Abstract
BackgroundThe purpose of this study was to investigate plasma levels of thrombin activatable fibrinolysis inhibitor (TAFI) and TAFI’s relationship with coagulation markers (prothrombin fragment 1 + 2) in gastric cancer patients.MethodsThirty-three patients with gastric adenocarcinoma and 29 healthy control subjects were prospectively enrolled in the study. Patients who had a history of secondary malignancy, thrombosis related disease, oral contraceptive use, diabetes mellitus, chronic renal failure or similar chronic metabolic disease were excluded from the study. A fasting blood sample was drawn from patients to determine the plasma levels of TAFI and Prothrombin Fragment 1 + 2 (F 1 + 2). In addition, data on patient age, sex, body mass index (BMI) and stage of disease were recorded. The same parameters, except stage of disease, were also recorded for the control group. Subsequently, we assessed the difference in the levels of TAFI and F 1 + 2 between the patient and control groups. Moreover, we investigated the relation of TAFI and F 1 + 2 levels with age, sex, BMI and stage of disease in the gastric cancer group.ResultsThere were no statistical differences in any demographic variables (age, gender and BMI) between the groups (Table 1). The mean plasma TAFI levels of the gastric cancer group (69.4 ± 33.1) and control group (73.3 ± 27.5) were statistically similar (P = 0.62). The mean plasma F 1 + 2 level in the gastric cancer group was significantly higher than for those in the control group (549.7 ± 325.3 vs 151.9 ± 67.1, respectively; P < 0.001). In the gastric cancer group, none of the demographic variables (age, gender and BMI) were correlated with either TAFI or F 1 + 2 levels. Also, no significant associations were found between the stage of the cancer and either TAFI or F 1 + 2 levels.ConclusionIn our study, TAFI levels of gastric cancer patients were similar to healthy subjects. The results of our study suggest that TAFI does not play a role in pathogenesis of the hypercoagulable state in gastric cancer patients.
Highlights
The purpose of this study was to investigate plasma levels of thrombin activatable fibrinolysis inhibitor (TAFI) and TAFI’s relationship with coagulation markers in gastric cancer patients
No significant associations were found between the stage of the cancer and either TAFI or F 1 + 2 levels (Table 3)
Reduction of TAFI levels was reported in disseminated intravascular coagulation (DIC) as well as in sepsis, in which a significant depletion of TAFI was observed in the presence of pathogens in plasma [16]. These results suggest that the consumption of TAFI is an important contributing factor in the pathogenesis of DIC and sepsis
Summary
The purpose of this study was to investigate plasma levels of thrombin activatable fibrinolysis inhibitor (TAFI) and TAFI’s relationship with coagulation markers (prothrombin fragment 1 + 2) in gastric cancer patients. Venous thromboembolism (VTE), which includes both deep vein thrombosis (DVT) and pulmonary embolism (PE), is the second leading cause of death in hospitalized and ambulatory cancer patients [1,2,3,4]. The probability of thrombosis occurring in a cancer patient is dependent on several factors, including the type of cancer, the clinical stage, accompanying medical problems, performance status and the treatment modalities employed. Effective fibrinolysis results from the formation of a ternary complex among tPA, plasminogen and C-terminal lysine residues on fibrin. Plasmin degradation of fibrin generates additional C-terminal lysine residues thereby amplifying the system locally. Increased plasma levels of TAFI were reported to be a contributing factor of thrombotic disorders in some kinds of cancers, such as breast and lung cancers
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