Fondaparinux: Should It Be Studied in Patients with COVID-19 Disease?

Marongiu, Francesco; Barcellona, Doris

doi:10.1055/s-0040-1719232

Cited by 5 publications

(5 citation statements)

References 25 publications

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“…Fondaparinux (a synthetic heparin pentasaccharide with a sequence identical with that found in anticoagulant heparin) is a well-known antithrombotic agent for the prevention and treatment of VTE and in ischaemic heart disease without significant bleeding risk [ 711 ]. It has also been suggested that Fondaparinux should be used in the treatment of COVID-19 coagulopathies [ 712 ]. As well as its role as an anticoagulant in decreasing mortality with acute COVID-19 [ 713 ] it was recognised early in the piece [ 714 ] that heparin binds to the SARS-CoV-2 spike protein and can thus inhibit its entry into cells [ 715 ].…”

Section: Anticoagulants Platelet Inhibitors and The Triple Treatmentmentioning

confidence: 99%

The potential role of ischaemia–reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications

Kell

2022

Biochemical Journal

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Ischaemia–reperfusion (I–R) injury, initiated via bursts of reactive oxygen species produced during the reoxygenation phase following hypoxia, is well known in a variety of acute circumstances. We argue here that I–R injury also underpins elements of the pathology of a variety of chronic, inflammatory diseases, including rheumatoid arthritis, ME/CFS and, our chief focus and most proximally, Long COVID. Ischaemia may be initiated via fibrin amyloid microclot blockage of capillaries, for instance as exercise is started; reperfusion is a necessary corollary when it finishes. We rehearse the mechanistic evidence for these occurrences here, in terms of their manifestation as oxidative stress, hyperinflammation, mast cell activation, the production of marker metabolites and related activities. Such microclot-based phenomena can explain both the breathlessness/fatigue and the post-exertional malaise that may be observed in these conditions, as well as many other observables. The recognition of these processes implies, mechanistically, that therapeutic benefit is potentially to be had from antioxidants, from anti-inflammatories, from iron chelators, and via suitable, safe fibrinolytics, and/or anti-clotting agents. We review the considerable existing evidence that is consistent with this, and with the biochemical mechanisms involved.

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Section: Anticoagulants Platelet Inhibitors and The Triple Treatmentmentioning

confidence: 99%

The potential role of ischaemia–reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications

Kell

2022

Biochemical Journal

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“…Although it rarely causes thrombocytopenia, some cases have reported HIT associated with fondaparinux [14,15]. Morangiu stated that fondaparinux had a low chance of causing HIT, but we found that two patients developed thrombocytopenia after the administration of fondaparinux [16]. In this study, three patients experienced thrombocytopenia after 6-7 days of treatment with UFH.…”

Section: Discussionmentioning

confidence: 46%

Comparison between unfractionated heparin (UFH) and fondaparinux on platelets and D-dimer level in COVID-19 patients with hypercoagulation

et al. 2022

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Introduction:This study aimed to compare the clinical effects between UFH and fondaparinux in COVID-19 patients with hypercoagulation. Material and methods: This was a prospective cohort study. Samples were taken consecutively from hospitalized COVID-19 patients with hypercoagulation who received UFH or fondaparinux based on the standardized guidelines. A total of 71 patients met the inclusion criteria. Patients were evaluated for platelet and D-dimer values before and after administration of UFH or fondaparinux. Results: Although there was no difference in D-dimer reduction between the two groups (p = 0.44), fondaparinux showed a greater reduction, 26% against 22% for UFH. While on platelets, there was a significant difference (p = 0.04) between fondaparinux and UFH. Fondaparinux showed a reduced thrombocytopenia impact, as seen by an increase in pre-and post-therapy platelets of up to 50%, compared to 16% in UFH. In regard to the incidence of Heparin-Induced Thrombocytopenia (HIT), there was no significant difference between post-UFH therapy and post-fondaparinux therapy (p = 0.361). Conclusion: Fondaparinux did not reduce platelet levels as much as UFH, but there was no difference between the fondaparinux group compared to the UFH group in the effect of decreasing D-dimer levels and the sign of HIT.

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“… 111 Nevertheless, fondaparinux, bivalirudin or argatroban might be a considerable option in patients with heparin induced thrombocytopenia. 112 Two clinical trials are being conducted to investigate the safety and efficacy of these drugs in patients with COVID-19. 113 , 114 The use of direct oral anticoagulants (DOAC) in patients with COVID-19 is a matter of great debate.…”

Section: Antithrombotic Therapy In Covid-19 Positive Patientsmentioning

confidence: 99%

Prothrombotic Milieu, Thrombotic Events and Prophylactic Anticoagulation in Hospitalized COVID-19 Positive Patients: A Review

Cryer

Farhan

Kaufmann

et al. 2022

Clin Appl Thromb Hemost

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The Coronavirus Disease 2019 (COVID-19) pandemic has resulted in significant morbidity and mortality worldwide. Although initial reports concentrated on severe respiratory illness, emerging literature has indicated a substantially elevated risk of thromboembolic events in patients with COVID-19 disease. Pro-inflammatory cytokine release has been linked to endothelial dysfunction and activation of coagulation pathways, as evident by elevated D-dimer levels and deranged coagulation parameters. Both macrovascular and microvascular thromboses have been described in observational cohort and post-mortem studies. Concurrently, preliminary data have suggested the role of therapeutic anticoagulation in preventing major thromboembolic complications in moderately but not critically ill patients. However, pending results from randomized controlled trials, clear guidance is lacking regarding the intensity and duration of anticoagulation in such patients. Herein, we review the existing evidence on incidence and pathophysiology of COVID-19 related thromboembolic complications and guide anticoagulation therapy based on current literature and societal consensus statements.

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Fondaparinux: Should It Be Studied in Patients with COVID-19 Disease?

Cited by 5 publications

References 25 publications

The potential role of ischaemia–reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications

The potential role of ischaemia–reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications

Comparison between unfractionated heparin (UFH) and fondaparinux on platelets and D-dimer level in COVID-19 patients with hypercoagulation

Prothrombotic Milieu, Thrombotic Events and Prophylactic Anticoagulation in Hospitalized COVID-19 Positive Patients: A Review

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