Allergic Rhinitis: Basic Facts and Treatment

Allergic rhinitis is an inflammation of the nasal mucosa triggered by contact with environmental allergens and maintained by an immediate-type hypersensitivity immune response involving immunoglobulin E and inflammatory cells. Typical symptoms include sneezing, itching, watery nasal discharge, and nasal congestion; eyes are often affected simultaneously (itching, tearing, and redness). The disease is common among people of all ages, often accompanies asthma, and impacts sleep, school, and work performance, so it has long been considered a significant global health problem. [1]

Modern approaches emphasize that this is not a "minor seasonal affliction," but a chronic inflammatory process of the upper respiratory tract that impairs quality of life, mental performance, and the control of underlying asthma. Allergic rhinitis is closely associated with conjunctivitis and bronchial asthma, and their simultaneous control improves outcomes. [2]

In recent years, climate change, urbanization, and air pollution have been shown to lengthen and intensify pollen seasons, increasing sensitization and symptom severity in susceptible individuals. This adds an important layer to prevention and treatment, including monitoring pollen calendars and adapting therapy. [3]

The diagnosis is established based on a combination of: characteristic complaints, connection with allergens, objective examination and confirmation of sensitization by skin tests or specific antibodies in the blood; in complex cases, molecular allergy diagnostics or nasal allergen provocation are used to distinguish “truly significant” allergens from accidental sensitization. [4]

Code according to ICD-10 and ICD-11

Below are the clinically applicable categories. For general practice, basic codes are often sufficient; for reporting and insurance reimbursement, some countries use expanded subcategories.

ICD-10 (WHO) codes and examples (basic level):

Code	Name
J30.1	Allergic rhinitis due to pollen (hay fever)
J30.2	Other seasonal allergic rhinitis
J30.3	Other allergic rhinitis
J30.4	Allergic rhinitis, unspecified
Note: J30.0 - vasomotor rhinitis - not an allergic form, although it is included in block J30. [5]

ICD-11 codes (MMS, v2025-01) - more detailed:

Code	Name
CA08.0	Allergic rhinitis (supraheading)
CA08.00	Allergic rhinitis due to pollen
CA08.01	Allergic rhinitis due to other seasonal allergens
CA08.02	Allergic rhinitis due to house dust mites
CA08.03	Other forms of allergic rhinitis
CA08.0Z	Allergic rhinitis, unspecified

Epidemiology

Allergic rhinitis is one of the most common chronic human ailments. According to systematic reviews from 2020 to 2024, it occurs in 10-30% of the adult population and up to 40% of children; the median prevalence in adult studies worldwide is approximately 18%. In some regions and for certain criteria, the prevalence is higher. [6]

In recent decades, an increase in the frequency and severity of symptoms has been observed, particularly in urban areas. Environmental factors have been implicated: longer pollen seasons and increased pollen grain concentrations place increased strain on the mucous membranes and lead to longer periods of illness. [7]

In children and adolescents, the disease particularly impacts school attendance and academic performance; failure to treat the condition leads to a decline in the family's quality of life. In large epidemiological studies, the proportion of adolescents with symptoms of rhinoconjunctivitis reaches 20-30%, with severe forms occurring in 7-8%. [8]

At the same time, awareness of “hidden” morbidity is growing – many people are treated symptomatically without seeking medical attention, and official statistics underestimate the real burden on public health and the economy. [9]

Table 1. Prevalence estimates

Population / source	Prevalence assessment
Adults (survey median, 2022)	18.1%
Range by country	1-54%
Children/teenagers (different countries)	14-40%
Overall Rating (Guides and Reviews)	10-30% of adults, up to 40% of children

Reasons

The main reason is immunological sensitization to inhaled allergens (plant pollen, house dust mites, animal hair and epithelium, mold fungi, etc.) with the formation of immunoglobulin E antibodies. Repeated contacts trigger a cascade of mediators and a cellular response of the nasal mucosa. [10]

Genetic predisposition plays a significant role: the presence of allergic diseases in parents increases the risk of sensitization in the child; many genes involved in the regulation of the epithelial barrier and immune response are associated with respiratory atopy. [11]

Occupational factors (flour, latex, livestock farming, chemical aerosols) and the home environment (dust mites, mold) can contribute. In some cases, allergic rhinitis develops against the background of a "local" allergy in the nasal mucosa with negative systemic tests—so-called local allergic rhinitis. [12]

