19 research outputs found
ΠΠ°ΠΊΡΠ°Ρ ΠΈ Π»Π΅Π³ΠΊΠΈΠ΅: ΠΎΡ ΡΠ΅ΠΎΡΠΈΠΈ ΠΊ ΠΏΡΠ°ΠΊΡΠΈΠΊΠ΅
Lactate (lactic acid) is an end product of glycolysis and cell anaerobic metabolism indicator. Reducing oxygen delivery to the cells leads to increased lactate production and blood concentration. Blood lactate concentration is usually measured to monitor tissue hypoxia and to assess oxygen transport efficacy in critically ill patients (with severe pneumonia, acute respiratory distress-syndrome, shock, etc.) Change in the blood lactate level could also indicate training intensity and post-exertional recovery and allows increase in peak work rate and endurance, individual training schedule, prevention physical overload and sport injuries. Exhaled breath condensate (EBC) is a complex mixture under influence both of respiratory pathology and environmental factors. Key metabolites concentration in EBC including lactate is much lower than that in the blood. This provides a need in novel diagnostic methods including biosensors with high stability, sensitivity and selectivity. Recently, biosensors are the leading methods in this field so as substrate specificity of lactate dehydrogenase underlying biosensor technique allows direct measurement in a biological sample without previous handling. Biosensors based on ferric ferrocyanide as an electrocatalizator have been developed in the M.V.Lomonosov Moscow State University; they have maximal selectivity for lactate and other markers exceeding that of platina-based biosensors used worldwide.ΠΠ°ΠΊΡΠ°Ρ (ΠΌΠΎΠ»ΠΎΡΠ½Π°Ρ ΠΊΠΈΡΠ»ΠΎΡΠ°) ΠΊΠ°ΠΊ ΠΊΠΎΠ½Π΅ΡΠ½ΡΠΈΜ ΠΏΡΠΎΠ΄ΡΠΊΡ Π³Π»ΠΈΠΊΠΎΠ»ΠΈΠ·Π° ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΈΠ½Π΄ΠΈΠΊΠ°ΡΠΎΡΠΎΠΌ Π°Π½Π°ΡΡΠΎΠ±Π½ΠΎΠ³ΠΎ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΊΠ»Π΅ΡΠΎΠΊ. ΠΡΠΈ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠΈ Π΄ΠΎΡΡΠ°Π²ΠΊΠΈ ΠΊΠΈΡΠ»ΠΎΡΠΎΠ΄Π° ΠΊ ΠΊΠ»Π΅ΡΠΊΠ°ΠΌ ΡΠ²Π΅Π»ΠΈΡΠΈΠ²Π°Π΅ΡΡΡ ΠΏΡΠΎΠ΄ΡΠΊΡΠΈΡ Π»Π°ΠΊΡΠ°ΡΠ° ΠΈ ΠΏΠΎΠ²ΡΡΠ°Π΅ΡΡΡ Π΅Π³ΠΎ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ Π² ΠΊΡΠΎΠ²ΠΈ. Π‘ΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ Π»Π°ΠΊΡΠ°ΡΠ° Π² ΠΊΡΠΎΠ²ΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ΅ΡΡΡ ΠΏΡΠΈ ΠΌΠΎΠ½ΠΈΡΠΎΡΠΈΡΠΎΠ²Π°Π½ΠΈΠΈ ΡΡΠΎΠ²Π½Ρ ΡΠΊΠ°Π½Π΅Π²ΠΎΠΈΜ Π³ΠΈΠΏΠΎΠΊΡΠΈΠΈ Ρ ΡΠ΅Π»ΡΡ ΠΎΡΠ΅Π½ΠΊΠΈ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ ΡΡΠ°Π½ΡΠΏΠΎΡΡΠ° ΠΊΠΈΡΠ»ΠΎΡΠΎΠ΄Π° ΠΏΡΠΈ ΠΊΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠΎΡΡΠΎΡΠ½ΠΈΡΡ
(ΡΡΠΆΠ΅Π»ΠΎΠΈΜ ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΠΈ, ΠΎΡΡΡΠΎΠΌ ΡΠ΅ΡΠΏΠΈΡΠ°ΡΠΎΡΠ½ΠΎΠΌ Π΄ΠΈΡΡΡΠ΅ΡΡ-ΡΠΈΠ½Π΄ΡΠΎΠΌΠ΅, ΡΠ΅ΠΏΡΠΈΡΠ΅, ΡΠΎΠΊΠ΅ ΡΠ°Π·Π»ΠΈΡΠ½ΠΎΠΈΜ ΡΡΠΈΠΎΠ»ΠΎΠ³ΠΈΠΈ ΠΈ ΠΏΡ.).Β ΠΠΈΠ½Π°ΠΌΠΈΠΊΠ° ΡΡΠΎΠ²Π½Ρ Π»Π°ΠΊΡΠ°ΡΠ° Π² ΠΊΡΠΎΠ²ΠΈ ΡΠ°ΠΊΠΆΠ΅ ΡΠΊΠ°Π·ΡΠ²Π°Π΅Ρ Π½Π° ΠΈΠ½ΡΠ΅Π½ΡΠΈΠ²Π½ΠΎΡΡΡ ΡΡΠ΅Π½ΠΈΡΠΎΠ²ΠΎΡΠ½ΠΎΠΈΜ Π½Π°Π³ΡΡΠ·ΠΊΠΈ ΠΈ ΡΡΠ΅ΠΏΠ΅Π½Ρ Π²ΠΎΡΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΈΡ ΠΏΠΎΡΠ»Π΅ Π½Π΅Π΅: ΠΏΡΠΈ Π΄ΠΎΡΡΠ°ΡΠΎΡΠ½ΠΎΠΌ ΡΡΠΎΠ²Π½Π΅ ΠΏΠΎΠ²ΡΡΠ°Π΅ΡΡΡ ΠΏΡΠ΅Π΄Π΅Π» ΡΠ°Π±ΠΎΡΠΎΡΠΏΠΎΡΠΎΠ±Π½ΠΎΡΡΠΈ ΠΈ Π²ΡΠ½ΠΎΡΠ»ΠΈΠ²ΠΎΡΡΡ, ΠΏΡΠΈ ΡΡΠΎΠΌ ΠΏΠΎΡΠ²Π»ΡΠ΅ΡΡΡ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΡ Π½Π΅ ΡΠΎΠ»ΡΠΊΠΎ ΠΏΠ΅ΡΡΠΎΠ½Π°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΏΠ»Π°Π½ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΈ ΠΊΠΎΠ½ΡΡΠΎΠ»Ρ ΡΡΠ΅Π½ΠΈΡΠΎΠ²ΠΎΡΠ½ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡΠ°, Π½ΠΎ ΠΈ Π·Π°ΡΠΈΡΡ ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌΠ° ΠΎΡ ΡΠΈΠ·ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΏΠ΅ΡΠ΅Π½Π°ΠΏΡΡΠΆΠ΅Π½ΠΈΡ ΠΈ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΡ ΡΡΠΎΠ²Π½Ρ ΡΡΠ°Π²ΠΌΠ°ΡΠΈΠ·ΠΌΠ° Π² ΡΠΏΠΎΡΡΠ΅. ΠΠΎΠ½Π΄Π΅Π½ΡΠ°Ρ Π²ΡΠ΄ΡΡ
Π°Π΅ΠΌΠΎΠ³ΠΎ Π²ΠΎΠ·Π΄ΡΡ
Π° (ΠΠΠ) ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΠ΅Ρ ΡΠΎΠ±ΠΎΠΈΜ ΡΠΌΠ΅ΡΡ ΡΠ»ΠΎΠΆΠ½ΠΎΠ³ΠΎ ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΎΠ³ΠΎ ΠΈ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΎΠ³ΠΎ ΡΠΎΡΡΠ°Π²Π°, Π½Π° ΠΊΠΎΡΠΎΡΡΠΈΜ Π²Π»ΠΈΡΡΡ ΠΊΠ°ΠΊ Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π»Π΅Π³ΠΊΠΈΡ
, ΡΠ°ΠΊ ΠΈ ΡΠ°ΠΊΡΠΎΡΡ ΠΎΠΊΡΡΠΆΠ°ΡΡΠ΅ΠΈΜ ΡΡΠ΅Π΄Ρ. Π‘ΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ ΠΊΠ»ΡΡΠ΅Π²ΡΡ
ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΡΠΎΠ², Π² Ρ. Ρ. Π»Π°ΠΊΡΠ°ΡΠ° Π² ΠΠΠ Π½Π°ΠΌΠ½ΠΎΠ³ΠΎ Π½ΠΈΠΆΠ΅, ΡΠ΅ΠΌ Π² ΠΊΡΠΎΠ²ΠΈ. ΠΡΠΈΠΌ ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½Π° Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎΡΡΡ ΡΠ°Π·ΡΠ°Π±ΠΎΡΠΊΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ², Π² ΡΠ°ΡΡΠ½ΠΎΡΡΠΈ Π±ΠΈΠΎΡΠ΅Π½ΡΠΎΡΠΎΠ² Ρ Π²ΡΡΠΎΠΊΠΎΠΈΜ ΡΡΠ°Π±ΠΈΠ»ΡΠ½ΠΎΡΡΡΡ, ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡΡ ΠΈ ΡΠ΅Π»Π΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΡΡ. Π Π½Π°ΡΡΠΎΡΡΠ΅Π΅ Π²ΡΠ΅ΠΌΡ Π±ΠΈΠΎΡΠ΅Π½ΡΠΎΡΡ Π·Π°Π½ΠΈΠΌΠ°ΡΡ ΠΎΠ΄Π½Ρ ΠΈΠ· Π»ΠΈΠ΄ΠΈΡΡΡΡΠΈΡ
