bubble_chart Overview

Allergic rhinitis, commonly known as hay fever, is an allergic reaction that occurs in the nasal mucosa and is a common manifestation of respiratory allergies. It sometimes coexists with bronchial asthma. The incidence of this disease has shown a significant increasing trend over the past 20 years, particularly in developed countries. It primarily affects young adults, but it is now observed more frequently in children as well. Although there is no significant gender difference in incidence, female hormones can exacerbate allergic reactions.

bubble_chart Etiology

This disease is caused by the following three factors:

(1) Genetic Factors

Individuals with a family history of allergies are more prone to this condition. Many patients have a family history of asthma, urticaria, or drug allergies. Previously, such individuals were referred to as atopic, as their bodies produce higher levels of IgE antibodies compared to normal individuals. However, recent studies have found no significant difference in the incidence rate between twins and the general population.

(2) Susceptibility of the Nasal Mucosa

Susceptibility arises from frequent stimulation by antigens, but the degree of susceptibility depends on the number of mast cells and basophils in the nasal mucosa tissue and their ability to release chemical mediators. It has been confirmed that allergic rhinitis patients have not only a higher number of these cells in their nasal mucosa than normal individuals but also a stronger capacity to release chemical mediators.

(3) Antigenic Substances

Antigens that stimulate the body to produce IgE antibodies are called allergens. When these allergens re-enter the nasal mucosa, they bind to the corresponding IgE, triggering an allergic reaction. The allergens causing this disease are divided into two major categories based on their mode of entry into the body: inhalant and food allergens:

1. Inhalant Allergens

These enter the nasal cavity through respiration and are often suspended in the air.

(1) Pollen Not all plant pollen can trigger the disease. Only pollen that is abundant, widespread, highly allergenic, and wind-dispersed is most likely to become an allergen. Due to differences in vegetation, the allergenic pollen varies by region. For example, birch and timothy grass pollen dominate in Northern Europe, ragweed in North America, and cedar pollen in Japan. In China, due to its vast territory, the sensitizing pollen differs by region, with wild Artemisia pollen being predominant in the north. However, ragweed has been found both north and south of the Yangtze River, warranting attention. Recent studies suggest that increasing industrialization and higher concentrations of harmful substances like sulfur dioxide in the air may alter the protein structure of airborne pollen, enhancing its allergenicity. This could be one of the main reasons for the significant rise in incidence rates. The types and levels of airborne pollen vary seasonally, with spring and summer-autumn being peak dispersal periods.

(2) Fungi Widely distributed in nature, fungi are mainly found in soil and decaying organic matter. Both their hyphae and spores are allergenic, with spores being more potent. Spores can spread widely via wind, and their airborne levels sometimes exceed those of pollen, especially in rural areas compared to urban ones. The most common fungal genera include Cladosporium, Alternaria, Penicillium, Aspergillus, and yeast. Among these, Cladosporium and Alternaria exhibit significant seasonal variation, with their spore counts peaking in summer. Indoor warmth, darkness, and humidity favor fungal growth, and the soil in potted houseplants often serves as an ideal breeding ground.

(3) House Dust Mites Belonging to the arthropod class Arachnida, adult mites typically measure 300–500 μm. They primarily inhabit various corners of homes, especially in dust from bedding, pillows, and sofa cushions. Mite feces, eggs, shed skins, and fragmented body parts can all act as allergens.

(4) Animal Dander Animal dander is one of the strongest allergens. Prolonged exposure to relevant animals can sensitize susceptible individuals. Once sensitized, even minimal exposure to dander can trigger nasal symptoms. The animal dander causing respiratory allergies mainly comes from animals closely associated with humans, such as pets (e.g., dogs, cats) and livestock (e.g., dogs, cows, horses, sheep). For instance, one case involved a pathology lab technician who experienced sneezing, profuse nasal discharge, and grade I asthma upon contact with lab guinea pigs.

(5) Feathers: Feathers from poultry or those found in bedding, pillows, and clothing, as well as feathers shed by domestic ornamental birds, can all be allergens.

(6) House dust is one of the common allergens that cause perennial allergic rhinitis. Its composition is quite complex, being a mixture of various substances including animal, plant, and chemical materials.

