tetano
Editor, Senior Moderator
BMC Infect Dis
. 2022 Mar 22;22(1):277.
doi: 10.1186/s12879-022-07228-2.
Pulmonary embolism after dexamethasone treatment for COVID-19: a case report
Hidenori Takahashi[SUP] 1 [/SUP], Yoshinobu Iwasaki[SUP] 2 [/SUP], Takayasu Watanabe[SUP] 2 [/SUP], Naoki Ichinose[SUP] 3 [/SUP], Toshimi Oda[SUP] 3 [/SUP]
Affiliations
Abstract
Background: Although the RECOVERY trial showed that dexamethasone was efficacious for the treatment of coronavirus disease 2019 (COVID-19), its impact on the risk of pulmonary embolism (PE) and other serious procoagulant events was not assessed.
Case presentation: Here we report the case of a previously healthy 83-year-old woman with COVID-19, without any genetic predisposition to thrombosis. She developed moderate respiratory distress 12 days after symptom onset and a 10-day course of dexamethasone therapy was initiated. Her clinical condition and imaging findings improved initially; however, they deteriorated after the completion of dexamethasone therapy, despite the improvement in her pneumonia and viral clearance. Laboratory tests showed markedly raised serum D-dimer, ferritin, and sIL-2R levels, and contrast-enhanced computed tomography showed deep vein thrombosis (DVT) in the left iliac vein and PE of the right pulmonary artery. The DVT and PE were successfully treated using intravenous heparin administration.
Conclusions: This case illustrates the potential risk of rebound inflammation and procoagulant events following dexamethasone withdrawal. We believe that COVID-19-induced DVT and PE can be affected by dexamethasone therapy. Although dexamethasone reduces procoagulant factors, increases anticoagulant factors, and modulates cytokines, which can suppress/delay thrombus formation during treatment, it confers the risk for rebound cytokine production after treatment completion, triggering cytokine and coagulation cascades that can lead to thromboembolic diseases. In this critical clinical period, the patient's deteriorating condition may be overlooked because of the masking effects of dexamethasone treatment on fever and other clinical conditions and laboratory changes. Clinicians should follow-up coagulation markers carefully and contrast-enhanced computed tomography is useful for detecting coagulation; and, if PE occurs, therapeutic heparin administration is essential because emboli can also generate cytokines.
Keywords: Anticoagulation; COVID-19; Cytokine; Dexamethasone; Pulmonary embolism; SARS-CoV-2.
. 2022 Mar 22;22(1):277.
doi: 10.1186/s12879-022-07228-2.
Pulmonary embolism after dexamethasone treatment for COVID-19: a case report
Hidenori Takahashi[SUP] 1 [/SUP], Yoshinobu Iwasaki[SUP] 2 [/SUP], Takayasu Watanabe[SUP] 2 [/SUP], Naoki Ichinose[SUP] 3 [/SUP], Toshimi Oda[SUP] 3 [/SUP]
Affiliations
- PMID: 35317729
- DOI: 10.1186/s12879-022-07228-2
Abstract
Background: Although the RECOVERY trial showed that dexamethasone was efficacious for the treatment of coronavirus disease 2019 (COVID-19), its impact on the risk of pulmonary embolism (PE) and other serious procoagulant events was not assessed.
Case presentation: Here we report the case of a previously healthy 83-year-old woman with COVID-19, without any genetic predisposition to thrombosis. She developed moderate respiratory distress 12 days after symptom onset and a 10-day course of dexamethasone therapy was initiated. Her clinical condition and imaging findings improved initially; however, they deteriorated after the completion of dexamethasone therapy, despite the improvement in her pneumonia and viral clearance. Laboratory tests showed markedly raised serum D-dimer, ferritin, and sIL-2R levels, and contrast-enhanced computed tomography showed deep vein thrombosis (DVT) in the left iliac vein and PE of the right pulmonary artery. The DVT and PE were successfully treated using intravenous heparin administration.
Conclusions: This case illustrates the potential risk of rebound inflammation and procoagulant events following dexamethasone withdrawal. We believe that COVID-19-induced DVT and PE can be affected by dexamethasone therapy. Although dexamethasone reduces procoagulant factors, increases anticoagulant factors, and modulates cytokines, which can suppress/delay thrombus formation during treatment, it confers the risk for rebound cytokine production after treatment completion, triggering cytokine and coagulation cascades that can lead to thromboembolic diseases. In this critical clinical period, the patient's deteriorating condition may be overlooked because of the masking effects of dexamethasone treatment on fever and other clinical conditions and laboratory changes. Clinicians should follow-up coagulation markers carefully and contrast-enhanced computed tomography is useful for detecting coagulation; and, if PE occurs, therapeutic heparin administration is essential because emboli can also generate cytokines.
Keywords: Anticoagulation; COVID-19; Cytokine; Dexamethasone; Pulmonary embolism; SARS-CoV-2.