ΠΏΠΎΠ·ΠΈΡΠΈΠΈΜ, Ρ. ΠΊ. ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ½ΠΎΡΡΡ ΠΈΠΌΠΌΠΎΠ±ΠΈΠ»ΠΈΠ·ΠΎΠ²Π°Π½Π½ΠΎΠ³ΠΎ Π² Π±ΠΈΠΎΡΠ΅Π½ΡΠΎΡΠ΅ ΡΠ΅ΡΠΌΠ΅Π½ΡΠ° Π»Π°ΠΊΡΠ°ΡΠΎΠΊΡΠΈΠ΄Π°Π·Ρ ΠΊ ΡΠ²ΠΎΠ΅ΠΌΡ ΡΡΠ±ΡΡΡΠ°ΡΡ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΠ΅Ρ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΡΡ ΠΈΠ·ΠΌΠ΅ΡΠ΅Π½ΠΈΡ Π½Π΅ΠΏΠΎΡΡΠ΅Π΄ΡΡΠ²Π΅Π½Π½ΠΎ Π² Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠΌ ΠΎΠ±ΡΠ°Π·ΡΠ΅ Π±Π΅Π· ΠΏΡΠ΅Π΄Π²Π°ΡΠΈΡΠ΅Π»ΡΠ½ΠΎΠΈΜ ΠΏΡΠΎΠ±ΠΎΠΏΠΎΠ΄Π³ΠΎΡΠΎΠ²ΠΊΠΈ, Π½Π΅ΡΠΌΠΎΡΡΡ Π½Π° ΡΠ»ΠΎΠΆΠ½ΠΎΡΡΡ Π΅Π³ΠΎ ΡΠΎΡΡΠ°Π²Π°. ΠΠΈΠΎΡΠ΅Π½ΡΠΎΡΡ Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΡΠ»Π΅ΠΊΡΡΠΎΠΊΠ°ΡΠ°Π»ΠΈΠ·Π°ΡΠΎΡΠ° β Π±Π΅ΡΠ»ΠΈΠ½ΡΠΊΠΎΠΈΜ Π»Π°Π·ΡΡΠΈ, ΡΠ°Π·ΡΠ°Π±ΠΎΡΠ°Π½Π½ΡΠ΅ ΡΠΏΠ΅ΡΠΈΠ°Π»ΠΈΡΡΠ°ΠΌΠΈ ΠΠΠ£ ΠΈΠΌ. Π.Π.ΠΠΎΠΌΠΎΠ½ΠΎΡΠΎΠ²Π°, ΠΎΠ±Π»Π°Π΄Π°ΡΡ ΠΌΠ°ΠΊΡΠΈΠΌΠ°Π»ΡΠ½ΠΎΠΈΜ ΡΠ΅Π»Π΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΡΡ Π² ΠΎΡΠ½ΠΎΡΠ΅Π½ΠΈΠΈ Π»Π°ΠΊΡΠ°ΡΠ° ΠΈ Π΄ΡΡΠ³ΠΈΡ
ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ΅ΠΌΡΡ
ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ², ΡΡΠΎ Π΄Π΅Π»Π°Π΅Ρ ΠΈΡ
ΡΠ½ΠΈΠΊΠ°Π»ΡΠ½ΡΠΌΠΈ ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ Π°Π½Π°Π»ΠΎΠ³Π°ΠΌΠΈ Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΠΏΠ»Π°ΡΠΈΠ½ΠΎΠ²ΡΡ
ΡΠ»Π΅ΠΊΡΡΠΎΠ΄ΠΎΠ², ΡΠΈΡΠΎΠΊΠΎ ΠΈΡΠΏΠΎΠ»ΡΠ·ΡΠ΅ΠΌΡΡ
Π·Π° ΡΡΠ±Π΅ΠΆΠΎΠΌ. ΠΠΎ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ°ΠΌ Π½Π΅Π΄Π°Π²Π½ΠΎ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½Π½ΡΡ
ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΈΜ ΠΏΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ Π»Π°ΠΊΡΠ°ΡΠ° Π² ΠΊΡΠΎΠ²ΠΈ ΠΊΠΎΡΡΠ΅Π»ΠΈΡΡΠ΅Ρ Ρ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠ΅ΠΈΜ Π»Π°ΠΊΡΠ°ΡΠ° Π² ΠΠΠ. Π’Π°ΠΊΠΈΠΌ ΠΎΠ±ΡΠ°Π·ΠΎΠΌ, Π½Π°ΠΌΠ΅ΡΠΈΠ»Π°ΡΡ ΡΠ΅Π½Π΄Π΅Π½ΡΠΈΡ ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π° ΠΎΡ ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΌΠ΅ΡΠΎΠ΄Π° (Π°Π½Π°Π»ΠΈΠ·Π° ΠΊΡΠΎΠ²ΠΈ) ΠΊ Π½Π΅ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΠΎ ΡΠΎΠ±ΠΈΡΠ°Π΅ΠΌΠΎΠΌΡ ΠΠΠ.
Π‘ΠΎΠ²ΡΠ΅ΠΌΠ΅Π½Π½ΡΠ΅ ΠΏΠΎΠ΄Ρ ΠΎΠ΄Ρ ΠΊ Π²Π΅Π΄Π΅Π½ΠΈΡ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π±ΡΠΎΠ½Ρ ΠΎΡΠΊΡΠ°Π·ΠΈΠ΅ΠΉ
The bronchoectasia (BE) is a chronic heterogeneous lung disease characterized by recurrent infection, inflammation, persistent cough and sputum discharge. The early BE diagnosis is one of the main recommendations of the European Respiratory Society (ERS) guidelines, which requires medical history collection and multispiral computed tomography (MSCT) of thoracic organs. Despite the complex examination, in most patients BE is classified as idiopathic. The minimum set of tests, including serum immunoglobulins, allergic bronchopulmonary aspergillosis tests and hematology is proposed in ERS guideline for detection of BE causes. Other examinations are recommended to perform based on disease history and radiological characteristics, indicating the importance of BE clinical phenotype identification by different healthcare specialists, for which special examinations are required. Initial examination algorithms and management of patients with BE, in particular, MSCT-semiotics and clinical features, which could help to identify specific reasons are presented in the article.ΠΡΠΎΠ½Ρ
ΠΎΡΠΊΡΠ°Π·ΠΈΡ (ΠΠ) β ΡΡΠΎ Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ΅ Π³Π΅ΡΠ΅ΡΠΎΠ³Π΅Π½Π½ΠΎΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅ Π»Π΅Π³ΠΊΠΈΡ
, Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΠ·ΡΡΡΠ΅Π΅ΡΡ ΡΠ΅ΡΠΈΠ΄ΠΈΠ²ΠΈΡΡΡΡΠ΅ΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ, Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΠ΅ΠΌ, ΠΏΠΎΡΡΠΎΡΠ½Π½ΡΠΌ ΠΊΠ°ΡΠ»Π΅ΠΌ ΠΈ ΠΎΡΠ΄Π΅Π»Π΅Π½ΠΈΠ΅ΠΌ ΠΌΠΎΠΊΡΠΎΡΡ. Π Π°Π½Π½ΡΡ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ° ΠΠ ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΎΠ΄Π½ΠΎΠΉ ΠΈΠ· ΠΎΡΠ½ΠΎΠ²Π½ΡΡ
ΡΠ΅ΠΊΠΎΠΌΠ΅Π½Π΄Π°ΡΠΈΠΉ ΡΡΠΊΠΎΠ²ΠΎΠ΄ΡΡΠ²Π° ΠΠ²ΡΠΎΠΏΠ΅ΠΉΡΠΊΠΎΠ³ΠΎ ΡΠ΅ΡΠΏΠΈΡΠ°ΡΠΎΡΠ½ΠΎΠ³ΠΎ ΠΎΠ±ΡΠ΅ΡΡΠ²Π° (European Respiratory Society β ERS). ΠΠ»Ρ ΡΡΠΎΠ³ΠΎ Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎ Π²ΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠ΅ΠΉ ΠΈΡΡΠΎΡΠΈΠΈ Π±ΠΎΠ»Π΅Π·Π½ΠΈ ΠΈ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΠ΅ ΠΌΡΠ»ΡΡΠΈΡΠΏΠΈΡΠ°Π»ΡΠ½ΠΎΠΉ ΠΊΠΎΠΌΠΏΡΡΡΠ΅ΡΠ½ΠΎΠΉ ΡΠΎΠΌΠΎΠ³ΡΠ°ΡΠΈΠΈ (ΠΠ‘ΠΠ’) ΠΎΡΠ³Π°Π½ΠΎΠ² Π³ΡΡΠ΄Π½ΠΎΠΉ ΠΊΠ»Π΅ΡΠΊΠΈ. ΠΠ΅ΡΠΌΠΎΡΡΡ Π½Π° ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠ½ΠΎΠ΅ ΠΎΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅, Ρ Π±ΠΎΠ»ΡΡΠ΅ΠΉ ΡΠ°ΡΡΠΈ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² ΠΊΠ»Π°ΡΡΠΈΡΠΈΡΠΈΡΡΠ΅ΡΡΡ ΠΈΠ΄ΠΈΠΎΠΏΠ°ΡΠΈΡΠ΅ΡΠΊΠ°Ρ ΠΠ. Π ΡΡΠΊΠΎΠ²ΠΎΠ΄ΡΡΠ²Π΅ ERS Π΄Π»Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΠΏΡΠΈΡΠΈΠ½ ΠΠ ΠΏΡΠ΅Π΄Π»Π°Π³Π°Π΅ΡΡΡ ΠΌΠΈΠ½ΠΈΠΌΠ°Π»ΡΠ½ΡΠΉ Π½Π°Π±ΠΎΡ Π°Π½Π°Π»ΠΈΠ·ΠΎΠ², Π²ΠΊΠ»ΡΡΠ°ΡΡΠΈΠΉ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΠΈΠΌΠΌΡΠ½ΠΎΠ³Π»ΠΎΠ±ΡΠ»ΠΈΠ½ΠΎΠ² ΡΡΠ²ΠΎΡΠΎΡΠΊΠΈ, ΡΠ΅ΡΡΡ Π½Π° Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΉ Π±ΡΠΎΠ½Ρ
