Clinical and experimental advances related to the detection, magnitude and pathobiology of subclinical portal hypertension in nonalcoholic fatty liver disease (NAFLD), primarily observed in the presence of nonalcoholic steatohepatitis (NASH),… Click to show full abstract
Clinical and experimental advances related to the detection, magnitude and pathobiology of subclinical portal hypertension in nonalcoholic fatty liver disease (NAFLD), primarily observed in the presence of nonalcoholic steatohepatitis (NASH), prompt us to revisit current disease paradigms. Hepatic venous pressure gradient (HVPG) has been reported to underestimate portal pressure in NASH-cirrhosis and inaccuracy is more likely in non-cirrhotic liver, indicating a potential need for new and preferably noninvasive methods of measurement. Although clinically significant portal hypertension (HVPG ≥ 10 mmHg) retains is prognostic significance in NASH Subclinical portal hypertension (HVPG, 6-9.5 mm Hg) in NAFLD has been repeatedly detected in the absence of cirrhosis or even significant fibrosis, although the impact of these findings on disease outcomes remains unclear. Mechanocrine signaling pathways in various types of liver cells offer molecular basis for the adverse effects of subclinical portal hypertension and suggest a bidirectional relationship between portal pressure and fibrosis. These findings may guide efforts to improve risk assessment and identify novel therapeutic targets in NAFLD.
               
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