antibioticsАнтибиотики и ХимиотерапияAntibiot Khimioter = Antibiotics and Chemotherapy0235-2990ООО «Издательство ОКИ»antibiotics-44Research ArticleОБЗОРЫREVIEWSЯтрогенные события при антибактериальной терапии (поражение лёгких)Iatrogenic Events During Antibiotic Therapy (Pulmonary Disease)ДворецкийЛ. И.DvoretskyL. I.noemail@neicon.ruСувороваМ. П.SuvorovaM. P.noemail@neicon.ruЯковлевС. В.YakovlevS. V.noemail@neicon.ruПервый московский государственный медицинский университет им. И.М. СеченоваРоссияI.M. Sechenov First Moscow State Medical UniversityRussian Federation201706052020627-88088Copyright © Дворецкий Л.И., Суворова М.П., Яковлев С.В., 20202020Дворецкий Л.И., Суворова М.П., Яковлев С.В.Dvoretsky L.I., Suvorova M.P., Yakovlev S.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.antibiotics-chemotherapy.ru/jour/article/view/44

Антибактериальные препараты (АБП) занимают лидирующие позиции среди лекарств, вызывающих нежелательные лекарственные реакции (НЛР), в том числе в нашей стране. Особое место среди НЛР при антибактериальной терапии занимает поражение лёгких, индуцированное антибиотиками (ПЛИА), которое наименее изучено. Имеются закономерные сложности в диагностике таких осложнений антибактериальной терапии, особенно у больных с хронической бронхолёгочной патологией и получающих АБП в связи с инфекцией дыхательных путей. АБП занимают третье место (4,4%) после противоопухолевых (53%) и антиревматических (15%) лекарственных препаратов в ряду других групп лекарств, применение которых сопровождается осложнениями со стороны лёгких. Клинические варианты ПЛИА разнообразны. АБП, при которых отмечено развитие ПЛИА, представлены (в порядке уменьшения риска) нитрофуранами, даптомицином, тетрациклинами (миноциклин), цефалоспоринами (цефтаролин, цефтриаксон, цефотаксим, цефепим), фторхинолонами (ципрофлоксацин, левофлоксацин). Крайне разнообразны формы ПЛИА при применении нитрофуранов (в основном нитрофурантоина) - от острой эозинофильной пневмонии (ЭП) до хронического интерстициального пневмонита и фиброза («нитрофурановое лёгкое»). ПЛИА на фоне применения липопетидного АБП даптомицина хорошо изучены и клинически представлены ЭП с благоприятным исходом после отмены препарата и назначения глюкокортикоидов; риск развития ПЛИА прямо зависит от суммарной дозы даптомицина. Многочисленные клинически варианты ПЛИА отмечены при применении тетрациклинов (преимущественно миноциклина, в меньшей степени доксициклина): ЭП, облитерирующий бронхиолит с организующейся пневмонией, плеврит, перикардит. При применении некоторых цефалоспориновых антибиотиков (цефотаксим, цефтриаксон, цефепим, цефтаролин) отмечено развитие ЭП, а также гиперчувствительного пневмонита; развитие последнего связано с генетической предрасположенностью, так как встречается преимущественно у жителей Японии. Крайне редкие случаи ПЛИА на фоне фторхинолонов (ципрофлоксацин, левофлоксацин) представлены гиперчувствительным пневмонитом. Согласно классификации НЛР, большинство ПЛИА относится к реакциям типа В (непредсказуемые, дозонезависимые, не связанные с фармакологическим действием); в то же время поражение лёгких на фоне даптомицина можно отнести к реакциям типа С (связь с кумуляцией и дозой препарата, но не связанные с фармакологическим действием). Следующие клинические данные позволяют заподозрить ПЛИА у пациента, получающего АБП: лечение АБП, для которых возможно развитие поражения лёгких; появление лёгочной симптоматики у пациента, получающего АБП в связи с инфекцией другой локализации, или усугубление лёгочной симптоматики, несмотря на проведение адекватной антибактериальной терапии; двусторонний и интерстициальный характер лёгочных поражений и наличие системных проявлений; эозинофилия крови и БАЛ. Для диагностики ПЛИА рекомендовано проведение компьютерной томографии высокого разрешения, исследование эозинофилов в крови в динамике, цитология БАЛ, в особо сложных ситуациях - прицельная тонкоигольная биопсия лёгкого.

Antibiotics occupy a leading position among drugs that cause adverse drug reaction (ADR), in Russia as well. Drug-induced pulmonary disease (DIPD), which is the least studied, takes a special place among ADR in antibiotic therapy. There are difficulties in diagnosing such complications of antibiotic therapy, especially in patients with chronic bronchopulmonary pathology and receiving antibiotics due to an infection of the respiratory tract. Antibiotics occupy the third place (4.4%), after antitumor (53%) and antirheumatic (15%) drugs, among other groups of drugs that cause lung damage. Clinical options for DIPD are diverse. Antibiotics, which cause DIPD, are represented (in order of descending risk) by nitrofurans, daptomycin, tetracyclines (minocycline), cephalosporins (ceftaroline, ceftriaxone, cefotaxime, cefepime), fluoroquinolones (ciprofloxacin, levofloxacin). The forms of DIPD are extremely diverse when using nitrofurans (mainly nitrofurantoin) - from acute eosinophilic pneumonia (EP) to chronic interstitial pneumonitis and fibrosis («nitrofuran lung»). DIPD during treatment with lipotetic antibiotic daptomycin are well studied and are clinically presented by EP with a favorable outcome after discontinuation of the drug and the appointment of glucocorticoids; the risk of DIPD development directly depends on the total dose of daptomycin. Numerous clinical variants of DIPD have been observed with the use of tetracyclines (mainly minocycline, to a lesser extent doxycycline): EP, obliterating bronchiolitis with organizing pneumonia, pleurisy, pericarditis. With the use of certain cephalosporin antibiotics (cefotaxime, ceftriaxone, cefepime, ceftarolin), development of EP and hypersensitive pneumonitis has been noted; the development of the latter is associated with a genetic predisposition, since it is found predominantly among the inhabitants of Japan. Extremely rare cases of DIPD due to fluoroquinolones (ciprofloxacin, levofloxacin) are represented by hypersensitive pneumonitis. According to the classification of ADR, most DIPD belong to type B reactions (unpredictable, dose-independent, unrelated to pharmacological action); at the same time, lung damage due to daptomycin can be attributed to type C reactions (association with cumulation and dose of the drug, but not related to pharmacological action). The following clinical data allow to suspect DIPD in a patient receiving antibiotics: antimicrobial treatment, for which the development of lung damage is possible; the appearance of pulmonary symptoms in a patient receiving antibiotics due to infection of other localization, or exacerbation of pulmonary symptoms, despite the conduct of adequate antibiotic therapy; bilateral and interstitial nature of pulmonary lesions and the presence of systemic manifestations; eosinophilia of blood and BAL fluid. For the diagnosis of DIPD, a high-resolution CT scan, a dynamic study of eosinophils in the blood, a cytology of BAL fluid, and, in particularly difficult situations, a targeted fine needle biopsy of the lung are recommended.

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The authors declare that there are no conflicts of interest present.