The mechanisms of the hypercoagulable state in cirrhotics with and without hepatocellular carcinoma are incompetently comprehended. Objective: We aimed to explore the plasma Annexin A5/PS + MP ratio in these patients. Higher levels of Annexin A5 and PhosphatidylSerine bearing microparticles have been observed in cases of inflammation and increased coagulation but there are no studies which explore if there is an association between them and PVT in cirrhotics with and without HCC. So, our goal is to estimate their role in predicting PVT within HCV cirrhotics with and without HCC. 91 HCV cirrhotics with and without HCC and 20 healthy people (controls) were enlisted. Cirrhotics with and without HCC who developed PVT displayed higher levels of PS + MPs and lower Annexin A5/PS + MPs ratio (38.73 ± 1.92) and (0.00238 ± 0.00047) than cirrhotics who didn't develop PVT (22.19 ± 10.58) and (0.00451 ± 0.0023) (P < 0.001). Among the tested factors, lower Annexin A5/PS + MPs ratio show higher performance in predicting PVT in total cirrhotics, AUC, 0.919 followed by PS + MPs level, 0.876, Portal flow velocity, 0.842, Plasma Annexin A5 level, 0.509. In our hypothesis, As phosphatidylserine exposure increase due to increased level of circulating microparticles in cirrhotics with and without HCC, anenxin-A5 may be secreted by platelets and endothelial cells into the circulation as a physiological response to inactivate the elevated levels of PS bearing MPs produced in these patients but the increase in anenxin-A5 level isn't equivalent to the increase in PS bearing MPs levels. The equilibrium between plasma annexin A5 and PS bearing MPs levels is defected.

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Background: Protein S100A14 has recently been implicated in the progress of several types of cancers. This study aimed to investigate the clinical significance of S100A14 in the diagnosis of hepatocellular carcinoma (HCC). Results: S100A14 was significantly elevated in the HCC group. A cut-off value for serum S100A14 between the HCC group and cirrhosis group is > 0.47 with a sensitivity of 100% and specificity of 88.57%. S100A14 level was a significant diagnostic factor for HCC and a good reference for HCC progression. Conclusion: These results suggest that S100A14 is a good diagnostic marker for HCC.

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Background: Nephrotoxicity is considered one of the most serious and dose-limiting factors for restricting clinical use of Cisplatin and anticancer efficacy. Gallic acid is a non-toxic substance that has a wide range of therapeutic roles with high antioxidant activity. So, the present study aims to investigate the concurrent protective action of Gallic acid against inflammatory and oxidative damage caused by Cisplatin in rat kidneys. Material and methods: Thirty-two male albino rats were classified into four groups, eight per each as follows: Group 1 (Normal control group): without treatment. Group 2 (Gallic acid group): healthy rats were given Gallic acid. Group 3 (Cisplatin group): healthy rats were injected with Cisplatin. Group 4 (Gallic acid + Cisplatin) treated group. Kidney functions, Paraoxonase-1, and inflammatory cytokines such as Tumor Necrosis Factor α, respectively were determined. Results: Cisplatin was induced kidney damage with a high significance (P <0.001) regarding kidney function tests and the group of Cisplatin + Gallic acid demonstrated a broad range in the prevention and/or management of kidney damage with a high significance (P <0.001) compared to cisplatin group. Conclusion: Gallic acid has a protective role against kidney dysfunction and renal damage in Cisplatin therapy.