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AIM To investigate serum omentin and vaspin levels in cirrhotic patients; and to assess the relationship of these levels with hemostatic parameters, metabolic abnormalities, cirrhosis severity and etiology.METHODS Fifty-one cirrhotic patients(17 with portal vein thrombosis) were analyzed. Serum omentin and vaspin levels were measured with commercially available direct enzyme-linked immunosorbent assays(ELISAs). To assess platelet activity, the following tests were performed using a MULTIPLATE?PLATELET FUNCTION ANALYZER:(1) an ADP-induced platelet activation test;(2) a cyclooxygenase dependent aggregation test(ASPI test);(3) a von Willebrand factor and glycoprotein Ibdependent aggregation(using ristocetin) test(RISTO test); and(4) a test for thrombin receptor-activating peptide-6 induced activation of the thrombin receptor, which is sensitive to Ⅱb/Ⅲa receptor antagonists. RESULTS Omentin, but not vaspin, serum concentrations were significantly decreased in patients with portal vein thrombosis(PVT)(P = 0.01). Prothrombin levels were significantly increased in patients with PVT(P = 0.01). The thrombin receptor activating peptide(TRAP) test results were significantly lower in the PVT group(P = 0.03). No significant differences in adipokines serum levels were found regarding the etiology or severity of liver cirrhosis assessed according to the Child-Pugh or Model of End-Stage Liver Disease(MELD) scores. There was a significant increase in the TRAP(P = 0.03), ASPI(P = 0.001) and RISTO high-test(P = 0.02) results in patients with lower MELD scores. Serum omentin and vaspin levels were significantly down-regulated in patients without insulin resistance(P = 0.03, P = 0.02, respectively). A positive relationship between omentin and vaspin levels were found both when all of the patients were analyzed(r = 0.41, P = 0.01) and among those with PVT(r = 0.94, P < 0.001).CONCLUSION Serum omentin levels are increased in patients without PVT. Cirrhosis origin and grade do not affect omentin and vaspin levels. The analyzed adipokines do not influence platelet activity.
AIM To investigate serum omentin and vaspin levels in cirrhotic patients; and to assess the relationship of these levels with hemostatic parameters; metabolic abnormalities, cirrhosis severity and etiology. METHODS Fifty-one cirrhotic patients (17 with portal vein thrombosis) were analyzed. Serum omentin The following tests were performed using a MULTIPLATE® PLATELET FUNCTION ANALYZER: (1) an ADP-induced platelet activation test; (2) a cyclooxygenase dependent aggregation test (ASPI test); (3) a von Willebrand factor and glycoprotein Ibdependent aggregation (using ristocetin) test (RISTO test); and (4) a test for thrombin receptor-activating peptide-6 induced activation of the thrombin receptor, which is sensitive to Ⅱb / Ⅲa receptor antagonists. RESULTS Omentin, but not vaspin, serum concentrations were significantly decreased in patients with portal vein Prothrombin levels were significantly increased in patients with PVT (P = 0.01). The thrombin receptor activating peptide (TRAP) test results were significantly lower in the PVT group (P = 0.03). No significant differences in adipokines serum levels were found regarding the etiology or severity of liver cirrhosis assessed according to the Child-Pugh or Model of End-Stage Liver Disease (MELD) scores. There was a significant increase in the TRAP (P = 0.03), ASPI (P = 0.001) and RISTO high-test (P = 0.02) results in patients with lower MELD scores. Serum omentin and vaspin levels were significantly down-regulated in patients without insulin resistance (P = 0.03, P = 0.02, respectively). A positive relationship between omentin and vaspin levels were found both when all of the patients were analyzed (r = 0.41, P = 0.01) and among those with PVT (r = 0.94, p <0.001) .CONCLUSION Serum omentin levels were increased in patients without PVT. Cirrhosis origin and grade do not aff ectomentin and vaspin levels. The analyzed adipokines do not influence platelet activity.