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Sara Montagnese

Researcher at University of Padua

Publications -  190
Citations -  5517

Sara Montagnese is an academic researcher from University of Padua. The author has contributed to research in topics: Cirrhosis & Hepatic encephalopathy. The author has an hindex of 33, co-authored 165 publications receiving 3846 citations. Previous affiliations of Sara Montagnese include University College London.

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EASL Clinical Practice Guidelines on nutrition in chronic liver disease

TL;DR: These Clinical Practice Guidelines review the present knowledge in the field of nutrition in chronic liver disease and promote further research on this topic, with recommendations provided in specific settings such as hepatic encephalopathy, cirrhotic patients with bone disease, patients undergoing liver surgery or transplantation and critically ill cirrhosis patients.
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The nutritional management of hepatic encephalopathy in patients with cirrhosis: International society for hepatic encephalopathy and nitrogen metabolism consensus

TL;DR: Effective management of these patients requires an integrated multidimensional approach, however, further research is needed to fill the gaps in the current evidence base to optimize the nutritional management of patients with cirrhosis and HE.
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Characteristics of Minimal Hepatic Encephalopathy

TL;DR: The neuropsychological features of minimal hepatic encephalopathy point to a disorder of executive functioning, particularly selective attention and psychomotor speed, but other abnormalities may be observed, although the specificity of the changes observed is unclear at present.
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The PREDICT study uncovers three clinical courses of acutely decompensated cirrhosis that have distinct pathophysiology.

Jonel Trebicka, +126 more
TL;DR: Acute decompensation without ACLF is a heterogeneous condition with three different clinical courses and two major pathophysiological mechanisms: systemic inflammation and portal hypertension.
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Blood metabolomics uncovers inflammation-associated mitochondrial dysfunction as a potential mechanism underlying ACLF.

TL;DR: Among patients with ACLF, the intensity of the fingerprint increased across ACLF grades, and was similar in patients with kidney failure and in those without, indicating that the fingerprint reflected not only decreased kidney excretion but also altered cell metabolism.