Delayed Recognition of Glycoprotein IIb/IIIa Antibody-Associated Platelet Dysfunction in Chronic Liver Disease: A Platelet-Mediated Bleeding-Thrombosis Dysregulation.

Recurrent bleeding in chronic liver disease is frequently attributed to structural gastrointestinal pathology, often without detailed interrogation of platelet function. We report a patient with prolonged transfusion-dependent gastrointestinal bleeding in whom repeated endoscopic findings failed to account for the severity and persistence of hemorrhage. The clinical course was characterized by a reproducible pattern in which bleeding episodes led to temporary withdrawal of aspirin with partial hematologic stabilization, whereas recurrent cardiac biomarker elevation prompted reintroduction of antiplatelet therapy, precipitating further bleeding. This pattern was consistent with platelet-mediated impairment of primary hemostasis amplified by pharmacologic platelet inhibition. Platelet-focused evaluation ultimately demonstrated glycoprotein IIb/IIIa antibody reactivity, indicating qualitative platelet dysfunction rather than isolated thrombocytopenia. Recognition of this possible platelet-mediated mechanism reframed the illness as a dynamic hemostatic instability state operating within chronic liver disease. Permanent withdrawal of aspirin resulted in cessation of overt bleeding, elimination of transfusion requirements, and sustained hematologic stabilization over more than three months of follow-up. This case illustrates a reproducible clinicophysiologic pattern, referred to here as a platelet-mediated hemostatic instability cycle, in which competing bleeding and thrombotic priorities perpetuate recurrent clinical instability. The report emphasizes the importance of platelet function assessment, longitudinal pattern recognition, and mechanism-based clinical reasoning in complex multisystem disease.