ΠΎΠ»Π΅Π³ΠΎΡΠ½ΡΠΉ Π°ΡΠΏΠ΅ΡΠ³ΠΈΠ»Π»Π΅Π· ΠΈ ΠΎΠ±ΡΠΈΠΉ Π°Π½Π°Π»ΠΈΠ· ΠΊΡΠΎΠ²ΠΈ. ΠΡΡΠ³ΠΈΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΡΠ΅ΠΊΠΎΠΌΠ΅Π½Π΄ΡΠ΅ΡΡΡ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΡΡ Π½Π° ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΠΈ Π°Π½Π°ΠΌΠ½Π΅Π·Π° Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ ΠΈ ΡΠ΅Π½ΡΠ³Π΅Π½ΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠ΅ΠΉ, ΡΡΠΎ ΡΠΊΠ°Π·ΡΠ²Π°Π΅Ρ Π½Π° Π²Π°ΠΆΠ½ΠΎΡΡΡ ΡΠ°ΡΠΏΠΎΠ·Π½Π°Π²Π°Π½ΠΈΡ Π²ΡΠ°ΡΠ°ΠΌΠΈ ΡΠ°Π·Π½ΡΡ
ΡΠΏΠ΅ΡΠΈΠ°Π»ΡΠ½ΠΎΡΡΠ΅ΠΉ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ΅Π½ΠΎΡΠΈΠΏΠΎΠ² ΠΠ, ΠΏΡΠΈ ΠΊΠΎΡΠΎΡΡΡ
ΡΡΠ΅Π±ΡΠ΅ΡΡΡ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΠ΅ ΡΠΏΠ΅ΡΠΈΠ°Π»ΡΠ½ΡΡ
ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΉ. Π ΡΡΠ°ΡΡΠ΅ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»Π΅Π½Ρ Π°Π»Π³ΠΎΡΠΈΡΠΌΡ ΠΏΠ΅ΡΠ²ΠΎΠ½Π°ΡΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΎΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΠΈ Π²Π΅Π΄Π΅Π½ΠΈΡ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΠ, Π² ΡΠ°ΡΡΠ½ΠΎΡΡΠΈ ΠΠ‘ΠΠ’-ΡΠ΅ΠΌΠΈΠΎΡΠΈΠΊΠ° ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ, ΠΏΡΠΈ ΠΏΠΎΠΌΠΎΡΠΈ ΠΊΠΎΡΠΎΡΡΡ
ΠΌΠΎΠΆΠ½ΠΎ ΡΡΡΠ°Π½ΠΎΠ²ΠΈΡΡ ΠΊΠΎΠ½ΠΊΡΠ΅ΡΠ½ΡΠ΅ ΠΏΡΠΈΡΠΈΠ½Ρ
Π‘ΠΎΠ²ΡΠ΅ΠΌΠ΅Π½Π½ΡΠ΅ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»Π΅Π½ΠΈΡ ΠΎΠ± ΠΈΠ΄ΠΈΠΎΠΏΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠΌ Π»Π΅Π³ΠΎΡΠ½ΠΎΠΌ ΡΠΈΠ±ΡΠΎΠ·Π΅: Π² ΡΠΎΠΊΡΡΠ΅ β Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΡ
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease with a poor prognosis. In recent years, the development of international diagnostic criteria based on clinical, physiological, radiological, and histopathological appearances, improved diagnosis of IPF. However, currently available clinical data do not accurately predict the course of the disease, which can vary from a slowly progressing to rapidly progressive, and, in 5% of cases, is punctuated by episodes of rapid acute exacerbation. These challenges highlight the need for the development and validation of diagnostic biomarkers specific to IPF and prognostic biomarkers of future disease behavior to guide treatment decisions, including referral for transplant. The recent approval of pirfenidone and nintedanib and the identification of new potential therapeutic targets have created an urgent need for theragnostic markers, i.e. biomarkers able to assess, ideally at an early stage, therapeutic response to a given drug. This will avoid the side effects and increase efficacy of treatment. In addition, the currently available methods are not able to identify the IPF in the early stage to predict the course of disease, and to assess response to antifibrotic therapy. Recent advances in understanding the multiple interrelated pathogenic pathways underlying IPF have identified various molecular phenotypes resulting from complex interactions among genetic, epigenetic, transcriptional, post-transcriptional, metabolic, and environmental factors. The development and validation of diagnostic and prognostic biomarkers are necessary to enable a more precise and earlier diagnosis of IPF and to improve prediction of future disease behavior.ΠΠ΄ΠΈΠΎΠΏΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΠΉ Π»Π΅Π³ΠΎΡΠ½ΡΠΉ ΡΠΈΠ±ΡΠΎΠ· (ΠΠΠ€) β Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΡΡΡΠ΅Π΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅ Π»Π΅Π³ΠΊΠΈΡ
Ρ Π½Π΅Π±Π»Π°Π³ΠΎΠΏΡΠΈΡΡΠ½ΡΠΌ ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΎΠΌ. Π ΠΏΠΎΡΠ»Π΅Π΄Π½ΠΈΠ΅ Π³ΠΎΠ΄Ρ Π±Π»Π°Π³ΠΎΠ΄Π°ΡΡ ΡΠ°Π·ΡΠ°Π±ΠΎΡΠΊΠ΅ ΠΌΠ΅ΠΆΠ΄ΡΠ½Π°ΡΠΎΠ΄Π½ΡΡ
Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΊΡΠΈΡΠ΅ΡΠΈΠ΅Π², ΠΎΡΠ½ΠΎΠ²ΠΎΠΉ ΠΊΠΎΡΠΎΡΡΡ
ΡΠ²ΠΈΠ»ΠΈΡΡ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅, ΡΠΈΠ·ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅, ΡΠ΅Π½ΡΠ³Π΅Π½ΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ, Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ° ΠΠΠ€ ΡΠ»ΡΡΡΠΈΠ»Π°ΡΡ. Π’Π΅ΠΌ Π½Π΅ ΠΌΠ΅Π½Π΅Π΅ ΠΈΠΌΠ΅ΡΡΠΈΠ΅ΡΡ Π² Π½Π°ΡΡΠΎΡΡΠ΅Π΅ Π²ΡΠ΅ΠΌΡ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π΄Π°Π½Π½ΡΠ΅ Π½Π΅ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΡΡ ΡΠΎΡΠ½ΠΎ ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°ΡΡ Π±ΠΎΠ»Π΅Π·Π½Ρ, ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΠΊΠΎΡΠΎΡΠΎΠΉ ΠΌΠΎΠΆΠ΅Ρ ΠΏΡΠΎΡΠ΅ΠΊΠ°ΡΡ Π½Π΅ΠΏΡΠ΅Π΄ΡΠΊΠ°Π·ΡΠ΅ΠΌΠΎ β ΠΊΠ°ΠΊ ΠΌΠ΅Π΄Π»Π΅Π½Π½ΠΎ, ΡΠ°ΠΊ ΠΈ Π±ΡΡΡΡΠΎ. Π 5 % ΡΠ»ΡΡΠ°Π΅Π² ΠΠΠ€ ΠΏΡΠΎΡΠ΅ΠΊΠ°Π΅Ρ Ρ ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ. Π£ΠΊΠ°Π·Π°Π½Π½ΡΠΌΠΈ ΠΏΡΠΎΠ±Π»Π΅ΠΌΠ°ΠΌΠΈ ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½Π° Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎΡΡΡ ΡΠ°Π·ΡΠ°Π±ΠΎΡΠΊΠΈ ΠΈ Π²Π°Π»ΠΈΠ΄Π°ΡΠΈΠΈ Π½Π΅ ΡΠΎΠ»ΡΠΊΠΎ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ², ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ½ΡΡ
