Transjugular intrahepatic portosystemic shunt (TIPS) implantation is an effective treatment of portal hypertension in patients with decompensated liver cirrhosis. However, some patients develop TIPS thrombosis with recurrence of portal hypertension. The role of platelets in TIPS thrombosis and the necessity of antiplatelet therapy is unclear. Therefore, we aimed to study platelet function in patients with liver cirrhosis prior to and after TIPS implantation. Platelet aggregation was tested in peripheral and portal-vein blood patient samples on the day (D) of TIPS implantation (D0), D4 and D30 following the procedure (platelet count above 100 × 103/µL, aspirin starting on D5) using whole-blood impedance aggregometry (WBIA) and light transmission aggregometry (LTA). In addition, surface platelet activation markers (P-selectin, activated GPIIb/IIIa) and platelet–neutrophil complexes (PNCs) were assessed by flow cytometry. Thrombin receptor activating peptide 6 (TRAP-6), adenosine diphosphate (ADP) and arachidonic acid (AA) were used as agonists. Healthy subjects were included as controls. Agonist-induced platelet aggregation was reduced (WBIA: TRAP-6 p < 0.01, ADP p < 0.01, AA p < 0.001; LTA: TRAP-6 p = 0.13, ADP p = 0.05, AA p < 0.01) in patients (D0, n = 13) compared with healthy subjects (n = 9). While surface activation markers at baseline were negligibly low, the percentage of PNCs was higher in patients than in controls (p < 0.05). ADP-induced P-selectin expression was increased (p < 0.001), whereas TRAP-6-induced GPIIb/IIIa activation was impaired (p < 0.001) in patients versus controls. PNC formation in response to agonists was not different between groups. Results did not differ between peripheral and portal-vein blood of patients (D0, n = 11) and did not change over time (D0, D4, D30) following TIPS implantation (n = 9). In summary, patients with decompensated liver cirrhosis display in vitro platelet aggregation defects in response to various agonists. Defective aggregation persists upon TIPS implantation. Therefore, we conclude that antiplatelet treatment to prevent TIPS thrombosis is questionable.

Background leptin (LEP) and leptin receptor (LEPR) genes have been correlated to the pathophysiology of obesity, diabetes, metabolic syndrome and associated complications. LEP G2548A (rs7799039) is a single nucleotide polymorphism (SNP) in leptin gene, the association between G2548A and increased leptinemia is controversial. Aim to study the correlation between LEP G2548A and leptin resistance and their accompaniment with insulin resistance among obese Egyptians. Patients & Methods: Forty-four obese patients and 44 normal controls were included, and polymerase chain reaction restriction fragment length polymorphism method were used. Serum lipid profile, blood glucose, serum leptin and insulin were also measured. Results Statistically significant positive correlations between insulin resistance and age, diabetes mellitus, hypertension, family history of cardiac disease, hyperlipidemia, family history of obesity, BMI, serum cholesterol, serum triglycerides, serum LDL cholesterol and allele G (for all p-value =0.0001 except cardiac disease p-value =0.006 and allele G p-value=0.001) were found. The percentages of heterozygous AG and homozygous AA genotypes were statistically significantly higher among obese group than among non-obese group (52.3% and 25% vs. 18.2 and 2.3%, respectively) (p=0.001). In contrast, non-obese group showed statistically significant higher percentage of homozygous genotype GG (Wild type) in comparison to obese group (79.5% vs. 25%, respectively) which is statistically significant (p=0.001). Conclusion Current results concluded that leptin gene G2548A polymorphism could be a genetic marker of obesity in Egypt. The correlation between (SNP) in the leptin gene (G2548A) and insulin resistance among obese Egyptians would help in improving knowledge and management of obesity among Egyptian patients.