Portal hypertension (PP) is the chief consequence of cirrhosis and
is responsible for the majority of its complications. In seventy
percentage of cases, PP increases at first as a result of an
increased intrahepatic resistance to portal flow attributed to
structural mechanisms e.g., fibrous tissue, regenerative nodules,
and micro thrombi. Yet, at least one third of the increased
intrahepatic resistance is attributed to an increased intrahepatic
vascular tone, which, results from endothelial dysfunction mostly
mediated from reduced nitric oxide (NO) bioavailability. The onset
of portal hypertension may not always be associated with specific
symptoms, however, the main symptoms and complications of
portal hypertension include; gastrointestinal bleeding due to the
spontaneous rupture and bleeding from varices, ascites, hepatic
encephalopathy and decreased levels of platelets or decreased
white blood cell count. It is currently possible to diagnose liver
cirrhosis and portal hypertension accurately by non-invasive
methods in a reasonable proportion of patients with chronic liver
disease. Recent, more complicated non-invasive diagnostic
methods such as MRE, CT images and dynamic techniques on
MRI are emerging tools further improving this possibility.