Π΄Π»Ρ ΠΠΠ€, Π½ΠΎ ΠΈ ΠΏΡΠΎΠ³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ² ΡΠ΅ΡΠ΅Π½ΠΈΡ Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π΄Π»Ρ ΠΏΡΠΈΠ½ΡΡΠΈΡ ΡΠ°ΠΊΡΠΈΠΊΠΈ Π»Π΅ΡΠ΅Π½ΠΈΡ, Π² Ρ. Ρ. ΡΡΠ°Π½ΡΠΏΠ»Π°Π½ΡΠ°ΡΠΈΠΈ Π»Π΅Π³ΠΊΠΈΡ
. ΠΠΎΡΠ»Π΅ ΡΠ΅Π³ΠΈΡΡΡΠ°ΡΠΈΠΈ ΠΏΡΠΎΡΠΈΠ²ΠΎΡΠΈΠ±ΡΠΎΠ·Π½ΡΡ
ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠΎΠ² (ΠΏΠΈΡΡΠ΅Π½ΠΈΠ΄ΠΎΠ½Π° ΠΈ Π½ΠΈΠ½ΡΠ΅Π΄Π°Π½ΠΈΠ±Π°) ΠΈ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ Π½ΠΎΠ²ΡΡ
ΠΏΠΎΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΡΡ
ΡΠ΅ΡΠ°ΠΏΠ΅Π²ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠΈΡΠ΅Π½Π΅ΠΉ ΠΏΠΎΡΠ²ΠΈΠ»Π°ΡΡ Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎΡΡΡ Π² ΠΏΠΎΠΈΡΠΊΠ΅ ΡΠ΅ΡΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ² β Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ², ΡΠΏΠΎΡΠΎΠ±Π½ΡΡ
ΠΎΡΠ΅Π½ΠΈΡΡ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ° Π² Π½Π°ΡΠ°Π»Π΅ Π»Π΅ΡΠ΅Π½ΠΈΡ, ΡΡΠΎ ΠΏΠΎΠ·Π²ΠΎΠ»ΠΈΡ ΠΈΠ·Π±Π΅ΠΆΠ°ΡΡ Π½Π΅ΠΆΠ΅Π»Π°ΡΠ΅Π»ΡΠ½ΡΡ
ΡΠ²Π»Π΅Π½ΠΈΠΉ ΠΈ ΠΏΠΎΠ²ΡΡΠΈΡΡ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ Π»Π΅ΡΠ΅Π½ΠΈΡ. ΠΡΠΎΠΌΠ΅ ΡΠΎΠ³ΠΎ, Ρ ΠΏΠΎΠΌΠΎΡΡΡ ΠΈΠΌΠ΅ΡΡΠΈΡ
ΡΡ Π² Π½Π°ΡΡΠΎΡΡΠ΅Π΅ Π²ΡΠ΅ΠΌΡ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² Π½Π΅ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΠ΅ΡΡΡ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΡΠΌ Π²ΡΡΠ²ΠΈΡΡ ΠΠΠ€ Π² ΡΠ°Π½Π½Π΅ΠΉ ΡΡΠ°Π΄ΠΈΠΈ, ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°ΡΡ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ Π±ΠΎΠ»Π΅Π·Π½ΠΈ, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΎΡΠ΅Π½ΠΈΡΡ ΠΎΡΠ²Π΅Ρ Π½Π° ΠΏΡΠΎΡΠΈΠ²ΠΎΡΠΈΠ±ΡΠΎΠ·Π½ΡΡ ΡΠ΅ΡΠ°ΠΏΠΈΡ. ΠΠ»Π°Π³ΠΎΠ΄Π°ΡΡ ΠΏΠΎΡΠ»Π΅Π΄Π½ΠΈΠΌ Π΄ΠΎΡΡΠΈΠΆΠ΅Π½ΠΈΡΠΌ Π² ΠΏΠΎΠ½ΠΈΠΌΠ°Π½ΠΈΠΈ Π½Π΅ΡΠΊΠΎΠ»ΡΠΊΠΈΡ
Π²Π·Π°ΠΈΠΌΠΎΡΠ²ΡΠ·Π°Π½Π½ΡΡ
ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΏΡΡΠ΅ΠΉ, Π»Π΅ΠΆΠ°ΡΠΈΡ
Π² ΠΎΡΠ½ΠΎΠ²Π΅ ΠΠΠ€, Π²ΡΡΠ²Π»Π΅Π½Ρ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠ΅ ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΡΠ΅ ΡΠ΅Π½ΠΎΡΠΈΠΏΡ Π² ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ΅ ΡΠ»ΠΎΠΆΠ½ΠΎΠ³ΠΎ Π²Π·Π°ΠΈΠΌΠΎΠ΄Π΅ΠΉΡΡΠ²ΠΈΡ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
, ΡΠΏΠΈΠ³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
, ΡΡΠ°Π½ΡΠΊΡΠΈΠΏΡΠΈΠΎΠ½Π½ΡΡ
, ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ°ΠΊΡΠΎΡΠΎΠ², Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΎΠΊΡΡΠΆΠ°ΡΡΠ΅ΠΉ ΡΡΠ΅Π΄Ρ. ΠΠ»Ρ Π±ΠΎΠ»Π΅Π΅ ΡΠΎΡΠ½ΠΎΠΉ ΠΈ ΡΠ°Π½Π½Π΅ΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ ΠΈ ΡΠ»ΡΡΡΠ΅Π½ΠΈΡ ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠ΅ΡΠ΅Π½ΠΈΡ ΠΠΠ€ Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠ° ΡΠ°Π·ΡΠ°Π±ΠΎΡΠΊΠ° ΠΈ ΠΎΠ±ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΠ΅ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ ΠΏΡΠΎΠ³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ²
Pulmonary vasculitis: diagnosis and treatment
Pulmonary vasculitis is a group of rapidly progressing severe diseases characterized by vascular inflammation, destruction and necrosis of the pulmonary tissue. The pathological process in the lungs varies from diffuse alveolar hemorrhage to inflammation of the parenchyma, pleural effusion, thrombotic and thromboembolic complications. Depending on the size of the affected vessels, vasculites are divided into vasculites of large, medium and small vessels. Most frequently the lung is found in the small vessels vasculitis, including ANCA-associated vasculitis [granulomatosis with polyangiitis (GP), eosinophilic granulomatosis with polyangiitis (EGPA) and microscopic polyangiitis (MPA)] and the disease is glomerular basement membrane (goodpasture syndrome). Clinical examination of other systems and organs involved in the pathological process, including the skin and kidneys, as well as the detection of autoantibodies can improve approaches to early diagnosis and treatment of vasculitis. Treatment of life-threatening pulmonary bleeding and irreversible damage to organs, especially the kidneys, requires rapid diagnosis of these conditions. Vasculitis is a rare disease with lesions of many organs, and methods of their treatment, including biological, are rapidly developing, which requires the cooperation of doctors of various specialties and specialized centers to achieve better control of the disease
ΠΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΊΠΎΠ½Π΄Π΅Π½ΡΠ°ΡΠ° Π²ΡΠ΄ΡΡ Π°Π΅ΠΌΠΎΠ³ΠΎ Π²ΠΎΠ·Π΄ΡΡ Π° Π² ΠΏΡΠ»ΡΠΌΠΎΠ½ΠΎΠ»ΠΎΠ³ΠΈΠΈ
ΠΠ΅Π³ΠΎΡΠ½ΡΠ΅ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΈΠΈ: Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ°, ΠΏΠΎΠ΄Ρ ΠΎΠ΄Ρ ΠΊ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ
