LPS may be responsible for platelet activation and potentially contributes to thrombotic complications occurring in cirrhosis. (Hepatology 2017;65:571-581).

Platelet count does not predict unprovoked major or minor bleeding in cirrhotic patients.

We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound‐detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross‐sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, −0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and controls, soluble clusters of differentiation (CD)40‐ligand ( P = 0.0238), soluble Nox2‐derived peptide (sNox2‐dp; P < 0.0001), and urinary excretion of isoprostanes ( P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD40L (Spearman’s rank correlation coefficient [ r s ], −0.33; P < 0.001), sNox2‐dp ( r s , −0.57; P < 0.0001), and urinary excretion of isoprostanes ( r s , −0.48; P < 0.0001) levels. The in vivo study showed a progressive decrease in platelet aggregation, sNox2‐dp, and urinary 8‐iso prostaglandin F2α‐III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2‐dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through interference with mechanisms regulating platelet activation.

Cirrhosis has been long considered a risk factor for bleeding due to the coexistence of the so-called 'coagulopathy'. 1,2 More recently, however, compelling evidences have been provided on the occurrence of thrombotic events in the portal and systemic circulation. 3-5 Portal vein thrombosis (PVT) is predominantly observed in patients with moderate to severe liver failure with a variable prevalence ranging from 0.6 to 25%. 6-8 Only few studies have provided a longitudinal assessment of the PVT incidence and its sequelae, including recurrence and survival. 9-14 Due to the variability of PVT incidence and the paucity of data regarding recurrence and survival, 15-20 we prospectively analysed the incidence and the recurrence of PVT in the population of Portal vein thrombosis Relevance On Liver cirrhosis: Italian Venous thrombotic Events Registry (PRO-LIVER), a multi-centre study, 8 which involved 43 enrolling centres in Italy (ClinicalTrials.gov Identifier: NCT01470547). The presence of PVT at baseline was assessed with Doppler ultrasound examination.

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BackgroundThe Canadian Syncope Risk Score (CSRS) has been proposed for syncope risk stratification in the emergency department (ED). The aim of this study is to perform an external multicenter validation of the CSRS and to compare it with clinical judgement.MethodsUsing patients previously included in the SyMoNE database, we enrolled subjects older than 18 years who presented reporting syncope at the ED. For each patient, we estimated the CSRS and recorded the physician judgement on the patients’ risk of adverse events. We performed a 30-day follow-up.ResultsFrom 1 September 2015 to 28 February 2017, we enrolled 345 patients; the median age was 71 years (IQR 51–81), 174 (50%) were men and 29% were hospitalised. Serious adverse events occurred in 43 (12%) of the patients within 30 days. The area under the curve of the CSRS and clinical judgement was 0.75 (95% CI 0.68 to 0.81) and 0.68 (95% CI 0.61 to 0.74), respectively. The risk of adverse events of patients at low risk according to the CSRS and clinical judgement was 6.7% and 2%, with a sensitivity of 70% (95% CI 54% to 83%) and 95% (95% CI 84% to 99%), respectively.ConclusionThis study represents the first validation analysis of CSRS outside Canada. The overall predictive accuracy of the CSRS is similar to the clinical judgement. However, patients at low risk according to clinical judgement had a lower incidence of adverse events as compared with patients at low risk according to the CSRS. Further studies showing that the adoption of the CSRS improve patients’ outcomes is warranted before its widespread implementation.

Peripheral arterial disease (PAD) is a hallmark of generalized atherosclerosis. Depending on the specific diagnostic criteria that are being used, the prevalence of PAD may be as high as 30 % in the population of people 70 or more years old. Unfortunately, although PAD is prevalent and has many important consequences for patients, it is often under-detected and under-treated by primary care physicians. The aim of this review is to provide an overview of the available literature on epidemiology and antiplatelets management of PAD patients. In particular, we focus on the "hidden" side of PAD burden, the asymptomatic patients, who are at high risk of negative cardiovascular outcomes. Identification of such PAD patients is therefore an important clinical goal to reduce mortality and morbidity and reduce the social cost of atherosclerotic disease. Early screening of PAD and an evidence-based antithrombotic approach are also discussed as potential strategies to counteract the negative impact of such condition in general population, as well as, in patients with other cardiovascular diseases.

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