This study in 102 patients with acute PVT prospectively enrolled over a period of 2 years clarifies manifestations, etiology, and outcome of anticoagulation therapy in this disease. Previously reported studies on acute PVT (most of them coming from centers participating to this consortium)8, 10, 11 yielded relatively consistent results which have based the current recommendation for management.2 However, these and subsequent studies7, 9, 16 all suffered from limitations that questioned the validity

of their interpretation, and inspired the design of the present collaborative study. First, the number of patients Talazoparib price given anticoagulation therapy was low (27 in the largest of these former studies).11 Second, the time period for patients’ accrual spanned 7 to 17 years. Third, a formal evaluation of the initial aspect of acute thrombosis and of the extent of the obstructed segments was not Veliparib cell line based on predefined standardized criteria and expert review. Fourth, investigations for causes were neither comprehensive, nor did they always use the most accurate tests (such as the assessment of V617F JAK2 mutation). Finally, a referral bias in tertiary

centers could not be ruled out, whereas the present study was based on patients’ identification through nationwide networks. Our study is a prospective, multicenter European study including 4 times as many patients as any of the previous studies, in a defined period of 2 years. All patients had a clearly visible thrombus in the absence of cavernoma (which usually develops in a few weeks in the absence of recanalization) and most had symptoms of an acute illness. Although extension of the thrombus was not a criterion

for inclusion, enrolled patients suffered from a severe form of the disease. Indeed, the extrahepatic portal vein was completely blocked in approximately 90% of patients who were thus at risk of permanent portal hypertension. Furthermore, two-thirds of the patients had superior mesenteric vein involvement and were thus at of risk intestinal infarction. The present cohort differs from previous reports by a yet unnoticed, high prevalence of ascites and spleen enlargement. This finding is probably related in a large part to a systematic central review of images. Ascitic fluid was frequently detected at early imaging, although clinically detectable ascites was rare. Ascites has been reported Glutamate dehydrogenase to herald intestinal infarction in patients with mesenteric vein thrombosis,17 which was confirmed in the present study with respect to clinically detectable ascites, although not with ascites that could be detected only at imaging. Spleen enlargement was shown here to be related in part to an underlying MPD, and possibly to acute congestion. Liver biopsy was not routinely performed for obvious ethical reasons in candidates for early anticoagulation. However, underlying cirrhosis was ruled out as an explanation for ascites and spleen enlargement.