Научная статья на тему 'CURRENT PROBLEM AND SOLUTION ALLERGIC RHINITISA'

CURRENT PROBLEM AND SOLUTION ALLERGIC RHINITISA Текст научной статьи по специальности «Фундаментальная медицина»

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allergic rhinitis / diagnosis / treatment / intranasal glucocorticoids budesonidase regions.

Аннотация научной статьи по фундаментальной медицине, автор научной работы — Sharofat Sevindikovna Jumarova

Воver the past 30 years, there has been an increase in the prevalence of allergic diseases (AD), in the structure of which one of the leading places is occupied by allergic rhinitis (AR). This pathology has a significant impact on the physical and mental health of patients, and is of great social importance. In the United States, the number of patients with AR is 25-30 million people, while AZ is registered in more than 40 million people. In England, the prevalence of AR is 16%, in Denmark-19%, in Germany-13-17%.

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Текст научной работы на тему «CURRENT PROBLEM AND SOLUTION ALLERGIC RHINITISA»

CURRENT PROBLEM AND SOLUTION ALLERGIC RHINITISA

Sharofat Sevindikovna Jumarova

Bukhara State Medical Institute

ABSTRACT

Bover the past 30 years, there has been an increase in the prevalence of allergic diseases (AD), in the structure of which one of the leading places is occupied by allergic rhinitis (AR). This pathology has a significant impact on the physical and mental health of patients, and is of great social importance. In the United States, the number of patients with AR is 25-30 million people, while AZ is registered in more than 40 million people. In England, the prevalence of AR is 16%, in Denmark-19%, in Germany-13-17%.

Keywords: allergic rhinitis, diagnosis, treatment, intranasal glucocorticoids budesonidase regions.

In the Republic of Uzbekistan, the prevalence of AR ranges from 12.7 to 24% [1]. However, not all patients suffering from this disease seek medical help, and therefore it can be imagined that the real prevalence of it is much higher. The data of official statistics on the number of visits to medical and preventive institutions do not correspond to the true values of the incidence and prevalence of allergic diseases among the population Uzbekistan: allergic rhinitis affects from 0.1 to 0.4% of the population, and according to research data, from 7 to 12% (according to international statistics, up to 20% of the population). It is important to take into account that in the practice of ENT doctors, who are often visited by patients with AR, among all chronic rhinitis, the share of AR is about 25%, i.e. approximately 1 out of 4 patients will have sensitization to any inhaled allergens. Despite the fact that AR is a global medical and social problem today, its role as a cause of suffering and deterioration in the quality of life of patients is clearly underestimated. This nosology is common in the practice of doctors of all specialties, however, making the correct diagnosis and prescribing adequate therapy can take many months and years [2]. The pathogenesis of AR is based on type 1 hypersensitivity (according to Coombs, and Gell) [3-9]. It is characterized by the fact that in individuals with an atopic predisposition, primary contact with a causally significant allergen is accompanied by activation of type 2 T-helper cells and production of interleukins 4 (IL-4), 10 (IL-10), and 13 (IL-13). As a result, the vector of immune responses is switched in the direction of the predominance of the humoral response with the production of allergen-specific IgE by B-lymphocytes. Various allergens can act as causally significant factors inthis case: plant pollen, spores of lower fungi, insect particles, animal epidermis, house dust mites, etc. The resulting IgE is then fixed to

mast cells, binding to them via Fcreceptors. Mast cell receptors, especially, are not only highly affinity for IgE, but also protect them from destruction. Due to this, mast cells remain IgE-sensitized for a long time. Therefore, upon re-entry into the body, the causally significant allergen immediately binds to specific IgE fixed on mast cells [515]. As a result of this interaction, mast cells degranulate with the release of histamine, proteases, thromboxane, leukotrienes (LTC4, LTD4, LTB4), prostaglandin D2, and other pro-inflammatory substances. cytokines. The impact of these biologically active substances on the tissues in which an allergic reaction develops is accompanied by typical signs of inflammation - vasodilation, hyperemia, increased vascular permeability, edema and cellular infiltration. The activity of inflammation is supported by eosinophils, basophils, and neutrophils attracted to the lesion site, which also produce cytotoxic mediators and cytokines [3,9].

From the above description of the mechanism of allergy, an important generalizing conclusion follows. It consists in the fact that the allergic form of reactivity is an integral reaction of the body, composed of the activities of certain cellular and molecular participants in mutual relations with each other, ensuring the readiness of the barrier systems of integumentary tissues and histohematic barriers to the perception of allergens and the organization of allergen-specific processes [16-25].