Pulmonary eosinophilias, diagnosis and therapy approach.ΠΠ΅Π³ΠΎΡΠ½ΡΠ΅ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΈΠΈ: Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ°, ΠΏΠΎΠ΄Ρ
ΠΎΠ΄Ρ ΠΊ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ
ΠΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΠΉ Π³ΡΠ°Π½ΡΠ»Π΅ΠΌΠ°ΡΠΎΠ· Ρ ΠΏΠΎΠ»ΠΈΠ°Π½Π³ΠΈΠΈΡΠΎΠΌ: Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ ΡΠ΅ΡΠ°ΠΏΠ΅Π²ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠΎΠ±Π»Π΅ΠΌΡ
Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare systemic necrotizing vasculitis of small to medium-sized vessels associated with antineutrophil cytoplasmic antibodies (ANCA). EGPA is usually diagnosed in patients with bronchial asthma (BA) and is characterized by a predominant lesion of the lungs, skin, and peripheral nervous system. ANCAs to myeloperoxidase are detected in 1/3 of patients with EGPA. Presence or absence of ANCAs differentiates 2 disease phenotypes with different clinical characteristics and prognosis. New opportunities for the treatment of EGPA appeared after identification of the key role of eosinophils in EGPA and development of targeted drugs for the treatment of eosinophilic BA that are being studied now.Aim of the review is to highlight modern approaches to the diagnosis and treatment of patients with EGPA, primarily through the use of targeted biological therapy.Conclusion. EGPA is a multisystem disease with ambivalent manifestations associated with eosinophilic or ANCA-mediated small vessel injuries. Currently, there is no βgold standardβ for the diagnosis of EGPA, although the efficacy of pharmacological therapy is directly related to early detection and timely initiation of treatment. Monoclonal antibodies targeting interleukin-5 (IL-5) are an effective alternative to conventional systemic corticosteroids used alone or in combination with immunosuppressants (cyclophosphamide for induction and azathioprine for maintenance therapy) in patients with severe/refractory disease and unfavorable prognosis. The clinical benefits of the targeted anti-IL-5 drug mepolizumab were confirmed in a randomized controlled trial, and this drug was approved for the treatment of patients with EGPA. Currently, new drugs, including targeted ones, are being tested for induction and maintenance therapy. Pulmonologists and rheumatologists should coordinate patient management to improve the results of treatment and the prognosis of the disease.ΠΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΠΉ Π³ΡΠ°Π½ΡΠ»Π΅ΠΌΠ°ΡΠΎΠ· Ρ ΠΏΠΎΠ»ΠΈΠ°Π½Π³ΠΈΠΈΡΠΎΠΌ (ΠΠΠΠ) β ΡΠ΅Π΄ΠΊΠΈΠΉ ΡΠΈΡΡΠ΅ΠΌΠ½ΡΠΉ Π½Π΅ΠΊΡΠΎΡΠΈΠ·ΠΈΡΡΡΡΠΈΠΉ Π²Π°ΡΠΊΡΠ»ΠΈΡ ΡΠΎΡΡΠ΄ΠΎΠ² ΠΌΠ΅Π»ΠΊΠΎΠ³ΠΎ ΠΈ ΡΡΠ΅Π΄Π½Π΅Π³ΠΎ ΡΠ°Π·ΠΌΠ΅ΡΠ°, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΠΉ Ρ Π°Π½ΡΠΈΠ½Π΅ΠΉΡΡΠΎΡΠΈΠ»ΡΠ½ΡΠΌΠΈ ΡΠΈΡΠΎΠΏΠ»Π°Π·ΠΌΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ Π°Π½ΡΠΈΡΠ΅Π»Π°ΠΌΠΈ (ΠΠΠ¦Π). ΠΠΠΠ ΠΎΠ±ΡΡΠ½ΠΎ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΡΠ΅ΡΡΡ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π±ΡΠΎΠ½Ρ
ΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π°ΡΡΠΌΠΎΠΉ (ΠΠ) ΠΈ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΠ·ΡΠ΅ΡΡΡ ΠΏΡΠ΅ΠΈΠΌΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΌ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΠ΅ΠΌ Π»Π΅Π³ΠΊΠΈΡ
, ΠΊΠΎΠΆΠΈ ΠΈ ΠΏΠ΅ΡΠΈΡΠ΅ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ Π½Π΅ΡΠ²Π½ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ. Π£ 1/3 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΠΠΠ Π²ΡΡΠ²Π»ΡΡΡΡΡ ΠΠΠ¦Π ΠΊ ΠΌΠΈΠ΅Π»ΠΎΠΏΠ΅ΡΠΎΠΊΡΠΈΠ΄Π°Π·Π΅, ΠΈ ΠΈΡ
ΠΏΡΠΈΡΡΡΡΡΠ²ΠΈΠ΅ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΡΠ΅Ρ 2 ΡΠ΅Π½ΠΎΡΠΈΠΏΠ° Π±ΠΎΠ»Π΅Π·Π½ΠΈ Ρ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠΌΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠ°ΠΌΠΈ ΠΈ ΠΏΡΠΎΠ³Π½ΠΎΠ·Π°ΠΌΠΈ. ΠΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΊΠ»ΡΡΠ΅Π²ΠΎΠΉ ΡΠΎΠ»ΠΈ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΎΠ² ΠΏΡΠΈ ΠΠΠΠ ΠΈ Π½Π΅Π΄Π°Π²Π½ΠΎ ΡΠ°Π·ΡΠ°Π±ΠΎΡΠ°Π½Π½ΡΠ΅ ΠΈ ΠΏΡΠΎΡ
ΠΎΠ΄ΡΡΠΈΠ΅ Π°ΠΏΡΠΎΠ±Π°ΡΠΈΡ ΡΠ°ΡΠ³Π΅ΡΠ½ΡΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ Π΄Π»Ρ Π»Π΅ΡΠ΅Π½ΠΈΡ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΠΎΠΉ ΠΠ ΡΠΎΠ·Π΄Π°Π»ΠΈ Π½ΠΎΠ²ΡΠ΅ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΠΈ Π΄Π»Ρ Π»Π΅ΡΠ΅Π½ΠΈΡ ΠΠΠΠ.Π¦Π΅Π»ΡΡ ΠΎΠ±Π·ΠΎΡΠ° ΡΠ²ΠΈΠ»ΠΎΡΡ ΠΎΡΠ²Π΅ΡΠ΅Π½ΠΈΠ΅ ΡΠΎΠ²ΡΠ΅ΠΌΠ΅Π½Π½ΡΡ
ΠΏΠΎΠ΄Ρ
