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Published on: June 12, 2021
[CRP apheresis in acute myocardial infarction and COVID-19]
Michael Buerke1, Ahmed Sheriff2, Christoph D Garlichs3
1Kardiologie, Angiologie, Internistische Intensivmedizin, St. Marienkrankenhaus Siegen, Siegen, Deutschland.
Insights
C-reactive protein (CRP) is a key inflammation biomarker. While beneficial for external wounds, CRP can harm internal tissues during events like heart attacks or COVID-19, but CRP apheresis offers a new treatment to remove it.
Area of Science:
- Biochemistry
- Immunology
- Clinical Medicine
Background:
- C-reactive protein (CRP) is a vital acute phase protein and biomarker for inflammation and infection.
- CRP initiates phagocytosis by labeling damaged cells, activating complement pathways for pathogen elimination.
- However, CRP can paradoxically cause tissue damage in internal conditions like myocardial infarction, stroke, and COVID-19 by labeling regenerable ischemic tissue.
Purpose of the Study:
- To investigate the detrimental role of C-reactive protein (CRP) in internal tissue damage.
- To explore the potential of CRP apheresis as a therapeutic strategy for conditions with high CRP levels.
Main Methods:
- Review of CRP's biological functions and its role in various clinical conditions.
- Introduction of selective immunoadsorption (CRP apheresis) as a method to remove CRP from blood plasma.
Main Results:
- CRP's dual role: protective in external wounds but damaging in internal ischemic conditions.
- Demonstration that CRP labeling contributes to tissue damage in myocardial infarction, stroke, and COVID-19.
- Successful implementation of CRP apheresis for rapid and efficient reduction of pathological CRP levels.
Conclusions:
- CRP plays a complex role in disease, contributing to tissue damage in internal injuries.
- CRP apheresis represents a novel and effective pharmacotherapeutic approach to mitigate CRP-induced damage.
- This method offers a clinical solution for rapidly lowering excessive CRP loads.
Abstract:
C‑reactive protein (CRP) is the best-known acute phase protein. In humans, inflammation and infection are usually accompanied by an increase in CRP levels in the blood, which is why CRP is an important biomarker in daily clinical routine. CRP can mediate the initiation of phagocytosis by labeling damaged cells. This labeling leads to activation of the classical complement pathway (up to C4) and ends in the elimination of pathogens or reversibly damaged or dead cells. This seems to make sense in case of an external wound of the body. However, in the case of "internal wounds" (e.g., myocardial infarction, stroke), CRP induces tissue damage to potentially regenerable tissue by cell labeling, which has corresponding deleterious effects on cardiac and brain tissue or function. The described labeling of ischemic but potentially regenerable cells by CRP apparently also occurs in coronavirus disease 2019 (COVID-19). Parts of the lung become ischemic due to intra-alveolar edema and hemorrhage, and this is accompanied by a dramatic increase in CRP. Use of selective immunoadsorption of CRP from blood plasma ("CRP apheresis") to rapidly and efficiently lower the fulminant CRP load in the body fills this pharmacotherapeutic gap. With CRP apheresis, it is possible for the first time to remove this pathological molecule quickly and efficiently in clinical practice.
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