Abstract
The blood coagulation system (hemostasis) constitutes one of the most reactive and dynamically regulated mechanisms within the human organism; its equilibrium is rapidly altered under the influence of pathological states and pharmacological agents. The activation or inhibition of the hemostatic cascade can precipitate catastrophic events culminating in tissue ischemia, massive thrombosis, or lethal hemorrhage. This study aims to quantitatively evaluate the pathophysiological and iatrogenic shifts in hemocoagulation parameters against the backdrop of diverse somatic pathologies (sepsis, liver failure) and the administration of drugs directly affecting blood coagulation (anticoagulants, antiplatelets). Utilizing a prospective clinico-laboratory design, the coagulogram and fibrinolysis indicators of 215 patients were subjected to in-depth analysis over a 12-month period. The research outcomes demonstrated that under conditions of systemic inflammation and endothelial dysfunction (sepsis, severe infections), serum D-dimer levels experience a pathological surge, escalating 6-8 times above the norm (reaching 1850 ± 320 ng/mL), accompanied by a precipitous decline in fibrinogen (1.4 ± 0.3 g/L) driven by consumption coagulopathy. In the pharmacological intervention cohort, 22.4% of patients receiving warfarin exhibited an International Normalized Ratio (INR) deviation beyond the anticipated therapeutic window (2.0-3.0), soaring above 4.5. This phenomenon is primarily elucidated by the disruption of drug biotransformation consequent to the interaction of the hepatic cytochrome P450 enzyme system with comorbid diseases or non-steroidal anti-inflammatory drugs (NSAIDs). The integral monitoring of coagulogram metrics and platelet aggregation within a unified diagnostic panel (AUC = 0.892) equips clinical practitioners with an objective, highly informative substrate for the early detection of drug toxicity, the prediction of covert bleeding risks, and the strict personalization of pharmacotherapeutic regimens.
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