Serum Amyloid Beta42 Is Not Eliminated By The Cirrhotic Liver: A Pilot Study

Amyloid-beta (A beta) deposition in the brain is the main pathological hallmark of Alzheimer disease. Peripheral clearance of A beta may possibly also lower brain levels. Recent evidence suggested that hepatic clearance of A beta 42 is impaired in liver cirrhosis. To further test this hypothesis, serum A beta 42 was measured by ELISA in portal venous serum (PVS), systemic venous serum (SVS), and hepatic venous serum (HVS) of 20 patients with liver cirrhosis. Mean A beta 42 level was 24.7 +/- 20.4 pg/mL in PVS, 21.2 +/- 16.7 pg/mL in HVS, and 19.2 +/- 11.7 pg/mL in SVS. Similar levels in the three blood compartments suggested that the cirrhotic liver does not clear A beta 42. A beta 42 was neither associated with the model of end-stage liver disease score nor the Child-Pugh score. Patients with abnormal creatinine or bilirubin levels or prolonged prothrombin time did not display higher A beta 42 levels. Patients with massive ascites and patients with large varices had serum A beta 42 levels similar to patients without these complications. Serum A beta 42 was negatively associated with connective tissue growth factor levels (r = -0.580, p = 0.007) and a protective role of A beta 42 in fibrogenesis was already described. Diabetic patients with liver cirrhosis had higher A beta 42 levels (p = 0.069 for PVS, p = 0.047 for HVS and p = 0.181 for SVS), which is in accordance with previous reports. Present analysis showed that the cirrhotic liver does not eliminate A beta 42. Further studies are needed to explore the association of liver cirrhosis, A beta 42 levels, and cognitive dysfunction.