A Systematic Review Of D-Dimer Responses To Gram Positive And Gram Negative Infections With Focus On Oncotherapeutic Consequences

Abstract

Bacterial infection triggers a cascade of inflammatory and coagulative events that culminate in measurable shifts in fibrin formation and fibrinolysis, with D dimer serving as a widely used and clinically accessible indicator of this dynamic process. Evidence from diverse clinical settings reveals that D dimer elevation not only mirrors the severity of infection but also carries prognostic weight across age groups, including neonatal, adult, and oncology populations. A consistent observation across multiple cohorts is that Gram negative organisms tend to elicit higher D dimer responses than Gram positive organisms, a pattern rooted in endotoxin driven stimulation of tissue factor, endothelial perturbation, and amplified systemic inflammation. This mechanistic distinction produces a recognisable laboratory phenotype that aligns with greater hemodynamic instability, higher inflammatory load, and more frequent need for escalated antimicrobial support in Gram negative disease. In oncology patients the interpretive complexity deepens. Cancer biology itself produces a pro thrombotic environment through tumour related procoagulant expression, maladaptive cytokine activity, endothelial injury, and treatment induced vascular stress. As a result oncology patients often present with elevated baseline D dimer levels, and infectious stimuli further magnify these values. This creates a diagnostic and therapeutic dilemma, since rising D dimer may signal infection severity, occult thrombosis, or impending treatment related toxicity. The synthesis of thirteen representative clinical studies demonstrates that D dimer modifications influenced timing of chemotherapy and immunotherapy, decisions about anticoagulation, escalation of infection management, and imaging strategies. While D dimer consistently enhances risk stratification, it cannot function as a solitary determinant of oncologic decisions because assay variability, heterogeneity of clinical presentations, and confounding from malignancy related coagulation changes limit its specificity. This review highlights the need for rigorously designed prospective trials in cancer populations that use standardised sampling methods, stratified analyses by pathogen class, and clearly defined therapeutic algorithms informed by biomarker patterns. Such work is essential to clarify actionable thresholds, improve integration of infection care with oncological planning, and refine the clinical role of D dimer at the intersection of host immunity, microbial virulence, and cancer therapeutics.