Перспективным направлением является внедрение в практику лекарственных препаратов, сочетающих противовирусное, противовоспалительное и антигистаминное действие. Современные представления о патогенезе воспаления в верхних дыхательных путях основаны на понимании роли различных механизмов защиты, препятствующих проникновению возбу-дителя в толщу слизистой оболочки, ее колонизации, а также развитию сначала локального, а затем и диффузного воспали-тельного процесса. Применяемые в настоящее время препараты позволяют не только воздействовать непосредственно на возбудителя инфекции, но и модулировать воспалительный процесс, индуцировать местные и общие иммунные реакции, как специфические, так и неспецифические. К группе современных препаратов, активирующих неспецифические факторы про-тивовирусной защиты, можно отнести Анаферон, Анаферон детский и Эргоферон. Стоит отметить, что Эргоферон обладает комплексной (противовирусной, противовоспалительной и антигистаминной) фармакологической активностью. Многолетний опыт практического применения этих препаратов подтверждает их высокую эффективность и безопасность в лечении и про-филактике ОРВИ, включая грипп, у пациентов с хроническими обструктивными заболеваниями легких.Ключевые слова: ОРВИ, бронхиальная астма, ХОБЛ, Анаферон, Анаферон детский, Эргоферон. N.P. KNYAZHESKAYA, PhD in medicine, I.A. BARANOVA, MD, Prof., M.P. FABRIKA, PhD in medicine Pirogov Russian National Research Medical University NOVEL POTENTIALS FOR TREATMENT AND PREVENTION OF ARVI IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASEOne of prospective tendencies is introduction into the clinical practice combined medicines with antiviral, resolvent and antihistamine mechanisms of action. Contemporary glimpses of the inflammation pathogenesis are based on understanding different protective mechanisms, preventing invasion of pathogen into the mucous, its colonization and development of local, then systemic inflammation. Currently applicable medicines act not only against the pathogen, but also modulate inflammation process, induce local and systemic immune responce, both specific and non-specific. To the later group of medicines, acting through non-specific immune system factors relate Anaferon, Anaferon for children and Ergoferon. It should be noted that Ergoferon has complex (antiviral, resolvent and antihistamine) pharmacological action. Long-term experience of their usage corroborates their high effectiveness and safety in treatment and prevention of ARVI including flu in patients with chronic obstructive pulmonary disease.

Despite the obvious and simple diagnosis, in practice we meet patients who do not respond to standard therapy. Why does drug resistance occur? The answer to this question is not unambiguous and requires careful investigation in each clinical case. Here we present a clinical case of a patient with bronchial asthma, who had no bad habits and occupational hazards and received adequate drug therapy. However, her condition worsened from attack to attack. Whole exome sequencing by NGS allowed us to determine the spectrum of pathogenic mutations which contribute to the pathological process and drug resistance. Atopy due to dysfunction of filaggrin gene (FLG) triggered the disease and supported the pathological process that led to bronchial asthma. Furthermore, the patient’s body is not able to neutralize the bacterial flaggelin. The inflammatory response is reduced due to а Toll-like receptor 5 (TLR5) deficiency. This is one of the mechanisms underlying development of allergic bronchial asthma. In addition, the patient has reduced cross-presentation of antigens by dendritic cells, that is, a reduced immune response in the absence of infection, due to the complete loss of UNC93B1 gene function. Conclusion. Thus, an atopic reaction based on reduced adaptive immunity led to severe IgE allergy and torpid course of bronchial asthma. This conclusion supports atopic sensitization as the target for therapeutic action and the main core of pathological processes. For this purpose, we used a monoclonal antibody omalizumab that is capable of binding and reducing the amount of IgE. Targeted treatment of bronchial asthma made it possible to interrupt the symptoms and achieve complete remission.