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In disseminated intravascular coagulation (DIC), there is widespread activation of the coagulation cascade, leading to the formation of microclots throughout the vasculature. As these clots are formed and subsequently degraded, fibrin degradation products, including D-Dimer, are released into the circulation.

In DIC, the patient experiences a significant consumption of coagulation factors and platelets due to this hypercoagulable state, which is followed by a bleeding tendency as the body's ability to coagulability is overwhelmed. The production of D-Dimer reflects the breakdown of fibrin, and due to the increased coagulation and fibrinolysis occurring in DIC, elevated levels of D-Dimer are expected as the body attempts to manage the extensive clot formation and its subsequent breakdown.

Therefore, it is anticipated that a patient with DIC would demonstrate increased D-Dimer levels, consistent with the underlying pathophysiology of this complex coagulation disorder.