الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
PH is the most common found serious complication of CLD, leading to high morbidity and mortality. One of its major consequences is bleeding from EV and PHG. VH develops at a rate of around 10%-15% annually and is determined by thr severity of liver disease, size of EV, and the presence of red color marks. Six-week mortality, which is currently recognized as the key endpoint to evaluate the impact of treatment modalities for acute VH, is around 16%-24%.
Liver cirrhosis is considered to be the most common cause of PH worldwide and is associated with profound phenotypic modifications in the profibrogenic hepatic cell types. During the progression of CLD, hepatic stellate cells (HSCs) become activated, liver sinusoidal endothelial cells (LSECs) undergo capillarization, and hepatic resident macrophages (Kuppfer cells) polarize, leading to liver microvascular dysfunction. Therefore, the hepatic structure is distorted by the synthesis and deposition of ECM, which leads to fibrosis; and the hepatic vascular tone rises owing to stimulation of vasoconstrictors and inhibition of vasodilators, leading to increased IHVR and elevated portal venous pressure.
PH is accurately evaluated by measurement of the HVPG. However, the technique requires specific expertise, is costly, invasive, and not available in all centers. Consequently, it is not a standard of care for every cirrhotic patient. Nevertheless, endoscopy is the standard technique for the diagnosis and management of EV and VH. The guidelines do recommend screening for EV