Climate change and air pollution increase pollen production and allergenicity, lengthening the season, increasing the likelihood of sensitization and the severity of symptoms. [13]

Risk factors

The main factors include familial atopy, urban living, exposure to tobacco smoke and pollutants, damp and dusty environments, and contact with pet allergens and dust mites. Frequent viral respiratory infections and unfavorable environmental conditions increase the risk. [14]

A link has been demonstrated between climate change and increased length and intensity of pollen seasons, which increases the burden on susceptible individuals, especially children.[15]

Some dietary and behavioral factors (low physical activity, dietary habits) have been associated with risk in individual studies, but these data are heterogeneous and require careful interpretation. [16]

Professional exposures are important in industries where high aerosol loads are present (bakeries, agriculture, veterinary medicine, latex production, etc.). [17]

Table 2. Risk factors and level of evidence (summary)

Factor	Association with disease
Familial atopy	Moderate-strong association
High pollen/mite exposure	Strong association
Air pollution, urbanization	Moderate-strong association
Smoking/passive smoking	Moderate association
Professional allergens	Strong association
Environmental changes (climate)	Growing evidence base

Pathogenesis

Trigger: contact of an allergen with the nasal mucosa of a sensitized individual. Immunoglobulin E binds to mast cells; repeated exposure leads to their activation and the release of mediators (histamine, leukotrienes), which quickly causes itching, sneezing, and rhinorrhea—the so-called "early" phase. [18]

After a few hours, the "late" phase develops: T-helper type 2 cells, eosinophils, and basophils are recruited, and interleukins 4, 5, and 13 are released, maintaining inflammation, swelling, and nasal congestion. This explains why antihistamine therapy alone is often insufficient to control symptoms. [19]

Local mechanisms are also important: disruption of the epithelial barrier function, local synthesis of immunoglobulin E in the mucosa, and imbalance of innate immunity. Modern studies confirm the role of eosinophils as key effectors of the late phase and persistence of symptoms. [20]

The "single airway" concept explains why allergic rhinitis and asthma often coexist and influence each other; treating rhinitis can improve asthma control.[21]

Symptoms

The classic four: an itchy nose, a runny nose with watery discharge, repeated sneezing, and nasal congestion. Itchy and red eyes, watery eyes, and an itchy throat and ears are often associated. Symptoms can be seasonal or year-round, depending on the triggers and their concentrations. [22]

At night, severe nasal congestion impairs sleep and daytime performance; children experience learning and behavioral problems. Adults experience decreased attention and productivity, and increased daytime sleepiness. [23]

A cough is often present, especially in people with concomitant asthma; however, fever and severe pain are usually absent, which helps differentiate it from a viral infection. [24]

Severity ranges from mild to severe; the longer and more intense the exposure to allergens (eg, during peak pollen season), the more severe the symptoms and the higher the risk of complications.[25]

Classification, forms and stages

The historical division into "seasonal" and "year-round" is complemented by the ARIA (Allergic Rhinitis and its Impact on Asthma) classification: intermittent or persistent (based on duration) and mild or moderate-severe (based on impact on sleep, activity, work/school, and subjective burden). This system better reflects the patient's needs and determines treatment tactics. [26]

Intermittent - symptoms < 4 days per week or < 4 weeks; persistent - > 4 days per week and > 4 weeks. Mild - no disturbance of sleep or activity, "not many" symptoms; moderate-severe - there is disturbance of sleep, activity, work/school, or symptoms "really interfere". [27]

A distinction is also made between occupational allergic rhinitis (occupational allergic rhinitis) and local allergic rhinitis (a local allergic reaction in the mucous membrane with negative systemic tests). This is important when planning diagnosis and treatment, including allergen-specific immunotherapy. [28]

Table 3. ARIA classification (basis for therapy planning)

Axis	Criterion
Duration	Intermittent: < 4 days/week or < 4 weeks; Persistent: > 4 days/week and > 4 weeks
Heaviness	Mild: no effect on sleep, activity, school/work; Moderate-severe: effect on one or more items
Form	Seasonal, year-round, professional, local

Complications and consequences

Without adequate control, allergic rhinitis impairs quality of life, sleep, and cognitive function, and increases the risk of school and work maladjustment. This is one of the reasons for the "hidden" social and economic burden of the disease. [29]

The link with asthma is fundamental: uncontrolled rhinitis worsens asthma control; rhinitis therapy, especially with intranasal corticosteroids, can improve asthmatic symptoms and medication requirements. [30]

Sinusitis, otitis media (especially in children), olfactory impairment, increased snoring, and the risk of sleep disorders are possible. In pediatrics, allergic rhinitis is considered a risk factor for sleep disturbances and deterioration of daytime behavior, although data on the strength of associations vary. [31]

Chronic nasal congestion can contribute to mouth breathing, and in children, it can affect the development of the facial skeleton and bite; with concomitant polypous rhinosinusitis, the load on the sense of smell and taste increases. [32]

When to see a doctor

If symptoms persist for more than 2-4 weeks or interfere with sleep, school, or work, consult a doctor: proper treatment can significantly improve daily life. Self-medication with antihistamines is not always sufficient, especially with severe congestion. [33]

Immediate medical evaluation is required for severe shortness of breath, wheezing, recurrent sinusitis, facial pain, purulent discharge, fever, decreased vision, severe unilateral symptoms, or nosebleeds. These are "red flags" for possible complications or other pathology. [34]

Children should be examined if their condition affects sleep and school performance, as well as if otitis media, adenoid pathology, or concomitant asthma are suspected. For those with year-round symptoms, a consultation with an allergist is helpful to identify clinically significant allergens. [35]

If standard drugs do not help or there is doubt about the diagnosis, a clarifying diagnosis is carried out, including sensitization tests and, if necessary, nasal provocation with an allergen. [36]

Table 4. Red flags - when urgent consultation is needed

Sign	Possible cause
Unilateral severe congestion, pain, bleeding	Structural pathology, sinusitis, polyps
Fever, purulent discharge	Infectious complication
Shortness of breath, wheezing	Asthma exacerbation
Decreased vision/severe headache	Severe complication, requires exclusion of sinusitis/orbital problems

Diagnostics

Step 1. Interview and examination. The doctor clarifies when and under what circumstances the symptoms appear, whether there is a connection with seasons, pets, dust, or work. The doctor examines the nasal cavity (swelling, pale mucous membrane, watery discharge), and evaluates the eyes and ears. This sets the direction for further testing. [37]

Step 2. Confirmation of sensitization. Skin prick tests with standard extracts or blood tests for specific antibodies to individual allergens (pollen, dust mites, animal epithelium, etc.) are used. A positive test indicates the presence of sensitization, and its clinical significance is assessed based on the relationship between symptoms and exposure. Routine testing for food allergies in rhinitis is not indicated. [38]

Step 3. Clarification of the "main allergen." In adults and children with multiple positive tests, molecular allergy diagnostics are useful: antibodies to specific protein molecules of allergens are determined, which helps distinguish cross-reactions from "true" sensitization and select optimal immunotherapy. [39]

Step 4. In complex cases. If the history and testing are inconsistent (e.g., negative systemic tests with typical symptoms), nasal allergen challenge is performed under symptomatic and rhinometry monitoring. This is the "gold standard" for confirming the causative allergen in polysensitized patients, but it requires an experienced center. [40]

Table 5. Main diagnostic methods

Method	What does it show?	When is it useful?
Skin prick tests	Sensitization to allergen extracts	Primary verification
Specific antibodies in the blood	Sensitization when skin testing should not be done	Pregnancy, dermatitis, taking antihistamines
Molecular diagnostics	Sensitization to individual proteins	Choice of immunotherapy, cross-reactions
Nasal provocation	Clinical significance of a specific allergen	Polysensitization, "local" rhinitis

Differential diagnosis

The main “doubles” are non-allergic rhinitis (vasomotor), viral rhinosinusitis, drug-induced rhinitis from the abuse of vasoconstrictor drops, chronic rhinosinusitis with or without polyps, as well as anomalies of the nasal septum and hypertrophy of the turbinates. [41]

Allergic rhinitis is characterized by itching and repeated sneezing, a characteristic seasonality, a connection to allergens, and confirmation of sensitization by testing. Viral infections are often accompanied by aches, fever, and thick mucus; drug-induced rhinitis is characterized by "rebound" congestion after prolonged use of decongestant drops. [42]

