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Collagen proportionate area (CPA, %) is used to quantify liver fibrosis. Here, we assessed CPA performance to sub‐classify cirrhosis. CPA was measured in explanted livers from consecutively transplanted patients for hepatitis C virus‐related cirrhosis. Model for end‐stage liver disease (MELD), Child‐Pugh score and decompensating events (ascites, variceal bleeding, non‐obstructive jaundice and encephalopathy) were recorded at the time of liver transplant. Of the 154 patients, 24%, 12%, 35%, 24% and 5% had zero, one, two, three and four previous decompensating events. Patients with decompensation had significantly higher CPA than those without (25.1 ± 8.4 vs 15.8 ± 5.5, P <.001). Decompensation was independently associated with CPA, bilirubin and albumin or with CPA and MELD score. CPA did not differ between patients with one, two, three or four decompensating events (22.2 ± 6.3 vs 26.6 ± 8.9 vs 24.5 ± 7.7 vs 24.4 ± 10.9, P =.242). Overall, CPA correlates with the clinical severity of cirrhosis until the advent of decompensation but not with subsequent decompensating events. [ABSTRACT FROM AUTHOR]

Background & Aims: Mortality of patients who develop acute-on-chronic liver failure (ACLF) is unacceptably high but the predominant mode of cell death is unknown. The aim of this study was to evaluate whether plasma levels of caspase-cleaved cytokeratin M30 (marker of apoptosis) and uncleaved cytokeratin M65 (marker of total cell death) are altered in ACLF patients and relate this to liver histology. Methods: Twenty-seven patients with acute decompensation of liver disease were divided into two groups: no-ACLF (n = 11) or ACLF (n - 16). Healthy controls (n = 8) and acute liver failure (ALF) patients (n = 10) were also enrolled. Cell death was assessed in plasma using an ELISA kit (M30 and M65). Simultaneous biopsy samples were analysed for M30 and caspase-3 staining. Results: Plasma M30 value was significantly elevated in ACLF patients compared with healthy volunteers (P = 0.0001), it was also significantly higher in ACLF patients compared with no-ACLF patients (P = 0.002). M65 levels were higher in ALF compared with ACLF patients (P = 0.002) but the apoptotic index defined by M30/M65 ratio was significantly higher in ACLF patients. Patients with extra-hepatic failure had higher M30 levels compared with patients without organ failure (P = 0.03). M30 staining in liver was more marked in the patients with ACLF and was observed in all the patients that died. Conclusions: The results of this study suggest that hepatocyte apoptosis is the predominant mode of cell death in ACLF, which can be identified in the peripheral blood. Further studies are required to validate our findings and to determine whether M30 can be used as a biomarker of apoptosis or as a target for therapy. [ABSTRACT FROM AUTHOR]

Prothrombotic haematological disorders, in particular myeloproliferative disorders, are identified in a significant proportion of patients with Budd-Chiari syndrome and portal vein thrombosis (PVT). Multiple prothrombotic disorders may coexist. PVT is diagnosed in one fourth of patients with cirrhosis and is more common with advanced liver disease and hepatocellular carcinoma. PVT in cirrhosis can precipitate decompensation. Intrahepatic microthrombosis may play a role in the pathogenesis of hepatic fibrosis. Sinusoidal obstruction syndrome is usually a complication of myeloablative treatment before haematopoietic stem cell transplantation. Post-transplant lymphoproliferative disorders can complicate liver transplantation and are related to Epstein-Barr virus infection. Hepatitis B reactivation in patients receiving chemotherapy for haematological malignancies is very common without pre-emptive treatment, and can lead to liver failure. Liver involvement is common in primary haematological diseases, such as haemolytic anaemias, lymphomas and leukaemia. [ABSTRACT FROM AUTHOR]

Background In patients with chronic hepatitis C virus ( HCV) infection, the presence of peripheral blood cytopaenia may represent an obstacle to pegylated interferon and ribavirin treatment. Aims To evaluate the prevalence of anaemia, neutropaenia and thrombocytopaenia potentially limiting initiation of pegylated interferon and ribavirin treatment in patients with chronic HCV infection who were otherwise eligible for antiviral therapy. Methods We studied 3059 consecutive anti- HCV and HCV- RNA positive patients referred to our centre to be evaluated for antiviral therapy from June 2002 to May 2011. The European Association for the Study of Liver HCV guidelines were applied to assess eligibility for antiviral therapy. Results In the study cohort, 1,521 patients (49.7%) were not eligible for treatment because of reasons different from haematological abnormalities. In the remaining 1,538 patients the overall prevalence of any peripheral blood cytopaenia potentially preventing patients from being treated with antiviral therapy was 15.1%. In particular, anaemia (haemoglobin level < 12 g/dL for women, <13 g/dL for men) was a relative contraindication to treatment in 8.9% (137/1,538) of the patients, while thrombocytopaenia (platelet count cut-off, 90 × 109/L) and neutropaenia (absolute neutrophil count < 1.5 × 109/L) limited treatment in 6.5% (100/1358) and 3.2% (48/1358) of patients respectively. These haematological abnormalities were more prevalent in patients with older age ( P < 0.004) and cirrhosis ( P < 0.001). Conclusions The presence of peripheral blood cytopaenia may potentially limit initiation of antiviral therapy in one in every seven patients with chronic HCV infection who are otherwise eligible for treatment. [ABSTRACT FROM AUTHOR]