Bronchial asthma in the ICD-10. Clinic of exogenous – atopic bronchial asthma

According to ICD-10, the term bronchial asthma is applied to patients with completely reversible obstruction of the bronchi (without the presence of symptoms of CB and EL). But BA cannot be considered in isolation from COPD, since a certain portion of patients with COPD have sighting or even bronchial asthma (“there are asthmatics among patients with COPD, and patients with COPD among those with long-term asthma”). J.45. bronchial asthma (4 forms). Excluded: chronic asthmatic bronchitis; acute severe bronchial asthma (for the purpose of epidemiological examination); chronic obstructive asthma; eosinophilic infiltrate with AD; lung diseases caused by exposure to exogenous substances. J.45.0. Mostly atopic bronchial asthma (an external allergen with 5 options has been identified): includes allergic diseases – bronchitis, not designated as chronic, rhinitis with asthma, atopic asthma, exogenous (external) asthma and hay fever with asthma. J.45.1. Non-allergic bronchial asthma: includes endogenous (internal, idiopathic), drug-free non-allergic (e.g. aspirin) bronchial asthma. J.45.8. Mixed bronchial asthma (a combination of J.45.0 and J.45.1) J.45.9. Unspecified asthma: two options are included – asthmatic bronchitis and late arising asthma (one of the variants of dis.metabolic asthma). J.46. Asthmatic status (AS) – acute severe bronchial asthma (more correctly – a very severe, life-threatening exacerbation). AS emphasizes the main thing – the unusual severity of the attack, resistance to the therapy, but not the duration of the attack. This is a temporary diagnosis indicating a sudden onset, severe clinical bronchial asthma and the need for the use of corticosteroids. After stopping AS, it is necessary to find out the form and variant of bronchial asthma. Occupational bronchial asthma is also distinguished, which can be allergic (characterized by an increase in circulating IgE in response to an agent in the workplace) and non-allergic (mechanisms other than IgE-mediated). Exogenous, atopic (IgE-mediated) bronchial asthma occurs more often in childhood in people with atopy – allergic dermatitis, rhinitis and conjunctivitis (in almost 80% they are combined with bronchial asthma). Half of the patients have the first symptoms of AD up to 10 years (70% of patients noted the onset of the disease up to 30 years), from exposure to known air allergens (house dust, bed mites, dandruff of pets – cats, dogs and birds, mold, cockroach allergen), especially a recurrent infection of the bronchi. Attacks of suffocation often occur when cleaning rooms, cleaning carpets. Airway obstruction in these patients can also be exacerbated by exposure to tobacco smoke, hair spray, perfume, or infection (as in non-allergy sufferers). This form of bronchial asthma is well treated (hyposensitization is often effective), its course is transient, and may “subside” with age. Sometimes the period of remission is 10-20 years, with the subsequent appearance of symptoms in adulthood. But in half of the children, bronchial asthma does not go away with age. This is influenced by the allergic constitution, the nature of the significant allergen, the number and severity of seizures. Exogenous bronchial asthma is characterized by: a genetic predisposition to antigenic effects with excess IgE production (its level is increased in 60% of patients) and the formation of allergic reactions of the immediate type, a family history of bronchial asthma, positive skin (at least one of the following – grass pollen, house dust , hair of cats or dogs) and bronchial provocative tests, seasonality of symptoms (hay fever, seasonal rhinitis and eczema, which can appear long before bronchial asthma), the presence of other allergies symptoms (allergic rhinosinusitis without symptoms of infection); lack of infectious bronchopulmonary process. Many patients, long before the formation of bronchial asthma, repeatedly received AB courses for respiratory tract infections. This form of bronchial asthma is aggravated by the appearance of a polyvalent allergy andlayering of the infectious component.

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