1 Introduction Primary biliary cholangitis (PBC), formerly called primary biliary cirrhosis, is a chronic cholestatic disease of autoimmune origin, presenting as destructive lymphocytic cholangitis, affecting mainly the biliary epithelial cells (BEC) of the small-bile ducts of the liver ( Antimitochondrial antibodies (AMA) targeting the E2 subunit of the pyruvate dehydrogenase complex (PDC-E2) of the inner mitochondrial membrane are highly specific for PBC and are present in more than 90% of patients, while certain antinuclear antibodies, namely antiglycoprotein 210 (anti-gp 210) and anti-sp100, occur in up to 50% of AMA negative PBC patients, highlighting the complexity of PBC pathogenesis ( PBC treatment has long been a clinical problem with less than 2/3 of all patients responding to first-line treatment, namely ursodeoxycholic acid ( Recent evidence further suggests that persistent elevation of multiple liver biochemical markers (AST, ALT, ALP and bilirubin) and non-invasive fibrosis indices such as APRI and FIB-4 are associated with poorer outcomes, supporting the concept of a deep biochemical response, defined by complete normalization of ALP and bilirubin, as an emerging therapeutic target ( Lastly, transient elastography has become an important tool for disease monitoring, as both baseline liver stiffness and its progression over time correlate strongly with the risk of clinical complications, including hepatic decompensation and cirrhosis ( In recent years, several different drugs, targeting various disease-modifying pathways, have been used in patients with PBC with promising results
A.KepeV.LiuJ.GhezziC.SatyamurthyN.et al (2015)
Su MrBiceps susidriau iekodama patikim, kokybik produkt tiek sau, tiek savo klientams
When IGF1 LR3 binds to IGF-1 receptors on target cells, it starts a cascade of intracellular signaling pathways, including the PI3K/Akt pathway and the MAPK/ERK pathway, which regulate protein synthesis, glucose body function, and cell survival mechanisms
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J.BrachT.MartyL.KreyeS.RouhierN.JacquotJ.-P.et al
