of the nose and sinuses that last less than 4 weeks. Chronic rhinitis and sinusitis persist for more than 3 months despite treatment. Recurrent acute rhinitis and sinusitis are defined by exacerbations that occur four or more times per year and last 7 to 10 days per episode. Subacute rhinitis and sinusitis define symptoms that persist between 4 and 12 weeks and resolve completely with treatment.

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Allergic Rhinitis and Conjunctivitis

Jonathan Corren, in Middleton's Allergy Essentials, 2017

Rhinitis related to the workplace is characterized by intermittent or persistent nasal symptoms attributable to exposures incurred in a particular work environment.41 Work-related rhinitis may be due to immunologic hypersensitivity, including the presence of IgE, or may be non-allergic in etiology. Occupations that carry a high risk for development of work-related rhinitis include laboratory workers, furriers, and bakers (Table 8-1). Diagnosis of work-related rhinitis relies heavily on a history of symptomatic worsening during the work week, with improvement over the weekend and during vacations, when the putative trigger is absent. Eventually, symptoms may persist during periods away from work as mucosal inflammation becomes more established. In situations in which the workplace exposure is a protein, skin or blood testing for specific IgE may be very helpful (see Ch. 14 for detailed commentary).

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Is inflammation of nasal mucosa caused by allergies?

Allergic rhinitis is caused by the immune system reacting to an allergen as if it were harmful. This results in cells releasing a number of chemicals that cause the inside layer of your nose (the mucous membrane) to become swollen and excessive levels of mucus to be produced.

What causes the inflammation associated with allergies?

Allergic inflammation is caused by the development of an allergen-induced immune response and can lead to several diseases, including asthma, allergic rhinoconjunctivitis, anaphylaxis, urticaria and atopic dermatitis1.

Why is there pale mucosa in allergic rhinitis?

This is the first study to report that a pale nasal mucosa is related to severe allergic rhinitis, nasal eosinophilic inflammation, and airflow limitations in the upper and lower airways of asthmatic children. Some reports have indicated that a nasal allergen challenge can induce bronchial inflammation [14,15].

Why is nasal mucosa blue in allergic rhinitis?

Allergic rhinitis patients' nasal mucosa is infiltrated with eosinophils, neutrophils, lymphocytes and basophilic cells. As we know, there is high amount of eosinophil infiltration in allergic rhinitis patients' nasal mucosa, which is probably the cause of bluish-grey discolouration.