2. Ingested allergens

refer to allergen substances that enter the human body through the digestive tract and cause nasal symptoms. Their mechanism of action on the nasal mucosa is highly complex and remains poorly understood. Milk, eggs, fish, shrimp, meat, fruits, and even certain vegetables can become allergens.

bubble_chart Pathogenesis

The pathogenesis of allergic rhinitis is essentially a type I allergic reaction occurring in the nasal mucosa. Allergens enter the body through the respiratory tract, are processed by macrophages, and stimulate B lymphocytes to transform into plasma cells, which produce specific IgE antibodies. It has been demonstrated that the specific IgE antibodies in the nasal mucosa primarily originate from the tonsils. IgE travels through the bloodstream to the nasal mucosa, where its Fc segment binds to the cell membranes of mast cells and basophils in the nasal mucosa, sensitizing the nasal mucosa. When allergens re-enter the nasal mucosa, they bind to the Fab segments of IgE antibodies, causing bridging between adjacent IgE molecules. This results in structural changes in the membranes of mast cells and basophils, leading to the release of various chemical mediators, primarily histamine, kinins, leukotrienes, eosinophil chemotactic factors, prostaglandins, platelet-activating factors, and serotonin. These mediators act on their respective receptors in the blood vessels, glands, and nerve endings of the nasal mucosa, causing vasodilation, increased vascular permeability, enhanced exudation, inflammatory cell infiltration (predominantly eosinophils), tissue edema, and heightened excitability of nerve endings. These pathological changes give rise to the corresponding clinical symptoms and signs.

bubble_chart Pathological Changes

Edema is present in the interstitial spaces of the nasal mucosa, with dilation of small blood vessels and hyperplasia of goblet cells in the mucosal epithelium. Glandular dilation can also be observed. The mucosa shows infiltration by numerous eosinophils, lymphocytes, monocytes, and plasma cells. When stained with toluidine blue, an increased number of mast cells can be seen in the mucosal tissue, along with a higher concentration of basophils in the superficial layer. Some studies have found that mast cells in the lamina propria of the mucosa may migrate to the superficial layer upon repeated exposure to allergens. The mechanism behind this chemotactic behavior of mast cells remains unclear. The presence or quantity of eosinophils in the tissue is related to recent allergen exposure. However, once the nasal mucosa is sensitized, the number of mast cells and basophils is generally higher than in healthy individuals.

bubble_chart Clinical Manifestations

Based on whether the onset has seasonal characteristics, it is clinically divided into seasonal rhinitis and perennial rhinitis:

(1) Seasonal Rhinitis

Mainly caused by mongolian snakegourd root, hence also known as mongolian snakegourd root disease. It is also referred to as hay fever, but it has no connection with summer hay and no fever, making this term a misnomer.

A significant seasonal pattern of onset is the clinical hallmark of seasonal rhinitis. Patients begin to experience symptoms during the mongolian snakegourd root dispersal season. During the attack, they experience itchy eyes, conjunctival congestion, and in severe cases, edema, which can lead to misdiagnosis as common conjunctivitis. Patients suffer from frequent sneezing fits, often with multiple sneezes in a row. Daily nasal congestion is accompanied by copious watery nasal discharge, requiring multiple handkerchief changes. The unbearable nasal itch forces them to frequently rub their eyes and nose. Once the flowering season passes, most patients recover without treatment. In the first year of onset, patients often mistake it for a common cold or a "heat common cold," but when the same "common cold" recurs in the same season and time in the second or third year, they begin to suspect the nature of the disease and seek further diagnosis and treatment. Another characteristic is its regionality. Some patients may not experience symptoms when moving to an area with different climatic or geographical conditions due to variations in plant species, but after several years, they may develop symptoms again due to repeated sensitization by a local mongolian snakegourd root.

(2) Perennial Allergic Rhinitis

This type of rhinitis is mainly caused by perennial exposure to certain allergens, such as house dust, dust mites, fungi, animal dander, or feathers. The onset is not seasonal, though those allergic to fungi may experience seasonal exacerbations. Patients experience symptoms year-round, similar to seasonal rhinitis but generally less severe. Ocular symptoms are mild or absent, with the main manifestations being episodic sneezing, nasal congestion, and runny nose.

Rhinoscopy Findings In perennial rhinitis, the nasal mucosa shows no characteristic changes; it may appear dark red and congested, or pale, pallid, or bluish. However, in seasonal rhinitis, especially in summer mongolian snakegourd root cases, the nasal mucosa often appears markedly pale and edematous.

Turbinate swelling is present, though not in all cases. In long-standing cases, edema or polypoid changes may appear at the anterior end or lower edge of the middle turbinate. Hyperplastic or markedly edematous turbinates show a weaker response to 1% Ephedrine.

bubble_chart Diagnosis

Allergic rhinitis is characterized by increased reactivity of the nasal mucosa, but increased nasal mucosal reactivity is not necessarily allergic rhinitis. Only through comprehensive analysis of medical history and various examination results can a correct diagnosis be made.