Over the past 30 years, there has been an increase in the prevalence of allergic diseases (AD), in the structure of which one of the leading places is occupied by allergic rhinitis (AR). This pathology has a significant impact on the physical and mental health of patients, and is of great social importance. In the United States, the number of patients with AR is 25-30 million people, while AZ is registered in more than 40 million people. In England, the prevalence of AR is 16%, in Denmark-19%, in Germany-13-17%.Despite the fact that AR is now a global меrцнкосоцнапbнуromedical and social problem, its role as a cause of suffering and deterioration in the quality of life of patients is clearly underestimated by inflammation. It is easy to seethat what has been said corresponds to the understanding of allergy as a systemic process. The central molecular link of this system, which determines its specificity, is the allergen-specific IgE molecule. Its formation and accessibility to all tissues ensure the ability of all barrier systems to recognize an allergen that previously entered the body and induced IgE formation. The allergic reaction itself, localized by the action of an allergen in a particular organ or tissue, affects not only their function, but also the state of other organs and tissues. For example, patients with bronchial asthma have asymptomatic signs of allergic inflammation of the salivary glands and gallbladder. An allergic reaction to one allergen can facilitate the immune system's response, which is expressed in the production of allergen-specific IgE to other allergens entering the body. Thus, during an allergic reaction of tissue mast cells, cytokines (in particular, interleukin-4 and interleukin-13) are released from them, which are mandatory participants in the

induction of the IgE response. Allergic reactivity as a system is provided by mandatory complementary relationships with other systems of the body (primarily with the immune system, as well as the nervous, endocrine, etc.). Without touching on the whole variety of these relationships, we can recall the role of bone marrow as an illustrative example. Bone marrow is involved in the formation of major effector cells. cellular participants of allergy: mast cells, basophils, and eosinophils that are actively recruited into the tissues where the allergic reaction unfolds. Special attention should be paid to the fact that an increase in the formation of inflammatory cell precursors in the bone marrow is associated with the maintenance of allergic inflammation in tissues and their nonspecific hyperre activity [26-35]. This has been shown both in humans with naturally occurring AD and experimentally in sensitized animals. All this gives us the right to consider the allergic process and AD as a systemic pathology [10]. In cases where these processes occur in the nasal mucosa, AR develops, the clinical manifestations of which are rhinorrhea, sneezing, itching, and nasal congestion [4-9, 1113, 15]. And since allergic inflammation is a systemic process, AR can be characterized not only by the involvement of the nasal mucosa. Quite often, patients suffering from AR are diagnosed with foci of chronic infection and other diseases of the upper respiratory tract (sinusitis, nasal polyposis in combination with polypous sinusitis, usually sinusitis, otitis media). Studies confirm the existence of a direct link between AR and bronchial asthma (BA). Allergic inflammation of the nasal and bronchial mucosa plays a major role in their pathogenesis, and the same cells and mediators cause and maintain inflammation in the nasal and bronchial mucosa. A provocative bronchial test with a suspected causal allergen in patients with AR leads to an asthmatic response involving inflammatory cells and prion flammatory mediators in the nasal mucosa, and a provocative nasal test with exposure to an allergen on the nasal mucosa, in turn, causes the development of inflammation in the bronchi.

These facts support the concept of a "single airway", which demonstrates a close relationship between AR and AD and proves that the inflammatory response can be supported and enhanced by interrelated mechanisms. Therefore, patients with AR should be screened for the presence of AD. Also, patients with asthma should be diagnosed with AR, and treatment should be aimed at suppressing allergic inflammation in both the upper and lower respiratory tracts [16, 17].

Classification of allergic rhinitis is classified according to the form, nature and severity of the course and stage of the disease [2, 18]. There is a distinction between seasonal (observed in patients with sensitivity to pollen and fungal allergens) and year-round (found in patients with sensitivity to household, epidermal, mold, and occupational allergens) AR. By the nature of the course of AR, it can be intermittent (symptoms are disturbed less than 4 days a week or less than 4 weeks. per year) or persistent (symptoms are bothering you for more than 4 days a week or for more than 4

weeks. per year). The course of AR can be mild (the patient has only minor clinical manifestations of the disease that do not interfere with daytime activity and sleep), moderate and severe, which are characterized by the presence of at least one of the following signs: sleep disorders, violations of daily activity, professional activity or study, inability to play sports and normal rest. During AR, there are two stages: exacerbation and remission [2].

Diagnosis and differential diagnosis The nasal mucosa is the border zone that is exposed to a wide variety of foreign particles. Their removal from the nasal cavity occurs within about 20 minutes due to the action of the mucociliary system of the mucous membrane. However, allergen molecules penetrate extremely quickly