ΠΎΠ΄ΠΎΠ² ΠΊ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ΅ ΠΈ Π»Π΅ΡΠ΅Π½ΠΈΡ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΠΠΠ, ΠΏΡΠ΅ΠΆΠ΄Π΅ Π²ΡΠ΅Π³ΠΎ ΠΏΡΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠΈ ΡΠ°ΡΠ³Π΅ΡΠ½ΠΎΠΉ Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΠΠΠ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΠ΅Ρ ΡΠΎΠ±ΠΎΠΉ ΠΌΡΠ»ΡΡΠΈΡΠΈΡΡΠ΅ΠΌΠ½ΠΎΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅ Ρ Π΄Π²ΠΎΡΠΊΠΈΠΌΠΈ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡΠΌΠΈ, ΠΎΡΠ½ΠΎΠ²Π°Π½Π½ΡΠΌΠΈ Π½Π° ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΠΎΠΌ ΠΈΠ»ΠΈ ΠΠΠ¦Π-Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΌ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΡΡ
ΠΌΠ΅Π»ΠΊΠΈΡ
ΡΠΎΡΡΠ΄ΠΎΠ². Π Π½Π°ΡΡΠΎΡΡΠ΅Π΅ Π²ΡΠ΅ΠΌΡ Π½Π΅Ρ Β«Π·ΠΎΠ»ΠΎΡΠΎΠ³ΠΎ ΡΡΠ°Π½Π΄Π°ΡΡΠ°Β» Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ ΠΠΠΠ, Ρ
ΠΎΡΡ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ Π΅Π³ΠΎ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½Π½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π½Π°ΠΏΡΡΠΌΡΡ ΡΠ²ΡΠ·Π°Π½Π° Ρ ΡΠ°Π½Π½ΠΈΠΌ Π²ΡΡΠ²Π»Π΅Π½ΠΈΠ΅ΠΌ ΠΈ ΡΠ²ΠΎΠ΅Π²ΡΠ΅ΠΌΠ΅Π½Π½ΡΠΌ Π½Π°ΡΠ°Π»ΠΎΠΌ Π»Π΅ΡΠ΅Π½ΠΈΡ. ΠΠΎΠ½ΠΎΠΊΠ»ΠΎΠ½Π°Π»ΡΠ½ΡΠ΅ Π°Π½ΡΠΈΡΠ΅Π»Π°, Π½Π°ΡΠ΅Π»Π΅Π½Π½ΡΠ΅ Π½Π° ΠΈΠ½ΡΠ΅ΡΠ»Π΅ΠΉΠΊΠΈΠ½-5 (IL-5), ΡΠ²Π»ΡΡΡΡΡ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΠΉ Π°Π»ΡΡΠ΅ΡΠ½Π°ΡΠΈΠ²ΠΎΠΉ ΡΡΠ°Π΄ΠΈΡΠΈΠΎΠ½Π½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ ΡΠΈΡΡΠ΅ΠΌΠ½ΡΠΌΠΈ ΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠΈΠ΄Π°ΠΌΠΈ, ΠΈΡΠΏΠΎΠ»ΡΠ·ΡΠ΅ΠΌΡΠΌΠΈ Π² ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ ΠΌΠΎΠ½ΠΎΡΠ΅ΡΠ°ΠΏΠΈΠΈ ΠΈΠ»ΠΈ Π² ΡΠΎΡΠ΅ΡΠ°Π½ΠΈΠΈ Ρ ΠΈΠΌΠΌΡΠ½ΠΎΠ΄Π΅ΠΏΡΠ΅ΡΡΠ°Π½ΡΠ°ΠΌΠΈ (ΡΠΈΠΊΠ»ΠΎΡΠΎΡΡΠ°ΠΌΠΈΠ΄ Π΄Π»Ρ ΠΈΠ½Π΄ΡΠΊΡΠΈΠΎΠ½Π½ΠΎΠΉ ΠΈ Π°Π·Π°ΡΠΈΠΎΠΏΡΠΈΠ½ Π΄Π»Ρ ΠΏΠΎΠ΄Π΄Π΅ΡΠΆΠΈΠ²Π°ΡΡΠ΅ΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ) Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΡΠΆΠ΅Π»ΠΎΠΉ / ΡΠ΅ΡΡΠ°ΠΊΡΠ΅ΡΠ½ΠΎΠΉ ΡΠΎΡΠΌΠΎΠΉ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ ΠΈ ΠΏΠ»ΠΎΡ
ΠΈΠΌ ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΎΠΌ. ΠΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠ΅ΠΈΠΌΡΡΠ΅ΡΡΠ²Π° ΡΠ°ΡΠ³Π΅ΡΠ½ΠΎΠ³ΠΎ Π°Π½ΡΠΈ-IL-5 ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ° ΠΌΠ΅ΠΏΠΎΠ»ΠΈΠ·ΡΠΌΠ°Π±Π° Π±ΡΠ»ΠΈ ΠΏΠΎΠ΄ΡΠ²Π΅ΡΠΆΠ΄Π΅Π½Ρ Π² ΡΠ°Π½Π΄ΠΎΠΌΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΌ ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈΡΡΠ΅ΠΌΠΎΠΌ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΈ, ΠΈ ΡΡΠΎΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°Ρ Π±ΡΠ» ΠΎΠ΄ΠΎΠ±ΡΠ΅Π½ Π΄Π»Ρ Π»Π΅ΡΠ΅Π½ΠΈΡ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΠΠΠ. Π Π½Π°ΡΡΠΎΡΡΠ΅Π΅ Π²ΡΠ΅ΠΌΡ ΠΏΡΠΎΡ
ΠΎΠ΄ΡΡ Π°ΠΏΡΠΎΠ±Π°ΡΠΈΡ Π½ΠΎΠ²ΡΠ΅ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½Π½ΡΠ΅, Π² Ρ. Ρ. ΡΠ°ΡΠ³Π΅ΡΠ½ΡΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ Π΄Π»Ρ ΠΈΠ½Π΄ΡΠΊΡΠΈΠΎΠ½Π½ΠΎΠΉ ΠΈ ΠΏΠΎΠ΄Π΄Π΅ΡΠΆΠΈΠ²Π°ΡΡΠ΅ΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ. ΠΠ»Ρ ΡΠ»ΡΡΡΠ΅Π½ΠΈΡ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠ² Π»Π΅ΡΠ΅Π½ΠΈΡ ΠΈ ΠΏΡΠΎΠ³Π½ΠΎΠ·Π° Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎ ΡΠΎΠ³Π»Π°ΡΠΎΠ²Π°Π½Π½ΠΎΠ΅ Π²Π΅Π΄Π΅Π½ΠΈΠ΅ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Π²ΡΠ°ΡΠ°ΠΌΠΈ-ΠΏΡΠ»ΡΠΌΠΎΠ½ΠΎΠ»ΠΎΠ³Π°ΠΌΠΈ ΠΈ ΡΠ΅Π²ΠΌΠ°ΡΠΎΠ»ΠΎΠ³Π°ΠΌΠΈ
ΠΡΡΡΡΠ΅ ΡΠΎΡΠΌΡ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΠΈ ΡΠ΅ΡΠ΄ΡΠ° ΠΏΡΠΈ ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΠΈ Ρ ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΎΠ±ΡΡΡΡΠΊΡΠΈΠ²Π½ΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π»Π΅Π³ΠΊΠΈΡ : ΡΠΏΠΈΠ΄Π΅ΠΌΠΈΠΎΠ»ΠΎΠ³ΠΈΡ, Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ° ΠΈ Π»Π΅ΡΠ΅Π½ΠΈΠ΅
Chronic obstructive pulmonary disease (COPD) is a major public health problem worldwide. COPD is closely related to comorbid cardiovascular diseases, which contribute to the worsening of COPD and increased mortality. The frequency and prevalence of cardiovascular diseases in patients with COPD is about 64%. Approximately 30% of patients with COPD die from cardiovascular complications. Recent evidence suggests an increased risk of acute myocardial infarction in severe exacerbations of COPD. Tachycardia, increased oxidative stress and systemic inflammation in patients with COPD may contribute to an increased risk of developing cardiovascular complications. Several studies may be useful for early diagnosis, including electrocardiography, imaging methods, and biomarker blood tests. Some drugs that have changed the prognosis for cardiovascular disease, in particular, cardioselective beta-blockers, are underused in patients with COPD, despite proven benefits. This review focuses on some aspects of COPD exacerbation and the risk of cardiovascular disease.Π₯ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠ°Ρ ΠΎΠ±ΡΡΡΡΠΊΡΠΈΠ²Π½Π°Ρ Π±ΠΎΠ»Π΅Π·Π½Ρ Π»Π΅Π³ΠΊΠΈΡ
(Π₯ΠΠΠ) ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΎΠ΄Π½ΠΎΠΉ ΠΈΠ· ΠΎΡΠ½ΠΎΠ²Π½ΡΡ
ΠΏΡΠΎΠ±Π»Π΅ΠΌ Π·Π΄ΡΠ°Π²ΠΎΠΎΡ
