查看文章

KARDIOLOGIA POLSKA 2021; 79 (2) 218 alongside other acute inflammatory plasma markers such as fibrinogen, C‑reactive pro‑tein, and serum ferritin. 1 Therefore, an alterna‑tive hypothesis was proposed, which suggests that the origin of D‑dimers is a direct conse‑quence of the acute lung injury seen in COV‑ID‑19 pneumonia. 5

However, it is important that intra‑alveolar fi‑brin deposition is the hallmark of acute lung in‑jury. The levels of fibrin are controlled by alveo‑lar epithelial cells which produce urokinase and regulate extravascular proteolysis by regulating expression of urokinase‑type plasminogen ac‑tivator, its receptor, and plasminogen activator inhibitor‑1 at post‑transcriptional levels. 5 Uro‑kinase then converts plasminogen to plasmin, which cleaves local fibrin. 5 Based on the above evidence, we suggest that D‑dimer levels are not only related to coagulopathy but also, sim‑ilarly to other acute‑phase proteins such as C‑‑reactive protein, ferritin, and fibrinogen, with the severity of COVID‑19, represent the degree of lung inflammation in SARS‑CoV‑2 infection. 5 In addition, the analysis of the single bio‑chemical parameter must be interpreted very carefully, especially in the context of cardiovas‑cular complications of SARS‑CoV‑2 infection. Only the complex analysis of clinical state as well as imaging and biochemical tests can pro‑vide valuable information about organ and sys‑temic consequences, and indicate particularly vulnerable patient subgroups and be useful in choosing the most beneficial therapy. Moreover, the interpretation of D‑dimers lev‑els is limited due to several factors. There is no single standardized D‑dimer assay …