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Ayah Ghazi Al-Qasrawi: Could Modulation of Factor VIII Be Beneficial in DIC?

Ayah Ghazi Al-Qasrawi/LinkedIn

May 3, 2026, 13:10

Ayah Ghazi Al-Qasrawi: Could Modulation of Factor VIII Be Beneficial in DIC?

Ayah Ghazi Al-Qasrawi, Pediatric Resident at Jordanian Royal Medical Services, shared on LinkedIn:

”I’ve been exploring a conceptual question in Disseminated Intravascular Coagulation that may open the door for further discussion and research collaboration

Factor VIII (FVIII) is released from endothelial cells (ECs) without Factor VII (FVII).

In Disseminated Intravascular Coagulation, laboratory findings commonly demonstrate prolongation of thrombin time (TT), reflecting impaired interaction between thrombin and fibrinogen.

This abnormality typically indicates reduced or functionally compromised fibrinogen levels as a result of ongoing consumption.

Multiple coagulation factors are affected during DIC.

Certain factors, such as factor VII, are rapidly depleted, while others may exhibit variable levels depending on the stage and severity of the condition.

Recombinant therapies, including Recombinant Factor VIIa, have been investigated as potential treatment strategies; however, robust evidence from randomized controlled trials remains limited.

In contrast, during inflammatory or stress states—such as infection or trauma – levels of factor VIII often increase rather than decrease.

This reflects its role as an acute-phase reactant, with enhanced production and release from activated endothelial cells alongside other acute-phase proteins.

This paradox has important implications in the context of DIC.

From a theoretical standpoint, it is worth questioning whether a relative reduction or dysfunction of factor VIII contributes to DIC progression.

Accordingly, one could consider therapeutic approaches aimed at restoring factor VIII activity, either through direct replacement or by enhancing endogenous release using agents such as Desmopressin, a synthetic analogue of antidiuretic hormone known to increase circulating factor VIII levels.

From a theoretical perspectiv too, could modulation of factor VIII be beneficial?

For instance, strategies such as enhancing endogenous release using Desmopressin, or targeted replacement, might offer unexplored avenues.

At the same time, therapies like Recombinant Factor VIIa highlight how single-factor interventions are already being considered, though evidence remains limited.

This leads to a critical question: could modulation of factor VIII represent a viable therapeutic target in DIC, or is the syndrome fundamentally driven by systemic consumption of coagulation components, making single-factor correction insufficient?

I would greatly value insights, critiques, or potential collaboration from clinicians, hematology researchers, and critical care specialists interested in coagulation disorders.”

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