(1) Non-specific diagnosis

Non-specific diagnosis involves analyzing medical history and general examination results to determine whether rhinitis is allergic.

1. Medical history The medical history is an important basis for diagnosing allergic rhinitis. When collecting the medical history, attention should not only be paid to symptoms but also to whether the onset is seasonal, whether there are obvious triggers (temperature changes, searching through boxes for clothes, dust, odors, etc.), whether there are allergenic factors in the living environment (pets, birds, excessive indoor ornamental flowers, etc.), whether the house is dark and damp, and the response to previous treatments. Through detailed inquiry and brief discussion with the patient, an impression diagnosis of allergic rhinitis can be made in nearly half of the patients.

2. Cytological examination of nasal secretions Under normal circumstances, nasal secretions contain only a small number of epithelial cells and lymphocytes. In allergic rhinitis, nasal secretions may show increased eosinophils, basophils, and goblet cells. Scrapings from the nasal mucosa may also reveal more mast cells.

Proper preparation of nasal secretion smears and appropriate staining are crucial for this examination. Using a small ear curette under anesthesia, gently scrape the surface of the anterior end of the inferior turbinate, spread the scrapings evenly on a slide, immediately fix with 95% ethanol, and then stain with Wright's stain, strictly controlling the time to 30–60 seconds.

If the patient has recently been exposed to allergens, microscopy often reveals numerous eosinophils, basophils (mast cells), and goblet cells.

(2) Specific diagnosis

Specific diagnosis involves identifying the allergen responsible for the condition in the presence of specific IgE in the patient. There are two main categories: in vivo and in vitro methods.

1. In vivo methods In vivo methods involve stimulating the body with allergens (allergens) and observing the allergic reactions. For diagnosing allergic rhinitis, the main methods are allergen skin tests and nasal provocation tests.

(1) Allergen skin tests This method introduces an appropriate allergen into the skin, allowing the allergen to bind to specific IgE on the surface of mast cells in the skin, causing the mast cells to release mediators such as histamine, leading to local vasodilation, plasma exudation, tissue edema, and the appearance of papules or wheals (urticaria-like reactions) on the skin. Clinically, two types of skin tests are commonly used:

① Intradermal method Inject 0.01–0.02 ml of a certain concentration (1:1000) of allergen solution intradermally and observe for 15–20 minutes. A wheal-like reaction (diameter ≥0.5 cm) at the injection site indicates a positive result.

② Prick method Apply a drop of a certain concentration (1:10) of allergen solution to the skin surface, then prick the skin at the droplet with a needle tip, breaking the epidermis without bleeding. Observe the result after 15–20 minutes; local swelling and redness indicate a positive result.

Both methods should use allergen solvent and histamine solution (0.1%) as negative and positive controls, respectively. The intradermal method is more sensitive but less specific than the prick method. The prick method is more specific and safer, and is increasingly adopted by most physicians.

The advantages of skin tests are speed, simplicity, and strong specificity, allowing multiple allergens to be tested simultaneously, though generally no more than 15. By carefully analyzing the medical history, only suspected allergens need to be tested.

Skin tests generally do not cause severe reactions, but highly sensitive individuals may occasionally experience them. The main symptoms include facial flushing, itchy palms, eyelid edema, chest tightness, cough, panting, and in severe cases, laryngeal edema may occur. If a reaction occurs, it can be managed similarly to penicillin allergy. With timely treatment, no serious danger will arise.

The allergen solutions used for skin tests are mostly commercially available in developed countries with certain quality standards. Currently, there is no nationwide unified quality standard in China, and most of the allergen solutions used are prepared by the allergy departments of several major hospitals.

(2) Nasal Provocation Test The nasal provocation test is a highly sensitive and specific method. This test involves applying approximately 200μl of an allergen solution (1:1000) to a round filter paper disc with a diameter of 0.5cm, which is then placed on the surface of the inferior turbinate mucosa. If the patient is allergic to the allergen, typical allergic rhinitis symptoms can be induced within 3 minutes, and highly sensitive individuals may even experience an asthma attack. Only one allergen can be tested at a time with this method, so it is mainly used when skin tests are negative but there is still suspicion of an allergy to a specific allergen, or when further verification of skin test results is required under special circumstances. Similar to skin tests, a control should be set before nasal provocation to exclude false positives.

