Acute liver failure is a life-threatening condition commonly caused by drug-induced hepatotoxicity or viral hepatitides. However, there are a number of rarer causes such as haemophagocytic lymphohistiocytosis. Haemophagocytic lymphohistiocytosis is a syndrome of uncontrolled immune cell activation, triggered by infection or malignancy, which carries a high mortality. Whilst mild to moderate liver injury is commonly seen with haemophagocytic lymphohistiocytosis, acute liver failure has rarely been reported in adults. We present a case of a 74-year-old man with acute liver failure secondary to haemophagocytic lymphohistiocytosis triggered by undiagnosed large B-cell lymphoma. Initially treated for biliary sepsis, there was a delay in the diagnosis of haemophagocytic lymphohistiocytosis and despite initiating chemotherapy, he died soon after. This case highlights the importance of considering haemophagocytic lymphohistiocytosis as a rare cause of acute liver failure, as given the life-threatening potential of haemophagocytic lymphohistiocytosis, a prompt diagnosis may allow early initiation of chemotherapy for any chance of survival.
was in close proximity to B cell rich areas. TSPAN6 expression was highly variable between primary liver cancer tumour tissues, but increased expression was linked to higher patient survival. Our preliminary data suggest that TSPAN6 could play a role in the tumour microenvironment of primary liver cancers and further investigation is warranted.
over 48 hours increased the epithelial cell proliferation rate by up to 56% in Caco-2 (p<0.01) and 42% in HT-29 (p<0.001) cells. Conclusion Our data demonstrates that IL-27 enhances epithelial barrier wound healing. Gene expression data suggests that cell-cell adhesion is enhanced through increased E-cadherin expression, with a reduction in permeability through decreased expression of claudin-2 (pore forming) and increase in claudin-4 (pore closing). Tight junction function is enhanced through increased expression of occludin and tight junctional protein-1. Further studies will define the IL-27 driven permeability related protein expression profile and impact on functional permeability in organoids and whether IL-27 is a potential new treatment for IBD.
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