Published online Apr 14, 2017. doi: 10.3748/wjg.v23.i14.2613
Peer-review started: September 12, 2016
First decision: November 21, 2016
Revised: February 24, 2017
Accepted: March 15, 2017
Article in press: March 15, 2017
Published online: April 14, 2017
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.
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 Ib-dependent 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.
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).
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.
Core tip: Accumulating data suggest that obesity and insulin resistance are related to a more rapid progression of chronic liver diseases, the development of cirrhosis and its complications. Some adipokines have been suggested to contribute to the complicated pathophysiology of hepatic injury and repair. Ongoing research has revealed alterations in the levels and expression of various adipokines in cirrhosis. Portal vein thrombosis (PVT) has been considered to be a complication of more advanced liver cirrhosis. The data regarding novel adipokines in liver cirrhosis is scare and ambiguous. The current study evaluated the serum concentrations of omentin and vaspin in patients with liver cirrhosis of different origins and stages with and without PVT. The relationships of these measures with disease severity and etiology, platelet activity, hemostatic parameters and potential complications were also assessed. The study included 51 patients with cirrhosis of different etiologies (alcohol in 30 patients, hepatitis C virus infection in 15, autoimmune hepatitis in 6). Seventeen these patients manifested portal vein thrombosis confirmed by contrast-enhanced computed tomography.