Both skin tests and nasal provocation tests require discontinuation of antihistamines and corticosteroids 48–72 hours prior to testing. If the patient is experiencing a severe asthma episode, these tests should not be performed.

2. In Vitro Methods These methods involve laboratory testing for the presence of specific IgE against certain allergens in the patient’s serum or secretions. The earlier method was the radioallergosorbent test (RAST), but enzyme-linked immunosorbent assay (ELISA) has gradually become more widely adopted by laboratories. Other methods include histamine release tests and basophil degranulation tests. In vitro methods are primarily used in pathological and clinical pharmacological research.

To make the diagnosis more precise and objective, a scoring system based on the above test results can be applied, and a diagnosis of allergic rhinitis can be made if a certain score is reached. The scoring criteria should be concise and take testing conditions into account. Currently, a 3-point scoring system is commonly used, as described below:

0 points: No symptoms;

1 point: Grade I symptoms, skin test (+),

Nasal smear (+);

2 points: Grade II symptoms, skin test (++),

Specific IgE (+), nasal smear (+);

3 points: Severe nasal symptoms, skin test (+++),

Specific IgE (+), nasal smear (+).

The diagnostic scoring can be performed according to the following table:

Table 1 Diagnostic Scoring for Allergic Rhinitis

A total score ≥5 points can diagnose allergic rhinitis; if it is below 1–2 points, a nasal provocation test can be performed, and a positive reaction confirms the diagnosis. Some statistics show that among patients with Mongolian snakegourd root disease, about 5% require a nasal provocation test, while in perennial rhinitis, 10–20% require the test.

bubble_chart Treatment Measures

(1) Avoidance Therapy

For identified allergens, contact should be minimized as much as possible. Patients with Mongolian snakegourd root symptoms should reduce outdoor activities during the dispersal period of Mongolian snakegourd root. Those with perennial rhinitis should improve their living environment by measures such as removing pets like cats and dogs, eliminating flowers and birds, replacing carpets and feather bedding, ensuring indoor ventilation, and reducing dust, all of which can be beneficial.

(2) Drug Therapy

1. Drug Treatment for Seasonal Allergic Rhinitis

Since the onset of this type of rhinitis occurs at a relatively fixed time, it provides an opportunity for preventive medication. Proper use of drugs can not only alleviate nasal symptoms during the Mongolian snakegourd root period but also help some patients get through the Mongolian snakegourd root period more comfortably without requiring lengthy desensitization injections.

(1) Sodium Cromoglycate: By inhibiting Ca²⁺ entry into cells and stabilizing mast cell membranes, it prevents the release of mediators like histamine. Clinically, it is applied as a 2% nasal drop or aerosol, or sometimes as a powder sprayed into the nasal cavity. It should be started two weeks before the onset of symptoms, administered three times daily, with each nostril receiving a dose equivalent to 2.5mg.

(2) Ketotifen: This drug has both antihistamine effects and prevents the release of inflammatory mediators from leukocytes. Taken orally at 1mg twice daily, it should be started two weeks before the onset and continued throughout the symptomatic period. Drowsiness may occur in the first two weeks of use but tends to diminish thereafter. Therefore, drivers, operators of precision machinery, and similar workers should exercise caution.

(3) Adrenocorticosteroids: These can suppress symptoms of nasal allergic reactions at various levels. One week before the onset season, an intramuscular injection of triamcinolone acetonide suspension or intranasal application (aerosol or nasal drops) can be administered. Intranasal application can continue until the end of the symptomatic period. The dose of beclomethasone dipropionate is 400μg/day. Some clinicians often prepare dexamethasone solutions temporarily. Pharmacokinetic studies show that this type of corticosteroid is highly absorbable through the nasal route.

During the entire symptomatic period, the following medications may be added depending on the specific condition:

(1) Antihistamines: These are highly effective in controlling nasal and ocular itching, as well as frequent sneezing. Oral formulations are commonly used. In recent years, intranasal topical formulations have been developed abroad, reportedly with excellent efficacy.

(2) Sodium Cromoglycate Eye Drops: Patients with prominent ocular symptoms due to Mongolian snakegourd root can use these drops, alternating with dexamethasone eye drops if necessary.

(3) Nasal Decongestants: If the nasal turbinate tissues are congested and swollen, 1% ephedrine nasal drops can be used. To prevent drug-induced rhinitis, intermittent or alternating administration is recommended, or adenosine triphosphate sodium may be added.

