The authors considered a number of interesting hypotheses.[10] Among them the most plausible includes the fact that some of the patients may have had a subclinical partial portal vein thrombosis at the study entry, which was undetected because Doppler ultrasonography of the abdomen was not performed at enrollment. Perhaps the sustained platelet increase following treatment with eltrombopag, risk factors such as an imbalance of coagulation,[16] portal hypertension Liproxstatin-1 cell line and reduced blood flow, local inflammation or endothelial injury could have acted in combination to exacerbate subclinical portal vein thrombosis in these patients. Another interesting hypothesis

could be that platelets in cirrhosis are overactivated, as shown by the increased urinary excretion of markers of in vivo platelet activation observed in these patients. It is possible that the relatively rapid increase Navitoclax supplier of the number of overactivated platelets may have acted as a trigger for thrombosis.[17] In conclusion, the study of Afdhal et al.[10] shows that the strategy of using eltrombopag in patients with cirrhosis undergoing elective invasive procedures is effective in increasing the platelet count and thus avoiding platelet transfusion, but carries

the risk of increasing the rate of thrombotic events. On the other hand, the benefit of increasing platelet counts in this population in order to prevent hemorrhagic events has not yet been established. Hence, the benefit of improving hemostasis at the expenses of increasing thrombotic risk should be carefully evaluated in individual patients. Armando Tripodi, Ph.D. “
“Background and Aim:  Studies on normal values of liver stiffness (LS) in subjects at “low risk” for liver disease are scant. The aim of the present study was to assess liver stiffness values in the subjects without overt liver disease with normal alanine aminotransferases (ALT)

and to determine potential factors, which may influence these MCE values with special reference to newly suggested updated upper limits of normal for ALT. Methods:  Liver stiffness measurements were performed in 445 subjects without overt liver disease (mean age, 41.1 ± 13.6; male, 73.5%) and normal liver enzymes. Results:  Mean LS value was 5.10 ± 1.19 kPa. LS values were higher in men than in women (5.18 ± 1.67 vs 4.86 ± 1.24 kPa, respectively, P = 0.008); in subjects with higher body mass index (BMI) category (Normal, overweight and obese subjects; 4.10 ± 0.75, 5.08 ± 0.66, and 6.05 ± 1.28 kPa, respectively; P < 0.001); in subjects with metabolic syndrome than in those without (5.63 ± 1.37 vs 5.01 ± 1.14 kPa, P = 0.001); and in subjects with ALT levels more than updated limits of normal compared to subjects with ALT levels less than updated limits of normal (5.68 ± 1.21 vs 4.77 ± 1.05 kPa, P < 0.001). On multiple linear regression, BMI and ALT was found to be significant predictor of LS.