In clinical terminology, it is one of the most common forms of the cold, which is equal in both adults and children. A distinctive feature of this pathology is its ability to skillfully mask for an ordinary cold.
Allergic rhinitis is a disease characterized by paroxysmal rhinorrhea, sneezing, nasal obstruction, itching in the nose and eyes, headache and observed at any age.
There is no final classification of this disease. Some authors subdivide it for etiology and pathogenesis into non-infectious-allergic, infectious-allergic and mixed, and for course into heavy (subcompensated) and burdened (decompensated), combined with other forms of allergy of the respiratory tract: allergic bronchitis, bronchial asthma, etc. According to morphological changes, there may be several stages of the disease: paroxysmal, catarrhal, vasodilator (correspond to mild course), chronic edema, polyposis, nest of hyperplasia (corresponding to severe course). Other researchers distinguish allergic rhinitis, caused mainly by inhalation allergens and mediated by allergic reactions of immediate type, rhinitis vasomotor and non-allergic (cryptogenic) year-round rhinitis. To non-allergic one, they include diseases with unclear etiology, in which immunological reactions do not play a significant role. Although such forms often combine with secondary infection, and nasal secretion reveals a large number of eosinophils.
The cause of noninfectious allergic rhinitis is the effect of inhaled exoallergens (allergens of household, fungal, plant and animal allergens) and food allergens (sensitization can develop with the use of allergenic products and even inhalation of them). Infectious-allergic one is caused by microbial allergens, mainly staphylococcus and streptococcus, and secondary factors – dry, hot climate, hypovitaminosis, air pollution.
The heart of non-infectious-allergic rhinitis is the immediate-type hypersensitivity mediated by antibodies related to immunoglobulin E. The prominent mediators lead to vasodilation, increased capillary permeability, hypersecretion, eosinophilia, and disruption of the autonomic nervous system. There is an imbalance between adrenergic and cholinergic regulatory mechanisms with a blockade of adrenergic effects and a violation of the control of nasal vascularization (ischemia of the mucosa due to arteriolar contraction and venule relaxation). Cholinergic stimulation promotes vasodilatation, hypersecretion and enhanced reactions, mediated immunoglobulins E. Previous sensitization to a single antigen can provoke a response to lower doses of other inhaled antigens (“priming effect”) and the formation of hyperreactivity on nonspecific stimuli. Tthe heart of infectious-allergic rhinitis is a bacterial allergy, manifested by the immediate-type and delayed-type hypersensitivity.
Allergic rhinitis causes hyperimia metaplasia of the epithelium, thickening of the basal membrane, infiltration of lymphocytes, eosinophils, monocytes, histiocytes, fibroblasts, increased number of mast cells and hypertrophied glands. With a progressive process, patients can develop polyps or join infectious diseases.
For allergic rhinitis, morning seizures are typical. Dysfunction of the Eustachian tube is often observed, the tympanic membrane can be involved in the process. Manifestations of allergic rhinitis are amplified in the position on the back, with the head lowered 20 ° below the horizontal (this helps to reveal the latent nasal obstruction). Infectious-allergic one is characterized by frequent exacerbations arising after acute respiratory infections, the presence of foci of chronic infection, mainly in the adnexal nasal cavity. Patients constantly have a bunged-up nose, even in the period of remission. They suffer from mucoid and suppurative discharges. The disease is seasonal in the pollen etiology of allergic rhinitis and year-round with both domestic and epidermal one. Some patients have nasal polyps; the disease is often complicated by allergic otitis and sinusitis. 3-10% of patients with allergic rhinitis have bronchial asthma. Persons with hyperreactivity of bronchial tubes to methacholine have high risk of bronchial asthma are. Patients with allergic rhinitis are also prone to respiratory infections, sinusitis.
To establish the diagnosis of allergic rhinitis different methods of examination of patients are used: allergological anamnesis, allergological diagnostic tests of cutaneous, allergological diagnostic tests provocative (with decisive importance) with specific antigens, nasal secretion and sine content analysis, riposcopy, functional, laboratory and radiographic studies.
