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Review
. 2023 Nov 20;15(22):5477.
doi: 10.3390/cancers15225477.

The Risk of Venous Thromboembolism in Neuroendocrine Neoplasms

Monika Wójcik-Giertuga  1 , Anna Malczewska-Herman  1 , Beata Kos-Kudła  1
Affiliations
Review

The Risk of Venous Thromboembolism in Neuroendocrine Neoplasms

Monika Wójcik-Giertuga et al. Cancers (Basel). .

Abstract

Neuroendocrine neoplasms (NENs) differ from other malignancies in their ability to produce hormones and biogenic amines, as well as offer a better prognosis in well-differentiated tumors. There are no definite data on the occurrence of thromboembolic events in NENs and no recommendations regarding the use of antithrombotic prophylaxis in this group. Accurate assessment of the thromboembolic risk in NENs represents an important issue, in order to reduce morbidity and mortality due to complications of VTE. The aim of this work was to review the occurrence of thromboembolic events in NENs and the use of antithrombotic prophylaxis in this group. A total of 28 studies identified on PubMed were analyzed. NENs, especially of pancreatic primary, exhibit an increased thrombotic risk. Atypical VTE locations are quite common in NENs. Hormonally active NENs are associated with a significantly increased thromboembolic risk. Further studies in NENs are needed to evaluate the parameters of coagulation and fibrinolysis as predictive biomarkers for VTE complications.

Keywords: cancer-associated thrombosis; neuroendocrine neoplasms; thromboembolic risk; thrombosis; venous thromboembolism.

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Conflict of interest statement

All authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The potential mechanisms of the pathogenesis of thrombosis in NENs. The figure illustrates the role of endothelial and plasma hemostasis in thrombus formation in NENs. NENs can exhibit rich internal vascularity. Pro-angiogenic factors that occur in NENs can support local activation of blood coagulation. Dysfunction of the vascular endothelium can lead to the loss of its anticoagulant features and may cause the reduction of the efficiency of the fibrinolysis process. The activation of coagulation occurs mainly through the activation of the extrinsic pathway, which is especially dependent on tissue factor (TF)—the main initiator of blood coagulation in vivo. Cancer cells also may release TF-positive microparticles (MP-microparticles) into the bloodstream, which may increase the risk of venous thrombosis, but this requires further research in NENs. TF—tissue factor, VEGF—vascular endothelial growth factor.
Figure 2
Figure 2
Groups of neuroendocrine neoplasms that exhibit an increased thromboembolic risk and the types of thromboembolic events in NENs. VTE—venous thromboembolism.
See this image and copyright information in PMC

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