ПАТОФІЗІОЛОГІЧНІ МЕХАНІЗМИ СИНДРОМУ СТІЙКОГО ЗАПАЛЕННЯ, ІМУНОСУПРЕСІЇ І КАТАБОЛІЗМУ
(ОГЛЯД ЛІТЕРАТУРИ)
DOI:
https://doi.org/10.11603/1811-2471.2020.v.i2.11300Ключові слова:
хронічний критичний стан, запалення, імуносупресія, катаболізмАнотація
Завдяки прогресу в галузі інтенсивної терапії рівень виживання тяжкохворих пацієнтів різко покращився. На теперішній час багатьох пацієнтів виписують з відділень інтенсивної терапії. Проте у частини таких хворих розвивається хронічний критичний стан, який характеризується постійним слабким запаленням, пригніченням імунітету і м’язовим виснаженням. У 2012 році цей стан був описаний як синдром стійкого запалення, імуносупресії і катаболізму, який може виникати після тяжкої травми і опіків, сепсису, некротичного панкреатиту.
Мета – висвітлення сучасних поглядів на механізми розвитку синдрому стійкого запалення, імуносупресії і катаболізму.
Матеріал і методи. Пошук літературних джерел проводився за базою MEDLINE.
Результати. Розмноження мієлоїдних клітин-супресорів, дисрегуляція у вродженому і адаптивному імунітеті, розвиток саркопенії є основними патофізіологічними механізмами хронічного критичного стану після тяжких запальних процесів.
Висновок. Синдром стійкого запалення, імуносупресії і катаболізму забезпечує пояснення основних патофізіологічних механізмів при хронічному критичному стані. Це є підґрунтям для визначення патогенетично спрямованого лікування, яке повинно бути багатомодальним і фокусуватися на перериванні циклу запалення/імуносупресії.
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