The imaging manifestations of hepatic lymphoma, both in its primary and secondary form, are extremely variable and overlap with a number of other more common hepatic diseases. However, in the appropriate clinical context, combining the imaging and laboratory features can aid in making the correct diagnosis. Since the management and prognosis of lymphomas are significantly different from other malignancies, early diagnosis and prompt commencement of therapy is of paramount importance. The various morphological appearances of hepatic lymphoma on imaging have been described here along with their possible differentials. Teaching points • Primary hepatic lymphoma is extremely rare. • Secondary liver involvement occurs in 50 % of patients with non-Hodgkin lymphoma. • The imaging manifestations of hepatic lymphoma are largely non-specific. • Some imaging features may be helpful in the appropriate clinical setting. • Management and prognosis of lymphoma is significantly different from other malignancies.

Since the Asian Pacific Association for the Study of the Liver (APASL) published guidelines on non-cirrhotic portal fibrosis/idiopathic portal hypertension in 2007, there has been a surge in new information, especially with the introduction of the term porto-sinusoidal vascular disorder (PSVD). Non-cirrhotic intra-hepatic causes of portal hypertension include disorders with a clearly identifiable etiology, such as schistosomiasis, as well as disorders with an unclear etiology such as non-cirrhotic portal fibrosis (NCPF), also termed idiopathic portal hypertension (IPH). This entity is being increasingly recognized as being associated with systemic disease and drug therapy, especially cancer therapy. An international working group with extensive expertise in portal hypertension was assigned with formulating consensus guidelines to clarify the definition, diagnosis, histological features, natural history, and management of NCPF/IPH, especially in the context of PSVD. The guidelines were prepared based on evidence from existing published literature. Whenever there was paucity of evidence, expert opinion was included after detailed deliberation. The goal of this manuscript, therefore, is to enhance the current understanding and help create global consensus on the issues surrounding NCPF/IPH.

Given the important role of angiogenesis in liver pathology, the current study investigated the role of Runt-related transcription factor 1 (RUNX1), a regulator of developmental angiogenesis, in the pathogenesis of non-alcoholic steatohepatitis (NASH). Quantitative RT-PCRs and a transcription factor analysis of angiogenesis-associated differentially expressed genes in liver tissues of healthy controls, patients with steatosis and NASH, indicated a potential role of RUNX1 in NASH. The gene expression of RUNX1 was correlated with histopathological attributes of patients. The protein expression of RUNX1 in liver was studied by immunohistochemistry. To explore the underlying mechanisms, in vitro studies using RUNX1 siRNA and overexpression plasmids were performed in endothelial cells (ECs). RUNX1 expression was significantly correlated with inflammation, fibrosis and NASH activity score in NASH patients. Its expression was conspicuous in liver non-parenchymal cells. In vitro, factors from steatotic hepatocytes and/or VEGF or TGF-β significantly induced the expression of RUNX1 in ECs. RUNX1 regulated the expression of angiogenic and adhesion molecules in ECs, including CCL2, PECAM1 and VCAM1, which was shown by silencing or over-expression of RUNX1. Furthermore, RUNX1 increased the angiogenic activity of ECs. This study reports that steatosis-induced RUNX1 augmented the expression of adhesion and angiogenic molecules and properties in ECs and may be involved in enhancing inflammation and disease severity in NASH.

Parvovirus B19 infection can present with myriads of clinical diseases and syndromes; liver manifestations and hepatitis are examples of them. Parvovirus B19 hepatitis associated aplastic anemia and its coinfection with other hepatotropic viruses are relatively underrecognized, and there is sufficient evidence in the literature suggesting that B19 infections can cause a spectrum of liver diseases from elevation of transaminases to acute hepatitis to fulminant liver failure and even chronic hepatitis. It can also cause fatal macrophage activation syndrome and fibrosing cholestatic hepatitis. Parvovirus B19 is an erythrovirus that can only be replicate in pronormoblasts and hepatocytes, and other cells which have globosides and glycosphingolipids in their membrane can also be affected by direct virus injury due to nonstructural protein 1 persistence and indirectly by immune mediated injury. The virus infection is suspected in bone marrow aspiration in cases with sudden drop of hemoglobin and onset of transient aplastic anemia in immunosuppressed or immunocompetent patients and is confirmed either by IgM and IgG positive serology, PCR analysis, and in situ hybridization in biopsy specimens or by application of both. There is no specific treatment for parvovirus B19 related liver diseases, but triple therapy regimen may be effective consisting of immunoglobulin, dehydrohydrocortisone, and cyclosporine.

Introduction. Liver disease patients have complex hemostatic defects leading to a delicate, unstable balance between bleeding and thrombosis. Conventional tests such as PT and APTT are unable to depict these defects completely. Aims. This study aimed at analyzing the abnormal effects of liver disease on sonoclot signature by using sonoclot analyzer (which depicts the entire hemostatic pathway) and assessing the correlations between sonoclot variables and conventional coagulation tests. Material and Methods. Clinical and laboratory data from fifty inpatients of four subgroups of liver disease, including decompensated cirrhosis, chronic hepatitis, cirrhosis with HCC and acute-on-chronic liver failure were analyzed. All patients and controls were subjected to sonoclot analysis and correlated with routine coagulation parameters including platelet count, PT, APTT, fibrinogen, and D-dimer. Results. The sonoclot signatures demonstrated statistically significant abnormalities in patients with liver disease as compared to healthy controls. PT and APTT correlated positively with SONACT ( and <0.0015, resp.) while platelet count and fibrinogen levels depicted significant positive and negative correlations with clot rate and SONACT respectively. Conclusion. Sonoclot analysis may prove to be an efficient tool to assess coagulopathies in liver disease patients. Clot rate could emerge as a potential predictor of hypercoagulability in these patients.