ΡΠ°Π½Π΅Π½ΠΈΡ Π² ΠΌΠΈΡΠ΅. Π₯ΠΠΠ ΡΠ΅ΡΠ½ΠΎ ΡΠ²ΡΠ·Π°Π½Π° Ρ ΠΊΠΎΠΌΠΎΡΠ±ΠΈΠ΄Π½ΡΠΌΠΈ ΡΠ΅ΡΠ΄Π΅ΡΠ½ΠΎ-ΡΠΎΡΡΠ΄ΠΈΡΡΡΠΌΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡΠΌΠΈ (Π‘Π‘Π), ΡΡΡΠΆΠ΅Π»ΡΡΡΠΈΠΌΠΈ Π₯ΠΠΠ ΠΈ ΠΏΠΎΠ²ΡΡΠ°ΡΡΠΈΠΌΠΈ ΡΠΈΡΠΊ ΡΠΌΠ΅ΡΡΠΈ. Π§Π°ΡΡΠΎΡΠ° ΠΈ ΡΠ°ΡΠΏΡΠΎΡΡΡΠ°Π½Π΅Π½Π½ΠΎΡΡΡ Π‘Π‘Π ΠΏΠΈ Π₯ΠΠΠ ΡΠΎΡΡΠ°Π²Π»ΡΠ΅Ρ ΠΎΠΊΠΎΠ»ΠΎ 64 %. ΠΡΠΈΠΌΠ΅ΡΠ½ΠΎ Ρ 30 % ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π₯ΠΠΠ Π½Π°ΡΡΡΠΏΠ°Π΅Ρ Π»Π΅ΡΠ°Π»ΡΠ½ΡΠΉ ΠΈΡΡ
ΠΎΠ΄ ΠΎΡ ΡΠ΅ΡΠ΄Π΅ΡΠ½ΠΎ-ΡΠΎΡΡΠ΄ΠΈΡΡΡΡ
ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½ΠΈΠΉ (Π‘Π‘Π). ΠΠΎΡΠ»Π΅Π΄Π½ΠΈΠ΅ Π΄Π°Π½Π½ΡΠ΅ ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²ΡΡΡ ΠΎ ΠΏΠΎΠ²ΡΡΠ΅Π½Π½ΠΎΠΌ ΡΠΈΡΠΊΠ΅ ΠΎΡΡΡΠΎΠ³ΠΎ ΠΠ ΠΏΡΠΈ ΡΡΠΆΠ΅Π»ΠΎΠΌ ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΠΈ Π₯ΠΠΠ. Π ΠΈΡΠΊ ΡΠ°Π·Π²ΠΈΡΠΈΡ Π‘Π‘Π ΡΠ²Π΅Π»ΠΈΡΠΈΠ²Π°Π΅ΡΡΡ ΠΏΡΠΈ ΡΠ°Ρ
ΠΈΠΊΠ°ΡΠ΄ΠΈΠΈ, ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠΈ ΠΎΠΊΠΈΡΠ»ΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ ΡΡΡΠ΅ΡΡΠ° ΠΈ ΡΠΈΡΡΠ΅ΠΌΠ½ΠΎΠΌ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΠΈ. ΠΠΎ Π΄Π°Π½Π½ΡΠΌ ΡΡΠ΄Π° ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΉ, Π΄Π»Ρ ΡΠ°Π½Π½Π΅ΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ Π‘Π‘Π ΠΌΠΎΠ³ΡΡ Π±ΡΡΡ ΠΏΠΎΠ»Π΅Π·Π½Ρ Π½Π΅ ΡΠΎΠ»ΡΠΊΠΎ ΠΌΠ΅ΡΠΎΠ΄Ρ Π²ΠΈΠ·ΡΠ°Π»ΠΈΠ·Π°ΡΠΈΠΈ, Π½ΠΎ ΠΈ ΡΠ»Π΅ΠΊΡΡΠΎΠΊΠ°ΡΠ΄ΠΈΠΎΠ³ΡΠ°ΡΠΈΡ, Π° ΡΠ°ΠΊΠΆΠ΅ Π°Π½Π°Π»ΠΈΠ· ΠΊΡΠΎΠ²ΠΈ Π½Π° Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΡ. ΠΠ΅ΡΠΌΠΎΡΡΡ Π½Π° Π΄ΠΎΠΊΠ°Π·Π°Π½Π½ΡΠ΅ ΠΏΡΠ΅ΠΈΠΌΡΡΠ΅ΡΡΠ²Π°, Π½Π΅ΠΊΠΎΡΠΎΡΡΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ, ΠΎΠ±Π»Π°Π΄Π°ΡΡΠΈΠ΅ ΡΠΏΠΎΡΠΎΠ±Π½ΠΎΡΡΡΡ ΠΈΠ·ΠΌΠ΅Π½ΠΈΡΡ ΠΏΡΠΎΠ³Π½ΠΎΠ· ΠΏΡΠΈ ΡΠ΅ΡΠ΄Π΅ΡΠ½ΠΎ-ΡΠΎΡΡΠ΄ΠΈΡΡΠΎΠΉ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΠΈ, Π² ΡΠ°ΡΡΠ½ΠΎΡΡΠΈ ΠΊΠ°ΡΠ΄ΠΈΠΎΡΠ΅Π»Π΅ΠΊΡΠΈΠ²Π½ΡΠ΅ Ξ²-Π°Π΄ΡΠ΅Π½ΠΎΠ±Π»ΠΎΠΊΠ°ΡΠΎΡΡ, Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Π₯ΠΠΠ ΠΈΡΠΏΠΎΠ»ΡΠ·ΡΡΡΡΡ Π½Π΅Π΄ΠΎΡΡΠ°ΡΠΎΡΠ½ΠΎ. ΠΠ°Π½Π½ΡΠΉ ΠΎΠ±Π·ΠΎΡ ΠΏΠΎΡΠ²ΡΡΠ΅Π½ Π½Π΅ΠΊΠΎΡΠΎΡΡΠΌ Π°ΡΠΏΠ΅ΠΊΡΠ°ΠΌ ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΡ Π₯ΠΠΠ ΠΈ ΡΠΈΡΠΊΠ° Π‘Π‘Π
ΠΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΠΉ Π³ΡΠ°Π½ΡΠ»Π΅ΠΌΠ°ΡΠΎΠ· Ρ ΠΏΠΎΠ»ΠΈΠ°Π½Π³ΠΈΠΈΡΠΎΠΌ: ΡΡΠΈΠΎΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·, ΠΊΠ»Π°ΡΡΠΈΡΠΈΠΊΠ°ΡΠΈΡ ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΡΠ΅Π½ΠΎΡΠΈΠΏΡ
Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare systemic disease that can be classified as both a hypereosinophilic condition and an antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis and is characterized by granulomatous inflammation. The pathogenesis of EGPA is not completely understood. It is likely that this disease is Th2-mediated, and blood and tissue eosinophilia serves as the main diagnostic criterion. The hallmarks and main effectors of organ damage in EGPA include asthma-associated necrotizing vasculitis of small-to-medium vessels and eosinophilic proliferation. Endothelial injury and vascular inflammation in EGPA is caused by ANCA via activation of circulating neutrophils. Two clinical phenotypes of the disease have been described based on the detection of ANCA: ANCA-negative with manifestations of hypereosinophilia (for example, pulmonary infiltrates and cardiomyopathy) and ANCA-positive with clinical signs of vasculitis (for example, glomerulonephritis, purpura, and mononeuritis multiplex). Both phenotypes were confirmed by histological and genomic research. However, these two coexisting mechanisms cannot be separated in clinical practice. The aim of the article is to present current knowledge of eosinophilic and ANCA-mediated aspects of the pathogenesis, classification and clinical phenotypes of EGPA, and consider prospects for future research. Conclusion. The development of EGPA is based on eosinophilic dysfunction. This dysfunction means that patients with a genetically determined predisposition to recognize the ANCA antigen and with HLA-DQ (human leukocyte antigen DQ) alleles produce anti-myeloperoxidase autoantibodies and later develop an aberrant autoimmune process. Further comprehensive post-genomic studies are needed to identify the pathogenetic mechanisms and characterize molecular features of EGPA clinical phenotypes. The elaboration of molecular endotypes will lead to the identification of new activity biomarkers and therapeutic targets that can improve the diagnosis of EGPA and the treatment outcomes.ΠΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΠΉ Π³ΡΠ°Π½ΡΠ»Π΅ΠΌΠ°ΡΠΎΠ· Ρ ΠΏΠΎΠ»ΠΈΠ°Π½Π³ΠΈΠΈΡΠΎΠΌ (ΠΠΠΠ) β ΡΠ΅Π΄ΠΊΠΎΠ΅ ΡΠΈΡΡΠ΅ΠΌΠ½ΠΎΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅, ΠΎΡΠ½ΠΎΡΡΡΠ΅Π΅ΡΡ ΠΊΠ°ΠΊ ΠΊ Π³ΠΈΠΏΠ΅ΡΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΠΌ ΡΠΎΡΡΠΎΡΠ½ΠΈΡΠΌ, ΡΠ°ΠΊ ΠΈ ΠΊ Π²Π°ΡΠΊΡΠ»ΠΈΡΠ°ΠΌ, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΠΌ Ρ Π°Π½ΡΠΈΠ½Π΅ΠΉΡΡΠΎΡΠΈΠ»ΡΠ½ΡΠΌΠΈ ΡΠΈΡΠΎΠΏΠ»Π°Π·ΠΌΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ Π°Π½ΡΠΈΡΠ΅Π»Π°ΠΌΠΈ (ΠΠΠ¦Π), ΠΈ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΠ·ΡΡΡΠ΅Π΅ΡΡ Π³ΡΠ°Π½ΡΠ»Π΅ΠΌΠ°ΡΠΎΠ·Π½ΡΠΌ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΠ΅ΠΌ. ΠΠ°ΡΠΎΠ³Π΅Π½Π΅Π· ΠΠΠΠ ΠΏΠΎΠ»Π½ΠΎΡΡΡΡ Π½Π΅ ΡΡΠ΅Π½. ΠΠ΅ΡΠΎΡΡΠ½ΠΎ, ΡΡΠΎ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅ ΡΠ²Π»ΡΠ΅ΡΡΡ Th2-ΠΎΠΏΠΎΡΡΠ΅Π΄ΠΎΠ²Π°Π½Π½ΡΠΌ, Π° ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΈΡ ΠΊΡΠΎΠ²ΠΈ ΠΈ ΡΠΊΠ°Π½Π΅ΠΉ β Π΅Π³ΠΎ Π³Π»Π°Π²Π½ΡΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠΉ ΠΊΡΠΈΡΠ΅ΡΠΈΠΉ. ΠΡΠ»ΠΈΡΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΠΏΡΠΈΠ·Π½Π°ΠΊΠΈ ΠΈ ΠΎΡΠ½ΠΎΠ²Π½ΡΠ΅ ΡΡΡΠ΅ΠΊΡΠΎΡΡ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΡ ΠΎΡΠ³Π°Π½ΠΎΠ² Π² ΡΠ»ΡΡΠ°Π΅ ΠΠΠΠ β ΡΡΠΎ Π½Π΅ΠΊΡΠΎΡΠΈΠ·ΠΈΡΡΡΡΠΈΠΉ Π²Π°ΡΠΊΡΠ»ΠΈΡ ΠΌΠ΅Π»ΠΊΠΈΡ
ΠΈ ΡΡΠ΅Π΄Π½ΠΈΡ
ΡΠΎΡΡΠ΄ΠΎΠ², Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΠΉ Ρ Π±ΡΠΎΠ½Ρ
ΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π°ΡΡΠΌΠΎΠΉ, ΠΈ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½Π°Ρ ΠΏΡΠΎΠ»ΠΈΡΠ΅ΡΠ°ΡΠΈΡ. ΠΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΠ΅ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΡ ΠΈ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΠ΅ ΡΠΎΡΡΠ΄ΠΎΠ² ΠΏΡΠΈ ΠΠΠΠ Π²ΡΠ·Π²Π°Π½ΠΎ ΠΠΠ¦Π β ΠΏΡΡΠ΅ΠΌ Π°ΠΊΡΠΈΠ²Π°ΡΠΈΠΈ ΡΠΈΡΠΊΡΠ»ΠΈΡΡΡΡΠΈΡ
Π½Π΅ΠΉΡΡΠΎΡΠΈΠ»ΠΎΠ². Π ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²ΠΈΠΈ Ρ ΠΎΠ±Π½Π°ΡΡΠΆΠ΅Π½ΠΈΠ΅ΠΌ ΠΠΠ¦Π ΠΎΠΏΠΈΡΠ°Π½Ρ 2 ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ΅Π½ΠΎΡΠΈΠΏΠ° Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ: ΠΠΠ¦Π-Π½Π΅Π³Π°ΡΠΈΠ²Π½ΡΠΉ Ρ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡΠΌΠΈ Π³ΠΈΠΏΠ΅ΡΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΈΠΈ (Π½Π°ΠΏΡΠΈΠΌΠ΅Ρ, Π»Π΅Π³ΠΎΡΠ½ΡΠ΅ ΠΈΠ½ΡΠΈΠ»ΡΡΡΠ°ΡΡ ΠΈ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΡ) ΠΈ ΠΠΠ¦Π-ΠΏΠΎΠ·ΠΈΡΠΈΠ²Π½ΡΠΉ Ρ ΠΊΠ»ΠΈΠ½ΠΈΠΊΠΎΠΉ Π²Π°ΡΠΊΡΠ»ΠΈΡΠ° (Π½Π°ΠΏΡΠΈΠΌΠ΅Ρ, Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡ, ΠΏΡΡΠΏΡΡΠ° ΠΈ ΠΌΠ½ΠΎΠΆΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΉ ΠΌΠΎΠ½ΠΎΠ½Π΅Π²ΡΠΈΡ), β ΠΊΠΎΡΠΎΡΡΠ΅ Π±ΡΠ»ΠΈ ΠΏΠΎΠ΄ΡΠ²Π΅ΡΠΆΠ΄Π΅Π½Ρ Π³ΠΈΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΈ Π³Π΅Π½ΠΎΠΌΠ½ΡΠΌΠΈ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡΠΌΠΈ. ΠΠ΄Π½Π°ΠΊΠΎ Π² ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΏΡΠ°ΠΊΡΠΈΠΊΠ΅ Π½Π΅Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎ ΡΠ°Π·Π΄Π΅Π»ΠΈΡΡ ΡΡΠΈ Π΄Π²Π° ΡΠΎΡΡΡΠ΅ΡΡΠ²ΡΡΡΠΈΡ
ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΠ°. Π¦Π΅Π»Ρ ΡΠ°Π±ΠΎΡΡ β ΠΏΡΠ΅Π΄ΡΡΠ°Π²ΠΈΡΡ ΡΠΎΠ²ΡΠ΅ΠΌΠ΅Π½Π½ΡΠ΅ Π·Π½Π°Π½ΠΈΡ ΠΎΠ± ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΡ
ΠΈ ΠΠΠ¦Π-ΠΎΠΏΠΎΡΡΠ΅Π΄ΠΎΠ²Π°Π½Π½ΡΡ
Π°ΡΠΏΠ΅ΠΊΡΠ°Ρ
ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π°, ΠΊΠ»Π°ΡΡΠΈΡΠΈΠΊΠ°ΡΠΈΠΈ ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ΅Π½ΠΎΡΠΈΠΏΠ°Ρ
ΠΠΠΠ, Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ°ΡΡΠΌΠΎΡΡΠ΅ΡΡ ΠΏΠ΅ΡΡΠΏΠ΅ΠΊΡΠΈΠ²Ρ Π±ΡΠ΄ΡΡΠΈΡ
ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΉ. ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. Π ΠΎΡΠ½ΠΎΠ²Π΅ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΠΠΠ Π»Π΅ΠΆΠΈΡ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½Π°Ρ Π΄ΠΈΡΡΡΠ½ΠΊΡΠΈΡ, ΠΏΡΠΈ ΠΊΠΎΡΠΎΡΠΎΠΉ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈ Π΄Π΅ΡΠ΅ΡΠΌΠΈΠ½ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΠΏΡΠ΅Π΄ΡΠ°ΡΠΏΠΎΠ»ΠΎΠΆΠ΅Π½Π½ΠΎΡΡΡΡ ΠΊ ΡΠ°ΡΠΏΠΎΠ·Π½Π°Π²Π°Π½ΠΈΡ Π°Π½ΡΠΈΠ³Π΅Π½Π° ΠΠΠ¦Π ΠΈ ΠΈΠΌΠ΅ΡΡΠΈΡ
Π°Π»Π»Π΅Π»ΠΈ HLA-DQ (Human Leukocyte Antigen DQ) Π²ΡΡΠ°Π±Π°ΡΡΠ²Π°ΡΡΡΡ Π°ΡΡΠΎΠ°Π½ΡΠΈΡΠ΅Π»Π° ΠΊ ΠΌΠΈΠ΅Π»ΠΎΠΏΠ΅ΡΠΎΠΊΡΠΈΠ΄Π°Π·Π΅, Π° ΠΏΠΎΠ·Π΄Π½Π΅Π΅ ΡΠ°Π·Π²ΠΈΠ²Π°Π΅ΡΡΡ Π°Π±Π΅ΡΡΠ°Π½ΡΠ½ΡΠΉ Π°ΡΡΠΎΠΈΠΌΠΌΡΠ½Π½ΡΠΉ ΠΏΡΠΎΡΠ΅ΡΡ. ΠΠ΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΡ Π΄Π°Π»ΡΠ½Π΅ΠΉΡΠΈΠ΅ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠ½ΡΠ΅ ΠΏΠΎΡΡΠ³Π΅Π½ΠΎΠΌΠ½ΡΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ Π΄Π»Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΠΎΠ² ΠΈ ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎΠΉ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ΅Π½ΠΎΡΠΈΠΏΠΎΠ² ΠΠΠΠ. ΠΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΡΡ
ΡΠ½Π΄ΠΎΡΠΈΠΏΠΎΠ² ΠΏΠΎΠ·Π²ΠΎΠ»ΠΈΡ ΠΈΠ΄Π΅Π½ΡΠΈΡΠΈΡΠΈΡΠΎΠ²Π°ΡΡ Π½ΠΎΠ²ΡΠ΅ Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΡ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ ΠΈ ΡΠ΅ΡΠ°ΠΏΠ΅Π²ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΌΠΈΡΠ΅Π½ΠΈ, ΠΊΠΎΡΠΎΡΡΠ΅ ΠΌΠΎΠ³ΡΡ ΡΠ»ΡΡΡΠΈΡΡ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΡ ΠΠΠΠ ΠΈ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ Π»Π΅ΡΠ΅Π½ΠΈΡ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΡΠΈΠΌ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅ΠΌ