Factor V Leiden was the most common risk factor, i.e., 14 of 53 (26.4%) in BCS cases followed by protein C, as compared with PVT cases, i.e., 2 of 33 (6.06%) and controls, i.e., 5 of 223 (2.3%).
A clonal mutation in JAK2 tyrosine kinase (JAK2V617F) occurs in a high proportion of patients with MPD and is of use in the characterization of latent MPD in BCS.
Additional imaging findings and patient characteristics, including alpha-fetoprotein serum level, can help determine the probability of a nodule being HCC in patients with BCS.
Associations of coagulation factor V Leiden and prothrombin G20210A mutations with Budd-Chiari syndrome and portal vein thrombosis: a systematic review and meta-analysis.
Based on the high alpha-fetoprotein (AFP) level and the ultrasonography findings, the patient was diagnosed as having hepatocellular carcinoma (HCC) with a RHV, IVC, and RA tumor thrombus and secondary Budd-Chiari syndrome (BCS).
By resolving the sensitivity bias of the JAK2 mutation with the results of BM histology and clonality assay, CMPD was diagnosed in 53% of patients with EHPVO or BCS.
Chronic BCS children were analysed in four subgroups: (i) SI: successful intervention (primary or secondary stent patency) (ii) PO: poor outcome (refractory stent block or requirement of liver transplantation), (iii) NU: naïve unintervened (awaiting RI) and (iv) DBI: died before intervention.
Determination of the JAK2V617F mutation may be useful to recognize patients with Budd-Chiari syndrome with or at risk for the subsequent development of overt myeloproliferative diseases.
Expression of three genes was significantly different in acute versus chronic BCS (increase in matrix metalloproteinase 7 and SCG10, decrease in thrombospondin-1 for chronic BCS).
Expression of three genes was significantly different in acute versus chronic BCS (increase in matrix metalloproteinase 7 and SCG10, decrease in thrombospondin-1 for chronic BCS).
Expression of three genes was significantly different in acute versus chronic BCS (increase in matrix metalloproteinase 7 and SCG10, decrease in thrombospondin-1 for chronic BCS).
Here, a 22 year old female with angiographically proven BCS secondary to JAK2/V617F positive Polycythemia vera on therapeutic warfarin presented with acute liver failure (ALF).
In conclusion, several DEGs including secreted protein acidic and cysteine rich, lipocalin‑2, GFI1B and proteasome‑associated DEGs may be associated with the pathological process of BCS.
In conclusion, several DEGs including secreted protein acidic and cysteine rich, lipocalin‑2, GFI1B and proteasome‑associated DEGs may be associated with the pathological process of BCS.