It's important to distinguish between localized allergic rhinitis, where systemic tests are negative but the local nasal reaction is positive; nasal provocation is helpful. A separate category is occupational rhinitis, characterized by worsening symptoms on weekdays and improvement on vacation. [43]

Table 6. Allergic vs. non-allergic rhinitis - key differences

Sign	Allergic	Non-allergic
Itching, multiple sneezing	Often	Rarely
Tearing, itchy eyes	Often	Rarely
Seasonality/triggers	Expressed	There are no clear
Sensitization tests	There is (or local)	No
Response to antihistamines	Good	Often weak

Treatment

Therapy is based on four pillars: reducing exposure to allergens, intranasal corticosteroids, antihistamines, and allergen-specific immunotherapy. The choice depends on the severity and duration of symptoms (according to ARIA), age, and comorbidities. In mild intermittent cases, second-generation antihistamines on demand are often sufficient; in persistent cases, intranasal corticosteroids are considered first-line drugs. [44]

Intranasal corticosteroids offer the best efficacy-to-safety ratio for most symptoms, including nasal congestion, and are recommended as basic therapy for persistent nasal congestion. Recent reviews confirm their superiority over oral antihistamine monotherapy. With proper injection technique and dosage, the risk of systemic side effects is minimal. [45]

The combination of an intranasal antihistamine with an intranasal corticosteroid (azelastine + fluticasone fixed spray) provides faster and more pronounced improvement compared to either component alone, especially for severe symptoms, including ocular ones. This has been confirmed by randomized trials and network meta-analyses in recent years. This approach is appropriate as an initial treatment for moderate-to-severe cases or for "breakthrough" symptoms with monotherapy. [46]

Second-generation oral antihistamines are useful for mild symptoms or as an adjunct to intranasal corticosteroids; they relieve itching, sneezing, and rhinorrhea, but are less effective at reducing congestion. Intranasal antihistamines act more quickly and may be preferred as an adjunct to corticosteroids than oral antihistamines, according to current guidelines.[47]

Ipratropium nasal spray is appropriate when rhinorrhea is predominant, and cromones may be an adjunctive option in some patients (especially as a prophylactic treatment before exposure), although they are inferior in effectiveness to corticosteroids and combination sprays. Seawater and saline irrigation reduce mucus viscosity and alleviate symptoms; major modern studies support their adjunctive role, especially in conjunction with drug therapy. [48]

Decongestant drops and sprays are used short-term (for a few days) for severe congestion, strictly as a "bridge" to basic anti-inflammatory therapy to avoid triggering drug-induced rhinitis. Oral decongestants are used with caution due to possible systemic side effects, especially in people with cardiovascular problems. Long-term courses of injectable glucocorticosteroids for rhinitis are not recommended due to an unfavorable safety profile. [49]

Leukotriene antagonists occupy a limited niche: they are considered when other agents are ineffective or intolerable, or when asthma and nocturnal symptoms coexist. In 2020, regulators added strict warnings about the risk of neuropsychiatric adverse reactions to montelukast and recommend avoiding it in mild forms of rhinitis; prescribing decisions require weighing the benefits and risks. [50]

Allergen-specific immunotherapy is the only method that addresses the underlying causes of the disease: with the correct selection of the "culprit allergen" and a sufficiently long course (usually at least 3 years), it reduces symptoms and the need for medications, and may also reduce the risk of future asthmatic symptoms. Immunotherapy is administered as subcutaneous injections or as tablets/drops under the tongue for standardized allergens (cereal pollen, ragweed, dust mites, etc.). The choice is based on the clinical significance of sensitization and patient preference. [51]

Modern personalization involves the use of molecular allergy diagnostics to select an extract and predict the response to immunotherapy, as well as digital symptom diaries and pollen trackers to assess effectiveness. Biological agents (e.g., anti-immunoglobulin E) are being studied in severe, refractory cases of rhinitis with comorbid asthma/polyposis, but for "pure" rhinitis without these conditions, they are not yet the standard of care. [52]