Allergic rhinitis is characterized by pronounced eosinophilia of the nasal secretion, however the absence of eosinophils does not exclude allergic rhinitis, since eosinophilia may not be detected in secondary infection (neutrophils predominate in secret) and treatment with glucocorticosteroid drugs. The ratio of eosinophil and neutrophil levels is an important indicator of the role of infection. A half of patients has mast cells, basophils, in large numbers, immunoglobulin A, G andE is often increased. In the acute phase of allergic rhinitis rhinoscopy helps to reveal the pallor of the mucous membrane, diffuse edema of the lower and middle nasal concha (lubrication with vasoconstrictive solutions does not reduce their volume), mucocutaneous watery discharge. In the chronic phase, non-infectious-allergic form of allergic rhinitis is characterized by hypersecretory-vasodilator disorders, infectious-allergic-edema of the mucous membrane, hyperplasia of nasal concha, or polyposis of their degeneration, mucopurulent discharge. Using the methods of functional diagnostics in patients with allergic rhinitis, there is a violation of the respiratory, suction and transport functions of the nose. A part of patients has an increase in the level of immunoglobulin E in the blood serum and positive reactions of leukocytolysis. In severe rhinitis a part of the patients has subclinical bronchospasm. With the help of X-ray examinations, the fuzzy darkening of the frontal and lattice accessory nasal cavities can be detected.
Allergic rhinitis differentiates with rhinitis with vasomotor, medicinal rhinopathies, hormonally caused rhinitis, nasal mastocytosis. Allergic rhinitis in hay fever rarely causes diagnostic difficulties. Medicamentous rhinitis is observed when using (local) for the treatment of allergic rhinitis vasoconstrictors, aerosols, hormones (oral contraceptives), derivatives of reserpine, hydralazine. Symptoms of it gradually disappear after the abolition of drugs. Hormonal rhinitis occurs during pregnancy (disappears after birth), before menstruation and is combined with metabolic disorders and endocrinopathies. The mechanisms of its development are not known. Symptoms of nasal mastocytosis are identical to those of allergic rhinitis. The diagnosis is established by biopsy of the nasal mucosa.
Therapy of allergic rhinitis is subject to the rules for the treatment of allergic diseases: elimination of contact with antigen, hyposensitization, desensitizing non-specific therapy with unknown etiology and contraindications to hyposensitization, which is most effective in treating pollen allergic rhinitis. Principles of nonspecific therapy: regular use of antihistamines and rational use of decongestants (sympathomimetic drugs). H-1-blocking and antihistamines H-2-blocking are the most effective combination of antihistamine preparations. They inhibit rhinorrhea, sneeze, and have little effect on nasal obstruction. With tachyphylaxis, the effect may come to one group of agents from others. Most decongestants contain adrenaline. These are fast acting agents, effective for the removal of nasal obstruction. They are assigned for a short time with the dominance of nasal obstruction; their prolonged use (more than 3-4 days) causes secondary hyperemia with the progression of nasal obstruction. Oral sympathomimetics in combination with antihistamines also effectively reduce obstruction. For non-specific therapy of allergic rhinitis, it is necessary to use cc-adrenoagonists (reduce vascular permeability), anticholinergic drugs, in particular atropine (eliminate rhinorrhea, but have side effects), intall locally (short-term effect, not always observed), glucocorticosteroid drugs. Long-term systemic glucocorticosteroid therapy for the treatment of allergic rhinitis is rarely used (only in severe allergic rhinitis, resistant to other forms of therapy). High-performance local glucocorticosteroid drugs can be used for a long time.
The patient with allergic rhinitis shows various hormonal preparations in the form of drops, powders, aerosols: their effectiveness is different; side effects are rare; used with caution in viral and fungal diseases of the nose. Highly active and rapidly metabolized drugs (beclomethasone dipropionate, flunisolide acetate, budesonide, triamsinolonopetonide), effective in the treatment of allergic rhinitis, are used by intermittent regimens for the therapy of year-round and vasomotor rhinitis, nasal polyposis, and may be useful in the treatment of drug rhinitis caused by vasoconstrictor agents. Histaglobulin (parenterally or by electrophoresis), intranasal electrophoresis of solutions (1% calcium chloride, 1% dimedrol, 5% vitamin C), cryotherapy, and the introduction of an ultrasound probe into the tissues of the inferior nasal concha are also used to treat allergic rhinitis.