2. Drug Treatment for Perennial Allergic Rhinitis

Antihistamines, sodium cromoglycate, adrenocorticosteroids, and anticholinergic drugs can all be used. However, this type of rhinitis often presents with one predominant symptom, so the choice or switch of medication should be based on symptom changes. A previously effective drug may lose efficacy over time, and switching to another drug (with a different pharmacological mechanism) may prove beneficial. Below is a comparison of the inhibitory effects of these drugs on nasal symptoms for clinical reference:

Table 2 Comparison of Drug Efficacy for Rhinitis

(3) Specific Immunotherapy

Specific immunotherapy, also known as desensitization therapy, involves administering injections of allergen extracts based on the results of allergen testing. Starting with a low concentration, the dose and concentration are gradually increased over time to achieve specific desensitization. There are three forms of desensitization injections:

1. Perennial Desensitization Injections

After determining the initial concentration based on skin test results, injections start at 0.1ml and are administered every 2–3 days, incrementally increasing the dose. Each course consists of 10 injections at a single concentration. The concentration typically ranges from 1:10⁶ to 10:10⁸, increasing with each course until the maintenance concentration and dose are reached. The maintenance concentration and dose refer to the maximum concentration and dose the patient can tolerate without experiencing local or systemic reactions, usually 1:10² to 1:10³, with a dose of 0.5ml per injection. The frequency of injections is gradually reduced from twice weekly to once weekly, biweekly, or monthly. This method is safe, with rare systemic reactions, and offers stable, long-lasting efficacy. However, it requires a long duration and may inconvenience the patient.

2. Rapid Desensitization Injections

This method achieves the maintenance dose in a short period. It is convenient for patients and shows significant efficacy. However, it often causes local reactions (swelling, itching at the injection site) and systemic reactions (nasal symptoms, chest tightness, or asthma). Therefore, it should be conducted under close supervision by an experienced physician.

3. Preseasonal Desensitization Injections

Primarily used for seasonal rhinitis, injections begin 3 months before the pollen season, with increased frequency to ensure sufficient concentration is reached by the time the season starts. Injections can be discontinued after the season ends. The efficacy of this method varies.

The efficacy of specific immunotherapy is most significant in Mongolian snakegourd root disease, with reports indicating an effectiveness rate as high as over 90%. The therapeutic effect develops slowly, so it should be used in combination with medication during treatment. The mechanism of this immunotherapy is not yet fully understood and may be related to the production of blocking antibodies in the body and reduced sensitivity of mast cells.

(IV) Surgical Therapy

In nasal allergies, the parasympathetic nerve activity is heightened, and severing the sympathetic nerve supply to the nasal cavity can reduce this activity. Such surgical procedures include vidian neurectomy, anterior ethmoidal neurectomy, and greater superficial petrosal neurectomy. These surgeries have shown significant short-term efficacy, but reports on long-term outcomes vary.

In some patients with long-standing perennial rhinitis, the inferior turbinate may undergo hyperplastic hypertrophy, exacerbating symptoms such as stuffy nose. Additionally, middle turbinate enlargement or polypoid changes may occur, leading to obstruction of the middle meatus drainage. Partial resection of the turbinate can significantly alleviate nasal symptoms. Some practitioners achieve notable results by removing only a small portion of the anterior end of the inferior turbinate.

Applying chemical (20% silver nitrate cauterization) or physical (electrothermal) local cauterization to the nasal mucosa, or using laser irradiation, can also markedly reduce nasal mucosal sensitivity and achieve symptom control.

bubble_chart Complications

Common complications are as follows:

1. Epistaxis—Mostly manifests as blood-streaked nasal discharge or minor dripping, more commonly seen in children. Previously thought to be caused by violent sneezing, it is now speculated to be related to reduced thrombus formation due to metabolic disorders of membrane peanut arachidonic acid in mast cells.

2. Allergic sinusitis—Because the sinus membrane is connected to the nasal membrane, allergic inflammation of the nasal mucosa can easily spread to the sinus membrane, leading to allergic sinusitis. The main symptoms include headache and dizziness. If secondary infection occurs, purulent nasal discharge may appear, and symptoms worsen.

3. Pharyngitis—Due to long-term stuffy nose and recurrent episodes, patients often breathe through their mouths, which can lead to chronic pharyngitis.

4. Bronchial asthma—May coexist with allergic rhinitis. Some asthma patients often experience attacks following episodes of sneezing.

5. Exudative otitis media—Nasal allergic reactions can spread to the middle ear via the Eustachian tube. Edema of the mucosal membrane at the pharyngeal opening of the Eustachian tube in the nasopharynx or allergens entering the middle ear through this tube can lead to exudative otitis media.