Table 7. Comparison of the main antisymptomatic agents

Class	Strengths	Restrictions
Intranasal corticosteroids	Better control of all symptoms including congestion	The effect develops over several days, technique is important
Intranasal antihistamines	Fast effect, good as a supplement	Less effect on congestion than corticosteroids
Oral antihistamines	Easy to use, itching and sneezing control	Weaker when congested
Ipratropium (nasal)	Reduces rhinorrhea the most	Does not affect itching/sneezing
Cromones	Preventive effect with predictable exposure	They are less effective

Table 8. Allergen-specific immunotherapy (general points)

Parameter	Subcutaneous	Sublingual
Proven effectiveness	High	High for standardized tablets
Course duration	≥ 3 years	≥ 3 years
Pros	Flexibility in allergens, accumulated experience	Convenience of home use
Cons	Clinic visits	Requires strict daily commitment

Prevention

A completely "sterile" life is impossible, but reducing exposure to clinically significant allergens helps: regular wet cleaning and dust mite barrier covers, washing bedding at a high temperature, humidity control, ventilation without pollen peaks, and, if possible, air purifiers with high-efficiency filters. For pollen allergies, pollen forecast apps and sensible planning of outings are helpful. [53]

For seasonal symptoms, it's best to begin basic therapy 1-2 weeks before the expected pollen peak. Barrier sprays and saline rinses help reduce contact and flush allergens from mucous membranes; protective goggles and masks reduce allergen exposure in windy weather. [54]

In children and adolescents, immunotherapy to the “correct” allergen, started early and completed in full, can reduce the risk of asthmatic symptoms and provide a long-lasting effect after completion of treatment. [55]

At the city and community level, "green" strategies are being discussed that take into account the impact of climate and urban flora on pollen load. Individually, avoid smoking and secondhand smoke, maintain physical activity, and get adequate sleep. [56]

Forecast

With correct diagnosis and modern therapy, the prognosis is favorable: most patients achieve good control of symptoms and daily activities. Selecting therapy according to the ARIA classification and considering individual triggers is key to success. [57]

Allergen-specific immunotherapy provides long-term benefits, reduces the need for symptomatic medications, and, according to clinical studies, reduces the risk of asthmatic symptoms in children with pollen allergy. The effect depends on the correct selection of the allergen and adherence. [58]

In cases of uncontrolled asthma, concomitant asthma, polypous rhinosinusitis, and other comorbidities, a multidisciplinary approach involving an allergist and otolaryngologist is required. Regular assessment of control and adjustment of therapy improve long-term outcomes. [59]

Table 9. Factors of good and unfavorable prognosis

Factor	Influence
Early initiation of basic therapy	Improves control
Adherence to treatment	Critical to the outcome
Full course of immunotherapy	Long-lasting benefits
Uncontrolled asthma/polyposis	They make it difficult to manage

FAQ - Frequently Asked Questions

Is it possible to treat the condition with just an "allergy pill"? Antihistamines help with itching and sneezing, but are less effective at relieving congestion; for persistent cases, intranasal corticosteroids are considered the mainstay, often in combination with an intranasal antihistamine. [60]

Are steroid nasal sprays dangerous? With proper technique and dosage, systemic effects are minimal; these are the medications with the best balance of effectiveness and safety for nasal symptoms. Follow spray instructions and do not exceed the dose. [61]

What does allergen-specific immunotherapy offer? It's a targeted treatment that reduces symptoms and the need for medications, and in children with pollen allergies, it reduces the risk of asthmatic symptoms over the long term. The course lasts at least 3 years. [62]

Is montelukast worth taking for rhinitis? It is prescribed only if other medications are ineffective or intolerable, taking into account the warning about the risk of neuropsychiatric reactions; the decision is made by a doctor after assessing the benefits and risks. [63]

Why is every year "worse than before"? Climate change plays a role: pollen seasons are becoming longer and more intense, increasing the burden on sensitized people. Plan prevention and treatment in advance. [64]

Summary Table: Quick Tactic Selection

Scenario	First line	Alternative/enhancement
Light intermittent	Oral or intranasal antihistamine as needed	Irrigation, barrier measures
Moderate to severe intermittent	Intranasal corticosteroid or fixed combination with intranasal antihistamine	Add a second component; a short course of decongestant
Persistent (any severity)	Intranasal corticosteroid daily (combination possible)	Consider immunotherapy for a proven allergen
Poorly controlled/comorbid asthma	Combination of nasal agents, evaluation of immunotherapy; multidisciplinary approach	Specialized center, individualization