Allergic reaction, localized action of the allergen in a particular organ or tissue affected not only their functionality, but also on the condition of other organs and tissues through the superficial layers of the nasal mucosa in the submucosal space, and become available to the cells of the immune system and cause an allergic reaction, resulting in a minute after contact with the allergen arise sneezing, itching in the nose, runny nose. Damage to the ciliated and secreting epithelium occurs in both allergic and non-allergic inflammatory processes. In the season of exacerbation of pollen AR, hypersecretion of mucus occurs, combined with a defect in its release due to structural and functional changes in the ciliated epithelium. The activity of cilia decreases by more than one and a half times. The epithelium of the nasal mucosa contains mast cells and basophils, and the number of these cells increases with AR. Other equally important participants in allergic inflammation are eosinophils, lymphocytes, and endothelial cells. The diagnostic value of the above information lies in the fact that the symptoms of AR develop very quickly, literally in a matter of minutes after contact with a causally significant allergen, which can also be attributed to the criteria for differential diagnosis with non-allergic rhinitis. AR can be detected not only with the help of allergological diagnostic methods, but also with available diagnostic tools in polyclinic settings. At an early stage of AR diagnosis, a general practitioner, ENT specialist, pediatrician, or family doctor (general practitioner) can identify AR. Moreover, the diagnosis of AR does not require special expensive equipment, long-term training, etc. The examination scheme should include a thorough collection of general clinical and allergological anamnesis, ENT examination, cytological examination of a nasal smear, visual check of the patency of the nasal passages, and a check of the sense of smell. However, to establish a definitive diagnosis, it is certainly necessary to consult an allergist and conduct an allergological examination. On the other hand, for the differential diagnosis of AR and the exclusion of frequently occurring concomitant pathology of ENT organs (polyposis, sinusitis, sinus cysts, etc.) often, endoscopy, computed tomography, and morphological research methods should be used. 1) and consider the basic principles of differential diagnosis of allergic and non-allergic rhinitis [19]. The greatest difficulty is

the differential diagnosis of year-round AR and year-round rhinitis of a non-allergic nature [2, 20]. The most important signs for the differential diagnosis of these types of rhinitis are presented in Table 1 [2]. Given that the symptoms of AR are non-specific, the disease is often overlooked under the guise of frequent acute respiratory infections. Therefore, in all cases where the clinical manifestations of rhinitis are not accompanied by other catarrhal symptoms and there are no manifestations of infectious toxicosis, it is necessary to exclude other causes of the disease. First of all, a differential diagnosis is made between allergic, vasomotor, drug-induced and non-allergic rhinitis with eosinophilic syndrome. At the same time, to clarify the diagnosis and choose adequate therapy, it is necessary to clarify the hereditary burden of atopy, clarify the anamnesis of the disease and detail the clinical manifestations. A laboratory examination (clinical blood test, etc.) and consultation with an otolaryngologist and allergist are required, which will determine the range of necessary special studies (cytological examination of nasal secretions, determination of general and specific IgE, skin tests, and in some cases provocative tests) [4, 6, 7, 9, 11,].

ONew approaches to the treatment of allergic. In accordance with the principles of evidence-based medicine, the use of medicines for different forms of AR is distributed. In the absence of a sufficient number of research results in this table are not given the levels of evidence of the effectiveness of drugs in persistent rhinitis - reliable data exist only in relation to the oral administration Differential diagnosis of rhinitis Symptom of Allergic rhinitis non-allergic rhinitis Causes of the disease Allergens household, epidermal, pollen, food, insectia, medicinal Anatomical defects, diseases of the nasopharynx, strong odors, sudden temperature changes, regular use of decongestants, pregnancy, hypothyroidism, primary ciliary dyskinesia, immunodeficiency States, granulomatosis Wegener's Allergological history Positive Negative Skin tests with allergens Positive Negative Cytological examination of the nasal mucosa The content of eosinophils in the smear is more than 2-4% Eosinophils are usually absent (however, with возможна NARES, eosinophilia up to 60% is possible). With infectious rhinitis-high neutrophil count Total serum IgE level IgE is more frequent-elevated More often -normal Presence of specific IgE in the blood serum Yes No Other allergy symptoms (eye) are observed Often Occur much less frequently NARES - from English) - non-allergicrhinitis with eosinophilia syndrome H1-histamine receptor blockers (level of evidence A). Pharmacotherapy of AR consists in influencing the pathogenetic and symptomatic link in the development of the disease, since in many cases etiotropic treatment is impossible (allergen elimination). The following groups of medications are prescribed: antihistamines; topical intranasal glucocorticosteroids; cromoglycic acid preparations (cromones); decongestants. Antihistamines (H1-receptor blockers). The main pharmacological effect is anti-allergic, so antihistamines are often used in the treatment of allergic rhinitis. According to the current classification, H1 blockers are

divided into two groups: I generation (classic or traditional, with noticeable sedative properties) and II generation ("new"non-sedative, with minimal sedative effect). Antihistamines of the first generation (diphenhydramine, chloropyramine, clemastine, promethazine, mebhydroline, dimethindene, ciproheptadine, etc.) are competitive blockers of H1-receptors and therefore bind to them quickly and reversibly. In this regard, to achieve the main pharmacological action, it is necessary to use relatively high doses of the drug. In addition, most traditional H1-histamine blockers have a short-term effect.

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